C

progresses to transient ischemic attacks (TIA), and recur-

C/NC rent strokes. The migraine attacks are often reported to be
particularly long lasting or severe and may even include
▶ Coma/Near Coma Scale symptoms of hemiplegia. The strokes are typically lacu-
nar, occurring in subcortical white matter or basal ganglia
and, in some cases, occur in the brain stem and spinal
cord. Recurrent subcortical infarcts lead to cognitive de-
CABG cline, pseudobulbar palsy, motor impairment, psychiatric
symptoms (most commonly depression), and ultimately
▶ Coronary Artery Bypass Graft total motor impairment and subcortical vascular demen-
tia. Cognitive decline is most prominently seen as execu-
tive dysfunction, slowed processing speed, and reduced
attentional abilities. As the disease progresses, memory
Cadasil and other areas of cognitive functioning begin to decline.
The total amount of white matter involvement associated
A NGELA E ASTVOLD, YANA S UCHY
with the lacunar lesions and the degree of atrophy predict
University of Utah
severity of cognitive and motor impairment.
Salt Lake, UT, USA
Cause: CADASIL is caused by mutations or deletions in
the Notch3 gene on chromosome 19, which plays an
important role in cell differentiation during development.
Synonyms
While the pathogenetic mechanism has yet to be deter-
mined, the resulting pathophysiology includes thickening
Agnogenic medial arteriopathy; Chronic familial vascular
of arterial walls, accumulation of granular osmiophilic
encephalopathy; Familial Binswanger’s disease; Familial
material (GOM) in arterial walls (this distinguishes it
disorder with subcortical ischemic strokes, dementia, and
from arterial hypertension), gradual destruction of vascu-
leukoencephalopathy; Hereditary multi-infarct dementia
lar smooth muscle cells leading to fibrosis, progressive
thickening of arterial walls, and narrowing of the lumen
Short Description or Definition of cerebral arteries. This eventually causes thrombosis,
reduced blood flow, destruction of small- and medium-
Cerebral autosomal dominant arteriopathy with subcor- sized arteries, and consequently focal infarcts. MRI typi-
tical infarcts and leukoencephalopathy (CADASIL) is a cally reveals characteristic periventricular or white matter
rare autosomal dominant, adult-onset inherited cerebral hyperintensities, as well as infarcts in the basal ganglia and
vascular disease, characterized by migraines, recurrent brain stem. The cerebral cortex remains relatively intact.
transient ischemic attacks, and strokes leading to cogni- Diagnosis: Identification of a Notch3 mutation provides
tive decline and dementia. the most certain diagnosis, in addition to the presence of
GOM in arterial walls, which can be detected with a skin
biopsy. Positive MRI findings are often detected in even
Current Knowledge asymptomatic individuals. History of particularly severe
migraines may be the earliest indication.
Clinical Manifestation: The typical age of onset is Treatment and prognosis: Currently, there is no cure or
30–500 years of age. The initial clinical manifestation disease-modifying therapy for CADASIL, and only symp-
often begins with migraines with aura, and slowly tom management and supportive care are available for

Jeffrey S. Kreutzer, John DeLuca, Bruce Caplan (eds.), Encyclopedia of Clinical Neuropsychology, DOI 10.1007/978-0-387-79948-3,
# Springer Science+Business Media LLC 2011
470 C CAGE Questionnaire

affected individuals. Death typically occurs 10–20 years to steady your nerves or to get rid of a hangover (eye-
after the onset of symptoms. Angiography and anticoagu- opener)?’’ Individual item responses are scored in a binary
lants should be avoided as they may provoke cerebrovascu- fashion (‘‘0’’ = ‘‘no’’ and ‘‘1’’ = ‘‘yes’’). The total score can
lar accidents. range from 0 to 4. A score of 2 or greater is typically
considered a positive finding, that is, an indication of
alcohol misuse.
Cross References

▶ Binswanger’s Disease Historical Background

▶ Lacunar Stroke
▶ Small Vessel Ischemic Disease The CAGE was developed by Ewing and Rouse (1968)
for detection of ‘‘alcoholism’’ and was first introduced
as a formal screening instrument 2 years later (Ewing &
References and Readings Rouse, 1970). Final item selection for the CAGE was
based on examination of 130 randomly selected, general
Kalaria, R. N., Viitanen, M., Kalimo, H., Dichgans, M., & Tabira T. hospital patients; items selected were those that resulted
(2004). The pathogenesis of CADASIL: An update. Journal of Neu- in a ‘‘minimal’’ set of items that ‘‘usefully divided’’
rological Sciences, 226, 35–39.
responders into two groups, patients with ‘‘alcoholism’’
Kalimo, H., Ruchoux, M. M., Viitanen, M., & Kalaria, R. N. (2002).
CADASIL: A common form of hereditary arteriopathy causing
(confirmed by physician impressions and chart
brain infarcts and dementia. Brain Pathology, 12(3), 371–384. study) and patients without indication of ‘‘alcoholism’’
Kalimo, H., Viitanen, M., Amberia, K., Juvonen, V., Marttila, R, (Ewing, 1984).
Poyhonen, M., et al. (1999). CADASIL: Hereditary disease of arteries Over the years, several modifications to the original
causing brain infarcts and dementia. Neuropathology and Applied
instrument have been recommended, including placing a
Neurobiology, 25, 257–265.
time frame reference on the four questions (e.g., in the last
year), as well as adding questions regarding frequency of
use, tolerance, and perceived history of drinking problems
(Bradley, Kiviahan, Bush, McDonell, & Fihn, 2001;
National Institute on Alcohol Abuse and Alcoholism,
CAGE Questionnaire 1995; McQuade et al., 2000).
M YRON G OLDBERG
University of Washington Medical Center
Seattle, WA, USA Psychometric Data

Test–retest reliability of the CAGE over a 7-day period was

Definition 0.80 in a psychiatric sample and 0.95 in a nonclinical
sample (Teitelbaum & Carey, 2000); mean CAGE score
The CAGE is one of a number of brief screening changes for each group across this same time period
instruments designed to help in the detection of alcohol were nonsignificant. Convergent validity has been reason-
misuse. The instrument’s name is an acronym for ably good, though somewhat variable, with reported
questions about Cutting down on drinking, Annoyance correlations ranging from 0.48 to 0.70 with other
at other’s concern about drinking, feeling Guilty about alcohol-screening instruments (see Dhalla & Kopec,
drinking, and using alcohol as an Eye-opener in the 2007 for review).
morning. The CAGE can be rapidly administered in an A number of studies have examined the validity of
interview format or written format and consists of the CAGE in detecting alcohol misuse. Aertgeerts, Buntinx,
following four items: (1) ‘‘Have you ever felt that you and Kester (2004) performed a meta-analysis of 10 studies
should cut down on your drinking?’’; (2) ‘‘Have people of the utility of the CAGE in detecting alcohol abuse or
annoyed you by criticizing your drinking?’’; (3) ‘‘Have alcohol dependency in general clinical populations using
you ever felt bad or guilty about your drinking?’’; and criteria from the Diagnostic and Statistical Manual for
(4) ‘‘Have you ever had a drink first thing in the morning Mental Disorders (DSM-III-R’ APA, 1987). With a cutoff
 CAGE Questionnaire C 471

score at
2, pooled sensitivities across studies were 0.87 in Cross References
hospital inpatients, 0.71 in primary care patients, and 0.60
in ambulatory medical patients; specificities were 0.77, ▶ Alcohol Abuse
0.91, and 0.92, and positive predictive validities were ▶ Alcohol Dependence
0.57, 0.74, and 0.82, respectively. Aertgeerts et al. (2004) ▶ Alcoholic Brain Syndrome C
concluded that the CAGE is only of ‘‘limited value’’ as a ▶ Alcoholism
screening instrument using a cutoff score of
2 and ▶ Blood Alcohol Level
recommended that additional information about alcohol ▶ Fetal Alcohol Syndrome
use patterns be obtained from any patient who gives one ▶ Korsakoff ’s Syndrome
positive answer on the instrument. ▶ Michigan Alcoholism Screen Test
Dhalla and Kopec (2007) provided a more recent ▶ Substance Abuse
review of the CAGE validity literature, considering, in ▶ Substance Abuse Disorders
part, the sensitivity, specificity, and positive predictive ▶ Wernicke–Korsakoff ’s Syndrome
value associated with different cutoff scores. The authors
concluded that the CAGE has ‘‘adequate validity’’ in
References and Readings
screening medical and surgical inpatients, psychiatric
inpatients, and ambulatory medical patients for alcohol
Aertgeerts, B., Buntinx, F., & Kester, A. (2004). The value of the CAGE in
misuse and that use of a cutoff score of
2 affords the screening for alcohol abuse and alcohol dependence in general
best combination of sensitivity, specificity, and positive clinical populations: A diagnostic meta-analysis. Journal of Clinical
predictive value. At the same time, they cautioned that the Epidemiology, 57, 30–39.
CAGE has not performed well with Caucasian women, American Psychiatric Association (1987). Diagnostic and statistical man-
ual of mental disorders (3rd rev. ed.). Washington, D.C.: American
prenatal women, and college students.
Psychiatric Press.
Fiellin, Carrington, and O’Conner (2000) also provide Bradley, K., Kiviahan, D., Bush, K., McDonell, M., & Fihn, S. (2001).
a noteworthy review of validity studies, concluding that in Variations on the CAGE alcohol screening questionnaire: Strengths
primary care settings, the CAGE questionnaire was more and limitations in VA general medical patients. Alcoholism: Clinical
effective in identifying patients with alcohol abuse or and Experimental Research, 25, 1472–1478.
Cherpitel, C. J. (2000). A brief screening instrument for problem drinking
dependency than in detecting patients with at risk,
in the emergency room: The RAPS4. Journal of Studies on Alcoholism,
hazardous, or harmful drinking. 61, 447–449.
Dhalla, S., & Kopec, J. (2007). The CAGE questionnaire of alcohol
misuse: A review of reliability and validity studies. Clinical & Inves-
Clinical Uses tigative Medicine, 30, 33–41.
Ewing, J. A. (1984). Detecting alcoholism: The CAGE questionnaire.
Journal of the American Medical Association, 252, 1905–1907.
The CAGE has enjoyed wide popularity in primary care Ewing, J. A., & Rouse, B. A. (1970). Identifying the hidden alcoholic.
settings as an alcohol-screening instrument for a number Presented at the 29th international congress on alcohol and drug
of reasons, as it is brief, easy to administer, and can be dependence, Sydney, Australia, February 3, 1970.
incorporated into more extensive interviews or question- Fiellin, D., Carrington, R., & O’Conner, P. (2000). Screening for alcohol
problems in primary care: A systematic review. Archives of Internal
naires (Bradley et al., 2001). However, support for its
Medicine, 160, 1977–1989.
validity across different populations has been mixed. It National Institute on Alcohol Abuse and Alcoholism (1995). The physician’s
appears to perform best when used to screen for alcohol guide to helping patients with alcohol problems (NIH publication
abuse or dependence in clinical populations and less 95-3769). Bethesda: U.S. Department of Health and Human
well in detecting current hazardous drinking. Caution Services, Public Health Service, National Institutes of Health.
Pokorny, A., Miller, B., & Kaplan, H. (1972). The brief MAST: A short-
should be used especially when interpreting results for
ened version of the Michigan Alcoholism Screening Test. American
nonclinical respondents (i.e., general population) as well Journal of Psychiatry, 129, 342.
as for women and college students, as the CAGE has been Saunders, J. B., Aasland, O. G., Babor, T. F., De La Fuente, J. R., & Grant,
noted to under-perform in these populations. In addition, M. (1993). Development of the Alcohol Use Disorders Identification
as several authors have recommended, a positive finding Test (AUDIT): WHO collaborative project on early detection of
persons with harmful alcohol consumption-II. Addiction, 88,
on the CAGE, regardless of cutoff score level (i.e.,
1
791–804.
or 2), should be followed up by further examination Teitelbaum, L., & Carey, K. (2000). Temporal stability of alcohol
of alcohol consumption patterns, using established stan- screening measures in a psychiatric setting. Psychology of Addictive
dard criteria. Behaviors, 14, 401–404.
472 C CalCAP

(what) streams to the parieto-occipital association

CalCAP cortex and occipitotemporal association cortices,
respectively.
▶ California Computerized Assessment Package

Illness

Calcarine Cortex The calcarine cortex is perfused by the calcarine artery,

which is a limb off the posterior cerebral artery. Our
M ARY-E LLEN M EADOWS visual system has evolved such that damage to one eye
Brigham and Women’s Hospital does not result in blindness in one visual field. Damage
Boston, MA, USA to either the right or left calcarine cortex results in a
contralateral field cut, a hemianopia. Macular sparing
usually occurs because of collateral blood supply from
Synonyms branches of the middle cerebral artery. Isolated lesions
of the primary visual cortex results in discrete blind
Primary visual cortex; Striate cortex spots (scotomas) in the corresponding area of the
visual field.

Structure
Cross References
This is the term for the primary visual cortex, V1, or
▶ Calcarine Fissure
Brodmann’s area 17. The area encompasses the medial
▶ Calcarine Sulcus
surface and a small lateral surface of the occipital lobe,
▶ Occipital Lobe
and is within the calcarine sulcus. It is located at the most
▶ Scotoma
posterior portion of the cerebral hemisphere. The optic
▶ Unimodal Cortex
radiations terminate in layer IV of the calcarine cortex.
▶ Visual Cortex
Layer IV is rather thick and is subdivided into sublaminae.
The calcarine cortex is also sometimes referred to as
the striate cortex because of a strip of myelin (Stria of
Gennari) that can be visualized. The area is organized in References and Readings
a retinotopic fashion; that is, there is point-to-point
representation from the retina to the cortex. For instance, Netter, F. (1991). The CIBA collection of medical illustrations: Volume I –
fibers in the right half of each retina (perceives information nervous system, part I: anatomy and physiology. West Caldwell, NJ:
in the left visual field) project to the right calcarine cortex, CIBA-Geigy.
and fibers in the left half of each retina (perceives informa-
tion in the right visual field) project to the left calcarine
cortex.

Calcarine Fissure
Function J OHN E. M ENDOZA
Tulane University Medical Center
From a functional perspective, the calcarine cortex is im- New Orleans, LA, USA
portant in determining orientation, spatial-frequencies,
and color properties of the visual stimulus. The infor-
mation is then projected to other areas in the occip- Synonyms
ital lobe for further visual analysis. This occurs via
transmission to the dorsal (where) and the ventral Calcarine sulcus
 California Computerized Assessment Package C 473

California Computerized
Assessment Package
E RIC N. M ILLER C
UCLA Psychology Clinic
Los Angeles, CA, USA

Synonyms
CalCAP

Description
Calcarine Fissure. Figure 1 Mid-sagittal view of the brain
(MRI) showing calcarine fissure separating the cuneus and the The California Computerized Assessment Package (Cal-
lingual gyrus of the occipital lobe CAP; 1999) presents a series of brief reaction time tasks
designed to assess speeded information processing and
psychomotor functioning. The Standard CalCAP consists
Definition of 4 Simple and 6 Go–No Go reaction time subtests that
require 20–25 min to complete. The individual reaction
The calcarine fissure is a deep sulcus located on the medial time measures were designed to assess a number of cog-
surface of the occipital lobe (see Fig. 1). The superior nitive domains, including speed of processing (reaction
(cuneus) and inferior (lingual gyrus) banks of this sulcus time), lexical discrimination (real word vs. nonsense
represent the primary cortical projection area for vision. word), rapid visual scanning, form discrimination and
Visual information that is first received in the upper matching, working memory (1-back and 2-back tasks),
portions of the retina is represented along the upper and sustained and divided attention. Each task includes a
banks of the fissure (cuneus), while that derived from practice session that must be completed with 100% accu-
the lower retina projects to its lower bank. Thus, lesions racy to proceed to the main 2-min procedure, a method
confined to the upper bank (cuneus) will result in con- that ensures that subjects understand the task instructions
tralateral inferior visual field defects, while damage to and that minimizes practice effects in longitudinal study
the lower bank (lingual gyrus) will produce upper field designs. Subjects are asked to focus on a display field and
deficits. Lesions destroying tissue along both the upper respond only to specific types of visual stimuli. For exam-
and lower banks may result in a contralateral homony- ple, in the form discrimination task, they are asked to
mous hemianopia. press a key only when two out of three non-nameable
figures are identical.
The core measures of reaction time, hits and false-
positives, and signal detection parameters allow investiga-
Cross References tors to measure accuracy and general speed of processing,
as well as relative differences among conceptually distinct
▶ Cuneus decision tasks. Four iterations of a Simple reaction time
▶ Lingual Gyrus routine at various points in the test allow direct measure-
▶ Visual System ment of the subject’s ability to maintain focus throughout
the 20-min testing procedure. The computer scores each
task using age- and education-specific norms derived from
641 men ranging from 21 to 58 years of age, with a mean
education of 16 years. Final scores are available immediate-
Calcarine Sulcus ly in tabular and graphical formats. Additional norms have
been derived for elementary school children (3rd, 5th, and
▶ Calcarine Fissure 6th grades), women, and older individuals. The CalCAP
474 C California Computerized Assessment Package

also includes a 4-subtest language-independent abbreviated Go–No Go paradigms, the simple reaction time measures
battery weighted toward measures of speeded processing have relatively low test–retest reliability (0.20–0.29), sug-
and working memory. These test batteries are well suited gesting that the psychomotor skills measured by the sim-
for collecting reliable information on psychomotor func- ple reaction time tasks vary considerably depending on
tioning in a brief period of time, and can be used effectively state variables such as mood, attention, fatigue, and time
for assessing changes over time. Stimulus materials are of day (Miller, 2008).
available in English, Spanish, French, Norwegian, Danish, CalCAP reaction time correlates most highly with age,
and Flemish. and, to a lesser extent, with years of education. Two
studies of gender effects on CalCAP reaction time have
shown no differences between men and women on any of
Historical Background the CalCAP indices (Berg, 1994). The psychometric prop-
erties of the CalCAP are unstable for 3rd graders, but
The CalCAP was originally developed by Dr. Eric Miller essentially the same as found in adults by the 5th grade
in the late 1980s as an automated substitute for (Budzinski, 1994).
traditional neuropsychological testing. The Standard
battery, developed in consultation with Dr. Paul Satz
and Dr. Ola Selnes, was designed to measure aspects of Clinical Uses
language and visuoperceptual skills, working memory,
speeded information processing, attention, learning and The CalCAP has been widely used in cross-sectional and
memory, visual scanning, and reaction time. While the longitudinal studies of HIV/AIDS (Miller et al., 1991;
reaction time tasks that comprise the Standard CalCAP Gonzalez et al., 2003), drug abuse (Chang et al., 2002;
battery do assess many of these areas of cognitive func- Volkow et al., 2001), depression (Stordal et al., 2004),
tioning, studies have shown that the tasks correlate only epilepsy (Hessen, Lossius, M. I., Reinvang, I., & Gjerstad,
modestly (0.2–0.4) with traditional neuropsychological 2008), traumatic brain injury (Waterloo, Ingebrigtsen, &
measures (Miller, Satz, & Visscher, 1991). Factor analyses Romner, 1997), and hyperbaric oxygen treatments
using the CalCAP and other neuropsychological test (Hjalmarsen, Waterloo, Dahl, Jorde, & Viitanen, 1999;
batteries show that the reaction time indices form two Van Hoof, Coomans, De Becker, De Meirleir, & Cluydts,
primary factors best characterized as simple reaction 2002). It is particularly sensitive to the psychomotor
time and decision speed. These factors are distinct changes seen in these disorders and, unlike most psycho-
from traditional neuropsychological measures and motor tasks, has minimal practice effects, making it par-
most researchers and clinicians now use the CalCAP ticularly appropriate for research paradigms such as
and other reaction time measures primarily as indices clinical trials and epidemiologic studies that require re-
of these types of speeded information processing and peated testing.
attention. The abbreviated version of the CalCAP specif- The cognitive functions assessed by the CalCAP pro-
ically excludes measures designed to look at visuoper- gram are best described as timed psychomotor skills re-
ceptual and language skills and focuses primarily on quiring focused or sustained attention. Impaired reaction
these core indices of reaction time, working memory, time across multiple measures is usually indicative of
and attention. generalized motor slowing or slowed information pro-
cessing. Impaired reaction time on specific measures,
particularly when coupled with scores outside of normal
Psychometric Data bounds on true-positive responding, is suggestive of a
more specific functional deficit, such as language skills
All the subtests in the CalCAP have high internal consis- (lexical discrimination task), visuoperceptual deficits
tency reliability (0.77–0.96). Six-month test–retest reli- (form discrimination), or working memory (1-back and
ability for the Go–No Go paradigms is comparable with 2-back tasks).
levels seen for conventional neuropsychological proce- The standard CalCAP program classifies subjects as
dures (0.43–0.68), but there is less evidence of the practice ‘‘outliers’’ if they perform two standard deviations or
effects commonly seen with psychomotor measures. The lower on two or more of the tasks. Using these
reduced practice effects may be due to the requirement criteria, approximately 10% of subjects are classified as
that all subjects complete practice trials with 100% outliers. This base rate of 10% includes individuals with
accuracy before proceeding to the actual test. Unlike the premorbid conditions such as prior head injury, learning
 California Verbal Learning Test (California Verbal Learning Test-II) C 475

disability, preexisting neurologic conditions, as well as Waterloo, K., Ingebrigtsen, T., & Romner, B. (1997). Neuropsychological
function in patients with increased serum levels of protein S-100
individuals who are simply on the low end of normal
after minor head injury. Acta Neurochirurgica, 139, 26–32.
functioning.

Cross References
C
California Verbal Learning Test
▶ Attention/Executive Functions (California Verbal Learning
▶ Continuous Performance Tests
▶ Information Processing Speed Test-II)
▶ Speed of Information Processing
▶ Visual–Motor Function A NGELA Y I
Mount Sinai Medical Center
New York, NY, USA
References and Readings

Berg, D. (1994). Adults’ reaction time as affected by age and education level.
Synonyms
B.A. Honours Thesis supervised by Dr. Frank Spellacy, University of
Victoria. CVLT
Budzinski, L. M. (1994). An exploration of simple and choice reaction times
in children. B.A. Honours Thesis supervised by Dr. Frank Spellacy,
Victoria, B.C., University of Victoria.
Chang, L., Ernst, T., Speck, O., Petal, H., DeSilva, M., Leonido-Yee, M., Description
et al. (2002). Perfusion MRI and computerized cognitive tests
abnormalities in abstinent methamphetamine users. Psychiatry Re-
search, 114, 65–79.
The California Verbal Learning Test-II (CVLT-II) is the
Gonzalez, R., Heaton, R. K., Moore, D. J., Letendre, S., Ellis, R. J., latest (2000) version of a widely used verbal learning and
Wolfson, T., et al. (2003). HIV Neurobehavioral Research Center memory test. The current version contains recalling
Group. Computerized reaction time battery versus a traditional and recognition of two lists of words over immediate
neuropsychological battery: detecting HIV-related impairments. and delayed trials. List A includes 16 words and requires
Journal of International Neuropsychological Society, 9, 64–71.
Hessen, E., Lossius, M. I., Reinvang, I., & Gjerstad, L. (2008). Improve-
the examinee to recall the list over five trials. List B
ment in speeded cognitive processing after anti-epileptic drug with- (interference), which is also 16 words, is administered
drawal – a controlled study in mono-therapy patients. Progress in after List A for one trial. Short-delay free recall and
Neurotherapeutics and Neuropsychopharmacology, 3, 199–209. cued recall are administered after List B. A 20-min delay
Hjalmarsen, A., Waterloo, K., Dahl, A., Jorde, R., & Viitanen, M. (1999). follows the short-delay recalls, followed by nonverbal
Effect of long-term oxygen therapy on cognitive and neurological
dysfunction in chronic obstructive pulmonary disease. European
testing. Long-delay recall, long-delay-cued recall, and yes/
Neurology, 42, 27–35. no-recognition trials of List A follow the 20-min delay.
Miller, E. N. (1999). CalCAP California Computerized Assessment Package A revision of the CVLT-II is the addition of a forced choice
Manual (2nd ed.). Los Angeles: Norland Software. recognition after a 10-min delay following the yes/no trial.
Miller, E. N. (2008). CalCAP California Computerized Assessment Pack- Another revision of the CVLT-II is the inclusion of a
age. Retrieved October 16, 2008 from http://www.calcaprt.com
Miller, E. N., Satz, P., & Visscher, B. (1991). Computerized and conven-
short form (nine words) and an alternate form. The short
tional neuropsychological assessment of HIV-1 infected homosexual form was created for the purpose of screening or for
men. Neurology, 41, 1608–1616. patients who may have more severe brain damage and
Stordal, K. I., Lundervold, A. J., Egeland, J., Mykletun, A., Asbjornsen, A., may feel overwhelmed by the long form. This short form
Landro, N. I., et al. (2004). Impairment across executive functions takes 15 min to administer and also has a 15-min delay.
in recurrent major depression. Nordic Journal of Psychiatry, 58,
41–47.
The alternate form has been statistically equated with the
Van Hoof, E., Coomans, D., De Becker, O., De Meirleir, K., & Cluydts, R. standard form.
(2002). Hyperbaric oxygen therapy for chronic systemic infections in The CVLT-II was normed from a national standardi-
chronic fatigue syndrome. International Journal of Psychophysiology, zation sample of 1,087 of ages 16–89, which was demo-
45, 82–83. graphically matched to the US population. It takes 30 min
Volkow, N. D., Chang, L., Wang, G. J., Fowler, J. S., Leonido-Yee, M.,
Francesci, D., et al. (2001). Association of dopamine transporter
to administer and includes 30 min of delay. The test is
reduction with psychomotor impairment in methamphetamine administered with paper and pencil format, with the
abusers. American Journal of Psychiatry, 158, 377–382. examiner recording the responses. The responses are
476 C California Verbal Learning Test – Children’s Version

scored using the Comprehensive Scoring System, which of the literature of clinical populations from 1987 to
computes raw scores and standardized scores for over 1999, summarizing the key findings of CVLT perfor-
50 learning and memory variables. The raw scores can mance across various clinical populations, which include
be scored manually, although there are limits to how anterior temporal lobectomy, Korsakoff ’s syndrome,
much information can be derived. Alzheimer’s disease, Huntington’s disease, Parkinson’s
The CVLT-children’s (CVLT-C) version can be adminis- disease, head injury, schizophrenia, depression and
tered to children aged 5–16 and can assist professionals in other affective disorders, chronic alcohol and drug
diagnosing memory impairment secondary to learning dis- abuse, posttraumatic stress disorder, systemic medical
abilities, attention-deficit disorder, mental retardation, and disease (HIV, chronic fatigue syndrome, Lyme disease,
other neurological disorders and psychiatric problems. The eosinophilia myaligia syndrome, cardiac transplant can-
administration is similar to the format of the CVLT-II, didates), insufficient effort, and predictor for everyday
although forced choice recognition is not included. functioning.

Historical Background Cross References

The first edition of the CVLT was originally published in ▶ Buschke Selective Reminding Test
1987 from the work of Delis, Kramer, Kaplan, and Ober ▶ Children’s Memory Scale
(1987). They created one of the first tests to incorporate ▶ Hopkins Verbal Learning Test
principles from cognitive science to measure learning and ▶ Rey Auditory Verbal Learning Test
memory. This test provided a measurement of not only ▶ Rivermead Behavioral Memory Test
what an individual remembers, but how they remember ▶ Selective Reminding Test
and what errors are made. This refuted previous beliefs ▶ Wechsler Abbreviated Scale of Intelligence
that memory dysfunction was limited to recall and ▶ Wechsler Memory Scale All Versions
recognition.

References and Readings

Psychometric Data
Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. (1987). The California
verbal learning test: Research edition, adult version. San Antonio, TX:
CVLT-II: Split-half reliability coefficients based on split-
The Psychological Corporation.
ting immediate-recall trials ranged from 0.89 to 0.94. Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. (1993). The California
Coefficient alphas based on word category scores across verbal learning test for children. San Antonio, TX: The Psychological
immediate-recall trials ranged from 0.71 to 0.82. The split- Corporation.
half reliability based on the number of times each word was Elwood, R. W. (1995). The California verbal learning test: Psychometric
characteristics and clinical application. Neuropsychology Review, 5(3).
correctly recalled across immediate-recall trials ranged
from 0.68 to 0.79. The CVLT-II is correlated with the
Wechsler Abbreviated Scale of Intelligence (WASI).
CVLT-C: The internal consistency reliability across
five trials ranged from 0.84 to 0.91. Reliability coefficients California Verbal Learning Test –
for across-semantic category consistency ranged from Children’s Version
0.64 to 0.80.
E RIC M. F INE , D EAN C. D ELIS
University of California, San Diego, School of Medicine
Clinical Uses San Diego Veterans Affairs Healthcare System
La Jolla, CA, USA
The CVLT-II manual states that the test measures ‘‘multi-
ple aspects of how verbal memory occurs or fails to
occur, therefore providing a comprehensive assessment Synonyms
of each patient’s profile of verbal learning and memory
strengths and weaknesses.’’ The manual reports a review CVLT-C
 California Verbal Learning Test – Children’s Version C 477

Description false-positive errors in recognition memory (Table 1 for

CVLT-C variable definitions).
Overview of Test Procedures

The California Verbal Learning Test – Children’s Version Standardization Sample C

(CVLT-C) is a relatively brief, individually administered
measure designed to assess the strategies and processes The CVLT-C was normed on a sample of 920 children
involved in learning and remembering verbal materials from 12 age groups ranging from 5 through 16 years of
(Delis, Kramer, Kaplan, & Ober, 1994). Like the adult age. The sample was stratified based on data from the
versions of this measure (CVLT; Delis, Kramer, Kaplan, 1988 U.S. Census (for additional information regarding
& Ober, 1987; CVLT-II; Delis, Kramer, Kaplan, & Ober, the sample characteristics, see the test manual; Delis et al.,
2000; ▶ California Verbal Learning Test (California Verbal 1994). In addition, normative data for 4-year-olds was
Learning Test-II), the CVLT-C adopts a process-oriented provided by a study by Goodman, Delis, and Mattson
approach for parsing a variety of learning and memory (1999).
components, which facilitates the identification of dis-
tinct memory profiles associated with clinical disorders.
The CVLT-C uses words presented as part of two Score Conversions and Contrast Scores
shopping lists (i.e., a ‘‘Monday list’’ and a ‘‘Tuesday
list’’) and measures both recall and recognition of the Raw scores for the various CVLT-C indices are converted
words over a number of trials. The use of a ‘‘shopping- into an age-based T or z scores (see test manual for
list’’ format makes the procedure more relevant for a description of procedures used to derive these standar-
child and provides information regarding how the child dized scores; Delis et al., 1994). Although the test manual
approaches an everyday memory task. Specifically, in the includes tables for converting the numerous raw scores to
first five trials, the child is asked to recall words from the standardized scores, these scores are computed automati-
Monday list (List A), which consists of 15 words, with cally using the CVLT-C computer scoring software. The
five words from each of three semantic categories (i.e., standard score for List A trials 1–5 total is presented in a
fruits, clothing, and toys). An interference Tuesday list T-score metric, with a mean of 50 and a standard devia-
(List B) of 15 words is then presented on one trial. Words tion of 10. The remaining standardized scores are pre-
from the Tuesday list are divided equally across three sented in a z-score metric, with a mean of 0 and a
semantic categories (i.e., fruits, furniture, and desert). standard deviation of 1.
The Tuesday trial is followed by short-delay free- and Examination of contrast scores (i.e., z-score differ-
cued-recall trials of the first (Monday) list. For cued- ences between two variables) allows for the assessment of
recall trials, the examinee is asked to recall words from particular learning and memory processes. For example,
the three semantic categories contained in List A. A comparing List B (Tuesday list) recall with List A (Monday
20 min delay occurs next, during which nonverbal mea- list) Trial 1 recall provides a measure of a child’s suscep-
sures should be administered. After the delay interval, tibility to proactive interference. As another example, con-
long-delay free-recall, long-delay cued-recall, and yes/no trasting List A long-delay free recall with List A short-delay
recognition memory trials of the Monday list (List A) are free recall can be used to identify rapid forgetting across
administered. delays (Delis et al., 1994; Delis et al., 2000; Donders &
With these procedures, the CVLT-C evaluates not only Minnema, 2004).
the level of a child’s memory performance, but also the
learning strategies used and types of errors made (Delis
et al., 1994). Numerous learning and memory variables Historical Background
are quantified on the CVLT-C, including level of total
recall and recognition on all trials, type of learning strate- In the past, the clinical neuropsychological assessment of
gy employed (e.g., semantic clustering and serial cluster- memory relied on tests designed primarily to assess the
ing), serial position effects, degree of vulnerability to presence or absence of memory dysfunction per se. This
proactive and retroactive interference, retention of infor- goal was accomplished by scoring memory tests only in
mation over short and longer delays, enhancement of terms of the level of correct recall or recognition. Howev-
recall performance by category cuing and recognition er, over the past 25 years or so, numerous studies from
testing, perseveration and intrusion errors in recall, and cognitive neuropsychology have documented qualitatively
478 C California Verbal Learning Test – Children’s Version

California Verbal Learning Test – Children’s Version. Table 1 CVLT-C variable definitions

Variable
List A total Total number of words recalled across the five learning trials
List A1 Number of words recalled from the first trial
List A5 Number of words recalled from the fifth trial
List B Number of words recalled from the interference list (List B)
List A short-delay free Number of words recalled from List A immediately after the presentation of the interference list
recall (List B)
List A short-delay cued Number of words recalled from List A with semantic cueing
recall
List A long-delay free Number of words recalled from List A after a 20 min delay
recall
List A long-delay cued Number of words recalled from List A with semantic cueing after a 20 min delay
recall
Semantic clustering Number of consecutively recalled words from the same semantic category (i.e., consecutive words
from the same semantic category), which reflects the extent to which the subject has actively
imposed a semantic organization on the list of words
Serial clustering Number of consecutively recalled words in the same order as they were presented (i.e., a serial
cluster)
Primacy % Percentage of words correctly recalled from the beginning of List A (first four words)
Middle % Percentage of words correctly recalled from the middle of List A (middle seven words)
Recency % Percentage of words correctly recalled from the end of List A (last four words)
Learning slope Average number of new words acquired across the five List A immediate-recall trials (e.g., a score of 1
means that the examinee learned approximately one new word per trial)
Consistency % Percentage of target words recalled once on each of the four learning trials that were also recalled on
the very next trial; reflects ability to maintain a consistent learning strategy
Perseverations Total number of target words repeated within a trial (called ‘‘repetitions’’ on the CVLT-II; Delis et al.,
2000)
Free-recall intrusions Total number of extra-list intrusions on all the free-recall trials
Cued intrusions Total number of extra-list intrusions on all the cued-recall trials
Total intrusions Total number of extra-list intrusions made on free- and cued-recall trials
Recognition hits Total number of target words correctly identified on recognition testing as belonging to List A
(yes/no format)
Recognition Accuracy of distinguishing target from distracter words on recognition testing; calculated using
discriminability signal detection methods
False positives Total number of distractor words incorrectly identified as belonging to List A during recognition
testing
Response bias Tendency to favor ‘‘yes’’ or ‘‘no’’ responses on recognition testing (positive scores reflect a ‘‘yes’’ bias)

distinct patterns of memory dysfunction associated with neuroscience, and modeled in part after the Rey Auditory
various neurological and psychiatric populations. These Verbal Learning Test (Rey AVLT; Rey, 1964), the CVLT-C,
findings emphasize the multicomponential nature of like its adult counterpart (▶ California Verbal Learning
learning and memory, and, as such, the importance of Test (California Verbal Learning Test-II)), was developed
developing clinical memory tests that allow for the to facilitate the quantification of multiple learning and
evaluation of both qualitative and quantitative features memory parameters (Delis et al., 1987; Delis, Freeland,
of memory performance. Informed by principles of Kramer, & Kaplan, 1988; Delis et al., 1994; Delis et al.,
learning/memory from cognitive science and cognitive 2000).
 California Verbal Learning Test – Children’s Version C 479

Psychometric Data Because the reliability characteristics of the primary

CVLT-C performance indices (e.g., the total words
Reliability and Validity recalled during the learning trials) are stronger than for
the ‘‘process’’ or strategy-use variables (e.g., semantic
The reliability of the CVLT-C was assessed using measures clustering), it has been recommended that clinicians C
of internal consistency and test–retest reliability (Delis place greater emphasis on the main performance variables
et al., 1994). The internal consistency coefficient for the and interpret process-variables cautiously (Strauss et al.,
five trials of the Monday list ranged from .84 to .91 (with a 2006). In order to evaluate learning and memory in other
mean of .88) and the across-semantic-category consisten- formats (e.g., story memory) or modalities (visual), the
cy coefficient ranged from .64 to .80 (with a mean of .72). CVLT-C can be complemented with measures from other
Test–retest stability (median retest interval of 28 days) standardized children’s memory assessment batteries
ranged from .90 to .17, with higher test–retest correlations (e.g., Children’s Memory Scale and Wide Range Assess-
typically occurring for measures of overall level of perfor- ment of Memory-Second Edition).
mance (e.g., total words recalled during the five learning
trials and long-delay free recall). Practice effects were
fairly large for certain conditions. For example, trials Cross References
1–5 total recall improved by an average of five words for
8-year-olds, by six words for 12-year-olds, and by nine ▶ California Verbal Learning Test (California Verbal
words for 16-year-olds. The average improvement on List B, Learning Test-II)
the short-delay, and long-delay trials ranged from one to ▶ Children’s Memory Scale
two words across all the groups. ▶ Rey Auditory Verbal Learning Test
Evidence supporting the validity of CVLT-C comes
from factor analyses of the original standardization
sample and studies of CVLT-C performance in various References and Readings
neurological and neurodevelopmental populations. As
described in the test manual, exploratory principal com- Delis, D. C., Freeland, J., Kramer, J. H., & Kaplan, E. (1988). Integrating
ponents analysis of the primary CVLT-C performance clinical assessment with cognitive neuroscience: Construct valida-
tion of the California Verbal Learning Test. Journal of Consulting and
indices produced a six-factor solution that closely paral-
Clinical Psychology, 53(1), 123–130.
leled the adult version (CVLT; Delis et al., 1987). In Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. (1987). The
addition, Donders (1999) employed confirmatory factor California verbal learning test - Adult version. San Antonio, TX:
analysis to reanalyze the CVLT-C standardization sample, The Psychological Corporation.
and found a five-factor solution that included attention Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. (1994). The
California verbal learning test-Children’s version. San Antonio, TX:
span (List A, Trial 1; List B; middle region recall), learning
The Psychological Corporation.
efficiency (List A, Trial 5; semantic clustering; recall Delis, D. C., Kramer, J., Kaplan, E., & Ober, B. A. (2000). California verbal
consistency), free delayed recall (ahort-delay free recall, learning test - Second Edition. San Antonio, TX: The Psychological
long-delay free recall), cued-delay recall (short-delay cued Corporation.
recall, long-delay cued recall), and inaccurate recall (total Donders, J. (1999). Structural equation analysis of the California verbal
learning test - Children’s version in the standardization sample.
intrusions, recognition false positives).
Developmental Neuropsychology, 15, 395–406.
Donders, J., & Minnema, M. (2004). Performance discrepancies on the
California verbal learning test - Children’s version (CVLT-C) in
Clinical Uses children with traumatic brain injury. Journal of the International
Neuropsychological Society, 10, 482–488.
Goodman, A. M., Delis, D. C., & Mattson, S. N. (1999). Normative data
The CVLT-C was designed to assess subtle to severe verbal
for 4-year-old children on the California verbal learning test -
learning and memory deficits in child clinical populations. Children’s version. The Clinical Neuropsychologist, 13(3), 274–282.
The extant literature indicates that the CVLT-C has utility Miller, L. J., & Donders, J. (2003). Prediction of educational outcome
for characterizing the learning and memory deficits asso- after pediatric traumatic brain injury. Rehabilitation Psychology, 48,
ciated with a wide-range of clinical disorders (for review, see 237–241.
Rey, A. (1964). L’examen clinique en psychologie. Paris: Presses Universi-
Strauss, Sherman, & Spreen, 2006). In addition, CVLT-C
taires de France.
performance has been shown to be predictive of long- Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A compendium
term educational outcomes in children who have suffered of neuropsychological tests (3rd ed.). New York: Oxford University
a traumatic brain injury (Miller & Donders, 2003). Press.
480 C Callosal Apraxia

Current Knowledge
Callosal Apraxia
The CANTAB includes two products: CANTABeclipse
▶ Alien Hand Syndrome and CANTABelect. The CANTABeclipse is composed
▶ Apraxia of 22 tests grouped in specific functional dimensions
measuring executive functioning, visual memory, atten-
tion, semantic/verbal memory, and decision making/
response control. A sixth functional category labeled ‘‘in-
Callosal Disconnection Syndrome duction’’ is comprised of two very short tests whose pur-
pose is to familiarize examinees with the general idea of
▶ Split-Brain responding by touching the screen and to identify those
examinees who cannot reliably participate in the exami-
nation. Details of each subtest are described in Table 1.
The CANTAB offers users flexibility by providing subtests
that can be selected for administration based upon the
Cambridge Neuropsychological specific clinical question. All subtest stimuli are delivered
Testing Automated Battery nonverbally, although adequate receptive language func-
tions are necessary to understand task demands. The
M ARK A. S ANDBERG publisher regards the majority of CANTAB tests to be
Independent Practice independent of language and culture.
Smithtown, NY, USA CANTABelect is described as a ‘‘bespoke service’’
geared toward conducting pharmaceutical clinical trials.
In this case, CCL configures a battery to meet the specific
Synonyms research needs and requirements of the investigator.
Research supporting the use of the CANTAB in the
CANTAB evaluation of brain–behavior relations is reasonably ex-
tensive, with many peer reviewed articles available for
review on the company’s website www.cantab.com. Stud-
ies are available supporting the validity and utility of
Description the CANTAB in measuring the impact of pharmaco-
therapy on neuropsychological performance, and in the
The Cambridge Neuropsychological Testing Automated assessment of Attention Deficit Hyperactivity Disorder,
Battery (CANTAB) is a neuropsychological measure de- affective disorders, schizophrenia, senile dementia of the
veloped at the University of Cambridge and currently Alzheimer’s type and Parkinson’s disease. Although consid-
marketed by Cambridge Cognition Limited (CCL). The erable research is available attesting to the usefulness of the
CANTAB is a theoretically derived instrument, predomi- CANTAB with adult populations, it has not been studied to
nantly measuring non-language functions. The current the same extent in the assessment of brain-behavior rela-
version is a Windows-based program operating on a PC tions and their developmental evolution among children.
platform utilizing interactive touch screen technology. More recent is the investigation of the CANTAB as
CANTAB tests are described as having sufficient sensitiv- a tool to assess the neuropsychological functioning of
ity to discern changes in cognitive functioning brought children. Luciana (2003) noted that because the format
about by CNS disorders and medications. and test items can be used in the assessment of all age
groups, the test allows for complex cognitive functions to
be measured from the time they developmentally emerge
Historical Background to the point where they begin to diminish. DeLuca and
colleagues (2003) studied the development of executive
Originally created in the late 1980s to diagnose dementia capacities during childhood and beyond. Using a sample
in elderly individuals (Fray et al., 1996), the CANTAB is of participants ranging in age from 8 to 64 years, they
used, and has been studied, across age groups and with found functional gains in the efficiency of working mem-
patients presenting with both psychiatric and neurologi- ory capacity, planning, and problem solving abilities be-
cal conditions. tween ages 15 and 19 and again from ages 20–29 years. In
 Cambridge Neuropsychological Testing Automated Battery C 481

Cambridge Neuropsychological Testing Automated Battery. Table 1 CANTAB tests

Subtest Functional category Skill measured

Motor screening Induction Capacity to undergo CANTAB assessment
Big little circle Induction Rule following C
Delayed matching to sample Visual memory Forced choice recognition
Paired associates learning Visual memory Episodic memory
Pattern recognition memory Visual memory Recognition memory for patterns
Spatial recognition memory Visual memory Recognition memory for spatial locations
Intra-extra dimensional set shift Executive function Attentional set shifting
One touch stockings of Cambridge Executive function Planning and working memory
Stockings of Cambridge Executive function Planning and motor control (Tower of London task)
Spatial span Executive function Working memory capacity
Spatial working memory Executive function working memory/strategic thinking
Choice reaction time Attention Alertness and motor speed
Reaction time Attention Simple reaction time
Match to sample visual search Attention Visual search and discrimination
Rapid visual information processing Attention Continuous performance task
Simple reaction time Attention Alertness and motor speed
Graded naming test Semantic/verbal memory Lexical access/naming
Verbal recognition memory Semantic/verbal memory Immediate and delayed verbal memory
Affective go/no-go Decision making/response control Information processing
Cambridge gambling task Decision making Decision making and risk taking
Response control
Information sampling task Decision making Pre-decisional contemplation
Response control
Stop signal task Decision making Inhibition of prepotent responses
Response control

contrast, the developmental vulnerability of executive cost will also be prohibitive to many private practitioners
skills was suggested by a decline in CANTAB performance and organizations.
among subjects in the 50–64 year old sample (Luciana & Software requirements described by the publisher
Nelson, 2002). include Microsoft Windows® 2000 or Windows® XP
Reliability studies have been completed internally by operating systems, with minimal hardware requirements
Cambridge Cognition which described test-retest reli- being a PC with 800 MHz Pentium III processor, 256 MB
ability coefficients ranging from 0.4–0.87. Those findings of RAM, 100 MB free disk space, sound card and speakers,
are consistent with stability coefficients reported by CD-ROM drive, serial port and USB port. A touch screen is
Lowe and Rabbitt (1998). Luciana (2003) reported con- also required, which Cambridge Cognition offers to supply.
sistency coefficients ranging from .73 for a measure of
reaction time latency to .95 for performance on the self-
ordered search task. Future Directions
Limitations of CANTAB include its exclusion of
language based measures, thus leaving the examiner to Pharmaceutical companies have been using CANTAB
supplement the battery with additional tests to assess internationally in multi-site clinical trials for more than
relevant brain-behavior issues such as those involving 20 years. The company is in the process of developing a
laterality (e.g., auditory-verbal memory). CANTAB’s version of CANTAB for the health care market.
482 C Cancellation Tests

References and Readings individuals make few, if any, errors (Weintraub, 2000).
Standardized versions of cancellation tests, such as the
Elliott, R., McKenna, P. J., Robbins, T. W., & Sahakian, B. J. (1995). Ruff 2 & 7, show good test–retest reliability. In addition,
Neuropsychological evidence for frontostriatal dysfunction in on the Ruff 2 & 7 younger adults performed better than
schizophrenia. Psychological Medicine, 25, 619–630.
older adults and performances improved with higher
Luciana, M. (2003). Practitioner review: Computerized assessment of
neuropsychological function in children: Clinical and research appli-
levels of education. There were no gender effects
cations of the Cambridge Neuropsychological Testing Automated (Mitrushina, Boone, Razani, & D’Elia, 2005).
Battery (CANTAB). Journal of Child Psychology and Psychiatry,
44(5), 649–663.
Luciana, M., & Nelson, C. A. (2002). Assessment of neuropsychological Clinical Uses
function through use of the Cambridge Neuropsychological Testing
Automated Battery: Performance in 4- to 12-year-old children. Cancellation tests have been shown to be sensitive in
Developmental Neuropsychology, 22(3), 595–624.
detecting deficits in attention related to right hemisphere
Prouteau, A., Verdoux, H., Briand, C., Lesage, A., Lalonde, P., Nicole, L.,
Reinharz, D., & Stip, E. (2004). The crucial role of sustained
lesions, traumatic brain injuries, schizophrenia, and
attention in community functioning in outpatients with schizo- AIDS-related cognitive impairment. Cancellation tests
phrenia. Psychiatry Research, 129, 171–177. are particularly useful in assessing visuospatial neglect.
Sweeney, J. A., Kmiec, J. A., & Kupfer, D. J. (2000). Neuropsychologic Unlike normal individuals who begin searching for target
impairments in bipolar and unipolar mood disorders on the
stimuli on the left side of the page and systematically
CANTAB neurocognitive battery. Biological Psychiatry, 48, 674–685.
move rightward, neglect patients begin on the right
using a disorganized search pattern omitting many targets
on the left side of the page (Weintraub, 2000). By decreas-
Cancellation Tests ing the attentional demands of a letter cancellation test by
reducing the number of nontarget stimuli, right hemi-
R ICHARD F. K APLAN sphere damaged patients showed decreased left-sided ne-
UConn Health Center glect, suggesting that the neglect syndrome is the result of
Farmington, CT, USA an attentional bias (Kaplan et al., 1991).

Synonyms Cross References

Vigilance tests ▶ Attention

▶ Neglect and Hemi-inattention
▶ Neglect Syndrome
Description ▶ Vigilance

Cancellation tests are designed to measure sustained and

selective attention. References and Readings
Kaplan, R. F., Verfaellie, M., Meadows, M. E., Caplan, L. R., Pessin, M. S., &
Historical Background DeWitt, L. D. (1991). Changing attentional demands in left hemi-
spatial neglect. Archives of Neurology, 48, 1263–1266.
Mitrushina, M., Boone, K. B., Razani, J., & D’Elia, L. F. (2005). Handbook
Numerous variations of cancellation tests have been
of normative data for neuropsychological assessment (2nd ed.,
developed to assess sustained, selective attention, and pp. 160–170). New York: Oxford.
spatial inattention following hemispheric lesions. The Weintraub, S. (2000). Neuropsychological assessment of mental state. In
patient is typically required to scan through an array M. Mesulam (Ed.), Principles of behavioral neurology (2nd ed.,
of stimuli and find (cancel) specific target stimuli (e.g., pp. 121–173). New York: Oxford.

bells).

Psychometric Data CANTAB

There is relatively little normative data for cancellation ▶ Cambridge Neuropsychological Testing Automated
tests, and most comparative studies show that normal Battery
 Capacity Limitations C 483

Capacity Capacity Limitations

R OBERT L. H EILBRONNER A NNA M AC K AY-B RANDT
Chicago Neuropsychology Group Brown University Medical School
Chicago, IL, USA Providence, RI, USA
C

Synonyms Definition

Competency The constraints on processing of internal and external

stimuli dependent upon the structure of, and the processes
related to, the cognitive system.
Definition

In the most basic sense, capacity refers to the ability to

make decision(s) with regard to oneself. Specifically, this
Historical Background
refers to one’s ability to understand and appreciate the
Fundamental research in attention emerged in the
consequences of one’s actions. Legal capacity remains
1950s with information processing theories. D.E. Broad-
in effect until death, unless a court rules that one is ‘‘inca-
bent published an influential book in 1958, Perception
pacitated.’’ If a person is ruled by a court of law to be legally
and Communication, which was in turn influenced by
incapacitated, this can remove all or part of a person’s right
the contemporary work of communication theorists in
to make decisions. Specifically, one can be deemed incapa-
engineering. Broadbent used the communication sys-
ble of managing financial affairs, but ruled capable of
tem as a metaphor for relationships within the human
making medical decisions, for example. If a person is
brain. Each brain system (i.e., sensory, memory, re-
ruled to lack full legal capacity, then they are prohibited
sponse generation) was conceptualized in terms of a
from entering into a contract, giving a power of attorney,
communication system, with an information source, a
creating a will, or consenting to medical treatment. A ruling
transmission channel(s), and a receiver. The channel by
of legal incapacity typically results in the appointment of a
which a message is transmitted has a capacity, which
guardian or conservator to make decisions for the person.
limits the rate by which information can be transmitted.
There are several types of capacity that are relevant to
A property of communication systems is that the
forensic neuropsychology including: capacity to consent
transmission of information within a system can never
to treatment, to manage financial affairs, and others.
exceed the capacity of the channel divided by the
information source output. This theoretical conceptu-
alization sets the stage for future research, describing the
Cross References limits in sensory and cognitive systems and mechanisms
to deal with the processing of information in these
▶ Testamentary Capacity
systems.

References and Readings Current Knowledge

Marson, D. C., & Hebert, K. (2005). Assessing civil competencies in older
In response to the observation that one is not able to
adults with dementia: Consent capacity, financial capacity, and
testamentary capacity. In G. Larrabee (Ed.), Forensic neuropsychology:
attend to all stimuli in the environment at the same
A scientific approach. New York: Oxford University Press. time, hypotheses have developed to explain the limita-
Marson, D. C., Sawrie, S., Snyder, S., McInturff, B., Stalvery, T., tions on the capacity for cognitive processing, particularly
Boothe, A., et al. (2000). Assessing financial capacity in patients in the areas of attention and memory (Broadbent, 1971;
with Alzheimer’s disease: A conceptual model and prototype
Miller, 1956; Shiffrin & Schnieder, 1977; Kahneman,
instrument. Archives of Neurology, 57, 877–884.
Willis, S. (1996). Everyday cognitive competence in elderly persons:
1973). Cohen (1993) organized attentional capacity in
Conceptual issues and empirical findings. The Gerontologist, 36, terms of structural and energetic limitations. Structural
595–601. capacity limitations can be thought of in terms of
484 C CAPD

optimal processing characteristic of the system such as References and Readings

channel capacity, working-memory capacity, processing
speed, and temporal–spatial characteristics of the sys- Broadbent, D. E. (1958). Perception and communication. London:
tem. These structural elements are influenced by vari- Pergamon.
Broadbent, D. E. (1971). Decision and stress. London: Academic Press.
ables such as performance required on more than one
Cohen, R. (1993). The neuropsychology of attention. New York: Plenum.
task (e.g., dual task): task complexity, memory de- Duncan, J., & Humphreys, G. W. (1989). Visual search and stimulus
mand, high or low rate of target event occurrence, similarity. Psychological Review, 96, 433–458.
and task duration. Energetic capacity limitations are Jacoby, L. L. (1991). A process dissociation framework: Separating auto-
considered to be natural or imposed variations within matic from intentional uses of memory. Journal of Memory and
Language, 30, 513–541.
an individual that includes arousal, motivation, and
Kahneman, D. (1973). Attention and effort. Englewood Cliffs, NJ: Pren-
generated effort. A clear indicator of the influence of tice-Hall.
energetic factors on performance is performance varia- Miller, G. A. (1956). The magical number seven, plus or minus two: Some
bility over time. limits on our capacity for processing information. Psychological
Researchers of cognition have used the debate over Review, 63, 81–97.
Shiffrin, R. M., & Schnieder, W. (1977). Controlled and automatic
whether particular processes are limited or unlimited in
human information processing: 2. Perceptual learning, automatic
capacity as a fruitful ground for study. For example, attending and a general theory. Psychological Review, 84, 127–190.
theories of serial and parallel processing have emerged Treisman, A., & Gelade, G. (1980). A feature integration theory of
in both the attention and memory literature in support attention. Cognitive Psychology, 12, 97–136.
and rejection of capacity limited processes. Although not Wolfe, J. M. (1994). Guided search 2.0: A revised model of visual search.
Psychonomic Bulletin & Review, 1, 202–238.
strictly coupled, serial processing is often considered in
the context of limited capacity, whereas paral-
lel processing is thought to be unlimited in capacity.
This coupling bears out in visual search studies that
have found preattentive processes that are thought
CAPD
to be parallel and unlimited in capacity, versus focal
▶ Central Auditory Processing Disorder
attentive processes that are serial and limited in capacity
(Duncan & Humphreys, 1989; Treisman & Gelade, 1980;
Wolfe, 1994). Similarly, in memory research, Jacoby
(1991) distinguished automatic from controlled proces- Capgras Syndrome
sing, with similar parallel and unlimited capacity (auto-
matic) versus serial and limited capacity (controlled) PAUL M ALLOY
distinctions. Alpert Medical School of Brown University
Providence, RI, USA

Future Directions
Synonyms
A relatively recent emphasis has been placed on the inter-
action of neural and cognitive limitations with factors Reduplication delusion; Reduplicative paramnesia
such as arousal, motivation, and effort.
Short Description or Definition

Cross References Delusions are defined as false beliefs based on incorrect

inference about external reality, and firmly sustained in
▶ Attention spite of the opinions of others or contrary evidence
▶ Attention/Executive Function (American Psychiatric Association, 1987).
▶ Parallel Processing Capgras syndrome (Capgras & Reboul-Lachaux, 1923)
▶ Serial/Sequential Processing is a type of reduplication delusion involving the belief that
▶ Short-Term Memory persons well-known to the patient, such as family
▶ Span Test members, have identical doubles or are imposters. The
▶ Working Memory double or imposter is sometimes perceived as differing
 Capgras Syndrome C 485

slightly in some physical characteristic from the found that the delusion actually had a 15% incidence in
‘‘genuine’’ person, but the patient may have difficulty their sample of adult inpatients previously diagnosed as
verbalizing the precise nature of this ‘‘difference.’’ having schizophrenia. Several researchers have found
that about 25% of Alzheimer patients display delusions
involving misidentification of people (e.g., Mendez, C
Categorization Martin, Smyth, & Whitehouse, 1992). Large-scale
epidemiological studies are lacking to date.
Several variations of Capgras syndrome have been identi-
fied. Doppleganger or subjective doubles is the belief that
the patient himself has a double or impersonator
(Christodoulou, 1978). Fregoli syndrome is the belief that
Natural History, Prognostic Factors,
a person is capable of taking on the appearance of others,
Outcomes
while retaining his/her own psychological identity (Courbon
About 58% of Capgras patients who receive adequate
& Fail, 1927). Intermetamorphosis is the belief that people
neurodiagnostic workups are found to display primary
are changing in both physical and psychological identity
psychiatric disorder, uncomplicated by demonstrable
to become another person (Courbon & Tusques, 1932).
neurologic disease (Dohn & Crews, 1986). Although
Capgras syndrome must be distinguished from purely
psychological factors can be important in the production
perceptual or hallucinatory disturbances, and from
of delusions, a critical review of the literature by Malloy
generalized disturbance of cognition. That is, in order to
and Richardson (1994) demonstrated that delusions can
be properly and convincingly diagnosed as a delusion, the
also result from identifiable neurologic disease, from
disturbance must involve a mistaken belief (not merely a
generalized disturbances to focal lesions.
misperception) and must be persistent (not a transitory
They found that Capgras and its variants have been
effect of confusion). For example, in autoscopy, the patient
reported in association with a variety of systemic diseases
experiences a second self, as in the subjective doubles
and diffuse neurologic disorders. Systemic etiologies have
variant of Capgras. However, the phenomena differ in
included: Metabolic disturbances such as myxedema,
that the double is actually seen in autoscopy, rather than
pseudohypoparathyroidism, anemia, hepatic dysfunction,
believed to be active elsewhere, as in subjective doubles. The
B12 deficiency; intoxication and reactions to drugs inclu-
prosopagnosic person may fail to recognize his wife, where-
ding cocaine, chloroquine, disulfiram, digoxin, and
as the Capgras patient will insist that the present person is
lithium; cerebral infections such as encephalitis and
an imposter and that the ‘‘real’’ wife is somewhere else.
AIDS; subarachnoid hemorrhage; migraine; post-ECT
Patients in confusional states or dementia may express
confusion; minor head trauma; and degenerative dementia.
strange beliefs, but the beliefs typically change from hour
In terms of focal lesions such as tumors and stroke,
to hour and do not persist once the confusion resolves. Thus
that review demonstrated that the right hemisphere or
this problem should not be termed delusional.
bilateral lesions were invariably found on neuroimaging,
Patients with Capgras syndrome are usually described
with no exclusively left-hemisphere lesions. EEG and neu-
as forthcoming and cooperative. Although they insist that
rologic exam findings also implicated right-hemisphere
their delusional beliefs are true, they often admit to puzzle-
pathology. In terms of specific localization, 72% of cases
ment or bemusement regarding aspects of the delusion.
with CT or MRI scans had right frontal, temporal, or
Rather than escalate their defenses by becoming hostile,
frontotemporal involvement. Neuropsychological testing
they are more likely to confabulate an explanation. For
documented spatial, executive, and nonverbal memory
example, a patient with a delusion of duplication (Malloy,
problems, consistent with the right frontotemporal
1991) was asked how she could have two sets of children
localization on neuroimaging studies.
with identical names. She appeared momentarily puzzled
and then stated, ‘‘My husband was in the Navy, and we
moved around a lot; it was hard to keep that straight.’’
Neuropsychology and Psychology of
Capgras Syndrome
Epidemiology
Capgras and its variants represent either underidentifica-
Dohn and Crews (1986) observed that Capgras syndrome tion or overidentification of the object of the delusion
was frequently overlooked in psychiatric patients and (Vie, 1930). Thus, in Capgras syndrome, the patient
486 C Capgras Syndrome

mistakenly perceives the person as unfamiliar due to Treatment

underidentification. In Fregoli syndrome, on the other
hand, the patient misperceives diverse persons as the In degenerative dementia, duplication delusions are usually
same person due to overidentification. transitory phenomena, occurring in the early-to-middle
Feinberg and Shapiro (1989) emphasized the stages and disappearing when cognitive deficits become
importance of the right temporal lobe in producing severe. In other etiologies such as cerebrovascular disease,
misidentification delusions. They reviewed the evidence they often occur acutely and persist for many months or
from stimulation and seizure studies indicating that the years. Prognosis appears to vary with the type of delusion
right temporal lobe plays an important role in producing and the underlying etiology.
the experience of familiarity. Cutting (1991) has put forth Many underlying systemic causes (e.g., infections,
a similar argument regarding the role of the right toxic reactions, metabolic disturbances) of duplication
hemisphere in identification. delusions are readily treated, resulting in elimination of
Crucial factors in the persistence of delusions may be the delusion. For example, Santiago, Stoker, Beigel, Yost,
the length of time the perceptual distortion continues, and Spencer (1987) reported resolution of Capgras
and the ability of the patient to correct the misperception following treatment of underlying thyroid disease.
on the basis of new information. Frontal lesions may Spontaneous resolution of Capgras delusions has also
impact on the latter self-corrective function, making it been reported (Ruff & Volpe, 1981).
impossible to resolve conflicting information, resulting On the other hand, Joseph (1987) described a patient
in unconcern and confabulation when the conflicts are whose chronic psychosis and intermittent psychotic mis-
confronted (Joseph, 1986). Alexander, Stuss, and Benson identification of the Capgras and intermetamorphosis
(1979) were the first to report a Capgras delusion clearly types were refractory to neuroleptic treatment. Upon
related to a specific neurologic structural lesion, involving administration of a trial of clorazepate, complete
the right hemisphere with predominantly frontal and remission of psychotic symptoms was achieved for the
temporal lobe damage. They noted the importance of first time in 19 years, but these recurred when the patient
frontal damage in Capgras, both in terms of the inability discontinued her clorazepate.
to resolve conflicts, and confabulation of a second The effectiveness of psychological interventions may
persona. vary with the type of delusion, and the degree to which
Psychodynamic or functional interpretations for the neurologic factors are involved. Unfortunately, there has
development of delusions are not incompatible with this been no systematic treatment follow-up research, and
neuropsychological explanation. data are limited to uncontrolled case studies.

Evaluation Cross References

Careful clinical interview with both patient and family ▶ Reduplicative Paramnesia
members will help to elicit evidence of Capgras delusions.
In the course of family disputes and initial evaluations,
patients may learn to minimize or deny their delusions. References and Readings
Demented patients may forget instances of misidentifica-
tion. Hence, family informants may be extremely helpful. Alexander, M., Stuss, D. T., & Benson, D. F. (1979). Capgras syndrome:
The literature is replete with case reports positing a A reduplicative phenomenon. Neurology, 29, 334–339.
American Psychiatric Association. (1987). Diagnostic and statistical
psychodynamic explanation for Capgras, but with no
manual of mental disorders-third edition-revised (DSM-III-R).
workup to rule out neurologic etiology. Since Capgras is Washington, DC: American Psychiatric Press.
commonly associated with neurologic illness; full workup Capgras, J., & Reboul-Lachaux, J. (1923). L’illusion des ‘‘sosies’’ dans
including neuroimaging and neuropsychological testing is un delire systematise. Bulletin de Societe Clinical Medicine Mentale,
essential. Neuropsychological testing often reveals deficits 11, 6–16.
Christodoulou, G. N. (1978). Syndrome of subjective doubles. The
in frontal/executive and visuospatial functions (Malloy &
American Journal of Psychiatry, 135, 249–251.
Richardson, 1994). Facial recognition and memory Courbon, P., & Fail, G. (1927). Syndrome ‘‘d’illusion de Fregoli’’ et
should be tested to rule out alternative explanations for schizophrenie. Bulletin de Societe Clinical Medicine Mentale, 88,
the patient’s problems, such as prosopagnosia. 214–237.
 Carbamazepine C 487

Courbon, P., & Tusques, J. (1932). L’illusion de intermetamorphose et de Brand Name

charme. Annales Médico-Psychologiques, 90, 401–406.
Cutting, J. (1991). Delusional misidentification and the role of the right
hemisphere in the appreciation of identity. The British Journal of
Tegretol, Carbatrol
Psychiatry, 159(Suppl. 14), 70–75.
Dohn, H. H., & Crews, E. L. (1986). Capgras syndrome: A literature review
C
and case series. The Hillside Journal of Clinical Psychiatry, 8, 56–74. Class
Feinberg, T. E., & Shapiro, R. M. (1989). Misidentification-reduplication
and the right hemisphere. Neuropsychiatry, Neuropsychology, and
Behavioral Neurology, 2, 39–48.
Anticonvulsant
Foerstl, H. (1990). Capgras’ delusion: An example of coalescent psycho-
dynamic and organic factors. Comprehensive Psychiatry, 31, 447–449.
Joseph, A. B. (1987). Delusional misidentification of the Capgras and Proposed Mechanism(s) of Action
intermetamorphosis types responding to clorazepate. A case report.
Acta Psychiatrica Scandinavica, 75, 330–332.
Carbamazepine is a use-dependent blocker of voltage-
Joseph, R. (1986). Confabulation and delusional denial: Frontal lobe and
lateralized influences. Journal of Clinical Psychology, 42, 507–520.
sensitive sodium channels, it interacts with the open chan-
Malloy, P. (1991). Differential diagnosis of primary and secondary nel conformation of voltage-sensitive sodium channels, it
Capgras delusions. Neuropsychiatry, Neuropsychology, and Behavioral interacts at alpha pore-forming subunit of voltage-sensitive
Neurology, 4, 90–108. sodium channels, and inhibits release of glutamate.
Mendez, M. F., Martin, R. J., Smyth, K. A., & Whitehouse, P. J. (1992).
Disturbances of person identification in Alzheimer’s disease. A retro-
spective study. The Journal of Nervous and Mental Disease, 180, 94–96.
Ruff, R. L., & Volpe, B. T. (1981). Environmental reduplication associated Indication
with right frontal and parietal lobe injury. Journal of Neurology,
Neurosurgery, and Psychiatry, 44, 382–386. Complex partial seizures, generalized tonic–clonic seizures,
Santiago, J. M., Stoker, D. L., Beigel, A., Yost, D., & Spencer, P. (1987).
mixed seizure patterns, and trigeminal neuralgia pain.
Capgras’ syndrome in a myxedema patient. Hospital & Community
Psychiatry, 38, 199–201.
Vie, J. (1930). Un trouble de l’identification des personnes: L’illusion des
sosies. Annales Médico-Psychologiques, 88, 214–237. Off Label Use

Glossopharyngeal neuralgia, bipolar disorder, psychosis,

schizophrenia, and personality disorders.
Capital Punishment
▶ Death Penalty Side Effects

Serious

CARB Aplastic anemia, agranulocytosis, Stevens Johnson Syn-

drome, cardiac problems, induction of psychosis or
▶ Computerized Assessment of Response Bias mania, and increased frequency of seizures.

Common
Carbamazepine
Sedation, dizziness, confusion, headache, nausea, and
J OHN C. C OURTNEY vomiting.
Children’s Hospital of New Orleans
New Orleans, LA, USA
References and Readings

Physicians’ Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson

Generic Name PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The prescriber’s guide –
Carbamazepine Second edition. New York, NY: Cambridge University Press.
488 C Carbon Monoxide Poisoning

Additional Information Exposure to carbon monoxide is the most common

form of poisoning worldwide. With increased awareness
Drug Interaction Effects: http://www.drugs.com/drug_interactions.html of its potential dangers, the majority of these exposures
Drug Molecule Images: http://www.worldofmolecules.com/drugs/ can be prevented.
Free Drug Online and PDA Software: www.epocrates.com
Gene-Based Estimate of Drug interactions: http://mhc.daytondcs.
com:8080/cgi bin/ddiD4?ver=4&task=getDrugList Natural History, Prognostic Factors,
Pill Identification: http://www.drugs.com/pill_identification.html Outcomes

Compared to normal oxyhemoglobin (i.e., when oxygen

binds to hemoglobin), carboxyhemoglobin is bright red;
thus, an early sign of carbon monoxide poisoning is a
Carbon Monoxide Poisoning cherry-red skin color.
Acute exposure to lower concentrations of carbon
G EORGE C. WAGNER monoxide will result in a slowly developing hypoxia that
Rutgers University triggers peripheral vasodilation. Paradoxically, when there
New Brunswick, NJ, USA is a slow increase in carboxyhemoglobin saturation, com-
pensatory changes in respiratory rate may lag. Thus, the
symptoms of dizziness, weakness, headache, and nausea
Synonyms will precede fainting. Once unconscious, increased respi-
ration and tachycardia will be followed by convulsions
Carboxyhemoglobinemia and coma, and death will ensue as the carboxyhemoglobin
climbs and remains above 50% saturation.
Chronic exposure to low concentrations of carbon
Short Description monoxide can occur in heavy smokers as well as in indi-
viduals whose occupations involve protracted exposure to
Carbon monoxide (CO) is a colorless, odorless gas gen- exhaust fumes. The binding of carbon monoxide to he-
erated during the combustion of carbon-containing fuels. moglobin is fully dissociable though these individuals
When inhaled into the lungs, it readily competes with may manifest carboxyhemoglobin saturation at 10%,
oxygen for binding sites on hemoglobin. The affinity of which is 20-fold higher than normal. Symptoms asso-
carbon monoxide binding to hemoglobin is more than ciated with chronic exposure include headache, fatigue,
200-fold greater than that of oxygen. Thus, at atmospheric nausea, difficulty in concentrating, and impaired memory
concentrations as low as 0.1%, carbon monoxide will (Kao & Nanagas, 2005).
achieve a 50% saturation of the hemoglobin, resulting in
carboxyhemoglobinemia and a significant reduction in Neuropsychological Assessment
the blood oxygen levels.
Acute carbon monoxide poisoning, for example, fol- The Carbon Monoxide Neuropsychological Screening
lowing exposure to automobile exhaust (which generates Battery (CONSB) has been developed to screen for cogni-
about 5% to 7% carbon monoxide) will rapidly saturate tive impairment following acute carbon monoxide poi-
the hemoglobin and cause death within minutes with soning (Messier & Myers, 1991). The CONSB battery
virtually no prior symptoms. begins with an assessment of general orientation of the
patient, and this is followed by the Digit Span, Trail
Making, Digit Symbol, Aphasia Screening, and Block De-
Epidemiology sign tests. Use of this battery in an emergency room
setting allows for the early detection of cerebral im-
Exposure to low concentrations of carbon monoxide con- pairment in the exposed individuals.
sequent to the operation of faulty furnaces or gas-powered
engines is the leading cause of accidental poisoning in the Evaluation
United States. Exposure to high concentrations of carbon
monoxide is the most common form of intentional poi- The long-term consequences of acute carbon monoxide
soning in the United States. poisoning may, in part, be consequent to the damage to
 Carotid Angiography C 489

the blood–brain barrier during the period of hypoxic Messier, L. D., & Myers, R. A. M. (1991). A neuropsychological screening
battery for emergency assessment of carbon-monoxide-poisoned
coma. Following apparent recovery from the acute expo-
patients. Journal of Clinical Psychology, 47(5), 675–684.
sure, a delayed toxicity with abrupt onset may appear Prockop, L. D., & Chichkova, R. I. (2007). Carbon monoxide intoxica-
with symptoms of confusion together with motoric tion: an updated review. Journal of the Neurological Sciences, 262,
symptoms resembling Parkinson’s disease (incoordina- 122–130.
C
tion, muscular weakness, and muscular rigidity). These
neurological signs reflect extensive damage to the basal
ganglia and white matter of the brain with a demyelin-
ation that spares the neuronal axons. Neuroimaging Carboxyhemoglobinemia
scans will most likely appear normal 24 h after exposure;
lesions may begin to appear 2 weeks later. Functional ▶ Carbon Monoxide Poisoning
changes associated with these later-appearing lesions are
variable but attempts have been made to relate these to
the severity of the initial exposure. Acute exposure result-
ing in carboxyhemoglobin saturation of 25% or more will
result in later onset cognitive impairments in as many as Cardiac Ultrasound
50% of the patients. The cognitive deficits include agno-
sia, aphasia, and apraxia as well as impaired memory, ▶ Echocardiogram
impaired executive function, and a general decrease
in intellect. In addition, visuomotor performance dete-
rioriates. Finally, late-appearing changes in affect are
frequently reported as are obsessive–compulsive tenden- Career Counseling for Individuals
cies and anxiety (Hopkins & Woon, 2006). with Disabilities
▶ Vocational Counseling
Treatment

Effective treatment entails removal from the source of the

carbon monoxide and providing oxygen; when breathing
Career Maintenance
air, the half-life of carboxyhemoglobin is about 5 h and
this time can be reduced to 1.5 h with oxygen supplemen-
▶ Job Retention
tation. Indeed, supplementation with oxygen immediately
after exposure remains as the most effective strategy for
reducing the severity of the later-appearing neural and
functional consequences following carbon monoxide poi-
soning (Prockop & Chichkova, 2007). Carotid Angiography
PAUL E. K APLAN
Capitol Clinical Neuroscience
Cross References Folsom, CA, USA

▶ Neurotoxins
Synonyms
References and Readings Angio

Hopkins, R. O., & Woon, F. L. M. (2006). Neuroimaging, cognitive

and neurobehavioral outcomes following carbon monoxide Definition
poisoning. Behavioral and Cognitive Neuroscience Reviews, 5(3),
141–155.
Kao, L. W., & Nanagas, K. A. (2005). Carbon monoxide poisoning. Angiography is the evaluation of the blood vessels
Medical Clinics of North America, 89, 1161–1194. of the central nervous system and associated
490 C Carotid Artery

cervicocerebral vasculature applying radiography to the

simultaneous injection of intravascular contrast media. Carotid Artery
Femoral or axillary nonselective approaches can be
used to catheterize the aortic arch or selective means ▶ Internal Carotid Artery
employed to catheterize the carotid artery. Contrast
media is then injected through the catheter and X-
rays taken. Digital subtraction, computed tomography
(CT) scanning, and MRI techniques too can be applied Carotid Endarterectomy
at this point. Obstructions, stenosis, aneurysms, and
A-V malformations can all be identified. Finer and A NUJ S HARMA
more selective views are realized by using microcath- Virginia Commonwealth University
eters. Some of the disease entities studied include is- School of Medicine
chemic cerebrovascular disease, aneurysms, vascular Richmond, VA, USA
malformations, neoplasms, and brain injuries. Two
special carotid lesions could be evaluated with carotid
angiography. Arterial dissections develop when blood Synonyms
is extravasated within the arterial wall itself narrowing
the arterial lumen. The carotid artery between C2 and CEA
the base of the skull is frequently a target for the
formation of a pseudoaneurysm. Pain, bruits, with
cranial nerve palsies will be present. Angiography will Definition
be useful. Another condition where carotid angiogra-
phy is useful is the carotid-cavernous fistula – a high CEA is an elective surgical procedure that removes plaque
pressure, high-flow connection between the carotid from the lumen of the carotid artery. After anesthesia, the
artery and the cavernous sinus veins. Patients will surgeon clamps the carotid artery proximal and distal to
present with visual loss, a bruit, proptosis. the stenosis temporarily. The surgeon may place a shunt
proximal to the clamp to reroute blood to the brain. Next,
an incision is made over the area of blockage. The plaque
is scraped out and separated from the inner lining of the
Current Knowledge
artery. After it is removed, the artery is sutured together,
the clamps are removed, and any bleeding is stopped.
Can be part of the evaluation process of patients with
Finally, the skin incision is closed.
cerebrovascular disease.

Current Knowledge
Cross References
The arch of the aorta gives off three branches: the
▶ Angioma innominate, the left common carotid, and the left sub-
▶ Glioma clavian. The innominate artery, also known as the bra-
▶ Hemangioma chiocephalic artery, gives rise to the right subclavian
▶ Hemiplegia artery and the right common carotid artery. The com-
mon carotid arteries bilaterally split into internal and
external carotid arteries. The right and left internal ca-
References and Readings rotid arteries, along with the vertebral arteries, branches
of the subclavian artery, are the major blood vessels
Dumolin, C. L., & Hart, H. R. (1986). Magnetic resonance angiography. supplying the brain.
Radiology, 161, 717. As plaque builds in the carotid artery, atherosclerosis,
Faro, S. H., Haselgrove, J. C., Wang, Z., et al. (1993). Carotid MR or hardening of arteries, develops. Carotid stenosis, or
angiography. Radiology, 189, 243.
narrowing of the carotid artery, may also develop and is
Love, B. B., & Biller, J. (2003). Neurovascular System. In C. G. Goetz (Ed.),
Textbook of clinical neurology (2nd ed.) (pp. 395–424). Philadelphia: most common at the origin of the internal carotid artery
Saunders. or less commonly, at the distal common carotid artery.
 Case Coordination C 491

If the stenosis is severe, it may result in decreased is inserted through the groin and is guided until it
perfusion of brain tissue, and consequently ischemia. reached the site of stenosis. After the location of the
Another mechanism by which ischemia can develop is catheter is confirmed, a balloon inflates and attaches a
by the development of a thrombus over the plaque. metal-mesh stent into the artery. The balloon is then
When this occurs, an embolus may break off and may deflated and the catheter is gently removed. However, C
result in the occlusion of a vessel distally. long-term studies have not proven this method to be
A stroke may develop if the brain is deprived of its superior to a CEA.
blood supply, resulting in a sudden loss of neurologic
function. However, transient ischemic attacks (TIA)
may be the diagnosis if symptoms, such as loss of sensory
or motor function in the extremities, inability to com- Cross References
prehend or initiate speech, or loss of vision in one
eye described a shade coming down over one eye (amau- ▶ Ischemia
rosis fugax), last for a few minutes to hours and ▶ Magnetic Resonance Angiography
resolve completely in twenty-four hours. Patients with ▶ Stroke
a history of stroke or TIA are at increased risk of a
subsequent stroke and should be further evaluated with
imaging studies. According to the North American
Symptomatic Carotid Endarterectomy Trial (NASCET),
References and Readings
patients with symptomatic carotid artery stenosis of
Chaturvedi, S., Bruno, A., Feasby, T., Holloway, R., Benavente, O.,
greater than 70% have a 26% risk of recurrent stroke Cohen, S. N. et al. (2005). Carotid endarterectomy – an evidence-
over two years. based review: Report of the Therapeutics and Technology Assess-
The diagnosis of a TIA is made by carotid duplex ment Subcommittee of the American Academy of Neurology.
ultrasound. This type of imaging bounces high-frequency Neurology, 65, 794–801.
Roffi, M., & Lüscher, T. F. (2008). Management of carotid artery stenosis.
sound waves off blood vessels and the blood within the
Herz, 33, 490–497.
lumen to determine blood flow and any abnormalities Rothwell, P. M., Eliasziw, M., Gutnikov, S. A., Fox, A. J., Taylor, D. W.,
within the vessels themselves. Other modalities useful in Mayberg, M. R. et al. (2003). Analysis of pooled data from the
the diagnosis of a TIA include computed tomography randomised controlled trials of endarterectomy for symptomatic
angiography (CTA), magnetic resonance angiography carotid stenosis. Lancet, 361, 107–116.
(MRA), and angiography. In each of these, a contrast
dye, or gadolidium in the case of MRA, is injected into
the arteries. This helps identify any areas of poor blood
flow and determine the degree of stenosis.
If there is greater than 70% blockage of the carotid CARS
artery, a CEA is recommended if the patient is symptomatic
with a history of TIA or nondisabling stroke, or even if ▶ Childhood Autism Rating Scales
the patient is asymptomatic. However, a CEA should not
be performed during a stroke or TIA or if the patient
experiences a stroke that leaves him severely disabled.
If there is less than a 70% blockage and the patient
is asymptomatic, a CEA is not recommended. In this
case, the patient should be treated medically with a baby
CAS
aspirin daily. In addition, other risk factors that may cause
▶ Cognitive Assessment System
further damage to the vessels, such as smoking, diabetes,
hypertension, and hypercholesterolemia, should be treated
medically. A CEA is only recommended for 50–69% steno-
sis if the patient has had recurrent TIAs unresponsive to
medical management.
For patients that are high risk for the CEA, other Case Coordination
surgical interventions, such as angioplasty and stenting,
can be considered. During this procedure, a catheter ▶ Case Management
492 C Case Management

patients or ‘‘cases.’’ People with disabilities often find the

Case Management term, ‘‘case manager,’’ to be pejorative as in, ‘‘I am not a
case and I will not be managed.’’ Case managers do not
B RIAN T. M C M AHON manage patients, but instead, they manage the rehabilita-
Virginia Commonwealth University tion process. Indeed, the planning, organizing, directing,
Richmond, VA, USA and controlling of the rehabilitation process from the
initial point of contact to the realization of outcomes is
the ultimate mission of the case manager. For example,
Synonyms life-care planning (▶ Life Care Planning) is often depicted
as the ultimate case management plan because of its
Case coordination; Case planning inherently comprehensive nature. It is hard to conceive
of a successful life-care planner who is not a professional
case manager.
Definition Another appropriate way to understand case manage-
ment is to review the core body of knowledge for CCMs.
‘‘Case management’’ is a widely used (and often misused) These include: case management concepts, principles, and
term that has become commonplace in health care and strategies; psychosocial and support systems; health-care
human services. In its most professional use, case manage- management and service delivery; health-care reimburse-
ment is a collaborative process that assesses, plans, imple- ment; and vocational concepts and interventions. Case
ments, coordinates, monitors, and evaluates the options management requires one to go well beyond the direct
and services required to meet the patient’s health and/or patient services of one’s core profession and intervene
human service needs. It is characterized by advocacy, com- in the systems, services, and supports available in the
munication, and resource management and promotes community to achieve intended outcomes. For example,
quality and cost-effective interventions and outcomes. it is not unusual for a case manager to work with multi-
ple stakeholders in a single case including payers,
service providers, family members, attorneys, employers,
Current Knowledge advocacy organizations, and, of course, the patient. The
case manager sees all of these parties as important and
In recent years, case management has become a freestand- is keenly aware that any single individual in this
ing profession, but it is actually an overlay upon one’s core system has the wherewithal to completely sabotage a
profession. The certified case manager (CCM) must first well-conceived plan if neglected or marginalized. In
hold a professional license or certification in a recognized essence, the case manager is not only the primary architect
health care or human service profession before he or she of the rehabilitation plan, but must also sell that plan to all
is eligible for case management certification. The core of the key stakeholders in order to maximize the plan’s
profession must involve a postsecondary degree in a field implementation and outcomes.
that promotes the psychological, medical, or vocational ‘‘Case management’’ is among the most misused
well-being of the person being served. The license or terms in health care. Because it is unprotected by most
certification that follows the degree in one’s core profession state departments of professional regulation, the term is
must be one that is required by law for independent often used in reference to discharge planners, utilization
practice without the supervision of another licensed reviewers, claims adjusters, and a host of paraprofes-
professional. Most CCMs are graduate-trained in rehabili- sionals. However, CCMs are professionally prepared and
tation counseling, rehabilitation or occupational health evaluated along the lines described above. They are also
nursing, or clinical social work. held to strict scope-of-practice guidelines, ethics, and
The essential functions of a case manager include continuing education requirements.
assessment and coordination; development, monitoring,
implementation and evaluation of the rehabilitation plan;
and achievement of outcomes. It is worth noting that case
managers are managers in a very real sense. Generally Cross References
speaking, management theory states that the primary
functions of a manger are to plan, organize, direct, and ▶ Life Care Planning
control. This is precisely what case managers do but not to ▶ Recommendation
 Catatonic Behavior C 493

References and Readings that has become too difficult or is perceived as being too
difficult. Typically, persons experiencing catastrophic
Case Management Society of America (2002). CMSA standards of reactions are not fully aware of their increasing lability
practice. Little Rock, AR: Case Management Society of America. and cannot respond to logic and reason, but they
Chan, F., & Leahy, M. (2005). Health care and disability case management,
benefit from decreased demands and calm reassurance. C
(2nd ed.). Lake Zurich, IL: Vocational Consultants Press.
Huber, D. (2005). Disease management: A guide for case managers.
Catastrophic reactions were initially thought to be
St. Louis: Elsevier Saunders. associated only with dominant hemisphere damage and
Mullahy, C. (2004). The case manager’s handbook (3rd ed.). Sudbury, MA: accompanying language impairment, but they can follow
Jones and Bartlett. any neurological problem that interferes with adaptive
coping and executive functioning.

Case Planning Cross References

▶ Case Management ▶ Agitation

▶ De-Escalation
▶ Executive Functioning
▶ Frustration Tolerance
CAT Scan
References and Readings
▶ Computed Tomography
Callahan, C. D. (2009). The assessment and rehabilitation of executive
function disorders. In B. Johnstone & H. H. Stonnington (Eds.),
Rehabilitation of neuropsychological disorders (2nd edn., pp. 75–106).
Philadelphia, PA: Psychology Press.
Catastrophic Condition Goldstein, K. (1948). Language and language disturbances: Aphasic
symptom complexes and their significance for medicine and theory of
▶ Catastrophic Reaction language. New York: Grune and Stratton.
Holland, D., & Larimore, C. (2009). The assessment and rehabilitation of
language disorders. In B. Johnstone & H. H. Stonnington (Eds.),
Rehabilitation of Neuropsychological Disorders (2nd edn., pp. 137–166).
Philadelphia, PA: Psychology Press.
Catastrophic Reaction Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). Neuropsychological
Assessment (3rd edn., p. 62). New York: Oxford University Press.
DAWN E. B OUMAN
Drake Center
Cincinnati, OH, USA
Catatonia
Synonyms ▶ Catatonic Behavior

Catastrophic condition

Catatonic Behavior
Definition
S OLOMON K ALKSTEIN , FARZIN I RANI
This term coined by Goldstein (1948) describes acute University of Pennsylvania
distress, agitation, and disorganized behavior occurring Philadelphia, PA, USA
when overwhelmed by a situation with which the person
cannot cope, typically following brain injury or other
neurological impairment. Rapid and extreme anxiety, Synonyms
depression, and frustration can result when a person
becomes over-stimulated or overwhelmed with a task Catatonia
494 C Catatonic Behavior

Short Description Diagnostically, since catatonic behavior has numerous

disease causes (Gelenberg, 1976), care must be taken to
Catatonic behavior is characterized by marked distur- distinguish the above-listed conditions from other syn-
bances in psychomotor movements that occur within dromes, which may present with similar features. Specifi-
the context of a psychiatric or medical condition. Accord- cally, DSM-IV TR notes that a separate diagnosis is not
ing to the Diagnostic and Statistical Manual of the Mental given if the catatonia occurs exclusively during the course
Disorders–Fourth edition (DSM-IV TR) catatonic fea- of a delirium. Additionally, catatonic-like symptoms may
tures are identified, or the catatonic subtype is recognized, occur in the context of one of the medication-induced
when there are at least two of the following: movement disorders, such as neuroleptic-induced parkin-
sonism or neuroleptic malignant syndrome, or as a fea-
 Motoric immobility as shown during catalepsy (in-
ture of akinetic parkinsonism, malignant hyperthermia,
cluding waxy flexibility) or stupor
locked-in syndrome, stiff-person syndrome or elective
 Excessive motor activity (apparently purposeless and
mutism (Taylor & Fink, 2003).
independent of external stimuli)
 Extreme negativism (motiveless resistance to instruc-
tions, maintenance of rigid postures against attempts
to be moved) or mutism
Epidemiology
 Peculiarities of voluntary movement as shown during
Catatonia is currently rare in North America and Europe;
posturing (voluntary assumption of inappropriate or
however, reports of its prevalence vary widely among
bizarre postures)
studies. Bleuler’s initial estimates of catatonic
 Stereotyped movements, prominent mannerisms, or
symptomatology among schizophrenia patients were sig-
prominent grimacing
nificantly higher than those that are found today. Numer-
 Echolalia (repetition of a word or phrase just spoken
ous surveys of catatonia among psychiatric patients using
by another) or echopraxia (repetitive imitation of
duration criteria of several to 24 h have yielded prevalence
movements of others).
rates ranging from 7.6% to 38% (Taylor & Fink, 2003).
When including studies in which systematic rules of ex-
amination are used and catatonia rating scales are applied
Categorization this range narrows from 7% to 15% (Fink & Taylor, 2006).
Although numerous reports of catatonia among children
The DSM-IV TR lists three conditions during which cata-
and adolescents have been documented, particularly in
tonic features may be observed:
autistic and pervasive developmental disorders popula-
1. Schizophrenia – Catatonic Subtype (295.20) tion, the syndrome appears to be more common in adults
2. Mood Disorder – Catatonic Features Specifier with prevalence rates for children and adolescents ranging
3. Catatonia due to a General Medical Condition from approximately 1–17% (Weder, Muralee, Penland, &
(293.89) Tampi, 2008).
Catatonic subtype of schizophrenia: This is a subtype of
schizophrenia characterized by marked psychomotor
disturbance that involves at least two of the six symp- Natural History, Prognostic Factors,
toms identified above. Outcomes
Mood disorder – Catatonic features specifier: The speci-
fier ‘‘With Catatonic Features’’ can be applied to the Catatonia was first formally described in the late nine-
current (or most recent) episode in major depressive teenth century by the German physician, Dr. Karl Lud-
disorder and bipolar I or II disorder when at least two wig Kahlbaum, as a disorder characterized by mood
of the six symptoms listed above are present. symptoms, stupor, confusion, and eventually, dementia.
Catatonia due to a general medical condition: When Additionally, he noted unusual motor symptoms and
evidence is present that catatonic behavior, presenting carefully documented the character and course of the
as at least two of the six symptoms listed above, is illness. Subsequently, Kraepelin classified patients who
the direct physiological consequence of a general med- exhibited symptoms of catatonia within his dementia
ical condition, the syndrome is specified as ‘‘Catatonic praecox disorder and Bleuler, adopting this formulation,
Disorder Due to. . .’’ and the medical condition is interpreted catatonic symptoms as features of his newly
listed. named ‘‘schizophrenia.’’ This model of catatonia as a
 Catatonic Behavior C 495

subtype within schizophrenia persisted through early psychopharmacological studies. Neuroimaging studies have
and recent versions of the DSM. Only with the publica- not been conclusive and have revealed various cortical and
tion of DSM-IV was consideration given to catatonia subcortical brain regions to be associated with the illness, a
occurring within the context of other psychiatric and finding that may explain observed clinical differences
medical conditions. This was due to important articles in symptom presentation (Weder et al., 2008). Neuropsy- C
published in the 1970s, which established co-occurrence chological evaluation of catatonic psychiatric inpatients
of catatonia and mood disorders (Abrams & Taylor, as compared with a psychiatric control group revealed
1976) and emphasized the association between catatonia relatively poorer performance on measures of working
and neurological or general medical conditions (Gelen- memory and those visual–spatial abilities related to right
berg, 1976). Several reports have also suggested the pres- parietal functioning. Additionally, significant differences
ence of a genetic form of catatonia not captured by between catatonic patients and healthy controls were
DSM-IV TR criteria (Taylor & Fink, 2003). Thus, the observed on attentional and executive tests associated with
conceptualization and classification of catatonia con- frontal functioning. These results suggest attentional-motor
tinues to evolve. and frontoparietal dysfunction in catatonia (Northoff,
An additional area of controversy involves categoriza- Nagel, Danos, Leschinger, Lerche, & Bogerts, 1999).
tion. Advocates have argued for DSM reclassification of
catatonia into a syndrome rather than a subtype of schizo-
phrenia. They claim that the current model fails to ade- Evaluation
quately recognize catatonia in other psychiatric illnesses
and limits treatment of catatonic behavior to protocols Although DSM-IV requires two of the six symptoms of
focusing on antipsychotic drugs. Fink and Taylor (2003, catatonic behavior listed previously in order to establish
2006) have therefore proposed a change in nomenclature, presence of catatonia, definitions of catatonia, as well as
suggesting that catatonia be reclassified separately from its basic signs and symptoms, are still the subject of
other syndromes, akin to delirium or dementia, with three debate and no authoritative set of criteria has been uni-
syndrome subtypes (nonmalignant, delirious, and malig- versally accepted (Caroff & Ungvari, 2007). Several rating
nant) and four specifiers (secondary to: mood disorders, scales have been developed to assess for the presence of
general medical conditions or toxic states, neurological dis- catatonia; however, the number of signs and symptoms
orders, or psychotic disorders). However, this reclassifica- that are included range from 10 to 40 for almost all
tion system remains controversial. instruments (Taylor & Fink, 2003). Several reviews have
Numerous risk factors for catatonia have been listed the most commonly listed signs and symptoms of
reported including history of perinatal infections, epilep- the syndrome as mutism, posturing, negativism, staring,
sy, medication effects, and frontal or basal ganglia dis- rigidity, echophenomena, stereotypes, grimacing, and
eases (Weder et al., 2008). Additionally, various aspects of perseveration (Weder et al., 2008). In terms of the num-
comorbid psychiatric conditions including age of onset ber of symptoms required to justify a diagnosis, mini-
and severity of symptoms are considered risk factors and mum thresholds vary among scales. While some scales
contribute significantly to prognosis. Although highly resemble the DSM-IV TR in requiring the presence of
variable, overall prognosis appears to be relatively better 2 or 3 symptoms out of a list of 11 or 12 (Lohr &
for recurrent catatonia and mood disorders with cat- Wisniewski, 1987; Rosebush, Hildebrand, Furlong, &
atonia as compared with catatonic schizophrenia. One Mazurek, 1990), other instruments assign greater weight
review study indicated that while acute treatment prog- to certain cardinal symptoms over other secondary symp-
nosis is excellent, long-term prognosis depends on the toms (Bush, Fink, Petrides, Dowling, & Francis, 1996).
underlying condition that elicited catatonia (Taylor & Other scales group symptoms by category (i.e., motor,
Fink, 2003). affective, and behavioral) and require a symptom from
each category in order to establish a diagnosis (Northoff
et al., 1999). Most authors accept a range from several
Neuropsychology and Psychology to 24-hours duration as being necessary in order to defin-
of Catatonic Behavior itively establish the presence of catatonia (Weder et al.,
2008). Attempts have been made to identify individual
Although the pathophysiology of catatonia remains poorly clusters within the catatonia syndrome based on dis-
understood, both the GABA and dopaminergic neurotrans- crete symptom-groups and duration of illness (acute/
mitter systems have been implicated in numerous chronic); however, further research in this area is
496 C Catecholamines

necessary before the existence of subtypes can be estab- Bush, G., Fink, M., Petrides, G., Dowling, F., & Francis, A. (1996).
Catatonia. I. Rating scale and standardized examination. Acta Psy-
lished (Weder et al., 2008).
chiatrica Scandanavica, 93, 129–136.
Caroff, S. N., & Ungvari, G. S. (2007). Expanding horizons in catatonia
research. Psychiatric Annals, 37(1), 7–9.
Treatment Fink, M., & Taylor, M. A. (2003). Catatonia: A clinician’s guide to diagnosis
and treatment. Cambridge: Cambridge University Press.
Fink, M., & Taylor, M. A. (2006). Catatonia: Subtype or syndrome in
Treatment for catatonic symptoms differs depending on DSM? American Journal of Psychiatry, 163, 1875–1876.
the underlying cause. Catatonia is currently viewed by Gelenberg, A. J. (1976). The catatonic syndrome. Lancet, 1(7973),
most clinicians from a predominantly biological frame- 1339–1341.
work (Penland, Weder, & Tampi, 2006). Generally, benzo- Lohr, J., & Wisniewski, A. A. (1987). Catatonia. In J. Lohr & A. A.
Wisniewski (Eds.), Movement disorders: A neuropsychiatric approach.
diazepines such as lorazepam are considered to be the first
New York: Guilford Press.
treatment of choice. If patients fail their initial trial, the Northoff, G., Nagel, D., Danos, P., Leschinger, A., Lerche, J., & Bogerts, B.
use of bilateral electroconvulsive therapy is usually con- (1999). Impairment in visual-spatial function in catatonia:
sidered. Although these are the best-studied treatments A neuropsychological investigation. Schizophrenia Research, 37,
of the syndrome, the efficacy of other approaches, such 133–147.
Penland, H. R., Weder, N., & Tampi, R. R. (2006). The catatonic dilemma
as transcranial magnetic stimulation, continues to be
expanded. Annals of General Psychiatry, 5(14), 1–9.
explored. Catatonic schizophrenia may be treated by a Rosebush, P. I., Hildebrand, A. M., Furlong, B. G., & Mazurek, M. F.
variety of pharmacotherapeutic and psychotherapeutic (1990). Catatonic syndrome in a general psychiatric inpatient popu-
methods. Hospitalization may be necessary to protect lation: Frequency, clinical presentation, and response to lorazepam.
the patient’s safety and supportive psychotherapy and Journal of Clinical Psychiatry, 51, 357–362.
Taylor, M. A., & Fink, M. (2003). Catatonia in psychiatric classification:
family education may help patients and their families
A home of its own. American Journal of Psychiatry, 160, 1233–1241.
adjust to problems created by the illness. Other support- Weder, N. D., Muralee, S., Penland, H., & Tampi, R. R. (2008). Catatonia:
ive services as sheltered workshops and special education A review. Annals of Clinical Psychiatry, 20(2), 97–107.
may also be helpful. When catatonic symptoms are due to
a mood disorder, episodes may be treated with mood
stabilizers or antidepressant medications. Catatonic
symptoms caused by a medical disorder require correct Catecholamines
diagnosis of the underlying medical condition, followed
by appropriate treatment. For example, levodopa and M ARLA S ANZONE
amantadine (symmetrel) have shown some effectiveness Independent Practice
in reducing catatonic symptoms due to postencephalitic Annapolis, MD, USA
Parkinson’s disease. Hospitalization and careful supervi-
sion of persons with catatonic symptoms may be neces-
sary to ensure that they do not harm themselves or others Synonyms
and to prevent malnutrition, exhaustion, or fever.
Adrenergic agonists; Direct- and indirect-acting adrenergic
receptor agonists; Dopamine agonists; Dopaminergic
Cross References agonists; Sympathomimetic amines/drugs/agents/
compounds
▶ Delusion
▶ Mood Disorder
▶ Schizophrenia Definition

Catecholamines are a class of biologically active water

soluble hormones comprising catechol and amine
References and Readings compounds. They are derivatives of the amino acid
tyrosine. Tyrosine is converted from phenylalanine as a
Abrams, R., & Taylor, M. A. (1976). Catatonia: A prospective clinical
function of the hydroxylation by the enzyme phenylala-
study. Archives of General Psychiatry, 33(5), 579–581.
American Psychiatric Association. (2000). Diagnostic and statistical man-
nine hydroxylase, and can also be directly ingested from
ual of mental disorders (4th edn., text revised). Washington, DC: dietary proteins (Catecholamines, 2002; Catecholamines,
American Psychiatric Association. 2008; Catecholamines, 2009a, b).
 Catecholamines C 497

Catecholamines are sympathomimetic amines, a group involuntary movement disorder and tends to develop
of compounds including dopamine, epinephrine, and during middle adulthood. Anxiety can precipitate and
norepinephrine whose molecular structure is similar to exacerbate the amplitude of the tremor. It is generally
that of a larger class of neurotransmitters, the monoa- treated with beta blockers such low doses of propranolol
mines. The specific molecular structure of catecholamines and with lesser efficacy with Atenolol and anxiolytics C
is a benzene ring with two hydroxyl groups, an intermedi- such as alprazolam (Kaufman, 2007).
ate ethylamine to the side and an amine terminal group. Chemodectoma (nonchromaffin paraganglioma) –
The chromaffin cells in the adrenal medulla and sympa- Benign chemoreceptor system tumors. The most common
thetic nervous system postganglionic fibers are the primary types are glomus jugulare tumor and carotid body tumor.
site of catecholamine production (Hoffman, 2004). Dopamine-b-hydroxalase Deficiency – Severe orthostatic
During times of physiological and/or psychological hypotension of a congenital nature caused by the inability
stress neurons in the central and peripheral sympathetic to generate the enzyme, dopamine-b-hydroxalase.
nervous systems secrete catecholamines via hypothalamic Familial Paraganglioma Syndrome – Genetic slow-
and adrenomedullary activation. Catecholamine toxicity, growing chromosomal (11q23) benign tumors primarily
also referred to as catecholamine dump or storm can of the head and neck. These unusual conditions are inher-
occur from trauma, causing over-stimulation, excessive ited from the father. Disfiguring facial swelling, hearing
production and circulation of catecholamines in the loss, tinnitus, pain, persistent cough, or other head/neck
central nervous system, and/or lesions of nuclei affecting anomalies as a function of cranial nerve damage from
the sympathetic nervous system in the brainstem. the tumor.
Catecholamines affect metabolic rate, temperature Neuroblastoma, produces catecholamines, and follow-
regulation, smooth muscle functions, cardiovascular and ing brain tumors is the second most common solid tumor
nervous systems. Epinephrine and norepinephrine auto- in childhood. Testing for the catecholamine metabolites,
nomically prepare the body for crisis such as cold, fatigue, vanillylmandelic acid and homovanillic acid, are
danger, and shock. Dopamine is produced as an interme- identified in the urine.
diate process in the synthesis of epinephrine and is critical Pheochromocytoma is a benign tumor that secretes
to the regulation of many neurological processes, includ- norepinephrine and epinephrine. It originates in
ing smooth fine and gross motor movements, energy sympathetic paraganglia or adrenal medulla.
regulation, motivation, executive functioning and formal Tetrahydrobiopterin deficiency is a genetic condition
thought regulation. Sympathomimetic drugs used to treat that results in the inability to manufacture the enzymes
conditions associated with these biological functions required to synthesize catecholamines. This leads to a defi-
mimic the actions of epinephrine, norepinephrine or do- ciency of the neurotransmitters, norepinephrine, epineph-
pamine (Sympathomimetic drug, 2008; Venes, Thomas, rine, and dopamine (Catecholamines, 2002; Myers, 2006).
Egan, Houska, 2001). Such drugs include those used to
treat a variety of abnormalities associated with central and
sympathetic nervous system processes (e.g., blood pressure, Mechanisms of Action
cardiac anomalies, premature labor, glaucoma, bronchitis,
asthma, emphysema, blood glucose metabolism, movement The adrenergic or sympathomimetic drugs act at
disturbances and psychosis). In addition, numerous disor- sympathetic postganglionic terminal by activating the
ders involve catecholamine disturbances of congenital, ge- catecholaminergic hormones, epinephrine (adrenaline),
netic, or familial origin such as dopamine-b-hydroxalase norepinephrine (noradrenaline), and/or dopamine in
deficiency, paraganglioma syndrome, and tetrahydrobiop- various ways. Some compounds have cross-reactivity
terin deficiency, but also those with unknown precipitating such that they act on catecholamines by more than one
mechanisms, including chemodectina, neuroblastoma, and mechanism of action (Sympathomimetic drug, 2008).
pheochromocytoma (Catecholamines, 2002). Directly activating adrenergic postsynaptic receptors
(Direct-Acting Adrenergic Agonists) include a-adrenergic
agonists and b-adrenergic agonists. There are five types:
Catecholamine-Related Conditions a1, a2, b1, b2, and b3. Adrenergic agonists stimulate one or
more of these receptor types. Adrenergic antagonists
Benign Familial Tremor/Essential Tremor is an inherited inhibit one or more of the actions of these receptors.
autosomal dominant condition suggestive of excessive Some agents have stimulating and blocking actions on
systemic adrenergic activity. It is the most common different receptors simultaneously. Receptor selectivity
498 C Catecholamines

Catecholamines. Table 1 Sympathomimetic Action & Function

Primary
neurotransmitter
actions Mechanism of action Examples of compounds Clinical uses
Alpha (a) Direct-acting alpha- Alpha (a1, a2) – adrenergic Used to treat glaucoma by decreasing the
adrenergic adrenergic agonists – agonists production of aqueous fluid; as vasopressors, nasal
agonists Promote decongestants and to dilate the pupil for eye
vasoconstriction, exams
mydriasis, body
tissue-building,
inhibition
of endogenous
testosterone release
a1 Agonists a1 Agonists – Oxymetazoline, Used to treat anemias caused by deficient
stimulate phenylephrine production of red blood cells, aplastic anemia,
phospholipase C hypotension, shock, paroxysmal supraventricular
activity tachcardia
a2 Agonists a2 Agonists – inhibit Clonidine – (a2 and a2 Agonists reduce sympathetic nervous system
adenylyl cyclase imidazoline-I1 agonist) activation. They are used to treat opiate and
activity Guanfacine – (affinity for alcohol withdrawal symptoms, as
preference for a2a antihypertensives, gestational hypertension, to
adrenoceptor) decrease peripheral resistance and as sedatives.
More recently they are being used to treat
Methyldopa is
neuropathic pain, sleep hyperhidrosis, and off-
approximately 50%
label, to counter the side effects of stimulant
absorbed from the gut,
medications
metabolized in the
intestines and liver and
alpha-methylnorepineprine,
its metabolite, stimulates
central a2- receptors
Mixed a, b1, Undetermined or Epinephrine, amidephrine, Mixed alpha- beta- agonists such as epinephrine
b2 agonists mixed alpha- beta- ergotamine, are used to treat anaphylaxis, acute asthmatic
stimulation norepinephrine, synephrine reactions, cardiac arrest, open-angle glaucoma
and nasal congestion. It stimulates alpha, beta1
and beta2 adrenergic receptors, increasing cardiac
output, dilating bronchials, skeletal muscle
vasulature, and pupils dilation due to constriction
of dilatory muscles
b Antagonists Direct-acting beta- Cardiac stimulants Beta blockers are used to treat heart block,
(beta blockers) – adrenergic agonists – ventricular tachcardia, cardiac arrest, asthma,
block the action of stimulate adenylyl chronic bronchitis, emphysema, hypovolemic and
epinephrine and cyclase activity and septic shock, low cardiac output or hypoperfusion,
norepinephrine open calcium congestive heart failure
channels
b1 Agonists Direct-acting b1- Albuterol, dobutamine Asthma, Chronic Obstructive Pulmonary Disease
adrenergic agonists (COPD), sinus congestion
 Catecholamines C 499

Catecholamines. Table 1 (Continued)

Primary
neurotransmitter
actions Mechanism of action Examples of compounds Clinical uses
b2 Agonists Direct-acting b2- Metaproterenal, formoterol, A moderately selective b2 – agonist. It acts on C
adrenergic agonists – salmeterol, terbutaline smooth muscle in the lungs, uterus, and skeletal
stimulate muscle vasculature. Used to treat asthma, COPD,
postsynaptic premature labor
b2 receptors of the The enzyme intracellular adenyl cyclase catalyzes
intracellular enzyme, the conversion of ATP to cAMP. Elevated cAMP
adenylyl cyclase. levels are associated with bronchial
Closes calcium smooth muscle relaxation and regulation of mast
channels, relaxing cells activation
smooth muscle
Mixed b Isoproterenol (b1 and Cardiogenic shock, bradyarrhythmias, heart block,
antagonists b2 agonist) cardiac arrest, brochospasm associated with
anesthesia, asthma, chronic
bronchitis, emphysema, hypovolemic and
septicemic shock
COMT-inhibitors Indirectly inhibiting Entacapone, tolcapone Adjunctive Parkinson’s treatment
epinephrine and
norepinephrine
metabolism
Dopamine Stimulate production Bromocriptine, Hypertensive crisis through vasodilation in
agonists and release at D1 apomorphine, fenoldopam coronary, renal, mesenteric and peripheral arteries
receptors Pramipexole – (pre- and Pramipexole used to treat idiopathic parkinsonism
postsynaptic D2 and 3 signs. It stimulates caudate neurons
receptor agonism) by D3 agonism
Prolongs Levodopa (I-Dopa) Parkinsonianism – Levodopa’s efficacy is as a
dopaminergic activity prodrug. It is a precursor of catecholamines
when combined with
COMT-inhibitors
and dopa
decarboxylase
inhibitors
(e.g., benserazide
or carbidopa)
Dopamine Increase Cocaine, Methylphenidate Cocaine used recreationally and highly subject to
Reuptake norepinephrine Amphetamines abuse. Ophthalmically used as local anesthetic.
Inhibitors (DRIs) release at central Amphetamines and methylphenidate are used
noradrenergic primarily to treat ADHD, narcolepsy, occasionally
neurons. Release of in geriatric depression, post-stroke and cancer
dopamine at to increase alertness and counteract
mesolimic areas in chemotherapy lethargy. All DRIs and stimulant-
high doses. acting drugs elevate mood, increase focusing
ability and physical energy in most, increase
respiration and heart rate, blood pressure and
decrease appetite. They can cause euphoria,
rebound depression and anxiety particularly
if over-used or used inappropriately to treat
depressive disorders
500 C Catecholamines

Catecholamines. Table 1 (Continued)

Primary
neurotransmitter
actions Mechanism of action Examples of compounds Clinical uses
Dopamine Blockade of Antipsychotic agents Schizophrenia, Bipolar I, mania
antagonists dopamine (more D2
than D1 receptor
affinity).
Moderate a
adrenergic and
histaminic
antagonism.
Monoamine Stimulate production Phenelzine (Nardil) Treatment resistant depression, atypical
Oxidase Inhibitors and release of depression, panic disorder
(MAOIs) catecholamines in
CNS
Chronic use Tranylcypromine (Parnate)
downregulates a2 or
b adrenergic and
serotonin receptors
Norepinephrine Prevent re-uptake of Most non-SSRI Atypical depression, dysthymia, anxiety, ADD, post
reuptake norepinephrine at antidepressants: Tricyclic traumatic stress disorder
inhibitors postsynaptic antidepressants (TCAs –
receptors mixed catecholamine
stimulation and inhibition)
Atomoxetine (Strattera) –
serotonin and
norepinephrine reuptake
inhibition Duloxetine
(Cymbalta) Venlafaxine
(Effexor) – selective
norepinephrine reuptake
inhibition
Norepinephrine- Increase availability of Bupropion, pyrovalerone, ADHD, depression, chronic fatigue, obesity
dopamine monoamines, mazindol (also classified as a
reuptake inhibitor dopamine and TCA), phenethylamines
norepinephrine, due
to inhibiting re-
uptake, causing a
stimulating effect
Norepinephrine Stimulate production Mirtazapine (classified as a Depression, mixed anxiety-depression with sleep
releasers and release of tetracyclic and a disruption
catecholamines noradrenergic specific
serotonergic antidepressant
– NaSSA)
Mianserin is a tetracyclic
antidepressant
 Catecholamines C 501

Catecholamines. Table 1 (Continued)

Primary
neurotransmitter
actions Mechanism of action Examples of compounds Clinical uses
Stimulants Stimulate direct Amphetamine salts, ADD/ADHD – increases alertness, concentration, C
production and methylphenidate, focus, attention, executive functions, endurance
release of dexamphetamine, mentally and physically. Diminishes verbal and
catecholamines, dextroamphetamine, physical impulsivity
particularly phentermine Narcolepsy – to help maintain alertness
norepinephrine and
Major depressive disorder – occasionally used to
dopamine from
augment antidepressant treatment
storage vesicles
Weight management – phentermine is used to
suppress appetite
Also increase Schedule IV controlled substances in the US
norepinephrine and
dopamine levels via
reuptake inhibition
and binding to the
MAO protein
transporter
Stimulate production Modafinil, adrafinil Narcolepsy – to maintain alertness, and counteract
and release of abnormal states that diminish alertness
catecholamines Night shift work – to counteract fatigue
Over-the-counter Synthetic and plant- Ephedrine, To suppress appetite, increase alertness, enhance
stimulants based herbal pseudoephedrine, MDMA, athletic performance
preparations with cocaine, ephedra, Ma huang, Cocaine, a tropane derivative, is made from South
significant abuse guarana American coca bush leaves. It is occasionally used
potential thought to legally as an ophthalmic local anesthetic, but no
stimulate release of longer prescribed for its stimulant properties
catecholamines
Aminoff (2004); Hoffman (2004); Kaufman (2007); Katzung (2004); Psychoactive drug (2009); Stimulant (2009); Sympathomimetic drug (2008);
Williams and Turner (2008).

addresses strength of affinity toward a particular receptor norepinephrine. If the enzyme is inhibited, it prevents the
rather than absolute specific selectivity of one receptor only. removal of epinephrine and norepinephrine from the sys-
Direct-acting dopamine agonists are used to treat tem which induces sympathomimetic effects. Similarly,
hypertensive crisis and parkinsonian signs and symptoms. with COMT-Inhibitors, the enzyme catechol-O-methyl
Indirect-acting, norepinephrine transporter antagonists transferase (COMT) is an intracellular enzyme in the
such as ephedra, cocaine, and amphetamines. They block postsynaptic neuron that degrades epinephrine and nor-
and reverse the activity of the norepinephrine transporter epinephrine. This enzyme effectively deactivates them by
proteins. These proteins functionally terminate the effects of inducing S-adenosyl methionine (SAM) to add a methyl
norepinephrine and to a lesser degree, dopamine, by remov- group to the catecholamines. The COMT-Inhibitors
ing these neurotransmitters from the synapse and repacka- prevent this deactivation by blocking the breakdown/
ging them in their vesicles for later use (Katzung, 2004). reuptake process, and enabling the utility of the catecho-
Indirectly inhibiting epinephrine and norepinephrine lamines (Catechol-O-methyl transferase, 2009).
metabolism such as COMT-Inhibitors (e.g., entacapone Stimulating production and release of catecholamines as
and tolcapone) and MAOIs such as Parnate and Nardil do MAOIs and amphetamines. These agents are known to
(Aminoff, 2004) that raise the level of all the catecholamines increase cardiac output and blood pressure as a function of
in the blood. Monoamine oxidase (MAO) is the enzyme constricting peripheral blood vessels which increases the
primarily responsible for metabolism of epinephrine and force and rate of cardiac muscle contractions. They can
502 C Categorical Data

also lead to elevations in blood lipid levels due to fat Catecholamines. (2009b). In Merriam-Webster online dictionary.
Retrieved January 13, 2009, from http://www.merriam-webster.
catabolism and blood glucose levels due to glycogenolysis
com/dictionary/catecholamines
of skeletal and hepatic muscle (Sympathomimetic drug, Hoffman, B. B. (2004). Adrenoceptor-activating & other sympathomi-
2008). As discussed above, monoamine oxidase (MAO) is metic drugs. In B. Katzung (Ed.), Basic and clinical pharmacology
the enzyme primarily responsible for degrading catechola- (9th ed., pp. 122–141). New York: Lange Medical Books/McGraw-
mines. It has a half-life of several minutes. MAOIs and Hill.
Katzung, B. G. (2004). Introduction to autonomic pharmacology.
psychoactive stimulants bind to the enzyme, inhibiting
In B. Katzung (Ed.), Basic and clinical pharmacology (9th ed.,
the break down of the catecholamines, and largely for this pp. 75–93). New York: Lange Medical Books/McGraw-Hill.
reason the effects of amphetamines last longer than those of Kaufman, D. M. (2007). Clinical neurology for psychiatrists (6th ed.,
cocaine or crack. Amphetamines are among the adrenergic pp. 97, 190, 193, 430–431). Philadelphia: Saunders Elsevier.
agents with dual mechanisms of action or cross-reactivity. Myers, T. (2006). Catecholamine (definition). In Myers, T. (Ed.),
Mosby’s dictionary of medicine, nursing & health professions
The production of all the catecholamines, dopamine, epi-
(7th ed., pp. 323). Missouri: Mosby Elsevier.
nephrine, and norepinephrine is stimulated and the reup- Psychoactive drug. (2009). In Wikipedia. Retrieved January 16, 2009, from
take, particularly of norepinephrine, is inhibited. http://en.wikipedia.org/wiki/Psychoactive_drug
Stimulant. (2009). In Wikipedia. Retrieved January 15, 2009, from http://
en.wikipedia.org/wiki/Stimulant
Specific Compounds and Properties Sympathomimetic drug. (2008). In Wikipedia. Retrieved January 13,
2009, from http://en.wikipedia.org/wiki/Sympathomimetic
Venes, D., Thomas, C., Egan, E., & Houska, A. (2001). Catecholamine
All sympathomimetic amines can be conceptualized to be (definition), In D. Venes, et al. (Eds.), Taber’s medical dictionary
part of a broad group of stimulant drugs due to their (19th ed., pp. 357). Philadelphia: FA Davis Company.
sympathetic nervous system and/or central nervous Williams, F. M., & Turner, T. J. (2008). Adrenergic pharmacology:
system activating properties. However, due to multiple Biochemistry & physiology of adrenergic function. In D. E. Golan,
A. H. Tashjian, E. J. Armstrong, & A. W. Armstrong (Eds.), Principles
mechanisms of action sympathomimetics are classified
of pharmacology: The pathophysiologic basis of drug therapy
accordingly and as a function of their use in the treatment (pp. 129–139). Philadelphia: Lippincott Williams & Wilkins.
of specific conditions (Table 1).

Cross References Categorical Data

▶ Adrenergic Agonists ▶ Qualitative Data
▶ Dopamine
▶ Epinephrine
▶ Monoamine Oxidase
▶ Norepinephrine Category Fluency
▶ Sympathomimetic Amines
▶ Controlled Oral Word Association Test
▶ Verbal Fluency
References and Readings

Aminoff, M. J. (2004). Pharmacologic management of parkinsonism &

other movement disorders. In B. Katzung (Ed.), Basic and clinical
pharmacology, (9th ed., pp. 447–461). New York: Lange Medical Category Test
Books/McGraw-Hill.
Catechol-O-methyl transferase. (2009). In Wikipedia. Retrieved January
15, 2009, from http://www.answers.com/topic/catechol-o-methyl-
N ICK A. D E F ILIPPIS
transferase Argosy University
Catecholamines. (2002). In MedicineNet. Retrieved January 15, 2009, Atlanta, GA
from http://www.medterms.com
Catecholamines. (2008). In Wikipedia. Retrieved January 13, 2009, from
http://en.wikipedia.org/wiki/Catecholamines
Catecholamines. (2009a). In The free dictionary by Farlex, Retrieved
Synonyms
January 13, 2009, from http://medical-dictionary.thefreedictionary.
com/Catecholamines BCT; CT; HCT
 Category Test C 503

Description which to base approaches to new and unfamiliar stimuli.

Although Halstead found his test to discriminate frontal
The Category Test (CT) was first published by Ward lobe-damaged patients from others, this finding was never
Halstead (Halstead & Settlage, 1943). Over the years, validated by other researchers. Various researchers have,
there have been several versions of the test, all retaining however, identified the CT as one of the most sensitive C
the essential format of the original and the goal of mea- measures of brain injury in the Halstead Reitan Battery
suring concept formation ability. All versions involve the (Choca, Laastch, Wetzel, & Agresti, 1993).
presentation of visual images of different shapes to the The existence of various versions of the CT has raised
examinee. The examinee is to determine which underly- the issue of comparability of these newer forms with the
ing concept is presented by the image and choose a num- original CT. To date, there has been no research indicating
ber from 1 to 4 to identify the concept. For example, the effects of CT test apparatus on the performance of exam-
examinee may choose the number corresponding to inees. Numerous studies demonstrated comparable
the number of items in the image, the proportion of the results, regardless of the test format. Kupke (1983) point-
image that is drawn continuously, etc. The examinee is ed out that the modification of a test apparatus in a purely
given feedback after each choice to indicate if he or she cognitive task, such as that presented by the CT, should
was correct in their decision. By a process of utilizing this have little effect on performance. However, this analysis
feedback to monitor performance, the examinee then would only pertain to versions that retain the original
learns the concepts. The number of errors is used to test stimuli and administration instructions. A self-
determine the overall performance. administered version of the test that drastically changed
The original version of the test was administered by instructions and allowed the examinee to view earlier
way of a drum with images on it and a slit for examinees responses does not meet this requirement. Also, various
to view them. Feedback was given with a bell (correct) or short forms of the CT have not been studied sufficiently to
buzzer (incorrect). Sometime during the 1940s or 1950s determine their comparability to the original length test.
(the exact date being unclear), the test was reduced from A number of investigators have attempted to determine
its original 360 items and 9 subtests to 208 items and if the CT can generate more scores than just the number of
7 subtests. The final subtest asks the examinee to recall errors. Factor analytic studies have indicated that there
previously presented concepts in order to respond cor- may be different abilities tapped by the test, prompting
rectly, constituting a memory component to the test. research into the possibility of developing scores for differ-
More recent versions have included a projection of images ent abilities. Scales for spatial positional reasoning, propor-
using slides, a card format, a self-administered version, tional reasoning, perseveration, loss of set, and memory,
a booklet version, and various computer versions. The have all been proposed, along with a measure of effort.
various versions are available from different publishers: Recent research has found concurrent validity for a num-
Slide projector version (Reitan Labs), Booklet version ber of these measures, and efforts to standardize them for
(Psychological Assessment Resources), and Computer ver- clinical use continue (Minassian et al., 2003).
sions (Psychological Assessment Resources and Mental
Health Systems). Feedback has varied by version and
includes the original bell or buzzer, computer approxima- Psychometric Data
tions of the bell or buzzer, or examiner feedback of ‘‘correct’’
and ‘‘incorrect.’’ Test administration time is 30–45 min. Demonstrated test–retest validity of the CT ranges from
0.60 in normal populations to 0.96 for brain-damaged
participants. A problem in identifying retest stability for
Historical Background the CT has to do with the substantial learning aspect of
the test. Although there has been no adequate analysis of
Halstead (1940) reported the preliminary findings of expected gain on re-administration of the test, reliability
studies dating back to the 1920s using concept formation data suggest an improvement of about 15 points for
tests in which brain-damaged participants grouped normal individuals and 25 points for brain-damaged
objects into categories. It was clear from subjective ana- individuals, with a retest interval of 2–3 months. Internal
lyses that brain damage affected this ability. Halstead consistency, perhaps a better marker of reliability for this
hypothesized that his test measured abstraction and the test, has been shown to be very high at 0.97, as is split half
process of developing sets or frames of reference on reliability at 0.98.
504 C Caudate Nucleus

Numerous studies have demonstrated the CT’s ability related to perseveration, attention, and possibly other
to discriminate brain damaged from normal examinees, aspects of their performance on the CT.
with analyses indicating statistically significant discrimi-
nation at the 0.05 to 0.001 levels. However, utilizing only
the suggested cut-off score of 50 errors to separate groups
Cross References
has resulted in a false positive rate of as high as 18%. The
need to correct for age and education has been firmly
▶ COWA
established, as these variables account for a significant
▶ Ruff Figural Fluency
variance of CT error scores. Including these corrections
▶ Tower of London
significantly reduces classification errors (Heaton, Grant,
▶ Trail Making Test
& Matthews, 1991).
▶ Wisconsin Card Sorting Test
The original intent of Halstead to utilize the CT as a
measure of frontal lobe functioning has not been vali-
dated by researchers. Also, the CT has been found to be
relatively ineffective in lateralizing damage to the brain. References and Readings
The test, as is the case with many neuropsychological
instruments, is significantly impacted by severe psychiat- Choca, J. P., Laastch, L., Wetzel, L., & Agresti, A. (1993). The
ric disturbance and inadequate effort. Halstead Category Test: A fifty year perspective. Paper presented at
the annual meeting of the American Psychological Association,
Toronto, Canada.
Halstead, W. C. (1940). Preliminary analysis of grouping behavior in
Clinical Uses patients with cerebral injury by the method of equivalent and non-
equivalent stimuli. American Journal of Psychiatry, 96, 1263–1294.
The category test is generally grouped in most textbooks Halstead, W. C., & Settlage, P. H. (1943). Grouping behavior of normal
persons and of persons with lesions of the brain. Archives of Neurol-
in the field with other measures of ‘‘executive function-
ogy and Psychiatry, 49, 489–503.
ing.’’ This concept can be loosely defined as the ability to Heaton, R. K., Grant, I., & Matthews, C. G. (1991). Comprehensive norms
utilize feedback to organize and plan one’s approach to for an expanded Halstead-Reitan Battery: Demographic corrections,
deal with a novel problem-solving task. Taking this defi- research findings, and clinical applications. Odessa, FL: Psychological
nition, the CT seems to qualify as a measure of this Assessment Resources.
Kupke, T. (1983). Effects of subject sex, examiner sex, and test apparatus
ability. In fact, clinicians who use the test typically in-
on Halstead Category and Tactual Performance Tests. Journal of
clude it in their battery of tests as an executive function- Consulting and Clinical Psychology, 51, 624–626.
ing measure. This approach is supported by the test Minassian, A., Perry, W., Carlson, M., Pelham, M., & DeFilippis, N.
format and some research, but should not involve reli- (2003). The Category Test Perseveration, Loss of Set, and Memory
ance on the CT as the sole measure of executive func- scales: Three new scales and their relationship to executive function-
ing measures. Assessment, 10, 213–221.
tioning. As previously discussed, the test does not
identify only frontal lobe dysfunction, but is sensitive
to any type of brain injury.
Unfortunately, the only validated and normed score
for the CT is the total error score. The original cut-off of
50 errors should not be used without also looking at age Caudate Nucleus
and education adjusted scores. The sex of the examinee
does not appear to have a significant effect on test per- S EEMA S HROFF
formance, and although norms are frequently broken Virginia Commonwealth University
down by sex, this demographic variable can largely be Richmond, VA, USA
ignored. The clinician can view CT performance as in-
dicative of the overall cortical integrity of his or her
patient. There is also some evidence that the test assesses Definition
fluidity of thinking and may be related to rehabilitation
outcome. The caudate nucleus is an arcuate mass deep into the
Ongoing research will hopefully provide the clinician cortical hemispheres forming a part of the basal ganglia.
more information concerning his or her patient’s abilities Apart from being involved in the smooth orchestration of
 Caudate Nucleus C 505

motor actions, it has been recently implicated in other the ‘‘direct pathway’’ that increases motor activity. An
functions like learning, memory, emotion, and language. indirect pathway, involving the subthalamic nucleus,
decreases motor activity. The activity of these pathways
is further modulated by dopamine from the nigrostrial
Nomenclature tract and ACh from the interneurons. C
Striatum/Neostriatum = Caudate Nucleus (nucleus
caudatus) + Putamen Physiology and Pathophysiology
Corpus striatum (Dorsal division) = Caudate Nucleus +
Putamen + Globus Pallidus The caudate nucleus is mainly involved in motor planning
and execution of smooth movement. Degeneration of the
caudate is associated with dyskinesias and involuntary
Current Knowledge movements. Caudate pathology manifests in choreiform
movements (brisk, jerky, and purposeless), as seen in
Anatomy Sydenham’s chorea (minute caudate hemorrhages and
capillary emboli post streptococcal infection in children)
The caudate nucleus has a globular head, tapering body, or Huntington’s disease (an adult onset degenerative he-
and down curving tail. The head lies in the floor and reditary disorder). Athetosis (slow, sinuous, and aimless
lateral wall of the anterior horn of the lateral ventricle, movements involving distal musculature) is also seen in
whereas the body runs in the floor. Medially, the caudate striatal pathology. Loss of nigrostriatal input in Parkin-
nucleus abuts the thalamus; in the floor of the ventricle, son’s disease leads to akinesia and rigidity characteristic of
this junction forms a groove known as the sulcus the disease.
terminalis that lodges the stria terminalis of the choroids Recently, the caudate nucleus has been implicated in
plexus. The corpus callosum runs above the head and functions other than motor planning. Using functional
body. The caudate nucleus is separated from the lenti- imaging, Crinion et al. (2006), have shown activation of
form nucleus by the anterior limb of the internal capsule. the caudate nucleus during language processing in bilin-
gual persons. Initial degeneration in the caudate is
thought to be responsible for the dysphoria in early Hun-
Histology tington’s disease (Paradiso et al., 2008). The caudate nu-
cleus has also been theorized to envision positive
The caudate nucleus and putamen show similar histology. emotional events in the near future (D’Argembeau et al.,
Small and large neurons (in a 20:1 ratio) with spherical or 2007) and provide complimentary information of the
ovoid dendritic fields populate the neostriatum making outcomes of actions (Lau & Glimcher, 2007).
connections within the nucleus or with the globus palli-
dus. Most small neurons contain GABA and either
enkephalin or substance P. Enkephalinergic neurons ex- Cross References
press D2 dopamine receptors whereas those with sub-
stance P have D1 receptors. Large neurons with spiny ▶ Globus Pallidus
dendrites contain acetylcholine esterase (AChE) and cho- ▶ Putamen
line acetyltransferase (CAT). ▶ Thalamus

Circuitry
References and Readings
Corticostriate, thalamostriate, and nigrostriate fibers
form the major input to the striatum. Cortical areas Crinion, J., Turner, R., Grogan, A., Hanakawa, T., Noppeney, U.,
Devlin, J. T., et al. (2006). Language control in the bilingual brain.
involved in motor planning and execution project to the
Science, 312(5779), 1537–1540.
caudate and putamen. Striatal neurons relay to the globus D’ Argembeau, A., Xue, G., Lu, ZL., Van der Linden, M., & Bechara, A.
pallidus that sends information to the thalamus (VA/VL), (2007). Neuroimage [Epub ahead of print].
which in turn feeds back to cortical motor areas forming Gray’s Anatomy (1995). (38th ed.). Pearson Professional Limited.
506 C Causal Modeling

Lau, B., & Glimcher, B. W. (2007). Action and outcome encoding in

the primate caudate nucleus. Journal of Neuroscience, 27(52), CDR
14502–14514.
Murray, B., & John, K. (1983). The human nervous system – An anatomical
▶ Clinical Dementia Rating
viewpoint (4th ed.). Philadelphia: Harper and Row, Publishers, Inc.
Paradiso, S., Turner, B. M., Paulsen, J. S., Jorge, R., Ponto, L. L., &
Robinson, R. G. (2008). Neural bases of dysphoria in early Hunting-
ton’s disease. Psychiatry Research, 162(1), 73–87.

CEA
▶ Carotid Endarterectomy
Causal Modeling
▶ Path Analysis

Ceiling Effect
S ANDRA B ANKS
Cavernoma Allegheny General Hospital
Pittsburgh, PA, USA
▶ Angioma, Cavernous Angioma

Synonyms
Cavernous Hemangioma Ceiling level

▶ Angioma, Cavernous Angioma

Definition

A ceiling effect is observed when an examinee obtains very

Cavernous Venous Malformation high or maximum scores on a particular test. This may
lead to an underestimation of the examinee’s true ability
▶ Angioma, Cavernous Angioma level because the test does not allow for higher levels of
performance to be assessed.

CBCL Current Knowledge

▶ Child Behavior Checklist A ceiling effect in a large number of participants in a

normative sample may prevent the examiner’s ability to
gauge a particular individual’s personal ceiling, or highest
level of performance, when compared with others in the
standardization sample because the maximum level of
CBCT performance within the sample cannot be assessed.
For example, on a list-learning memory test that con-
▶ Cognitive Behavioral Couples Therapy tains only four words, the majority of examinees will most
likely recall most or all of the words. Four ‘‘bits’’ of
information (in this case, words in a list) place very little
demand on the average person’s memory ability. To say
CCT that any particular examinee who learns all four words is
demonstrating intact memory abilities may underesti-
▶ Children’s Category Test mate that examinee’s actual memory span. Adding at
 Center for Epidemiological Studies–Depression C 507

least five more words would allow for an investigation of cut-off scores may be more appropriate with medical
that individual’s upper limit of learning or memory populations.
capacity.

Historical Background C
Cross References
In 1971, the National Institute of Mental Health (NIMH)
▶ Floor Effect began development of the CES-D to measure depressive
▶ Testing the Limits symptoms in epidemiological research (Brantley,
Mehan, & Thomas, 2000). Selection of original compo-
nents of depressive symptomatolgy (e.g., depressed
mood, worthlessness) was based on factor analytic stud-
Ceiling Level ies and clinical literature (Radloff, 1977); specific items
were chosen from established measures. Following
▶ Ceiling Effect minor revisions, items were added to the NIMH
structured interview and used in a large-scale study
(Brantley et al., 2000).
Follow-up studies support use of the CES-D with
diverse populations, including those with neurological
Center for Epidemiological compromise. Recent efforts have also focused on creating
Studies–Depression shorter versions of this measure (e.g., Iowa, Boston) to
facilitate use and decrease participant burden. Kohout
L ISA A. B RENNER and colleagues (1993) found that when assessing older
VISN 19 MIRECC adults (65 and older) shorter versions adequately evalu-
Denver, CO, USA ated the same symptom dimensions as the original mea-
sure. Findings from Carpenter et al. (1998), who pooled
data from 832 women (6 population), support use of the
Synonyms Iowa form over the Boston.

CES-D
Psychometric Data
Description Psychometric properties of the CES-D were initially
established with members of the general population
The Center for Epidemiological Studies – Depression (household interview survey) and those receiving ser-
Scale (CES-D; Radloff, 1977) is a 20-item self-report vices in a psychiatric setting (Radloff, 1977). Validity
measure that assesses the presence and severity of depres- (content, construct, and criterion) was confirmed via
sive symptoms over the previous week. The CES-D has item choice and patterns of correlations with clinical
been used with adult and adolescents. Individuals com- ratings and alternate self-report measures. CES-D scores
pleting the Scale rate each item on a four-point Likert differentiated between psychiatric inpatients and mem-
scale ranging from 0 (rarely or none of the time) to 3 (most bers of the general population (Radloff, 1977): 70% of
or all of the time). Four items require reverse scoring. the patients versus 21% of the general population scored
Administration time is approximately 5 min. Responses above 16. Internal consistency, based on coefficient
are summed to obtain a total score of 0–60, with higher alpha and Spearman-Brown split-halves method, is gen-
scores indicating a greater frequency of symptoms. Scores erally high – approximately 0.85 in the general population
of 16 or higher were suggested to identify subjects with and approximately 0.90 in the patient sample. Consistent
depressive illness (Radloff, 1977). Work by Pandya, Metz, with the expectation that shorter test-retest intervals
and Patten (2005) supports the use of this cut-off in those would produce higher correlations, test-retest reliabilities
with multiple sclerosis (MS). Earlier work by Zich, ranged from 0.32 (12 months) to 0.67 (4 weeks). Follow-
Attkisson, and Greenfield (1990) suggest that alternate up studies appear to support Radloff ’s (1977) original
508 C Center for Epidemiological Studies–Depression

reliability and validity statistics (Brantley et al., 2000). A Cross References

four factor structure (depressed affect, positive affect,
somatic and retarded activity, and interpersonal) was ▶ Beck Depression Inventory
initially reported (Radloff, 1977), and has been supported ▶ Geriatric Depression Scale
by subsequent confirmatory analyses. However, findings ▶ Hamilton Rating Scale of Depression
suggest that among minority populations alternate mod- ▶ Structured Clinical Interview for DSM-IV (SCID)
els may provide a better fit (Brantley et al., 2000). ▶ Zung Self-Rating Depression Scale

Clinical Uses References and Readings

Bay, E., Hagerty, B. M., & Williams, R. A. (2007). Depressive symptom-

The CES-D is a widely accepted measure of depressive
atology after mild-to-moderate traumatic brain injury: A compari-
symptoms that has been used with a range of popula- son of three measures. Archives of Psychiatric Nursing, 21(1), 2–11.
tions, including those with a history of neuropsycholog- Brantley, P. J., Mehan, J., & Thomas, J. L. (2000). The beck depression
ical impairments secondary to disease (e.g., MS), inventory (BDI) and the center for epidemiological studies depres-
acquired insult (e.g., stroke), or injury (e.g., traumatic sion scale (CES-D). In M. E. Maruish (Ed.), Handbook of psychologi-
cal assessment in primary care settings (pp. 391–422). Mahwah, NJ:
brain injury, TBI). The CES-D has been relied on to
Lawrence Erlbaum Associates, Inc.
document the incidence and severity of depression in Bush, B. A., Novack, T. A., Schneider, J. J., & Madan, A. (2004). Depres-
individuals with MS, including those who received dis- sion following traumatic brain injury: The validity of the CES-D as a
ease-modifying treatments (Patten, Fridhandler, Beck, & brief screening device. Journal of Clinical Psychology in Medical
Metz, 2003; Chwastiak et al., 2002), and to assess for Settings, 11, 195–201.
Carpenter, J. S., Andrykowski, M. A., Wilson, J., Hall, L. A., Rayens, M. K.,
potential adverse psychiatric side effects of Interferon
Sachs, B., et al. (1998). Psychometrics for two short forms of the
treatment (Patten & Metz, 2001). It has also been used center for epidemiologic studies-depression scale. Issues in Mental
to explore the relationship between depression and cogni- Health Nursing, 19, 481–494.
tive complaints in individuals with MS (Maor, Olmer, & Chwastiak, L., Ehde, D. M., Gibbons, L. E., Sullivan, M., Bowen, J. D., &
Mozes, 2001), and study whether depression may be a Kraft, G. H. (2002). Depressive symptoms and severity of illness in
multiple sclerosis: Epidemiologic study of a large community sam-
risk factor for increased mortality after stroke (Gump
ple. The American Journal of Psychiatry, 159(11), 1862–1868.
et al., 2005). Dikmen, S. S., Bombardier, C. H., Machamer, J. E., Fann, J. R., & Temkin,
Confirmatory factor analysis supports the use of N. R. (2004). Natural history of depression in traumatic brain injury.
this measure for those with mild to moderate TBI Archives of Physical Medicine & Rehabilitation, 85(9), 1457–1464.
(McCauley et al., 2006); acceptable reliability of the Gump, B. B., Matthews, K. A., Eberly, L. E., Chang, Y. F., & MRFIT
Research Group. (2005). Depressive symptoms and mortality in
CES-D with individuals with TBI has also been docu-
men: Results from the multiple risk factor intervention trial. Stroke,
mented (Bush, Novack, Schneider, & Madan, 2004). 36(1), 98–102.
Moreover, Bay, Hagerty, and Williams (2007) argue that Kohout, F. J., Berkman, L. F., Evans, D. A., & Cornoni-Huntley, J. (1993).
the CES-D’s psychometric properties and ease of use Two shorter forms of the CES-D depression symptoms index. Jour-
render it an appropriate measure for depression screening nal of Aging and Health, 5, 179–193.
Maor, Y., Olmer, L., & Mozes, B. (2001). The relation between objective
in persons with TBI. The CES-D has also been used in
and subjective impairment in cognitive function among multiple
longitudinal research on the incidence of depression sclerosis patients–the role of depression. Multiple Sclerosis, 7(2),
following TBI (Dikmen et al., 2004) and in studies of 131–135.
depression in caregivers of individuals with TBI (Rivera McCauley, S. R., Pedroza, C., Brown, S. A., Boake, C., Levin, H. S.,
et al., 2007). Goodman, H. S., et al. (2006). Confirmatory factor structure of the
center for epidemiologic studies-depression scale (CES-D) in mild-
Of note, although findings from the CES-D may be
to-moderate traumatic brain injury. Brain Injury, 20, 519–527.
useful in identifying certain symptoms of depression, the Pandya, R., Metz, L., & Patten, S. B. (2005). Predictive value of the CES-D
measure only addresses mood during the week prior to in detecting depression among candidates for disease-modifying
administration and, therefore, does not permit the clini- multiple sclerosis treatment. Psychosomatics, 46, 131–134.
cian to assign a formal diagnosis of a mood disorder. As Patten, S. B., Fridhandler, S., Beck, C. A., & Metz, L. M. (2003). Depres-
sive symptoms in a treated multiple sclerosis cohort. Multiple Scle-
such, in a clinical setting it may be best used in conjunc-
rosis, 9, 616–620.
tion with additional findings (e.g., structured clinical in- Patten, S. B., & Metz, L. M. (2001). Interferon beta-1 a and depression in
terview, additional measures) to diagnose depressive relapsing-remitting multiple sclerosis: An analysis of depression data
disorders and assess treatment needs. from the PRISMS clinical trial. Multiple Sclerosis, 7(4), 243–248.
 Center for Medical Home Improvement C 509

Radloff, L. S. (1977). The CES-D Scale: A self-report depression scale for adults, and their families may require more than the
research in the general population. Applied Psychological Measure-
usual well child and/or adult, preventive care, and acute
ment, 1, 385–401.
Rivera, P., Elliott, T. R., Berry, J. W., Grant, J. S., & Oswald, K. (2007).
illness interventions. It involves explicit changes in the
Predictors of caregiver depression among community-residing families roles of providers and office staff aimed at improving).
living with traumatic brain injury. Neurorehabilitation, 22(1), 3–8.
Zich, J. M., Attkisson, C. C., & Greenfield, T. K. (1990). Screening for
1. Access to needed services C
depression in primary care clinics: The CES-D and the BDI. Interna- 2. Communication with specialists, schools, and other
tional Journal of Psychiatry in Medicine, 20, 259–277. resources
3. Outcomes for children and families

Landmark Contributions
Center for Medical Home
Improvement The ‘‘story’’ of the medical home extends from the 1935
Social Security Legislation Act that called for Maternal
W. C ARL C OOLEY, J EANNE W. M C A LLISTER and Child Health (MCH) Title V Programs to ‘‘locate,
Crotched Mountain diagnose, and treat crippled children’’ to today’s emphasis
Concord, NH, USA on providing planned primary health care in the context
of the families and communities in which patients live.
Community-based care in a medical home is increasingly
Membership accepted as one of the means of achieving optimal out-
comes for children, youth, adults, and their families. The
The Center for Medical Home Improvement (CMHI) is a term ‘‘medical home’’ was coined in 1967 by the Council
nonprofit organization affiliated with Crotched Mountain. on Pediatric Practice, a subgroup of the American Acade-
(Crotched Mountain is a charitable organization employing my of Pediatrics, and has been described with a variety of
more than 900 people, whose mission is to serve individuals applications and definitions since then. The CMHI began
with disabilities and their families, embracing personal its efforts in 1993 with a capacity building endeavor for
choice and development, and building communities of pediatric practices serving children with special healthcare
mutual support. It provides specialized education, rehabili- needs. In 1997, the CMHI developed and implemented an
tation, community and residential support services for improvement model with multiple New Hampshire, Ver-
more than 2,000 individuals living in New England and mont, and Maine healthcare teams. These teams (physi-
New York.) It is founded in 1993 by Dr. Carl W. Cooley, cian leader and practice-based care coordinator)
Medical Director and Ms. Jeanne W. McAllister, R.N., M.S., partnered with patients and families to redesign primary
M.H.A., Director. Along with the founders, Dr. Cooley and care services. In 2003, the CMHI published the Medical
Ms. McAllister, the CMHI is staffed by Lora Council, M.D. Home Index (MHI) as a validated measurement to assess
(Quality Consultant), Lori Keehl-Markowitz, R.N., B.S.N. quality and monitor improvements in a primary care
(Program Manager), Leah Reed (Program Coordinator), practice (this tool is now available for adult care). Practice
and Kathleen Sherrieb, R.N., M.S., M.P.H. (Data Manage- improvement activities in multiple states have consistent-
ment Consultant). ly demonstrated sustained increases of greater than 30%
in MHI scores overall. A companion Medical Home Fam-
ily Index and Survey used by these practices has shown
Major Areas or Mission Statement significant improvement in clinical, functional, satisfac-
tion, and cost outcomes and an increase in the use of
The mission of the CMHI is to promote high-quality written and portable care plans. During 2001–2004, the
primary care in the medical home and secure health CMHI spread its model to ten additional practices in
policy changes critical to the future of primary care. The Vermont and New Hampshire and partnered with the
CMHI defines the medical home ‘‘as a community-based National Initiative for Children’s Healthcare Quality
primary care setting which provides and coordinates high (NICHQ) in two national medical home learning collabora-
quality, planned, family-centered health promotion, acute tives. These efforts ‘‘spread’’ the CMHI’s model to 20 state
illness care and chronic condition management’’ (chronic Title V Programs, 40 primary care practices, and multiple
condition management acknowledges that children, family advocacy organizations. The CMHI and NICHQ
510 C Center for Medical Home Improvement

adapted the widely recognized Chronic Care Model as 2. Develop supports for primary care practices to im-
the ‘‘Care Model for Child Health in a Medical Home.’’ prove their ‘‘medical homeness’’
A health resources and services administration 3. Align statewide efforts toward an investment in the
(HRSA) systems grant was awarded to the CMHI in future of primary care
2004 and a contract for a medical home outcomes re-
Following initial Council meetings, the New Hampshire
search study. Early findings from this research show that
Endowment for Health funded the CMHI to convene and
enhanced chronic condition management and care coor-
lead the New Hampshire Primary Care Task Force. This
dination, as outlined in the MHI, are associated with
group will issue consensus statements crafted to further
reductions in emergency room use, hospitalizations, and
detail the resources and supports necessary to develop and
visits to specialists. Starting in 2007, the CMHI Medical
provide relationship-centered primary care. The Task
Director, Dr. Carl Cooley began convening and chairing a
Force will comment on what they would like a future
Medical Home Work Group to design and develop a pilot
medical home pilot effort to look like in New Hampshire.
program to test a new process of primary care medical
The CMHI plans to develop and provide technical assis-
home-based, longitudinal care of children with genetic
tance to help primary care practices pass the National
conditions identified through newborn screening includ-
Committee for Quality Assurance (www.ncqa.org) medi-
ing the potential use of registries, planned care methods,
cal home recognition measure, a requirement to enter a
decision support mechanisms, comanagement with spe-
medical home pilot demonstration and receive enhanced
cialists, and application of family-and-patient-centered
payment. The CMHI is working with the New Hampshire
practices. This project is called the New England Genetics
Citizen’s Health Initiative and a public private multi-
Collaborative (NEGC) and is funding through the Uni-
payer and stakeholders group to craft New Hampshire’s
versity of New Hampshire’s Office of Sponsored Research.
pilot to stimulate a transformative process in primary care
A similar medical home project entitled ‘‘Leadership Edu-
for the twenty-first century. In conclusion, the CMHI
cation in Autism Spectrum Disorders’’ (LEASD) will begin
provides content expertise, education, and consultation
in the fall of 2008. The CMHI will work in partnership with
focused on medical home development to a variety of states,
Dartmouth Medical School (DMS) and the University of
centers, and initiatives including the American Academy of
New Hampshire Leadership in Education in Neurodeve-
Pediatrics, the commonwealth fund, various HRSA gran-
lopmental and Related Disabilities (LEND) program to
tees, and numerous state and regional programs.
assure that all children in New Hampshire are screened
for autism and spectrum disorders at 18 and 24 months to
assure early diagnosis and access to early intervention and
Major Activities
family-centered care for optimal development outcomes.
The providence for the medical home model has gained
2001: Medical Home Index (MHI), pediatric version, a
substantial momentum that in 2007, the American Acade-
validated measurement to assess quality and monitor
my of Pediatrics, American Academy of Family Physicians,
improvements in a primary care practice (available at
and the American College of Physicians as well as Family
www.medicalhomeimprovement.org). 2001: Developed
Voices and the National Association of Pediatric Nurse
a companion Medical Home Family Index and Survey
Practitioners endorsed the medical home as the model
(available at www.medicalhomeimprovement.org). 2001:
for twenty-first-century primary care (www.pcpcc.org).
Medical Home Improvement Tool Kit (available at www.
States are looking for better ways to effectively support
medicalhomeimprovement.org). 2003: Parent Partners
the healthcare needs of its citizens and the organizational
Creative Forces on Medical Home Improvement Teams’’
and operational needs of those providing health care.
(available at www.medicalhomeimprovement.org).
However, there is a looming crisis in primary care that
2006–current: New Hampshire Council on the Future of
raises concerns about current and future capacity, recruit-
Primary Care Medical Home. 2007–current: New Hamp-
ment, and reimbursement. In response to the current
shire Primary Care Task Force 2007: Medical Home Prac-
struggle inherent to primary care, the CMHI, in partner-
tice-Based Care Coordination, Workbook (available at
ship with New Hampshire Special Medical Services regu-
www.medicalhomeimprovement.org). 2007–2008: New
larly convenes the New Hampshire Council on the Future
England Genetics Collaborative (NEGC), Regional Genet-
of the Primary Care Medical Home with explicit goals to:
ics and Newborn Screening Collaborative. 2008: Leader-
1. Build and spread awareness of the medical home ship Education in Autism Spectrum Disorders (LEASD).
model of primary care 2008: ‘‘Extra-Ordinary Care: Improving Your Medical
 Center for Outcome Measurement in Brain Injury (COMBI) C 511

Home,’’ Guide and Workbook (available at www.medical- measures for persons with brain injury. The measures
homeimprovement.org). included in the COMBI are commonly used in the field
2008: Medical Home Index (MHI), Adult version of brain injury rehabilitation and assessment. The
(available at www.medicalhomeimprovement.org). COMBI is a collaborative project of 16 brain injury
facilities or centers, with each center contributing infor- C
mation on one or more measures. For most supported
References and Readings
measures, there are syllabus and training information,
rating forms, background information on validity and
Cooley, W. C., McAllister, J. W., Sherrieb, K., & Clark, R. (2003).
The medical home index: Development and validation of a new
reliability, a reference list of published studies, and test-
practice-level measure of implementation of the medical home ing materials. A Frequently Asked Question (FAQ) sec-
model. Ambulatory Pediatrics, 3, 173–180. tion is also included, compiled from past training
Cooley, W. C., & McAllister, J. W. (2004). Building medical homes:
Improvement strategies in primary care for children with special
health care needs. Pediatrics, 113, 1499–1506.
Dillon, A., & McAllister, J. W. (2006). Do you have a medical home? EP Center for Outcome Measurement in Brain Injury (COMBI).
Magazine (www.eparent.com), August, 22–28.
Table 1 COMBI-featured scales/measures
Joint Principles of the Patient-Centered Medical Home (2007). http://
www.aafp.org/online/etc/medialib/aafp_org/documents/policy/fed/ Agitated Behavior Scale (ABS)
jointprinciplespcmh0207.Par.0001.File.dat/022107medicalhome.pdf
Apathy Evaluation Scale (AES)
McAllister, J. W., Pressler, E., & Cooley, W. C. (2007). Practice-based care
coordination: A medical home essential. Pediatrics, 120, e723–e733. Awareness Questionnaire (AQ)
doi: 10.1542/peds.2006-1684. Cognitive Log (Cog-Log)
Takachand, M., Kaye, N., & Beesla, R. (2008). Strategies states can use to
Coma/Near Coma Scale (CNC)
support the infrastructure of medical homes. State Health Policy
Briefing. www.nashp.org/Files/shpbriefing_pcmhsupport.pdf. Coma Recovery Scale-Revised(CRS-R)
Confusion Assessment Protocol (CAP)
Community Integration Questionnaire (CIQ)
The Craig Handicap Assessment and Reporting Technique
Center for Outcome Measurement (CHART)
The Craig Handicap Assessment and Reporting Technique
in Brain Injury (COMBI) Short Form (CHART SF)
The Craig Hospital Inventory of Environmental Factors
J ERRY W RIGHT
(CHIEF)
Santa Clara Valley Medical Center
Disability Rating Scale (DRS)
San Jose, CA, USA
The Family Needs Questionnaire (FNQ)
Functional Assessment Measure (FAM)
Membership Functional Independence Measure (FIM)(TM)
Glasgow Outcome Scale (GOS)
The Center for Outcome Measurement in Brain Injury Extended Glasgow Outcome Scale (GOS-E)
(COMBI) is a collaborative project of 16 brain injury High Level Mobility Assessment Tool (HiMAT)
facilities or centers, most of them Traumatic Brain
Level of Cognitive Functioning Scale (LCFS)
Injury Model Systems (funded by the National Institute
Mayo Portland Adaptability Inventory (MPAI)
on Disability and Rehabilitation Research). The product is
an informational web site that is oriented primarily to- Mississippi Aphasia Screening Test (MAST)
wards clinicians and researchers, but is also freely avail- Neurobehavioral Functioning Inventory (NFI)
able to the general public. The Orientation Log (O-Log)
The Patient Competency Rating Scale (PCRS)
Participation Objective, Participation Subjective
Major Areas Satisfaction With Life Scale (SWLS)
Service Obstacle Scale (SOS)
The COMBI is an online resource for those needing
Supervision Rating Scale (SRS)
detailed information and support in regards to outcome
512 C Centers for Medicare and Medicaid Service

information and submitted questions. The COMBI was

designed to provide accessible and consistent informa- Centers for Medicare and
tion regarding brain injury outcome measures to clini- Medicaid Service
cians and researchers.
R OBERT G. F RANK
Kent State University
Landmark Contributions Kent, OH, USA

The COMBI is coordinated by Santa Clara Valley Medical

Center and is supported by funds from the National Membership
Institute on Disability and Rehabilitation Research
(NIDRR). It has been a collaborative project of the The Centers for Medicare and Medicaid (CMS) served
NIDRR-funded Traumatic Brain Injury Model Systems 102 million Americans enrolled in Medicare, Medicaid,
since 1998. and the Children’s Health Insurance Program (CHIP)
in FY 11.

Major Activities
Major Areas
Currently, the COMBI has 28 featured scales, with 25
scales available for immediate download. Table 1 shows CMS is part of the Department of Health and Human
the COMBI-featured scales as of August 2008. Additional Services. The primary offices are not located in Washing-
information is available about measuring employment ton D.C. but in Baltimore. With a budget of approximate-
and substance abuse after brain injury. The COMBI web ly $650 billion, serving almost 90 million beneficiaries,
site also conducts testing and certification for the Disabil- CMS has a dominant role in American health care. The
ity Rating Scale (DRS). The COMBI web site (www.tbims. top position in CMS, the Administrator, is nominated by
org/combi) receives over 1,200 visitors per day, with well the President of the USA but must be confirmed by the
over one million visits in total. Senate. Most administrators have come to CMS from
academia or have been industry lobbyists. The position
of Administrator is complex and demanding. Nancy-Ann
DePearle, who served as Administrator at the end of the
Cross References Clinton administration, during one of the few periods in
which federal spending for CMS declined, noted that
▶ Agitated Behavior Scale (ABS) the Administrator has ‘‘. . .many bosses, including 535
▶ Coma/Near Coma Scale (CNS) members of Congress, the White House, the Inspector
▶ Coma Recovery Scale (CRS) General, the US Government Accountability Office
▶ National Institute on Disability and Rehabilitation (GAO)’’ (Health Affairs: W-5–337).
Research (NIDRR) The Department of Health and Human Services,
▶ Neurobehavioral Functioning Inventory (NFI) through CMS, issues regulations and policy clarifications
▶ Orientation Log guiding the provision of services for Medicare benefici-
▶ Rancho Los Amigos Scale aries. All psychologists who provide health-care services
▶ Traumatic Brain Injury to Medicare recipients, particularly neuropsychologists,
▶ Traumatic Brain Injury Model System interact with CMS. Each psychologist who provides ser-
vices to Medicare beneficiaries must obtain National Pro-
vider Identification (NPI) from CMS. Medicare fiscal
intermediaries oversee payment for Medicare services
References and Readings including the electronic fund transfer. Each state has a
fiscal intermediary overseeing Medicare Part A (inpatient
http://www.tbims.org/combi
services) and Part B (professional services). CMS regula-
Wright, J. M., Bushnik, T., & O’Hare, P. (2000). The center for outcome
measurement in brain injury (COMBI): An internet resource you
tions now guide the care of all Medicare beneficiaries. In
should know about. Journal of Head Trauma Rehabilitation, 15(8), addition, the size and impact of Medicare have made the
734–738. agency a predictor of many coverage choices by private
 Centigray C 513

insurers. When CMS issues proposed rules in the Federal Medicare program (health insurance for people aged 65
Register (the federal government’s daily journal), all and over, younger people receiving social security disabil-
providers have the opportunity to comment. Final rules ity benefits, and persons with end-stage kidney disease)
that guide reimbursement by CMS’s fiscal intermediaries as well as the Medicaid program (providing medical
are then issued. assistance from state and federal governments for eligible C
low-income persons). Although the federal government
regulates Medicaid, state governments actually operate
Landmark Contributions the program). HCFA also provided federal oversight for
quality control initiatives.
In July 1965, at the home of President Harry Truman, Between 1989 and 2000, the number of Medicare
President Lyndon B. Johnson signed the Social Security claims rose from 70% to more than 800 million claims.
Act of 1965. Titles XVIII and XIX of the Act fostered a new Despite this staggering volume, Medicare’s administrative
view of health care in the USA, responding to more than costs were only 2%. HCFA was viewed as having a bias
20 years of legislative initiatives aimed at creating an toward providers. In 2001, the Bush administration,
insurance program to cover hospitalization, health ser- believing that HCFA was perceived as bureaucratic, unre-
vices, and skilled nursing care for the elderly as well as sponsive, and biased toward physicians and hospitals,
coverage for low-income children. When implemented in sought a new image for the agency. In an effort to improve
1966, Medicare (created by Title XVIII) provided cover- the agency’s image, the Bush administration changed the
age for more than 19 million elderly Americans. Medicaid name to the Centers for Medicare and Medicaid – CMS
(created in Title XIX), covered almost 15 million people (Scully, 2005), heralding an effort to streamline the many
and was administered by the Social Rehabilitation administrative processes overseen by CMS. Despite the
Administration, an agency managing poverty and welfare new name, CMS continued the responsibilities of HCFA:
programs. Medicare, end-stage renal disease, quality, and coordina-
The inclusion of Medicare and Medicaid within the tion of Medicaid with the states.
Social Security Act reflected political compromises need-
ed for the passage of both programs. Wage and price
controls imposed during World War II prompted many
References and Readings
employers to offer health-care coverage. This ‘‘de facto’’
DePearle, N. A. (2005). What does it take to run Medicare and Medicaid?
wage increase determined that health insurance became a Health Affairs, W-5–337–338.
common employer benefit, but one that excluded the Derzon, R. A. (2005). The Genesis fo HCFA. Health Affairs, W5–326.
elderly and unemployed. By 1960, the inadequacy of Scully, T. A. (2005). Policy high oints: Medicare and medicaid in the New
health services for older Americans had become a political Millennium. Health Affairs, W5–339.
issue. In order to secure enough votes to pass Medicare,
President Johnson created the concept of the ‘‘medically
indigent’’ thereby linking welfare to health care for the
elderly. Centigray
Medicare and Medicaid were administered separately
during the Johnson and Nixon administrations. Joseph B RAM G OLDSTEIN
Califano, Secretary of Health Education and Welfare Hoag Hospital Cancer Center
(HEW) under Jimmy Carter, believed that ineffective Newport Beach, CA, USA
oversight of health programs permitted spiraling health
costs and health-care spending inflation (Derzon, 2005).
Califano knew the separate administration of Medicare Synonyms
and Medicaid reflected the political compromises needed
to create coverage for the elderly and the poor through cGY
linking coverage for the elderly to welfare. The split ad-
ministration of Medicare and Medicaid, however, made Definition
the two mammoth programs less manageable. Califano
moved quickly, in secret and combined Medicare and Centigray (cGY) is the preferred measurement of
Medicaid, forming the Health Care Financing Admin- absorbed radiation and is equivalent to one-hundredth
istration (HCFA). HCFA provided oversight to the (10-2) of a gray, or 1 rad. The gray measures the deposited
514 C Central Auditory Processing Disorder

energy of radiation. The daily dose of radiation is also symptoms diagnosed by audiologists and/or speech and
referred to as a fraction, since each dose is a percentage of language specialists using the audiology code of ICD-9
the cumulative prescribed dose. The dose is given in code 388.4 (Abnormal Auditory Processes).
sublethal fractions, which protracts the dose to facilitate The American Speech-Language Hearing Association
the occurrence of repair kinetics. Hence, radiation oncol- (ASHA, 2005) defines CAPD as difficulties in the per-
ogists use fractions to take advantage of the differential ceptual processing of auditory information in the central
recovery rates for normal and neoplastic tissue, thereby nervous system (CNS). It presents in the form of poor
permitting repopulation of normal cells and inducing performance in one or more of the following abilities
radiosensitivity via increased oxygen to the remaining or skills: sound localization and lateralization, auditory
tumor cells. Fractionated dose radiotherapy enhances discrimination, auditory pattern recognition, temporal
the treatment efficacy by targeting the cancer cells aspects of audition (including temporal integration,
while mitigating the damage to healthy tissue. This is temporal discrimination/gap detection, temporal order-
determined using a therapeutic ratio, which compares ing, and temporal masking), auditory performance in
the damage to both cancerous and healthy cells (Potters, competing acoustic signals (including dichotic listen-
Timmerman, & Larson, 2005). Moreover, the biological ing), and auditory performance with degraded acoustic
effects on the relevant tissue vary according to the signals.
radiation type and intensity.

Categorization
Cross References
Neither CAPD nor SI is listed in the DSM-IVor DSM-IV-TR
▶ Radiation Therapy manuals which provide diagnostic codes for psychologists,
psychiatrists, and speech and language specialists. When
References and Readings individuals from these fields assess problems that are
language based, they use language tests and assign diag-
Potters, L., Timmerman, R., & Larson, D. (2005). Stereotactic body
nostic codes associated with specific language disorders
radiation therapy. Journal of the American College of Radiology, 2, (e.g., ICD-9: 315.3, Developmental Speech or Language
676–680. Disorder; ICD-9: 389.9, Unspecified Hearing Loss).
While the diagnosis of CAPD has a 50-year history,
there is much controversy about its legitimacy (Carneol,
2008). In part, this stems from its extensive comorbidity
Central Auditory Processing with a variety of impairments in attention/concentration,
Disorder language, memory, IQ, academic achievement, and other
behavioral/emotional disorders. Children with the CAPD
J UDITH A. S HECHTER 1, S ARAH J. L EINEN 2 diagnosis typically demonstrate poor listening skills,
1
Wynnewood, PA, USA difficulty filtering linguistic information from back-
2
Widener University ground noise, problems following oral instructions, poor
Chester, PA, USA auditory discrimination skills, distractibility/inattentive-
ness, and often need additional time to complete tasks
(Bloom & Hynd, 2008). In addition, there is no compel-
Synonyms ling research that reliably provides specific neurobiologi-
cal bases for CAPD when compared to findings that
Auditory perceptual disorder (APD); Auditory processing link specific brain regions with language-based learning
disorder (APD); CAPD; Sensory integration-C/APD disabilities and Attention Deficit Hyperactivity Disorder
(SI-C/APD) (Bloom & Hynd, 2008). Together, these factors have
called into question the validity of CAPD as a distinct
diagnosis.
Short Description or Definition It is important to understand the complicated neuro-
physiological constructs of hearing to better understand
Central Auditory Processing Disorder (CAPD) is not a the etiological basis of CAPD. That is, one must know
neuropsychological diagnosis. It refers to an amalgam of how sound travels from the outer ear through the middle
 Central Auditory Processing Disorder C 515

and inner ear structures through the eighth auditory contribute to outcome trajectories (e.g., comorbid
nerve to Heschl’s gyrus in the left temporal lobe of the ADHD, LD) (Bloom & Hynd, 2008).
brain. At that point, the brain begins to recognize nerve
impulses as sound and then initiates interpretation of
these impulses as either speech or nonverbal auditory C
stimuli. These stimuli are then analyzed bilaterally by Neuropsychology and Psychology
auditory stimulus networks distributed within the brain of CAPD
(Carneol, 2008).
Some researchers have proposed CAPD subgroups The immense overlap of CAPD symptoms with other de-
such as Auditory Decoding Deficit (primary left auditory velopmental disorders such as ADHD continues to fuel
cortex dysfunction), Prosodic Deficit (nonprimary right debate among psychologists, neuropsychologists, audiolo-
auditory cortex and associated areas dysfunction), and gists, and speech-language pathologists over the existence of
Integration Deficit (corpus callosum dysfunction) (Bellis, this diagnosis. While a definition of CAPD as a unimodal
2003; Bellis & Ferre, 1999; Katz, 1992). These subtypes disorder is a useful tool in the conceptualization of the
may help clinicians design intervention strategies specific symptoms associated with it, the notion of CAPD as sepa-
to an individual’s presenting problems However, these rate and distinct from language-based LD and ADHD has
models are theoretical in nature and not universally not been well documented in the literature.
agreed upon (ASHA, 2005; Jutras et al., 2007). In a sample of 30 9–13-year-olds, approximately 50%
of children diagnosed with CAPD also met diagnostic
criteria for ADHD (Riccio, Hynd, Cohen, Hall, & Molt,
1994). Based on ratings from audiologists and pediatri-
Epidemiology
cians, Chermak, Tucker, and Seikel (2002) identified
exclusive behavior sets characterizing CAPD and ADHD.
No truly authoritative population or prevalence studies
CAPD was not characterized by hyperactivity and
regarding CAPD are available (Castrogiovanni, 2008).
difficulties with impulse control.
Chermak and Musiek (1997) estimate a prevalence rate
Some individuals with CAPD may have difficulties
of 2–3% in children, with the disorder occurring twice as
with speech and language. Varying combinations of audi-
frequently in males than females. Cooper and Gates
tory processing deficits may be associated with different
(1991) estimate that the prevalence in older adults is
functional deficits in speech and language. Differential
10–20%.
diagnosis between CAPD and language disorders can be
quite challenging due to shared symptomatology. For
example, a core deficit in phonological processing under-
Natural History, Prognostic Factors, lies dyslexia. Similarly, children with CAPD may have
and Outcomes difficulty discriminating and manipulating the phonetic
aspects of auditory input. It has been suggested that
The etiology of CAPD is unknown. CAPD may present as auditory processing problems in developmental dyslexia
a developmental or acquired disorder. The maturation of are specific to the encoding of speech, whereas CAPD is
the central auditory pathway may be delayed (Bamiou, characterized by a general dysfunction encoding all
Musiek, & Luxon, 2001). Prenatal or perinatal factors auditory stimuli.
(e.g., hyperbilirubenemia, anoxia or hypoxia, ototoxic Academic difficulties are often a characteristic of
drugs, Rh incompatibility, prematurity/low birth weight, children who carry a CAPD diagnosis (ASHA, 2005).
birth complications, maternal diabetes, or infections), ear They may have a difficult time encoding/learning spoken
infections, heavy metal exposure, cerebrovascular disor- information or information presented with background
ders, epilepsy, Lyme disease, and traumatic brain injury noise. They are more likely to have behavioral, emotional,
may be risk factors for the constellation of symptoms that and social difficulties secondary to poor communica-
characterize the CAPD diagnosis (Bamiou, Musiek, & tion skills (ASHA, 2005). The preceding, combined
Luxon, 2001; Musiek & Chermak, 2009; Riccio & with associated learning difficulties, can compromise
Hynd, 1996). self-esteem and contribute to emotional withdrawal, so-
It is not clear if problems in auditory processing matization, conduct disorders, depression, anxiety, and
resolve with age, if children are able to compensate for interpersonal problems (Riccio, Cohen, Garrison, &
auditory processing deficits, and what factors may Smith, 2005).
516 C Central Auditory Processing Disorder

Evaluation educational programming. These would be written in the

form of an Individual Education Program (Individuals
Since CAPD is an auditory deficit, an audiologist is the with Disabilities Education Improvement Act of 2004,
professional best-qualified to diagnose CAPD (ASHA, 20 U.S.C. 1400; Public Law 108–446) that would provide
2005). Although psychologists and speech-language such accommodations under the category of Other
pathologists (SLPs) may screen for auditory processing Health Impaired.
difficulties, speech-language and psychological measures
should not be used to diagnose CAPD (ASHA, 2005).
Screening processes involve systematically observing lis- Cross References
tening behavior and assessing performance on tests of
auditory function (ASHA, 2005). Multidisciplinary as- ▶ ADD
sessment including other professionals such as psycholo- ▶ ADHD
gists and SLPs should be conducted to help delineate ▶ American Speech-Language-Hearing Association (ASHA)
cognitive communication and language-related factors ▶ Americans with Disabilities Act
associated with CAPD, determine the functional impact ▶ Auditory System
of CAPD, and guide treatment (ASHA, 2005). ▶ Cognitive Communication Disorder
The audiologist’s central auditory diagnostic test ▶ D-amphetamine
battery, which aims to examine the integrity of the central ▶ Dyslexia
auditory nervous system (ASHA, 2005) may include au- ▶ Executive Functioning
ditory discrimination tests, auditory temporal processing ▶ Learning Disability
and patterning tests, dichotic speech tests, monaural ▶ Section 504 of the Rehabilitation Act of 1973
low-redundancy speech tests, binaural interaction tests, ▶ Stimulants
electroacoustic measures, and electrophysiologic mea-
sures (ASHA, 2005). Auditory processing tests include
elements of attention and memory, but also appear to References and Readings
assess processes not tapped by measures of these con-
structs (Riccio et al., 2005). A diagnosis of CAPD typically American Speech-Language-Hearing Association. (2005). (Central)
auditory processing disorders [Technical Report]. Available from
requires performance, two standard deviations below the
www.asha.org/policy.
mean on two or more auditory processing tests. The Bamiou, D., Musiek, F., & Luxon, L. (2001). Aetiology and clinical
audiologist must also consider the confounding effects presentations of auditory processing disorders – A review. Archives
of fatigue, poor attention, memory, and motivation on of Disease in Childhood, 85, 361–365.
test performance. Bellis, T. J. (2003). Assessment and management of central auditory proces-
sing disorders in the educational setting: From science to practice
(2nd ed.). Clifton Park, NY: Delmar Learning.
Bellis, T. J., & Ferre, J. M. (1999). Multidimensional approach to the
differential diagnosis of auditory processing disorders in children.
Treatment Journal of the American Academy of Audiology, 10, 319–328.
Bloom, J. S., & Hynd, G. (2008). Dysfunctions of attention, learning, and
central auditory processing: What’s the difference? In K. McBurnett &
Collaboration among educators, school psychologists,
L. Pfiffner (Eds.), ADHD, concepts, controversies, new directions.
speech-language pathologists, audiologists, neuropsy- (pp. 63–70). New York: Informa Health Clinic USA Inc.
chologists, and physicians may be necessary to identify Carneol, S. O. (2008). Elusive, inclusive, or conclusive? (central)
and implement interventions aimed at ameliorating auditory processing disorder. In J. Apps, R. F. Newby, &
symptoms that resemble those associated with the L. W. Roberts (Eds.), Pediatric neuropsychology case studies: From
the exceptional to the commonplace. (pp. 307–323). New York, NY:
CAPD diagnosis.
Springer Business & LLC.
While there is some evidence that methylphenidate Castragiovanni, A. (2008). Incidence and prevalence of hearing loss and
may ameliorate symptoms in children with the diagnosis hearing aid used in the United States – 2008 Edition. Available from
of CAPD, research is inconclusive. More typical interven- www.asha.org/research/reports/hearing.
tions for CAPD symptoms include perceptual training, Chermak, G., & Musiek, F. (1997). Central auditory processing disorders:
New perspectives. San Diego: Singular Publishing Group.
instruction in linguistic and cognitive compensatory stra-
Chermak, G., Tucker, E., & Seikel, J. (2009). Behavioral considerations of
tegies, environmental modifications (e.g., preferential auditory processing disorder and attention-deficit hyperactivity dis-
seating, use of a stereo system in the classroom, use of order: Predominantly inattentive type. Journal of American Academy
area rugs), assistive technology alternatives, and specific of Audiology, 13, 332–338.
 Central Executive C 517

Cooper, J., & Gates, G. (1991). Hearing in the elderly – the Framingham several types of memory in the intact human mind.
cohort, 1983–1985: Part II. Prevalence of central auditory processing
Although philosophers have long been theorizing about
disorders. Ear and Hearing, 12, 304–311.
Jutras, B., Loubert, M., Dupuis, J., Marcoux, C., Dumont, V., & Baril, M.
distinctions within memory, there has been experimental
(2007). Applicability of central auditory processing disorder models. evidence supporting the divisions of memory for only the
American Journal of Audiology, 16, 100–106. past 30–40 years (Baddeley, 1999). C
Katz, J. (1992). Classification of auditory processing disorders. In J. Katz,
N. Stecker, & D. Henderson (Eds.), Central auditory processing:
A transdisciplinary view (pp. 81–91). Baltimore: Mosby-Yearbook.
Musiek, F., & Chermak, G. (2009). Diagnosis of (central) auditory
Historical Background
processing disorder in traumatic brain injury: Psychophysical
and electrophysiological approaches. Washington, DC: The ASHA
Leader. Retrieved from http://www.asha.org/publications/leader/ Baddeley and Hitch (1974) developed a theory of a WM
2009/091124/CAPD.htm. system that has become the dominant theory in cognitive
Riccio, C., Cohen, M., Garrison, T., & Smith, B. (2005). Auditory pro- psychology for the organization of WM (Fig. 1). Baddeley’s
cessing measures: correlation with neuropsychological measures of
model addressed weaknesses of previous short-term
attention, memory, and behavior. Child Neuropsychology, 11,
363–372.
memory (STM) models, including the failure to address
Riccio, C., & Hynd, G. (1996). Relationship between ADHD and central nonverbal processing. Baddeley’s model, which has
auditory processing disorder: A review of the literature. School undergone changes throughout the years, is a theoretical
Psychology International, 17, 235–252. concept and was not originally developed to directly cor-
Riccio, C., Hynd, G., Cohen, M., Hall, J., & Molt, L. (1994). Comorbidity
respond with specific neuroanatomical regions, though
of central auditory processing disorder and attention-deficit hyper-
activity disorder. Journal of the American Academy of Child and
research that attempts to do so has been completed. The
Adolescent Psychiatry, 33, 849–847. original theory proposed the existence of three compo-
nents (Fig. 1). Baddeley envisioned this system as consist-
ing of a central executive, which is a limited capacity
subsection that controls certain subsystems. The central
executive controls ‘slave’ systems, which are mainly used
Central Executive for the temporary storage of information. Information
that is not needed right now, but will soon be needed,
N ICOLE C. R. M C L AUGHLIN can be stored within these ‘slave’ systems to free up the
Butler Hospital, central executive for other tasks. One of the slave systems
Alpert Medical School of Brown University is the articulatory or phonological loop, which is a verbal
Providence, RI, USA store. Subvocalization of verbal material creates a record
in a phonological buffer. The central executive then reads
the phonological buffer, and the cycle begins again. For
Definition most of this cycle, the central executive is not needed.
Another slave system is the visuospatial sketchpad, which
Working memory (WM) has been defined as the is used to rehearse visual or spatial materials. Manipulation
‘‘blackboard of the mind’’ and the ‘‘mental sketchpad’’ of information within either the phonological loop or vi-
(Baddeley, 1986). It enables the online holding and mental suospatial sketchpad does not affect information being
manipulation of information. Human beings use WM retained in the other system; they have been shown to be
processes all the time. For example, WM is used to distinct systems in regard to interference effects (Brooks,
perform rapid mathematical functions in our heads and 1968). Another component, the episodic buffer
to understand the inherent meaning in speech and (described in detail below), was added in 2000 to address
writing. WM is also important for reasoning and problem some of the perceived weaknesses of the earlier model.
solving (Baddeley, 1999). Psychologists have posited The current multicomponent model describes ‘fluid’

Visuospatial Central executive Phonological

sketchpad loop

Central Executive. Figure 1 Initial three-component model of working memory (WM) (Baddeley & Hitch, 1974)
518 C Central Executive

Central executive

Phonological Loop Episodic buffer Visuospatial sketchpad

Visual Episodic Language

semantic long-term memory

Central Executive. Figure 2 Multicomponent model of working memory (WM) (Baddeley, 2000)

capabilities (such as temporary storage) and ‘crystallized’ are prevented from rehearsing items by being required to
abilities that are involved in long-term knowledge (Fig. 2). state an irrelevant word (such as the. . .the. . .the), perfor-
Phonological Loop. The phonological loop is most mance declines. There also appears to be a word-length
similar to the earlier concept of STM (Baddeley, 1992) effect such that longer words are more difficult to remem-
and is the most studied component within this theory. ber, potentially because participants are subvocalizing
There are two components within the phonological loop: words, and thus, there is more time for information to
a phonological store and an articulatory rehearsal system. deteriorate (Baddeley, 2000).
The phonological store can temporarily hold acoustic People frequently use the phonological store in every-
material for 1–2 s and is involved in speech perception. day life, subvocalizing when counting and when reading.
The articulatory rehearsal system can maintain material Adult fluent readers use this component less than poor
by subvocal repetition and can take visually presented readers, or individuals learning to read, but show diffi-
material and register this material by subvocalization. culties picking up errors in written text when their sub-
There are several pieces of evidence that have supported vocalization capabilities are disrupted (Baddeley, 1999).
the presence of the phonological loop. The simplest piece The phonological store may also be important for new
of evidence is that it appears clear that our verbal store language acquisition as well as native language acquisition
holds only a limited amount of information. The phono- (Baddeley, 1999); some researchers have indicated that the
logical similarity effect indicates that sequences of items phonological loop’s primary purpose is for language
with similar phonological sounds are more difficult to acquisition (Baddeley, Gathercole, & Papagno, 1998).
remember than those with disparate sounds (e.g., ‘‘mad A deficit in phonological STM appears to stem from a
can cap man’’ is more difficult than ‘‘pen day cow bar rig’’) defective phonological store. Articulatory rehearsal appears
(Baddeley, 1966b). In addition, it demonstrates the ten- to be defective in aphasic patients with dyspraxia, as they
dency for participant errors to be phonologically similar are unable to carry out the speech motor codes needed for
to the correct item (i.e., F for S and B for G). Similarity of articulation (Waters, Rochon, & Caplan, 1992). Dysarthric
meaning does not seem to be important for the phono- patients do not appear to have a deficit in articulatory
logical store (Baddeley, 1966b), whereas long-term stor- rehearsal, likely because their deficits are peripheral, not
age is affected by similarity of meaning, but not sound central (Baddeley & Wilson, 1985). Neuroanatomically,
(Baddeley, 1966a). The irrelevant speech effect shows that based upon lesion studies, the inferior parietal cortex
exposure to irrelevant speech either at the same time or appears to be related to the temporary phonological store,
directly after stimuli material can disrupt immediate re- whereas the articulatory rehearsal system uses brain areas
call of the stimulus; meaningless noise does not disrupt necessary for speech production, such as Broca’s area and/
stimuli material. This effect is the same for phonologically or the supplementary motor area (Muller & Knight, 2006).
similar or dissimilar items (Salame & Baddeley, 1987). Visuospatial Sketchpad. Similar to the function of the
Preventing rehearsal (articulatory suppression) further phonological loop for verbal material, the visuospatial
decreases performance (Baddeley, 1999); when participants sketchpad allows for the maintenance of temporary
 Central Executive C 519

representations of visuospatial information. The visuo- ‘‘override’’ the CS when the CS fails or no known schema
spatial sketchpad is involved in such tasks as visual imag- exists (Shallice, 1982).
ery and mental rotation. Evidence for this system comes Additional attentional processes that have been ascribed
from the finding that visuospatial immediate memory can to the central executive include focusing, dividing, and
be disrupted by visual tracking, but not by verbal coding switching attention, as well as serving as the interface be- C
(Baddeley, 1999). There seems to be separate subsystems tween the subsystems described above and long-term mem-
involved in the maintenance of visual information (shape, ory (Baddeley, 2001). With regard to focusing attention,
color) and spatial information, independent of the central participants in a chess game were impaired by interference
executive (Klauer & Zhao, 2004). In addition, there also from a random digit generation task; this was thought to
appears to be a dissociation of this system into two com- place a heavy load on the central executive (Robbins et al.,
ponents, a passive store that maintains information, and 1996). With regard to dividing attention, participants
a more active device that manipulates it (Bruyer & with Alzheimer’s disease who have long-term memory and
Scailquin, 1998). attentional deficits are impaired on dual-task paradigms,
The visuospatial sketchpad appears to be principally yet are able to do the same tasks individually (MacPherson
represented within the right hemisphere (Baddeley, 2000). et al., 2007). There is a question as to whether switching is
Within this component, as noted above, past research has primarily an executive process, though there also appears
indicated that there is a neuroanatomical differentiation to be a strong relationship between the phonological loop
between object and spatial information. Using evidence and switching.
from the parietal and temporal visual streams, it is likely Research has indicated that the prefrontal cortex,
that the parietal lobe (dorsal stream) processes spatial especially the dorsolateral prefrontal region, is critical
information (i.e., where – the relation of objects across for executive functioning (Collette et al., 1999; D’Esposito
coordinates) while the temporal lobe (ventral stream) et al., 1995; Owen, Evans, & Petrides, 1996; Salmon et al.,
processes nonspatial (i.e., what – as in a visual image or 1996). However, more recent studies have indicated that,
object information); this subdivision also possibly although the PFC appears essential for executive function-
extends into dorsal and ventral regions of the prefrontal ing, other brain regions may also be important for these
cortex, and these regions are most relevant for short-term, functions (Baddeley & Wilson, 1988; Baker et al., 1996;
or working memory processes (Goldman-Rakic & Leung, Berman et al., 1995; Nagahama et al., 1996).
2002). Episodic Buffer. As mentioned above, the episodic buff-
Central Executive. The central executive has been er was developed in response to a need for a component to
described as a ‘‘homunculus,’’ or ‘‘little man’’ who makes relate between working and long-term memory (Baddeley,
decisions as to how the slave systems should be used. It is a 2000). The episodic buffer is envisioned as a temporary
limited capacity attentional system that is in charge of the storage system controlled by the central executive, as well
phonological loop and visuospatial sketchpad (Baddeley, as an interface between multiple systems. The central
1999). Although the central executive may be considered executive can retrieve information from the store, and
the most important component of this model, given the potentially manipulate or modify it. There were multiple
apparent complexity of this system, it is difficult to investi- weaknesses to the initial three-component theory that this
gate. Baddeley (1986) coined the term dysexecutive syn- multicomponent model has attempted to address. For
drome (DES) to describe dysfunctions of the central example, with articulatory suppression (interference of
executive. encoding of numbers) of the phonological loop, short-
Baddeley has compared the central executive to Norman term span becomes shorter, but does not completely dis-
and Shallice’s ideas of the supervisory attentional system appear (Baddeley, 1984). In addition, participants can
(SAS; Shallice, 1982), which is used in planning, decision- remember more in sentences or in paragraphs than
making, novel situations, and difficult situations. Cont- would be anticipated solely based upon the phonological
ention scheduling (CS) is a process that chooses one store. There appears to be a distinction between immedi-
response and inhibits another, in a ‘‘crude and fast’’ way. ate recall and delayed prose recall, with disparate subsys-
CS modulates the selection of an action schema when it is tems implicated in each (Wilson & Baddeley, 1988). The
routine, or unconscious, selecting the schema with the episodic buffer appears to be preserved in patients with
‘‘strongest triggers.’’ The SAS is a higher level system that impaired LTM (Baddeley, 2000), and plays an important
is ‘‘slow and flexible.’’ It is utilized when a selection is role in sending information to and retrieving information
more complex, and adjusts the activation level of the from LTM. Although there is minimal research specifically
action schemas. Therefore, the SAS can actually examining the neuroanatomical basis of this component,
520 C Central Executive

it appears likely that the frontal lobes are involved in Berman, K. F., Ostrem, J. L., Randolph, C., Gold, J., Goldberg, T. E.,
Coppola, R., et al. (1995). Physiological activation of a cortical
these processes. Specifically, there appears to be greater
network during performance of the Wisconsin card sorting test: A
right frontal activation for integration of information positron emission tomography study. Neuropsychologia, 33(8),
(Prabhakaran, Narayanan, Zhao, & Gabrieli, 2000). 1027–1046.
Baddeley’s theory provided a framework for the Brooks, L. R. (1968). Spatial and verbal components of the act of recall.
initial study of working memory processes, addressing Canadian Journal of Psychology, 22, 349–368.
Bruyer, R., & Scailquin, J. C. (1998). The visuospatial sketchpad for
weaknesses of earlier models of STM that did not suffi-
mental images: Testing the multicomponent model of working
ciently account for many important pieces of information. memory. Acta Psychologica (Amsterdam), 98(1), 17–36.
Although there have been additions to the model since its Collette, F., Salmon, E., Van der Linden, M., Chicherio, C., Belleville, S.,
initial conception, Baddeley’s ideas continue to be relevant Degueldre, C., et al. (1999). Regional brain activity during tasks
today, and this work has informed, and continues to in- devoted to the central executive of working memory. Cognitive
Brain Research, 7(3), 411–417.
form, multiple avenues of research within the field.
D’Esposito, M., Detre, J. A., Alsop, D. C., Shin, R. K., Atlas, S., &
Grossman, M. (1995). The neural basis of the central executive
system of working memory. Nature, 378(6554), 279–281.
Cross References Goldman-Rakic, P. S., & Leung, H. (2002). Functional architecture of the
dorsolateral prefrontal cortex in monkeys and humans. In D. T. S. R.
T. Knight (Ed.), Principles of frontal lobe function (pp. 85–95). New
▶ Attention/Executive Functions
York: Oxford University Press.
▶ Controlled Attention Klauer, K. C., & Zhao, Z. (2004). Double dissociations in visual and
▶ Dysexecutive Syndrome spatial short-term memory. Journal of Experimental Psychology: Gen-
▶ Working Memory eral, 133(3), 355–381.
MacPherson, S. E., Della Sala, S., Logie, R. H., & Wilcock, G. K. (2007).
Specific AD impairment in concurrent performance of two memory
tasks. Cortex, 43(7), 858–865.
References and Readings Muller, N. G., & Knight, R. T. (2006). The functional neuroanatomy of
working memory: Contributions of human brain lesion studies.
Baddeley, A. D. (1966a). The influence of acoustic and semantic similarity Neuroscience, 139(1), 51–58.
on long-term memory for word sequences. Quarterly Journal of Nagahama, Y., Fukuyama, H., Yamauchi, H., Matsuzaki, S., Konishi, J.,
Experimental Psychology, 18(4), 302–309. Shibasaki, H., et al. (1996). Cerebral activation during performance
Baddeley, A. D. (1966b). Short-term memory for word sequences as a of a card sorting test. Brain, 119(Pt 5), 1667–1675.
function of acoustic, semantic and formal similarity. Quarterly Jour- Owen, A. M., Evans, A. C., & Petrides, M. (1996). Evidence for a two-
nal of Experimental Psychology, 18(4), 362–365. stage model of spatial working memory processing within the lateral
Baddeley, A. D. (1984). Exploring the articulatory loop. Quarterly Journal frontal cortex: A positron emission tomography study. Cerebral
of Experimental Psychology, 36, 233–252. Cortex, 6(1), 31–38.
Baddeley, A. (1986). Working memory. Oxford: Clarendon. Prabhakaran, V., Narayanan, K., Zhao, Z., & Gabrieli, J. D. (2000).
Baddeley, A. (1992). Working memory. Science, 255(5044), 556–559. Integration of diverse information in working memory within the
Baddeley, A. D. (1999). Essentials of human memory. East Sussex: frontal lobe. Nature Neuroscience, 3(1), 85–90.
Psychology Press. Repovs, G., & Baddeley, A. (2006). The multi-component model
Baddeley, A. (2000). The episodic buffer: A new component of working of working memory: Explorations in experimental cognitive psy-
memory? Trends in Cognitive Science, 4(11), 417–423. chology. Neuroscience, 139(1), 5–21.
Baddeley, A. D. (2001). Is working memory still working? American Robbins, T. W., Anderson, E. J., Barker, D. R., Bradley, A. C., Fearny-
Psychologist, 56(11), 851–864. hough, C., Henson, R., et al. (1996). Working memory in chess.
Baddeley, A. D., & Hitch, G. (1974). Working memory. In G. A. Bower Memory & Cognition, 24(1), 83–93.
(Ed.), Recent advances in learning and motivation. New York: Salame, P., & Baddeley, A. (1987). Noise, unattended speech and short-
Academic. term memory. Ergonomics, 30(8), 1185–1194.
Baddeley, A. D., & Wilson, B. (1985). Phonological coding and short- Salmon, E., Van der Linden, M., Collette, F., Delfiore, G., Maquet, P.,
term memory in patients without speech. Journal of Memory and Degueldre, C., et al. (1996). Regional brain activity during working
Language, 24, 490–502. memory tasks. Brain, 119(Pt 5), 1617–1625.
Baddeley, A., & Wilson, B. (1988). Frontal amnesia and the dysexecutive Shallice, T. (1982). Specific impairments of planning. Philosophical Trans-
syndrome. Brain and Cognition, 7(2), 212–230. actions of the Royal Society of London. Series B, Biological Sciences, 298
Baddeley, A., Gathercole, S., & Papagno, C. (1998). The phonological (1089), 199–209.
loop as a language learning device. Psychological Review, 105(1), Waters, G. F., Rochon, E., & Caplan, D. (1992). The role of high-level
158–173. speech planning in rehearsal: Evidence from patients with apraxia of
Baker, S. C., Rogers, R. D., Owen, A. M., Frith, C. D., Dolan, R. J., speech. Journal of Memory and Language, 31, 54–73.
Frackowiak, R. S., et al. (1996). Neural systems engaged by planning: Wilson, B., & Baddeley, A. (1988). Semantic, episodic, and autobiograph-
A pet study of the tower of London task. Neuropsychologia, 34(6), ical memory in a postmeningitic amnesic patient. Brain and Cogni-
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 Cerebellar Cognitive Affective Syndrome C 521

pressure results from the thrombosis, then surgical

Central Neurocytoma placement of a ventriculoperitoneal shunt is considered.
Survival rate exceeds 90%, full recovery occurs in 88% of
▶ Neurocytoma the survivors, and recurrence rate is about 2%.
C
Cross References
Central Venous Thrombosis
▶ Anticoagulation
E LLIOT J. R OTH ▶ Antiplatelet Therapy
Northwestern University ▶ Cerebrovascular Disease
Chicago, IL, USA ▶ Heparin
▶ Ischemic Stroke
▶ Thrombolysis
Synonyms ▶ Thrombosis
▶ Venous Thrombosis
Cerebral thrombophlebitis; Cerebral venous thrombosis; ▶ Warfarin
Dural sinus thrombosis; Intracranial venous thrombosis;
Sagittal sinus thrombosis; Sinus thrombosis
References and Readings

Ferro, J. M., Canhão, P., Bousser, M. G., Stam, J., & Barinagarrementeria,
Definition F. (2005). Cerebral vein and dural sinus thrombosis in elderly
patients. Stroke, 36, 1927–1932.
Central venous thrombosis is a rare form of stroke Stam, J. (2005). Thrombosis of the cerebral veins and sinuses.
that results from thrombosis (blood clot) of the veins in New England Journal of Medicine, 352(17), 1791–1798.
the dura mater that surround and drain blood from
the brain.

Current Knowledge Cephalalgia

▶ Headache
Symptoms may include headache, abnormal vision,
▶ Post-traumatic Headache
seizures, and any of the symptoms of stroke such as
weakness of the face and limbs on one side of the body.
Diagnosis is usually made by computed tomography
(CT/CAT) or magnetic resonance imaging (MRI) scan-
ning, using radiocontrast to demonstrate obstruction of
the venous sinuses by thrombus. In about 80% of patients CERAD
with this condition, it occurs in the setting of a preexisting
underlying clotting disorder such as Protein C deficiency, ▶ Consortium to Establish a Registry on Alzheimer’s
Protein S deficiency, hyperhomocysteinemia, nephrotic Disease
syndrome, antiphospholipid antibody syndrome, preg-
nancy, oral contraceptive use, systemic lupus erythemato-
sus, Wegener’s granulomatosis, and sarcoidosis, and
infections such as otitis, mastoiditis, and meningitis. For
this reason, a search for these conditions should be Cerebellar Cognitive Affective
undertaken. Syndrome
Treatment relies on the administration of anticoagu-
lants, or rarely, thrombolytic agents. If raised intracranial ▶ Cognitive Affective Syndrome
522 C Cerebellar Hemorrhage

Salvati, M., Cervoni, L., Raco, A., & Delfini, R. (2001). Spontaneous
Cerebellar Hemorrhage cerebellar hemorrhage: Clinical remarks on 50 cases. Surgical
Neurology, 55, 156–161.

E LLIOT J. R OTH
Northwestern University
Chicago, IL, USA
Cerebellar Mutism
Synonyms J ACQUELINE L. C UNNINGHAM
The Children’s Hospital of Philadelphia
Posterior fossa hemorrhage Philadelphia, PA, USA

Definition
Definition
A cerebellar hemorrhage is a bleeding into the cerebellum,
A transient speech disorder typically associated with re-
the portion of the brain located posteriorly, that controls
section of cerebellar tumors, particularly medullo-
balance, coordination, and related functions.
blastomas involving the cerebellar vermis. Cerebellar
mutism can also result from stroke in the cerebrovascular
Current Knowledge distribution, affecting the cerebellar peduncles and brain-
stem. Cerebellar mutism forms part of a syndrome of
It is estimated that 10% of all intracerebral hemorrhages, or deficits, known as the posterior fossa syndrome (PFS).
about 1–2% of all strokes, are cerebellar hemorrhages. It
can be caused by high blood pressure, heavy alcohol con-
sumption, cocaine use, anticoagulant use, clotting disor- Current Knowledge
ders, cerebral vascular abnormalities such as arteriovenous
malformations and aneurysms, and cerebral amyloid Symptoms
angiopathy. Approximately two-thirds are thought to result
from hypertension. Symptoms of the hemorrhage include As part of PFS, cerebellar mutism is associated with de-
headaches, especially at the posterior and inferior area of creased or absent speech, irritability, hypotonia, ataxia,
the skull, nausea and emesis, stiff neck, dizziness and verti- and the inability to coordinate voluntary movements,
go, blurred or double vision, balance and coordination including the volitional motor aspects of speech. Mutism
deficits, speech difficulty, and altered consciousness. The occurs within the first week of surgery (or cerebrovascular
onset of symptoms is generally abrupt and dramatic. This event) and its duration may be a matter of days or weeks.
is a medical emergency, requiring immediate neurosurgical It is expected to resolve within 4 months. However, even
attention. It is diagnosed using CTor MRI scanning. Treat- with the return of functional speech, the quality of voca-
ment relies on reducing intracranial pressure and surgically lizations may lack normalcy in being hypernasal, mono-
removing the hemorrhage as quickly as possible. tone, high pitched, slowed, and/or sparse.

Cross References
Pathophysiology
▶ Hemorrhagic Stroke
▶ Intracerebral Hemorrhage Information obtained from single photon emission
▶ Intracranial Hemorrhage computerized tomography (SPECT) studies have sup-
ported the theory that cerebellar mutism results from
the effects of decreased cerebral and cerebellar blood
References and Readings
flow upon cell functioning in particular brain pathways.
These cause disruption in the cerebellar modulation
Kirollos, R. W., Tyagi, A. K., Ross, S. A., van Hille, P. T., &
Marks, P. V. (2001). Management of spontaneous cerebellar hema-
of neural circuits that link prefrontal, posterior parietal,
tomas: A prospective treatment protocol. Neurosurgery, 49, superior temporal, and limbic cortices with the
1378–1386. cerebellum.
 Cerebellum C 523

Treatment voluntary movements as well as the control of

equilibrium.
The treatment of cerebellar mutism resides in speech–
language therapy, with early goals of therapy including
the teaching of nonverbal communication as a compen- Current Knowledge C
satory strategy as well as the direct strengthening of oral-
motor functioning through the systematic practicing Embryology
of tongue and lip movements. Moreover, since cerebellar
mutism occurs within a context of broad cognitive The cerebellum originates from the metenencephalic
and affective change, a comprehensive assessment of division of the rhombencephalon, sharing the same
speech and language skills is important to identify embryologic origin with the pons.
and treat language deficits more broadly. Problems in
higher-level cognitive–linguistic functioning can include
difficulty in areas like planning and initiating communi- Anatomy
cation, verbal fluency, abstract reasoning, and working
memory. The cerebellum consists of three main lobes: anterior
(paleocerebellum or spinocerebellum), posterior (neocer-
ebellum or cerebrocerebellum), and flocculonodular
Cross References (archicerebellum or vestibulocerebellum). These lobes
are further divided to ten small lobules: lingula, folium,
▶ Brain Tumor central lobule, tuber, culmen, pyramid, declive, uvulae,
▶ Cerebellum and tonsils.
▶ Cognitive Affective Syndrome
▶ Medulloblastoma Cerebellar Peduncles
▶ Posterior Fossa The cerebellar peduncles are bundles of nerve fibers,
▶ Posterior Fossa Syndrome connecting the cerebellum with the brain stem. There
are three bundles: inferior, middle, and superior cerebellar
peduncles.
The inferior cerebellar peduncle (ICP) contains the
References and Readings dorsal spinocerebellar tract (DSCT), cuneocerebellar tract
(CCT), olivocerebellar tract (OCT), and vestibulocerebel-
Keating, R. F., Goodrich, J. T., & Packer, R. J. (2001). Tumors of the
lar tract (VCT). DSCT fibers arise from cells in the ipsi-
pediatric central nervous system. New York: Thieme.
Schmahmann, J. D., & Caplan, D. (2006). Cognition, emotion and the lateral Clarke’s column in the spinal cord (C8-L3). CCT
cerebellum. Brain, 129, 290–292. fibers arise from the ipsilateral accessory cuneate nucleus.
Schweizer, T. A., Levine, B., Rewilak, D., et al. (2008). Rehabilitation of The largest component of the OCT fibers arises from the
executive functioning after focal damage to the cerebellum. Neuror- contralateral inferior olive. VCT fibers arise from cells in
ehabilitation and Neural Repair, 22, 72–77.
both the vestibular ganglion and the vestibular nuclei, and
pass in the inferior cerebellar peduncle to reach the
cerebellum.
The middle cerebellar peduncle (MCP) contains the
Cerebellum pontocerebellar tract (PCT). These fibers arise from the
contralateral pontine gray matter.
I SLAM Z AYDAN The superior cerebellar peduncle (SCP) is the prima-
Virginia Commonwealth University ry efferent peduncle of the cerebellum. It contains fibers
Richmond, VA, USA that arise from several deep cerebellar nuclei. These
fibers pass ipsilaterally and then cross at the level of the
inferior colliculus to form the decussation of the SCP.
Definition From the SCP, these fibers will then continue rostrally
to terminate in the red nucleus and the motor nuclei of
The cerebellum, one of the three major portions of the ventral anterior (VA) and ventral lateral (VL)
the brain, is involved with the coordination of thalamus.
524 C Cerebellum

To thalamus and red nucleus cells. Golgi cells are intermediary cells located in the
Corticopontine granular layer. They receive stimulatory input (GABA)
fibers Superior cerebellar from the granular layer to inhibit granule cells.
peduncle
Cerebellum
Nuclei
Pons Purkinje cells can transmit inhibitory signals to the deep
To vestib. nuclei of the cerebellum. The most lateral nucleus,
nuclei
Pontine dentate, receives its input from the OCT and PCT and
Dentate
mossy fibers Interposed
carries planning information from the posterior parietal
Fastigial area. The interpositus nucleus (globose and emboliform)
Middle receives its Purkinje cell input from the OCT and PCT
cerebellar fibers carrying information from primary motor cortex
peduncle (area 4), DSCT, and CCT. Medially located fastigial
Inferior cerebellar nucleus receives input from the DSCT and CCT. Vestibu-
peducncle lar nuclei receive proprioceptive input from the spinal
Climbing fibers Proprioceptive cord and medullary olive.
from inferior olive information from
spinocerebellar tract
(mossy fibers) Fibers
Climbing fibers go to all parts of the cerebellum. They are
Cerebellum. Figure 1
not restricted to a particular zone. A climbing fiber sends
a collateral synapse to the deep cerebellar nuclei, which is
excitatory. The climbing fiber then ‘‘climbs up,’’ synapsing
Histology on the dendrites of the Purkinje cell. Each Purkinje cell
receives input from only one climbing fiber axon, but
Cortex each climbing fiber axon can split to innervate several
The cerebellar cortex consists of three layers from outer- Purkinje cells. The climbing fiber-Purkinje cell synapses
most to innermost: molecular, Purkinje (pyriform), and are excitatory. The OCT terminates directly on Purkinje
granular layers. The molecular layer consists mainly of cells, by-passes granule cells, and causes complex spikes in
neuropil and is the site of synapses. The majority of cells Purkinje cells.
in this layer are stellate and basket cells in addition to a Mossy fibers are the axons of DSCT, CCT, vestibulo-
few neurons. Purkinje cell layer consists of a single layer of cerebellar (VCT) and PCT carrying input to the cerebellar
large (25 micrometer) pear-shaped neurons. It is consid- cortex. They terminate and excite granule cells. Each
ered the largest cells in the nervous system. The granular mossy fiber branches profusely in the white matter. Each
layer is dense with 3–7 million neurons per cubic mm, Purkinje cell receives input from approximately >20,000
consisting of small cells with a granular cytoplasm. mossy fibers and only one climbing fiber.
Beneath the cortex lies white matter that forms the core Parallel fibers are the long axons of granule cells that
of the foliae. pass dorsally through the granule and Purkinje cell layers
to reach the molecular layer of the cerebellar cortex,
Cells where they bifurcate and run parallel to the long axis of
The cerebellum is formed of several complex cells. Stellate the folium. Parallel fibers excite a row of Purkinje cells
cells project local inhibitory output (taurine). Basket cells and in addition to a few basket cells that in turn will
also project local inhibitory output (GABA). They feed inhibit distant Purkinje cells outside the field of
forward inhibition on Purkinje cells. Purkinje cells are excitation.
stimulatory, transmitting impulses from the cerebellar The aminergic fibers originate in the Raphe nuclei and
cortex via efferent pathways. They project inhibitory out possess serotonergic input, modulating the granule and
(GABA). Granule cells have axons that run parallel to the molecular layers. This category of fibers also includes
longitudinal axis of the lobes. Granule cell excite by way of those originating from the locus ceruleus possessing
glutamate. Granule cells are only excitatory in the cere- noradrenergic input and terminating in all three cortical
bellar cortex, terminating on Golgi, basket, and Purkinje layers.
 Cerebral Amyloid Angiopathy C 525

Function References and Readings

The cerebellum receives input from all areas of the Albus, J. S. (1971). A theory of cerebellar function. Mathematical
central and peripheral nervous systems. Continuous Biosciences, 10, 25–61.
Miller, N., & Newman, N. (2005). Walsh and Hoyt’s clinical neuro-
flow of information from the spinal centers and cortical C
ophthalmology (6th ed.). Philadelphia, Pennsylvania: Lippincott
areas are integrated in the cerebellar cortex. The cere- Williams and Wilkins.
bellar output then guides the precision of different cere- Ramnani, N. (2006). The primate cortico-cerebellar system: anatomy and
bral functions namely equilibrium, planned voluntary function Nature Reviews Neuroscience, 7, 511–522.
movements, and muscle tone. The cerebellar modula- Ropper, A., & Brown, R. (2005). Adams and Victor’s principles of
neurology (11th ed.). USA: McGraw-Hill Inc.
tion of motor control is executed through its inhibitory
Strick, P. L., Dum, R. P., & Fiez, J. A. (2009). Cerebellum and nonmotor
output to the motor cortex and the descending motor function. Annual Review Neuroscience, 32, 413–434.
tracts. Guided by visual, proprioceptive, and vestibular
spinal input, the cerebellum compares the intended
force needed to execute a planned voluntary movement
with the appropriate muscle power needed to execute it. Cerebral Amyloid Angiopathy
It then modulates the tone of the agonist and antagonist
muscles through inhibitory input to the motor cortex, E LLIOT J. R OTH
the pyramidal and extrapyramidal tracts, aiming at the Northwestern University
execution in a precise manner. While this voluntary Chicago, IL, USA
movement is executed, maintenance of equilibrium re-
gardless of movement or body position is achieved
through the cerebellar output to the antigravity muscles Definition
and the vestibular centers. Eye movements are also
maintained during body movement via extensive con- Cerebral amyloid angiopathy is a syndrome characterized
nections with the occulomotor nuclei in the brain stem. by recurrent spontaneous lobar cerebral hemorrhages of
More recent data has shown that the cerebellum is various sizes and in various locations. Each hemorrhage
involved in cognitive, behavioral, and emotional proces- may be asymptomatic or may cause all of the symptoms
sing, including executive control, attention, working of lobar hemorrhages resulting from increased intracranial
memory, learning, language, pain, and emotion (Strick pressure, including severe headache, seizure, stiff neck, and
et al., 2009). vomiting; altered consciousness; paralysis or weakness and
sensory loss; cognitive and language dysfunction, often
Lesions leading to dementia after multiple episodes.
Damage to the cerebellar center or to either its inflow
or outflow tracts leads to loss of cerebellar fine tuning
Current Knowledge
modulation on different cerebral functions. Vestibulocer-
ebellar lesions can result in disequilibrium, nystagmus,
The pathological process that causes this disease is the depo-
abnormal gait, and recurrent falls. Truncal ataxia and
sition of a protein, beta-amyloid, in the walls of the arteries of
scanning speech are seen with spinocerebellar lesions.
the brain. Interestingly, this protein is identical to the one
Patients with corticocerebellar lesions can display signs
found in high quantities in the brains of patients with Alz-
of dysmetria, asynergia (decomposition of the voluntary
heimer’s disease. The incidence of cerebral amyloid angio-
movement), hypotonia, dysdiadochokinesia, and inten-
pathy is difficult to estimate, but is known to increase with
tion tremors.
advancing age. It is thought to account for 15% of all intra-
cerebral hemorrhages in patients over 60 years and up to
Cross References one-half of lobar intracerebral hemorrhages in patients older
than 70, totaling about 20 per 100,000 per year in that group.
▶ Ataxia Diagnosis is usually made based on the clinical presentation
▶ Dysdiadochokinesia and imaging of recurrent spontaneous lobar hemorrhages,
▶ Glutamate with no other predisposing problems, usually associated with
▶ Nystagmus progressive decline in function, and most often associated
▶ Proprioception with dementia. The recurrences can occur simultaneously,
526 C Cerebral Angiitis

clustered in time, or separated by years. The definitive normal, but magnetic resonance imaging of the brain is
diagnosis, based on pathological findings, is most typically abnormal in more than 90% of patients. However, the
made postmortem. Treatment is usually supportive, consist- pattern of abnormal findings is not specific. Cerebrospi-
ing of observation, symptom relief, and rehabilitation. nal fluid analysis usually reveals elevations in total protein
level or white blood cell count. Angiography has a low
sensitivity and low specificity. Treatment usually includes
Cross References cyclophosphamide and prednisone.
▶ Hemorrhagic Stroke
▶ Lobar Hemorrhage
Cross References

References and Readings ▶ Lupus Cerebritis

▶ Moyamoya Disease
Kinnecom, C., Lev, M. H., Wendell, L., et al. (2007). Course of cerebral ▶ Vasculitis
amyloid angiopathy-related inflammation. Neurology, 68, 1411–1416. ▶ Vasospasm

References and Readings

Cerebral Angiitis
Birnbaum, J., & Hellmann, D. B. (2009). Primary angiitis of the central
nervous system. Archives of Neurology, 66, 704–709.
E LLIOT J. R OTH Calabrese, L. H., Duna, G. F., & Lie, J. T. (1997). Vasculitis in the central
Northwestern University nervous system. Arthritis & Rheumatism, 40, 1189–1201.
Chicago, IL, USA Younger, D. S. (2004). Vasculitis of the nervous system. Current Opinion
in Neurology, 17, 317–336.

Synonyms

Cerebral vasculitis Cerebral Artery

▶ Anterior Cerebral Artery
Definition ▶ Internal Carotid Artery
▶ Middle Cerebral Artery
Cerebral angiitis or cerebral vasculitis is a relatively rare ▶ Posterior Cerebral Artery
disease, characterized by inflammation of the blood ves-
sels inside and leading to the brain. It may be caused
either by a primary disease of the blood vessel walls
producing inflammation or as a secondary phenomenon Cerebral Autoregulation
resulting from a systemic inflammatory disease such as
systemic lupus erythematosus or certain infections. ▶ Cerebral Blood Flow

Current Knowledge
Cerebral Blood Flow
Angiitis that is confined to the brain is relatively uncom-
mon, and is called primary angiitis of the central nervous E LLIOT J. R OTH
system (PACNS), isolated CNS vasculitis, primary CNS Northwestern University
vasculitis, or granulomatous angiitis of the nervous sys- Chicago, IL, USA
tem. It usually affects small- and medium-sized cerebral
blood vessels, but does not involve blood vessels outside
of the CNS. Headache and encephalopathy are the most Synonyms
frequent symptoms. Stroke occurs in about 20% of
patients. Blood tests reflecting inflammation are usually Cerebral autoregulation; Cerebral perfusion pressure
 Cerebral Cortex C 527

Definition
Cerebral Cortex
Cerebral blood flow is the amount of blood that goes
through the arterial tree in the brain in a given amount K IMBERLE M. J ACOBS
of time. Virginia Commonwealth University
Richmond, VA, USA
C

Current Knowledge Synonyms

In adults, cerebral blood flow is typically 750 ml per Cerebrum surface; Cortex
minute, or about 50 ml per 100 grams of brain tissue
per minute. This amount is equivalent to about 15% of
the total cardiac output. Cerebral blood flow is highly
Definition
regulated, through ‘‘autoregulation,’’ in order to meet
the metabolic demands of the functioning brain. If it is
The cerebral cortex is a structure lying on the outer
too high, it can cause elevated intracranial pressure, which
surface of the vertebrate cerebrum that is responsible for
will compress and damage brain tissue. If it is too low, it
consciousness and higher brain functions.
will fail to meet the demands of the brain, resulting
in cerebral ischemia if blood flow is less than 20 ml per
100 grams of brain tissue per minute and in cerebral
infarction if blood flow is less than 10 ml per 100 grams
Historical Background
of brain tissue per minute. Cerebral blood flow is affected
The cerebral cortex is a structure lying on the outer
by blood viscosity, blood vessel size, intracranial pressure
surface of the vertebrate cerebrum that is responsible for
level, and systemic blood pressure.
consciousness and higher brain functions, including sen-
sory perception, voluntary movement, language,
reasoning, memory, and planning. Cerebral comes from
Cross References the Latin word cerebrum, meaning brain. Cortex comes
from the Latin word for bark, which is typically an outer
▶ Atherosclerosis layer or covering. In large mammals, this structure is
▶ Diffusion-Weighted Imaging folded forming ridges known as gyri and grooves known
▶ Ischemic Penumbra as sulci. Gyri and sulci normally form in the same relative
▶ Ischemic Stroke locations from one individual to another. This folding
▶ Perfusion-Weighted Imaging increases the cortical surface area while allowing for con-
▶ Transcranial Doppler Ultrasonography straints on skull circumference. Abnormal folding of the
▶ Vasospasm cortex is associated with neurological deficits. Absent or
reduced folding in humans is known as lissencephaly
(smooth brain) and is associated with mental retardation
References and Readings and epilepsy (Leventer, Mills, & Dobyns, 2000). The ab-
normality of small regions of increased folding is known
Aaslid, R., Lindegaard, K. F., Sorteberg, W., & Nornes, H. (1989). Cerebral as polymicrogyria (many small ridges), and can also be
autoregulation dynamics in humans. Stroke, 20, 45–52.
associated with developmental delay and epilepsy (Piao
Kandel, E. R., Schwartz, J. H., & Jessell, T. M. (2000). Principles of neural
science (4th ed., p. 1305). New York: McGraw-Hill.
et al., 2005).

Current Knowledge
Cerebral Cavernous Malformation Structurally, the cerebral cortex can be divided into four
(CCM) lobes named after the overlying cranial bones: frontal,
parietal, temporal, and occipital. Prominent sulci define
▶ Angioma, Cavernous Angioma the borders of these lobes. Primary functions of the lobes
528 C Cerebral Cortex

can be ascribed as follows: occipital: vision; parietal: sense

of touch (somatosensation) and body position; frontal:
planning of action and control of movement; and tempo-
ral: hearing, visual identification, and memory. These
lobes are present in each of the two hemispheres (left
and right).
The cerebral cortex can also be divided on the basis of
phylogeny into archicortex, paleocortex, and neocortex
(oldest to newest). Archicortex consists of the hippocam-
pus, which is associated with the acquisition of memories.
Paleocortex is primarily associated with the function of
olfaction. Only mammals have neocortex. In humans, the
majority of the cerebral cortex is made up of neocortex. In
addition, as a percentage of total brain tissue, humans have
more neocortex than other species (see for example,
human relative to rat, Swanson, 1995). This is unique to
the neocortex, since evolution has not increased the size of
other brain structures, such as the cerebellum (Clark,
Mitra, & Wang, 2001). This increase in proportion is due
to increased surface area, and not to a change in the thick-
ness of the cortex, which is from 1–3 mm thick in all species. Cerebral Cortex. Figure 1 Cortical Lamination. Cresyl Violet
Cortex is made up of gray matter, where cell bodies stained coronal section from rat, showing neocortex above
predominate, and white matter that consists primarily of hippocampus (archicortex). Neocortical layers are indicated by
myelinated axons. All cortex is laminated, but the gray Roman numerals. Layer V is commonly divided into subparts
matter of neocortex has six layers (Fig. 1), while that of with layer Va containing callosal projection neurons, and Vb
the older archi-and paleocortices has three layers. Cortical containing the largest pyramidal neurons that project to
layers are differentiated based on their cellular compo- spinal cord and other subcortical locations. Within this section
nents. The basic components and lamination of cortex are of neocortex, slight differences in cytoarchitectonics can be
consistent across phylogeny. Within neocortex, the layers seen between the somatosensory cortex (Brodmann’s area 3)
are given names that represent the predominant neuronal to the right and motor cortex (Brodmann’s area 4) to the left.
cell type. The outermost layer (identified by Roman nu- Most obvious is the lack of a clear layer IV within motor cortex.
meral I), contains mainly dendrites and axons and is WM neocortical white matter; s.o. stratum oriens; s.p. stratum
called the molecular layer. Layer II is called the external pyramidale; s.r. stratum radiatum, all of the CA1 region of the
granule layer and consists of small, spherical cells. Layer hippocampus
III primarily contains small to medium pyramidal neu-
rons and is called the external pyramidal layer. Layer IV instance sending the result of motor cortical processing to
contains spiny stellate neurons and is called the internal the motor neurons of the spinal cord. Layer VI provides a
granule cell layer. Layer V contains large pyramidal neu- return feedback to the thalamus.
rons and is called the internal pyramidal layer. Layer VI Different functional regions of cortex are considered
has a variety of morphological cell types and is therefore to have primary, secondary, and association components.
called the polymorphic cell layer. These layers have differ- In sensory cortex, the primary cortical area is the region
ential functions that are consistent across different neo- that first receives information about that sense from the
cortical areas (Fig. 2). Layer I is a modulatory region and periphery (traveling by way of the thalamus). The second-
receives input from higher order cortical regions. Layers II ary cortical area is considered ‘‘higher order’’ because the
and III perform intracortical processing, receiving input input it receives is the result of cortical processing from
from the deeper layer IV, as well as from adjacent layers II the primary cortical area. Association cortex receives
and III and from the homologous cortical region in the input from several different cortical regions.
opposite hemisphere. Layer IV is the major input layer The general function of the layers is maintained across
and receives specific thalamocortical afferents in sensory cortical regions; however, there are slight changes in cell
areas of cortex. Layer V is the major cortical output, for size and packing density (cytoarchitecture) from one
 Cerebral Cortex C 529

cortical area to another. These cytoarchitectonic differ-

ences were used by Korbinian Brodmann in 1909 to draw
I boundaries presumed to identify functionally different
cortical areas.
Perpendicular to the plane of the cortical layers are C
II
functional modules called cortical columns. The idea that a
column of cortex represents a fundamental processing unit
Callosal was brought to light by Vernon Mountcastle of Johns
Hopkins University (Mountcastle, 1957). Within a column,
III neurons tend to have similar response properties. For
instance, within somatosensory cortex, the neurons within
a column have similar receptive fields (area of the receptive
surface that causes the neuron to fire action potentials).
IV Neurons of different columns have nonoverlapping recep-
tive fields. The result of evolution then has been to add
cortical columns or additional processing units.
Head trauma, stroke, and tumor may all result in
Callosal lesions of the cerebral cortex. The function lost will be
V dependent on the location of the lesion. For example,
lesion of Brodmann’s area 17 will result in loss of vision,
while lesion of Brodmann’s area 3 will result in some loss
of somatosensation including touch and pain discrimina-
tion. Damage to Brodmann’s area 4 will result in loss of
VI motor function. Lesions of the frontal cortex can cause
severe personality changes. Memory loss is typically asso-
Modulatory ciated with cortical lesions. The inability to speak occurs
Specific Nonspecific
DA
Thalamic
after destruction of Broca’s area in the ventral portion of
NE To Thalamic
Afferents the frontal lobe, typically in the left hemisphere
5-HT Spinal Cord Afferents
Superior Colliculus (Brodmann’s areas 44 and 45). Incoherent speech or
ACh
‘‘word salad’’ results from the destruction of Wernicke’s
Cerebral Cortex. Figure 2 Diagram of typical excitatory area in the upper portion of the temporal lobe (part of
neuronal cell types and connections of neocortex. Layer I, the Brodmann’s area 22).
modulatory cell layer, contains the tufts of deeper lying
pyramidal neurons, nonspecific thalamic afferents, and input
from brainstem modulatory transmitter systems. Layer II Cross References
contains primarily small granule cells. Layer III has small
pyramidal neurons that perform intracortical processing, ▶ Association Cortex
sending their axons horizontally within layer III. Layer IV ▶ Auditory Cortex
contains spiny stellate neurons that send their output to layer ▶ Brodmann’s Areas of the Cortex
III. Specific thalamic afferents make excitatory synapses within ▶ Heteromodal Cortex
layer IV on the spiny stellate cells as well as on the apical ▶ Homotypic Cortex
dendrites of deeper lying pyramidal neurons. These specific ▶ Neocortex
thalamic afferents have a smaller projection to layer VI, near ▶ Prefrontal Cortex
the border with layer V. Layer V is the major output layer for ▶ Primary Cortex
the cortex, and contains medium and large pyramidal ▶ Secondary Cortex
neurons. Layer VI contains neurons with a variety of shapes. ▶ Somatosensory Cortex
Note that inhibitory cells that make up 20% of the neurons ▶ Striate Cortex
in the neocortex are not shown here. Modulatory: Modulatory ▶ Tertiary Cortex
neurotransmitters; DA: Dopamine; NE: Norepinephrine; 5-HT: ▶ Unimodal Cortex
Serotonin; and ACh: Acetylcholine ▶ Visual Cortex
530 C Cerebral Dominance

References and Readings Vasogenic edema involves a disruption in the blood–

brain barrier with leakage of fluid from the intravascular
Clark, D. A., Mitra, P. P., & Wang, S. S. (2001). Scalable architecture in space.
mammalian brains. Nature, 411, 189–193. In cytotoxic edema, the blood–brain barrier is
Jones, E. G., & Peters, A. (Eds.). (1990). Cerebral cortex: Volume 8A:
intact, and there is an increase in the intracellular fluid
Comparative structure and evolution of the cerebral cortex, part I.
New York: Springer.
compartment.
Jones, E. G., & Peters, A. (Eds.). (1990). Cerebral cortex: Volume 8B:
Comparative structure and evolution of the cerebral cortex, part II.
New York: Springer. Cross References
Leventer, R. J., Mills, P. L., & Dobyns, W. B. (2000). X-linked malforma-
tions of cortical development. American Journal of Medical Genetics, ▶ Cerebral Perfusion Pressure
97, 213–220.
▶ Intracranial Pressure
Mountcastle, V. B. (1957). Modality and topographic properties of single
neurons in cat’s somatic sensory cortex. Journal of Neurophysiology,
20, 408–434.
Piao, X., Chang, B. S., Bodell, A., Woods, K., Benzeev, B., Topcu, M., et al. References and Readings
(2005). Genotype-Phenotype analysis of human frontoparietal poly-
microgyria syndromes. Annals of Neurology, 58(5), 680–687. Beaumont, A., Marmarou, A., & Ward, J. D. (2001). Intracranial Hyper-
Rasmussen, W., & Penfield, T. (1957). The cerebral cortex of man: A tension Mechanisms and Management. In D. G. McClone (Ed.),
clinical study of localization of function. New York: Macmillan Pediatric Neurosurgery (pp. 619–633). Philadelphia: W. B. Saunders.
Company. Greenberg, M. S. (1997). Handbook of Neurosurgery. Lakeland, FL:
Swanson, L. W. (1995). Mapping the human brain: Past, present, and Greenberg Graphics.
future. Trends in Neuroscience, 418, 471–474. Rosenblum, W. I. (2007). Cytotoxic edema: monitoring its magnitude
and contribution to brain swelling. J Neuropathol Exp Neurol, 66(9),
771–778.

Cerebral Dominance
Cerebral Embolism
▶ Hemispheric Specialization
E LLIOT J. R OTH
Northwestern University
Chicago, IL, USA

Cerebral Edema
Synonyms
G ARY T YE 1, J OHN B ROWN 2
1
Virginia Commonwealth University Embolic stroke
Richmond, VA, USA
2
Medical College of Georgia
Augusta, GA, USA Definition
A cerebral embolism is a blood clot (thrombus) that starts
Synonyms from the heart or blood vessel where the clot originates
and stops in an artery that leads to or rests within the
Cytotoxic edema; Vasogenic edema brain. The result is occlusion of the vessel and obstruction
of the flow of oxygen and blood to the brain tissue
supplied by that artery.

Definition
Current Knowledge
Cerebral edema is an increase in the water content of the
brain that leads to brain swelling. It may be divided into Cerebral embolisms cause about 15–20% of all strokes and
two broad categories: vasogenic and cytotoxic. about one-quarter of all ischemic strokes. It occurs most
 Cerebral Palsy C 531

frequently in patients who have known heart disease, in-

cluding atrial fibrillation and other arrhythmias, valve dis- Cerebral Hemisphere
ease, ‘‘mural thrombus’’ (a blood clot sitting in the left
ventricle of the heart), or other conditions. It causes symp- ▶ Frontal Lobe
toms similar to those of thrombotic strokes, but the pre- ▶ Occipital Lobe
▶ Parietal Lobe
C
sentations of embolic strokes tend to be more abrupt and
dramatic. These can include sudden onset of hemiplegia, ▶ Temporal Lobe
sensory loss, facial weakness, cognitive deficits, or speech
disturbance. Seizures or headaches are relatively common in
embolic strokes, and both of these symptoms are relatively
rare in ischemic strokes. In addition, there may be multiple Cerebral Hemorrhage
diffuse simultaneous neurological findings, which may re-
sult from multiple simultaneous emboli, known as ‘‘showers ▶ Hemorrhagic Stroke
of emboli.’’ Usually, management requires addressing the
cardiac condition and preventing subsequent emboli by
using anticoagulants, in addition to the treatment of the
cerebral infarction and its neurological consequences. Cerebral Infarction
▶ Ischemic Stroke
Cross References

▶ Anticoagulation
▶ Echocardiogram Cerebral Leukencephalopathy
▶ Infarction
▶ Ischemic Stroke ▶ Periventricular Leukomalacia
▶ Myocardial Infarction
▶ Thrombosis
▶ Warfarin
Cerebral Malformation
References and Readings ▶ Arteriovenous Malformation (AVM)

DiTullio, M. R., & Homma, S. (2002). Mechanisms of cardioembolic

stroke. Current Cardiology Reports, 4, 141–148.
Fuster, V., Rydén, L. E., Cannom, D. S., Crijns, H. J., Curtis, A. B., &
Ellenbogen, K. A. (2006). ACC/AHA/ESC 2006 Guidelines for the Cerebral Microvasculature
Management of Patients with Atrial Fibrillation: A report of the
American College of Cardiology/American Heart Association Task
Force on Practice Guidelines and the European Society of Cardiolo- ▶ Blood-Brain Barrier
gy Committee for Practice Guidelines (Writing Committee to Revise
the 2001 Guidelines for the Management of Patients With Atrial
Fibrillation): Developed in collaboration with the European Heart
Rhythm Association and the Heart Rhythm Society. Circulation,
114, e257–e354. Cerebral Palsy
Hart, R. G., Pearce, L. A., & Aguilar, M. I. (2007). Meta-analysis:
antithrombotic therapy to prevent stroke in patients who have non- K ATHLEEN K EELY M C C ANN D EIDRICK
valvular atrial fibrillation. Annals of Internal Medicine, 146, 857–867. University of Missouri-Columbia
Columbia, MO, USA

Cerebral Evoked Potentials Synonyms

▶ Event-Related Potentials Static encephalopathy
532 C Cerebral Palsy

Short Description or Definition birth raises the risk of CP, with a recent study reporting a
diagnosis of cerebral palsy among 20% of children born at
As defined by the International Workshop on the Definition or before 27 weeks of gestation versus diagnosis of 5–6%
and Classification of Cerebral Palsy, Cerebral Palsy (CP) is: of children born between 28 and 31 weeks (Ancel et al.,
2006). Reviewers note that overall rates of CP are climb-
" a group of permanent disorders of the development of
ing, while rates of CP among full-term infants have
movement and posture, causing activity limitation, that
remained stable (1.1/1,000). This suggests that increases
are attributed to non-progressive disturbances that oc-
are largely due to greater survival of preterm infants
curred in the developing fetal or infant brain. The motor
(Mukherjee & Gaebler-Spira, 2007).
disorders of cerebral palsy are often accompanied by
disturbances of sensation, perception, cognition, commu-
nication, and behavior, by epilepsy, and by secondary Natural History, Prognostic Factors,
musculoskeletal problems (Rosenbaum et al., 2007). and Outcomes

Etiology varies by birth status (preterm or full-term) and

Categorization type of CP (Menkes & Sarnat, 2000). For preterm infants,
the most common causes of CP are intraventricular hemor-
Classification schemes are critical to providers attempt-
rhage and/or periventricular leukomalacia. Risk factors for
ing to describe the disorder, measure change in func-
CP in full term infants include prenatal infections, anoxic or
tion, and provide prognostic information (Rosenbaum
ischemic injuries, genetic syndromes, brain malformations,
et al., 2007). Historically, classification has focused on two
or stroke. Atypical CP with athetoid movements is typically
features: (a) tone and (b) body part involvement (Menkes
caused by basal ganglia damage secondary to hyperbiliru-
& Sarnat, 2000). Table 1 for a summary.
binema (Mukherjee & Gaebler-Spira, 2007). A variety of
Spastic forms of CP are more common, with spastic
symptoms are associated with CP, which vary by severity
diplegia being the most common (Menkes & Sarnat, 2000).
and type of CP (Menkes & Sarnat, 2000; Mukherjee &
However, there is disagreement regarding classification
Gaebler-Spira, 2007). See Table 2 for a summary.
schemes, largely due to poor reliability (Accardo & Hoon,
2008). Recent attempts to improve classification schemes
include: (a) development of standardized examination pro- Neuropsychology and Psychology
cedures and diagnostic algorithms and (b) use of the Gross of Cerebral Palsy
Motor Functional Classification System (GMFCS), which
focuses on functional mobility without identifying abnor- As many as 30–50% of children with CP may have a
malities of tone or affected limbs (Rosenbaum et al., 2007). diagnosis of mental retardation, with increased incidence
for children with quadriplegia, more severe motor deficits,
Epidemiology full-term birth, and/or a coexisting seizure disorder
(Menkes & Sarnat, 2000; Mukherjee & Gaebler-Spira,
Prevalence rates vary from 1.3 to 3/1,000 and are stable 2007). Estimates of intellectual functioning can be diffi-
across country of origin (Clark & Hankins, 2003). Preterm cult to obtain, as apraxic speech, visual difficulties, and

Cerebral Palsy. Table 1 Traditional categorization of cerebral palsy

Type Description
Spastic cerebral palsy Increased muscle tone with movement
Spastic quadriplegia Spasticity of upper and lower limbs
Spastic diplegia Greater involvement of the legs than the arms
Spastic hemiparesis Greater involvement of one side of the body (more often the right); greater impairment
of the arm than the leg
Extrapyramidal cerebral palsy Involuntary and abnormal muscle movements: dystonia (fluctuating tone and abnormal
body postures) and/or athetoid movements (writhing movements in the extremities)
Hypotonic cerebral palsy Persistent, low muscle tone
Mixed and atypical cerebral palsy Mixture of spasticity and extrapyramidal symptoms
 Cerebral Palsy C 533

Cerebral Palsy. Table 2 Symptoms associated with CP

Domain Symptoms
Secondary muscular and Delayed development of adaptive motor skills
orthopedic symptoms Gait abnormalities C
Oral-motor difficulties and problems with speaking and drooling
Contracture (shortening of the muscle)
Bone deformities (e.g., hip subluxation/dislocation)
Scoliosis
Osteoporosis
Reduced limb growth
Neurologic symptoms Seizure disorder
Sensory Visual problems
Homonomous hemianopsia (in spastic hemiplegia)
Strabismus
Nystagmus
Visual sequela related to prematurity
Tactile/perceptual deficits
Stereognosis
Poor two-point discrimination (in spastic hemiplegia)
Neglect of affected side of the body (in spastic hemiplegia)
Hearing loss
Feeding/gastrointestinal Dysphagia and aspiration
Malnutrition requiring gastrostomy
Gastroesophageal reflux
Constipation
Incontinence or difficulty voiding
Dental Malocclusion
Poor tooth enamel
Pain and fatigue Pain associated with primary (e.g., spasticity and contractures) and secondary
(e.g., constipation) disease processes
Pain related to medical procedures
Fatigue secondary to poor mobility

fine motor deficits can limit participation in traditional disability (e.g., attractiveness, social interaction, athletics,
tests (Fennell & Dikel, 2001). Little is known about cog- academics) (Miyahara & Cratty, 2004). Adolescent girls
nitive functioning among children with CP who do not may be at particularly increased risk for low self-concept
have a diagnosis of mental retardation, reports of deficits (Shields, Murdoch, Loy, Dodd, & Taylor, 2006). Studies of
in learning (specifically arithmetic), visual-perceptual Quality of Life (QOL) suggest lower QOL for children
processing (particularly in spastic diplegia), working with CP, particularly in areas associated with CP and its
memory, and executive functioning are emerging (Blon- sequella (e.g., academics, social interaction) and most
dis, 2004; Jenks et al., 2007). notably for children with quadriplegia/more severe CP
The empirical literature regarding mental health in (Livingston, Rosenbaum, Russell, & Palisano, 2007).
children with CP is sparse. Overall, studies of children Transition to adulthood is understudied, but issues re-
with physical disabilities suggest that difficulties with garding reduced involvement in age-appropriate social
adjustment are atypical, with the exception of poor self- activities and roles, employment, and leisure activities
concept in areas directly impacted by the physical are of concern (Liptak, 2008).
534 C Cerebral Palsy

Evaluation Jongerius, & Rotteveel, 2007). Pain can be life-limiting

and may be underrecognized due to communication def-
Given the broad variability in etiology and the sparse icits and atypical pain responses in children with CP
knowledge base regarding neuropsychological function- (Houlihan, O’Donnell, Conaway, & Stevenson, 2004).
ing in CP, evaluations should be tailored to the child and Adaptation of common self-report pain assessment scales
situation. Prior to the evaluation, medical evaluations and/or use of measures that have been developed for
clarifying the child’s vision and hearing will be critical. children who have communication problems may help
Assessment measures should be chosen carefully to avoid the team to adequately evaluate and treat pain (Hadden
underestimates of function due to motor or verbal output & von Baeyer, 2005). Fatigue due to increased energy
problems (e.g., use of nonverbal tests of intelligence that expenditure during daily tasks can also impact function
minimize requirements for motor output) (Fennell & and should be addressed (Berrin et al., 2007).
Dikel, 2001). In children with marked communication
deficits, parents and educators may be interested in possi-
ble methods for alternative communication (e.g., picture Cross References
exchange systems, complex computerized devices), a
question which can be addressed through a multi-disci- ▶ Assistive Technology
plinary evaluation including a psychologist, speech–lan- ▶ Augmentative and Alternative Communication
guage pathologist, and occupational therapist. For ▶ Constraint Induced Therapy
children who are less impaired, evaluations should in- ▶ Encephalopathy
clude a broad overview of neuropsychological functions ▶ Hemiparesis
with attention to executive functioning, visual-perceptual ▶ Hemiplegia
processing, and academics. Assessments should include ▶ Interdisciplinary Team Rehabilitation
formal or informal evaluation of pain, fatigue, and psy- ▶ Periventricular Leukomalacia
chological and behavioral functioning. ▶ Prematurity and Low Birthweight

Treatment References and Readings

Accardo, P. J., & Hoon, A. H., Jr. (2008). The challenge of cerebral
Multidisciplinary treatment is considered the standard of palsy classification: The ELGAN study. Journal of Pediatrics, 153,
care for children with CP (Braddom, 2007). Children are 451–452.
involved in medical and therapeutic treatments designed Ancel, P.-Y., Livinec, F., Larroque, B., Marret, S., Arnaud, C., Pierrat, V.,
to decrease spasticity and increase function (e.g., botox et al. (2006). Cerebral palsy among very preterm children in relation
to gestational age and neonatal ultrasound abnormalities: The
injections, baclofen pump, surgical interventions, splinting
EPIPAGE cohort study. Pediatrics, 117, 828–835.
and casting, physical and occupational therapies, early inter- Berrin, S. J., Malcarne, V. L., Varni, J. W., Burwinkle, T. M., Sherman,
vention services). Although promising, treatment efficacy is S. A., Artavia, K., et al. (2007). Pain, fatigue, and school functioning
unknown for many of these interventions (Tupper, 2007). in children with cerebral palsy: A path-analytic model. Journal of
Interventions developed from a rehabilitation psy- Pediatric Psychology, 32(3), 330–337.
Blondis, T. A. (2004). Neurodevelopmental motor disorders: Cerebral
chology perspective are integral to the treatment
palsy and neuromuscular diseases. In D. Dewey & D. E. Tupper
plan, including behaviorally-based treatments to increase (Eds.), Developmental motor disorders: A neuropsychological approach
function and assessment and intervention of pain and (pp. 113–136). New York: Guilford Press.
fatigue. Constraint-induced movement therapy (CIMT) Braddom, R. L. (Ed.). (2007). Physical medicine and rehabilitation (3rd
is a promising approach that attempts to overcome ed.). Philadelphia: Elsevier, Inc.
Clark, S. L., & Hankins, G. D. V. (2003). Temporal and demographic
learned non-use of the affected limb and to promote use
trends in cerebral palsy – fact and fiction. American Journal of
of the affected limb through brain re-organization Obstetrics and Gynecology, 188, 628–633.
(Hoare, Wasiak, Imms, & Carey, 2007). Patients are re- Fennell, E. B., & Dikel, T. N. (2001). Cognitive and neuropsychological
strained from using the unaffected limb through a sling or functioning in children with cerebral palsy. Journal of Child Neurol-
glove for 2–3 weeks and behavioral techniques (e.g., shap- ogy, 16, 58–63.
Hadden, K. L., & von Baeyer, C. L. (2005). Global and specific behavioral
ing, massed practice, scaffolding, and positive reinforce-
measures of pain in children With Cerebral Palsy. Clinical Journal of
ment) are used to encourage use of the affected limb. Pain, 21(2), 140–146.
Also promising are behavioral treatments that address Hoare, B. J., Wasiak, J., Imms, C., & Carey, L. (2007). Constraint-induced
problems with drooling (Van der Burg, Didden, movement therapy in the treatment of the upper limb in children
 Cerebral Ventricles C 535

with hemiplegic cerebral palsy. Cochrane Database of Systematic the mean arterial pressure (MAP) and the intracranial
Reviews (2), CD004149.
pressure (ICP).
Houlihan, C. M., O’Donnell, M., Conaway, M., & Stevenson, R. D.
(2004). Bodily pain and health-related quality of life in children
with cerebral palsy. Developmental Medicine and Child Neurology,
46(5), 305–310.
Jenks, K. M., de Moor, J., van Lieshout, E. C. D. M., Maathuis, K. G. B.,
Cross References C
Keus, I., & Gorter, J. W. (2007). The effect of cerebral palsy on
arithmetic accuracy is mediated by working memory, intelligence, ▶ Cerebral Blood Flow
early numeracy, and instruction time. Developmental Neuropsycholo- ▶ Intracranial Pressure
gy, 32, 861–879.
Liptak, G. S. (2008). Health and well being of adults with cerebral palsy.
Current Opinion in Neurology, 21, 136–142.
Livingston, M. H., Rosenbaum, P. L., Russell, D. J., & Palisano, R. J. References and Readings
(2007). Quality of life among adolescents with cerebral palsy: What
does the literature tell us? Developmental Medicine and Child Neu-
Diringer, M. N., & Axelrod, Y. (2007). Hemodynamic manipulation
rology, 49(3), 225–231.
in the neuro-intensive care unit: cerebral perfusion pressure therapy
Menkes, J. H., & Sarnat, H. B. (2000). Perinatal asphyxia and trauma.
in head injury and hemodynamic augmentation for cerebral vaso-
In J. H. Menkes & H. B. Sarnat (Eds.), Child neurology (6th ed.,
spasm. Current Opinion in Critical Care, 13(2), 156–162.
pp. 401–466). Philadelphia: Lippincott Williams & Wilkins.
Wright, W. L. (2007). Multimodal monitoring in the ICU: when could
Miyahara, M., & Cratty, B. J. (2004). Psychosocial functions of children
it be useful? Journal of the Neurological Sciences, 261(1–2), 10–15.
and adolescents with movement disorders. In D. Dewey & D. E.
Tupper (Eds.), Developmental motor disorders: A neuropsychological
perspective (pp. 427–442). New York: Guilford.
Mukherjee, S., & Gaebler-Spira, D. J. (2007). Cerebral palsy. In R. L.
Braddom (Ed.), Physical medicine and rehabilitation (3rd ed.,
pp. 1243–1267). Philadelphia: Elsevier. Cerebral Seizures
Rosenbaum, P., Paneth, N., Leviton, A., Goldstein, M., Bax, M., Damiano,
D., et al. (2007). A report: The definition and classification
▶ Epilepsy
of cerebral palsy April 2006. Developmental Medicine and Child
Neurology – Supplementum, 109, 8–14.
Shields, N., Murdoch, A., Loy, Y., Dodd, K. J., & Taylor, N. F. (2006).
A systematic review of the self-concept of children with cerebral
palsy compared with children without disability. Developmental
Medicine and Child Neurology, 48, 151–157. Cerebral Thrombophlebitis
Tupper, D. E. (2007). Management of children with disorders of motor
control. In S. J. Hunter & J. Donders (Eds.), Pediatric neuropsycho- ▶ Central Venous Thrombosis
logical intervention: A critical review of science and practice
(pp. 338–365). Cambridge, UK: Cambridge University Press.
Van der Burg, J. J. W., Didden, R., Jongerius, P. H., & Rotteveel, J. J.
(2007). Behavioral treatment of drooling: A methodological critique
of the literature with clinical guidelines and suggestions for future
research. Behavior Modification, 31, 573–594. Cerebral Vasculitis
▶ Cerebral Angiitis
Cerebral Perfusion Pressure
G ARY T YE 1, J OHN B ROWN 2
1
Virginia Commonwealth University
Cerebral Venous Thrombosis
Richmond, VA, USA
2
Medical College of Georgia
▶ Central Venous Thrombosis
Augusta, GA, USA

Definition
Cerebral Ventricles
Cerebral perfusion pressure (CPP) is the net pressure of
flow of blood to the brain, which is the difference between ▶ Ventricles
536 C Cerebrovascular Accident (CVA)

injury is irreversible, this causes a completed ‘‘stroke,’’

Cerebrovascular Accident (CVA) which is defined as the neurological manifestations of
disease of blood vessels of the brain. Other forms of
▶ Stroke cerebrovascular disease also can occur. Inflammation
of blood vessel walls (‘‘vasculitis’’), bleeding into the
cerebral vessel walls (‘‘dissection’’), and hemorrhage, or
extravasation of blood outside of the vessels themselves
and into the brain tissue, also can cause brain damage.
Cerebrovascular Dementia These can give rise to strokes.

▶ Multi-infarct Dementia

Cross References

▶ Atherosclerosis
▶ Cerebral Angiitis
Cerebrovascular Disease ▶ Cerebral Embolism
▶ Dissection
E LLIOT J. R OTH ▶ Hemorrhagic Stroke
Northwestern University ▶ Infarction
Chicago, IL, USA ▶ Intracerebral Hemorrhage
▶ Ischemic Stroke
▶ Stroke
Definition ▶ Subarachnoid Hemorrhage
▶ Thrombosis
Cerebrovascular disease refers to the group of conditions ▶ Transcranial Doppler Ultrasonography
characterized by disease of the blood vessels that supply ▶ Vascular Dementia
blood to the brain. It can occur in the blood vessels that ▶ Vascular Malformation
lead to the brain or in the blood vessels inside the brain. ▶ Vasculitis
While it usually presents with symptoms of a stroke (the
group of clinical manifestations of cerebrovascular disease),
it can be asymptomatic, in which case it is usually detected
either by physical examination or selected imaging References and Readings
techniques.
The term ‘‘cerebrovascular accident’’ (or CVA) is Wolf, P. A., & Grotta, J. C. (2000). Cerebrovascular disease. Circulation.
incorrect and should be avoided, as there is nothing 102, IV-75.
accidental about a stroke. The term ‘‘cerebrovascular
disease’’ is a more general term than is ‘‘stroke,’’ because
‘‘cerebrovascular disease’’ includes asymptomatic or sub-
clinical disease, in addition to the clinically manifest
strokes.
Most cerebrovascular disease is obstructive in nature,
Cerebrum Surface
caused by atherosclerotic plaques that line the blood
▶ Cerebral Cortex
vessel walls and block the blood flow. If the blockage is
only partial, and is not severe enough to impair brain
function, then the disease remains asymptomatic. How-
ever, if the obstruction is severe enough to reduce blood
supply to the extent that brain injury occurs, then symp-
toms suggesting a stroke ensue. If these symptoms are CES-D
temporary and completely reversed, the phenomenon is
known as a ‘‘transient ischemic attack.’’ If the brain ▶ Center for Epidemiological Studies–Depression
 Chapple v. Ganger C 537

involved, especially neuropsychologists. These types of

CFL Test challenges question the scientific basis of one or more
of the expert’s methods, measures, or conclusions. Chal-
▶ Controlled Oral Word Association Test lenges to specific methods are brought under Frye v.
▶ F-A-S Test United States (1923) and Daubert v. Merrell Dow (1993)
▶ Verbal Fluency
C
rulings.

Cross References
CGY
▶ Daubert v. Merrell Dow
▶ Centigray

References and Readings

Chandler Exterminators Inc. v. Morris, 200 Ga. App. 816 (1992).
Chandler Exterminators v. Morris Schudel v. General Electric, 120 F. 3d 991 (1995).
(1992)
R OBERT L. H EILBRONNER
Chicago Neuropsychology Group
Chicago, IL, USA Chapple v. Ganger
R OBERT L. H EILBRONNER
Definition Chicago Neuropsychology Group
Chicago, IL, USA
The testimony of neuropsychologists is commonly
challenged by defense attorneys in cases relating to infer-
ences of subtle brain changes associated with neurotoxic Historical Background
brain injury. In the case of Schudel v. General Electric
(1995), plaintiffs accepted neuropsychological evidence In the cause of Daubert v. Merrell Dow (1993), it was ruled
for brain damage caused by organic solvents and poly- that for scientific testimony to be admissible, it has to be:
chlorinated biphenyls (PCBs). However, the federal (a) scientifically valid, and (b) relevant to the case at
appeals court from the Ninth Circuit ruled that neuro- hand. The court provided a list of guidelines intended
psychological testimony is limited only to damages and to aid in the determination of scientific validity (e.g.,
cannot determine physical causation. The court opined peer reviewed, fasifiability, acceptable error rate, etc.).
that determination of causation is relegated to medical The Daubert ruling along with subsequent related rulings
doctors (MDs) or left to the discretion of the jury to (e.g., General Electric v. Joiner, 1997, Kumho Tire v.
make connections between neurocognitive deficits pre- Carmichael, 1999), generated significant debate among
sented and exposure to toxins. In the case of Chandler psychologists and neuropsychologists, and many other
Exterminators v. Morris (1992), the Georgia Supreme disciplines. Specifically, Reed (1996) viewed the Daubert
Court ruled in favor of the trial court’s decision to ruling to necessitate the utilization of commercially avail-
prohibit neuropsychological testimony that proposed a able fixed batteries only, such as the Halsteid–Reitan Bat-
link between neurotoxicants and impaired neuropsycho- tery. However, most neuropsychologists employ a flexible
logical test scores. In response to this case, Georgia legis- battery approach; thus, contradicting Reed’s assertions
lature wrote a new law permitting neuropsychologists to implying that most neuropsychologists would not be suit-
provide testimony related to causation of brain injuries ed for involvement in forensic work. In support of his
in Georgia. Challenges to specific neuropsychological conclusion, Reed referenced the case of Chapple v. Ganger
tests and test batteries occur with some degree of fre- (1998), a brain injury claim. Review of the judge’s written
quency, and they should be taken seriously by all parties decision in Chapple v. Ganger outlined that all
538 C Charles Bonnet Syndrome

neuropsychological testimony (even partial HRB proto- Categorization

cols from two other neuropsychologists) was admitted
into evidence and the fact that the judge had placed The images associated with CBS are often rich in detail,
more emphasis on testimony from a fixed battery advo- and their clarity frequently contrasts sharply with suf-
cate was completely unrelated to the determination of the ferers’ blurred perception of real objects (Menon, Rah-
test battery. Indeed, there was no Daubert challenge to a man, Menon, & Dutton, 2003). They are sometimes
flexible test battery approach. In this particular case, only referred to as ‘‘pseudo-hallucinations’’ to indicate that
the testimony of a vocational specialist who conducted no the person experiencing them is aware that the images
testing and provided no evidence in the form of a peer- are not real. Hallucinations may vary greatly in terms of
reviewed study to support his claims, was subject to a color, clarity, movement, and bizarreness (Plummer, Klei-
Daubert hearing from the defense. nitz, Vroomen, & Watts, 2007). Nevertheless, common
themes and figures have been described, including
humans and animals, extended landscapes, and ornate
References and Readings structures (Plummer et al., 2007). Ffytche and Howard
(1999) classified their patients’ hallucinations into eight
Chapple v. Ganger, 851 F. Supp. 1481, E.D. of Washington (1994). categories (Table 1).
Daubert v. Merrell Dow Pharmaceuticals, 509 U.S. 579 (1993). While the clinical validity of this classification system
General Electric co. v. Joiner, 522 U.S. 136 (1997).
has not yet been established, it does share some simila-
Greiffenstein, M. F., & Cohen, L. (2005). Neuropsychology and the law:
Principles of productive attorney-neuropsychologists relations. In
rities with known functional and anatomical networks
G. Larrabee (Ed.), Forensic neuropsychology: A scientific approach. within the visual association cortex (Plummer et al.,
New York: Oxford University Press. 2007).
Kumho Tire Co. v. Carmichael, 526 U.S. 137 (1999).
Reed, J. E. (1996). Fixed versus flexible neuropsychological test batteries
under the Daubert standard for the admissibility of scientific
Epidemiology
evidence. Behavioral Sciences and the Law, 14, 315–322.

1. Prevalence: Once considered rare, CBS is becoming

increasingly more common (Rovner, 2006). The larger
number of reported CBS cases may be related to the
Charles Bonnet Syndrome growing population of older adults and the more
common occurrence of visual disorders such as age-
M ELISSA B UTTARO related macular degeneration, glaucoma, and cataracts
Brown University (Rovner, 2006). It has also been argued that past prev-
Providence, RI, USA alence estimates of CBS were spuriously low due to a

Synonyms/Associated Terms Charles Bonnet Syndrome. Table 1

Bonnet syndrome Hallucination Category Description

Tessellopsia Regular, overlapping patterns

Short Description or Definition Hyperchromatopsia Hyperintense, vivid, brilliant

colors
Charles Bonnet syndrome (CBS) is characterized by the Prosopometamorphopsia Facial distortions
following features (Eperjesi & Akbarali, 2004): Dendropsia Branching forms
Perseveration True percept that persists after
1. The presence of well-formed, complex, repetitive or the individual looks away
persistent visual hallucinations
Illusory visual spread Spread of a non-hallucinated
2. Full or partial retention of insight into the unreal
pattern
nature of the hallucinations
Polyopia Multiple copies of a percept
3. Absence of hallucinations in other sensory modalities
(e.g., auditory, olfactory) Micropsia/macropsia Miniaturized/‘‘larger than life’’
images
4. Absence of delusions
 Charles Bonnet Syndrome C 539

general lack of awareness of the syndrome in the medi- Charles Bonnet Syndrome. Table 2
cal community, as well as patients’ reluctance to dis-
Factors Favoring the Recurrence of Hallucinations
close their hallucinatory symptoms for fear of being
labeled psychotic or demented (Plummer et al., 2007). Dimly lit conditions
One estimate suggests that the prevalence of complex States of drowsiness C
visual hallucinations in patients with visual impairment Physical and social isolation
is between 11% and 15% (Menon et al., 2003).
2. Age of onset: CBS may occur at any age, but it is more
common in the elderly. Average age of onset tends to be
in the 70s and 80s (Plummer et al., 2007). The
increased prevalence of CBS in older adults is likely Charles Bonnet Syndrome. Table 3
related to the greater incidence of sudden visual loss
Factors that May Help Relieve Hallucinations
and/or isolation in this age group (Menon et al., 2003).
Rapid blinking
Sustained eye closure
Natural History, Prognostic Factors, Diversionary activities
Outcomes Limiting exposure to dim lighting
Walking away
Historical background: Charles Bonnet syndrome is
Looking at or approaching images
named after the eminent Swiss philosopher and naturalist
who first described this phenomenon in 1760 (Hedges,
2007). In a book entitled Essai Analytique sur les Faculties
de L’Ame [Analytical Essays Concerning the Faculties of
the Mind], Charles Bonnet described how his cognitively It has been argued that CBS is more commonly asso-
intact, 89-year-old grandfather with failing eyesight began ciated with higher degrees of visual impairment, and with
to experience well-formed visual hallucinations, which he bilateral as opposed to unilateral ocular pathology
was aware were not actually physically present. Interest- (Menon et al., 2003). It has also been suggested that it is
ingly, Charles Bonnet began to have similar experiences not the specific lesion site or the severity of impairment,
later in his own life. At the age of 22, he began to experi- but rather the rate of development of the visual im-
ence severe eye pain and progressively worsening loss of pairment that best predicts CBS (Plummer et al., 2007).
vision that made it difficult for him to use a microscope, That is, hallucinations may be more common in the
and he ultimately turned to more abstract philosophical context of sudden or unexpected decrease in visual func-
pursuits and theoretical questions in biology. In his re- tion (Menon et al., 2003).
tirement, he experienced formed visual hallucinations Outcomes: The course of CBS can be unpredictable.
associated with many of the common attributes of the While the onset is generally sudden, it may also be gradual
syndrome that shares his name, including blindness, in- (Menon et al., 2003). Hallucinations can last from seconds
tact cognition, and occurrence in quiet and reflective to hours, or even days. Clustering of episodes across days
settings. Another native of Geneva, George de Morsier, or weeks is not unusual. Three patterns of the syndrome
proposed in 1967 that visual hallucinations in older men have been described (Menon et al., 2003). The episodic
without mental deficiency be designated the syndrome of pattern, characterized by hallucinations that happen over
Charles Bonnet. a period of days to months and then permanently cease, is
Current thinking/prognostic factors: The question of reportedly the least common. In the periodic pattern,
whether visual impairment is necessary for the develop- phases of hallucinatory activity alternate with phases of
ment of CBS has been the matter of debate. Some argue remission. The continuous pattern, as its name suggests, is
that CBS is almost invariably associated with impaired characterized by unremitting hallucinations (i.e., no hal-
vision, and it may occur whenever sensory input to the lucination-free intervals) (Menon et al., 2003). Overall,
brain is decreased sufficiently to allow release phenomena. the duration of CBS can extend from days to years, and
Other researchers report that visual dysfunction, though spontaneous recurrence after a symptom-free interval is
common, is not mandatory for diagnosis, and note that possible. Interestingly, some sufferers have reported per-
CBS has been found in individuals with intact vision manent remissions of CBS in conjunction with ongoing
(Terao & Collinson, 2000). visual decline (Plummer et al., 2007).
540 C Charles Bonnet Syndrome

Neuropsychology and Psychology of Treatment

Charles Bonnet Syndrome
Treatment for CBS may not always be necessary, since
The exact pathophysiology of CBS is unclear. Although visual hallucinations often resolve spontaneously, either
Charles Bonnet suggested that the primary pathology in response to improvement or further deterioration of
was restricted to the eye, subsequent research has suggest- visual function (Menon et al., 2003). In addition, many
ed that complex hallucinations can occur in the context of patients are not distressed by their hallucinations and may
visual impairment secondary to pathology anywhere along even enjoy them. However, if hallucinations are frequent
the central visual pathway, from the orbit to the occipital or distressing, the following treatment options are
cortex (Menon et al., 2003). A leading hypothesis is that available:
complex visual hallucinations result from deafferentation
1. Optimizing visual acuity: Patients should initially
of the visual association cortex following lesions among
be referred to a low-vision specialist, who may be
the central visual pathway. Age-related macular degenera-
able to reduce or alleviate hallucinations by optimiz-
tion is a commonly cited cause of CBS, but other ocular
ing visual function (e.g., via prescription eyeglasses or
pathologies include glaucoma, central retinal artery oc-
visual aids). If appropriate, the patient might be con-
clusion, and optic neuritis (Plummer et al., 2007). Extrao-
sidered for surgery (e.g., cataract surgery or neurosur-
cular and central visual axis pathologies associated with
gical procedures). Several reports indicate that
CBS include lesions of the pituitary and optic chiasm,
improvement of visual function, either spontaneously
meningioma, and occipital stroke.
or by intervention, can effectively decrease or even
eliminate hallucinations (Menon et al., 2003).
Evaluation 2. Supportive treatment: A key component in the man-
agement of CBS is supportive. Patients may derive
The evaluation of CBS should begin with a clinical comfort from sympathetic explanations that their hal-
interview, which should be approached carefully in lucinations are not uncommon, are not necessarily a
light of sufferers’ frequent reluctance to disclose hallu- marker of psychiatric disease, and may represent a
cinatory experiences. The clinician should assess the release phenomenon in the context of visual im-
nature of the hallucinations, the modalities in which pairment. Using the analogy of ‘‘phantom visions,’’
they occur, the presence of delusions, and the patient’s similar to a phantom limb syndrome, may be helpful
insight. It is important to note that insight into the (Rovner, 2006).
illusory nature of the hallucinations may not occur 3. Psychotherapeutic strategies: Psychotherapeutic techni-
immediately; in fact, there may be a period of initial ques used for phantom limb pain, including distrac-
deception, especially if the perceived images are not tion, hypnosis, relaxation training, and cognitive
uncommon and fit realistically into the patient’s sur- restructuring can help reduce the unpleasant effects
roundings (Menon et al., 2003). Referrals to an ophthal- of intrusive and upsetting visual hallucinations
mologist, low-vision specialist, and neuropsychiatrist may (Menon et al., 2003). Support or psychoeducational
be helpful. groups are useful settings in which sufferers can meet,
A key issue for clinical neuropsychologists is the differ- obtain reassurance, and be given advice about specific
ential diagnosis of CBS from other causes of visual hallu- techniques for reducing hallucinations (Eperjesi &
cinations. Conditions belonging in the differential include Akbarali, 2004).
migraine, occipital seizures, peduncular hallucinosis (usu- 4. Behavioral/environmental modifications: Approaches
ally from rostral brainstem infarct), drug-induced states, such as rapid eye blinking, sustained eye closure,
psychiatric disease, delirium, and dementia. In particular, minimizing fatigue and stress, and engaging in dis-
CBS may occur in the early stages of dementia with Lewy tracting activities (e.g., listening to the radio and
bodies (DLB), and as cognitive function declines, insight attending to household chores) may help reduce hal-
about the unreal nature of the hallucinations vanishes lucinations. Limiting exposure to dim lighting (e.g.,
(Terao & Collinson, 2000). Some have suggested the by increasing lighting in the home in the evening) and
term Charles Bonnet Plus or CBS plus to describe visual taking steps to reduce glare may also be helpful. Look-
hallucinations that occur in the presence of a neuropsy- ing directly at the images, attempting to approach
chiatric disorder (Eperjesi & Akbarali, 2004; Menon et al., them, and conversing with them have also been
2003). reported to stop hallucinations (Menon et al., 2003).
 CHART Short Form C 541

Since solitude and loneliness, particularly during the

evening hours, tend to heighten hallucinations, CHART
strengthening social networks and increasing the
amount of time spent interacting with others may be ▶ Craig Handicap Assessment and Reporting Technique
useful (Plummer et al., 2007). C
5. Pharmacological interventions: Referral to a specialist
for pharmacological therapy may be helpful. A few
case studies have reported efficacy of pharmacological
agents in alleviating symptoms, such as sodium
CHART Short Form
valproate, olanzapine, and carbamazepine (Plummer
G ALE G. W HITENECK
et al., 2007). Use of other medications (e.g., risperi-
Craig Hospital
done, gabapentin, and diazepam) has also been
Englewood, CO, USA
described (Eperjesi & Akbarali, 2004).
6. Follow-up: Since some cases of CBS do go on to devel-
op dementia, it is recommended that clinicians follow
patients with complex visual hallucinations carefully
Synonyms
over time (Menon et al., 2003). Though most patients
CHART-SF; Craig handicap assessment and reporting
experience no practical problems associated with CBS,
technique (CHART) short form
continuous visual hallucinations can interfere with
navigation and driving, and patients’ ability to per-
form daily activities safely should be monitored over
time (Menon et al., 2003).
Definition

The Craig Handicap Assessment and Reporting

Technique Short Form (CHART-SF) is a 19-item measure
Cross References of handicap or level of societal participation. Released in
1998, the CHART-SF is the short version of the 32-item
▶ Dementia with Lewy Bodies CHART instrument designed to provide a simple,
▶ Macropsia objective measure of the degree to which impairments
▶ Micropsia and disabilities result in handicaps (societal participation
▶ Visual Hallucinations limitations) for adolescents and adults (15 years and
older) in the years after initial rehabilitation. Like its
precursor, the CHART-SF includes six subscales (physical
independence, cognitive independence, mobility, occupa-
References and Readings tion, social integration, and economic independence),
which closely reflect the disablement model developed
Eperjesi, F., & Akbarali, N. (2004). Rehabilitation in Charles Bonnet by the World Health Organization, published in 1980
syndrome: A review of treatment options. Clinical and Experimental
and revised in 2001. Each subscale contains from 2 to 5
Optometry, 87(3), 149–152.
Ffytche, D. H., & Howard, R. J. (1999). The perceptual consequences of
questions, which together quantify the extent to which
visual loss: ‘Positive’ pathologies of vision. Brain, 122(Pt 7), individuals fulfill various social roles. CHART-SF focuses
1247–1260. on objective, observable criteria that are easily quantifi-
Hedges, T. R. (2007). Charles Bonnet, his life, and his syndrome. Survey of able and unlikely to be open to subjective interpretation.
Ophthalmology, 52(1), 111–114.
Each of the domains or subscales of the instrument have a
Menon, G. J., Rahman, I., Menon, S. J., & Dutton, G. N. (2003). Complex
visual hallucinations in the visually impaired: The Charles Bonnet
maximum score of 100 points, which is considered the
Syndrome. Survey of Ophthalmology, 48(1), 58–72. level of performance typical of the average non-disabled
Plummer, C., Kleinitz, A., Vroomen, P., & Watts, R. (2007). Of Roman person. High subscale scores indicate less handicap, or
chariots and goats in overcoats: The syndrome of Charles Bonnet. higher social and community participation.
Journal of Clinical Neuroscience, 14(8), 709–714.
Although originally developed for use with persons
Rovner, B. W. (2006). The Charles Bonnet syndrome: A review of recent
research. Current Opinion in Ophthalmology, 17(3), 275–277.
with spinal cord injury, the CHART and the CHART-SF
Terao, T., & Collinson, S. (2000). Charles Bonnet syndrome and demen- have proven to be appropriate measures of societal
tia. Lancet, 355(9221), 2168. participation that can be used with individuals having a
542 C CHART-SF

range of physical or cognitive impairments. The CHART-

SF was designed to be administered by interview, either in CHEIs
person or by telephone and takes approximately 5–7 min
to administer. There is no set time period for administering ▶ Cholinesterase Inhibitors
the CHART-SF; however, it is recommended that multiple
measurements be taken over the course of a person’s
lifetime to assess the changes with adaptation to the
disability and to gain insight into changes in participation, Chelation
which may occur over time.
The 19-item CHART-SF with subscales closely B RUCE J. D IAMOND, A MANDA FAULHABER
approximating the subscale scores for the CHART long William Paterson University
form is recommended for those populations for whom Wayne, NJ, USA
time is at a minimum.

Synonyms
Current Knowledge EDTA therapy

In an effort to reduce the number of items in the original

CHART, a short form was developed. A multidimension- Short Description or Definition
al analysis was performed which showed that fewer vari-
ables were needed to obtain CHART scores. Regression Chelation therapy has been used in allopathic and in
analyses were performed on each subscale with the complementary and alternative (CAM) forms of medi-
dependent measure being the scale score and the variables cine. Claims that chelation therapy with ethylene diamine
contributing to the subscale acting as the predictor variables. tetraacetic acid (EDTA) is an effective technique for
All CHART subscale scores could be reduced by fewer controlling and treating cardiovascular disease are not
questions to reach 90% explained variance except Economic supported by systematic reviews of the literature (Ernst,
Self-Sufficiency, which using the main variables could Pittler, Stevinson, White & Eisenber, 2001; Seely, Wu &
only explain 45%. Mills, 2005). However, Chelation therapy does appear to
be highly effective and is the treatment of choice in treat-
ing heavy metal poisoning (Ernst et al., 2001). Recent
research also suggests that Chelation therapy may have
Cross References applications in the treatment of malaria (Mabeza, Love-
vsky, Gordeuk & Weiss, 1999). The therapy involves the
▶ Craig Handicap Assessment and Reporting Technique
intravenous administration of EDTA, which binds ions in
the blood, and is often used in combination with vita-
mins, trace elements, and iron supplements.
References and Readings

Whiteneck, G., Brooks, C. A., Charlifue, S., Gerhart, K. A., Mellick, D.,
Categorization
Overholser, D., et al. (1998). Guide for use of the CHART: Craig
handicap assessment and reporting technique. www.craighospital. While Chelation therapy has been used for treating lead
org/Research/CHART December 28, 2009. poisoning and vascular occlusive disease, oral chelation ther-
apy with the a-ketohydroxypyridine chelator 1,2-dimethyl-
3-hydroxypyrid-4-one (L1, INN/BAN: deferiprone) has
also been used in iron- and aluminum-overloaded patients.
A number of iron(III) chelators have also shown antimalar-
CHART-SF ial activity in vitro with the proposed mechanism of activ-
ity involving the withholding of iron from metabolic
▶ CHART Short Form pathways of the intra-erythrocytic parasite and the forma-
▶ Craig Handicap Assessment and Reporting Technique tion of toxic complexes with iron.
 Chemical AIDS C 543

History levels (Kontoghiorghes, 1995). Toxic side effects include

six cases of reversible agranulocytosis, 0–30% incidence of
Chelation therapy began in the early 1950s and was pri- transient musculoskeletal and joint pains, 0–6% of gastric
marily used to treat metal poisoning of the blood. How- intolerance, and 0–2% zinc deficiency. In the treatment of
ever, both allopathic and CAM practitioners have claimed malaria, iron chelation therapy with desferrioxamine, C
that the technique can be used to reverse the arterioscle- which is the only compound of this nature that is available
rotic disease process (e.g., peripheral arterial occlusive for use in humans, has shown clinical activity in both
disease (PAOD)). uncomplicated and severe malaria in humans (Mabeza
et al., 1999).

Evaluation
Adverse Side Effects
Studies examining the efficacy of Chelation therapy have
shown mixed results. In one authoritative systematic re-
In one systematic review, adverse effects were character-
view, it was stated that proponents of chelation therapy
ized as rare but cases of hypocalcemia and a single case of
adhere to pathophysiological models of arteriosclerosis,
increased creatinine was noted in a patient on the EDTA
which are inconsistent with current knowledge and prac-
intervention (Seely, Wu & Mills, 2005). Moreover, it was
tice (Ernst et al., 2001). In a systematic review of chelation
emphasized that if the treatment is used in lieu of proven
therapy in the treatment of malaria, it was concluded that
therapies, indirect harm to the patient could result. In
when used via oral administration, its efficacy and low
another systematic review, it was reported that EDTA
cost make it more accessible than desferrioxamine for the
treatment may be associated with life-threatening adverse
majority of patients needing iron chelation (Mabeza et al.,
effects, such as hypocalcemia and severe kidney damage,
1999).
in addition to prolonged bleeding and respiratory distress
(Ernst et al., 2001).
Treatment and Mechanisms

Typically, Chelation therapy is administered in multiple Cross References

sessions with each treatment lasting for over an hour. The
putative mechanism underlying chelation therapy is the ▶ Lead Exposure
binding of ions in the blood by EDTA. The therapy is,
generally, considered to be effective in heavy metal poi-
soning. In CAM applications, it has been used as an References and Readings
alternative to bypass surgery, based on the idea that che-
lation therapy removes harmful plaque build-up in the Ernst, E., Pittler, M. H., Stevinson, C., White, A., & Eisenber, D.
arteries (unblocking arteriosclerotic arteries) and helps (Eds.) (2001). The desktop guide to complementary and alternative
medicine: An evidence based approach. Amsterdam: Elsevier Health
prevent strokes. The mechanism is believed to involve
Sciences.
the extraction of calcium out of arteriosclerotic plaques Kontoghiorghes, G. J. (1995). New concepts of iron and aluminum
via the chelating mechanism. In a systematic review of chelation therapy with oral L1 (deferiprone) and other chelators:
randomized, placebo-controlled, double-blind trials, it A review. Analyst, 120, 845–851.
was concluded that Chelation therapy for PAOD is not Mabeza, G. F., Loyevsky, M., Gordeuk, V. R., Weiss, G. (1999). Iron
chelation therapy for Malaria: A review. Pharmacology & Therapeu-
superior to placebo, that it is associated with considerable
tics, 81, 53–75.
risks and costs, and that it should now be considered Seely, D. M., Wu, P., & Mills, E. J. (2005). EDTA Chelation therapy for
obsolete (Ernst et al., 2001). However, it should also be cardiovascular disease: A systematic review. BMC Cardiovascular
noted that using oral chelation therapy, in doses ranging Disorders, 5, 32–38.
from 55 to 100 mg kg–1 of L1 (a-ketohydroxypyridine
chelator 1,2-dimethyl-3-hydroxypyrid-4-one (L1, INN/
BAN: deferiprone)), a majority of iron-loaded patients
showed urinary iron excretion levels greater than those Chemical AIDS
accumulating from transfusions (15–35 mg d–1) and also
reductions in serum ferritin and liver iron to near normal ▶ Multiple Chemical Sensitivity
544 C Chemical Hypersensitivity Syndrome

-thalidomide. The specific manner in which chemothera-

Chemical Hypersensitivity py achieves the intended effect is contingent upon the
Syndrome particular drug(s) employed. However, cytotoxicity
usually occurs when the cell attempts to divide and before
▶ Multiple Chemical Sensitivity the repair occurs (Chabner & Longo, 2004). The proba-
bility of the intended effect on the targeted molecules
reflects the appropriate concentration of drugs, amount
or dose and timing of drug administration. Drug absorp-
tion, distribution, and penetration are also significant
Chemotherapy factors inherent in the efficacy of chemotherapy. The
precise drug dosage can be complicated because if
B RAM G OLDSTEIN the amount is too low, it may be ineffective against the
Hoag Hospital Cancer Center tumor. Conversely, if the dosage is too high, patients may
Newport Beach, CA, USA suffer from excessive toxicity. Since chemotherapy
damages healthy cells during the therapeutic process, the
treatment is associated with several harmful side effects,
Synonyms such as myelosuppression. For example, bone marrow,
which produces white blood cells, red blood cells, and
Systemic therapy blood platelets, can be damaged during chemotherapy
treatment. In particular, white blood cells and platelets
frequently drop transiently after chemotherapy, so that
Definition patients are at increased risk for infection and bleeding
during and post chemotherapy. Many chemotherapy
Chemotherapy is a systemic treatment for cancer, com- patients also suffer from nausea and vomiting because
prising cytoxic agents that target cancer cells. Normally, the drugs irritate the stomach lining and bowel. Certain
cells develop and die in an orderly and determined chemotherapy drugs also cause alopecia, or hair loss. This
fashion. However, when cancer manifests itself, the cells condition results from the chemotherapy agent adversely
intractably divide and proliferate. Chemotherapy drugs affecting the growth of hair cells, causing them to become
target these cancer cells by destroying them before they brittle and eventually break. Several chemotherapies also
continually multiply and divide. In particular, chemo- result in anorexia, severe loss of appetite, and significant
therapy interferes with or impairs the targeted molecules weight loss. Fatigue, diarrhea, and constipation are also
(e.g., DNA, proteins) during designated cellular stages, very common side effects from cancer and chemotherapy.
such as synthesis or mitosis. The majority of chemothera- Additionally, specific chemotherapy agents can cause
py drugs damage or interfere with the replication of DNA stomatitis, a condition that results in sores manifesting
and/or RNA, and are used to treat several malignancies, inside the mouth or throat. Chemotherapy is most often
particularly brain tumors, lymphomas, and leukemias. given intravenously, whereby a thin needle is inserted
Some of the chemotherapies include: alkylating agents into a patient’s vein on the hand or lower arm. Intrave-
(such as cisplatin, carboplatin, cyclophosphamide, and nous chemotherapy can also be delivered through cathe-
temozolomide) to treat brain tumors, lymphomas, and ters, ports, and pumps. The treatment is frequently given
leukemias; nitrosoureas (e.g., carmustine and lomustine) in cycles (i.e., specified treatment periods) that reflect
are indicated for the treatment of brain tumors and alternating rest periods. This is necessary because
lymphomas; antimetabolites (such as methotrexate) to patients require substantial relief to permit the body to
treat leukemias; anthracycline and related drugs recuperate, build healthy new cells, and restore strength.
(e.g., doxorubicin), which have toxic effects on the Treatment regimens may be given daily, weekly, or
heart; topoisomerase inhibitors (such as topotecan, monthly and are based upon a drug’s efficacy or toxicity.
irinotecan, and etoposide); mitotic inhibitors (e.g., vin- Chemotherapy is usually administered before (neo-ad-
blastine and vincristine), which can cause peripheral juvant) surgery or post (adjuvant) surgery. Neoadjuvant
nerve damage; and corticosteroid hormones, which can chemotherapy is intended to decrease the primary
be used to kill or slow the growth of cancer cells. There tumor’s size. This potentially mitigates the harmful
are other chemotherapies that are excluded from these effects of surgery or radiotherapy and enhances the effi-
categories, namely L-asparaginase, -hydroxyurea, and cacy of chemotherapy.
 Chemotherapy C 545

Adjuvant chemotherapy may also reduce the proba- the cell attempts to divide and before repair occurs
bility of tumor resistance to drug therapy in the event of (Chabner & Longo, 2004).
disease recurrence (Chabner & Longo, 2004). Further- The probability of the intended effect on the targeted
more, adjuvant chemotherapy is effective at destroying molecules reflects the appropriate concentration of drugs,
residual cancer cells that have spread to distal parts of amount or dose and timing of drug administration. Drug C
the body (i.e., metastasis), particularly because rapidly absorption, distribution, and penetration are also signifi-
proliferating lesions are very amenable to treatment. cant factors inherent in the efficacy of chemotherapy.
Palliative chemotherapy is indicated when the curative The precise drug dosage can be complicated because if
potential is very low and the primary goals are to decrease the amount is too low, it may be ineffective against the
the patient’s tumor burden and prolong life expectancy. tumor. Conversely, if the dosage is too high, patients may
suffer from excessive toxicity.
Since chemotherapy damages healthy cells during the
Current Knowledge therapeutic process, the treatment is associated with
several harmful side effects, such as myelosuppression.
Recent neuropsychological research has indicated that For example, bone marrow, which produces white blood
chemotherapy can also adversely impact cognitive cells, red blood cells, and blood platelets, can be damaged
functioning, both short-term and delayed. In particular, during chemotherapy treatment. In particular, white
neuropsychological research studies have provided blood cells and platelets frequently drop transiently after
evidence discussing the impact of chemotherapy on atten- chemotherapy, so that patients are at increased risk for
tion, memory, and concentration (Armstrong, Gyato, infection and bleeding during and after chemotherapy.
Awadalla, Lustig, & Tochner, 2004). Consequently, many Many chemotherapy patients also suffer from nausea
of these chemotherapy-induced cognitive impairments and vomiting because the drugs irritate the stomach lining
can significantly impair patients’ daily activities, such as and bowel. Certain chemotherapy drugs also cause alope-
working, being involved in a committed relationship, and cia or hair loss. This condition results from the chemo-
attending to personal responsibilities. Research has therapy agent adversely affecting the growth of hair cells,
suggested that many of these impairments are temporary causing them to become brittle and eventually break.
but some may be more long-term, or even permanent. Several chemotherapies also result in anorexia, severe
The cognitive effects are not uniform, and the severity loss of appetite, and significant weight loss. Fatigue, diar-
appears to reflect a higher concentration and/or larger rhea, and constipation are also very common side effects
dose of chemotherapy. from cancer and chemotherapy. Additionally, specific
Most of the different types of chemotherapy drugs chemotherapy agents can cause stomatitis, a condition
damage or interfere with the replication of DNA and/or that results in sores manifesting inside the mouth or throat.
RNA, and are used to treat several malignancies, particu- Chemotherapy is most often given intravenously,
larly brain tumors, lymphomas, and leukemias. Some of involving a thin needle, which is inserted into a patient’s
the chemotherapies include: alkylating agents (such as vein on the hand or lower arm. Intravenous chemotherapy
cisplatin, carboplatin, cyclophosphamide, and temozolo- can also be delivered through catheters, ports, and pumps.
mide) to treat brain tumors, lymphomas, and leukemias; The treatment is frequently given in cycles that reflect
nitrosoureas (e.g., carmustine and lomustine) to treat brain specified treatment periods which are alternated with
tumors and lymphomas; antimetabolites to treat leukemias rest periods. This is necessary because patients require
(such as methotrexate); anthracycline and related drugs substantial relief to permit the body to recuperate, build
(e.g., doxorubicin), which have toxic effects on the heart; healthy new cells, and restore strength.
topoisomerase inhibitors (such as topotecan, irinotecan, Treatment regimens may be given daily, weekly,
and etoposide); mitotic inhibitors (e.g., vinblastine and or monthly and are based upon a drug’s efficacy or
vincristine), which can cause peripheral nerve damage; toxicity. Chemotherapy is usually administered before
and corticosteroid hormones, which can be used to kill or (neo-adjuvant) surgery or post (adjuvant) surgery.
slow the growth of cancer cells. There are other che- Neo-adjuvant chemotherapy is intended to decrease the
motherapies that are excluded from these categories, such primary tumor’s size. This potentially mitigates the harm-
as L-asparaginase, -hydroxyurea, and -thalidomide. The ful effects of surgery or radiotherapy and enhances the
specific manner in which chemotherapy achieves the efficacy of chemotherapy.
intended effect is contingent upon the particular drug(s) Adjuvant chemotherapy is employed when there is
employed. However, cytotoxicity usually occurs when scant evidence of residual disease, but there is an increased
546 C Chief Sensory Nucleus of V

risk of cancer recurrence. Adjuvant chemotherapy may cuneatus and gracilis in the medulla, which mediate simi-
also reduce the probability of tumor resistance to drug lar input from the trunk and extremities. It gives rise to
therapy in the event of disease recurrence (Chabner & trigeminothalamic fibers, which terminate in the ventral
Longo, 2004). Furthermore, adjuvant chemotherapy is posterior medial nucleus of the thalamus.
effective at destroying residual cancer cells that have
spread to distal parts of the body (i.e., metastasis), partic-
ularly since rapidly proliferating lesions are very amenable Current Knowledge
to treatment. Palliative chemotherapy is indicated when
the curative potential is very low and the primary goals Because of its size and density, it is rare for brainstem
are to decrease the patient’s tumor burden and prolong lesions to be isolated to a single nucleus or pathway.
life expectancy. Theoretically, lesions which involve this nucleus might
most readily be distinguished on a routine neurological
exam by changes (asymmetries) in two-point discrimina-
Cross References tion on the ipsilateral face. In practice, however, such
lesions are likely to involve other brainstem nuclei and
▶ Systemic Therapy pathways, including the adjacent motor nucleus of V,
spinal trigeminal tract and/or nucleus, spinal thalamic
tracts, lateral portions of the medial lemniscus, and mid-
dle cerebellar peduncles resulting in ipsilateral muscle
References and Readings weakness of the jaw muscles, ipsilateral changes in pain
and temperature in the face and diminished or abolished
Armstrong, C. L., Gyato, K., Awadalla, A. W., Lustig, R., & Tochner, Z. A. corneal reflex, contralateral loss of pain and temperature
(2004). A critical review of the clinical effects of therapeutic irradia-
in the extremities, diminished or loss of proprioception,
tion damage to the brain: the roots of controversy. Neuropsychology
Review, 14, 65–86. stereognosis, and vibration in the contralateral extremities
Chabner, B. A., & Longo, D. L. (2004). Cancer chemotherapy and biother- (leg > arm), and ipsilateral cerebellar signs.
apy: Principles and practice. Hagerstown, MD: Lippincott, Williams &
Wilkins.
References and Readings

Gilman, S., & Newman, S. W. (2003). Manter and Gatz’s essentials of

clinical neuroanatomy and neurophysiology. Philadelphia: F.A. Davis.
Chief Sensory Nucleus of V Wilson-Pauwek, L., Akesson, E. J., Stewart, P. A., & Spacey, S. D. (2002).
Cranial nerves in health and disease. Hamilton, ON: B.C. Decker.
J OHN E. M ENDOZA
Tulane University Medical Center
New Orleans, LA, USA
Child Behavior Checklist
Synonyms T HOMAS M. A CHENBACH
University of Vermont
Principal sensory nucleus of the trigeminal nerve; Princi- Burlington, VT, USA
pal sensory nucleus of V

Synonyms
Definition
ASEBA; CBCL
Nucleus responsible for proprioceptive feedback from the
muscles of facial expression, stereognosis or fine tactual
discrimination, and vibratory sensations from the face. Description
Located in the dorsolateral pons just medial to the middle
cerebellar peduncle and inferior to the superior cerebellar The Achenbach System of Empirically Based Assessment
peduncle, it is the functional equivalent of the nuclei (ASEBA) comprises a family of forms for rating
 Child Behavior Checklist C 547

behavioral/emotional problems and adaptive characteris- interviewer who administers the SCICA to 6- to 18-year-
tics. For ages 1½ to 90þ years, developmentally appropri- olds and the Test Observation Form (TOF), which test
ate forms are designed to be completed by collaterals who examiners use to rate the behavior observed during the
know the person who is being assessed. These forms administration of individual ability and achievement tests
include versions of the Child Behavior Checklist to 2- to 18-year-olds. Table 1 summarizes the ASEBA C
(CBCL), completed by parent figures for 1½- to 5-year- forms, ages covered, who completes the forms, and refer-
olds and for 6- to 18-year-olds; the Caregiver-Teacher Re- ences to manuals for each form.
port Form (C-TRF) for ages 1½–5, completed by daycare
providers and preschool teachers; the Teacher’s Report
Form (TRF) for ages 6–18, completed by teachers and Normed Profiles
other school personnel; the Adult Behavior Checklist
(ABCL) for ages 18–59, completed by spouses, partners, Scores obtained from all ASEBA forms are displayed on
family members, friends, therapists, and other collaterals; profiles in relation to norms that are based on distribu-
and the Older Adult Behavior Checklist (OABCL) for ages tions of scale scores obtained by large samples of peers.
60 and older, completed by caregivers as well as by For the collateral and self-report forms for ages 1½ to
collaterals. 90þ years, norms are based on a US national probability
The ASEBA also includes parallel forms completed by sample of people who had not received mental health or
the people being assessed, including the Youth Self-Report substance abuse services in the preceding 12 months. For
(YSR) for ages 11–18, the Adult Self-Report (ASR) for the CBCL/6–18, TRF, and YSR, norms are provided for
ages 18–59, and the Older Adult Self-Report (OASR) for many cultures in addition to the USA, as detailed later
ages 60 and older. The collateral and self-report forms (Achenbach & Rescorla, 2007a, b). Multicultural norms
assess functioning in everyday contexts over periods of for the CBCL/1½–5 and C-TRF were released in 2010. For
2–6 months. the DOF, SCICA, and TOF, norms are based on ratings of
In addition to the collateral and self-report forms, children observed in the contexts for which these instru-
other ASEBA forms are designed for rating behavior ob- ments are designed.
served in specific situations. These forms include the Each profile displays an individual’s scale scores in
Direct Observation Form (DOF), which is completed by terms of standard scores (T scores) and percentiles based
observers who rate two or more 10-min samples of chil- on the normative sample of that individual’s peers, as
dren’s behavior observed in classrooms and other group rated by a particular type of informant (e.g., parent,
settings; the Semistructured Clinical Interview for Chil- teacher, self). The profiles also display demarcations be-
dren and Adolescents (SCICA), which provides an inter- tween the normal range, borderline clinical range, and
view protocol and a rating form completed by the clinical range on each scale. Figure 1 illustrates a profile

Child Behavior Checklist. Table 1 ASEBA assessment instruments

Instrument Ages Completed by Reference

CBCL/1½–5 1½–5 Parent figures Achenbach and Rescorla (2000)
C-TRF 1½–5 Daycare providers, preschool teachers Achenbach and Rescorla (2000)
CBCL/6–18 6–18 Parent figures Achenbach and Rescorla (2001, 2007a)
TRF 6–18 Teachers Achenbach and Rescorla (2001, 2007a)
YSR 11–18 Youths Achenbach and Rescorla (2001, 2007a)
TOF 2–18 Psychological examiner McConaughy and Achenbach (2004)
DOF 6–11 Observer McConaughy and Achenbach (2009)
SCICA 6–18 Interviewer McConaughy and Achenbach (2001)
ASR 18–59 Adults Achenbach and Rescorla (2003)
ABCL 18–59 Collaterals Achenbach and Rescorla (2003)
OASR
60 Older adults Achenbach, Newhouse, and Rescorla (2004)
OABCL
60 Collaterals Achenbach, Newhouse, and Rescorla (2004)
 548
YSR/11–18 - Syndrome scale scores for Boys (2001 version)
C
ID: 2301251405–003 Date filled: 01/08/2001 Informant: Self
Gender: Male
Name: Wayne webster Birth date: 03/03/1986 Relationship: Self
Age: 15
Clinician: Dr. Barrett Agency: CMHC
Internalizing Verified: Scanned Externalizing
100
C
95
L
90 I
T 85 N
I
S 80
C
C 75 A
O
Child Behavior Checklist

70 L
R
E 65
N
60 O
55 R
M
≤50
Anxious/ Withdrawn/ Somatic Social Thought Attention Rule-breaking Aggressive A
L
depressed depressed complaints problems problems problems behavior behavior
Total score 12 12 6 14 14 9 5 14
T score 70-C 83-C 64 80-C 77-C 63 56 67-B
Percentile >97 >97 92 >97 >97 90 73 96
1 14.Cries 2 5.EnjoysLittle 2 47.Nightm ares 2 11.Dependent 2 9.MindOff 0 1.ActsYoung 1 2.Alcohol 2 3.Argues
0 29.Fears 2 42.PreferAlone 1 51.Dizzy 2 12.Lonely 0 18.HarmSelf 0 4.FailsToFinish 0 26.NoGuilt 1 16.Mean
0 30.FearSchool 2 65.Won’tTalk 1 54.Tired 1 25.NotGetAlong 1 40.HearsThings 2 8.Concentrate 0 28.BreaksRules 0 19.DemAtten
0 31.FearDoBad 2 69.Secretive 0 56a.Aches 0 27.Jealous 2 46.Twitch 0 10.SitStill 0 39.BadFriends 1 20.DestroyOwn
0 32.Perfect 0 75.Shy 1 56b.Headaches 2 34.OutToGet 0 58.PicksSkin 2 13.Confused 0 43.LieCheat 0 21.DestroyOther
2 33.Unloved 0 102.LacksEnergy 0 56c.Nausea 2 36.GetsHurt 2 66.RepeatsActs 1 17.Daydream 0 63.PreferOlder 1 22.DisobeyHome
2 35.Worthless 2 103.Sad 0 56d.EyeProb 1 38.Teased 0 70.SeesThings 1 41.Impulsive 0 67.RunAway 1 23.DisobeySchl
2 45.Nervous 2 111.Withdrawn 1 56e.SkinProb 2 48.NotLiked 2 76.SleepsLess 1 61.PoorSchool 1 72.SetsFires 1 37.Fights
0 50.Fearful 0 56f.Stomach 1 62.Clumsy 0 83.StoresUp 2 78.Inattentive 0 81.StealsHome 0 57.Attacks
0 52.Guilty 0 56g.Vomit 1 64.PreferYoung 1 84.StrangeBehav 0 82.StealsOther 0 68.Screams
1 71.SelfConsc 0 79.SpeechProb 2 85.StrangeIdeas 1 90.Swears 1 86.Stubborn
2 91.ThinkSuic 2 100.SleepProb 1 96.ThinksSex 2 87.MoodChang
2 112.Worries 0 99.Tobacco 2 89.Suspicious
0 101.Truant 0 94.Teases
1 105.UsesDrugs 2 95.Temper
0 97.Threaten
0 104.Loud

Copyright 2001 T.M. Achenbach B = Borderline clinical range; C = Clinical range Broken lines = Borderline clinical range

Child Behavior Checklist. Figure 1 Syndrome profile scored from the Youth Self-Report completed by 15-year-old Wayne Webster (From Achenbach & Rescorla, 2001, p. 33)
 Child Behavior Checklist C 549

of syndrome scales scored from the YSR completed by McConaughy, & Howell, 1987). Consequently, profes-
15-year-old Wayne Webster (not his real name). sionals who work with children recognize the need to
obtain reports from multiple informants. Meta-analyses
of correlations between collateral and self-reports of
Scales on Which ASEBA Instruments adult psychopathology have also revealed only modest C
Are Scored correlations that argue for using multi-informant data to
assess adults (Achenbach, Krukowski, Dumenci, &
ASEBA problem items are scored on scales for syn- Ivanova, 2005).
dromes derived empirically via exploratory factor ana- Because each informant may provide valid and useful
lyses (EFAs) and confirmatory factor analyses (CFAs). information that differs from what other informants
These empirically derived syndromes reflect patterns of provide, data from multiple informants should be com-
problems found to co-occur in ratings by each kind of pared. Software for scoring ASEBA forms facilitates cross-
informant. informant comparisons by printing scores obtained from
In addition to the syndrome scales, each form is parallel forms on parallel profiles. In addition, it prints
scored on DSM-oriented scales constructed by having side-by-side comparisons of ratings by up to eight infor-
experts from many cultures select ASEBA problem items mants on all problem items that have counterparts on
that are very consistent with particular diagnostic cate- forms completed by different informants. It also prints Q
gories of the American Psychiatric Association’s (1994) correlations that measure the degree of agreement be-
Diagnostic and Statistical Manual-Fourth Edition (DSM- tween each pair of informants and compares them with
IV). Like the syndrome scales, the DSM-oriented scales Q correlations between pairs of informants in large refer-
are displayed on profiles in terms of T scores, percentiles, ence samples.
and normal, borderline clinical, and clinical ranges. Most An especially useful kind of comparison between
forms are also scored on scales comprising critical items informants’ reports is illustrated in Fig. 2. This is a com-
that are of particular concern to clinicians. parison between syndromes scored from the YSR com-
The collateral and self-report forms are additionally pleted by Wayne Webster, CBCLs completed by Wayne’s
scored on scales for favorable characteristics, such parents, and TRFs completed by three of Wayne’s tea-
as competence, adaptive functioning, and personal chers. For each syndrome, such as the Anxious/Depressed
strengths. The particular items and scales are geared to syndrome shown in the upper left-hand corner, the bars
the developmental level of people being assessed and to reflect the magnitude of standard scores (T scores)
the informants’ knowledge of people being assessed. For obtained from ratings by each kind of informant. Because
example, parents of 6- to 18-year-olds provide data re- the T scores are based on ratings by each kind of infor-
garding their children’s involvement in sports, nonsports mant for a normative sample of children, the height of the
activities, organizations, jobs and chores, friendships, and bar indicates the level of the problems reported by a
relationships with parents, siblings, and peers. Teachers particular kind of informant compared to problems
provide data on children’s academic performance and reported by that kind of informant for a normative sam-
adaptive characteristics at school. For adults, data are ple of children. For example, the leftmost bars indicate
requested regarding friendships, relations with spouse or that the Anxious/Depressed syndrome scores obtained
partner, children, job, and enrolment in educational pro- from CBCL ratings by Wayne’s parents are above the top
grams. Only the items relevant to the adult being assessed broken line compared to parents’ CBCL ratings of a
are scored. For example, adults who lack a spouse or normative sample of adolescent boys. As scores above
partner, children, job, or enrolment in educational pro- the top broken line are in the clinical range, the CBCL
grams are not scored on those items. Adult forms also bars indicate that Wayne’s parents reported more pro-
have normed scales for substance use. blems of this syndrome than were reported by parents of
97% of boys in the normative sample.

Cross-Informant Comparisons
Multicultural Norms
Meta-analyses have revealed that correlations between
parent, teacher, and self-reports of children’s problems Norms obtained in one society may not be generalizable
are typically only low to moderate (Achenbach, to other societies. To determine the degree of
 550
Cross-informant comparison - CBCL/TRF/YSR Syndrome scale T Scores (2001 version)
C
ID: 2301251405 Name: Wayne webster Gender: Male Birth date: 03/03/1986 Comparison date: 04/13/2001
Form Eval ID Age Informant name Relationship Date Form Eval ID Age Informant name Relationship Date
CBC1 001 15 Alice N. Webster Biological mother 04/04/2001 TRF5 005 15 Carmen Hernandez Classroom teacher {F} 04/11/2001
CBC2 002 15 Ralph F. Webster Biological father 04/05/2001 TRF6 006 15 Charles Dwyer Classroom teacher {M} 04/12/2001
YSR3 003 15 Self Self 04/08/2001
TRF4 004 15 George jackson Classroom teacher {M} 04/10/2001

Anxious/depressed Withdrawn/depressed Somatic complaints

100

90
Child Behavior Checklist

80

70

60

≤50
72–C 72–C 70–C 68–B 61 63 82–C 70–C 83–C 79–B 74–C 74–C 58 61 64 50 58 62
CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6

Social problems Thought problems Attention problems

100

90

80

70

60

≤50
69–B 69–B 80–C 70–C 65–B 69–B 69–B 66–B 77–C 70–C 60 66–B 71–C 76–C 63 68–B 65–B 64
CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6

Rule-breaking behavior Aggressive behavior

100
B = Borderline clinical range; C = Clinical range
90 Broken lines = Borderline clinical range

80 {F} = Female {M} = Male

70

60

≤50
57 62 56 63 53 53 73–C 73–C 67–B 82–C 65–B 67–B
CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6

Child Behavior Checklist. Figure 2 Cross-informant comparisons of syndrome scores for Wayne Webster (From Achenbach & Rescorla, 2001, p. 39)
 Child Behavior Checklist C 551

generalizability across societies, the same assessment instruments, theory, and applications, as well as directions
instruments must be administered to large representative in which the ASEBA is now moving. Translations are
samples of people in different societies. This has been available in 85 languages. Over 6,500 publications by
done with ASEBA instruments in many societies. CFAs some 9,000 authors report use of the ASEBA in 80 cultural
of CBCL, TRF, and YSR data from many societies support groups and societies (Bérubé & Achenbach, 2010). ASEBA C
the generalizability of syndromes that were initially instruments are available in paper and Internet-based
derived from US samples. Comparisons of scale scores electronic versions in many countries around the world
show that the distributions of CBCL, TRF, and YSR scores for practical assessment in clinical, educational, forensic,
in many societies approximate those obtained in the USA. and other services, as well as for research on countless
However, some societies have substantially lower or topics, such as genetics, medical conditions, outcome
higher mean scores. To take account of societal differences evaluations, epidemiology, development, diagnosis, and
in scale scores, separate sets of norms have been con- multicultural comparisons. Because the ASEBA’s concep-
structed for the societies obtaining relatively low scores, tual framework is open ended and generative, it continues
societies obtaining intermediate scores, and societies to advance in multiple directions (Achenbach, 2009).
obtaining relatively high scores. Because parent, teacher,
and self-ratings often yield different scores, the multicul-
tural CBCL, TRF, and YSR norms were constructed sepa- Psychometric Data
rately. For some societies, problem scores obtained from
one kind of informant are relatively low, while scores Table 2 summarizes psychometric data for all ASEBA
obtained from another kind of informant are intermedi- instruments in terms of mean alphas, test-retest reliability,
ate or high. For example, CBCL and TRF problem scores and the percentage of variance in ASEBA scale scores
obtained from Japanese parents and teachers are in the accounted for by clinical referral status, after partialing
low range, whereas YSR scores obtained from self-ratings out demographic effects. Many additional psychometric
by Japanese youths are in the intermediate range. findings – including goodness of fit obtained from CFAs
To enable practitioners and researchers to compare in diverse samples – are reported in ASEBA manuals and
CBCL, TRF, and YSR scores with culturally appropriate in refereed publications listed by Bérubé and Achenbach
norms, the scoring software provides options for displaying (2010).
problem scale scores in relation to norms for low-scoring,
intermediate-scoring, and high-scoring societies. For ex-
ample, CBCL and TRF scores for a Japanese youth would Clinical Uses
typically be displayed in relation to norms for low-scoring
societies. However, the youth’s YSR scores would be dis- ASEBA instruments have numerous clinical uses. Bérubé
played in relation to norms for intermediate-scoring socie- and Achenbach (2010) list publications reporting use of
ties. If the Japanese youth lived in the USA and attended an the ASEBA in relation to over 150 medical conditions.
American school, the TRF scores would be displayed in Some 600 publications report use of the ASEBA for eval-
relation to US norms for teachers’ ratings. If the youth’s uating treatments and outcomes for many kinds of psy-
parents were well acculturated to the USA, the CBCL scores chopathology and other problems.
could be displayed in relation to US norms and also in ASEBA instruments can be used at many stages of
relation to Japanese norms to see whether the scores were clinical processes, including screening to identify needs
clinically deviant according to either set of norms. for help, documentation of problems and adaptive func-
tioning for use in clinical referrals, and intake assessment
on which to base treatment decisions. During the course
Historical Background of treatment, ASEBA instruments are useful for determin-
ing whether goals are being met. Following the treatment,
The ASEBA stems from Achenbach’s (1966) factor- ASEBA instruments can be readministered to evaluate
analytic derivation of syndromes of child and adolescent outcomes and subsequent functioning. At any point,
psychopathology. Since then, over 4 decades of research ASEBA instruments can be used to assess behavioral/
and practical experience have produced ASEBA instru- emotional concomitants of neuropsychological and med-
ments for ages 1½ to 90þ years. Achenbach (2009) docu- ical disorders. The availability of similar ASEBA instru-
ments the historical development of ASEBA research, ments for children and adults facilitates family
552 C Child Behavior Checklist

Child Behavior Checklist. Table 2 Summary of ASEBA psychometric data

Alphaa Reliabilityb Validityc

Instrument Narrow Broad Narrow Broad Narrow Broad
CBCL/1½–5 0.76 0.92 0.82 0.89 11 17
C-TRF 0.80 0.94 0.78 0.85 13 20
CBCL/6–18 0.83 0.94 0.88 0.92 24 32
TRF 0.86 0.94 0.84 0.90 15 20
YSR 0.78 0.92 0.78 0.85 10 14
TOF 0.82 0.90 0.76 0.84 9 14
DOF 0.68 0.79 0.51 0.72 7 20
SCICA 0.70 0.84 0.75 0.80 9 16
ASR 0.78 0.93 0.84 0.91 10 14
ABCL 0.80 0.94 0.84 0.88 6 8
OASR 0.80 0.96 0.86 0.95 13 20
OABCL 0.83 0.97 0.94 0.95 19 29
Narrow, mean for syndrome and DSM-oriented scales; broad, mean for internalizing, externalizing, and total problems. Data are from manuals
listed in the Further Reading.
a
Cronbach’s coefficient alpha for the internal consistency of scales.
b
Pearson rs for test-retest reliability over 8- to 16-day intervals. SCICA rs are between ratings by different interviewers who interviewed children
over intervals averaging 12 days.
c
Percentage of variance accounted for by clinical referral status (referred vs. nonreferred) in multiple regressions of referral status on ASEBA scale
scores with demographic variables partialed out.

assessment, as well as close coordination between inter- Achenbach, T. M., & Rescorla, L. A. (2003). Manual for the ASEBA adult
forms & profiles. Burlington, VT: University of Vermont, Research
ventions for parents and their children.
Center for Children, Youth, and Families.
Achenbach, T. M., & Rescorla, L. A. (2007a). Multicultural supplement to
the manual for the ASEBA school-age forms & profiles. Burlington,
References and Readings VT: University of Vermont Research Center for Children, Youth, and
Families.
Achenbach, T. M. (1966). The classification of children’s psychiatric symp- Achenbach, T. M., & Rescorla, L. A. (2007b). Multicultural understanding
toms: A factor-analytic study. Psychological Monographs, 80, (No. 615). of child and adolescent psychopathology: Implications for mental health
Achenbach, T. M. (2009). The Achenbach system of empirically based assessment. New York: Guilford Press.
assessment (ASEBA): Development, findings, theory, and applications. Achenbach, T. M., & Reescorla, L. A. (2010). Multicultural guide to the
Burlington, VT: University of Vermont, Research Center for manual for the ASEBA preschool forms & profilies. Burlington, Ver-
Children, Youth, and Families. mont, University of Vermont Research Center for Children, Youth,
Achenbach, T. M., Krukowski, R. A., Dumenci, L., & Ivanova, M. Y. and Families.
(2005). Assessment of adult psychopathology: Meta-analyses and American Psychiatric Association (1994). Diagnostic and statistical man-
implications of cross-informant correlations. Psychological Bulletin, ual of mental disorders (4th ed.). Washington, DC: Author.
131, 361–382. Bérubé, R. L., & Achenbach, T. M. (2010). Bibliography of published
Achenbach, T. M., McConaughy, S. H., & Howell, C. T. (1987). Child/ studies using the Achenbach system of empirically based assessment
adolescent behavioral and emotional problems: Implications of (ASEBA). Burlington, VT: University of Vermont, Research Center
cross-informant correlations for situational specificity. Psychological for Children, Youth, and Families.
Bulletin, 101, 213–232. McConaughy, S. H., & Achenbach, T. M. (2001). Manual for the semi-
Achenbach, T. M., Newhouse, P. A., & Rescorla, L. A. (2004). Manual for structured clinical interview for children and adolescents (2nd ed.).
the ASEBA older adult forms & profiles. Burlington, VT: University of Burlington, VT: University of Vermont, Research Center for Chil-
Vermont, Research Center for Children, Youth, and Families. dren, Youth, and Families.
Achenbach, T. M., & Rescorla, L. A. (2000). Manual for the ASEBA McConaughy, S. H., & Achenbach, T. M. (2004). Manual for the test
preschool forms & profiles. Burlington, VT: University of Vermont, observation form for ages 2–18. Burlington, VT: University of
Research Center for Children, Youth, and Families. Vermont, Research Center for Children, Youth, and Families.
Achenbach, T. M., & Rescorla, L. A. (2001). Manual for the ASEBA school- McConaughy, S. H., & Achenbach, T. M. (2009). Manual for the ASEBA
age forms & profiles. Burlington, VT: University of Vermont, direct observation form for ages 6–11. Burlington, VT: University of
Research Center for Children, Youth, and Families. Vermont, Research Center for Children, Youth, and Families.
 Childhood Autism Rating Scales C 553

and the CARS was published as an appendix to the 1980

Childhood Autism article by Schopler, Reichler, DeVellis, and Daly. It was
originally intended for use by trained diagnosticians
▶ Autistic Disorder making ratings based on observation; however, the mea-
sure has been expanded for use by others (e.g., physicians, C
speech–language pathologists, special educators, and
audiologists) as well as to include information from
Childhood Autism Rating Scales other sources such as parent report and classroom obser-
vations. It is important to note that the CARS was devel-
M AUREEN G RISSOM
oped prior to the DSM-IV concept of Autism as a
University of Missouri
spectrum of disorders (Magyar & Pandolfi, 2008).
Columbia, MO, USA

Synonyms Psychometric Data

The CARS Manual (1988) describes high internal consis-

CARS
tency reliability (alpha = 0.94) and an average interrater
reliability of 0.71 for two independent raters across 280
Description cases. Test–retest reliability for 91 cases rated 1 year apart
by two separate raters was 0.88. The sensitivity of the
The childhood autism rating scale (CARS) is a 15 item CARS was 100% for a sample of 54 children with autistic
measure intended to assist in distinguishing children with disorder in a study by Rellini et al. (2003). However, there
autism spectrum disorder (ASD) from children with other is concern that the CARS may overdiagnose children with
types of delays. It is an observational scale in which each cognitive impairments as having autism with lower IQ
item is rated from 1 (within normal limits) to 4 (severely scores correlating with higher CARS scores (Perry, Con-
abnormal) and ratings include consideration of ‘‘peculiarity, dillac, Freeman, Dunn-Geier, & Belair, 2005). In addition,
frequency, and duration’’ of the behavior rated (Schopler, sensitivity in the Rellini et al. study was not as great for
Reichler, & Renner, 1988). It yields a total score ranging distinguishing children with Asperger’s disorder and per-
from 15 to 60. Scores of 30–36.5 suggest mild to moderate vasive developmental disorder-not otherwise specified
Autism and 37–60 suggest severe Autism. However, when (PDD-NOS) from children with attention-deficit/hyper-
used with adolescents and adults, the cut-off has been activity disorder (ADHD) and language delay. Despite the
decreased to 28 (Schopler et al., 1988). fact that the CARS was initially published during the time
The CARS was initially developed using a sample of of the DSM-III, the CARS has shown good agreement
1,606 children, approximately three quarters of whom were with clinical diagnosis with the DSM-IV/ICD-10 criteria
male. Sixty seven percent of the sample was white, 30% (Perry, Condillac, Freeman, Dunn-Geier, & Belair, 2005).
African American, and 3% was of other racial descent. Several studies have looked at the relations between
Within the male and female samples, the age distribution the CARS and other measures intended to assist in the
was similar with 56% age 5 years or younger, 32% between diagnostic process. In one study, the CARS and the Au-
ages 6 and 10 years, and 11% age over 10 years. Seventy one tism Diagnostic Interview-Revised (ADI-R) were found
percent of the sample had an IQ (as determined by one of to correlate 91.8% for cases in which a child received a
various measures) below 70, 17% with an IQ between 70 and diagnosis of Autism and 44.4% for those in which an
84, and 13% with an IQ above 84 (Schopler et al., 1988). Autism diagnosis was not given (Pilowsky, Yirmiya, Shul-
man, & Dover, 1998). More recently, Saemundsen, Mag-
nusson, Smari, and Sigurdardottir (2003) found a
Historical Background correlation of 0.81 between the CARS (having a total
score greater than 30) and the ADI-R (meeting cut-offs
The CARS was developed at the University of North in all three domains) in a study that included 54 children.
Carolina at Chapel Hill and was used to evaluate children Several factor analyses of the 15 items comprising the
referred to the TEACCH program. The CARS has been in CARS have been conducted. Magyar and Pandolfi
use since 1971 (Reichler & Schopler, 1971) at which point (2007) found that four components: (1) a social com-
it was called the childhood psychosis rating scale (CPRS) ponent, (2) a negative emotionality construct, (3) a
554 C Childhood Epileptic Encephalopathy with Diffuse Slow Spike-and-waves

sensory and stereotypy construct, and (4) an ‘‘activity Rating Scale (CARS). Journal of Autism and Developmental Disorders,
10, 91–103.
level and consistency of intellectual response’’ compo-
Schopler, E., Reichler, R. J., & Renner B. (1988). The Childhood Autism
nent, accounted for 57% of the variance in ratings. Rating Scale (CARS). Los Angeles, CA: Western Psychological
Services.

Clinical Uses

The CARS can be used as part of multimodal approach to

the diagnosis of ASD that ‘‘includes observation of the Childhood Epileptic
child, caregiver interview, assessment of developmental
levels, detailed developmental history, and screening
Encephalopathy with Diffuse
for associated disorders such as Fragile X’’ (Magyar & Slow Spike-and-waves
Pandolfi, 2007, p. 1787).
▶ Lennox–Gastaut Syndrome

Cross References

▶ Autism Diagnostic Interview-Revised

▶ Asperger’s Disorder Childhood or Adolescent Brain
▶ Attention-Deficit/Hyperactivity Disorder Injury
▶ Autism Diagnostic Observation Schedule
▶ Autistic Disorder ▶ Pediatric Traumatic Brain Injury
▶ Pervasive Developmental Disorder Not Otherwise
Specified
▶ TEACCH

Children’s Category Test

References and Readings
VANESSA L. R AMOS , K EITH O. Y EATES
Magyar, C. I., & Pandolfi, V. (2007). Factor structure evaluation of the Nationwide Children’s Hospital
Childhood Autism Rating Scale. Journal of Autism and Developmen-
tal Disorders, 37, 1787–1794.
Columbus, OH, USA
Perry, A., Condillac, R. A., Freeman, N. L., Dunn-Geier, J., & Belair, J.
(2005). Multi-site Study of the Childhood Autism Rating Scale
(CARS) in Five Clinical Groups of Young Children. Journal of Autism Synonyms
and Developmental Disorders, 35, 625–634.
Pilowsky, T., Yirmiya, N., Shulman, C., & Dover, R. (1998). The Autism
Diagnostic Interview-Revised and the Childhood Autism Rating
CCT
Scale: Differences between diagnostic systems and comparison be-
tween genders. Journal of Autism and Development Disorders, 28,
143–151.
Reichler, R. J. & Schopler, E. (1971). Observations on the nature of Description
human relatedness. Journal of Autism and Childhood Schizophrenia,
1, 283–296. The Children’s Category Test (CCT) is an abbreviated
Rellini, E., Tortolani, D., Trillo, S., Carbone, S., & Montecchi, F. (2004). version of the original Halstead Category Test (HCT;
Childhood Autism Rating Scale (CARS) and Autism Behavior
Checklist (ABC) Correspondence and Conflicts with DSM-IV
Reitan & Wolfson, 1992). The CCT is an individually
Criteria in Diagnosis of Autism. Journal of Autism and Developmen- administered instrument designed to measure nonverbal
tal Disorders, 34, 703–708. learning and memory, concept formation, and problem-
Saemundsen, E., Magnusson, P., Smari, J., & Sigurdardottir, S. (2003). solving abilities. The CCT consists of two levels. Level 1 is
Autism Diagnostic Interview-Revised and the Childhood Autism given to children aged 5–8 and consists of five subtests
Rating Scale: Convergence and discrepancy in diagnosing Autism.
Journal of Autism and Developmental Disorders, 33, 319–328.
and 80 items. Level 2 is given to children aged 9–16 and
Schopler, E., Reichler, R. J., DeVellis, R. F., & Daly, K. (1980). Toward consists of six subtests and 83 items. The child’s task is to
objective classification of childhood autism: Childhood Autism identify the single conceptual rule underlying the items in
 Children’s Category Test C 555

each subtest. The last subtest on both levels requires the deficits or speech/language difficulties (Boll, 1993). The
child to remember and reapply the conceptual rules from CCT can provide insights regarding a child’s cognitive
previous subtests. abilities and learning strategies in terms of difficulties in
The CCT was normed on a stratified representative memory or shifting between conceptual ideas (MacNeil
sample of 920 children in 12 age groups ranging from Horton, 1996). However, a poor score on the CCT does C
5 years to 16 years, 11 months. Administration requires not necessarily indicate a neurologically based disorder;
approximately 15–20 min. The raw score is the total rather it indicates a disruption in mental processing
number of errors (CCT Total), which is converted into (Boll, 1993).
an age-normed T-score (M = 50, SD = 10). The CCT is Studies of the CCT’s sensitivity to brain dysfunction
easy to administer and score. indicate that the measure is not consistently sensitive to
structural brain damage or neurodevelopment disorders
in children (Bello, Allen, & Mayfield, 2008; Donders,
Historical Background 1996). Results from studies examining the sensitivity of
the CCT to various forms of brain dysfunction suggest
The CCT was developed in an effort to provide an efficient that the CCT assesses multiple dimensions of problem
and well-normed children’s version of the HCT, which is solving, rather than a general construct of abstraction
well documented to be sensitive to cerebral impairment (Nesbit-Greene & Donders, 2002), which has led some
(Reiten & Wolfson, 1992), and the previous children’s to caution against relying on the total error score as the
versions of the Category Test (Reiten & Wolfson, 1993). sole index of brain dysfunction (Allen, Knatz, & Mayfield,
Concerns about lengthy administration times and expen- 2006; Bello et al., 2008). The use of the CCT with brain-
sive, bulky equipment led to the development of various injured children may be hampered by the fact that the
short forms of these tests (e.g., Short Category Test Book- overall T-score is based on six different subtests that differ
let Format), with the most comprehensive of these efforts in their sensitivity to the severity of the injury (Nesbit-
resulting in the CCT (Boll, 1993). The CCT and California Greene & Donders, 2002). Another problem with using the
Verbal Learning Test-Children’s Version (CVLT-C) were CCT with brain-injured children is that it is untimed and
standardized and normed on the same population. children are provided with corrective feedback throughout
the test administration, and these features may compensate
for any deficits in processing speed or executive function
Psychometric Data that the child may be experiencing (Donders & Nesbit-
Greene, 2004). Overall, studies investigating the use of the
Median internal consistency reliability for the CCT Total CCT with brain-injured children suggest that caution is
score is 0.88 for Level 1 and 0.86 for Level 2, with average needed in interpreting the results, and that it should be
standard errors of measurement of 3.46 and 3.74, respec- supplemented with psychometric data from additional
tively (Boll, 1993). The separate age-level values and neuropsychological tests (Donders & Nesbit-Greene,
averaged coefficients indicate that the CCT possesses a 2004; Moore, Donders, & Thompson, 2004).
high degree of internal consistency across ages. The
manual reports a variety of studies demonstrating that
the CCT consistently and significantly correlates with Cross References
other measures of achievement or cognitive ability, such
as the WISC-R and CVLT-C. ▶ Concept Learning
▶ Delis-Kaplan Executive Function System
▶ Halstead-Reitan Neuropsychological Test Battery
Clinical Uses ▶ Memory (Including Memory Impairment)
▶ Nonverbal Learning Disabilities
The CCT is a widely used test of the ability to solve ▶ Problem Solving
problems by developing and modifying strategies of
responding to various visual designs and patterns References and Readings
(Nesbit-Greene & Donders, 2002). The CCT does not
require demonstration of acquired skills, ability, or Allen, D. N., Knatz, D. T., & Mayfield, J. (2006). Validity of the children’s
knowledge, and eliminates potential confounding vari- category test-level 1 in a clinical sample of heterogeneous forms of
ables because it can be used with children with motor brain dysfunction. Archives of Clinical Neuropsychology, 21, 711–720.
556 C Children’s Memory Scale

Bello, D. T., Allen, D. A., & Mayfield, J. (2008). Sensitivity of the children’s of both immediate and delayed (30 min) recall. Each
category test level 2 to brain dysfunction. Archives of Clinical
Auditory/Verbal subtest also provides a measure of recogni-
Neuropsychology, 23, 329–339.
Boll, T. (1993). Children’s category test. San Antonio, TX: Psychological
tion recall.
Corporation. After administration of the core subtests (Table 1), the
Donders, J. (1996). Validity of short forms of the intermediate Halstead examiner can derive eight index scores: Attention/Con-
category test in children with traumatic brain injury. Archives of centration, Verbal Immediate, Verbal Delayed, Delayed
Clinical Neuropsychology, 11, 131–137.
Recognition, Visual Immediate, Visual Delayed, Learning,
Donders, J., & Nesbit-Greene, K. (2004). Predictors of neuropsychologi-
cal test performance after pediatric traumatic brain injury.
and General Memory (Fig. 1). The learning Index is
Assessment, 11(4), 275–284. derived using subtest scores from the Auditory/Verbal
MacNeil Horton, A. (1996). Book and test reviews. Archives of Clinical (Word Pairs) and the Visual/Nonverbal (Dot Locations)
Neuropsychology, 11, 171–173. domains. The General Memory Index is a measure of
Moore, B. A., Donders, J., & Thompson, E. H. (2004). Validity of the
global memory functioning and is generated using both
children’s category test-level 1 after pediatric traumatic brain injury.
Archives of Neuropsychology, 19, 1–9.
the immediate and delayed memory indexes from the
Nesbit-Greene, K., & Donders, J. (2002). Latent structure of the children’s Auditory/Verbal and Visual/Nonverbal domains.
category test after pediatric traumatic head injury. Journal of Clinical The immediate portion of the core battery takes
and Experimental Neuropsychology, 24(2), 194–199. approximately 30–40 min to administer, with an additional
Reiten, R. M., & Wolfson, D. (1992). Neuropsychological evaluation of
10–20 min required for administration of the delayed
older children. South Tucson, AZ: Neuropsychology Press.
Reiten, R. M., & Wolfson, D. (1993). The Halstead-Reitan neuropsycho-
recognition sections. Two record forms are provided for
logical test battery: Theory and clinical interpretation (2nd ed.). South students of 5–8 and 9–16 years. Scoring tables in the
Tucson, AZ: Neuropsychology Press. manual or computer software allow for conversion of raw
scores to scaled scores (mean = 10; SD = 3) at the individ-
ual subtest level and standard scores (mean = 100; SD = 15)
at the index level. Table 1 provides a brief description of
the core subtests.
Children’s Memory Scale
M ORRIS J. C OHEN
Medical College of Georgia Historical Background
Augusta, Georgia, USA
Development of the CMS began in 1985 to provide clin-
icians with a comprehensive, well-standardized, individu-
Synonyms ally administered instrument that would assess the
important processes involved in learning and memory
CMS within the pediatric population. Prior to this, traditional
psychological evaluation of children with neurological and
neurodevelopmental disorders included tests of intelli-
gence, achievement, and behavior/emotional functioning
Description with little if any attention paid to the child’s ability to learn
and remember new information. This was the case despite
The Children’s Memory Scale (CMS), published in 1997,
the fact that most referrals were in some way related to the
provides a comprehensive assessment of learning and mem-
student’s inability to learn and remember school-related
ory in children and adolescents of ages 5 through 16 years.
content. As a result, the CMS was developed with five goals
The CMS is individually administered and designed to be
in mind:
used as part of a standard psychological or neuropsycho-
logical evaluation. It assesses declarative learning and mem- 1. The development of an instrument that was consistent
ory functions across three domains: Auditory/Verbal, with current theoretical models of learning and memory.
Visual/Nonverbal, and Attention/Concentration (working 2. The development of an instrument that was sensitive
memory). Each domain contains two core subtests and to developmental changes over time.
one supplemental subtest. The subtests comprising the 3. To evaluate the relationship between memory and
Attention/Concentration domain provide measures of at- intelligence and provide the clinician with a mecha-
tention and working memory. Each subtest in the Auditory/ nism to meaningfully evaluate discrepancies between
Verbal and Visual/Nonverbal domains provide measures IQ and learning/memory performance.
 Children’s Memory Scale C 557

Children’s Memory Scale. Table 1 Description of CMS core index and subtest components

Core
Core Index Subtest Subtest Description
Verbal Memory Indexes Stories Two stories (age-dependent 5–8-, 9–12-, and 13–16-year olds) are read.
(Immediate, Delayed, and Immediately after presentation of each story, the child is asked to repeat as
C
Recognition) much of the story as can be remembered. In the delayed portion, the child
retells the stories and then answers questions about the stories (recognition
recall).
Word Pairs A list of 10 or 14 (age-dependent 5–8-year olds; 9–16-year olds) related and
unrelated word pairs are read; thereafter the stem is read and the child recalls the
associate. Three learning trials are administered followed by a free recall. In the
delayed portion, the child is asked to recall the word pairs spontaneously
followed by a recognition section.
Visual/Non-Verbal Memory Dot The child is shown an array of dots (blue) located within a rectangle in a stimulus
Indexes (Immediate and Locations book. This page is removed and the client is asked to replicate the spatial location
Delayed) of the dots by placing chips on a 3  4 or 4  4 rectangular grid (depending on
age 6 dots for 5–8-year olds; 8 for dots 9–16-year olds). Three learning trials are
administered followed by presentation of a distractor array (red dots) after which
an immediate recall trial is presented. In the delayed portion, the child is asked to
reproduce the original blue dot array.
Faces The child is presented with a series of 12 (5–8-year olds) or 16 (9–16-year olds)
pictured human faces one at a time. In the immediate and delayed recall sections,
the child is asked to identify the stimulus faces from a different set of foils (36 or
48 colored photos).
Attention/Concentration Numbers A digit span forwards and backwards task (similar to the WISC-III subtest).
Index Sequences The client is asked to mentally sequence or manipulate information as quickly as
possible. The 12 items include such tasks as reciting numbers, days of the week
and months in forward and reverse order, and counting by 2s, 4s, and 6s. Scoring
is based upon accuracy and speed.

4. The inclusion of a diversified selection of clinically and Psychometric Data

educationally relevant tasks that would allow clini-
cians to indentify and characterize learning and mem- The CMS was standardized on a representative US sample
ory disorders in children and help them to design of 1,000 children. The sample was stratified according to age
remedial and compensatory programs based upon (10 age groups ranging in age from 5 to 16 years; 100 per age
the child’s performance. group), sex (equal number of males and females in each age
5. The development of an instrument that could be suc- group), race/ethnicity (White, African American, Hispanic,
cessfully administered within a standardized testing and other), geographic region (northeast, north central,
situation and also be child friendly. south, west), and parent education level (five categories
ranging from <8th grade to university degree). Further,
As such, the CMS focused upon the assessment of de-
the CMS is the only memory assessment instrument to
clarative memory with no attempt made to formally
provide a linking sample co-normed with an individually
evaluate procedural memory, which involves skill
administered intelligence scale (WISC-III and WPPSI-R).
learning and classical conditioning. Further, the CMS
This sample was comprised of 300 children (ages 5–16; 50%
was unable to provide measures of long-term memory
male 50% female) and provided the examiner with an
beyond 30 min due to the time restriction of a traditional
empirically grounded basis for predicting the level of mem-
assessment and the logistical problems inherent in the
ory performance from IQ and determining when a child’s
reevaluation of the standardization sample over a longer
memory performance deviated significantly from IQ
time interval.
558 C Children’s Memory Scale

Domain Subtests Indexes

Stories* Verbal
Word pairs* Immediate
Word lists**
Auditory/verbal

Stories 2* Verbal
Word pairs 2* Delayed
Word lists 2**

Delayed
Recognition

Learning

Dot locations* Visual

Faces* Immediate
Family pictures**
Visual/nonverbal

Dot locations 2* Visual

Faces 2* Delayed
Family pictures 2**

Numbers* Attention/
Attention/concentration Sequences* Concentration
Picture locations**
Note: *Core subtest; **Supplemental subtest

Children’s Memory Scale. Figure 1 Structure of the children’s memory scale

expectancy. With the release of the WISC-IV in 2004, a With respect to validity, the results of confirmatory
smaller correlation study was conducted involving 126 chil- factor analysis yielded a three-factor solution consisting of
dren of ages 6–16 years (Drozdick, Holdnack, Rolfhus, & Auditory/Verbal memory, Visual/Nonverbal memory,
Weiss, 2005). The authors provide tables which allow for and Attention/Concentration. The manual also provides
ability-memory discrepancy analysis using the predicted concurrent validity studies with different measures of
actual or simple difference methods and base rates. intelligence and achievement, which consistently show a
The CMS manual provides both split-half and test- moderate positive correlation. The CMS correlations with
retest reliability coefficients for the index scores and subt- measures of executive functioning and language were low
ests. For the indexes, average split-half reliability estimates to moderate. Finally, with respect to other measures of
ranged from .76 to .91. Average split-half reliability esti- memory, moderate to high correlation were obtained
mates for the subtests ranged from .71 to .91. Test-retest across the indexes of the CMS and Wechsler Memory
reliability (mean re-test interval 59.6 days) was assessed Scale–III, and low to moderate correlations were obtained
across three age bands using a sample of 125 students. across the indexes of the CMS and the Wide Range As-
Reliability estimates ranged from .29 to .89 for the indexes. sessment of Learning and Memory. More recently, perfor-
Due to the nature of memory assessment and psychometric mance on both the CMS and WRAML-2 was reported as
considerations (restriction of range), decision consistency low to moderate in the latter test’s Examiner’s Manual
test-retest coefficients were also calculated. These ranged (Sheslow & Adams, 2003).
from .61 to .93 for the indexes and from .71 to .93 for the
core subtests. Results indicated a general practice effect of
up to one standard deviation, similar to what was obtained Clinical Uses
on the WISC-III. Inter-rater reliability was also assessed on
subtests requiring subjective scoring (e.g., stories) and was As previously stated, the CMS was designed to be used as
found to be high. part of a standard psychological or neuropsychological
 Chlordiazepoxide C 559

evaluation in order to provide a comprehensive assess-

ment of learning and memory in children and adolescents Chi-square
of ages 5–16 years. The clinical sensitivity and usefulness of
the CMS was demonstrated by the inclusion of case studies M ICHAEL D. F RANZEN
and clinical validity studies in the test manual. These in- Allegheny General Hospital
Pittsburgh, PA, USA
C
cluded individual studies comparing the performance of
children with temporal lobe epilepsy, traumatic brain inju-
ry, brain tumors, learning disabilities, ADHD, and specific
language impairment to that of normal controls. Additional Definition
studies have been published examining learning and mem-
ory performance in children with dyslexia and/or ADHD Chi-square is a nonparametric statistic that evaluates the
(Kibby & Cohen, 2008), and specific language impairment likelihood that two observed distributions are different.
(Riccio, Cash, & Cohen, 2007). The relationship between The first step to calculating a chi-square is to construct a
continuous performance testing and performance on the contingency table in which observations are plotted
CMS has been investigated in a clinic sample (Riccio, on the basis of the values of the relevant variables. For
Garland, & Cohen, 2007). Studies have also been reported example, a contingency table might be constructed
on learning and memory performance of children with where one axis is gender and the other axis is diagnosis.
complex partial epilepsy of temporal origin, using an The chi-square would describe whether female and male
experimental version of the CMS (Cohen, 1992; Cohen, patients have approximately the same distribution of
Holmes, Campbell, Smith, & Flanigan, 1990). diagnoses.

Cross References
Cross References
▶ Memory
▶ Wechsler Memory Scale ▶ Correlation Coefficients
▶ Wide Range Assessment of Memory and Learning

References and Readings References and Readings

Cohen, M. J. (1992). Auditory/verbal and visual/spatial memory in chil- Castellan, N. J. Jr. (1965). On the partitioning of contingency tables.
dren with complex partial epilepsy of temporal lobe origin. Brain Psychological Bulletin, 64, 330–338.
and Cognition, 20, 315–326.
Cohen, M. J. (1997). Children’s memory scale. Administration manual.
San Antonio, Texas: The Psychological Corporation.
Cohen, M. J., Holmes, G. L., Campbell, R., Smith, J. R., & Flanigan, H. F.
(1990). Memory performance following unilateral electrical stimu-
lation of the hippocampus in a child with right temporal lobe
Chlordiazepoxide
epilepsy. Journal of Epilepsy, 3, 115–122.
Drozdick, L. W., Holdnack, J., Rolfus, E., & Weiss, L. (2005). Technical J OHN C. C OURTNEY
report #5 WISC-IV and children’s memory scale. San Antonio, Texas: Children’s Hospital of New Orleans
Harcourt Assessment. New Orleans, LA, USA
Kibby, M. Y., & Cohen, M. J. (2008). Memory functioning in children
with reading disorders and/or attention-deficit/hyperactivity disor-
der: A clinical investigation of their working memory and long-term
memory functioning. Child Neuropsychology, 14, 525–546. Generic Name
Riccio, C. A., Cash, D. L., & Cohen, M. J. (2007). Learning and memory
performance of children with specific language impairment (SLI). Chlordiazepoxide
Applied Neuropsychology, 14, 255–261.
Riccio, C. A., Garland, B. H., & Cohen, M. J. (2007). Relations between
the test of variables of attention (TOVA) and the children’s memory
scale (CMS). Journal of Attention Disorders, 11, 167–171.
Sheslow, D., & Adams, W. (2003). Wide range assessment of memory
Brand Name
and learning -2. Administration manual. Wilmington, DE: Jastak
Associates. Librium, Librax
560 C Chlorpromazine

Class
Chlorpromazine
Anxiolytic
J OHN C. C OURTNEY 1, C RISTY A KINS 2
1
Children’s Hospital of New Orleans
New Orleans, LA, USA
Proposed Mechanism(s) of Action 2
Mercy Family Center
Metarie, LA, USA
Chlordiazepoxide binds to the GABA-A ligand-gated
chloride channel complex and, thereby, enhances the in-
hibitory effects of GABA. Generic Name

Chlorpromazine
Indication

Anxiety disorders, symptoms of anxiety, preoperative ap- Brand Name

prehension and anxiety, and withdrawal from acute
alcoholism. Thorazine

Side Effects Class

Serious Conventional antipsychotic

Respiratory depression, kidney dysfunction, and liver

disorders (rare).
Proposed Mechanism(s) of Action

Blocks dopamine 2 receptors; dopamine D2, histamine

Common H1, and cholinergic M1 blockade in the vomiting center
(area postrema)
Sedation, dizziness, depression, forgetfulness, confusion,
and hyperexcitability.
Indication

References and Readings Schizophrenia, nausea, vomiting, restlessness before sur-

gery, manic episodes of bipolar disorder, tetanus
Physicians’ Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson
PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The prescriber’s guide
(2nd ed.). New York, NY: Cambridge University Press. Off Label Use

Bipolar disorder

Additional Information
Side Effects
Drug Interaction Effects: http://www.drugs.com/drug_interactions.html
Drug Molecule Images: http://www.worldofmolecules.com/drugs/
Free Drug Online and PDA Software: www.epocrates.com
Serious
Gene-Based Estimate of Drug interactions: http://mhc.daytondcs.
com:8080/cgi bin/ddiD4?ver=4&task=getDrugList Neuroleptic malignant syndrome, jaundice, agranulocy-
Pill Identification: http://www.drugs.com/pill_identification.html tosis, seizures
 Cholesterol C 561

Common cholesterol. In the presence of high circulating concentra-

tions, LDL-cholesterol gradually builds up in and on the
Neuroleptic-induced deficit syndrome, akathisia, extrapy- walls of the coronary, cerebrovascular, or peripheral
ramidal symptoms, priapism, amenorrhea arteries. Together with coagulation factors and platelets,
cholesterol deposits on the vessel walls can form thick C
hard ‘‘plaques’’ which, over time, can occlude the blood
References and Readings vessels in a process called ‘‘atherosclerosis.’’ Therefore,
a high level of LDL-cholesterol (usually greater than
Physicians’ Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson 160 mg/dL) indicates an increased risk of heart disease
PDR. and, to a lesser extent, stroke. For this reason, LDL-choles-
Stahl, S. M. (2007). Essential psychopharmacology: the prescriber’s guide
terol is often called ‘‘bad cholesterol.’’ About one-third of
(2nd ed.). New York, NY: Cambridge University Press.
the circulating cholesterol is transported by high-density
lipoprotein (HDL), which more commonly carries the cho-
lesterol away from the arteries, and toward the liver where
Additional Information
it is metabolized and eliminated. It has been suggested
that HDL removes excess cholesterol from plaques, and
Drug Interaction Effects: http://www.drugs.com/drug_interactions.html
Drug Molecule Images: http://www.worldofmolecules.com/drugs/
consequently HDL-cholesterol is known as ‘‘good choles-
Free Drug Online and PDA Software: www.epocrates.com terol’’ because a high HDL-cholesterol level seems to
Gene-Based Estimate of Drug interactions: http://mhc.daytondcs. protect against coronary heart disease. Typically, the
com:8080/cgi bin/ddiD4?ver=4&task=getDrugList liver meets all of the body’s requirements for cholesterol
Pill Identification: http://www.drugs.com/pill_identification.html
by manufacturing it, which means that dietary cholesterol
is not needed for nutritional purposes. In foods, saturated
fatty acids, and to a lesser extent, trans fats, are the main
sources of elevated blood cholesterol levels. Measures to
Cholesterol reduce elevated cholesterol levels include reductions in
dietary cholesterol intake, cholesterol-lowering medica-
E LLIOT J. R OTH tions, increases in physical activity levels (which increase
Northwestern University HDL-cholesterol), and cessation of smoking.
Chicago, IL, USA

Cross References
Synonyms
▶ Atherosclerosis
Fats; Lipids ▶ Cerebrovascular Disease
▶ Coronary Disease
▶ Ischemic Stroke
Definition ▶ Myocardial Infarction
▶ Peripheral Vascular Disease
Cholesterol is a naturally occurring lipid found in the ▶ Stent
bloodstream and in cells throughout the body. It is an ▶ Thrombosis
important component of cell membranes and some hor-
mones. However, hypercholesterolemia, or high blood References and Readings
concentrations of cholesterol, is a major risk factor for
heart disease and stroke. Fletcher, B., Berra, K., Ades, P., Braun, L. T., Burke, L. E., Durstine, J. L.
et al. (2002). Managing abnormal blood lipids: A collaborative
approach. Circulation, 112, 3184–3209.
Current Knowledge National Cholesterol Education Program Expert Panel on Detection,
Evaluation, and Treatment of High Blood Cholesterol in Adults
(Adult Treatment Panel III): Third Report of the National Choles-
Cholesterol does not typically exist on its own in the blood; terol Education Program (NCEP) Expert Panel on Detection, Evalu-
it is transported to and from cells by lipoprotein molecules. ation, and Treatment of High Blood Cholesterol in Adults (Adult
Low-density lipoprotein (LDL) is the major carrier of Treatment Panel III). (2002). Circulation, 106, 3143–3421.
562 C Cholinergic System

When acetylcholine binds to the nicotinic receptor, it

Cholinergic System generates the opening of the ion pore, causing a rapid
influx of cations. There are four nicotinic receptor
C OLLEEN E. J ACKSON subtypes (N1, N2, N3, and N4), as well as a, b, d, and g
University of Connecticut subunits for each subtype.
Storrs, CT, USA Muscarinic: The muscarinic acetylcholine receptor
type forms G protein-coupled channels in the membranes
of neurons receptive to acetylcholine. When acetylcholine
Synonyms binds to one of these metabotropic channels, it generates a
cascade of information transduction within the cell via
Acetylcholinergic system intracellular proteins. There are five muscarinic receptor
subtypes (M1, M2, M3, M4, and M5). All five receptor
subtypes are present in the central nervous system;
Definition however, M1, M2, and M4, are more predominant.

The cholinergic system is composed of organized nerve

cells that use the neurotransmitter acetylcholine in
the transduction of action potentials. These nerve cells Cholinergic Projections
are activated by or contain and release acetylcholine dur-
ing the propagation of a nerve impulse. The cholinergic The cholinergic system is formed by a broadly projecting
system has been associated with a number of cognitive circuitry, as well as local circuitry. Long-projection cho-
functions, including memory, selective attention, and linergic neurons originating in the nuclei of the basal
emotional processing. forebrain project widely throughout the brain. For exam-
ple, the nucleus basalis of Meynert and the diagonal band
of Broca, both structures within the basal forebrain, trans-
Current Knowledge mit acetylcholine to the cerebral cortex. In addition, cho-
linergic projections exist between the septal nucleus and
Acetylcholine Synthesis and Metabolism the hippocampus. Local cholinergic circuitry within the
striatum has important interactions with nigrostriatal
The synthesis of acetylcholine, the neurotransmitter used dopamine neurons and striatal GABAergic neurons
by nerve cells in the cholinergic system, requires choline, a involved in extrapyramidal movement.
natural amine found in the lipid bilayer of the cell mem-
brane, and acetyl coenzyme A (acetyl-CoA), a thioester
used in metabolic reactions and an acceptor and donor of Cognitive Role of the Cholinergic System
acetyl groups. These molecules are catalyzed by choline
acetyltransferase, an enzyme found only in acetylcholiner- The cholinergic system has been implicated in a number
gic cells, in order to produce acetylcholine. of cognitive abilities, including attention, memory, and
In the metabolism of acetylcholine, acetylcholinester- emotional processing. Both human and animal studies
ase degrades the molecule to produce choline and acetic indicate that cholinergic input originating in the basal
acid. The choline molecules generated through this reac- forebrain mediates sustained attentional performance
tion are transported, via a high-affinity choline uptake (see Sarter, Givens, & Bruno, 2001 for review). In addi-
protein, back to the nerve terminal. They are then used to tion, the cholinergic system also acts as a modulator of
synthesize new acetylcholine molecules. level of processing (e.g., primitive responses such as
reflexes vs. limbic system responses vs. evaluative and
discriminative executive functioning processes). Broadly,
Cholinergic Receptor Types and Subtypes activation of the cholinergic system supports attentional
processing of threat-related stimuli (Berntston, Sarter, &
Nicotinic: The nicotinic acetylcholine receptor type forms Cacioppo, 1998), while specific projections to the medial
ligand-gated ion channels in the membranes of neurons prefrontal cortex influence anxious responses to contex-
receptive to acetylcholine. As an ionotropic receptor, the tual stimuli (Hart, Sarter, & Bernston, 1999). By influen-
nicotinic receptor is directly linked to an ion channel. cing arousal and attention, acetylcholine also impacts
 Cholinergic System C 563

working memory and the attentional processes required agent is currently being assessed as a treatment for schizo-
for error detection (see Sarter, Gehring, & Kozak, 2006 for phrenia (Lameh et al., 2007).
review). Emotional processing is also intricately related to
the cholinergic system; additionally, cholinergic inputs
to the frontoparietal cortex may influence how attention Future Directions C
is directed toward emotional information (Bentley, Vuilleu-
mier, Thiel, Driver, & Dolan, 2003). As would be expected Future research focused on the interaction between the
from a system influencing such a variety of cognitive cholinergic system and other neurotransmitters (e.g., nor-
functions, decreased cholinergic tone, associated with epinephrine, dopamine, and serotonin), and neuromodu-
Alzheimer’s disease, results in impaired cognitive perfor- lators (e.g., substance P) will be important in
mance broadly extending to memory, attention, and understanding the complexities that exist within the
executive functioning (Terry & Buccafusco, 2003). brain and body regarding the communication of chemical
signals. Further development of biomarkers (e.g., behav-
ioral, electrophysiological, and neuroimaging) associated
Pharmacological Agents Acting on the with cholinergic decline will allow for improved identifi-
Cholinergic System cation of disorders associated with the cholinergic system.
A continued focus on the role of the cholinergic system in
Pharmacological agents impact the cholinergic system in Alzheimer’s disease, as well as the development of phar-
a number of different ways. At the receptor level, nicotinic maceutical interventions targeting the cholinergic system
acetylcholine agonists stimulate cholinergic activity large- in the treatment of this disease (e.g., alpha-7 subunit
ly in peripheral acetylcholine neurons. However, nicotine, nicotinic agonists), remains critical, particularly with the
a nicotinic acetylcholine agonist acts at nicotinic receptors continued rise in the elderly population. Finally, research
in the central nervous system. Nicotinic acetylcholine on the role of the cholinergic system in a number of
antagonists acting on cells in the central nervous system psychological disorders, including stress, affective and
are rarely used in clinical practice. panic disorders, and schizophrenia, will continue to high-
Pilocarpine is an example of a muscarinic acetylcho- light the broad implications on mental health that this
line agonist that acts on the parasympathetic nervous system has.
system. While pilocarpine is not used clinically to treat
central nervous system disorders, it has a range of side
effects, including excessive sweating and salivation, which Cross References
are related to its action on muscarinic receptors in the
parasympathetic nervous system. Muscarinic acetylcho- ▶ Alzheimer’s Disease
line antagonists, such as scopolamine and atropine, block ▶ Cholinesterase Inhibitors
muscarinic receptors. Their anticholinergic effects on the ▶ Memory
parasympathetic nervous system result in side effects such ▶ Memory Impairment
as dry mouth, constipation, and tachycardia. ▶ Mild Cognitive Impairment
Acetylcholinesterase inhibitors, such as tacrine and
donepezil, block the breakdown of acetylcholine in the
synaptic cleft. The result is sustained levels of acetylcho- References and Readings
line in the synapse that are capable of transmitting
chemical information to other cells. Acetylcholinester- Bentley, P., Vuilleumier, P., Thiel, C., Driver, J., & Dolan, R. (2003).
ase inhibitors are commonly used in the treatment of Cholinergic enhancement modulates neural correlates of selective
attention and emotional processing. Neuroimage, 20, 58–70.
Alzheimer’s disease, as well as Lewy Body dementia.
Bodick, N. C., Offen, W. W., Levey, A. I., Cutler, N. R., Gauthier, S. G.,
Presently, there is a developing focus on the choliner- Satlin, A., et al. (1997). Effects of xanomeline, a selective muscarinic
gic system in the treatment of schizophrenia. Xanomeline, receptor agonist, on cognitive function and behavioral symptoms in
an M1/M4 muscarinic acetylcholine agonist that was Alzheimer disease. Archives of Neurology, 54, 465–473.
initially assessed as a possible treatment for Alzheimer’s Lameh, J., Burstein, E. S., Taylor, E., Weiner, D. M., Vanover, K. E., &
Bonhaus, D. W. (2007). Pharmacology of N-desmethylclozapine.
disease, has shown efficacy in treating psychotic
Pharmacology & Therapeutics, 115, 223–231.
symptoms (Bodick et al., 1997). In addition, N-des- Sarter, M., Givens, B., & Bruno, J. P. (2001). The cognitive neuroscience of
methylclozapine (norclozapine, NDMC), a metabolite of sustained attention: Where top-down meets bottom-up. Brain Re-
the antipsychotic clozapine, is a partial M1 agonist. This search Reviews, 35, 146–160.
564 C Cholinesterase Inhibitors

Sarter, M., Gehring, W. J., & Kozak, R. (2006). More attention must be
paid: the neurobiology of attentional effort. Brain Research Reviews, Chorea
51, 145–160.
Terry, A., & Buccafusco, J. (2003). The cholinergic hypothesis of age
A NNA D E P OLD H OHLER 1, M ARCUS P ONCE DE LEON2
and Alzheimer’s disease-related cognitive deficits: recent challenges 1
and their implications for novel drug development. Journal of Phar- Boston University Medical Center
macology and Experimental Therapeutics, 306, 821–827. Boston, MA, USA
2
William Beaumont Army Medical Center
El Paso, TX, USA

Cholinesterase Inhibitors
Synonyms
J OA NN T. T SCHANZ
Utah State University Dance-like
Logan, UT, USA

Synonyms Definition
Acetylcholinesterase inhibitors; AchEIs; Anticholinester-
Chorea is characterized by brief, irregular muscle
ase inhibitors; CHEIs
contractions that are not repetitive or rhythmic,
but appear to flow from one muscle to the next.
Definition They may appear as dance-like movements of the
limbs, trunk, or head. Typical movements include facial
Cholinesterase inhibitors are a class of medications used in grimacing, shoulder adduction, and finger extension
the treatment of Alzheimer’s disease (AD) that targets the and contractions. They can be associated with snakelike
cholinergic neurotransmitter system. The treatment is writhing movements of the hands or feet known as
based on the observation of a cholinergic deficiency in athetosis.
AD. Cholinesterase inhibitors block the activity of acetyl-
cholinesterase, the primary enzyme that breaks down ace-
tylcholine, and allows the neurotransmitter substance to
remain in the synaptic cleft longer in order to stimulate Current Knowledge
postsynaptic receptors. These drugs do not prevent the
further degeneration of cholinergic neurons. They are mod- Chorea is a feature of Huntington’s disease, and may be
estly effective in the short-term improvement of attention, present with rheumatic fever. It can be seen as a side effect
concentration, memory, and some behavioural symptoms, of the medication levodopa or the dopamine agonists and
but are not thought to alter the progression of the disease. may result from metabolic disorders, endocrine disorders,
and vascular incidents.

Cross References

▶ Alzheimer’s Dementia Cross References

▶ Alzheimer’s Disease
▶ Anticholinesterase Inhibitors ▶ Huntington’s Disease

References and Readings

Orgogozo, J.-M. (2003). Treatment of Alzheimer’s disease with cholines-

References and Readings
terase inhibitors. An update on currently used drugs. In K. Iqbal &
B. Winblad (Eds.), Alzheimer’s disease and related disorders: Research Marshall, F. J. (2004). Clinical features and treatment of Huntington’s
advances (pp. 663–675). Bucharest, Romania: Ana Asian Interna- disease. In R. L. Watts, & W. C. Koller (Eds.), Movement disorders
tional Academy of Aging. (2nd ed., pp. 589–603). New York: McGraw-Hill.
 Christensen, Anne-Lise (1926– ) C 565

qualitatively oriented LNI continues to be used in Eur-

Christensen, Anne-Lise (1926– ) ope, and somewhat less frequently in the USA

A NTHONY Y. S TRINGER
Emory University Education and Training C
Atlanta, GA, USA
 1954–1955 – Visiting research fellow at Radcliffe
University
Landmark Clinical, Scientific, and  1956 – Master of Arts in Psychology, University of
Professional Contributions Copenhagen, Denmark
 1957 – Doctor of Philosophy, University of Copenha-
 In 1966, Anne-Lise Christensen reviewed a newly gen, Denmark
published English translation of Aleksandr Luria’s
Christensen began attending the University of Copenha-
(1966) Higher Cortical Functions in Man and instantly
gen in 1945, shortly after the liberation of Denmark from
realized its value in the clinical bedside examination of
the Nazi occupation. She writes about the ‘‘overwhelming
cognitive function in neurological patients. Luria
experience of freedom and peace . . . [when] the borders
provided a comprehensive theory of the brain organi-
were opened, and we were full of hope and expectations
zation, from which cognitive tasks could be developed
for the future’’ (Christensen, 2002, p. 119). Her studies
to measure various cortical functions. However, Lur-
were interrupted for 6 years by marriage and mother-
ia’s scholarly presentation required some adaptation
hood, but she returned to the university in 1952, dividing
before it could be practically applied by clinicians.
her time between literature and psychology. Christensen
Christensen began to translate Luria’s methods into
was accepted at Radcliffe University in 1954, where she was
her native Danish as well as adapt them for use in the
exposed to the work of Talcott Parsons, Gordon Allport,
clinic. Responding to Luria’s invitation, Christensen
Gardner Lindzey, and George Mandler. She cites, Jerome S.
visited him in Moscow and presented her Danish
Bruner, however, as her greatest influence. In his work,
translation. Luria labeled it a ‘‘vulgarization’’ of his
Christensen was exposed to ‘‘New Look Psychology’’
method, but added he had always wanted someone
which took the methods of the psychophysics laboratory
to do this. He encouraged Christensen to do an En-
and applied them to everyday perceptual experience.
glish translation. Five years later, Christensen pre-
Christensen returned to Denmark in 1955 and
sented the first English draft to Luria on her second
completed her doctoral studies at the University of
visit to Moscow. Luria made edits and provided a
Copenhagen in 1957. Bruner continued to influence
paper for Christensen to translate and include in the
Christensen’s career for more than a decade later when
final draft. Christensen published Luria’s Neuropsy-
he insisted she introduced herself to Luria at a 1969
chological Investigation (LNI) in 1975, including a
conference in London. Impressed with her attempts at
textbook, manual, and stimulus cards.
 using his method in Denmark, Luria invited Christensen
The LNI introduced a qualitative approach to neuro-
to visit him in Moscow, but a sudden heart attack pre-
psychological examination, which contrasted with the
vented his participation in the conference. Nonetheless,
predominant quantitative batteries used in the USA.
an official invitation arrived in Denmark, and Christensen
The LNI is one of the few theory-based assessment
made her visit to the Bourdenko Neurosurgical University
approaches in neuropsychology and has been lauded
Institute to work with Luria in September 1970 (Chris-
for its flexible administration, brevity, and qualitative
tensen, 2002). This began the collaboration between
focus (Kolb & Wishaw, 1990). It has also been criti-
the two, which resulted in the introduction of the LNI
cized for its lack of norms and insensitivity to mild
to the West.
impairment (Lezak, 1983). Though Christensen de-
clined to collaborate, Charles Golden and colleagues
(Golden, Purisch, & Hammeke, 1979) in the USA Major Appointments
attempted to standardize the administration of the
LNI and establish a normative base for interpretation.  University Hospital of Aarhus (Psychiatry and Neuro-
This unfortunately violated the original qualitative surgery Departments), Jutland, Denmark, 1959–1968
focus of the LNI and generated considerable contro-  University Hospital of Aarhus (Head of Clinical Psy-
versy and criticism. Nonetheless, Christensen’s original chological Department), Jutland, Denmark, 1969–1981
566 C Chromosome

 University of Copenhagen (Research Neuropsycholo- ▶ Luria, Alexander Romanovich (1902–1977)

gist), Denmark, 1981–1985 ▶ Luria Nebraska Neuropsychological Battery
 Center for Rehabilitation of Brain Injury (Founder ▶ Qualitative Neuropsychological Assessment
and Director), University of Copenhagen, Denmark,
1985–1998
 University of Copenhagen (Professor of Neuropsy-
References and Readings
chological Rehabilitation), Denmark, 1985–1998
Christensen, A.-L. (1975). Luria’s neuropsychological investigation. Manual
and test materials. New York: Spectrum Publications.
Major Honors and Awards Christensen, A.-L. (2002). Lifelines. In A. Y. Stringer, E. L. Cooley, & A.-L.
Christensen (Eds.), Pathways to prominence in neuropsychology:
 1987 – Lady of the Dannebrog Order (bestowed by the Reflections of twentieth-century pioneers (pp. 119–137). New York:
Psychology Press.
Queen of Denmark) Golden, C. J., Purisch, A. D., & Hammeke, T. A. (1979). The Luria-
 1994 – Philosophia Doctor Honoris Causa, University Nebraska neuropsychological battery. Lincoln: University of Nebraska
of Lund, Sweden Press.
Kolb, B., & Wishaw, I. Q. (1990). Fundamentals of human neuropsychology
(3rd ed.). New York: Freeman.
Lezak, M. (1983). Neuropsychological assessment (2nd ed.). New York:
Short Biography Oxford University Press.
Luria, A. R. (1966). High cortical functions in man (2nd ed.). New York:
A deep and lasting penchant for collaboration is evident Basic Books.
both in Anne-Lise Christensen’s personal and professional
lives. At 19, she married Niels Egmont Christensen, a
former classmate. Their careers progressed in tandem.
While Anne-Lise was at Radcliffe, Niels was at Harvard.
They were at the University of Aarhus together beginning Chromosome
in 1959, and Niels became the Chair of the Philosophy
Department just a year before Anne-Lise became the M ARTIN H AHN 1, R OHAN PALMER 2
1
Chair of Clinical Psychology. Over the course of her William Paterson University
career, Christensen has had many distinguished collabora- Wayne, NJ, USA
2
tors, colleagues, and mentors. Besides Bruner and Luria, University of Colorado at Boulder
she cites the noted neuropsychologists Elkhonon Gold- Boulder, CO, USA
berg (whom she met in Moscow while training with
Luria), Edith Kaplan, and Muriel Lezak, and neuroscien-
tists Donald Stein and Stanley Finger (Christensen, 2002). Definition
Her collaborations have always been international
in scope, stretching across Europe and the Americas. Chromosomes are threadlike structures made of proteins
Her collaboration with her husband Niels came to a sad and nucleic acids. They are found in the nucleus of
ending with his suicide in 1980 after battling bipolar eukaryotic cells and carry genetic information along
disorder. Yet, even after retiring, her international colla- their length in the form of genes. In the early 1900s, Walter
borations continued, with Christensen recently serving Sutton and Theodor Boveri argued that the understanding
on the Board of Consultants for the SARAH Network of chromosomes was consistent with Mendelian genetics,
Hospitals in Brazil, a complex of facilities, she believes and the result of their thinking is called the chromosome
bridge ‘‘the chasm between humanistic and empirical theory of heredity. A part of that theory is that Mendelian
scientific approaches’’ to rehabilitation (Christensen, genes have specific locations (or loci) on chromosomes – a
2002, p. 134). topic under heavy research since that time.
Chromosomes differ in overall length and the length
of their parts, and they have distinctive banding patterns
Cross References that allow them to be recognized. Humans have 23 pairs
or 46 chromosomes. Of those 23 pairs, one pair is called
▶ Kaplan, Edith (1924–2009) the sex chromosomes, and the remaining 22 pairs are
▶ Lezak, Muriel called autosomes.
 Chronic Fatigue Syndrome C 567

Cross References defined by the Centers for Disease Control (CDC) study
group (Holmes et al., 1988); they named the condition
▶ Deoxyribonucleic Acid (DNA) Chronic Fatigue Syndrome (CFS). In subsequent years,
▶ Gene case definitions for CFS were created in Australia, Great
Britain (Sharpe et al., 1991; Wessely, 1995), and Canada C
(Carruthers et al., 2003), and a pediatric case definition
for ME/CFS was published in 2006 (Jason et al., 2006).
Chronic Bronchitis Currently, the most common case definition used in the
United States for the clinical diagnosis of CFS is a version
▶ Chronic Obstructive Pulmonary Disease of the original 1988 CDC case definition revised in 1994
by an International CFS Study Group (Fukuda, Straus,
Hickie, Sharpe, Dobbins, & Komaroff, 1994).
The diagnosis of CFS cannot be made if the following
are present and could account for the presence of persis-
Chronic Familial Vascular tent fatigue: (1) permanent medical exclusions include
Encephalopathy organ failure, chronic infections, rheumatic and chronic
inflammatory diseases, major neurologic diseases requir-
▶ Cadasil ing systemic treatment, major endocrine diseases, and
primary sleep disorders; (2) temporary medical exclu-
sions include treatable conditions that require evaluation
over time to determine the extent to which they contrib-
Chronic Fatigue Immune ute to the fatiguing illness such as conditions discovered
at onset or initial evaluation (e.g., effects of medications,
Deficiency Syndrome (CFIDS) sleep deprivation, untreated hypothyroidism, untreated
or unstable diabetes mellitus, active infection), conditions
▶ Chronic Fatigue Syndrome that resolve (e.g., pregnancy), cardiac conditions, and
morbid obesity specified as BMI > 45; 3) permanent
psychiatric exclusions include lifetime diagnoses of bipo-
lar affective disorders, schizophrenia of any subtype, de-
Chronic Fatigue Syndrome lusional disorders of any subtype, dementias of any
subtype, organic brain disorders, and alcohol or substance
G UDRUN L ANGE abuse within 2 years before onset of the fatiguing illness,
UMDNJ-New Jersey Medical School any past or current diagnosis of major depressive disorder
Newark, NJ with psychotic or melancholic features, anorexia nervosa,
or bulimia.
If none of the exclusions apply, using the 1994 case
Synonyms definition, CFS is diagnosed based on the following cri-
teria: (1) fatigue is of new or definite onset, not due to
Chronic Fatigue Immune Deficiency Syndrome (CFIDS); exertion, not relieved by rest, and must result in substan-
Medically unexplained symptoms (MUS); Myalgic en- tial reductions in previous levels of educational, occupa-
cephalitis (ME); Post-infectious fatigue syndrome tional, social, or personal activities, (2) fatigue is of at least
(PFIS). Nomenclature used by patients or healthcare pro- 6 months duration, and (3) concurrent with at least four
viders is generally based on their etiologic perspective of the following eight symptoms that could not have
predated the onset of fatigue: impairment in short-term
memory or concentration severe enough to result in
Short Description or Definition substantial reductions in previous levels of educational,
occupational, social, or personal activities, painful lymph
Chronic fatigue syndrome is a complex illness defined by nodes in front or back of the neck or under the arms, sore
unexplained disabling fatigue and a combination of non- throat, muscle pain, pain in more than one joint without
specific accompanying symptoms that can have sudden or accompanying redness or swelling, headaches of a new
gradual onset. The diagnosis of the condition was initially type, unrefreshing sleep, postexertional malaise lasting
568 C Chronic Fatigue Syndrome

more than 24 h. These symptoms are nonspecific and dysfunction, cortisol dysregulation, small white matter
variable in both nature and severity over time. They lesions in the frontal regions of the brain, orthostatic
were selected on the basis of consensus clinical opinion and cognitive dysfunction. Most abnormalities are found
and were not identified empirically. in CFS patients who do not suffer from comorbid psychi-
atric disorder, most commonly depression. Treatments,
especially cognitive behavioral and graded exercise treat-
Categorization ments, enhance the prognosis for improvement. If un-
treated, complete recovery from CFS is rare.
Only a small percentage of patients complaining of fatigue
will be categorized as having CFS. Most patients either have
prolonged fatigue, defined as self-reported, persistent fa- Neuropsychology and Psychology of
tigue of 1 month or longer, or chronic fatigue defined as Chronic Fatigue Syndrome
self-reported persistent or relapsing fatigue of 6 or more
consecutive months (Fukuda et al., 1994). Other conditions CFS patients typically complain of difficulties with concen-
of unexplained etiology with similar symptom profiles tration, memory, and thinking, yet neuropsychological
are often comorbid with CFS and can include Fibromyalgia testing does not generally confirm the reported cognitive
Syndrome (FMS), Temporo-Mandibular Syndrome dysfunction. Available data suggest that the main cognitive
(TMS), Irritable Bowel Syndrome (IBS), Multiple Chemi- deficit in individuals with CFS is slowed information pro-
cal Sensitivity (MCS), Gulf War Syndrome (GWS), Major cessing, which can affect memory as well as executive
Depressive Disorder (MDD), and anxiety disorders. function. Depression is a very common comorbid condi-
tion (Tiersky, Johnson, Lange, Natelson, & DeLuca, 1997).
Epidemiology Neuroimaging data increasingly provide evidence for de-
creased cerebral blood flow and functional activation of
In the United States, CFS occurs in up to about 0.5% of brain areas suggesting increased cognitive effort (Lange,
the general population. It is most commonly found in Wang, Deluca, & Natelson, 1998; Lange et al., 2005).
middle-aged women and is most common in Latinos,
followed by African Americans, and Whites. The illness
affects women (predominantly between the ages of 40 Evaluation
and 59) more often than men (Reyes et al., 2003). In
general, the expression of the syndrome is not gender- A neuropsychological testing battery for individuals with
specific (Buchwald, Pearlman, Kith, & Schmaling, 1994). CFS should include measures of overall current and pre-
Chronic Fatigue Syndrome can also occur in children and morbid cognitive function (i.e., Wechsler Test of Adult
adolescents. While gender distribution is similar to that of Reading, Wechsler Adult Intelligence Scale III/IV), simple
adults, prevalence rates are significantly lower. and complex attention as well as information processing
and working memory (i.e., Continuous Performance
Test, Gordon, Trails, Paced Auditory Serial Addition
Natural History, Prognostic Factors, Test), executive function (i.e., subtests of Delis–Kaplan
Outcomes Executive Function System including verbal fluency,
towers test; Wisconsin Card Sort Test), memory
Disorders with similar symptom profiles have been des- (i.e., Wechsler Memory Scale III/IV, California Verbal
cribed for at least two centuries and have been known Learning Test II, Rey Osterrieth Complex Figure Test),
under a variety of names including neurasthenia, language function (i.e., Boston Naming Test), visual–
Akureyri disease, Epstein Barr Syndrome, and chronic perceptual function (i.e., Judgment of Line Orientation,
mononucleosis. Although many hypotheses exist about Hooper), and motor function (i.e., grip strength, finger
the causes for CFS, the etiology of the condition is still tapping, pegboard). It is also recommended to test the
unclear. Some believe that CFS is a latent form of depres- level of motivation and effort expanded during neuropsy-
sion and anxiety disorder, while others view the syndrome chological testing as well as emotional functioning to
as a sleep disorder, attribute it to endocrine dysfunction improve interpretability of test results.
or abnormalities within the central nervous system When an individual is diagnosed with CFS, it may be
(CNS). Abnormalities identified in individuals with desirable to evaluate the intensity and severity of symp-
CFS include Hypothalamic–Pituitary–Adrenal Axis toms associated with CFS using self-report
 Chronic Fatigue Syndrome C 569

questionnaires. To assess fatigue intensity, several mea- Dietrich, & Oxman, 2000). Medication management
sures have been used including the Chalder Fatigue Scale of fatigue is in its infancy; presently, there is no FDA
and the Krupp Fatigue Scale; both have acceptable psy- approved drug for fatigue. Over the counter medications
chometric properties. The Chalder Fatigue Scale is a 14- offer a first line of therapeutic possibilities. Stronger med-
item instrument with a 4-choice format and separates ications, including stimulants and antidepressants, re- C
mental and physical fatigue (Chalder et al., 1993). The quire a physician’s prescription. In general, medications
Krupp Fatigue Severity Scale includes nine items rated on used to treat depression, anxiety, and pain are very often
7-point scales and is sensitive to different aspects and used for the pharmacologic treatment of CFS. It is impor-
gradations of fatigue severity. Most items in the Krupp tant to recognize that fatigue is not solely due to disease
scale are related to behavioral consequences of fatigue processes, but can occur as an indirect consequence of
(Krupp, LaRocca, Muir-Nash, & Steinberg, 1989). The decreased physical activity and conditioning. Graded aer-
Checklist Individual Strength (CIS) is a 20-item inventory obic exercise training is a safe and effective treatment for
with four subscales commonly used to measure fatigue CFS and has been shown to improve quality of life. The
severity, concentration, reduced motivation, and physical primary goal of exercise is to avoid the spiral of decon-
activity. The CIS focuses on fatigue over the preceding ditioning that is common in most fatiguing diseases.
2 weeks (Vercoulen, Swanink, Fennis, Galama, Van der
Meer, & Bleijenberg, 1994). Another commonly used in-
strument to measure fatigue severity is the Multidimen- Cross References
sional Fatigue Inventory, also a 20-item questionnaire
providing scores for severity of general fatigue, physical ▶ Epstein Barr Syndrome
fatigue, mental fatigue, as well as reduced motivation and ▶ Gulf War Syndrome
activity (Smets, Garssen, Bonke, & De Haes, 1995). ▶ Neurasthenia
Another symptom that might warrant additional in- ▶ Unexplained Illness
vestigation is pain. Five of the eight CFS-defining symp-
toms reflect pain (headaches of a new type, pattern, or
severity, muscle pain, and multi-joint pain without
References and Readings
swelling or redness, sore throat, tender cervical/axillary
lymph nodes). In many cases, pain may be the primary
Buchwald, D., Pearlman, T., Kith, P., & Schmaling, K. (1994). Gender
determinant of disability for some individuals with CFS. differences in patients with chronic fatigue syndrome. Journal of
The McGill Pain Questionnaire (MPQ) is a well-validated General International Medicine, 9, 397–401.
questionnaire that can be used to further characterize Chalder, T., Berelowitz, G., Pawlikowska, T., Watts, L., Wessely, S., Wright,
pain or follow the course of pain in CFS (Melzack, 1975). D., et al. (1993). Development of a fatigue scale. Journal of Psychoso-
matic Research, 37, 147–153.
The MPQ includes four components: (1) a human figure
Carruthers, B. M., Jain, A. K., De Meirleir, K. L., Peterson, D. L., Klimas,
drawing on which patients are asked to mark the location N. G., Lerner, A. M. et al. (2003). Myalgic Encephalomyelitis/
of their pain; (2) a series of adjectives divided into groups Chronic Fatigue Syndrome: clinical Working Case Definition,
from which patients identify their experience by circling Deagnostic and Treatment Protocols. Journal of Chronic Fatigue
word descriptors; (3) questions about prior pain experi- Syndrome, 11, 7–115.
DeLuca, J. (2008). Fatigue as a window to the brain. London, UK: MIT
ence, pain location, and information on the use of pain
Press.
medication; and (4) a present pain intensity index. Fukuda, K., Straus, S. E., Hickie, I., Sharpe, M. C., Dobbins, J. G., &
Komaroff, A. (1994). The chronic fatigue syndrome: a comprehensive
approach to its definition and study. International Chronic Fatigue
Treatment Syndrome Study Group. Annals of Internal Medicine, 121, 953–959.
Holmes, G. P., Kaplan, J. E., Gantz, N. M., Komaroff, A. L., Schonberger,
L. B., Straus, S. E., et al. (1988). Chronic fatigue syndrome: a working
Effective treatment needs to be tailored to each individual case definition. Annals of Internal Medicine, 108, 387–389.
diagnosed with CFS and often consists of a combination Jason, L. A., Bell, D. S., Rowe, M. D., van Hoof, E. L. S. J. K., Lapp, C.,
of behavioral, pharmacological, and physical interven- et al. (2006). A pediatric case definition for myalgic encephalomyeli-
tions. Behavior modification or cognitive restructuring tis and chronic fatigue syndrome. Journal of Chronic Fatigue Syn-
drome, 13, 1–44.
are two cognitive behavioral therapy (CBT) approaches
Kroenke, K., Taylor-Vaisey, A., Dietrich, A. J., & Oxman, T. E. (2000).
used to treat CFS. Using this modality, reductions in Interventions to improve provider diagnosis and treatment of men-
the effect of fatigue on functional ability and quality of tal disorders in primary care. A critical review of the literature.
life have been shown in CFS (Kroenke, Taylor-Vaisey, Psychosomatics, 41, 39–52.
570 C Chronic Multisymptom Illnesses

Krupp, L. B., LaRocca, N. G., Muir-Nash, J., & Steinberg, A. D. (1989). Short Description or Definition
The fatigue severity scale. Application to patients with multiple
sclerosis and systemic lupus erythematosus. Archives of Neurology,
46, 1121–1123.
The Global Initiative for Chronic Obstructive Lung Disease
Lange, G., Steffener, J., Cook, D. B., Bly, B. M., Christodoulou, C., Liu, (GOLD) Workshop defines COPD as ‘‘a disease state char-
W. C., et al. (2005). Objective evidence of cognitive complaints in acterized by airflow limitation that is not fully reversible.
Chronic Fatigue Syndrome: a BOLD fMRI study of verbal working The airflow limitation is usually both progressive and asso-
memory. Neuroimage, 26, 513–524.
ciated with an abnormal inflammatory response of the
Lange, G., Wang, S., Deluca, J., & Natelson, B. H. (1998). Neuroimaging
in chronic fatigue syndrome. American Journal of Medicine, 105,
lungs to noxious particles or gases.’’ The GOLD committee
50S–53S. was organized by the World Health Organization (WHO)
Melzack, R. (1975). The McGill pain questionnaire: major properties and and the US National Heart Lung and Blood Institute
scoring methods. Pain, 1, 277–299. (NHLBI). Additional information about definitions, diag-
Reyes, M., Nisenbaum, R., Hoaglin, D. C., Unger, E. R., Emmons, C.,
nosis, treatment, and research can be found at www.gold
Randall, B., et al. (2003). Prevalence and incidence of chronic fatigue
syndrome in Wichita, Kansas. Archives of Internal Medicine, 163,
copd.com.
1530–1536.
Sharpe, M. C., Archard, L. C., Banatvala, J. E., Borysiewicz, L. K., Clare,
A. W., David, A., et al. (1991). A report–chronic fatigue syndrome:
guidelines for research. Journal of the Royal Society of Medicine, 84,
Categorization
118–121.
Smets, E. M., Garssen, B., Bonke, B., & De Haes, J. C. (1995). The
Multidimensional Fatigue Inventory (MFI) psychometric qualities COPD has traditionally been defined by severity of airflow
of an instrument to assess fatigue. Journal of Psychosomatic Research, limitation. Indeed, the GOLD COPD classification system
39, 315–325. relies on measures of airflow limitation to stratify COPD
Tiersky, L. A., Johnson, S. K., Lange, G., Natelson, B. H., & DeLuca, J.
severity (i.e., Forced Expiratory Volume in 1 Second (FEV1)
(1997). Neuropsychology of chronic fatigue syndrome: a critical
review. Journal of Clinical and Experimental Neuropsychology, 19,
and Forced Expiratory Volume in 1 Second/Forced Vital
560–586. Capacity(FEV1/FVC ratio)). This staging system is cur-
Vercoulen, J. H., Swanink, C. M., Fennis, J. F., Galama, J. M., Van der rently the primary determinant of treatment guidelines.
Meer, J. W., & Bleijenberg, G. (1994). Dimensional assessment of Heterogenity in the pathophysiology underlying COPD
chronic fatigue syndrome. Journal of Psychosomatic Research, 38,
has been increasingly recognized over the past decade
383–392.
Wessely, S. (1995). The epidemiology of chronic fatigue syndrome.
including chronic bronchitis, peripheral airways disease,
Epidemiological Review, 17, 139–151. and emphysema (Friedlander, Lynch, Dyar, & Bowler,
2007). At times, asthma has also been included in group-
ing of patients with COPD.

Chronic Multisymptom Illnesses

Epidemiology
▶ Unexplained Illness
COPD is the fourth leading cause of death in United
States. Worldwide mortality from COPD is predicted to
increase owing to the increased tobacco consumption in
third world countries, and COPD mortality among
Chronic Obstructive Pulmonary women is increasing faster than mortality among men
Disease (Anthonisen & Manfred, 2004). The third National
Health and Nutrition Examination Survey, conducted
E LIZABETH KOZORA , K ARIN F. H OTH between 1988 and 1994, demonstrated that between 5%
National Jewish Health and 8% of the US population had COPD as defined by
Denver, CO, USA physiological parameters (NHANES III). The worldwide
prevalence of COPD in 1990 was estimated by the WHO/
World Global Burden of Disease Study to be 9.34 per
Synonyms 1,000 in men and 7.33 per 1,000 in women. In the US,
COPD death rates are low among people under the age of
Chronic bronchitis; COPD; Emphysema 45, but increase with age.
 Chronic Obstructive Pulmonary Disease C 571

Natural History, Prognostic Factors, in daily activity, increased disease severity, and impaired
Outcomes health status (Hopkins & Bigler, 2001; McSweeny &
Labuhn, 1996).
Risk factors for COPD include both environmental and
host-related variables. Cigarette smoke has been identified C
as the most important external risk factor, followed by pipe
Evaluation
and cigar smoke, occupational dusts and chemicals, history
of severe childhood respiratory infections, HIV infection,
Neuropsychological evaluation for cognitive problems
outdoor pollution, and IV drug use. Host-related factors
associated with COPD typically involves measurement of
include airways hyper-responsiveness, genetic factors, se-
attention, learning and memory, reasoning and executive
vere hereditary alpha1-antitrypsin deficiency, low birth
functioning skills, visuomotor speed, and visuoperceptual
weight, and maternal cigarette smoking during gestation
function. Psychological evaluation typically involves mea-
(Anthonisen & Manfred, 2004).
sures of depression, anxiety, and health-related quality
of life.
Neuropsychology and Psychology of
COPD
Treatment
Empirical studies have documented neuropsychological
(i.e., cognitive) deficits in patients with chronic airway Research to date suggests that a variety of therapeuticap-
obstruction and COPD. Two of the largest studies proaches utilized in COPD patients (including oxygen
conducted in the 1980s were the Nocturnal Oxygen therapy, comprehensive rehabilitation programs, and
Therapy Trial (NOTT) and the Intermittent Positive surgical techniques) improve psychological and cognitive
Pressure Breathing Trial (Prigatano & Levin, 1988). The functioning. Long-term (greater than 6 months) use of
pattern and extent of cognitive dysfunction reported oxygen therapy improves cognitive performance in
in COPD vary across patients and appear to be associated COPD, probably due to direct effects of improved oxygen
with disease severity. In COPD patients with moderate delivery to the central nervous system (Prigatano & Levin,
to severe hypoxemia, deficits have been identified in sim- 1988). Early studies reported improvement in visual
ple motor movement and overall strength, perceptual- memory, verbal memory, and motor speed among the
motor integration, abstract reasoning, attention to COPD subjects following 6 months of continuous oxygen
auditory stimuli, learning and memory, and language therapy. Large multisite studies have also demonstrated
skills. In patients with mild hypoxemia, impairments in benefits of oxygen for cognitive function in COPD.
higher cerebral functioning include abstract reasoning, For example, in the Nocturnal Oxygen Therapy Trial,
auditory and visual attention, verbal and nonverbal COPD patients receiving continuous oxygen therapy for
learning and recall, and reasoning and motor skills 12 months experienced greater improvements in cognitive
(Kozora et al., 2008). There is some evidence that cogni- performance than did patients receiving only nocturnal
tive impairment has an independent impact on patients’ oxygen therapy.
daily functioning, medical regimen adherence, and quali- There is also evidence suggesting that comprehensive
ty of life, although results have been mixed (McSweeny & multidisciplinary rehabilitation programs can improve
Labuhn, 1996). cognitive functioning and psychological status in emphy-
Psychological changes and emotional distress have also sema patients. Comprehensive rehabilitation programs
been noted in COPD patients. To date, depression and for treatment of COPD are well established and typically
anxiety are the most commonly observed psychological include assessment, education, instruction on respiration,
problems in COPD (Hynninen, Breitve, Wiborg, Pallesen, & psychosocial support, and exercise training with the
Nordhus, 2005) with estimates of the prevalence of dep- goal of restoring patients to the highest level of indepen-
ression ranging from approximately 25% to 50%. Some of dent function (Make, 2004). As noted in a recent review
the discrepancies in prevalence estimates across studies article (Kozora et al., 2008), Emery and colleagues first
may be related to differences in the method used to assess reported in 1991 improved complex attention in COPD
depression. In addition to emotional distress, multiple patients following a 30-day exercise rehabilitation pro-
studies have demonstrated poor quality of life in patients gram that included instructional/educational compo-
with COPD, which has been associated with restrictions nents, psychosocial counseling, and stress reduction. In a
572 C Chronic Organic Brain Syndrome

subsequent study published in 1998, they reported im- J. B. Karlinsky, & T. E. King (Eds.), Baum’s textbook of pulmonary
diseases (7th ed.). Philadelphia: Lippincott, Williams & Wilkins.
provement in verbal fluency and reduction in symptoms
Friedlander, A. L., Lynch, D., Dyar, L. A., & Bowler, R. P. (2007). Pheno-
of anxiety and depression in a group participating in types of chronic obstructive pulmonary disease. COPD: Journal of
exercise, stress reduction, and education programs when Chronic Obstructive Pulmonary Disease, 4(4), 355–384.
compared to a control group participating in stress reduc- Hopkins, R. O., & Bigler, E. D. (2001). Pulmonary disorders. In R. E.
tion and education treatment only. This finding high- Tarter, M. Butters, & S. R. Beers (Eds.), Medical neuropsychology
(2nd ed., pp. 247–266). New York: Kluwer/Plenum.
lighted the utility of the exercise component toward
Hynninen, K. M., Breitve, M. H., Wiborg, A. B., Pallesen, S., & Nordhus,
improved cognitive and psychological functions. In I. H. (2005). Psychological characteristics of patients with chronic
2002, Kozora and colleagues also reported improvement obstructive pulmonary disease: A review. Journal of Psychosomatic
in visual attention and semantic fluency, among COPD Research, 59(6), 429–443.
patients following a 3-week comprehensive rehabilitation Kozora, E., Emery, C., Kaplan, R. M., Wamboldt, F. S., Zhang, L., & Make,
B. J. (2008). Cognitive and psychological issues in emphysema.
program when compared to untreated COPD and
Proceedings of the ATS, 5(4), 556–560.
healthy control subjects similar in age, education, and Make, B. (2004). Pulmonary rehabilitation. In J. D. Crapo, J. Glassroth,
gender. This program included exercise, educational, in- J. B. Karlinsky, & T. E. King (Eds.), Baum’s textbook of pulmonary
structional, and psychosocial components. In addition to diseases (7th ed., pp. 289–307). Philadelphia: Lippincott Williams
cognitive changes, significant improvement in depressive and Wilkins.
McSweeny, A. J., & Labuhn, K. T. (1996). The relationship of neuropsy-
symptoms was reported. Together, these studies indicate
chological functioning to health-related quality of life in systemic
improved cognitive performance and psychological medical disease: The example of chronic obstructive pulmonary
status following comprehensive rehabilitation with an disease. In I. Grant & K. M. Adams (Eds.), Neuropsychological assess-
exercise component. Many studies have also reported ment of neuropsychiatric disorders (pp. 577–602). New York: Oxford
increased quality of life following comprehensive reha- University Press.
Prigatano, G. P., & Levin, D. C. (1988). Pulmonary system. In R. E. Tarter,
bilitation (Make, 2004).
D. H. Van Theiel, & K. L. Edwards (Eds.), Medical neuropsychology
Finally, studies have suggested some improvement in (pp. 11–26). New York: Plenum.
cognition for moderate to severe COPD patients follow-
ing lung volume reduction surgery (LVRS). In an ancillary
study of the National Emphysema Treatment Trial
(NETT), Kozora and colleagues (Kozora et al., 2008)
examined neuropsychological and psychological func-
Chronic Organic Brain Syndrome
tioning of patients receiving LVRS when compared to
▶ Organic Brain Syndrome
patients receiving only medical therapy (MT). The LVRS
group showed significant improvement compared to the
MT group at 6 months on a measure of psychomotor
speed, delayed recall for verbal information, and trends
toward improved sequential thinking, and psychomotor Chronic Progressive Multiple
speed and naming to confrontation. LVRS patients Sclerosis
also experienced significant reduction in depression at
6 months, as reflected in total Beck Depression Inventory ▶ Primary Progressive Multiple Sclerosis
score. There was no direct evidence that improved cogni-
tion in LVRS was related to improved physical capacity
(workload and 6 min walk) or pulmonary function.
Chronic Widespread Pain
Cross References Disorder
▶ Fibromyalgia
▶ Anoxia

References and Readings

Cingulate Cortex
Anthonisen, N. R., & Manfred, J. (2004). Epidemiology of chronic
obstructive pulmonary disease. In J. D. Crapo, J. Glassroth, ▶ Cingulate Gyrus
 Cingulate Gyrus C 573

the more rostral olfactory piriform paleocortex unites the

Cingulate Gyrus orbitofrontal, insular, and temporopolar regions, while
the more caudal archicortex of the hippocampus provides
M ICHAEL M EGA the nidus for developmental spread through parahippo-
Providence Brain Institute campal and entorhinal regions into the posterior cingu-
Portland, OR, USA
C
late. Both paralimbic belts reflect a different emphasis
within the cingulate (Fig. 1). The orbitofrontal-centered
belt processes the internal affective state of the organism.
Synonyms The more recent hippocampal-centered belt is the exter-
nally directed evaluative arm of the limbic system.
Cingulate cortex; Subcallosal; Subgenual Both work in concert, enabling the selection of envi-
ronmental stimuli based on the internal relevance those
stimuli have for the organism. Although both areas 24 and
Structure 32 are part of the hippocampal belt, the more rostral
connections of area 24 contrast with the more caudal
The cingulate gyrus, first named by Burdach in 1822, was sensory connections of area 23, distinguishing the anteri-
combined with the anterior olfactory region and hippo- or executive from the posterior evaluative cingulate.
campus by Broca to form the ring of olfactory processing Appreciating that the major reciprocal connections
he termed the grand lobe limbique. Anatomic studies between the orbitofrontal trends are with the anterior
revealed extensive connections between the anterior cingulate, while the hippocampal trends are with the
thalamus, known to be associated with the hippocampus posterior cingulate, will assist the understanding of cin-
and hypothalamus, and the cingulate. In 1937, Papez gulate function.
combined these anatomic results with the clinical reports Three anterior effector regions and a posterior proces-
of emotional disturbances following lesions to the cingu- sing region also emerge through a review of the efferent
late and other limbic structures to propose a mechanism and afferent connections of the cingulate. The three ante-
of emotion based on a limbic circuit. For Papez, the rior regions include a visceral effector region inferior to the
integration of internal feelings and emotional responsive- genu of the corpus callosum encompassing area 25, the
ness with the functions of the lateral cerebral cortex oc- anterior subcallosal portions of 24a–b, and 32; a cognitive
curred in the cingulate. The limbic circuit of Papez effector region, which includes most of the supra-callosal
however did not find anatomical evidence to support area 24, and areas 24a’–b’ and 32’; and a skeletomotor
the closing connection of the cingulate to the hippocam- effector region within the depths of the cingulate sulcus
pus until 1975, when Shipley and Sørensen documented that includes areas 24c’/23c on the ventral bank, with
that the presubiculum, which receives a dense cingulate 24c’g and 6c on the dorsal bank. These three cingulate
outflow, projects heavily to layer III of the entorhinal effector regions integrate ascending input concerning the
cortex – the origin of the perforant pathway into hippo- internal milieu of the organism with visceral motor sys-
campal pyramidal cells. tems, cognitive-attentional networks, and skeletomotor
Understanding the function of the cingulate in the
integration of internal feelings and emotional responsive-
ness with movement and thought begins with an apprecia-
tion of its cytoarchitecture. Brodmann’s original
cytoarchitectonic separation of anterior and posterior
cingulate cortex into areas 24 and 23 based upon the
presence of agranular cortex in area 24 contrasted with
the granular cortex of area 23 has been refined by more
accurate studies of the progressive cytoarchitectonic elabo-
ration in the ventral to dorsal direction. Two main centers
of isocortical development can be traced phylogenetically
and through cytoarchitectonic progression. These two
developmental trends, termed paralimbic belts, are transi-
tional cortical zones from less-differentiated allocortex to Cingulate Gyrus. Figure 1 The Orbiotfrontal (red) and
more-differentiated isocortex with two functional centers: hippocampal (blue) paralimbic trends
574 C Cingulate Gyrus

centers to produce the affective motivation necessary for nucleus of the vagus, and the nucleus accumbens/olfacto-
the organism’s engagement in the environment. The pos- ry tubercle of the ventral striatum.
terior sensory processing region (areas 23a–b and 29/30) Brain areas that have reciprocal connections with the
assists in the memory and processing of environmental visceral effector region, except the claustrum that supplies
stimuli targeted as relevant to the organism based on their auditory input, also influence visceral function when sti-
motivational valence. The following sections will explore mulated. This results from their amygdalar connections
the connections of these four cingulate regions (Figs. 2 that convey the visceral state of the organism to paralimbic
and 3) and their function as observed from electrical areas. The orbitofrontal cortex mediates empathic, civil,
stimulation, imaging, and clinical data. and socially appropriate behavior. Rostral auditory associ-
ation cortex in the superior temporal area also provides
auditory information to the visceral effector region. No
Function visual information has direct access to the subcallosal area.
The dorsolateral prefrontal lobe, functioning as an
Visceral effector region. Major reciprocal connections with ‘‘executive processor,’’ provides nonreciprocal input
the visceral effector region are with the basal and accesso- from areas 9 and 46 to the subcallosal anterior cingulate
ry basal amygdala, medial orbitofrontal cortex areas 11, region. Executive functions permit an organized behav-
12, and 13, anterior superior temporal pole area 38, and ioral response to solve a complex problem. This includes
the anterior ventral claustrum. Major nonreciprocal pro- the activation of remote memories, self-direction, and
jections from the visceral effector region target the para- independence from environmental contingencies, shifting
sympathetic nucleus of the solitary tract, the sympathetic and maintaining behavioral sets appropriately, generating
thoracic intermediolateral column, the dorsal motor motor programs, and using verbal skills to guide behavior.
Dorsolateral prefrontal efferents into the subcallosal cin-
gulate provide feedback inhibition on the basic drives of
hunger, aggression, and reproductive urges. Table 1 for a
summary of these anatomic connections.
Subcallosal cingulate processing modulates visceral
output from brain-stem sympathetic and parasympathetic
centers. Access to the basal ganglia, via the ventral striatum,
allows processing of the internal milieu of the organism to
influence the skeletal motor system as well. This visceral
motor network encompasses the bulk of the orbitofrontal-
centered paralimbic belt dedicated to assessing the emo-
Cingulate Gyrus. Figure 2 Cytoarchitectonic divisions of the tional valence of objects based upon internal motivating
cingulate and adjacent areas drives. Patients with lesions in this area are often

Cingulate Gyrus. Table 1 Major reciprocal connections and

nonreciprocal targets for the visceral effector region of the
cingulate cortex
Reciprocal connections
Basal and accessory basal amygdala
Medial orbitofrontal areas 11, 12, and 13
Superior temporal pole area 38
Anterior ventral claustrum
Nonreciprocal targets
Parasympathetic nucleus of solitary tract
Cingulate Gyrus. Figure 3 The four functional divisions of the Sympathetic intermediolateral column
cingulate. The visceral effector region (1), the cognitive
Dorsal motor nucleus of the vagus
effector region (2), the skeletomotor effector region (3), and
Nucleus accumbens and olfactory tubercle
the posterior cingulate (4)
 Cingulate Gyrus C 575

disinhibited with irritability, lability, tactlessness, and fatu- reticular activating system and its control over arousal.
ous euphoria. Patients act upon visceral drives without Table 2 for a summary of these anatomic connections.
regard to social decorum. Skeletomotor effector region. Major reciprocal connections
Cognitive effector region. Major reciprocal connections with the skeletomotor effector region are with the primary
with the cognitive effector region are with the basal amyg- and supplementary/premotor motor cortex areas 4 and 6, C
dala, prefrontal areas 8, 9, 10, and 46, caudal orbitofrontal prefrontal areas 8, 9, and 46, parietal areas 1, 2, 3a, 5, and
area 12, inferior temporal pole area 38, rostral insula, 7b, and caudal insula. Major nonreciprocal projections
anterior parahippocampal areas 35 and 36, and the ante- from the skeletomotor area target the lateral putamen,
rior medial claustrum. Areas reciprocally connected to the spinal cord, ventromedial parvocellular division of the red
cognitive effector region share a general similarity with nucleus, and the ventrolateral pontine gray matter.
the subcallosal anterior region underscoring their com- Primary motor cortex has very limited input. The me-
mon membership in the orbitofrontal paralimbic belt. dial supplementary, lateral premotor, and cingulate skeletal
The cognitive effector region is more developed in its motor regions are the only forebrain inputs to the primary
cytoarchitecture, than the subcallosal cingulate, and thus motor cortex. The skeletomotor region in the banks of the
has stronger connections with more phylogenetically re- cingulate sulcus conveys limbic influence to the medial
cent neocortex of dorsolateral prefrontal areas 8, 9, 10, supplementary, lateral premotor, and primary motor cor-
and 46 devoted to executive function. The amygdala pro- tex. Frontal eye fields in area 8 also share reciprocal connec-
vides internal affective input to the supracallosal anterior tions with the skeletal motor effector region. Areas 9 and 46
cingulate. The distribution of amygdala efferents deline- of the dorsolateral prefrontal cortex contribute executive
ates the dorsal boundary of the cingulate as a functional input to the limbic motor system. Thus, executive and
system. Auditory input arises from the anterior medial limbic systems gain access to primary motor area 4 indi-
claustrum as well as a minor link with the auditory asso- rectly. The cingulate skeletal motor region receives the
ciation area of the superior temporal gyrus. The rostral greatest outflow from executive prefrontal cortex than
insula and anterior parahippocampal areas provide addi- all other motor cortices underscoring its influence over
tional reciprocal connections with the cognitive effector goal-directed behavior. Sensory-motor parietal areas 1, 2,
region not associated with the subcallosal region. Rostral 3a, and 5 also have reciprocal connections with the skeletal
insular cortex is a transitional paralimbic region that motor center within the banks of the cingulate sulcus. The
integrates visceral alimentary input with olfactory and rostral parietal area 7b has a strong relationship with the
gustatory afferents. Connections with the anterior para- premotor cortex, while the granular cortex of the caudal
hippocampal areas 35 and 36 allow the supracallosal cin-
gulate to influence multimodal sensory afferents entering
the hippocampus. Cingulate Gyrus. Table 2 Major reciprocal connections and
Major nonreciprocal projections of the supracallosal nonreciprocal targets for the cognitive effector region of the
anterior cingulate include the auditory association cortex cingulate cortex
of anterior superior temporal area 22, allowing the cognitive
effector region to influence language and the access of Reciprocal connections
semantic stores. The posterior parietal area 7a and the Basal amygdale
dorsomedial head of the caudate are also targets. Parietal Prefrontal areas 8, 9, 10, and 46
area 7a is the sensory component in the extrapersonal Caudal orbitofrontal cortex area 12
attentional network linked with the dorsolateral prefrontal Inferior temporal pole area 38
‘‘executive system.’’ The head of the caudate is also a target Rostral insula
of this executive prefrontal cortex. Cingulate input to the
Anterior parahippocampal areas 35 and 36
caudate assists in the initiation of vocalization behavior as
Anterior medial claustrum
well as executive function. Emotional vocalizations occur-
ring during stimulation in monkeys requires intact cingu- Nonreciprocal targets
late efferents to the periaqueductal gray that produce Anterior superior temporal area 22
similar behaviors when stimulated. The most caudal amyg- Parietal area 7a
dalar projections to 24c, extending into anterior 24c’, inner- Dorsomedial head and body of caudate
vate a face representation region that may have direct
Periaqueductal gray
connections with the facial nucleus in the pons. Efferents
Dorsomedial pontine gray matter
to the dorsomedial pons provide cingulate influence on the
576 C Cingulate Gyrus

insula is a somatosensory limbic region. More corticospinal The posterior granular sensory cortices are distin-
neurons are found in the cingulate than are found in the guished from the anterior agranular executive cortices.
supplementary motor cortex, and the cingulate has about The posterior cingulate, with its prominent granular
40% of the amount found in primary motor cortex. Table 3 layer IV, is dedicated to visuospatial and memory proces-
for a summary of these anatomic connections. sing. Major reciprocal connections are with the dorsal
Sensory processing region. Major reciprocal connections visual system of the inferior parietal lobe dedicated to
with the sensory processing region are with caudal parie- spatial processing and with the frontal eye fields in area
tal area 7a, frontal eye fields area 8, posterior perirhinal 8. Reciprocal connections with lateral prefrontal area 46
area 35, presubiculum, posterior parahippocampal area allow an interaction between executive and sensory/mne-
36, prefrontal area 46, and the ventral caudal claustrum. monic processing, which may mediate perceptual work-
Major nonreciprocal projections from the sensory proces- ing memory tasks. Posterior parahippocampal and
sing region target the dorsal caudate, posterior superior perirhinal areas 36 and 35, as well as the presubiculum,
temporal gyrus area 22, and orbitofrontal area 11. These are reciprocally connected to the sensory processing re-
regions are shown in Table 4. gion of the posterior cingulate. These connections modu-
late the multimodal efferents entering the entorhinal layer
III cells that form the perforant pathway into the hippo-
Cingulate Gyrus. Table 3 Major reciprocal connections and campus. Feedback from these areas to the cingulate pro-
nonreciprocal targets for the skeletomotor effector region of vides highly processed sensory information, and the
the cingulate cortex ventral visual system involved in feature analysis can
Reciprocal connections influence the posterior cingulate through these connec-
Primary motor area 4 tions. Although in cats dorsal caudal claustrum is related
Supplementary motor area 6 to visual processing, while the ventral caudal claustrum
receives auditory input, it is possible that in primates
Prefrontal areas 8, 9, and 46
visual information may reach the posterior cingulate via
Parietal areas 1, 2, 3a, 5, and 7b
the ventral caudal claustrum.
Caudal insula The nonreciprocal targets of the posterior sensory
Nonreciprocal targets processing region include the dorsal caudate which also
Lateral putamen receives input from area 7a of the caudal inferior parietal
Spinal cord lobe. This shared connection between the dorsal head of
the caudate and the dorsal visual system of area 7a sup-
Red nucleus
ports the role of the posterior cingulate in visual atten-
Ventrolateral pontine gray matter
tion. Output to posterior superior temporal area 22 will
influence auditory association cortex. Limited efferents to
the rostral portion of area 11 provide the only overlap
with the orbitofrontal-centered belt.
Cingulate Gyrus. Table 4 Major reciprocal connections and Electrical stimulation of the cingulate. Electrical stimula-
nonreciprocal targets for the sensory processing region of the tion studies of the cingulate in humans and animals are
cingulate cortex difficult to interpret because differing techniques have
Reciprocal connections been used in these investigations. With varying intensity,
Caudal parietal area 7 time course, and location of stimulation, it is not
surprising that a spectrum of results is noted. Despite
Frontal eye fields area 8
technical variations, stimulation of the anterior cingulate
Prefrontal area 46
in humans regularly produces visceral motor and affective
Posterior parahippocampal areas 35 and 36 changes, speech alterations, and automatic motor beha-
Presubiculum viors (Meyer, McElhaney, Martin, & McGraw, 1973). In
Ventral caudal claustrum contrast to inhibitory responses elicited by the stimula-
Nonreciprocal targets tion of primary motor cortex, which cannot be controlled,
Dorsal caudate
respiratory arrest from cingulate stimulation can be over-
come volitionally (Penfield & Jasper, 1954). Automatic
Posterior superior temporal area 22
behaviors noted include unilateral and bilateral move-
Orbitofrontal area 11
ments and repetitive ‘‘tic like’’ movements of the hands,
 Cingulate Gyrus C 577

lips, or tongue. These movements can also be consciously cingulate skeletomotor region is also activated (Grafton,
suppressed; implicating the cingulate as an ‘‘unconscious’’ Woods, & Tyszka, 1994).
effector supports its role in the pathophysiology of
obsessive–compulsive disorder (behaviors that respond
well to cingulotomy). Fear, pleasure, agitation, euphoria, Illness C
and a sense of well being – affective phenomena also
common after limbic stimulation – have been reported Structural and functional abnormalities. Seizures originat-
(Meyer, McElhaney, Martin, & McGraw, 1973). Involun- ing in the anterior cingulate can alter visceral activity,
tary vocalizations and speech arrests are less common in produce involuntary skeletomotor output, result in dis-
humans than in animals with stimulation of areas 32, 24, turbed attention, and cause interictal behavior abnormal-
and the rostral part of 25 (Vogt & Barbas, 1988). ities. The severity and specific abnormality will depend
Functional activation of the cingulate. In functional activa- upon the location of the seizure focus and ensuing dam-
tion studies, the cognitive effector region of the anterior age that affects interictal brain function. A diverse assort-
cingulate is activated when sustained attention to novel ment of atonic, absence, speech arrest, autonomic, and
tasks is required. Tasks spanning motor, language, mem- complex partial seizures with secondary generalization
ory, and visuospatial paradigms all produce supracallosal have been described. Inaccessibility of the medial hemi-
anterior cingulate activation. When memory encoding is sphere to surface electrode recording is the greatest obsta-
combined with a motor task demanding sustained cle to the elucidation of cingulate seizures.
divided attention (Fletcher et al., 1995), only the anterior In a study involving 36 cases (Mazars, 1970), depth
cingulate is activated due to the sustained vigilance electrodes revealed near-instantaneous bilateral spread to
demanded by dividing effort between the two tasks. the frontal poles when the focus was in the anterior
When motivation to master a task is no longer required, cingulate; posterior foci spread to the contralateral cingu-
and accurate performance of a task becomes routine, the late within seconds, followed by involvement of the con-
anterior cingulate returns to a baseline activity level vexities with generalized tonic–clonic seizures. Emotional
(Raichle et al., 1994). The acquisition of novel cognitive stress often precipitated the seizures. Psychoses and
strategies requires the ‘‘dynamic vigilance’’ of the supra- episodic rage were common interictal behavioral abnorm-
callosal cingulate, but with practice the motivation re- alities that responded to the removal of the anterior cin-
quired to entrain new cognitive networks to a novel task gulate and occasionally the frontal pole as well.
is no longer necessary. A distinction between motivation Consciousness may be altered and automatisms can be
and attention is important. A task is still attended to and voluntarily inhibited or integrated with ongoing move-
completed correctly after the motivating influence of the ments (Geier et al., 1977).
supracallosal cingulate has initiated the acquisition of an An 11-year-old girl who initially had atonic seizures at
efficient cognitive routine. Through the activation of the age 30 months was reported to develop complex partial
anterior supracallosal cingulate limbic motivation directs seizures with blinking, lip smacking, automatisms, and
the selection of the best cognitive strategy among many humming (Levin & Duchowny, 1991). An obsessive–
competing contingencies. Thus, activation studies using compulsive disorder developed over a 5-year period, and
varied tasks consistently activate the cognitive effector by age 8, she became preoccupied with Satan and her
region in normals motivated to succeed in whatever task personal hygiene. Seizure focus, recorded from depth
is given them. The contribution to an extrapersonal at- electrodes, was in the right anterior cingulate. The
tentional network – involving direct links between the patient’s behavioral abnormalities responded well to a
anterior cingulate, dorsolateral executive frontal area, 4-cm ablation of the right anterior cingulate.
and the inferior parietal lobule – provided by the cogni- Another case of a right anterior cingulate focus with
tive effector region is the motivation to engage in a cogni- accompanying behavioral abnormalities has been de-
tive challenge. scribed (Devinsky, Morrell, & Vogt, 1995). One year
Functional imaging has also confirmed the role of the after mild head trauma, a 42-year-old male developed,
skeletomotor effector region in the preparation of motor over a 15-year period, sociopathic behavior and complex
output and motor learning. When a motor task is only partial seizures unresponsive to medical treatment. Sei-
imagined, the cingulate cortex inferior and anterior to the zures were usually nocturnal and frequent (10–20 per
supplementary motor area (dorsal bank of the cingulate night), with stereotypic motor output: facial contortions,
sulcus) shows significant activation. During the acquisi- tongue thrusting, a strangulated yell, flexion of the neck
tion of procedural learning in a rotory pursuit task, the and trunk, bilateral extremity extension, and thrashing
578 C Cingulate Gyrus

with preserved consciousness. Occasionally, generali- lesions, possibly affecting the ascending reticular core. Fail-
zation to tonic–clonic seizures developed with loss of ure of response inhibition on go-no-go tests is the major
consciousness. neuropsychological deficit in the patient with an anterior
Irritability, disinhibition, and sexual deviancy were medial frontal damage. The loss of spontaneous motor
behavioral complications in a police officer who was dis- activity results when the lesion involves the supplementary
missed from the force because of brutality and the use of motor area and the skeletomotor effector region. When
confiscated drugs. Surface and sphenoidal electroenceph- these two motor regions are spared, motor activity will be
alogram showed rhythmic bifrontal theta. Magnetic reso- normal but the patient will demonstrate profound indif-
nance imaging (MRI) and [18F]-fluorodeoxyglucose ference, docility, and the loss of motivation to engage in a
positron emission tomography (FDG-PET) were essen- task. They can be led by the examiner to engage in a task
tially normal, but depth electrodes revealed a right cingu- but will fail to self-generate sustained directed attention.
late focus which spreads to the ipsilateral orbitofrontal They lack cognitive motivation.
area and contralateral anterior cingulate in 300 ms. Re- The role of the anterior cingulate as a cognitive effec-
section of the right cingulate and anterior corpus callo- tor is appreciated within the realm of language. Language,
sum relieved 90% of the spells with only brief axial flexion a cognitive function, is distinguished from the motor
being the residual seizures. The behavioral abnormalities function of speech. Transcortical motor aphasia
were reported to improve with the patient married and (TCMA) is the usual result of left anterior medial or
employed as a fast-food restaurant manager. anterior dorsolateral prefrontal lesions. The classic syn-
Both stimulation and seizure activity can discharge drome of TCMA is initial mutism that resolves in days to
the functional centers of the cingulate to produce a vis- weeks, yielding a syndrome featuring delayed initiation of
ceral effect, a cognitive or behavioral change, and a speech brief utterances without impaired articulation, excellent
or motor output. Appreciating the functional centers repetition, inappropriate word selection, agrammatism,
within the cingulate assists the interpretation of the and poor comprehension of complex syntax. Activation
signs and symptoms exhibited when it discharges. The of dorsolateral prefrontal cortices enabling language and
interictal behavioral abnormalities of anterior cingulate speech arises from two sources: the anterior cingulate and
epilepsy reflects the dysfunction of limbic networks the supplementary motor area (with the cingulate skele-
which, if affecting infracallosal and orbitofrontal cortex, tomotor effector region). When the executive prefrontal
will result in visceral motor disturbances and disinhibi- cortex (areas 9, 10, and 46) is disrupted, cognitive lan-
tion with socially inappropriate behavior. Obsessive– guage deficits are prominent (TCMA, type I); when
compulsive features may occur with dysfunction of the motor neurons in area 4, devoted to the speech apparatus,
cognitive component of the supracallosal cingulate. This are disconnected from their activation, speech hesitancy
abnormal ‘‘dynamic vigilance’’ exerted by the cognitive and impoverished output ensues (TCMA, type II). These
effector region in obsessive–compulsive disorders can two functional realms are separable and can be discon-
occur from a well-circumscribed seizure focus in this nected anywhere along two pathways. Direct damage to
region (Levin & Duchowny, 1991) and is relieved by the supplementary motor area or its efferent pathway to the
surgical ablation of this region or its outflow (Tow & motor cortex traveling in the anterior superior paraventri-
Whitty, 1953). cular white matter will produce TCMA type II. Direct
Focal lesions and syndromes. Well-circumscribed lesions in damage to the anterior cingulate, its outflow to areas 9,
humans are rarely confined to one region of the cingulate. 10, and 46, or to the caudate – via the subcallosal fasciculus,
With an anterior lesion, both the cognitive, skeletomotor just inferior to the frontal horn of the lateral ventricle – will
and visceral effector regions are often affected. Bilateral disrupt frontal-subcortical circuits involved in motivation
lesions result in an akinetic mute state (▶ Akinetic Mut- and executive cognitive functions. The initial muteness has
ism). Patients are profoundly apathetic. Rarely moving, been described by a patient after recovering from an anteri-
and incontinent, they eat and drink only when fed, and if or cingulate/supplementary motor infarction as a loss of the
speech occurs it is limited to monosyllabic responses to ‘‘will’’ to reply to her examiners, because she had ‘‘nothing
questioning. Patients appear awake with eyes tracking to say,’’ her ‘‘mind was empty,’’ and ‘‘nothing mattered’’
objects. Displaying no emotions, even when in pain, (▶ Akinetic Mutism).
patients show complete indifference to their circumstance. The cingulum bundle has also been the site of surgical
Transient akinetic mutism with similar features occurs with lesions (cingulumotomy, or cingulotomy when cingulate
unilateral lesions. The akinetic mute state can also result cortex is also removed) to treat psychiatric and pain dis-
from bilateral paramedian diencephalic and midbrain orders. The cingulum contains the efferents and afferents
 Cingulate Gyrus C 579

of the cingulate to the hippocampus, basal forebrain, and the hippocampus during encoding and may also be
amygdala, and all cortical areas, as well as fibers of passage important in the storage of long-term information.
between hippocampus and prefrontal cortex, and from Synthesizing cytoarchitectonic refinements, nonhu-
the median raphé to the dorsal hippocampus. Surgical man primate tracer studies, clinical-behavioral correla-
ablation of the anterior portion (sparing fibers relevant tion data, and functional neuroimaging results have C
to memory function) is most successful when treating been refined – but have not significantly added to – the
aggression, extreme anxiety, obsessive–compulsive beha- basic description of cingulate function offered by Papez:
viors, and severe pain. Psychotic symptoms show only a
" It is thus evident that the afferent pathways from the recep-
temporary response. The three anterior cingulate regions,
tor organs split at the thalamic level into three routes, each
by virtue of the distinct functional systems they access, are
conducting a stream of impulses of special importance. One
the conduits through which limbic motivation can acti-
route conducts impulses through the dorsal thalamus and
vate feeling, thought, and movement.
the internal capsule to the corpus striatum. This route
Lesions of the posterior cingulate disrupt memory func-
represents ‘the stream of movement.’ The second conducts
tion in animals and humans. The closing link in the circuit
impulses from the thalamus through the internal capsule to
of Papez, from the anterior thalamic efferents traveling
the lateral cerebral cortex. This route represents ‘the stream
through the posterior cingulum to areas 32 and 29/30, is
of thought.’ The third conducts a set of concomitant
the cingulate projection sent to the presubiculum. Anterior
impulses through the ventral thalamus to the hypothala-
cingulotomy will not disrupt this memory circuit but rarely
mus and by way of the mamillary body and the anterior
pathologic lesions will extend into, and beyond, the poste-
thalamic nuclei to the gyrus cinguli, in the medial wall of the
rior cingulate. If the lesion extends inferior to the splenium
cerebral hemisphere. This route represents ‘the stream of
of the corpus callosum, it may also disrupt the fornix, thus
feeling.’ In this way, the sensory excitations which reach the
disconnecting the efferents from the hippocampus to the
lateral cortex through the internal capsule receive their
diencephalon. If the lesion extends posteriorly, it may dam-
emotional coloring from the concurrent processes of hypo-
age the supracommissural portion of the hippocampus –
thalamic origin which irradiate them from the gyrus cinguli.
the gyrus fasciolaris and the fasciola cinerea. A large left-
(Papez, 1937)
sided lesion that extended beyond the posterior cingulate
into the fornix and supracommissural hippocampus after
the surgical repair of an arteriovenous malformation
resulted in a persistent amnesia (Cramon & Schuri, 1992). References and Readings
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Tow, P. M., & Whitty, C. W. M. (1953). Personality changes after opera- Rose, S. E., McMahon, K. L., Janke, A. L., O’Dowd, B., de Zubicaray, G.,
tions of the cingulate gyrus in man. Journal of Neurology Neurosur- Strudwick, M. W., et al. (2006). Diffusion indices on magnetic
gery & Psychiatry, 16, 186–193. resonance imaging and neuropsychological performance in amnestic
Valenstein, E., Bowers, D., Verfaellie, M., Heilman, K. M., Day, A., & mild cognitive impairment. Journal of Neurology, Neurosurgery &
Watson, R. T. (1987). Retrosplenial amnesia. Brain, 110, 1631–1646. Psychiatry, 77(10), 1122–2112.
Vogt, B. A., & Barbas, H. (1988). Structure and connections of the Wakana, S., Jiang, H., Nagae-Poetscher, L. M., van Zijl, P. C. M., & Mori, S.
cingulate vocalization region in the rhesus monkey. In J. D. Newman (2004). Fiber tract-based atlas of human white matter anatomy.
(Eds.), The physiological control of mammalian vocalization (pp. Radiology, 23(1), 77–87.
203–225). New York: Plenum Press. Zhang, Y., Schuff, N., Jahng, G. H., Bayne, W., Mori, S., Schad, L., et al.
Von Cramon, D. Y., & Schuri, U. (1992). The septo-hippocampal path- (2007). Diffusion tensor imaging of cingulum fibers in mild
ways and their relevance to human memory: A case report. Cortex, cognitive impairment and Alzheimer disease. Neurology, 68(1),
28, 411–422. 13–19.

Cingulum
CIQ
I RENE P IRYATINSKY
Butler Hospital and Alpert Medical School of Brown ▶ Community Integration Questionnaire
University
Providence, RI, USA

Circadian Clock
Definition
▶ Circadian Rhythms
The cingulum is a collection of white matter fibers project-
ing from the cingulate gyrus to the entorhinal cortex in the
brain, allowing for communication between components
of the limbic system. The cingulum connects the medial
temporal lobe with the posterior cingulate gyrus. Diffusion
Circadian Rhythms
tensor imaging studies have reported cingulum bundle
B RUCE J. D IAMOND
disruption in mild cognitive impairment and Alzheimer’s
William Paterson University
disease. In addition, some research indicates that in Alzhei-
Wayne, NJ, USA
mer’s disease, the posterior cingulate cortex hypofunction
is due to the indirect effect of the degeneration of cingulum
fibers secondary to medial temporal lobe atrophy.
Synonyms
Cross References Biological cycles; Biorhythms; Circadian clock

▶ Cingulate Gyrus
Short Description or Definition
References and Readings
The pervasive characteristics of living organisms are
Catani, M., Howard, R. J., Pajevic, S., & Jones, D. K. (2002). Virtual
rhythmic biological and behavioral changes, which are
in vivo interactive dissection of white matter fasciculi in the human expressed at varying levels of organization ranging from
brain. NeuroImage, 17(1), 77–94. basic cellular to the highly complex level. These rhythms
 Circadian Rhythms C 581

are generally referred to as circadian rhythms and they Developmental factors may also mediate some of the
organize a variety of behaviors, including sleep, which is variations in circadian rhythms. For example, the aging
characterized by a 90-min Rapid Eye Movement (REM) process is often accompanied by changes in circadian
cycle and the wakefulness–sleep cycle, which is organized rhythms that may affect sleep and place older adults at a
around an approximate 24-h cycle (Carlson, 1999). higher risk for sleep disturbance (Lee-Chiong, 2005). C

Categorization History and Impact

The core body temperature rhythm and the sleep–wake Endogenous biological clocks were demonstrated over
cycle are among the most extensively studied of the 200 years ago (Kolb & Wishaw, 2005) and entrainment
human biorhythms (Waterhouse & DeCoursey, 2004b) was identified as the most important property for deter-
with the 24-h circadian rhythms represented most prom- mining the phase relationship of a circadian clock
inently in the research literature. This is because these (Johnson, Elliot & Foster, 2004). Circadian rhythms
rhythms impact daily life (e.g., work, school, medical– may confer an adaptive value on an organism, since the
psychological status) and are of relatively brief duration, organism can anticipate environmental changes (Clark,
so they are amenable to study (Clark, 2005). There is also 2005), and physiological functions synchronized with
a developmental progression in how rhythmicity is the time of day are associated with enhanced efficiency
expressed from birth to old age (Waterhouse & DeCour- (Quigg, 2006). Disruption in circadian rhythms can ad-
sey, 2004b). There are a number of biological rhythms versely impact individuals involved in shift and night work,
characterized by different time periods (Table 1). who suffer jet lag or whose schedules are temporally irregu-
lar. The impact is more profound when task demands
involve vigilance and reaction time (Costa, 1999) and are,
Mechanisms therefore, more vulnerable to the effects of fatigue. Atten-
tional regulation over both incoming information and
Circadian rhythms are modulated by both internal clocks outgoing responses may also be vulnerable to time of
(e.g., pacemakers) and external triggers that can entrain day effects. Disturbances in sleep–wake cycles and
biorhythms, acting as zeitgebers (e.g., changes in illumi- biological rhythms have been associated with affective
nation). The superchiasmic nucleus (SCN) of the hypo- disorders including depression.
thalamus has been identified as the principal biological
clock (Carlson, 1999) based on lesion studies and day–
night changes in activity levels. The mechanisms med- Evaluation
iating communication and synchronization between
neurons appear to be chemical in nature. Both the SCN There are large differences in circadian cycles between
and the pineal gland exert an influence on seasonal younger and older adults. Clinicians should assess the
rhythms with SCN-induced melatonin secretion involved quantitative and qualitative nature of cognitive decline
in synchronizing circadian rhythms (Carlson, 1999). in the elderly with attention to circadian influences
(with the elderly tending to be morning oriented)
(Hasher, Goldstein & May, 2005). In evaluating clients
for possible disruptions in circadian rhythms, clinicians
Circadian Rhythms. Table 1 Biological rhythms
would be well advised to determine if clients engage in
Biological shift work, have experienced jet lag or changes in sched-
rhythms Time period Activity ule, or exhibit fatigue, sleep disorders, excessive daytime
drowsiness, or decrements in job-related performance
Infradian Period of less Eating behaviors
than 24 h
(Costa, 1999).
Circadian Period of about Sleep–wake
24 h
Treatment
Ultradian Period of about Human female
28 days menstrual cycle
While the circadian clock of healthy humans is entrained
Circannual Yearly Migratory birds
to a period of about 24 h, the precise timing varies on an
582 C Circle of Friends

intraindividual and interindividual basis. At a certain Quigg, M. (2006). Circadian rhythms: Problems with the body clock.
In N. F. Watson & B. V. Vaughn (Eds.), Clinicians guide to sleep
point, these deviations may be considered clinical abnor-
disorders (pp. 277–304). Philadelphia: Taylor & Francis.
malities (i.e., seasonal affective disorder). In fact, seasonal Waterhouse, J. M., & DeCoursey, P. J. (2004a). Human circadian organi-
affective disorder has been treated using phototherapy, zation. In J. C. Dunlap, J. J. Loros, & P. J. DeCoursey (Eds.),
which involves the use of light boxes, whereby a patient Chronobiology: Biological timekeeping (pp. 291–323). Sunderland,
is exposed to light each winter morning or evening and MA: Sinauer.
Waterhouse, J. M., & DeCoursey, P. J. (2004b). The relevance of circadian
the circadian rhythm becomes entrained in ways that
rhythms for human welfare. In J. C. Dunlap, J. J. Loros, &
induce circadian phase shifts (Kolb & Wishaw, 2005). P. J. DeCoursey (Eds.), Chronobiology: Biological timekeeping
Individuals who make substantial changes to their sleep– (pp. 325–356). Sunderland, MA: Sinauer.
wake cycles during night work or after trans-meridian
travel could be helped using a chronobiological treatment.
The treatment would involve exposure to appropriate
circadian synchronizers and basing therapy on phase re-
sponse curves for light and melatonin (Waterhouse & Circle of Friends
DeCoursey, 2004a). By making accommodations in the
timing of work-related activities (Hasher et al., 2005), ▶ Circles of Support
performance efficiency can be improved and fatigue
decreased, thus enhancing health and safety (Costa, 1999).
And in treating patients with bipolar disorder, psychoso-
cial therapies should identify areas of vulnerability includ- Circle of Willis
ing unhealthy circadian rhythms (Newman, 2006).
E LLIOT J. R OTH
Northwestern University
Cross References
Chicago, IL, USA
▶ Fatigue
▶ Sleep Disturbance
Definition

References and Readings The circle of Willis is the anatomical name given to
the formation of arteries at the base of the brain that
Carlson, N. R. (1999). Foundations of Physiological Psychology (4th edn.).
contribute the overwhelming majority of blood supply
Boston: Allyn & Bacon. to the brain.
Clark, A. V. (Ed.). (2005). Causes, role and influence of mood states.
Hauppauge, NY: Nova Biomedical Books.
Costa, G. (1999). Fatigue and biological rhythms. In D. J. Garland, J. A.
Wise, & D. V. Hopkin (Eds.), Handbook of aviation human factors Current Knowledge
(pp. 235–255). Mahwah, NJ: Lawrence Erlbaum.
Hasher, L., Goldstein, D., & May, C. P. (2005). It’s about time: Circadian
rhythms, memory, and aging. In C. & Izawa N. Ohta (Eds.), Human The circle of Willis is formed by the connections between
learning and memory: Advances in theory and application: The 4th the predominantly horizontal branches that derive from
Tsukuba international conference on memory (pp. 199–217). the middle cerebral arteries anteriorly and from the
Mahwah, NJ: Lawrence Erlbaum. basilar artery posteriorly. The right and left middle cere-
Johnson, C. H., Elliot, J., & Foster, R. (2004). Fundamental properties of
bral arteries each give off an anterior cerebral artery
circadian rhythms. In J. C. Dunlap, J. J. Loros, & P. J. DeCoursey
(Eds.), Chronobiology: Biological timekeeping (pp. 67–105). Sunder- (forming the anterolateral borders of the circle of Willis),
land, MA: Sinauer Associates. which goes forward to supply blood to the frontal lobe.
Kolb, B., & Wishaw, I. Q. (2005). An introduction to brain and behavior. These anterior cerebral arteries are connected to each
New York: W. H. Freeman. other by the anterior communicating artery, which
Lee-Chiong, T. L. (2005). Sleep: A comprehensive handbook. Hoboken, NJ:
forms the front of the circle. Posteriorly, the basilar
Wiley.
Newman, C. F. (2006). Bipolar disorder. In F. Andrasik (Ed.), Compre- artery bifurcates into the right and left posterior cerebral
hensive handbook of personality and psychopathology: Vol. 2: Adult arteries, which supply the occipital and posterior tem-
psychopathology (pp. 244–261). Hoboken, NJ: Wiley. poral lobes and the cerebellum, forming the posterior
 Circles of Support C 583

border of the circle. Each posterior cerebral artery is personal goals. It is one of many tools addressing life
connected to the middle cerebral artery on its planning from a functional or strategic assessment ap-
corresponding side by a posterior communicating artery, proach known as person-centered planning. Person-
forming the posterolateral borders of the circle. There centered planning replaces more traditional assessment
are several clinical implications of the circle pattern approaches associated with the medical model of services. C
of these arteries. Perhaps most importantly, because Circles of support originated in Canada and have experi-
of the interconnectedness of the arteries that result enced widespread use in North America. Circles view
from this circle format, if one of the main arteries is people as individuals and assist them to attain self-
occluded, the distal smaller arteries that it supplies determination focusing upon empowerment and
can potentially receive blood from the other arteries not dependence of the individual. It is capacity oriented
that make up the circle, a phenomenon known as and identifies strengths, preferences, likes, and dislikes of
collateral circulation. This helps to prevent cerebral the individual. The circle will also identify support needs
ischemia and stroke. The circle of Willis also is a in order to achieve a particular goal.
common site for cerebral aneurysms, with the greatest The focus person leads the process and decides who
numbers involving the anterior communicating artery, will participate in the circle and the direction which the
posterior communicating arteries, and middle cerebral planning will take. Typically, a facilitator is selected
arteries. from within the circle to help energize the group. The
first circle is the circle of intimacy and includes
the people most intimate in the focus person’s life. The
Cross References second circle, the circle of friendship, includes good
friends and close relatives. The third circle, the circle
▶ Anterior Cerebral Artery of participation includes the people and organizations
▶ Anterior Communicating Artery the focus person is involved with. The fourth circle is the
▶ Basilar Artery circle of exchange and includes those that are paid to
▶ Internal Carotid Artery be in the focus person’s life. Members are not paid to be
▶ Middle Cerebral Artery involved in a circle of support, but are involved in the
▶ Posterior Cerebral Artery focus person’s life in some capacity. Members use their
▶ Posterior Communicating Artery skills, knowledge, and networks to help the focus person
▶ Vertebrobasilar System accomplish goals. The circle develops and monitors
the plan, making sure that it is current with the wishes
of the focus person. It is as ongoing process that is
dynamic.

Circles of Support
A MY J. A RMSTRONG Cross References
Virginia Commonwealth University
Richmond, VA, USA ▶ Inclusion
▶ Medical Model

Synonyms
References and Readings
Circle of friends
Falvey, M. A., Forest, M., Pearpoint, J., & Rosenberg, R. (1994). All my
life’s a circle. Using the tools: Circles, MAP’s and PATH. Toronto,
Definition Canada: Inclusion Press.
O’Brien, C. L., & O’Brien, J. (2000). The origins of person-centered
planning: A community of practice perspective. Retrieved from
A circle of support is a group of people that forms a http://thechp.syr.edu/PCP_History.pdf
community around a specific individual (focus person) O’Brien, J., & Lyle O’Brien, C., (Eds.). (1998). A little book about person
with significant disabilities to assist him or her to achieve centered planning. Toronto: Inclusion Press.
584 C Circumduction

are often used by persons with aphasia when having

Circumduction difficulty recalling or retrieving a word. In place of the
target word, a description of the word is used. Circumlo-
T HESLEE J OY D E P IERO cutions, or ‘‘substitutions of object description (e.g., snow/
Boston University School of Medicine soft, white/cold) and instrumental function (e.g., watch/
Braintree, MA, USA knowing the hour) can be observed in aphasic output’’
(Benson & Ardila, 1996; p. 53). They occur frequently
with a posterior (sensory) aphasia.
Synonyms Circumlocutions can represent a positive symptom
of anomia in which, upon failure to retrieve a word,
Spastic gait the subject talks around the word by defining it, describ-
ing a referent, or even making sound effects. Pointing
Definition to his wrist, a patient might say, ‘‘I wear it right here,
and I tell time with it; mine goes tick, tick.’’ The use
Circumduction describes the movement of the leg of a of circumlocutions ‘‘is indicative of intact semantic activa-
person with hemiplegia, hemiparesis or paraplegia, tion and a general capacity to retrieve lexical forms’’
paraparesis. Lesions of the pyramidal tract cause more (Davis, p. 109).
weakness in the flexors of the leg than the extensors
(hip and knee flexors and ankle dorsiflexors). Because of
this weakness, the foot cannot be raised from the floor, Cross References
and the leg cannot be advanced in a straight line forward,
as it would do normally. The leg moves away from the ▶ Anomia
trunk, then it is advanced toward it during walking, in a ▶ Aphasia
circular pattern. The medial side of the shoe scrapes the
floor, causing excessive wear in that area.
References and Readings
Cross References
Benson, D. F., & Ardila, A. (1996). Aphasia: A clinical perspective.
Chapter 4, Linguistic analysis of aphasia, 46–60. New York: Oxford
▶ Hemiparesis University Press.
▶ Hemiplegia Davis, G. A. (2000). Aphasiology: Disorders and clinical practice. Chap. 1,
▶ Pyramidal Tract Introduction to acquired language disorders, 1–19 (p. 7); Chap. 5,
Investigating symptoms and syndromes, (92–119). Needham Heights,
MA: Allyn & Bacon.
References and Readings
Victor, M., & Ropper, A. H. (2001). Adams and victor’s principals of
neurology (7th ed.). New York: McGraw-Hill.
Circumstantiality
R OBERT F RANK
Circumlocution Kent State University
Kent, OH, USA
C AROLE R. R OTH
Naval Medical Center
San Diego, CA, USA Definition

Circumstantiality is circuitous thinking and speech that

Definition digresses from the essential point. It differs from tangen-
tiality in which the individual ultimately fails to address
The use of an unnecessarily large number of words the main idea. In circumsatantiality, the main point is
to express an idea. Evasion in speech. Circumlocutions never lost but may be ‘‘clouded’’ and its appearance
 Civil Law C 585

delayed by excess and repeated material. Circumstantial Off Label Use

thinking is a characteristic of thought disorders.
Premenstrual dysphoric disorder, obsessive compulsive
disorder, panic disorder, generalized anxiety disorder,
Cross References posttraumatic stress disorder, and social anxiety disorder. C
▶ Tangentiality
Side Effects
Serious

Seizures, mania, and suicidal ideation (all rare).

Circumventricular Organ
▶ Subfornical Organ
Common

Sexual dysfunction, gastrointestinal upset, insomnia, se-

dation, tremor, headache, dizziness, sweating, bruising
Citalopram and very rare bleeding, rare hyponatremia, and a potential
for SIADH (syndrome of inappropriate antidiuretic hor-
J OHN C. C OURTNEY mone secretion).
Children’s Hospital of New Orleans
New Orleans, LA, USA
References and Readings
Generic Name Physicians’ Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson
PDR.
Citalopram Stahl, S. M. (2007). Essential psychopharmacology: The prescriber’s guide
(2nd ed.). New York, NY: Cambridge University Press.

Brand Name
Additional Information
Celexa
Drug Interaction Effects: http://www.drugs.com/drug_interactions.html
Drug Molecule Images: http://www.worldofmolecules.com/drugs/
Free Drug Online and PDA Software: www.epocrates.com
Class Gene-Based Estimate of Drug interactions: http://mhc.daytondcs.
com:8080/cgi bin/ddiD4?ver=4&task=getDrugList
Selective Serotonin Reuptake Inhibitor Pill Identification: http://www.drugs.com/pill_identification.html

Proposed Mechanism(s) of Action

Civil Action
Citalopram blocks the presynaptic serotonin reuptake
pump and desensitizes serotonin receptors, theoretically
▶ Litigation
increases serotonin neurotransmission, and is a mild
antihistamine.

Indication Civil Law

Depression. ▶ Personal Injury
586 C Civil Litigation

Civil Litigation CJD

M OIRA C. D UX ▶ Creutzfeldt-Jakob Disease
University of Maryland Medical Center/Baltimore VA
Baltimore, MD, USA

Definition Classical Model of Aphasia

Civil law is a division of the law that deals primarily with ▶ Wernicke–Lichtheim Model of Aphasia
disputes between individuals and/or organizations, in
which some form of compensation may be awarded to
the victim. Typically, civil law involves filing of a lawsuit
by a private party, called ‘‘the plaintiff.’’ Civil litigation
commonly involves hearing related to disputes regarding Classical Test Theory
torts, contracts, probate of wills, trusts, property, admin-
istrative law, commercial law as well as a plethora of other M ICHAEL D. F RANZEN
matters related to private parties and organizations. Allegheny General Hospital
Civil litigation primarily aims to correct an injustice, Pittsburgh, PA, USA
uphold an agreement, or settle a dispute. If compensation
is awarded to the victim, then the person/organization
responsible for the injustice is responsible for covering the
Definition
compensation. In civil litigation, the burden of proof is
usually placed on the plaintiff, though exceptions do exist.
Classical test theory is the body of concepts and methods
Punishment related to civil litigation is typically limited
that have formed the basis for psychological assessment.
to reimbursement for loses incurred by the plaintiff as a
Classical test theory posits that observed scores are the
result of actions/inactions committed by the defendant.
additive function of true scores and error terms. True
Incarceration is not a punishment rendered via civil liti-
scores are the ideal value of a construct in a particular
gation. Civil litigation and criminal litigation are not
person or situation. The error term is the effect of factors
mutually exclusive entities. For example, an individual
extraneous to the construct of interest. Error terms are
involved in a criminal case may seek compensation in
assumed to be independent of (or uncorrelated with)
civil court. For neuropsychologists, civil litigation typi-
the true scores. Analysis of the reliability of a score can
cally involves determination of causation, damages, and
be accomplished by manipulating factors thought to be
disability in disputes in which neuropsychological func-
influencing the error term. For example, in order to
tioning is of relevance (e.g., personal injury, medical
examine the effect of factors related to time or instance
malpractice).
of measurement, a test might be administered to the same
individuals on two different occasions. The relation
between the two observed scores, determined by calculat-
ing a correlation coefficient or by performing an analysis
References and Readings
of variance, helps to estimate the magnitude of the error
term and the proportion of the observed score that is
Greiffenstein, M. F. (2009). Basics of forensic neuropsychology. In
J. Morgan & J. Ricker (Eds.), Textbook of clinical neuropsychology. likely to be true score.
New York: Psychology Press.
Greiffenstein, M. F., & Cohen, L. (2005). Neuropsychology and the law:
Principles of productive attorney-neuropsychologists relations. Cross References
In G. Larrabee (Ed.), Forensic neuropsychology: A scientific approach.
New York: Oxford University Press.
Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin, C. (2007). ▶ Item Response Theory
Psychological evaluations for the courts (3rd ed.). New York: Guilford ▶ Reliability
Press. ▶ Sources of Error
 Clinical Dementia Rating C 587

References and Readings Cross References

Embretson, S. E. (Ed.). (2010). Measuring psychological constructs: ▶ Beyond Reasonable Doubt

Advances in model-based approaches. Washington, DC: American ▶ Burden of Proof
Psychological Association.
▶ Preponderance of Evidence C
Lord, F. M., & Novick, M. R. (2008). Statistical theories of mental test
scores. New York: Information Age Pub Inc.

References and Readings

Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin, C. (2007).

Psychological evaluations for the courts: A handbook for mental
Clear and Convincing Evidence health professionals and lawyers (3rd ed.). New York: Guilford
Press.
R OBERT L. H EILBRONNER
Chicago Neuropsychology Group
Chicago, IL, USA

Client Generated Index (CGI)

Definition
▶ Patient Generated Index
The burden of proof is the obligation to shift the as-
sumed conclusion away from an oppositional opinion
to one’s own position: it may only be fulfilled by evi-
dence. Under the Latin maxim, necessitas probandi Clinical Dementia Rating
incumbit ei qui agit, the general rule is that ‘‘the neces-
sity of proof lies with he who complains.’’ The burden of J ING E E TAN 1, E STHER S TRAUSS 1,
proof, therefore, usually lies with the party making the E LISABETH M. S. S HERMAN 2
1
claim. The exception to this rule is when a prima facie University of Victoria
case has been made. He who does not carry the burden Victoria, BC, Canada
2
of proof carries the benefit of assumption, meaning he Alberta Children’s Hospital, University of Calgary
needs no evidence to support his claim. Fulfilling the Calgary, AB, Canada
burden of proof effectively captures the benefit of as-
sumption, passing the burden of proof off to another
party. Clear and convincing evidence is a burden of Synonyms
proof required of a plaintiff for him to win the lawsuit.
This standard is higher than mere preponderance of the CDR
evidence. Proof of fraud, for example, usually requires
clear and convincing evidence. Clear and convincing
evidence is the higher level of burden of persuasion Description
and is most often employed in civil litigation. To
prove something by ‘‘clear and convincing evidence,’’ The Clinical Dementia Rating (CDR; Hughes, Berg, Dan-
the party with the burden of proof must convince the ziger, Coben, & Martin, 1982) is a semi-structured,
trier of fact that it is substantially more likely than clinician-rated interview widely used to stage the progres-
not that the thing is in fact true. This is a lesser require- sion of dementia using information provided by the pa-
ment than ‘‘proof beyond a reasonable doubt,’’ which tient and an informant. A global CDR score is generated
requires that the trier of fact be close to certain of the to stage the severity of dementia. It is based on ratings
truth of the matter asserted, but a stricter requirement of the patient’s functioning in six domains commonly
than proof by ‘‘preponderance of the evidence,’’ which affected in Alzheimer’s disease (AD): memory, orienta-
merely requires that the matter asserted seem more tion, judgment and problem solving, community affairs,
likely true than not. home and hobbies, and personal care. The CDR rates only
588 C Clinical Dementia Rating

impairments due to cognitive deficits rather than to phys- that uses a total score generated from the sum of boxes
ical disability. Based solely on clinical information (CDR-SB) has gained popularity to quantify progression
obtained from the patient and informant, and without of AD in longitudinal clinical trials of experimental thera-
reference to psychometric performance, a box score de- pies (e.g., Petersen et al., 2005).
scribing the level of impairment is generated for each
domain. The box score ranges from 0 to 3, representing
‘‘none’’ to ‘‘severe’’ impairment. Using a scoring algo- Psychometric Data
rithm, one of five possible stages is then derived from
the individual box scores as follows: CDR = 0 (no demen- Interrater Reliability
tia); CDR = 0.5 (questionable dementia); CDR = 1 (mild
dementia); CDR = 2 (moderate dementia); CDR = 3 (se- Most of the psychometric studies on the CDR have
vere dementia). Although not part of the original proto- focused on interrater reliability in multicenter clinical
col, CDR = 4 (profound) and CDR = 5 (terminal) can also trials. These studies have concluded that experience
be used to classify the later stages of dementia. An alter- using the CDR increases reliability estimates, although
native method that generates a total score (range 0–18) adequately trained inexperienced raters may also demon-
from the sum of boxes (CDR-SB) has also been used for strate a high level of agreement (kappa = 0.83 or higher;
quantification purposes in longitudinal studies (e.g., Schafer et al., 2004; Tractenberg, Schafer, & Morris, 2001).
Cortes et al., 2008). The CDR takes about 90 min to The CDR also shows good reliability among raters of
administer. various qualifications. There were no major differences in
The CDR has been used in clinical practice and mul- reliability among physicians, nurses, PhDs, social workers,
ticenter clinical trials, as well as in cross-cultural dementia psychometrists, or research assistant raters (85% for
studies around the world. The CDR protocol is available non-MDs and 82% for MDs; Oremus, Perrault, Demers,
in over 60 languages and dialects, including English, & Wolfson, 2000). Kappas between physician raters range
French, Spanish, Italian, Portuguese, Dutch, Czech, from 0.75 to 0.94 for the six individual domain scores and
Bulgarian, Russian, Tagalog, Afrikaans, Greek, German, CDR-SB score. Kappas between nurses, or between nurses
Hebrew, Indian dialects, Chinese dialects, Japanese, and and physicians, range from 0.66 to 0.77 (Oremus et al.,
Korean. These translations can be downloaded free of cost 2000).
on the CDR Web site (http://alzheimer.wustl.edu/cdr/
default.htm).
An online training video on the use of the CDR is Construct Validity
available free for individual users, and takes about 8–9 h to
complete. Detailed scoring algorithms, including ‘‘tie-break’’ Evidence for construct validity of the CDR appears solid.
rules, and an online scoring worksheet are available on the In the original study, the CDR had strong correlations
CDR Web site. with the Blessed Dementia Scale (BDS; r = 0.74) and the
Pfeiffer Short Portable Mental Status Questionnaire
(SPMSQ; r = 0.84) among individuals with CDR ratings
Historical Background between no dementia and very mild dementia (Hughes
et al., 1982). Correlations with various cognitive measures
The CDR was originally developed at the Washington ranged from small to large in community-dwelling sam-
University School of Medicine in 1979 to evaluate the ples (Folstein’s Mini-Mental State Examination = 0.33;
progression of AD (Hughes et al., 1982). The original BDS = 0.74; SPMSQ = 0.84). Similar correlations were
protocol has evolved somewhat over the years, with box found with neuropsychological measures such as the
descriptors updated to sharpen the distinction between CERAD Boston Naming Test, list learning, and verbal
severity levels within each domain, and new scoring rules fluency (Oremus et al., 2000).
added to resolve scoring ambiguity (Morris, 1993). Alter- In terms of neuropathology, CDR = 0.5 (a proxy for
native scoring methods have also been suggested to im- mild cognitive impairment; MCI) has been associated
prove scoring accuracy (Gelb & St. Laurent, 1993). An with multiple pathological signs including those related
extension of this scale to include CDR = 4 (profound) and to AD, Lewy body dementia, or vascular dementia, as
CDR = 5 (terminal) to classify the later stages of dementia well as nonspecific pathology (Saito & Murayama,
(Dooneief, Marder, Tang, & Stern, 1996) among nursing 2007). Further, increased microglia activation, an inflam-
home elderly has been proposed. As well, another method matory biomarker of AD, was seen with advancing CDR
 Clinical Dementia Rating C 589

stages (Xiang, Haroutunian, Ho, Purohit, & Pasinetti, populations (Lim, Chin, Lam, Lim, & Sahadevan, 2005;
2006). A negative association was also found between the Senanarong, Chen, & Orgogozo, 2006), although empiri-
CDR-SB score and glucose metabolism in the right poste- cal validation of various translations is needed.
rior cingulate gyrus (Perneczky, Hartmann, Grimmer, The CDR presents several advantages over psychomet-
Drzezga, & Kurz, 2007). ric tests. First, it is an assessment option for patients who C
are illiterate and/or have limited English language profi-
ciency. Moreover, it can also be used in the presence of
aphasia, a condition common among patients with
Predictive Validity
dementing disorders. Lastly, the administration of the
CDR does not require a standardized set of instructions,
There is evidence that individuals with higher CDR-SB
but is dependent upon a set of guidelines. As such, the
scores are more likely to develop dementia in the future
CDR is easily adapted for cross-cultural use (e.g., Lim
(Lynch et al., 2006). In addition, CDR scores predict
et al., 2005). A disadvantage of the CDR is that it is
survival in individuals with suspected dementia. Using
somewhat lengthy to administer.
survival as outcome, the median survival was 1 year for
CDR = 5, 2 years for CDR = 4, 2.5 years for CDR = 3,
3 years for CDR = 2, and 3.5 years for CDR = 1 (Dooneief
Cross References
et al., 1996). Use of the CDR as a screening tool for
dementia revealed a sensitivity of 92% and specificity of
▶ Alzheimer’s Disease
94% for mild dementia in a community sample of adults
▶ CERAD
older than age 75 (Juva et al., 1995).
▶ Dementia

Clinical Uses
References and Readings
The original focus of the CDR was to assess community-
dwelling older adults, since its anchor points probe for Cortes, F., Nourhashémi, F., Guérin, O., Cantet, C., Gillette-Guyonnet, S.,
examples of one’s engagement with the home and com- Andrieu, S., et al. (2008). Prognosis of Alzheimer’s disease today: A
two-year prospective study in 686 patients from the REAL-FR study.
munity. However, it has also been adapted for use in
Alzheimer’s and Dementia, 4(1), 22–29.
chronic long-term care facilities (Marin et al., 2001). Dooneief, G., Marder, K., Tang, M. X., & Stern, Y. (1996). The Clinical
The global CDR is widely used primarily for the staging Dementia Rating scale: community-based validation of ‘profound’
of AD. It has also been used to stage other dementing and ‘terminal’ stages. Neurology, 46, 1746–1749.
disorders such as Parkinson’s disease and frontotemporal Gelb, D. J., & St. Laurent, R. T. (1993). Alternative calculation of the
global clinical dementia rating. Alzheimer Disease & Associated
dementia. In recent years, CDR = 0.5 has been used to
Disorders, 7(4), 202–11.
characterize MCI; however, there is evidence that a large Hughes, C. P., Berg, L., Danziger, W. L., Coben, L. A., & Martin, R. L.
proportion (29.7%) of individuals at CDR = 0.5 also meet (1982). A new clinical scale for the staging of dementia. British
ICD-10 criteria for mild dementia (Lynch et al., 2006). Journal of Psychiatry, 140, 566–572.
In terms of longitudinal studies of AD progression, Juva, K., Sulkava, R., Erkinjuntti, T., & Ylikoski, R. (1995). Usefulness of
the Clinical Dementia Rating scale in screening for dementia. Inter-
both the global CDR and the CDR-SB appear to be
national Psychogeriatrics, 7(1), 17–24.
useful for tracking cognitive changes over a 2–3 year Lim, W. S., Chin, J. J., Lam, C. K., Lim, P. P. J., & Sahadevan, S. (2005).
period (e.g., Cortes et al., 2008; Meguro et al., 2004). Clinical Dementia Rating: experience of a multi-racial Asian
Of the two scoring methods, the CDR-SB is more population. Alzheimer Disease and Associated Disorders, 19(3),
commonly used in clinical drug trials because it was 135–142.
Lynch, C., Walsh, C., Blanco, A., Moran, M., Coen, R., Walsh, J., et al.
found to be sensitive to changes within 12 months follow-
(2006). The clinical dementia rating sum of box score in
ing baseline measurement in donepezil drug trials, where- mild dementia. Dementia and Geriatric Cognitive Disorders, 21(1),
as the global CDR was not (e.g., Petersen et al., 2005). 40–43.
There is also evidence that the CDR-SB is more useful Marin, D., Flynn, S., Mare, M., Lantz, M., Hsu, M., Laurans, M., et al.
than the global CDR in distinguishing mild cognitive (2001). Reliability and validity of a chronic care facility adaptation of
the Clinical Dementia Rating scale. International Journal of Geriatric
deficits from dementia (Lynch et al., 2006).
Psychiatry, 16(8), 745–750.
In addition to western populations, use of the CDR Meguro, K., Shimada, M., Yamaguchi, S., Sano, I., Inagaki, H.,
has also been accepted as an appropriate comprehensive Matsushita, M., et al. (2004). Neuropsychosocial features of very
measure for studies of dementia patients in Asian mild Alzheimer’s Disease (CDR 0.5) and progression to dementia
590 C Clinical Depression

in a community: The Tajiri Project. Journal of Geriatric Psychiatry

and Neurology, 17(4), 183–189. Clinical Interview
Morris, J. C. (1993). The clinical dementia rating (CDR): Current version
and scoring rules. Neurology, 43(11), 2412–2414.
K IMBERLY A. G ORGENS
Oremus, M., Perrault, A., Demers, L., & Wolfson, C. (2000). A review of
outcome measurement instruments in Alzheimer’s disease drug University of Denver
trials: Psychometric properties of global scales. Journal of Geriatric Denver, CO, USA
Psychiatry and Neurology, 13(4), 197–205.
Perneczky, R., Hartmann, J., Grimmer, T., Drzezga, A., & Kurz, A. (2007).
Cerebral metabolic correlates of the clinical dementia rating scale in
mild cognitive impairment. Journal Of Geriatric Psychiatry And
Synonyms
Neurology, 20(2), 84–88.
Petersen, R. C., Thomas, R. G., Grundman, M., Bennett, D., Doody, R., Diagnostic interview; Intake; Intake interview; Unstruc-
Ferris, S., et al. (2005). Vitamin E and Donepezil for the treatment tured clinical interview
of Mild Cognitive Impairment. New England Journal of Medicine,
352(23), 2379–2388.
Saito, Y., & Murayama, S. (2007). Neuropathology of mild cognitive
impairment. Neuropathology, 27(6), 578–584. Definition
Schafer, K., Tractenberg, R., Sano, M., Mackell, J., Thomas, R., Gamst, A.,
et al. (2004). Reliability of monitoring the clinical dementia rating in A skillfully conducted clinical interview is the cornerstone
multicenter clinical trials. Alzheimer Disease & Associated Disorders,
of psychological assessment. This interaction, typically a
18(4), 219–222.
Senanarong, V., Chen, C., & Orgogozo, J. (2006). Third Asia- face-to-face meeting that lasts between 30 min and 2 h,
Pacific Regional Meeting of the International Working Group generates a tremendous amount of data for the clinician via
on Harmonization of Dementia Drug Guidelines: Meeting both observation and direct questioning. Information
Report Summary. Alzheimer Disease & Associated Disorders, 20(4), obtained through observation during the clinical interview
311–312.
is considered qualitative or descriptive, and can include
Tractenberg, R., Schafer, K., & Morris, J. (2001). Interobserver disagree-
ments on clinical dementia rating assessment: Interpretation and impressions about cognition, attention, orientation, lan-
implications for training. Alzheimer Disease & Associated Disorders, guage, sensorimotor deficits, affect, insight, attitude toward
15(3), 155–161. assessment, acculturation, hygiene, interpersonal relations,
Xiang, Z., Haroutunian, V., Ho, L., Purohit, D., & Pasinetti, G. M. (2006). and coping mechanisms, among other variables. In addi-
Microglia activation in the brain as inflammatory biomarker of
tion, the verbal exchange between patient and clinician
Alzheimer’s disease neuropathology and clinical dementia. Disease
Markers, 22(1–2), 95–102. yields information about current life circumstances, in-
cluding the reason for referral and history of the presenting
problem, as well as an account of developmental/medical/
family history, educational and occupational achievement,
legal problems, sociocultural/religious considerations, sub-
stance abuse, and other relevant psychiatric issues. Together
Clinical Depression with test data and collateral information, interview materi-
al is an invaluable tool for clinical hypothesis formulation
▶ Major Depression
and testing, as well as treatment planning.

Current Knowledge
Clinical Extender There are three types of clinical interview, reflecting
the degree to which the content and questions are scripted:
▶ Psychometrician structured, semi-structured, and unstructured. A struc-
tured interview (e.g., the Structured Clinical Interview for
DSM-IV-Clinical Version [SCID-I]; First, Gibbon, Spitzer,
& Williams, 2001), like any standardized assessment tool,
gathers specific data that allows clinicians to make com-
Clinical Importance parisons between client and normative group function.
Criticisms of structured clinical interviews include a frus-
▶ Clinical Significance tration with lengthy questionnaires and the missed
 Clinical Neuropsychology C 591

opportunity for meaningful dialogue (Maruish, 2008). An ▶ Referral Question

unstructured clinical interview, on the other hand, is ▶ Self-Report Measures
principally reliant on clinical skill for direction. An opti- ▶ Structured Clinical Interview for DSM-IV (SCID-I)
mal unstructured clinical interview involves moving from ▶ Structured Interview of Reported Symptoms (SIRS)
broad content areas to more specific ones, from open- C
ended to more directive questions seeking yes/no re-
sponses. While the goals of clinical interviewing remain References and Readings
much the same regardless of format, critics have argued
that bias is more easily introduced into unstructured First, M., Gibbon, M., Spitzer, R. L., & Williams, J. B. W. (2001). User’s
clinical interviews than standardized approaches. A hy- guide for the Structured Clinical Interview for DSM-IV Axis I disor-
brid, the semi-structured clinical interview, offers many ders. New York: Biometrics Research.
of the benefits of its structured and unstructured counter- Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). Neuro-
parts, with breadth and depth chief among them. The psychological assessment, (4th ed.). New York, NY: Oxford
University Press.
semi-structured format ensures that all areas of potential Maruish, M. M. (2008). The clinical interview. In R. P. Archer & S. R.
clinical concern are assessed, while affording the clinician Smith (Eds.), Personality assessment. New York: Routledge.
the flexibility to dictate the degree of attention each con- Rogers, R. (2001). Diagnostic and structured interviewing. A handbook for
tent area receives. In addition, the semi-structured clinical psychologists. New York: Guilford Press.
interview can be altered to accommodate disabilities, it Sbordone, R. J. (2000). The assessment interview in clinical neuropsy-
chology. In G. Groth-Marnat (Ed.), Neuropsychological assessment in
can be abbreviated to meet the needs of the client (e.g., clinical practice (pp. 94–126). New York: Wiley.
fatigue) or the setting (e.g., bedside assessment), and it Shedler, J. (2002). A new language for psychoanalytic diagnosis. Journal of
can be amended to include additional lines of inquiry. the American Psychoanalytic Association, 50, 429–456.
As well as yielding information regarding patient Zimmerman, M. (1994). Interview Guide for Evaluating DSM-IV Psychi-
history and current functioning, a clinical interview offers atric Disorders and the Mental Status Examination. East Greenwich,
RI: Psych Products Press.
opportunities to build rapport and foster a working al- Zimmerman, M., & Mattia, J. I. (1999). Psychiatric diagnosis in clinical
liance. In addition to promoting satisfaction with the practice: Is comorbidity being missed? Comprehensive Psychiatry,
assessment process, the development of rapport may pro- 40(3), 182–191.
mote compliance from a reluctant patient and provide a
foundation for follow-up discussions and interventions
that may be indicated. Also, the dialogue during a clinical
interview allows a clinician to provide important patient
education. The initial conversation may explicitly address Clinical Neuropsychology
confidentiality, insurance/fee setting, the nature and pur-
pose of the examination, the intended use of assess- A NTHONY Y. S TRINGER
ment data, and a summary of follow-up plans including Emory University
feedback sessions (Lezak, Howieson, & Lorig, 2004). Atlanta, GA, USA
Despite routine use in clinical practice, there is consid-
erable debate about the reliability of clinical interviews.
Many believe the variability in questioning undermines the Definition
utility of the tool itself. Some research has suggested that
unstructured clinical interviews often fail to detect psychiat- Clinical neuropsychology is a specialty within psychology
ric and comorbid conditions (Zimmerman & Mattia, 1999). that applies the science of brain-behavior relations to the
Other researchers find ‘‘empirical rigor’’ in skillful clinical assessment, diagnosis, treatment, and rehabilitation of
interviewing (Shedler, 2002, p. 429). This argument not- patients across the life span with neurological, medical,
withstanding, the clinical interview remains a staple as- neurodevelopmental, psychiatric, or other cognitive and
sessment tool, as fallible or effectual as the clinician. learning disorders (Barth et al., 2003). The American
Psychological Association (APA) defines a clinical neu-
ropsychologist as ‘‘a professional psychologist who applies
Cross References principles of assessment and intervention based upon the
scientific study of human behavior as it relates to normal
▶ Behavioral Assessment and abnormal functioning of the nervous system’’ (APA,
▶ Mental Status Examination 1989, pp. 22).
592 C Clinical Neuropsychology

Clinical neuropsychology is recognized as a specialty intended to measure what he termed ‘‘biological intelli-
by APA, the American Board of Professional Psychology, gence.’’ The influence of Galton’s statistical methods is
and the Canadian Psychological Association. Though seen in Halstead’s factor analysis of his test battery. Hal-
there is no agreed upon date for the emergence of the stead proposed a four-factor theory of biological intelli-
field, clinical neuropsychology began to be recognized as a gence in his 1947 book Brain and Intelligence. Halstead’s
distinct professional discipline following a 1948 sympo- book was severely criticized by contemporary scholars,
sium at the APA annual meeting appropriately entitled and ultimately had little influence on theories of intelli-
‘‘Neuropsychology.’’ In this symposium, Hans-Lukas gence (Hartman, 1991). Halstead’s test battery, however,
Teuber described procedures he and Morris Bender devel- did prove highly influential. Ralph Reitan, a student of
oped to study the behavioral effects of penetrating missile Halstead, established a laboratory at the University of
wounds to the brain (Benton, 1987). Indiana Medical Center in 1950. Over the course of sever-
Clinical neuropsychology had many forerunners. In al decades, Reitan expanded upon Halstead’s initial bat-
the 1880s, Sir Francis Galton opened a laboratory in tery, adding procedures for detecting aphasia and sensory
London where for a few pennies, people could take tests perceptual impairments and for comparing performances
of visual acuity, reaction time, and various psychophysical of the two sides of the body. Reitan developed adaptations
abilities. A cousin of Charles Darwin, Galton’s ideas about of the original adult battery for children and adolescents,
eugenics have made him a historically controversial fig- collected normative data, and used discriminant function
ure. Nonetheless, factor analytic statistical methods grew analysis to validate the ability of the various batteries to
out of his work and became critical for the development discriminate brain damaged from neurologically healthy
and validation of mental ability tests. His work was put to individuals. The Halstead–Reitan Neuropsychological
practical use in early twentieth-century France when psy- Test Battery set a standard of excellence for test develop-
chologists Alfred Binet and Théodore Simon developed ment in neuropsychology and for a time was the most
intellectual tests to identify and place children in need of widely used approach in clinical neuropsychological
special education. World War I also stimulated interest in assessment.
his work in the USA, as the military sought tests that Reitan’s students were also prolific (Reed, 1985). They
could efficiently identify the strengths and weaknesses of include Hallgrim Kløve who studied with Reitan in the
large numbers of military recruits. As many as one million 1950s and then established a laboratory at the University
soldiers underwent mental ability testing during World of Wisconsin. Another student, Homer Reed, directed the
War I (Hartman, 1991). Neuropsychology Laboratory at the New England Medical
Just after World War I, the German American psychol- Center in Boston where he concentrated on use of the
ogist Shepherd Ivory Franz (1919) published detailed battery with pediatric patients. Phillip Rennick, who did
descriptions of tests of tactile sensation, motor coordina- fellowship training with Reitan, went on to establish a
tion, praxis, language, attention, memory, visuospatial laboratory at the former (now defunct) Lafayette Clinic
perception, reasoning, and intelligence. By 1924, hand in Detroit, and developed a repeatable neuropsychological
dynamometers, finger tapping keys, motor steadiness battery for situations in which serial testing is needed.
tests, form perception boards, and tests of color vision, Just as World War I provided an impetus for the
vibration sense, attention, and memory were available development of psychological ability tests, World War II
(Hartman, 1991). Though these tests were quickly stimulated the development of neuropsychological assess-
adopted by researchers (see Neuropsychology, Science of), ment and treatment methods because of the large number
clinical application came a few decades later. Franz advo- of veterans who returned having survived penetrating
cated for their clinical use in a series of lectures to the missile wounds to the brain. Reitan’s early work involved
Government Hospital for the Insane, starting in 1910 the examination of brain-injured World War II veterans.
(Hartman, 1991) and in 1904 was instrumental in estab- This population also provided the impetus for Hans-
lishing a psychological laboratory at Mclean Hospital in Lukas Teuber’s work in the USA and Aleksandr Romano-
Boston. This was the first such laboratory in a hospital vich Luria’s work in Russia.
setting in the USA Teuber immigrated from Germany and served as a
In 1935, the experimental psychologist Ward Halstead noncommissioned naval officer before establishing the
opened a laboratory at the University of Chicago for the Psychophysiological Laboratory with the neurologist
psychological study of neurology and neurosurgery Morris Bender at New York University (Weinstein,
patients. Adopting techniques used to test animals in 1985). Besides being the focal point for numerous seminal
ablation studies, Halstead designed a series of tests studies, Teuber’s laboratory was the incubator for many
 Clinical Neuropsychology C 593

neuropsychologists who went on to make important con- neuropsychology practitioners and researchers. Dr.
tributions including Joseph Altman, Lila Ghent, Rita Kaplan and her associates in Boston developed the pro-
Rudel, Josephine Semmes, and Sidney Weinstein. cess-approach to neuropsychological assessment, recog-
Meanwhile, working with Russian World War II veterans nizing that tests are complex and multifactorial and that
at the Burdenko Neurosurgical Institute in Moscow, Luria patients can take different paths to the same test score. C
developed a richly qualitative approach to neuropsycho- According to this approach, only by systematically analyz-
logical assessment that was in stark contrast to the quan- ing the process(es) by which patients arrive at their
titative and normatively based test batteries that were in responses, often by parsing a test into fine-grained com-
use in the USA Luria also was an exponent of neuropsy- ponents, can a neuropsychologist truly understand what
chological approaches to rehabilitation and to use of aspect of brain functioning is compromised.
pharmacologic agents to enhance recovery of function Activity was not confined to North America. Clinical
(Gualtieri, 1988). neuropsychology got its South American start when C.
Besides having cognitive disorders, many injured Mendilaharsu and S. Acevedo de Mendilaharsu established
World War II veterans were aphasic, sparking neuropsy- the first South American neuropsychological laboratory
chological interest in language and the brain. Kurt in 1958 at the Neurological Institute in Montevideo,
Goldstein’s (▶ Goldstein, Kurt) book Language and Lan- Uruguay (Ardila, 1990). Despite sometimes challenging
guage Disorders, published in 1948, combined his theories economic conditions, South American neuropsycholo-
about abstracting ability with neurology’s classic anato- gists conducted investigations of constructional ability,
mico-clinical syndrome approach to aphasia. The num- dementia, and language. The field spread to Mexico,
bers of aphasic veterans available for study along with Peru, Columbia, Chile, Argentina, Brazil, Honduras,
Goldstein’s influential book attracted experimental neu- Nicaragua, and elsewhere.
ropsychologists and psycholinguists to the study of lan- Clinical neuropsychology as a profession has be-
guage disorders (Goodglass, 1985). Aphasia research come increasingly organized since its inception. The
centers began to appear in the USA, among them being International Neuropsychological Society (INS), the
a laboratory established by Arthur Benton. National Academy of Neuropsychology (NAN), and
In 1948, the year of Teuber’s seminal APA presenta- the APA Division of Clinical Neuropsychology (Divi-
tion, Arthur Benton accepted an appointment as Profes- sion 40) are the most well-known professional neuro-
sor of Psychology at the University of Iowa, and by 1950 psychological organizations within the USA. Founded
established a neuropsychological testing unit at the Uni- in 1967, INS has a membership that exceeds 3,500.
versity of Iowa Hospitals (Hamsher, 1985). There, Benton NAN, formed in 1974, includes more than 3,000 mem-
and his students and colleagues conducted normative bers. Division 40 of the American Psychological Associ-
studies, examining the effects of age, gender, and educa- ation, incorporated in 1980, is the most recent of these
tion. They also developed a variety of tests for use in professional organizations, with a membership of over
studying what had previously been vaguely defined clini- 4,000 neuropsychologists. Although smaller in member-
cal disorders such as the Gerstmann syndrome ship, neuropsychologists have formed similar profes-
(▶ Gerstmann Syndrome). Over the next 2 decades, Ben- sional organizations throughout Europe, Asia, South
ton’s laboratory was home to numerous neuropsychology America, Australia, and Africa (see, for example, Jodzio,
pioneers including Max Fogel, Donald Shankweiler, Kerry 1998; Nihashi, 1998; Preilowski, 1997).
deS. Hamsher, Nils Varney, Scott Lindgren, Otfried Formal courses and organized programs of instruc-
Spreen, and Harvey Levin (Hamsher, 1985). Benton’s tion in clinical neuropsychology began to appear in the
laboratory conducted important studies of aphasia using 1960s, with one of the first offered in the Biological
control group designs, psychological test construction Psychology Doctoral Program at the University of
methods, statistical analysis, and psycholinguistic theory. Oklahoma Health Sciences Center (Parsons, 1991). Qual-
The behavioral neurologist Norman Geschwind, along ity and content of instruction varied from program to
with his colleagues Davis Howes and Harold Goodglass, program as they multiplied in the 1970s. In 1979,
established an aphasiology center at the Boston Veterans Dr. Manfred Meier initiated an effort to establish stan-
Administration Hospital, continuing the more rigorous dards of training and competence for neuropsychologists
neuropsychological approach to language disorders. The in the USA. This effort culminated first in the establish-
Boston VA became a major center for neuropsychological ment of the American Board of Clinical Neuropsychology
training and research with Dr. Edith Kaplan famously (ABCN) in 1981. A year later, the American Board of
serving there as ‘‘mother’’ to a generation of Professional Neuropsychology (ABN) was established
594 C Clinical Neuropsychology

with a similar goal of establishing standards of profes- ▶ International Neuropsychological Society

sional expertise in neuropsychology. These two certifica- ▶ Luria, Alexander Romanovich (1902–1977)
tion bodies continue to function autonomously, though ▶ National Academy of Neuropsychology
ABCN affiliated with the American Board of Professional ▶ Neuropsychiatry
Psychology (ABPP) in 1984, joining other boards that ▶ Neuropsychology, Science of
conduct peer review of the credentials, knowledge, and ▶ Reitan, Ralph (1922– )
practice of clinical psychologists seeking subspecialty cer- ▶ Teuber, Hans-Lukas (1916–1977)
tification in the USA.
In 1987, APA Division 40 published guidelines for
doctoral, internship, and postdoctoral training in neuro- References and Readings
psychology and a year later formally adopted the defini-
tion of a clinical neuropsychologist quoted above. American Psychological Association Division 40 (1989). Definition of a
clinical neuropsychologist. The Clinical Neuropsychologist, 3, 22.
Included in this definition (but not quoted) were explicit
Ardila, A. (1990). Neuropsychology in Latin America. The Clinical Neu-
training, supervision, licensing, and peer review require- ropsychologist, 4, 121–132.
ments that must be met by neuropsychologists. APA also Barth, J. T., Pliskin, N., Axelrod, B., Faust, D., Fisher, J., Harley, J. P., et al.
recognized attainment of the ABCN/ABPP diploma as (2003). Introduction to the NAN 2001 definition of a clinical neu-
‘‘the clearest evidence of competence as a Clinical Neu- ropsychologist. Archives of Clinical Neuropsychology, 18, 551–555.
Benton, A. (1987). Evolution of a clinical specialty. In K. M. Adams, &
ropsychologist’’ (APA Division 40, 1989). As of 2010, over
B. P. Rourke (Eds.), The TCN guide to professional practice in clinical
500 practicing clinicians have attained ABPP/ABCN dip- neuropsychology (pp. 1–4). Amsterdam: Swets & Zeitlinger.
lomate status in neuropsychology and over 350 neurop- Goldstein, K. (1948). Language and language disorders. Orlando, FL:
sychologists had attained ABN certification. Grune & Stratton.
Though ABCN and ABN initially differed in their Goodglass, H. (1985). Aphasiology in the United States. International
Journal of Neuroscience, 25, 307–311.
examination procedures, currently both boards require a
Groth-Marnat, G. (2000). Introduction to neuropsychological assessment.
peer review of credentials, a multiple-choice written In G. Groth-Marnat (Ed.), Neuropsychological assessment in clinical
exam, and a 1 h ethics oral exam. The two boards differ, practice: A guide to test interpretation and integration (pp. 3–25).
however, in other aspects of their oral examination. In New York, NY: Wiley.
particular, ABCN, but not ABN, conducts an oral ‘‘fact- Gualtieri, C. T. (1988). Pharmacotherapy and the neurobehavioural se-
quelae of traumatic brain injury. Brain Injury, 2, 101–129.
finding’’ examination in which candidates solicit informa-
Hamsher, K. D. (1985). The Iowa Group. International Journal of Neuro-
tion about a neuropsychological patient in order to arrive science, 25, 295–305.
at a diagnostic formulation and clinical recommenda- Hartman, D. E. (1991). Reply to Reitan: Unexamined premises and the
tions. Nonetheless, the two boards have grown more evolution of clinical neuropsychology. Archives of Clinical Neuropsy-
similar since their inception, and have discussed merger, chology, 6, 147–165.
Jodzio, K. (1998, Spring). Neuropsychology in Poland: Past and present.
but these efforts have been unsuccessful. One milestone
International Neuropsychological Society Liaison Committee Newslet-
likely to occur in the USA in the twenty-first century is the ter, 5, 1–3.
achievement of widespread ABCN or ABN diplomacy Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). The practice of
among those identifying neuropsychology as their prima- neuropsychological assessment. In Neuropsychological assessment
ry area of specialization. This milestone would signal (4th ed., pp. 3–14). New York, NY: Oxford University Press.
Nihashi, N. (1998, Spring). Neuropsychology in Japan. International
the professional and organizational maturity of clinical
Neuropsychological Society Liaison Committee Newsletter, 5, 1–3.
neuropsychology. Parsons, O. A. (1991). Clinical neuropsychology 1970–1990: A personal
view. Archives of Clinical Neuropsychology, 6, 105–111.
Preilowski, B. (1997). Establishing clinical neuropsychology in Germany:
Cross References Scientific, professional, and legal issues. Neuropsychology Review, 7,
187–199.
Reed, J. (1985). The contributions of Ward Halstead, Ralph Reitan and
▶ American Board of Clinical Neuropsychology (ABCN) their associates. International Journal of Neuroscience, 25, 289–291.
▶ American Board of Professional Neuropsychology Stringer, A. Y., & Cooley, E. L. (2002). Neuropsychology: A twentieth-
▶ American Psychological Association (APA), Division 40 century science. In A. Y. Stringer, E. L. Cooley, & A.-L. Christensen
▶ Benton, Arthur (1909–2006) (Eds.), Pathways to prominence in neuropsychology: Reflections of twen-
tieth century pioneers (pp. 3–26). New York, NY: Psychology Press.
▶ Forensic Neuropsychologist
Weinstein, S. (1985). The influence of Hans-Lukas Teuber and the
▶ Forensic Neuropsychology psychophysiological laboratory on the establishment and develop-
▶ Geschwind, Norman (1926–1984) ment of neuropsychology. International Journal of Neuroscience, 25,
▶ Halstead, Ward (1908–1968) 277–288.
 Clinical Practice Guidelines C 595

guide the allocation of health care resources, and

Clinical Practice Guidelines (5) reduce the risk of liability for negligent care
(IOM, 1992).
A NDREA M. L EE In addition to patients and their families, health care
University of Manitoba providers, and health care institutions, others such as
Winnipeg, Manitoba, Canada
C
payers, health care benefit providers, and public policy
makers have a stake in clinical practice guidelines. Legis-
lators, regulators, and health care purchasers take an
Synonyms interest in studying them to assist them in making deci-
sions that control health care costs. It is assumed that if
Practice guidelines the most appropriate care is administered, better health
outcomes will be achieved and health care costs will be
lowered. Although some guidelines could likely achieve
such hopes for decreased health care costs, other guide-
Definition lines may not.
The Agency for Healthcare Research and Quality
According to the Institute of Medicine’s 1990 report, (AHRQ), formerly known as the AHCPR, created a
Clinical Practice Guidelines: Directions for a New Program, central public resource for evidenced-based clinical prac-
clinical practice guidelines are ‘‘systematically developed tice guidelines called the National Guideline Clearing-
statements to assist practitioner and patient decisions house (NGC) that can be accessed at http://www.
about appropriate health care for specific clinical guideline.gov/
circumstances.’’ For a clinical practice guideline to be included on the
NGC, the following criteria must be met: (1) The guide-
line must contain systematically developed recommenda-
tions, strategies, or information that assist in the decision
Historical Background making of appropriate health care in specific clinical
situations by healthcare providers and patients; (2) the
Recommendations for appropriate care have been found guideline must be produced by a medical specialty associ-
in ancient writings (IOM, 1992). Modern guidelines have ation, professional societies, public or private organiza-
been developed by professional organizations for over tions, government agencies, or health care organizations
50 years. It was only in the 1990s, however, that the or plans; (3) a documentation should be produced that
systematic, evidence-based guidelines began to appear verifies that a systematic literature search and review of
with any regularity. In November 1989, the Agency for scientific literature was performed during the guideline
Health Care Policy and Research (AHCPR) was created development; (4) the guidelines should have been
with, among other responsibilities, a mandate to devel- reviewed or produced within 5 years and should be avail-
op, disseminate, and evaluate clinical practice guidelines. able in print or electronic format in the English language
The AHCPR then enlisted the Institute of Medicine (National Guideline Clearinghouse, 2009). These criteria
(IOM) for advice. The result was the 1990 report gener- ensure minimum quality of guidelines submitted to
ated by the IOM, called Clinical Practice Guidelines: the NGC.
Directions for a New Program, that aimed to encourage
standardization and consistency in the development of
guidelines.
Future Directions
An ongoing challenge is the implementation of clinical
Current Knowledge practice guidelines and ensuring their application by
health care providers. Factors such as information over-
The five major purposes of clinical practice guidelines load, habitual practice patterns, fears of malpractice, and a
are to: (1) aid in clinical decision-making by patients lack of economic incentives create barriers to guideline
and health care providers, (2) educate individuals application and each must be addressed on an individual
or groups, (3) assess and ensure quality of care, (4) and systemic level.
596 C Clinical Relevance

Cross References Clinical significance also refers to a static condition of

import – for example, a functionally relevant discrepancy
▶ AACN Practice Guidelines between cognitive abilities in different domains (e.g., lan-
guage vs. visual-perceptual abilities). The term can also
refer to the level of distress or impairment related to
References and Readings psychological symptoms as criteria for a DSM-IV TR
disorder diagnosis.
IOM. (1990). In M. J. Field & K. N. Lohr (Eds.), Clinical Practice guide- While clinical significance may be supported by sta-
lines: Directions for a new program. Washington, DC: National tistically significant differences on quantitative measures
Academy Press. of functioning, statistical significance cannot be equated
IOM. (1992). In M. J. Field & K. N. Lohr (Eds.), Guidelines for clinical
with clinical significance.
practice: From development to use. Washington, DC: National
Academy Press.
National Guideline Clearinghouse. (2009). Inclusion criteria. Retrieved
October 13, 2009, from the National Guideline Clearinghouse Web
site: http://www.guideline.gov/submit/inclusion.aspx Cross References
▶ Functional Assessment
▶ Premorbid Functioning
Clinical Relevance ▶ Quality of Life
▶ Reliable Change Index
▶ Clinical Significance ▶ Response to Intervention
▶ Statistical Significance

Clinical Significance References and Readings

M ONICA K URYLO 1, J ASON VAN A LLEN 2 American Psychiatric Association. (2000). Diagnostic and statistical man-
1
The University of Kansas Medical Center ual of mental disorders (Rev. 4th ed.). Washington, DC: American
Kansas, KS, USA Psychiatric Association.
2 Jacobson, N. S., Roberts, L. J., Berns, S. B., & McGlinchey, J. B. (1999).
University of Kansas
Methods for defining and determining the clinical significance of
Lawrence, KS, USA treatment effects: Description, application, and alternatives. Journal
of Consulting and Clinical Psychology, 67, 300–307.
Jacobson, N. S., & Truax, P. (1991). Clinical significance: A statistical
Synonyms approach to defining meaningful change in psychotherapy research.
Journal of Consulting and Clinical Psychology, 59, 12–19.
Kazdin, A. E. (1999). The meanings and measurement of clinical
Clinical importance; Clinical relevance significance. Journal of Consulting and Clinical Psychology, 67,
332–339.
Kazdin, A. E. (2003). Clinical significance: Measuring whether interven-
Definition tions make a difference. In A. E. Kazdin (Ed.), Methodological issues
and strategies in clinical research (3rd ed., pp. 691–710). Washington,
DC: American Psychological Association.
Clinical significance is a perceived, valued, and function- Spitzer, R. L., & Wakefield, J. C. (1999). DSM-IV diagnostic criterion for
ally relevant discrepancy in symptoms/abilities that clinical significance: Does it help solve the false positives problem?
reflects an important change in functioning. This can American Journal of Psychiatry, 156, 1856–1864.
involve either an improvement (usually as a result of
treatment or intervention) or a decline (typically due
progression of illness or disorder) as measured by symp-
toms or impairment level. The relevance and value of
this to difference may be determined by the client, mental Clinical Target Volume
health professional, and/or the client’s significant
other(s). ▶ Involved Field Radiotherapy
 Clock Drawing C 597

Disorders of Speech (1926), assessed aphasic patients using

Clock Drawing a wide number of drawing tests including ‘‘the clock test’’
(p. 214) to assess deficits in understanding and executing
DAVID J. L IBON 1, E DITH K APLAN 2, R OD S WENSON 3, complex propositional speech and deficits associated with
DANA L. P ENNEY 4 symbol formation. In describing propositional speech and
1
Drexel University College of Medicine
C
symbolic formation deficits associated with aphasia, Head
Philadelphia, PA, USA (1926) wrote ‘‘any act of mental expression, which
2
Suffolk University demands symbolic formulation, tends to be defective
Boston, MA, USA and the higher its propositional value the greater the
3
North Dakota School of Medicine difficulty it will present’’ (p. 212). Head (1926) provided
Fargo, ND, USA many examples of aphasic patients who demonstrated
4
The Lahey Clinic striking impairment in executing the propositional com-
Burlington, MA, USA mand to set the clock hands for a specified time. For
example, Head described an aphasic patient who was
able to set clock hands ‘‘correctly at 3:40,’’ but not when
Description he was told to place the hands at ‘‘20 minutes to 4.’’ For
this latter test condition (‘‘20 minutes to 4’’), Head com-
Clock Drawing Test (CDT) is a widely used and popular mented that his patient appeared ‘‘doubtful of the mean-
neuropsychological test. Rubin, Barr, and Burton (2005) ing of the words 20 minutes to.’’ Other researchers have
reported that the CDT appears in the top 40 tests most used the CDT to assess deficits in symbolic formation in
commonly used by neuropsychologists. The CDT is often neurologic patients (Mayer-Gross, 1935; McFie & Zangwill,
considered to be a visuoconstructional test. Modern ver- 1960; Van Horst, 1934).
sions of the CDT usually contain at least two parts – clock Classically trained neurologists often associate the
drawing to command and clock drawing to copy. In the CDT as a means to assess constructional apraxia. Kleist
command condition, patients are presented with a blank (1912, cited in Benton & Tranel, 1993) described con-
sheet of paper and are asked to ‘‘draw the face of a clock structional apraxia as deficits in formative activities nec-
showing the numbers and the two hands set for ten after essary to assemble parts into a meaningful whole. For
eleven.’’ In the copy condition, a pre-drawn model of a Kleist, the essential defect in constructional apraxia was
clock with numbers and hands set for 10 after 11 is the ineffective translation of visuoperceptual information
presented, and the patient is asked to copy the model. into an effective motor act. In this sense, the concepts of
Clock drawing with hands set for ten after eleven is Kleist are consistent with the constructs Head (1926) used
an innovation introduced by Edith Kaplan (Kaplan, to understand impaired clock drawings produced by
1988, 1990). aphasic patients. Interestingly, Kleist tended to associate
As described below, other versions of the CDT ask the constructional apraxia with lesions in the left posterior
patient to set the hands for other times. Also, some ver- cortex. This is in stark contrast to the anecdotal point of
sions of the CDT include a clock subtest in which patients view that tends to automatically associate defective clock
are presented with pre-drawn clock faces with and with- drawing (or any other impaired figure copying test for
out numbers and/or hands and are asked to either draw that matter) with a right parietal lesion. While it is cer-
clock hands to designate specific times or read the speci- tainly true that patients with right parietal lesions often
fied time (Borod, Goodglass, & Kaplan, 1980; Leach, produce very spatially impaired clock drawings, it is naive
Kaplan, Reweilak, Richards, & Proulx, 2000; Tuokko, to automatically associate impaired clock drawing with
Hadjustavropoulos, Miller, & Beattie, 1992). either a lesion in any single brain region, or as a measure
of any single cognitive operation. As described below,
defective clock drawings to command and copy can be
Historical Background associated with a wide array of neurologic lesions and
underlying cognitive disorders.
Since the late 1980s, a profusion of research using the Many time settings have been used in the CDT. Kaplan
CDT as an assessment tool for dementia has emerged. (1988, 1990) recommends using ‘‘ten after eleven.’’ First,
However, some of the more interesting historical roots clock setting for ten after eleven requires the patient to
of the CDT came from research with aphasic patients. disambiguate a complex propositional command. Sec-
Henry Head, in his magnum opus Aphasia and Kindred ond, since the numbers ‘‘10’’ and ‘‘11’’ are on the clock,
598 C Clock Drawing

patients need to resist the temptation to be pulled to the patients are presented with a blank page and asked to
numbers ‘‘10’’ and ‘‘11.’’ Thus, clock setting to ten after draw a clock with numbers and set the hands for ten
eleven tends to elicit a variety of stimulus-bound errors. after eleven, (3) a pre-drawn clock face where patients
In a survey of neuropsychologists and neurologists are asked to put in all the numbers and set the hands for
described by Freedman, Leach, Kaplan, Shulman, and 20 after 8, (4) a clock reading test with hands, but without
Delis (1994), other commonly used clock settings include numbers where patients are asked to identify a specified
‘‘20 after 8’’ and ‘‘3 o’clock.’’ time, and (5) a clock reading test with numbers and hands
where patients are, again, asked for the specified time. For
clock drawing to command and copy, behavior related to
Psychometric Data the drawing of the clock face, the numbers, and hands,
and the representation of the clock hands originating
Some scoring guidelines for the CDT can be found as part from the center of the clock are each scored using a
of the Boston Diagnostic Aphasia Examination supple- 13-point scoring system. The pre-drawn clock face condi-
mentary language tests (BDAE; Goodglass & Kaplan, tion is scored using an 11-point scoring system. Thus, for
1972, 1983; Goodglass, Kaplan, & Baresi, 2001). In this portion of the test scores have a 0–37 point range.
the original BDAE (with the rakishly purple cover [see Each clock reading subtest contains six test stimuli. Per-
Holland’s forward to the third edition of the BDAE, formance on the three clock drawing test conditions are
2001]), the CDT test was one of several tests believed to combined with a score measuring the copy of a complex
be sensitive to parietal lobe injury. As described in the figure for a combined age-corrected scale score. The two
BDAE corpus, clock drawing is one of six figures where clock reading subtests are scored separately (range 0–6).
patients are asked to draw to command and copy (i.e., a For these two tests, age-related percentile cut scores are
clock with hands set for 10 after 11, a daisy, an elephant, provided.
a red cross, a three-dimensional cube, and a house). For Freedman, Leach, Kaplan, Shulman, and Delis (1994)
the clock drawing portion of the test, a three-point described a very comprehensive clock scoring system
scoring system was described awarding a point for an using a variety of clock drawing conditions and clock
approximately circular clock face, symmetry of number settings. Normative data was collected and grouped by
placement, and correctness of numbers. No scoring for decade from age 20 to 80þ. Separate scales were devel-
the representation of the clock hands was suggested. oped to assess the drawing of the clock face, the drawing
Normative data for the entire figure drawing test of the numbers, the presence and drawing of the clock
(range 0–13 for the separate command and copy test hands, and the degree to which the clock hands emanated
conditions) is provided. Separate normative data for from the center of the clock face. Base rates for a wide
the CDT is not included. Additional normative informa- range of clock drawing behavior are provided. These data
tion is provided by Borod, Goodglass, and Kaplan show that certain errors occur more frequently with age.
(1980). In this report, norms are also provided for two For example, for clock setting using ‘‘ten after eleven,’’ the
additional clock assessment procedures – clock setting representation of the clock hands tends to be differentially
with numbers and clock setting without numbers. In affected by age.
both tests, the patient is presented with pre-drawn clock As noted above, a wide number of clock drawing
faces with and without numbers and are asked to draw the procedures have been reported (Lezak, Howison, & Lor-
hands to read 1:00, 3:00, 9:15, and 7:30. Performance is ing, 2004); however, most researchers follow Kaplan’s
assessed using a 12-point scoring system. Borod and col- (1988, 1990) suggestion and ask patients to set the
leagues (1980) described both age and educational effects hands for ‘‘ten after eleven’’ (Freedman et al., 1994). It is
for this clock assessment procedure. Other researchers important to understand that many CDT scoring proce-
have commented on the effects of education on clock dures are essentially atheoretical, that is, the administra-
drawing test performance (Marcopulos, McLean, & tion and scoring procedures were devised with an
Giuliano, 1997). eye toward sensitivity to brain damage or neurological
The Kaplan-Baycrest Neuropsychological Survey insult rather than to assess for deficits involving specific
(KBNS; Leach et al., 2000) contains a comprehensive cognitive constructs. Recent research, particularly in
clock test consisting of five parts: (1) clock drawing to using the CDT as part of a dementia evaluation, suggests
command where patients are asked to draw the face that the command and copy conditions are related to
of clock put in all the numbers and set the hands for different underlying cognitive mechanisms (Cosentino,
10 after 11, (2) a clock drawing to copy condition where Jefferson, Chute, Kaplan, & Libon, 2004; Libon, Swenson,
 Clock Drawing C 599

Barnoski, & Sands, 1993; Libon, Malamut, Swenson, & in the command condition may be due to a deficit in
Cloud, 1996; Rouleau, Salmon, Butters, Kennedy, & visuospatial memory. Tranel, Rudrauf, Vianna, and
McGuire, 1992). Equally important, different results are Damasio (2008) administered the CDT to a large group
obtained depending on test instruction (see Cosentino of focal lesioned patients. Imaging studies found errors on
et al., 2004 for a review). These considerations are criti- the CDT were associated with right parietal (supramargi- C
cally important when the task at hand is to differentiate nal gyrus) and left inferior frontal-parietal opercular
between say, dementia subtypes. brain damage. These researchers also noted that visuospa-
tial errors were predominant in patients with right hemi-
sphere damage, whereas time-setting errors were
Clinical Uses predominant in patients with left hemisphere lesions.
Dementia – As noted above, since the late 1980s, there
Focal lesions – Clock drawing has not been extensively has been a plethora of research demonstrating the value
studied in non-dementia, focal lesioned patients. None- of the clock drawing test as both a screening test for
theless, specific patterns of deficits can be associated with dementia as well as a means of investigating cognitive
specific neurologic lesions. Freedman et al. (1994) and constructs that may differentiate between dementia sub-
Kaplan (1988, 1990) provide some instructive exemplars. types (see Cosentino et al., 2004 for a review). Rouleau
For example, patients with left posterior brain lesion et al. (1992, 1996) examined patients with Alzheimer’s
resulting in a Wernicke’s aphasia often present with lan- disease (VaD) and Huntington’s disease (HD) adminis-
guage comprehension deficits. While these patients may tering a clock drawing test to command and copy with
demonstrate general understanding of the clock drawing hands set for ten after eleven. An analysis of errors proved
instructions, numbers may be omitted entirely with hatch effective in differentiating between dementia subtypes.
marks used as substitutes (Freedman et al., 1994). Patients AD patients made more conceptual errors while HD
with a left anterior lesion presenting with a Broca’s apha- patients produced more graphomotor errors. These
sia often have difficulty in understanding functor words authors speculated that semantic knowledge deficits
such as ‘‘to’’ and ‘‘after.’’ These patients, therefore, may be might underlie the deficits produced on the CDT by AD
apt to draw the clock hands pointing to the numbers ‘‘10’’ patients whereas executive dysfunction might underlie the
and ‘‘11.’’ Further assessment is required to see if this kind errors produced by HD patients. When the command and
of error is caused by a language-related deficit or repre- copy conditions were compared, AD, but not HD patients
sents an executive deficit. Patients with left hemisphere improved from the command to copy test conditions.
lesions might initiate their drawing on the left side of the Rouleau’s research was the impetus for a series of studies
clock, that is, on the side contralateral to their intact right conducted by Libon and colleagues (Cosentino et al., 2004;
hemisphere. Thus, numbers may be written correctly but Libon et al., 1993, 1996) that examined differences on
in a counterclockwise direction (Freedman et al., 1994). the CDT between patients with AD and vascular dementia
Interesting dissociations can be found in clock draw- (VaD). In their original study, Libon et al. (1993) found
ings to command versus copy in focal lesion patients. no difference in errors between AD and VaD patients in
Kaplan (1990) provides several instructive examples. An the command condition. However, similar to Rouleau,
analysis of clock drawings produced by a patient with a AD patients improved, that is, made fewer errors than
right parietal lesion demonstrates differential impairment VaD patients in the copy condition. These findings
in the copy versus the command test conditions. In the were replicated in a second study (Libon et al., 1996),
copy test condition, many numbers were omitted on the that is, AD patients generally improved from the com-
left side of the drawing. The clock drawing to command mand to copy test conditions compared to VaD patients.
did not demonstrate this behavior and was generally Cosentino et al. (2004) grouped dementia patients diag-
intact compared to the copy test condition. Kaplan nosed clinically with either AD or VaD on the basis of
(1988) demonstrated the opposite profile in a patient MRI white matter alterations (MRI-WMA). These groups
with a right temporal lesion. Here, there was differential were compared to dementia patients with Parkinson’s
impairment in the command condition. For this patient, disease (PD). Patients presenting with minimal to mild
the clock drawing to copy was generally intact. For the MRI-WMA continued to improve from the command to
right parietal lesioned patient, the differential impairment copy test conditions, that is, produce fewer errors in the
in the copy condition likely reflected a deficit involving copy versus the condition test conditions, compared to
visually mediated neglect of left hemi-space. For the left patients with moderate to severe MRI-WMA and PD
temporal lobe patient, the visuospatial impairment seen patients. Errors produced the copy condition were
600 C C-Log

correlated with poor performance on executive tests. Libon, D. J., Malamut, B. L., Swenson, R., & Cloud, B. S. (1996). Further
analyses of clock drawings among demented and non-demented
Errors produced in the command condition were corre-
subjects. Archives of Clinical Neuropsychology, 11, 193–211.
lated with overall dementia severity and tests related to Libon, D. J., Swenson, R., Barnoski, E., & Sands, L. P. (1993). Clock
semantic knowledge. Cahn-Weiner (2003) correlated CDT drawing as an assessment tool for dementia. Archives of Clinical
performance with MRI measures of atrophy and found Neuropsychology, 8, 405–416.
that impaired CDT performance was attributable to im- Marcopulos, B. A., McLean, A., & Giuliano, A. J. (1997). Cognitive
impairment or inadequate norms: A study of healthy, rural, older adults
pairment in multiple cognitive domains but was primarily
with limited education. The Clinical Neuropsychologist, 11, 111–131.
related to volume loss involving the right temporal cortex. Mayer-Gross, W. (1935). Some observations on apraxia. Proceeding of the
Taken as a whole, this research suggests that different Royal Society of Medicine, 28, 1203–1212.
cognitive constructs underlie impaired clock drawing in McFie, J., & Zangwill, O. L., (1960). Visuo-constructive disabilities asso-
patient with cortical versus subcortical dementia. ciated with lesions of the left cerebral hemisphere. Brain, 83,
243–260.
Rouleau, I., Salmon, D. P., & Butters, N. (1996). Longitudinal analysis of
Cross References clock drawing in Alzheimer’s disease patients. Brain and Cognition,
31, 17–34.
Rouleau, I., Salmon, D. P., Butters, N., Kennedy, C., & McGuire, K.
▶ Constructional Apraxia (1992). Quantitative and qualitative analyses of clock drawings in
Alzheimer’s and Huntington’s disease. Brain and Cognition, 18, 70–87.
Rubin, L. A., Barr, W. B., & Burton, L. A. (2005). Assessment practices of
References and Readings clinical neuropsychologists in the United States and Canada: A
survey of INS, NAN, and APA Division 40 members. Archives of
Benton, A., & Tranel, D. (1993). Visuoperceptual, visuospatial, and Clinical Neuropsychology, 20, 33–65.
visuoconstructional disorders. In K. M. Heilman & E. Valenstien, Tranel, D., Rudrauf, D., Vianna, E. P. M., & Damasio, H. (2008). Does the
(Eds.), Clinical neuropsychology (3rd ed.). New York: Oxford clock drawing test have focal Neuroanatomical correlates? Neuropsy-
University Press. chology, 22, 553–562.
Borod, J. C., Goodglass, H., & Kaplan, E. (1980). Normative data on the Tuokko, H., Hadjustavropoulos, T., Miller, J. A., & Beattie, B. L. (1992).
Boston diagnostic aphasia examination, parietal lobe battery, and the The clock test: A sensitive measure to differentiate normal elderly
Boston Naming Test. Journal of Clinical Neuropsychology, 2, 209–216. from those with Alzheimer disease. Journal of the American Geriatrics
Cahn-Weiner, D. A., Williams, K., Grace, J., Tremont, G., Westervelt, H., Society, 40, 579–584.
& Stern, R. A. (2003). Discrimination of dementia with lewy bodies Van der Horst, L. (1934). Constructional apraxia: Osychological views on
from Alzheimer disease and Parkinson disease using the clock draw- the conception of space. Journal of Nervous and Mental Disease, 80,
ing test. Cognitive and Behavioral Neurology, 16, 85–92. 645–650.
Cosentino, S., Jefferson, A. J., Chute, D. L., Kaplan, E., & Libon, D. L.
(2004). Clock drawing errors in dementia: Neuropsychological and
Neuroanatomic considerations. Cognitive and Behavioral Neurology,
17, 74–83. C-Log
Freedman, M., Leach, L., Kaplan, E., Shulman, K. I., & Delis, D. C. (1994).
Clock drawing: A neuropsychological analysis. New York: Oxford
University Press.
▶ Cognitive-Log
Goodglass, H., & Kaplan, E. (1972). Assessment of aphasia and related
disorders (1st ed.). Philadelphia, PA: Lea and Febiger.
Goodglass, H., & Kaplan, E. (1983). Assessment of aphasia and related
disorders (2nd ed.). Philadelphia, PA: Lea and Febiger. Clomipramine
Goodglass, H., Kaplan, E., & Baresi, B. (2001). Assessment of aphasia and
related disorders (3rd ed.). Philadelphia, PA: Lippincott, Williams. J OHN C. C OURTNEY
Head, H. (1926). Aphasia and kindred disorders of speech. New York:
Children’s Hospital of New Orleans
Macmillan.
Kaplan, E. (1988). A process approach to neuropsychological assessment. New Orleans, LA, USA
In T. Boll & B. K. Bryant (Eds.), Clinical neuropsychology and brain
function: Research, measurement, and practice. Washington, DC:
American Psychological Association. Generic Name
Kaplan, E. (1990). The process approach to neuropsychological assess-
ment of psychiatric patients. Journal of Neuropsychiatry and the
Clinical Neurosciences, 2, 72–87. Clomipramine
Leach, L., Kaplan, E., Rewilak, D., Richards, B., & Proulx, G.-B. (2000).
The kaplan baycrest neurocognitive assessment. San Antonio, TX: The
Psychological Corp.
Brand Name
Lezak, M., Howison, D. B., & Loring, D. W. (2004). Neuropsychological
assessment (4th ed.). New York: Oxford University Press. Anafranil
 Clonazepam C 601

Class Additional Information

Tricyclic antidepressant Drug Interaction Effects: http://www.drugs.com/drug_interactions.html

Drug Molecule Images: http://www.worldofmolecules.com/drugs/
Free Drug Online and PDA Software: www.epocrates.com
Gene-Based Estimate of Drug interactions: http://mhc.daytondcs. C
Proposed Mechanism(s) of Action com:8080/cgi bin/ddiD4?ver=4&task=getDrugList
Pill Identification: http://www.drugs.com/pill_identification.html
Boosts neurotransmitters serotonin and norepinephrine/
noradrelaline; blocks serotonin transporter; apparently
desensitizes both serotonin 1A receptors and beta adren-
ergic receptors Clonazepam
J OHN C. C OURTNEY
Indication Children’s Hospital of New Orleans
New Orleans, LA, USA
Obsessive-compulsive disorder, depression, cataplexy
syndrome
Generic Name

Off Label Use Clonazepam

Anxiety, insomnia, chronic pain

Brand Name

Side Effects Klonopin

Serious
Class
Paralytic ileus, hyperthermia, lowered seizure threshold
Anxiolytic
and rare seizures, orthostatic hypotension, sudden death,
arrhythmias, tachycardia, QTc prolongation, increased
intraocular pressure, hepatic failure, extrapyramidal
Proposed Mechanism(s) of Action
symptoms, mania, and suicidal ideation
Binds to benzodiazepine receptors at the GABA-A ligand-
gated channel, thus allowing for neuronal hyperpolariza-
Common tion. Benzodiazepines enhance the inhibitory action of
GABA via boosted chloride conductance.
Blurred vision, constipation, increased appetite, urinary
retention, dry mouth, nausea, diarrhea, heartburn,
strange taste in mouth, weight gain, fatigue, weakness, Indication
dizziness, headache, anxiety, nervousness, restlessness, se-
dation, sexual dysfunction, sweating Panic disorders (with or without agoraphobia), Lennox–
Gastaut syndrome, akinetic seizures, myoclonic seizure,
absence seizures
References and Readings
Off Label Use
Physicians’ Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson
PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The prescriber’s guide Atonic seizures and other anxiety disorders, acute psycho-
(2nd ed.). New York, NY: Cambridge University Press. sis, insomnia
602 C Clonidine

Side Effects Proposed Mechanism(s) of Action

Serious Centrally acting alpha 2 agonist

Respiratory depression, hepatic dysfunction (rare), renal

dysfunction and blood dyscrasias, Grand mal seizures Indication

Hypertension
Common

Sedation, fatigue, depression, dizziness, memory pro- Off Label Use

blems, dysinhibition, confusion, ataxia, slurred speech
Attention deficit hyperactivity disorder, Tourette’s syn-
drome, anxiety disorders including PTSD and social anx-
References and Readings iety disorder, substance withdrawal including opiates and
alcohol, menopausal flushing, clonadine-induced hyper-
Physicians’ Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson salavation, severe pain in cancer patients
PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The prescriber’s guide
(2nd ed.). New York, NY: Cambridge University Press. Side Effects

Serious
Additional Information
Sinus bradycardia, atrioventricular block during with-
Drug Interaction Effects: http://www.drugs.com/drug_interactions.html
drawal, hypertensive, encephalopathy, cerebrovascular
Drug Molecule Images: http://www.worldofmolecules.com/drugs/
Free Drug Online and PDA Software: www.epocrates.com
accidents, and death
Gene-Based Estimate of Drug interactions: http://mhc.daytondcs.
com:8080/cgi bin/ddiD4?ver=4&task=getDrugList
Pill Identification: http://www.drugs.com/pill_identification.html Common

Dry mouth, dizziness, constipation, sedation, major de-

pression, weakness, fatigue, impotence, loss of libido,
Clonidine insomnia, headache, dermatologic reactions, hypoten-
sion, occasional syncope, nervousness, agitation, tachy-
J OHN C. C OURTNEY cardia, nausea, vomiting
Children’s Hospital of New Orleans
New Orleans, LA, USA
References and Readings

Generic Name Physicians’ Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson
PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The prescriber’s guide
Clonidine
(2nd ed.). New York, NY: Cambridge University Press.

Brand Name
Additional Information
Duraclon, Catapres, Catapres-TTS, Clorpres
Drug Inter action Effects: http://www.drugs.com/drug_interactions.html
Drug Molecule Images: http://www.worldofmolecules.com/drugs/
Free Drug Online and PDA Software: www.epocrates.com
Class Gene-Based Estimate of Drug interactions: http://mhc.daytondcs.
com:8080/cgi bin/ddiD4?ver=4&task=getDrugList
Antihypertensive Pill Identification: http://www.drugs.com/pill_identification.html
 Closure C 603

Common
Clorazepate
Sedation, fatigue, depression, dizziness, memory pro-
J OHN C. C OURTNEY blems, dysinhibition, confusion, ataxia, and slurred
Children’s Hospital of New Orleans speech.
New Orleans, LA, USA
C

References and Readings

Generic Name
Physicians’ Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson
Clorazepate PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The prescriber’s guide
(2nd ed.). New York, NY: Cambridge University Press.

Brand Name

Azene, Tranxene Additional Information

Drug Interaction Effects: http://www.drugs.com/drug_interactions.html

Drug Molecule Images: http://www.worldofmolecules.com/drugs/
Class Free Drug Online and PDA Software: www.epocrates.com
Gene-Based Estimate of Drug interactions: http://mhc.daytondcs.com:
Anxiolytic 8080/cgi bin/ddiD4?ver=4&task=getDrugList
Pill Identification: http://www.drugs.com/pill_identification.html

Proposed Mechanism(s) of Action

Binds to benzodiazepine receptors at the GABA-A ligand- Closure
gated channel, thus allowing for neuronal hyperpolariza-
tion. Benzodiazepines enhance the inhibitory action of R ONALD A. C OHEN
GABA via boosted chloride conductance. Clorazepate is Brown University
also hypothesized to inhibit neuronal activity in amgy- Providence, RI, USA
dala-centered fear circuits.

Synonyms
Indication
Visual integration; Visual synthesis
Anxiety Disorder, symptoms of anxiety, and acute alcohol
withdrawal.
Definition
Off Label Use Visual closure refers to the ability to perceive and recog-
nize objects, shapers, features, or symbols from incom-
Partial seizures (as an adjunct). plete or degraded visual stimuli. It reflects the capacity of
humans to fill in missing information from incomplete
sensory input to achieve a meaningful percept.
Side Effects

Serious Historical Perspective

Respiratory depression, hepatic dysfunction (rare), renal The principle of visual closure had its roots in Gestalt
dysfunction and blood dyscrasias, and Grand mal psychology (Ellis, 1938; Harlow, 1938; Köhler, 1929).
seizures. Gestalt psychology theorized that operationally brain
604 C Clot Buster

functions (i.e., perception and cognition) are holistic impairments on tests such as the Gollin Figures and
consisting of analog processes that occur in a parallel Mooney Closure tests. This may reflect the fact that impair-
manner and are self-organizing. This led to the well- ments on this type of task tend to be embedded in other
known conclusion regarding perception, and cognition visual perception deficits that are more striking. However,
more generally, that ‘‘the whole is greater than the sum it is also clear that closure paradigms have not been system-
of its parts.’’ Based on this framework, all perceptual atically implemented into standard neuropsychological
processes act to achieve optimal organization and recon- batteries using modern computerized methods, so that
ciliation with the objects that are being perceived. A definitive conclusions regarding impairments of closure
critical principle driving Gestalt perception is prägnanz secondary to localized and global brain disorders cannot
(law of conciseness), which maintains that people orga- be reached at this point.
nize their experience in an orderly, symmetric, and simple
manner when possible. Visual closure was one of the
five laws of prägnanz, with others including the laws Cross References
of similarity, proximity, symmetry continuity, and com-
mon fate. ▶ Gollin Figures
While each of these laws has potential value in ac- ▶ Hooper Visual Organization Test
counting for elements of visual integration, the law of ▶ Simultanagnosia
visual closure seems to have had the most direct impact,
particularly with respect to clinical neuropsychology.
Early clinical studies of the effects of posterior cortical
lesions on visual perception indicated that certain patients
References and Readings
had difficulty in simultaneously processing all the ele-
Ellis, W. D. (1938). A source book of Gestalt psychology. New York:
ments of their visual sensorium to achieve a unified
Harcourt, Brace & World.
percept, a syndrome that was labeled simultagnosia Foreman, N. (1991). Correlates of performance on the Gollin and
(Poppelreuter, 1990). Mooney tests of visual closure. Journal of General Psychology, 118
(1), 13–20.
Harlow, R. F. (1938). Philosophy’s contribution to Gestalt psychology.
Journal of Psychology: Interdisciplinary and Applied, 5, 185–200.
Current Knowledge Holmes, D. S. (1968). Search for ‘‘closure’’ in a visually perceived pattern.
Psychological Bulletin, 70(5), 296–312.
The idea that visual perception occurs as a function by- Jones, E. C., & Dennis, M. E. (1972). Perceptual closure as a function of
product of active self-organizing processes is now widely gap size. Perceptual and Motor Skills, 35(1), 126.
accepted by most visual scientists, though many would Köhler, W. (1929). Gestalt psychology. New York: H. Liveright.
Mooney, C. M., & Ferguson, G. A. (1951). A new closure test. Canadian
reject a pure holistic view. Instead, visual perception and
Journal of Psychology/Revue Canadienne de Psychologie, 5(3),
higher-order visual processes tend to be conceptualized as 129–133.
the by-product of computational processes carried out by Poppelreuter, W. (1990). Disturbances of lower and higher visual capacities
modular neural networks responsible for specific opera- caused by occipital damage: with special reference to the psychopatho-
tions. Visual closure is thought to result from such pro- logical, pedagogical, industrial, and social implications. Oxford/New
York: Clarendon Press/Oxford University Press.
cesses occurring in extra-striatal systems found primarily
in the parietal cortex. Psychometric studies of closure
have tended to employ tests such as the Gollin Figures
and Mooney test (Foreman, 1991; Holmes, 1968; Jones &
Dennis, 1972; Mooney & Ferguson, 1951). In healthy Clot Buster
adults, the ability to recognize line drawings that have
been degraded has been shown to be a function of the ▶ Recombinant Tissue Plasminogen Activator
size of gaps in the drawing (Jones & Dennis, 1972), which
in turn reflects the amount of missing information. Per-
formance on closure tests has been shown to not be
strongly associated with visual search performance, sug-
gesting that these are distinct visual processes (Foreman, Clot Busting
1991). While tests of closure have existed for over 40 years,
there are relatively few studies demonstrating consistent ▶ Thrombolysis
 Clustering C 605

Side Effects
Clotting
Serious
▶ Thrombosis
Agranulocytosis, neuroleptic malignant syndrome, sei- C
zures, pulmonary embolism, myocarditis, hyperglycemia.

Clozapine Common

J OHN C. C OURTNEY 1, C RISTY A KINS 2 Increased risk for diabetes, sweating, and increased
1 salivation.
Children’s Hospital of New Orleans
New Orleans, LA, USA
2
Mercy Family Center References and Readings
Metarie, LA, USA
Physicians’ Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson
PDR.
Generic Name Stahl, S. M. (2007). Essential psychopharmacology: The prescriber’s guide
(2nd ed.). New York, NY: Cambridge University Press.
Clozapine
Additional Information

Brand Name Drug interaction effects: http://www.drugs.com/drug_interactions.html

Drug molecule images: http://www.worldofmolecules.com/drugs/
Free drug online and PDA software: www.epocrates.com
Clozaril, Leponex Gene-based estimate of drug interactions: http://mhc.daytondcs.
com:8080/cgi bin/ddiD4?ver=4&task=getDrugList
Pill identification: http://www.drugs.com/pill_identification.html

Class

Atypical Neuroleptic Clumsiness

▶ Ataxia
Proposed Mechanism(s) of Action

Blocks dopamine 2 receptors, inhibits serotonin 2A recep- Cluster Analysis

tors, thus increasing presynaptic release of related
catecholamines ▶ Clustering

Indication
Clustering
Schizophrenia (treatment-resistant), reduction of suicidal
M ICHAEL D. F RANZEN
behavior.
Allegheny General Hospital
Pittsburgh, PA, USA

Off Label Use

Synonyms
Bipolar disorder (treatment-resistant), violence, and ag-
gression associated with psychosis or brain dysfunction. Cluster analysis
606 C Cmax

Definition elimination. The maximum concentration of a drug in

blood plasma represents a drug’s peak effect. Cmax is one
Clustering can be thought of as the obverse of factoring. In of the primary pharmacokinetic measures for evaluating
factor analysis, observations are correlated with each other how the body acts upon a drug.
and the correlation matrix is examined to see which items The same dose of a drug may result on different
covary among themselves. In cluster analysis, the correla- plasma levels because the body is not a passive recipient.
tion matrix is examined to see which individuals or obser- Plasma levels of a drug can be altered by the route of
vations covary among themselves. Once the groups of administration, the ease of absorption, the distribution of
individuals are composed, they are compared to each the drug with the body, the bioavailability or accessible
other in order to see if some external correlate exists. concentration of the drug, and the efficiency with which a
For example, a large group of patients might be drug is metabolized or eliminated.
administered a series of cognitive measures. The scores Common factors that affect plasma levels of a drug
on those measures are examined to see which individuals could include the size of the molecule and its fat solubility;
seem to be most similar to each other. Once the groups the patient’s gastric pH, physical health or age, and
are empirically formed, their characteristics are examined the presence of other medications or foods that may expe-
to see if age or diagnosis or injury severity discriminates dite or slow absorption from the gastrointestinal tract into
among the groups. general circulation or alter the drug’s metabolism and
excretion. These factors may require changes in dosing in
order to achieve therapeutic levels of a drug or alterations
Cross References in diet, such as to take a drug with or without food. It may
also include recommendations to avoid particular foods
▶ Correlation Coefficients
that are known to induce or inhibit the specific enzyme
▶ Factor Analysis
pathways that metabolize the drug (e.g., grapefruit juice).
Drug–drug interactions can alter the plasma levels of a
References and Readings drug, including its peak effect.
There are also mediations that inhibit metabolism with-
Corter, J. (1996). Tree models of similarity and association. Thousand in a particular liver-mediated enzyme system, thus altering
Oaks, CA: Sage. the availability of other agents of that drug itself. This can
Kaufman, L., & Rousseeuw, P. (2005). Finding groups in data: An
alter the availability of a drug, including its Cmax. Fluox-
introduction to cluster analysis. Hoboken, NJ: Wiley.
McIntyre, R. M., & Blashfield, R. K. (1980). A nearest-centroid technique
etine’s impact on codeine is a good example. Codeine is
for evaluating the minimum-variance clustering procedure. ultimately synthesized into morphine and via a transforma-
Multivariate Behavioral Research 15, 2225–2238. tion that requires an enzyme that makes this change possi-
ble. Fluoxetine appears to inhibit this process, thus
dramatically reducing the pain control intended via the
administration of codeine.
Cmax For some drugs, there is no clear relationship be-
tween the concentration of a drug in blood plasma and
N ADIA W EBB its pharmacological effect. For other drugs, the concen-
Children’s Hospital of New Orleans tration must be tightly monitored, typically through
New Orleans, LA, USA regular plasma assessments of drug levels (assays). As a
rule of thumb, adverse drug reactions and side effects
become more likely as the dose of a drug increases.
Synonyms Consequently, adverse drug effects are more likely at
the time of Cmax.
Maximum concentration; Peak concentration
Cross References
Definition
▶ p450 Cytochrome System
Plasma concentrations reflect a time curve from the ad- ▶ Pharmacokinetics
ministration of a drug through its peak effect and eventual ▶ Side Effects
 Cochlear Nuclei (Dorsal and Ventral) C 607

References and Readings waves in the cochlea are transduced into bioelectrical
nerve impulses. The acoustic division of the eighth cranial
Brunton, L. B., Lazo, J. S., & Parker, K. L. (Eds.). (2005). Goodman & nerve has its cell bodies in the spiral ganglion of the
Gilman’s the pharmacological basis of therapeutics (11th ed.). cochlea.
New York: McGraw Hill.
Stahl, S. M. (2008). Stahl’s essential psychopharmacology: Neuroscientific C
basis and practical applications. New York: Cambridge University
Press.
Cross References

▶ Auditory System

CMS
References and Readings
▶ Children’s Memory Scale
Ropper, A. H., & Brown, R. J. (2005). Deafness, dizziness, and disorders
of equilibrium. In Adams and Victor’s principles of neurology.
New York: McGraw Hill.

CNC
▶ Coma/Near Coma Scale
Cochlear Nerve
▶ Vestibulocochlear Nerve

CNS Lupus
▶ Lupus Cerebritis
Cochlear Nuclei (Dorsal
and Ventral)
J OHN E. M ENDOZA
Cochlea Tulane University Medical Center
New Orleans, LA, USA
K ERRY D ONNELLY
University at Buffalo/SUNY
Buffalo, NY, USA
Definition
Cochlear nuclei is the nuclei that receive first-order
Definition auditory input from the organ of Corti in the cochlea of
the inner ear.
The cochlea, a small conical structure, is the part of the
inner ear that converts mechanical energy (vibrations)
into nerve impulses sent to the brain. It is also known as
the organ of hearing. The word cochlea is a Latin word Current Knowledge
derived from the Greek kokhlos, which refers to the land
snail. A coiled tube, the cochlea winds around a central The cochlear nuclei are divided into a dorsal and a
axis, forming the anterior part of the labyrinth. It contains ventral group. The dorsal cochlear nuclei give rise to
the organ of Corti, which includes the hair cells that the dorsal acoustic stria, which immediately cross the
constitute the primary mechanisms by which pressure midline and contribute fibers that ascend contralaterally
608 C Coding

in the lateral lemniscus. The ventral cochlear nuclei are

the source of two other auditory pathways, the interme- Cogniform Disorder
diate and the ventral acoustic stria. The former also
crosses the midline and, like the dorsal acoustic stria, D EAN C. D ELIS
ascends in the contralateral lateral lemniscus. Fibers San Diego School of Medicine
making up the ventral acoustic stria, the largest of these San Diego Veterans Affairs Healthcare System
three pathways, take three different paths after leaving La Jolla, CA, USA
the nucleus. They (1) synapse in both the ipsilateral or
contralateral superior olivary nuclei, which in turn send
tertiary fibers to the inferior colliculi via the ipsilateral Synonyms
and contralateral lateral lemniscus, and (2) send fibers
directly to the contralateral inferior colliculi, bypassing Conversion disorder; Malingering; Somatoform disorders
the superior olivary nuclei.
The crossing fibers of the ventral acoustic stria make
up what is known as the trapezoid body of the pontine Definition
tegmentum. The dorsal and ventral cochlear nuclei them-
selves are located laterally in the rostral medulla at the In neuropsychology, the assessment of test-taking effort
pontine–medullary junction near the vestibulocochlear has captured the focus of considerable research and de-
nerve. bate. In the past 20 years, over 500 studies have been
Since the first-order neurons from the auditory nerve published in peer-reviewed neuropsychological journals
terminate in the cochlear nuclei and the decussations that address the breadth and scope of this problem (see
within the auditory system only begin with the second- reviews by Hom & Denny, 2002; Iverson & Binder, 2000;
order neurons originating in the cochlear nuclei, these Larrabee, 2005; Sweet, 1999). Considerable advances have
nuclei receive input only from one ear. Hence, unilateral been made in the development of empirically based meth-
pontine lesions affecting the dorsal and ventral cochlear ods for identifying individuals who are simulating cogni-
nuclei would be expected to result in ipsilateral hearing tive problems, including the use of instruments designed
deficits (loss). specifically to assess cognitive validity (Binder, 1993;
Frederick, 1997; Green et al., 1999; Tombaugh, 1996),
analysis of atypical performances on standard ability
tests (Larrabee, 2003; Millis et al., 1995), and analysis of
Cross References
test–retest profile inconsistencies (Hom & Denny, 2002;
Iverson & Binder, 2000). In addition, specific guidelines
▶ Auditory System
and criteria have been developed for diagnosing subopti-
mal effort and malingering on neuropsychological tests
(e.g., Slick et al., 1999). Using these methods and guide-
References and Readings
lines, neuropsychologists have found that the frequency of
individuals exhibiting excessive or exaggerated cognitive
Wilson-Pauwek, L., Akesson, E. J., Stewart, P. A., & Spacey, S. D. (2002).
Cranial nerves in health and disease. Hamilton, ONT: B.C. Decker. symptoms in medicolegal evaluations often ranges from
20% to 40% (Miller, 2001; Millis et al., 1995; Mittenberg
et al., 2002). In light of the pervasiveness of this problem,
it is now generally accepted that cognitive validity testing
Coding is an important part of the neuropsychological assessment
process, particularly for evaluations that occur in the
▶ Digit Symbol Substitution Test context of medicolegal or disability-application settings
(Bush et al., 2005).
While considerable advances have been made in the
methods used to detect individuals who are exhibiting
inadequate effort and symptom exaggeration on cognitive
Cog-Log testing, neuropsychologists often find themselves in a quan-
dary in terms of the diagnostic labels to ascribe to these
▶ Cognitive-Log individuals once they have been identified. The DSM-IV
 Cogniform Disorder C 609

offers several possible categories for diagnosing individuals (b) Undifferentiated Somatoform Disorder requires
with excessive cognitive symptoms (e.g., Malingering and ‘‘one or more physical complaints,’’ with no reference
Conversion Disorder); however, shortcomings of these con- made to cognitive difficulties.
ditions have been noted in the literature. In particular, (c) Conversion Disorder requires ‘‘one or more symp-
Malingering has been the subject of considerable debate toms or deficits affecting voluntary motor or sensory C
and criticism, especially with regards to the objectivity with function’’ [emphasis added], without mention of
which clinicians can assess if feigned symptoms were inten- cognitive or memory difficulties among the specific
tionally or unintentionally produced. Improvements have criteria.
been made in establishing criteria for this condition (e.g., (d) Pain Disorder requires only excessive pain
Slick et al., 1999), but clinicians nevertheless often remain symptoms.
reluctant to use any diagnosis that requires them to make (e) Somatoform Disorder NOS could conceivably in-
judgments about intentionality of symptom exaggeration. clude individuals with predominantly excessive cog-
Clinicians often face three general problems in trying nitive symptoms; however, ‘‘soma’’ denotes physical
to use existing DSM-IV categories to classify individuals rather than cognitive problems, and the list of exam-
with excessive cognitive symptoms. These problems in- ple cases provided in the DSM-IV for this catchall
clude (a) lack of a diagnostic category that adequately category makes no reference to excessive cognitive
targets the specific features of this relatively common symptoms.
condition, (b) the use of criteria that require the clinician (f) Dissociative Amnesia requires one specific type of
to make judgments about internal states that are exceed- cognitive problem, namely, ‘‘an inability to recall
ingly difficult to evaluate in an objective manner (e.g., important personal information, usually of a trau-
intentional versus unintentional production of excessive matic or stressful nature’’ [emphasis added]. Howev-
symptoms), and (c) difficulties in determining the relative er, individuals presenting with excessive cognitive
role that external incentive and sick-role factors may play symptoms do so in a myriad of ways (Bush et al.,
in the symptom production. 2005; Delis & Jacobson, 2000; Larrabee, 2003). Some
Symptom Specificity. The existing DSM-IV cate- people endorse problems in all cognitive domains
gories addressing excessive symptomatology can be queried, including attention, language, math, visual-
divided into two general types: symptom-specific versus spatial functions, higher-level executive functions,
symptom-nonspecific conditions. Symptom-specific con- new learning and memory, and remote recall of im-
ditions are those that require amplification of only certain portant personal information. In contrast, other
types of symptoms. The DSM-IV offers a relatively small individuals endorse difficulties in only one or a few
number of symptom-specific categories, which fall only specific cognitive skills (e.g., short-term memory and
among the somatoform disorders (e.g., Somatization Dis- concentration), while denying problems in other cog-
order and Conversion Disorder) and dissociative disor- nitive domains, including recall of important person-
ders (e.g., Dissociative Amnesia and Dissociative Fugue). al information. In fact, cases of isolated difficulty in
In addition, the DSM-IV offers two symptom-nonspecific remembering important autobiographical informa-
conditions, Malingering and Factitious Disorder, which tion are relatively rare, illustrating the limited utility
are discussed in the next section. of this diagnostic category for the vast majority of
A major problem in trying to subsume individuals cases with excessive cognitive symptoms.
with excessive cognitive complaints or invalid test perfor- (g) Dissociative Fugue not only requires one specific
mances into one of the symptom-specific diagnoses is that cognitive difficulty (‘‘inability to recall some or all
the cognitive symptoms of many of these cases simply fail of one’s past’’), but carries the added stipulation that
to fit adequately in these categories. Following are expla- this difficulty must surface in the context of a ‘‘sud-
nations of this problem for each of the symptom-specific den, unexpected, travel away from home or one’s
categories provided in the DSM-IV: customary place of daily activities’’ [emphasis
added]. These cases are extremely rare among indi-
(a) Somatization Disorder requires at least four pain
viduals presenting with excessive cognitive symp-
symptoms, two gastrointestinal symptoms, one sex-
toms, thereby precluding the use of this category
ual symptom, and one pseudoneurological symp-
for almost all cases.
tom. However, many individuals who present with
(h) Dissociative Identity Disorder is thought to occur
primarily excessive cognitive symptoms have few if
in individuals with multiple personalities in which
any physical complaints (Larrabee, 2005).
they exhibit an inability to recall important
610 C Cogniform Disorder

information about one or more personality states goal-directed motivation. An individual may be both
when they are in a different personality state. How- conscious of producing feigned behavior (e.g., is capable
ever, cases of multiple personalities are relatively of admitting to self and others that he or she is simulating
rare, particularly in clinical–neuropsychological symptoms) and motivated to do so for some type of
practice, and thus this diagnosis is seldom applicable personal gain; these features would meet criteria for a
to individuals with excessive cognitive symptoms. DSM-IV diagnosis of Malingering. However, someone
(i) Dissociative Disorder NOS is another catchall cate- may be largely unconscious of the feigned behavior (e.g.,
gory that, conceivably, could encompass individuals has convinced himself or herself that the excessive symp-
with excessive cognitive complaints. However, the toms are real), yet the feigned behavior may still arise due
tenor of this category is for individuals who exhibit to a specific, goal-directed purpose. For example, it was
an inability to recall personal information that was of noted during World War II that some soldiers, when faced
a traumatic or stressful nature, thereby greatly limit- with the prospect of entering the frontlines of battle,
ing the utility of this category for most cases of would develop psychogenic paralysis (what would now
excessive cognitive symptoms. be diagnosed as Conversion Disorder given that the symp-
tom amplification occurred primarily in the motor do-
Taken together, the aforementioned nine symptom-spe-
main). These individuals often appeared to truly believe
cific categories either fail to include cognitive complaints,
they were paralyzed, thereby suggesting an unconscious
target only highly specific, relatively rare types of cogni-
(conversion) process. However, their exaggerated behav-
tive problems, or require that other, qualitatively different
ior (paralysis) was clearly goal-directed, because it was
symptoms or conditions also be present (e.g., extensive
manifested in the context of an external incentive (avoid-
physical symptoms for Somatization Disorder). For these
ance of danger). In these cases, the conscious component of
reasons, these diagnoses generally fail to capture the vast
intentionality may have been absent, but the goal-directed
majority of individuals presenting with excessive cogni-
motivational component for producing the symptom was
tive symptoms.
likely present.
Intentionality. Another difficulty in using existing
In neuropsychological practice, the same type of disso-
DSM-IV categories has to do with required criteria related
ciation may occur in which individuals may produce exces-
to intentional/unintentional or voluntary/involuntary
sive cognitive symptoms in reaction to an external incentive
control over the production of the excessive complaints
(e.g., litigation), thereby suggesting goal-directed motiva-
or symptoms. For example, a key required criterion for
tion for the symptom production. However, these indivi-
the two symptom-nonspecific categories – Malingering
duals may have nevertheless convinced themselves that their
and Factitious Disorder – is that the clinician must deter-
symptoms are real, thereby suggesting a lack of a conscious
mine if the excessive symptoms were generated in an
component to the symptom production. Thus, for these
intentional or volitional manner. The problem here is
individuals, only certain components of intentionality may
that this criterion reflects a causative internal state that,
be present, with the lack of conscious awareness calling
for the majority of cases, is difficult if not impossible to assess
into question whether they would adequately meet the
in an objective manner. That is, the degree to which a person
required criteria for a diagnosis of Malingering. Another
may be exhibiting excessive symptoms or behaviors in an
complicating factor in the assessment of intentionality is
intentional, voluntary, or conscious manner versus an un-
that conscious awareness likely exists on a continuum, with
intentional, involuntary, or unconscious manner represents
individuals varying from being fully conscious, to semicon-
an untestable diagnostic hypothesis for many cases (see also
scious, to largely unconscious of the production of the
Slick et al., 1999). A clinician may have a ‘‘hunch’’ about
feigned behavior. Although an operational definition of
whether an individual’s excessive complaints or symp-
intentionality is beyond the scope of this chapter, the im-
toms were under the voluntary or involuntary control of
portant point here is that intentionality of symptom pro-
the person, but usually these impressions are not substan-
duction not only refers to an elusive internal state, but
tiated by objective data, such as a disclosure or confession
it likely has component features that exist on a continuum
made by the individual to a clinician or other uninvolved,
(e.g., levels of conscious awareness), thereby making this
reliable third party.
construct exceedingly difficult for clinicians to assess in an
Another difficulty in this area of diagnosis is that
objective manner. Consequently, many clinicians are reluc-
intentionality is likely multifactorial in nature. For exam-
tant to use diagnoses such as Malingering, Factitious Disor-
ple, there may be at least two key components of inten-
der, and Conversion Disorder at least in part because of
tionality that can be dissociated: conscious awareness and
difficulty in objectively assessing the presence or absence
 Cogniform Disorder C 611

of intentionality in the generation of the excessive As another example, some individuals may begin to
symptom. feign symptoms intentionally and consciously in reaction
External Incentive. A third difficulty in using existing to an external incentive (e.g., a lawsuit). However,
DSM-IV categories to diagnose individuals with excessive these individuals may gradually, and perhaps uncon-
cognitive symptoms is related to another required criteri- sciously, assume a progressively worsening sick role due C
on for the two symptom-nonspecific categories – Malin- to (a) a prolongation in obtaining the external incentive
gering and Factitious Disorder – regarding the presence or (e.g., caused by delays in the lawsuit); and (b) increased
absence of external incentive in the production of the skepticism and questioning on the part of family mem-
symptoms. Specifically, external incentive is a required bers, coworkers, or health providers about the authentici-
inclusionary criterion for Malingering and required exclu- ty of the individual’s complaints. This prolonged scrutiny
sionary criterion for Factitious Disorder. (If there is an may be overwhelming to these individuals, compelling
absence of external incentive, then the clinician must them to adopt the sick role and exhibit illness behavior
make a further determination of whether or not an indi- in widespread areas of their lives, to the point where they
vidual has adopted the sick role in order to diagnose may even convince themselves of the authenticity of their
Factitious Disorders). However, the criterion of external symptoms. In other words, while the DSM-IV treats
incentive carries its own inherent difficulties for clinicians external incentive and sick role as mutually exclusive diag-
to identify when considering these diagnoses. First, for nostic criteria for differentiating Malingering and Facti-
many cases, practitioners may not have access to sufficient tious Disorder, in reality, as is the case for most psychiatric
background information about a person’s life to be able to conditions, they may co-occur in varying degrees (Slick
assess if external incentives are operative in the case. That et al., 1999).
is, a practitioner may be unaware that a patient has or is Given these limitations in the DSM-IV, the following
planning to apply for disability or to initiate a civil lawsuit two diagnostic categories were proposed by Delis and
in the future, or has committed a crime and fears that he Wetter (2007) to encompass cases of excessive cognitive
or she may soon be apprehended. This lack of knowledge complaints or poor (invalid) test performances in the
about possible covert sources of external incentives makes absence of sufficient evidence of intentionality of symp-
it difficult to utilize the diagnoses of Malingering or tom production to warrant a diagnosis of Malingering.
Factitious Disorder for a number of cases, especially
given that such information is a required criterion rather
than an optional one for these categories. Neuropsychology of Cogniform Disorder
Second, as currently written, the DSM-IV criteria do
not allow for the possibility that a comorbidity may occur The essential feature of Cogniform Disorder is a pattern of
between the adoption of the sick role and the presence cognitive complaints or low scores on psychometric cog-
of external incentives (see also Slick et al., 1999). nitive tests that are considered to be excessive because they
For example, some individuals may gradually develop cannot be fully explained by a neurological disorder, by
into a progressively worsening sick role without the pres- another mental disorder that is associated with CNS dys-
ence of external incentives. However, after a period of function (e.g., schizophrenia), by a general medical con-
time, these individuals may present as so ‘‘disabled’’ that dition known to affect CNS function (e.g., renal disease),
they begin to receive disability payments, without neces- by the direct effects of a substance (e.g., opioid medica-
sarily having actively sought out such compensation. The tions), or by other factors known to affect cognitive func-
financial gain, however, likely buttresses and propagates tioning (e.g., developmental learning disorder, insomnia,
the continuation of the sick role. According to the and normal aging process). If the cognitive complaints or
DSM-IV, these individuals would have started out as poor test performances occur in the presence of a known
having Factitious Disorder, but as soon as the external neurological or mental disorder or any other factor
incentive was initiated and became a reinforcing factor, known to affect CNS function (e.g., medication), the
the diagnosis of Factitious Disorder would be called into cognitive symptoms are in excess of what would be
question (again, because external incentive is a required expected from the history, physical examination, labora-
exclusionary criterion for this condition). However, for tory tests, or psychometric validity testing. Findings from
these cases, the predominant causative factor for the ex- the clinical interview or psychometric testing of cognitive
cessive symptomatology may still be the adoption of the functions do not substantiate the degree of cognitive
sick role, with the external incentive playing a secondary complaints or symptoms because of the presence of at
or supportive role in the continuation of the symptoms. least two of the following features:
612 C Cogniform Disorder

(a) Cognitive complaints or poor test performances that reporting significant cognitive complaints and dysfunction
are rare for patients with documented mild to mod- in their daily lives.
erate generalized brain damage (e.g., loss of remote The primary distinguishing feature between Cogniform
autobiographical memories and inability to perform Disorder and Cogniform Condition (see below) concerns
overlearned verbal skills like reading, spelling, or the degree to which the individual presents as cognitively
simple math) impaired in widespread areas of his or her life. Specifically, a
(b) Inconsistencies between the individual’s excessive diagnosis of Cogniform Disorder should be made if there is
cognitive complaints or poor test performances and reasonable evidence that the individual exhibits excessive
the relatively mild nature of the injury or illness as cognitive symptoms in most if not all areas of his or her life
documented in the medical records and seemingly at all times, thereby suggesting a conversion-
(c) Inconsistencies between the individual’s excessive like adoption of the sick role manifested primarily as cogni-
cognitive complaints or poor test performances and tive dysfunction. In addition, in Cogniform Disorder, the
observed behavior degree of claimed disability in performing activities of daily
(d) Delayed onset of excessive cognitive complaints or living will often parallel the individual’s complaints of cog-
symptoms after an injury and/or significant worsen- nitive dysfunction and poor (invalid) cognitive test perfor-
ing of symptoms over time without an adequate mance. For example, the individual not only obtains
explanation for the decline in functioning (e.g., severely deficient (and likely invalid) scores on tests of
subsequent neurological complications) visual-motor and visual-spatial functioning, but he or she
(e) Significant inconsistencies in cognitive test scores or also ceases to drive a vehicle because of the perceived cogni-
profiles across repeat evaluations tive problems. In many ways, Cogniform Disorder is analo-
(f) Patterns of cognitive test scores within an examina- gous to the somatoform condition of Conversion Disorder,
tion that are rare for brain-damaged patients but with the excessive symptoms manifested primarily in
(g) Significant inconsistencies in cognitive complaints or terms of cognitive dysfunction rather than deficits affecting
symptoms over time primarily motor or sensory functions (e.g., nonepileptic
(h) Evidence of insufficient test-taking effort or exagger- seizures). For this reason, Cogniform Disorder should be
ation on tests designed specifically to assess validity considered as a new subtype of the somatoform disorders.
of cognitive performance
(j) Evidence of insufficient test-taking effort or exagger-
ation on specific measures obtained from standard
Neuropsychology of Cogniform
ability tests that have been empirically found to assess
Condition
validity of cognitive performance
The essential features of Cogniform Condition are the
Considerable individual differences are found in the per- same as those of Cogniform Disorder in every respect,
formances of people with this condition on psychometric with the exception of the degree to which the individual
tests of cognitive skills (Larrabee, 2003; Slick et al., 1999). exhibits cognitive dysfunction in widespread areas of his
Some individuals obtain markedly low scores on most or her everyday life. That is, in Cogniform Condition,
cognitive tests administered; these individuals are often there is (a) a lack of reasonable evidence that the individ-
less sophisticated about medical and psychological condi- ual presents as cognitively dysfunctional in many areas of
tions and more blatant in their symptom amplification. his or her life, and (b) evidence of significant inconsis-
Other people may obtain low and invalid scores on only a tencies between the individual’s excessive cognitive com-
few tests administered (e.g., memory tasks); these indivi- plaints or poor test performances in an evaluation and his
duals may be more subtle in their symptom exaggeration or her higher level of everyday functioning. For example,
and, as a result, more difficult to identify. Occasionally, an an individual may obtain severely deficient (and likely
individual may perform within expected ranges on most invalid) scores on tests of visual-motor and visual-spatial
cognitive tests administered, including cognitive validity functioning and yet continues to drive a vehicle without
tests, and yet continue to complain of extensive cognitive apparent difficulty. In other words, in Cogniform Condi-
problems and dysfunction in their daily lives. These indivi- tion, the individual is not given a diagnosis of ‘‘disorder,’’
duals may have learned from other sources (e.g., Internet; because there is a lack of reasonable evidence that the
attorney coaching) that neuropsychological tests are capa- individual is acting out the ‘‘sick role’’ of being cognitively
ble of detecting poor test-taking effort, and consequently dysfunctional in widespread areas of his or her life despite
exert adequate effort on psychometric tests despite presenting to the clinician in a manner that suggests that
 Cogniform Disorder C 613

he or she should be markedly impaired in everyday As proposed here, a diagnosis of Cogniform Disorder or
functioning. Cogniform Condition does not exclude the possibility of
intentional production of the excessive symptoms; rather,
these categories imply only that there is insufficient evidence
Cogniform Disorder and Condition Versus at the time of the assessment to formulate a diagnosis of C
Malingering: Similarities and Differences intentionality and therefore Malingering. Indeed, an ad-
vantage of having diagnostic categories such as Cogni-
Cogniform Disorder, Cogniform Condition, and Malin- form Disorder and Cogniform Condition is that they
gering (when manifested in the form of cognitive dysfunc- allow the clinician to label the cognitive symptoms as
tion) are similar in that the individual may present with excessive using more neutral terms that avoid the accusa-
excessive cognitive complaints or exhibit evidence of tory implications of Malingering when there is a lack of
inadequate effort and exaggeration on formal neuropsy- clear evidence to make that diagnosis. In addition, as
chological testing. However, a diagnosis of Cogniform discussed above, intentionality is likely multifactorial in
Disorder or Cogniform Condition should not be made if nature and is comprised of at least two key components:
there is reasonable evidence that the excessive cognitive conscious awareness and goal-directed motivation. The
symptoms are produced in an intentional or volitional individual who has convinced himself or herself that the
manner, in which case a diagnosis of Malingering may be feigned behavior is real may not be fully or even partially
warranted. As noted above, however, this determination conscious of his or her symptom amplification, but this
can be difficult to make for many cases due to inherent person may nevertheless have developed the symptoms in
problems in objectively assessing the internal state of the reaction to the presence of external or interpersonal
intentionality of simulated behavior. For this reason, it is incentives for personal gain. The categories Cogniform
likely that many cases of excessive cognitive symptoms Disorder and Cogniform Condition allow the clinician
would receive the more neutral diagnosis of Cogniform to acknowledge the presence of incentives that may
Condition, and possibly a diagnosis of Cogniform Disor- have played a significant role in the goal-directed motiva-
der if the individual exhibits cognitively dysfunctional tion for the excessive symptomatology without having to
behavior in widespread areas of his or her life. However, make the difficult determination of whether the individu-
when evidence emerges that implicates at least a conscious al is conscious or unconscious of these dynamics.
component in the production of the excessive cognitive
symptoms, then a diagnosis of Malingering (or Malin-
gered Neuropsychological Dysfunction; Slick et al., 1999)
References and Readings
may be warranted. Following are different examples of
Binder, L. M. (1993). Assessment of malingering after mild head trauma
evidence that can be supportive of a diagnosis of with the Portland Digit Recognition Test. Journal of Clinical and
Malingering: Experimental Neuropsychology, 15, 170–182.
Binder, L. M., Storzbach, D., Anger, W. K., Campbell, K. A., & Rohlman,
(a) On psychometric testing, an individual obtains an D. S. (1999). Subjective cognitive complaints, affective distress, and
accuracy score on a forced-choice recognition memory objective cognitive performance in Persian Gulf War Veterans.
test that falls significantly below a chance level. Such a Archives of Clinical Neuropsychology, 14, 531–536.
score provides empirical evidence that the individual Bush, S. S., Ruff, R. M., Troster, A. I., Barth, J. T., Koffler, S. P., & Pliskin,
N. H. (2005). Symptom validity assessment: Practice issues and
correctly remembered the right answers above a
medical necessity. Archives of Clinical Neuropsychology, 20, 419–426.
chance level and used this knowledge to frequently Delis, D. C., & Jacobson, M. (2000). Neuropsychological testing. Encyclo-
select the wrong answer (Larrabee, 2003; Millis, 1992). pedia of Psychology. New York: American Psychological Association/
(b) A person who is involved in two separate personal- Oxford University Press.
injury lawsuits for different accidents complains of Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. (2000). The
California verbal learning test (2nd ed.). San Antonio: The Psycho-
one set of symptoms and injuries to doctors asso-
logical Corporation.
ciated with one lawsuit and different symptoms and Delis, D. C., & Wetter, S. R. (2007). Cogniform disorder and cogniform
injuries to other doctors associated with the second condition: Proposed diagnoses for excessive cognitive symptoms.
lawsuit. Such selective reporting of symptoms that Archives of Clinical Neuropsychology, 22, 589–604.
correspond to the different lawsuits suggests a con- Frederick, R. I. (1997). Validity indicator profile. Minnetonka: NCS
Assessments.
scious component to the symptom amplification.
Gervais, R. O., Russell, A. S., Green, P., Allen, L. M., Ferrari, R., & Pieschl,
(c) An individual ‘‘confesses’’ to intentionally per- S. D. (2001). Effort testing in patients with fibromyalgia and disabil-
forming poorly when taking cognitive tests. ity incentives. Journal of Rheumatology, 28, 1892–1899.
614 C Cognistat

Green, P., Rohling, M. L., Lees-Haley, P. R., & Allen, L. M. (2001). Effort for Level of Consciousness is also provided. The various
has a greater effect on test scores than severe brain injury in com-
subscales are modeled after more extensive and well-vali-
pensation claimants. Brain Injury, 15, 1045–1060.
Hom, J., & Denney, R. L. (2002). Detection of response bias in forensic
dated neuropsychological tests but in an abbreviated from.
neuropsychology. Journal of Forensic Neuropsychology, 2, 1–166. For example, Attention is assessed using digit repetition
Iverson, G. L., & Binder, L. M. (2000). Detecting exaggeration and similar to that used on the Wechsler scales. Unlike other
malingering in neuropsychological assessment. The Journal of Head screening procedures that yield a single summary score,
Trauma Rehabilitation, 15, 829–858.
Cognistat is designed to yield a score for each domain and
Iverson, G. L., & Franzen, M. D. (1996). Using multiple objective memory
procedures to detect stimulated malingering. Journal of Clinical and
thus produce a differentiated profile of cognitive abilities.
Experimental Neuropsychology, 18, 38–51. Cognistat also employs an adaptive testing approach (re-
Larrabee, G. J. (2003). Detection of malingering using atypical perfor- ferred to as a screen and metric approach) to decrease the
mance patterns on standard neuropsychological tests. The Clinical time spent in administration. In this approach, an item that
Neuropsychologist, 17, 410–425.
is of average difficulty is first administered for each subtest.
Larrabee, G. J. (2005). Assessment of malingering. In G. L. Larrabee (Ed.),
Forensic Neuropsychology. New York: Oxford University Press.
If that item is passed, no other items are administered from
Millis, S. R. (1992). The recognition memory test in the detection of that subtest, but if it is failed, additional easier items are
malingered and exaggerated memory deficits. The Clinical Neurop- administered. The raw scores for each subscale are then
sychologist, 6, 406–414. plotted on a standard profile form, and performance is
Millis, S. R., Putnam, S. H., Adams, K. M., & Ricker, J. H. (1995). The
classified as being in the average range or as indicative of
California verbal learning test in the detection of incomplete effort.
Psychological Assessment, 7, 463–471.
mild, moderate, or severe impairment.
Mittenberg, W., Patton, C., Canyock, E. M., & Condit, D. C. (2002). Base
rates of malingering and symptom exaggeration. Journal of Clinical
and Experimental Neuropsychology, 24, 1094–1102.
Slick, D. J., Sherman, E. M. S., & Iverson, G. L. (1999). Diagnostic criteria
Current Knowledge
for malingered neurocognitive dysfunction: Proposed standards for
clinical practice and research. The Clinical Neuropsychologist, 13, Because extensive validity and normative information
545–561. were not available when Cognistat was originally pub-
Sweet, J. J. (1999). Malingering: Differential diagnosis. In J. J. Sweet (Ed.),
lished, a number of studies have subsequently examined
Forensic Neuropsychology. Lisse: Swets and Zeitlinger.
Tombaugh, T. N. (1996). Test of memory malingering. New York: Multi
its sensitivity to brain damage as well as the influence
Health Systems. of demographic variables on test performance. Research
revealed that the Cognistat may be more sensitive to brain
damage than the Mini Mental State Exam, Cognitive Ca-
pacity Screening Examination, and Mattis Dementia Rating
Cognistat Scale (e.g., Drane et al., 2003). Cognistat has also been
found to be sensitive to a variety of neurological and
DANIEL N. A LLEN
psychiatric disorders, and to age-related changes
University of Nevada Las Vegas
in cognitive abilities (for brief review see Doninger,
Las Vegas, NV, USA
Ehde, Bode, Knight, Bombardier, & Heinemann, 2006).
Correlations between its various subtests and neuropsycho-
logical measures of similar abilities provide evidence for its
Synonyms construct validity (Nabors, Millis, & Rosenthal, 1997).
The Cognistat battery also has limitations. For exam-
Neurobehavioral cognitive status examination (NCSE)
ple, performance is influenced by demographic variables,
including age and education. Although the original valida-
Description tion study of the Cognistat demonstrated no differences in
performance between age groups (Kiernan, Mueller,
The Cognistat test battery (Kiernan, Mueller, & Langston, Langston, & Van Dyke, 1987), subsequent investigations
1995), formerly called the Neurobehavioral Cognitive found that increased age is associated with poorer perfor-
Status Examination, is a screening tool designed to as- mance on the Construction, Memory, Similarities, Atten-
sess a number of different cognitive domains including tion, and Calculation domains, with Construction and
Orientation, Attention, Language Abilities (Comprehen- Memory appearing to be the most consistently impacted
sion, Repetition, Naming), Construction, Memory, Calcu- by age (Drane & Osato, 1997). Additionally, years of
lations, and Reasoning (Similarities, Judgment). A rating education and low levels of educational attainment are
 Cognitive Affective Syndrome C 615

associated with diminished performance (Macauly et al.,

2003; Ruchinskas et al., 2001). With only limited norma- Cognition
tive data available to correct for these influences (Drane
et al., 2003), interpretation of performance in the elderly ▶ Cognitive Functioning
and those with limited education must be tentative. C
Finally, a recent study of community dwelling and hospi-
talized individuals with traumatic brain injury suggests Cognitive Affective Syndrome
that the Cognistat should not be used to profile neuro-
cognitive strengths and weaknesses because measurement R OBERT R IDER
error accounted for the majority of variance in subtest Drexel University
scores (Doninger et al., 2006). Thus, the Cognistat pro- Philadelphia, PA, USA
vides a useful method to screen patients with a variety of
neurological and psychiatric disorders for neurocognitive
impairment, although additional research appears war- Synonyms
ranted before that it can be used to make inferences
regarding impairment of discrete cognitive abilities, and Cerebellar cognitive affective syndrome
more extensive normative data is needed.

Definition
Cross References
First described by Schmahmann and Sherman (1997),
▶ Mattis Dementia Rating Scale (DRS)
cerebellar cognitive affective syndrome (CAS) refers to
▶ Mini Mental State Exam (MMSE)
a cluster of impairments involving higher-order cognitive
processes and affective functioning. Symptoms tend to
References and Readings cluster in executive dysfunction, including problems
with planning, set shifting, verbal fluency, abstract
Doninger, N. A., Ehde, D. M., Bode, R. K., Knight, K., Bombardier, C. H., & reasoning, perseveration, attentional dysregulation, hy-
Heinemann, A. W. (2006). Measurement properties of the neurobe- peractivity, impulsivity and disinhibition, and deficits in
havioral cognitive status examination (Cognistat) in traumatic brain working memory. However, symptoms may also include
injury rehabilitation. Rehabilitation Psychology, 51(4), 281–288.
Drane, D. L., & Osato, S. S. (1997). Using the neurobehavioral cognitive
visuospatial disorders, expressive language disorders,
status examination as a screening measure for older adults. Archive of affective abnormalities, difficulties with visuospatial orga-
Clinical Neuropsychology, 12(2), 139–143. nization, visual memory, logical sequencing, and blunted
Drane, D. L., Yuspeh, R. L., Huthwaite, J. S., Klingler, L. K., Foster, L. M., or inappropriate affect (Schmahmann & Sherman, 1997).
Mrazik, M., & Axelrod, B. N. (2003). Healthy older adult perfor-
mance on modified version of the Cognistat (NCSE): Demographic
issues and preliminary normative data. Journal of Clinical and Current Knowledge
Experimental Neuropsychology, 25(1), 133–144.
Kiernan, R. J., Mueller, J., & Langston, J. W. (1995). Cognistat (Neurobe- Causes and Correlates of CAS
havioral Cognitive Status Examination). Lutz, FL: Psychological
Assessment Resources.
Kiernan, R. J., Mueller, J., Langston, J. W., & Van Dyke, C. (1987). The The co-occurrence of these cognitive and affective symp-
Neurobehavioral Cognitive Status Examination: A brief but quanti- toms arises from the disruption of neuroanatomical cir-
tative approach to cognitive assessment. Annals of Internal Medicine, cuits connecting the cerebellum with frontal, parietal,
107(4), 481–485. temporal, and limbic cortices. Damage to these connec-
Macaulay, C., Battista, M., Lebby, P. C., & Mueller, J. (2003). Geriatric
performance on the Neurobehavioral Cognitive Status Examination
tions can occur in association with cerebellar infarct
(Cognistat) what is normal? Archives of Clinical Neuropsychology, 18, (Schmahmann and Sherman, 1997), cerebellar atrophy
463–471. associated with severe alcoholism (Fitzpatrick, et al.,
Nabors, N. A., Millis, S. R., & Rosenthal, M. (1997). Use of the Neuro- 2008), cerebellar tumor or tumor resection (Levihson,
behavioral Cognitive Status Examination (Cognistat) in traumatic
et al., 2000; Konczak, 2005), trauma, neurodegenerative
brain injury. Journal of Head Trauma Rehabilitation, 12(3), 79–84.
Schrimsher, G. W., Parker, J. D., & Burke, R. S. (2007). Relation between
disorders, or cerebellitis. Affective symptoms have been
cognitive testing performance and pattern of substance use in males associated with damage to the cerebellar vermis (Levihson,
at treatment entry. Clinical Neuropsychologist, 21(3), 498–510. et al., 1997). Lesions of the anterior lobe of the cerebellum
616 C Cognitive Archives

tend to produce only minor changes in executive and The Planning scale consists of: matching numbers,
visual–spatial functions. Children with a cognitive affective planned codes, and planned connections.
syndrome can also have autistic characteristics, and diag-
1. Matching numbers – The individual is asked to
nosis of autism can be confounded by cerebellar lesions.
locate and underline a pair of matching numbers.
The task begins with 1 digit and progressively moves
References and Readings into 7 digit numbers.
2. Planned codes – A client is requested to complete a
Schmahmann, J., & Sherman, J. (1998). The cerebellar cognitive affective series of boxes according to a corresponding code
syndrome. Brain, 121, 561–579. provided at the beginning of each item.
Schmahmann, J., Weilburg, J. D., Sherman, J. B., & Janet, C. (2007). The
3. Planned connections – This subtest is similar to
neuropsychiatry of the cerebellum - insights from the clinic. Cere-
bellum, 6(3), 254–267.
the original trail making task. In this subtest, both
numerical and alphabetical sequences are employed.
The Attention scale encompasses: number detection,
expressive attention, and receptive attention.
Cognitive Archives 1. Number detection – This subtest consists of rows of
numbers with both target and distracter stimuli.
▶ Cognitive Correctors
At the top of each item page, a key is printed with
the target numbers. Children are instructed to under-
line only the target specified.
Cognitive Assessment System 2. Expressive attention – Children aged 5–7 are to
identify the size of an assortment of animals, in spite
L EESA V. H UANG of the size depicted on the page. For children aged
California State University 8–17, this subtest is similar to the Stroop Test.
Chico, CA, USA Color words are presented in a different colors of ink
(e.g., the word ‘‘red’’ might be in blue ink) and the
children are requested to name the color of the ink.
Synonyms 3. Receptive attention – First, a series of pictures or words
are presented in which the client must identify and
CAS underline identical stimuli. Second, children are
requested to recognize and identify two items that
Description share a common characteristic. This subtest is omitted
for the Basic Battery.
The Das–Naglieri Cognitive Assessment System (CAS;
The Simultaneous Processing scale includes: nonverbal
Naglieri & Das, 1997a, 1997b) is a cognitive assessment
matrices, verbal–spatial relations, and figure memory.
to assess children aged 5 years, 0 months to 17 years,
11 months. Individual administration time is approximate- 1. Nonverbal matrices – A variety of pictures with
ly 1 h. The CAS is arranged in three separate, yet interrelat- geometrical shapes or patterns are shown to the
ed levels of scores: individual subtests, PASS (Planning, student. The student needs to select one option that is
Attention, Simultaneous, and Successive) composite scales, consistent with the presented relationship or pattern.
and a Full Scale quotient. Twelve subtests comprise the CAS 2. Verbal spatial relations – The individual receives
and each subtest generates a scaled score (M = 10; SD = 3). auditory information and determines which picture
The Standard Battery utilizes 12 subtests with three subt- best represents the verbal description given. Presented
ests per PASS process, while the Basic Battery includes in a multiple-choice format, the series of pictures
eight subtests, two subtests for each PASS process. Each of allows the student to demonstrate understanding of
the four PASS composite scores (M = 100; SD = 15) is a logical, grammatical, and spatial information.
combination of the subtests included in each respective 3. Figure memory – A client is required to trace geometric
process. Finally, the Full Scale Score (M = 100; SD = 15) is design previously observed, which is embedded within
the aggregate total of the four PASS cognitive processes a larger and more intricate geometrical design. This is
scales, which are equally weighed. omitted from the Basic Battery.
 Cognitive Assessment System C 617

The Successive Processing scale consists of: word series, position to a collective whole (Naglieri, 2005). Successive
sentence repetition, sentence questions, and speech rate. Processing is described as the unidirectional, consecutive
organization of stimuli (Naglieri & Das, 2005).
1. Word series – Individuals are instructed to repeat a
series of commonly used words in the same consecutive
order given. The difficulty level increases as the word C
list starts with two words and ends with nine words.
Psychometric Data
2. Sentence repetition – This subtest demands that
The standardization sample of 2,200 children is represen-
individuals repeat sentences that gradually become
tative of the US population on nine criteria (Naglieri &
longer. The sentences in this subtest utilized color
Das, 1997b). The internal consistency of the CAS subtests
words to reduce the contextual meaning and possible
range from 0.75 to 0.89, with a median reliability of 0.82.
interference with simultaneous processing. The score
The Standard Battery had average reliabilities of 0.88
is based on the total number of correctly repeated
(Planning), 0.88 (Attention), 0.93 (Simultaneous), and
items.
0.93 (Successive). The reliability coefficient range for the
3. Speech rate – This subtest is administered only to
Full Scale score was 0.95–0.97.
children aged 5–7. Children are verbally presented
The theoretical premise of the CAS was constructed
with a series of three word combinations and are
on a four-factor model; however, factor analyses
requested to repeat each combination as quickly and
generated empirical support for both three- and four-
as many times as possible within 30 s.
factor models depending upon the age category. Further
4. Sentence questions – Administered to children aged 8–17
research has provided support for the CAS as a measure of
instead of speech rate. In an extension of the sentence
g. Weak correlations were found between the CAS
repetition task, this subtest requires that children re-
Standard Battery Full Scale and PASS scales (ranging
spond to a question about a nonsensical sentence.
from 0.37 to 0.67) with the Wechsler Intelligence Scale
for Children-third edition (WISC-III; Wechsler, 1991).
Historical Background Predictive validity was moderately established with cluster
and subtest scores from the Woodcock–Johnson Psycho-
The CAS is one of few cognitive processing instruments Educational Battery-Revised Tests of Achievement
which incorporate a neuropsychological foundation. The (Woodcock & Johnson, 1989).
theoretical basis of the CAS is an extension of Alexander S.
Luria’s work relating to the brain’s three functional units
Clinical Uses
(Naglieri, 1999, 2005). It was modified and refined by Das,
Naglieri, and Kirby into four processing components:
The purpose of the CAS is to provide an analysis of an
Planning, Attention, Simultaneous, and Successive Pro-
individual’s cognitive abilities through the measurement
cessing, otherwise known as PASS, to explain differences
of the PASS processes (Naglieri, 2005). The authors
in cognitive processing of children (Das & Naglieri, 2001).
suggested that the CAS is a valuable alternative tool
The Planning subtests require individuals to engage in
to the traditional Wechsler or Stanford–Binet scales,
a problem-solving sequence to complete novel tasks
when assessing individuals who may have attention-
(Naglieri, 1999). The development, selection, application,
deficit/hyperactivity disorders (ADHD), LD, mental
and evaluation of strategies are crucial to the success of
retardation, traumatic brain injury, serious emotional
performance (Naglieri & Das, 1997b). Subtests in the
disturbance, giftedness, and planning problems (Naglieri
Attention scale require a combination of three com-
& Das, 1997b). Furthermore, possessing an under-
ponents: focused, selective, and sustained attention
standing of an individual’s PASS profile will provide
(Naglieri, 2005). Focused attention involves the act of
essential information for the selection and evaluation of
attending to presented stimuli in the environment.
instructional recommendations (Das & Naglieri, 2001;
Selective attention is the concentration of attention to
Naglieri & Das, 1997b).
chosen stimuli while disregarding nonessential or com-
peting stimuli. Sustained attention is the differential
effort (over time, especially) an individual applies to- References and Readings
ward task completion. Simultaneous Processing subtests
require the ability of an individual to incorporate and Das, J. P., & Naglieri, J. A. (2001). The Das-Naglieri cognitive assessment
comprehend unconnected entities and its relation/ system in theory and practice. In J. J. W. Andrews, D. H. Saklofske, &
618 C Cognitive Assessors

H. L. Janzen (Eds.), Handbook of psychoeducational assessment: Definition

Ability, achievement, and behavior in children (pp. 33–63).
San Diego, CA: Academic Press.
Naglieri, J. A. (1999). Essentials of CAS assessment. New York: Wiley.
Cognitive Behavioral Couples Therapy (CBCT) has
Naglieri, J. A. (2005). The cognitive assessment system. In D. P. Flanagan become one of the most well researched approaches for
& P. L. Harrison (Eds.), Contemporary intellectual assessment: the treatment of marital and couple distress, with growing
Theories, tests, and issues (2nd ed., pp. 441–460). New York: The empirical support for it effectiveness. Theoretically
Guilford Press.
grounded in both social learning and social exchange
Naglieri, J. A., & Das, J. P. (1997a). Cognitive assessment system:
Administration and scoring manual. Itasca, IL: Riverside Publishing.
theories, the premise of CBCT is that an individual’s
Naglieri, J. A., & Das, J. P. (1997b). Cognitive assessment system: behavior both influences and is influenced by his/her
Interpretive handbook. Itasca, IL: Riverside Publishing. environment. When applied to a marriage or other long-
Naglieri, J. A., & Das, J. P. (2005). Planning, attention, simultaneous, and term relationship, this premise suggests that one partner’s
successive (PASS) theory: A revision of the concept of intelligence.
behavior influences and is influenced by the actions of the
In D. P. Flanagan & P. L. Harrison (Eds.), Contemporary intellectual
assessment: Theories, tests, and issues (2nd ed., pp. 120–135).
other. CBCT typically focuses on two aspects of this
New York: The Guilford Press. process: (a) exchanges of positive and negative behaviors;
Wechsler, D. (1991). Wechsler intelligence scale for children-third edition. (b) communication skills that influence the interaction
San Antonio, TX: Psychological Corporation. process (Epstein, Baucom, & Daiuto, 1997).
Woodcock, R. W., & Johnson, M. B. (1989). Woodcock–Johnson psycho-
educational battery-revised, tests of achievement. Itasca, IL: Riverside.
Current Knowledge
Couples and Health
Cognitive Assessors
A patient’s ongoing, long-term relationship can influence
▶ Cognitive Correctors a range of psychosocial variables related to health
behaviors. The health-enhancing properties of intimate
and long-term relationships have been repeatedly
documented (Kiecolt-Glaser & Newton, 2001; Wilson,
Cognitive Assistive Technology 2001). Various mechanisms of action for this relationship
have been proposed, including selection and protection
▶ Prosthetic Memory Aids (Kiecolt-Glaser & Newton, 2001). That is, healthier people
are more likely to be in and stay in intimate relationships,
and they tend to have more resources and take care of
themselves better than their counterparts without such
Cognitive Awareness relationships. Additional research has investigated other
mechanisms for the protective benefits of long-term
▶ Metacognition relationships, including partner attitudes or behaviors, and
caretaking (Keefe et al., 1996; Wilson, 2001).

Treatment Procedures
Cognitive Behavioral Couples
Therapy A CBCT approach to treatment with both relationship
distressed and health impaired couples focuses on three
TAMARA G OLDMAN S HER factors: behavioral factors, affective/emotional factors,
Illinois Institute of Technology and cognitive factors. The behavioral component
Chicago, IL, USA includes increasing positive behaviors such as spending
more time together and decreasing negative behaviors
such as criticizing or nagging. In addition, because com-
Synonyms munication problems are the most commonly reported
presenting complaint of distressed couples, the behavior-
Behavioral marital therapy; CBCT; Cognitive behavioral al aspects of the treatment also typically involve a skills-
marital therapy; Couples therapy; Marital therapy oriented approach to communication change where the
 Cognitive Behavioral Therapy C 619

value and skills of working together to solve a problem References and Readings
are the foci.
Affect is a focus of therapy insomuch as it is an Baucom, D. H., Shoham, V., Mueser, K. T., Daiuto, A. D., & Stickle, T.
indicator of significant relationship distress and for its (1998). Empirically supported couple and family interventions
for marital distress and adult mental health problems. Journal of
ability to direct the therapist in exploring links between C
Consulting and Clinical Psychology, 66, 53–88.
the emotions of the partners and their behaviors. Affect Epstein, N. B., & Baucom, D. H. (2002). Enhanced cognitive-behavioral
can be approached with a skills approach in helping therapy for couples. Washington, DC: American Psychological
partners learn to express their own and listen to the Association.
other person’s emotions and by linking specific emotions Epstein, N. H., Baucom, D. H., & Daiuto, A. (1997). Cognitive-behavioral
couples therapy. In W. K. Halford, & H. J. Markman (Eds.), Clinical
to specific relationship issues.
handbook of marriage and couples intervention (pp. 415–449). West
The third factor in CBCT is cognition. As Epstein et al. Sussex, England: Wiley.
(1997) note, ‘‘the importance of cognitive factors in Halford, W. K., & Markman, H. J. (Eds.). (1997). Clinical handbook of
relationship functioning lies in the fact that objectively marriage and couples intervention. New York: Wiley.
observable behavioral events are often subjectively experi- Keefe, F. J., Caldwell, D. S., Baucom, D. H., Salley, A., Robinson, E.,
Timmons, K., et al. (1996). Spouse-assisted coping skills training
enced quite differently by the partners’’. The therapist
in the management of osteoarthritic knee pain. Arthritis Care and
works to uncover underling cognitive factors shaping the Research, 9(4), 279–291.
behavior and affect of the partners in order to increase Kiecolt-Glaser, J. K., & Newton, T. L. (2001). Marriage and health: His
understanding and promote behavioral change. and hers. Psychological Bulletin, 127(4), 472–503.
Schmaling, K., & Sher, T. G. (2000). The psychology of couples and illness:
Theory, research, and practice. Washington, D.C.: American Psycho-
logical Association.
Efficacy Information Shadish, W. R., & Baldwin, S. A. (2003). Meta-analysis of MFT inter-
ventions. Journal of marital and family therapy, 29, 547–570.
CBCT, and its predecessor, Behavioral Marital Therapy Shadish, W. R., & Baldwin, S. A. (2005). Effects of Behavioral Marital
(BMT) have been one of the most researched forms of Therapy: A Meta-analysis of randomized controlled trials. Journal of
couples therapy (Shadish & Baldwin, 2003, 2005). Results Consulting and Clinical Psychology, 73(1), 6–14.
Wilson, S. E. (2001). Socioeconomic status and the prevalence of health
of efficacy trials repeatedly demonstrate that those who
problems among married couples in later midlife. American Journal
receive either CBCT or BMT report less distress than those of Public Health, 91(1), 131–135.
who receive no treatment and that this finding remains
not only for couples presenting with general marital
distress, but also for depression, agoraphobia, and alcohol
abuse (Baucom, Shoham, Mueser, Daiuto, & Stickle,
1998). Based upon recent meta-analyses of studies using Cognitive Behavioral Marital
CBCT, Shadish and Baldwin (2003, 2005) reported an Therapy
overall mean effect size ranging from 0.59 to 0.84 for
couples therapy generally, with no differential effective- ▶ Cognitive Behavioral Couples Therapy
ness across theoretical orientation found.

Qualifications of Providers
Cognitive Behavioral Therapy
CBCT can be conducted by a variety of treatment
providers, specifically trained in its use with various TARYN M. S TEJSKAL
populations. This includes neuropsychologists, clinical Virginia Commonwealth University Medical Center
psychologists, marriage and family therapists, counselors, Richmond, VA, USA
social workers, and clergy.

Definition
Cross References
Cognitive behavioral therapy (CBT) is a theoretical
▶ Behaviorism framework based on the premise that a person’s
▶ Cognitive Behavior Therapy cognitions influence their emotions and behavior. CBT
620 C Cognitive Behavioral Therapy

provides considerable utility in addressing a variety of alleviation. To reduce the emotional experience of frustra-
common emotional consequences of neurological disor- tion, a neuropsychologist working with a brain-injured
ders including anxiety and depression, as well as behavior patient would encourage the patient to appreciate the
modification for brain injury survivors. gains made since the injury. In order to avoid unrealistic
expectations for post injury functioning that could create
frustration; the patient would be cautioned against com-
Historical Background paring present capabilities to preinjury functioning.

CBT grew out of Albert Ellis’s (Ellis, 1975) work on

Rational Emotive Behavioral Therapy (REBT) and Treatment Participants
examination of irrational beliefs in the 1950s. Ellis
concluded that irrational beliefs (e.g., I am powerless to CBT is broadly applicable to a variety of clinical neuro-
solve my problems; I am unlovable) were associated with logical diagnoses including anxiety, depression, obsessive
the development of mood disorders. Beck, Rush, Shaw, compulsive disorder (OCD), and posttraumatic stress
and Emery (1979) developed Cognitive Therapy on the disorder (PTSD). CBT can be used with individuals,
premise that cognitive errors (e.g., over-generalizing, couples, and families. Further, CBT can be used with
magnification, personalization) were associated with the patients at developmental levels from young children to
development of depression and anxiety. Further, they older adults. CBT therapists act more as coaches colla-
viewed depression as accompanied by of a triad of borating with patients alter processes of thinking, feeling,
negative cognitions consisting of a negative view of self, and action as opposed to an analyst making expert
the world, and the future. interpretations.
Arnold Lazarus (1971) was the first to introduce the
term ‘‘behavior therapy’’ into the professional literature.
Further expanding the lens of CBT, Lazarus and Folkman Treatment Procedures
(1984) developed the stress, appraisal, and coping
model (1984) that acknowledges the importance of how CBT encompasses a variety of clinical interventions for
an individual views the environment (primary appraisal) individuals with a neurological disorder as well as couples
and their available coping resources (secondary apprais- and families in which a member has a neurological
al). Finally, attribution theory, proposed by Fritz Heider diagnosis or injury. Within all CBT interventions,
(1958) posits that people can interpret events as caused by behaviors, cognitions, and emotions are integrally related;
internal (i.e., factors within the person such as a person’s though interventions may focus on behavior or cognition,
own intelligence and behavior) or external factors (i.e., these distinctions are often made for heuristic purposes
factors external to the person such as the weather or luck). (Epstein & Baucom, 2002). Further, CBT posits that
When internal attributions are made, people are said to change in one domain will produce changes in others
have an internal locus of control, or hold cognitions that domains. In the past, behavior-oriented therapies have
support their sense of efficacy in affecting what happens been ripe with skills training in areas such as problem-
to them. When external attributions are paramount, peo- solving, communication, and relaxation with the idea
ple are said to have an external locus of control, that being that maladaptive patterns arise around areas of
is, they believe that they exert less control over their skill deficits. Though CBT therapists also deliver a
environment. judicious amount of skills-based training, therapy moves
beyond behavior modification to the meaning and inter-
pretations made as a result of interactions and experience.
Goals and Objectives

Neuropsychologists using CBT as a conceptual framework Behavior-Focused Interventions

work toward modifying maladaptive cognitions such as
negative attributions, unattainable expectations and Patients with neurological diagnoses have a host of behav-
standards, and faulty belief systems. Through the modifi- ior patterns amenable to CBT intervention. One such
cation of these problematic (i.e., schemas), CBT seeks to pattern, negative reciprocity, is the idea that negative
alter people’s emotional and behavioral responses in behavior increases the propensity that a person will
service of symptom management, reduction, and respond to expressed negative behavior with more
 Cognitive Behavioral Therapy C 621

negative behavior (Epstein & Baucom, 2002). For exam- encouraging healthy compartmentalization of emotion
ple, family members may respond angrily toward a pa- (Epstein & Baucom, 2002). In cases of neurological diag-
tient who acts aggressively after a brain injury. Over time nosis or injury, emotions may either be exacerbated or
negative reciprocity pervades relationships, invading minimized. To enhance the expression of emotions, thera-
cognitions and emotions such that family members pists may ask probing questions to bring awareness to C
make global negative attributions about another person’s emotional experience such as: What happens to you
intentions and behavior (Epstein & Baucom, 2002). when. . .What is it like for you when. . .How do you feel
An important aspect of CBT is skills-based training; as you listen to your son expressing his experience. . .
meant to enhance positive behavior and decrease negative (Epstein & Baucom, 2002). In this way, individuals and
behavior. In an instance where a person receives a diagnosis family members can be encouraged to share their emo-
of schizophrenia, a CBT clinician may intervene with a tional experience in the context of a safer therapeutic
family to teach communication skills. Empirical literature environment.
has discussed the detrimental impact of expressed emotion
(EE) in families with a schizophrenic family member.
Further, the family members may be overwhelmed and Efficacy Information
have many questions, concerns, and emotions they need
to express surrounding the diagnosis. Communication CBT has been empirically validated for the treatment of
skills training teaches families how to communicate more many disorders including anxiety (Barlow, O’Brien, &
productively with one another about complex issues and Last, 1984), sexual dysfunction (Baucom, Shoham,
reduce detrimental patterns of interaction such as EE. Mueser, Daiuto, & Stickle, 1998), depression (Beach,
Sadeen, & O’Leary, 1990), bipolar disorder, schizophre-
nia, and bulimia nervosa (Baucom et al., 1998). CBT is
Cognition-Focused Interventions often used in conjunction with medication for a variety of
mental health concerns. In addition, CBT effectively
The manner in which a person cognitively ascribes mean- enhances coping skills for adults with chronic illness
ing to behavior is an important factor in CBT. Therapy (Rybarczyk, DeMarco, DeLaCruz, Lapidos, & Fortner,
often focuses on reassessing and amending these 2001) and caregivers (Gallagher-Thompson, Lovett,
cognitions. Areas of inquiry often include attributions, Rose, McKibbin, Coon, et al., 2000).
expectancies, assumptions, standards, and beliefs. In Recently, advances in computer software have given
order to evaluate and modify existing cognitions, clinicians rise to computerized versions of CBT. Though computer-
intervene using guided discovery during which clients are ized cognitive behavioral therapy (CCBT) is not meant t o
asked to identify and evaluate their cognitions (Epstein & replace face-to-face therapy, it does provide an additional
Baucom, 2002). When a patient is depressed about a treatment option. CCBT allows clients to participate in
neurological diagnosis or injury, clinicians may intervene therapy when there is a paucity of available therapists,
at the cognitive level challenging catastrophic thinking the associated costs are prohibitive, or the prospect of
(e.g., I will never get better). A therapist may focus speaking to someone face-to-face seems off-putting. In
decreasing negative self talk (e.g., I am worthless the way 2006, the United Kingdom’s National Institute of Health
I am now) by encouraging the patient to keep a journal of and Clinical Excellence (NICE) provided guidelines
thoughts occurred and the impact of the thoughts on the recommending CCBT as a result of randomized
patient’s mood (Epstein & Baucom, 2002). controlled trials for mild to moderate depression and
anxiety (NICE, 2006).

Emotion-Focused Interventions
Outcome Measurement
Interventions within the realm of emotions may range
from expanding minimized emotional experience to con- Many clinicians used standardized instruments to assess
taining heightened emotional experience. Clinicians may the presence and severity of a variety of neuropsychologi-
draw on a variety of strategies to access, heighten, or limit cal diagnoses. With regard to depression, clinicians may
emotional experience including normalizing emotional use self-report inventories such as the Beck Depression
responses, metaphor, acceptance of emotional expression, Inventory (BDI II; Beck, Steer, & Brown, 1996) Finally, the
enhancing tolerance for distressing emotions, and Beck Anxiety Inventory (BAI: Kabacoff, Segal, Hersen, &
622 C Cognitive Behaviorism

Van Hasselt, 1997) has shown considerable utility in Inventory and the State-Trait Anxiety Inventory with older adult
psychiatric outpatients. Journal of Anxiety Disorders, 11(1), 33–47.
diagnosing anxiety and identifying the severity of the
Lazarus, A. A. (1971). Behavior therapy and beyond. New York: McGraw-
anxiety symptoms. Hill.
Lazarus R. S., & Folkman, S. (1984). Stress, appraisal and coping.
New York: Springer.
Qualifications of Treatment Providers Leahy, R. L. (Ed.) (1997). Practicing cognitive therapy: A guide to inter-
ventions. Northvale, NJ: Jason Aronson.
National Institute of Health and Clinical Intervention (NICE). (2006).
CBT can be used by a variety of treatment providers such Depression and anxiety computerized cognitive behavioral therapy
as neuropsychologists, clinical psychologists, marriage (CCBT). Retrieved on July 17, 2007 at http://guidance.nice.org.uk/
and family therapists (MFTs), counselors, and social TA97
workers. Treatment providers using CBT should have O’Farrell, T. J., Choquette, K. A., Cutter, H. S. G., Brown, E. D., &
appropriate clinical training in the model. Further, McCourt, W. F. (1993). Behavioral marital therapy with and without
additional couples relapse prevention sessions for alcoholics and
clinical providers learning to use CBTas a conceptual frame- their wives. Journal of Studies on Alcohol, 54, 652–666.
work to guide therapy should seek supervision from an Rybarczyk, B., DeMarco, G., DeLaCruz, M., Lapidos, S., & Fortner, B.
experienced individual trained in the model of CBT. (2001). A classroom mind-body wellness intervention for older
adults with chronic illness: Comparing immediate and one year
benefits. Behavioral Medicine, 27, 15–27.
Cross References

▶ Behaviorism
▶ Behavior Modification Cognitive Behaviorism
▶ Psychotherapy
▶ Behaviorism

References and Readings

Barlow, D. H., O’Brien, G. T., & Last, C. G. (1984). Couples treatment of Cognitive Control
agoraphobia. Behavior Therapy, 15, 41–58.
Baucom, D. H., Shoham, V., Mueser, K. T., Daiuto, A. D., & Stickle, T. R.
(1998). Empirically supported couples and family therapies for
▶ Controlled Attention
adult problems. Journal of Consulting and Clinical Psychology, 66,
53–88.
Beach, S. R. H., Sadeen, E. E., & O’Leary, K. D. (1990). Depression in
marriage: A model for etiology and treatment. New York: Guilford
Press.
Cognitive Correctors
Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979). Cognitive therapy
of depression. New York: Guilford. R ICK PARENTE
Beck, A. T., Steer, R. A., & Brown, G. K. (1996). Manual for the Beck Towson University
Depression Inventory-II. San Antonio, TX: Psychological
Towson, MD, USA
Corporation.
Beck, J. S. (1995). Cognitive therapy: Basics and beyond. New York:
Guilford.
Dattilio, F. M., & Freeman, A. (Eds.). (2003). Cognitive-behavioral strate- Synonyms
gies in crisis intervention (3rd ed.). New York: Guilford.
Ellis, A. (1975). A new guide to rational living. Englewood Cliffs: Prentice
Behavioral memory aids; Behavioral prothestics; Cogni-
Hall.
Epstein, N. B., & Baucom, D. H. (2002). Enhanced cognitive-behavioral
tive archives; Cognitive assessors; Cognitive monitors;
therapy for couples. Washington: American Psychological Association. Cognitive orthotics; Cognitive robots; Cognitive trainers;
Gallagher-Thompson, D., Lovett, S., Rose, J., McKibbin, C., Coon, D., External aids; Prosthetic devices
Futterman, A., & Thompson, L.W. (2000). Impact of psycho-
educational interventions on distressed family caregivers. Journal of
Clinical Geropsychology, 6, 91–110.
Definition
Heider, F. (1958). The psychology of interpersonal relations. New York:
Wiley.
Kabacoff, R. I., Segal, D. L., Hersen, M., & Van Hasselt, V. B. (1997). A device, external to the mind, that enhances or replaces
Psychometric properties and diagnostic utility of the Beck Anxiety a memory or cognitive function.
 Cognitive Functioning C 623

Current Knowledge Cognitive trainers and archives teach a skill and/or

store large searchable databases. For example: academic
Parente and Herrmann (2010) defined several different remediation software teaches basic academic skills; cogni-
external aids that take over a deficient cognitive or memory tive remediation software provides drill and practice exer-
function. Table 1 surveys the various types of cognitive cises that improve cognitive skills; skills training software C
correction devices. teaches skills like typing or the use of specific software
Cognitive prosthetics refer to a general class of devices packages (e.g., Microsoft Office). Cognitive archives (e.g.,
that take over some memory process. Examples of partic- electronic encyclopedias) store large amounts of informa-
ularly useful prosthetics include: color coding, which cre- tion and provide a search engine for finding specific topics.
ates simplistic visual organization; checklists, which
improve consistency and sequential ordering; medication
organizers, – which organize medications and remind a References and Readings
person which ones to take on each day; notepads and post-
it notes, –which are useful for quickly writing a message or Parente, R., & Herrmann, D. (2010). Retraining cognition: Techniques and
for placing a written message somewhere where it will be applications. Austin, TX: ProEd Publishers.
seen later; appointment calendars and diaries, – which
remind the person of important appointments and pro-
vide a record of daily activities.
Cognitive robots carry out a repetitive task for an
individual. For example: calculators perform the same Cognitive Exercises
mathematical operations; cycling timers turn appliances
on and off at preset times; telememo wrist watches remind ▶ Homework
the person of appointments at the same time every day,
week, month, or year; motion-sensitive detectors automat-
ically turn lights on and off when motion or the lack
thereof is sensed; smart irons turn themselves off after a Cognitive Flexibility
short period of disuse.
Cognitive Orthotic Devices replace some cognitive ▶ Mental Flexibility
function. For example: spelling machines find the correct ▶ Stroop Effect
spelling by keying in a close match; internet search engines
search the internet using key words and Boolean logic;
grammar checkers check a document for accuracy of
grammar.
Cognitive Functioning
C HRISTINA A. PALMESE
Beth Israel Medical Center
Cognitive Correctors. Table 1 Kinds of cognitive correctors
New York, NY, USA
Behavioral Changes in behavior that are specifically
prosthetics designed to remind a person to do
something Synonyms
Cognitive Carries out the same task consistently and
robot correctly Cognition; Mentation; Thinking
Cognitive Performs a thinking task
orthotic
Cognitive Help the person to learn new skills and to Definition
trainers practice them
Cognitive Maintain knowledge and records of past ‘‘Cognitive functioning’’ is a general term used to describe
archives experience so that a person does not have the different ways that people think. It refers to faculties
to store and retain this information
such as attention, mental processing speed, executive
internally in his or her memory
functions, language, visual spatial skills, memory, and
624 C Cognitive Functioning

fine motor dexterity. Different cognitive functions are sup- radio or television nearby. Divided attention allows us to
ported by distinct cortical and subcortical brain regions. pay attention to two or more tasks simultaneously. At the
Disruption of neural processes in these brain regions can top of the hierarchy is alternating attention, which is the
result in a range of cognitive deficits and syndromes. most complex form of attention that involves shifting of
attention from one task to another.
Many neuropsychological measures have been
Historical Background designed to evaluate attention. One such measure is the
digit span test. This task assesses basic attention capacity
In the 1600s, Descartes, a philosopher, was one of the first through repetition of series of numbers of increasing
scholars to establish the idea that the brain controls be- length (e.g., 1-2-3-etc). Continuous performance tests
havior. In the late 1700s, Franz Gall, a forefather of phre- are computerized assessment tools that evaluate attention
nology (the study of behavior based on the size and shape capacity over an extended time period of 10–15 min.
of the skull) helped identify that different parts of the Higher level attention skills can be examined using tests
brain regulate distinct aspects of thought, personality, and involving mental arithmetic, more complex mental arith-
behavior. Later on in the 1800s and 1900s,Wilder Penfield, metic, connecting numbers and letters in alternating
Hughlings Jackson, Paul Broca, and Carl Wernicke, to sequence (e.g., 1-A-2-B-3-etc), and resequencing of
name only a few researchers who contributed significantly numbers and letters in numeric and alphabetic order
to the field of neuropsychology, used epilepsy and lesion (e.g., transform ‘‘8-K-2’’ to 2-8-K).
models to delineate distinct neuroanatomical correlates of Attention problems can be seen across the lifespan.
cognitive and motor functions. More recently, functional In children, poor concentration, distractibility, and trou-
(e.g., fMRI, PET) and structural (e.g., MRI, CT) neuro- ble regulating behavior can be related to an Attention
imaging techniques have provided an even more well Deficit Disorder, a diagnosis that is made when pervasive
defined understanding of brain-behavior relationships. attention difficulties are demonstrated prior to age seven
years and are observable in at least two different environ-
ments. However, attention difficulties in children also
Current Knowledge may develop secondary to anxiety, language disorders,
or neurological disorders such as epilepsy. In adults, at-
Attention tention deficits may manifest secondary to a variety of
neurological and medical conditions, including sub-
Attention refers to the ability to concentrate on informa- arachnoid hemorrhage, epilepsy, dementia, head injury,
tion that is heard and seen in the environment in both diabetes, and hypothyroidism. Stress, depression, and med-
the presence and absence of distractions. It also allows ication side effects often contribute to attention problems
us to concentrate on two things at once, such as balancing in adults, as well.
a checkbook while talking on the phone. It is regulated
by the frontal lobes, although pathways involving the
pons, parietal lobe, and thalamus are involved in the Mental Processing Speed
mediation of attention, as well. Dysfunction along these
pathways can contribute to various types of attention Mental processing speed, a term used synonymously with
problems. reaction time, refers to the speed at which an individual
Attention is hierarchically organized, and disruption thinks and completes activities. It is largely regulated by
of the most basic attention skills leads to disruption of the frontal lobes and subcortical regions, and it has global
more complex attention abilities. Focused attention is the effects on cognition. That is, if mental processing speed is
most rudimentary level of attention that permits us to poor slowness also is observed in areas of attention, lan-
concentrate or be vigilant to something in the environ- guage, and spatial processing abilities. This mental slow-
ment for a very brief time period. Sustained attention ing is referred to as bradyphrenia.
refers to maintenance of concentration for minutes or Reaction time can be evaluated in several ways. Mea-
hours. Selective attention requires even greater attention sures requiring manual transcription of numbers and
capacity that allows us to attend to a particular task while shapes are very sensitive to bradyphrenia. Other tasks
filtering out irrelevant, background information. For ex- may involve rapid reading of color names and naming
ample, this form of attention is used when we read the of colors, timed symbol search, and rapid generation of
newspaper and are not distracted by noises such as the words.
 Cognitive Functioning C 625

Bradyphrenia is commonly observed in medical and Cognitive Correctors. Table 1

neurological conditions across the lifespan, including de-
Aphasia
mentia, brain injury, and Parkinson’s disease.
syndrome Neuroanatomy Symptom(s)
Broca’s Posterior, Poor articulation,
(expressive) lateral frontal telegraphic, non-fluent,
C
Executive Functions
aphasia lobe limited speech, intact
comprehension
Executive functioning refers to some of the most highly
complex aspects of thinking. It includes skills such as Wernicke’s Anterior, lateral Poor comprehension,
(receptive) temporal lobe fluent speech, nonsensical
problem solving ability, task execution and efficiency,
aphasia speech content
self-monitoring, strategizing, mental flexibility, planning,
Anomic Temporal- Poor naming, intact
and conceptualization. Executive functions are largely
aphasia parietal border comprehension, intact
mediated by the frontal lobes, and they are highly sensitive
fluency
to cerebral dysfunction.
Deficits in executive functioning can occur secondary
to neurodevelopmental immaturity, such as seen in atten-
tion deficit disorder. For the most part, however, execu- commonly observed language problems in adults is a
tive dysfunction is either acquired through brain injury naming deficit (which is synonymous with word finding
(e.g., stroke, head injury) or associated with neurodegen- difficulty, dysnomia, and ‘‘tip of the tongue’’ experiences),
erative diseases, such as Alzheimer’s disease, multiple auditory naming tests have proven to be useful for identi-
sclerosis, and Huntington’s disease. fication of anomia, as well. Similar measures are used
during evaluation of pediatric populations. In addition,
examination of children also should include assessment of
Language phonics, grammar, syntax, language formulation, and
language organization skills.
At the most fundamental level, language can be broken
down into two categories: receptive and expressive lan-
guage. Receptive language refers to the ability to under- Visual Spatial Processing
stand language; it is mediated by the posterior region
of the superior temporal gyrus, which is known as Cognitive abilities such as basic spatial perception, visual
Wernicke’s area. Expressive language, on the other hand, construction, and nonverbal problem solving ability are
pertains to oral and written expression and it is regulated characterized as spatial processing skills. These faculties
by the posterior frontal/anterior temporal lobe. This re- involve identifying ‘‘what’’ and ‘‘where’’ items are in space.
gion commonly is referred to as Broca’s area. The ‘‘what,’’ or ventral, pathway is mediated by the right
Deficits in receptive and expressive language can be (nondominant) temporal lobe. Disruption of this pathway
idiopathic (i.e., of unknown origin) or acquired. If lan- by acquired brain injury can result in agnosia, which is a
guage problems are idiopathic, they typically are identi- loss of awareness and inability to recognize entities in the
fied during a child’s development and are referred to as a environment. Agnosias can be domain specific, affecting
developmental language delay. As some children mature, auditory, visual, or somatosensory functioning. Prosopag-
their language difficulties might resolve; however, other nosia is a unique agnosia in which there is an inability to
children experience residual language deficits throughout recognize faces.
adulthood. On the other hand, acquired language deficits The ‘‘where’’ or dorsal pathway is regulated by the
such as those resultant from stroke, head injury, and parietal lobe. Dysfunction in the parietal lobe can contrib-
tumor are characterized as aphasia. Depending on the ute to spatial neglect in which a portion of space is
location of brain injury, different aphasia syndromes can neglected or ignored. Neglect can be detected during
be observed. Listed below are three of the most commonly visual field screening and on line bisection and drawing
referenced syndromes. tasks. An individual with spatial neglect will not respond
Traditionally, language skills in adults are assessed to information presented in part or all of the visual field.
with an aphasia battery (e.g., Boston Diagnostic Aphasia Left hemispatial neglect, in which the entire left side of
Examination (BDAE)), letter and category fluency, and space is ignored, is the most commonly observed form of
visual confrontation naming tasks. As one of the most neglect that results from damage to the right parietal lobe.
626 C Cognitive Functioning in the Elderly

Memory Cross References

Memory involves learning, retrieval, retention, and recog- ▶ Agnosia

nition of information. Memory functions are lateralized, ▶ Agraphia
with verbal memory regulated by left (dominant) tempo- ▶ Alexia
ral regions and visual-spatial memory regulated by the ▶ Amnesia
right temporal lobe. In order for new learning to occur, we ▶ Anomia
must be able to attend to the material and store it tempo- ▶ Aphasia
rarily in our short-term memory. Consolidation of this ▶ Attention
information into long-term memory stores occurs within ▶ Learning
the CA1-CA3 regions of the hippocampus, a subcortical ▶ Memory
brain region rich in acetylcholine. Once learned, informa- ▶ Processing Speed
tion is then stored in various neural networks throughout ▶ Syndrome
the brain. ▶ Verbal Fluency
Learning deficits can be attributed to depletion of ▶ Visuoperceptual
acetylcholine or loss of brain cell within the hippocam-
pus. This type of memory problem typically is associated
with cortical dementia, such as Alzheimer’s disease. References and Readings
Cholinesterase inhibitors, which are medications that
promote cholinergic availability, are common treatment Hamberger, M. J., Goodman, R. R., Perrine, K., & Tamny, T. (2001).
options to delay or slow the progression of a learning Anatomic dissociation of auditory and visual naming in the lateral
temporal cortex. Neurology, 56(1), 56–61.
deficit. Retrieval deficits, on the other hand, are charac-
Heilman, K. M., & Valenstein, E. (2003). Clinical neuropsychology
terized by poor spontaneous recall, yet adequate recog- (4th ed.). New York, NY: Oxford University Press.
nition of newly learned material. They are associated Kolb, B., & Wishaw, I. (2008). Fundamentals of human neuropsychology
with cell loss and neurochemical depletion of dopamine (6th ed.). New York, NY: Worth Publishers, Inc.
and glutamate in the basal ganglia and other subcortical Lezak, M., Howieson, D. B., & Loring, D. W. (2004). Neuropsy-
chological assessment (4th ed.). New York, NY: Oxford University
regions. Retrieval deficits are observed in subcortical
Press.
dementias, including Parkinson’s disease and Hunting- Squire, L. R., & Schacter, D. L. (2002). Neuropsychology of memory
ton’s disease. Although cholinesterase inhibitors can be (3rd ed.). New York, NY: The Guilford Press.
used to treat subcortical memory dysfunction, their effi-
cacy is relatively weaker in subcortical versus cortical
dementia populations.

Cognitive Functioning in the

Elderly
Motor
▶ Normal Aging
Motor abilities refer to skills such as hand-eye coordina-
tion, manual dexterity, and visual-motor integration.
These skills all have contralateral representation within
the parietal lobes. That is, right sided motor functions Cognitive Impairment No
are regulated by left parietal lobe regions, and vice versa.
Motor dysfunction can be observed in children with de-
Dementia (CIND)
velopmental delay, as well as in adults and children with
▶ Mild Cognitive Impairment
medical conditions including cerebral palsy, spasticity,
and dementia. It often manifests as clumsiness, poor
handwriting, or trouble tying shoe laces and buttoning
shirts. Motor abilities can be evaluated using tasks requir-
ing rapid placement of pegs into a pegboard, drawing, Cognitive Log
imitation of hand movements, finger tapping, and grip
strength. ▶ Cognitive-Log
 Cognitive Processing Speed C 627

psychology approach to better understanding cognitive

Cognitive Monitors processing has been through the development of computa-
tional models, such as artificial intelligence.
▶ Cognitive Correctors In cognitive neuroscience research, cognitive proces-
sing concepts are used to explore the relation between C
brain and behavior, as exemplified by George Miller’s
research (1956) on the capacity of short-term memory
to hold seven plus or minus two items and Baddeley’s
Cognitive Orthotics theory (1974) of a central executive, phonological loop,
and visuospatial sketchpad.
▶ Cognitive Correctors
▶ Prosthetic Memory Aids

Current Knowledge

The cognitive processing model is currently used in

Cognitive Potential the assessment and treatment of learning disabilities,
alcohol and drug addictions, and trauma and abuse.
▶ Best Performance Method This model emphasizes how new information is pro-
cessed, internalized, and retrieved in the context of a
person’s existing mental representations of information,
and of his/her beliefs, desires, knowledge, preferences,
and intentions.
Cognitive Processing
D ENISE K RCH
Kessler Foundation Research Center Cross References
West Orange, NJ, USA
▶ Attention
▶ Cognitive Functioning
Definition ▶ Learning
▶ Memory
Cognitive processing is a general term to describe a ▶ Metacognition
series of cognitive operations carried out in the creation ▶ Perception
and manipulation of mental representations of informa- ▶ Reasoning
tion. Cognitive processes may include attention, per- ▶ Retrieval, Retrieval Techniques
ception, reasoning, emoting, learning, synthesizing, ▶ Short Term Memory
rearrangement and manipulation of stored information,
memory storage, retrieval, and metacognition. These
functions can be conscious (e.g., learning a concept) or References and Readings
unconscious (e.g., learning a skill) and can be internally
generated (e.g., recalling a memory) or initiated by a Coren, S., Ward, L., & Enns, J. (2004). Sensation and perception. New York:
novel sensory input from the environment (e.g., solving Harcourt Brace.
Groome, D., Brace, N., Edgar, H., Esgate, A., Pike, G., Stafford, T., et al.
a problem).
(2006). An introduction to cognitive psychology: Processes and disor-
From a cognitive psychology perspective, cognitive ders (2nd ed.). London: Routledge.
processing is approached as a sequence of ordered stages
wherein sensory input is transformed, reduced, elaborated,
stored, recovered, and utilized. Early views of cognitive
processing emphasized linear temporal processing, whereas
contemporary models assume a less linear, more complex Cognitive Processing Speed
flow of dynamics, including bottom-up (sensory-driven)
and top-down (concept-driven) processes. One cognitive ▶ Information Processing Speed
628 C Cognitive Rehabilitation

Rationale or Underlying Theory

Cognitive Rehabilitation
CR is multidisciplinary and draws from a range of fields,
M ARIANNE H RABOK , K IMBERLY A. K ERNS including neuropsychology, learning theory, cognitive
University of Victoria behavioral therapy and psychotherapy, among many
Victoria, BC, Canada others. One main category of theories underlying CR is
that specific to the cognitive or behavioral domain of CR
focus. For example, attention rehabilitation programs are
Synonyms based on theoretical models of attention, memory reha-
bilitation programs on theoretical models of memory, and
Cognitive Remediation so on. A theory-driven approach provides a rational and
empirical basis for intervention, and guidance on the
structure and delivery of CR (Levine & Downey-Lamb,
Definition 2002; Sohlberg & Mateer, 2001).
Another major theory underlying many forms of CR
Cognitive rehabilitation (CR) can be defined as efforts is neuroplasticity (Kolb & Cioe, 2004), the concept that
to promote maximal adaptive cognitive functioning in the brain is amenable to change in structure and func-
people with neurologically induced cognitive deficits tion. These changes occur at multiple levels, and are
(Barrett & Gonzalez-Rothi, 2002). manifest in various ways, including changes at the syn-
apse, changes in neurotransmitter systems, and changes
in neural networks (Barrett & Gonzalez-Rothi, 2002;
Historical Background Sohlberg & Mateer, 2001). Neuroplasticity has many
implications to CR, including the type and timing of
The field of CR has grown rapidly over the last few CR, and the effect of environmental factors on recovery
decades, but historically can be traced to the 1800s of cognitive function following brain injury (Barrett &
(Ponsford, 2004; Sohlberg & Mateer, 2001). For example, Gonzalez-Rothi, 2002).
Broca administered language rehabilitation in the 1800s
and until the 1980s most rehabilitation programs focused
on remediation of language deficits (as reviewed by Goals and Objectives
Ponsford, 2004). Many further developments in CR were
a result of the confluence of societal influences and CR aims to foster natural recovery, decrease the develop-
scientific and technological advances. During WWI, ment of maladaptive patterns, and increase functional
Goldstein established CR programs for brain-injured recovery (Sohlberg & Mateer, 2001). The primary goal
soldiers. During WWII, Luria advanced the field of CR of CR is to help people achieve an optimal level of func-
through his theoretical model of brain functioning, tioning in the context of impairments. CR emphasizes
recovery, and rehabilitation (Ponsford, 2004). improving function in everyday contexts, rather than on
Advances in medical practice and an increase in the specific cognitive tasks per se.
number of survivors of traumatic brain injury (TBI) led
to a greater awareness of the needs of people who sus-
tained TBI, and an expansion of the number and focus of Treatment Participants
CR programs (the ‘‘era of proliferation’’; Coelho, 1997, as
cited by Sohlberg & Mateer, 2001). However, current CR has been used with a variety of populations, including
trends in service delivery have resulted in an ‘‘era of but not limited to: TBI, stroke, acquired brain injury
consolidation,’’ a term describing the significant down- (ABI) of varying etiology, developmental disorders,
sizing of CR programs. It has been suggested that the Alzheimers’ dementia, and schizophrenia. CR has been
reduced length of inpatient stays, outpatient health most commonly used among people who have sustained
coverage, and more limited support for CR programs TBI and stroke. Research on CR aimed at neurocognitive
have made evidence and theory-based CR practices deficits associated with schizophrenia has been growing
increasingly relevant to contemporary practice (Cicerone over the last 10 years (Kurtz & Nichols, 2007).
et al., 2005; Levine & Downey-Lamb, 2002; Sohlberg & Variables contributing to the pattern and degree
Mateer, 2001). of recovery following brain injury include: demographic
 Cognitive Rehabilitation C 629

(e.g., age, education, gender, culture), injury-related (e.g., rapid recovery than diffuse injury (Sohlberg & Mateer,
time since injury, extent, and severity of injury), and 2001).
psychological characteristics (e.g., therapeutic alliance,
comorbid psychological disorders, awareness).
Psychological Factors C
Demographic Variables Therapeutic Alliance: CR should be an interactive partner-
ship between the client, their significant others, and the
Age : Younger adults show better levels of recovery therapist. Cultivating a relationship characterized by
than older adults (Teuber, 1975 as cited by Sohlberg & attentiveness, respect, trust, commitment, and rapport is
Mateer, 2001). ABI in older adults may be complicated a critical component of CR. Open communication and
by a number of factors, including the superimposition involvement of the client and family in goal setting can
of effects of ABI on declining cognitive abilities (Richards, also enhance engagement in rehabilitation (Sohlberg &
2000 as cited by Sohlberg & Mateer, 2001), and psycho- Mateer, 2001).
social difficulties more prevalent in the population, Comorbid Psychological Disorders: Depression and
including reduced levels of social support and financial anxiety are frequently associated with brain injury (e.g.,
resources (Goleburn & Golden, 2001). However, it Anson & Ponsford, 2006). These can impede CR and
has also been suggested that older adults often have a adjustment following injury due to their propensity
greater degree of stability, coping skills, fewer life to decrease motivation and contribute to a feeling of
demands, and effective compensatory techniques, which hopelessness (Sohlberg & Mateer, 2001).
may be helpful to promoting recovery (Sohlberg & Awareness: Lack of awareness can occur following
Mateer, 2001). brain injury, and has been associated with poor self-
Education and Intelligence: Premorbid intelligence and regulation, disengagement in CR programs (Allen &
education are significantly related to recovery and adjust- Ruff, 1990), and poorer outcome.
ment (Anson & Ponsford, 2006). Although these factors provide important informa-
Gender: Some research suggests that women have tion related to the pattern and degree of recovery follow-
better recovery following left hemisphere lesions than ing brain injury, it should also be noted that much more
men (Kimura, 1983), and circulating sex hormones have research is needed to better identify therapy factors and
also been shown to have neuroprotective effects (e.g., client characteristics that optimize clinical outcomes of
Roof, Duvdevani, & Stein, 1993). CR (Cicerone et al., 2005).
Culture: Culture influences beliefs regarding the
nature and cause of loss, service utilization, degree of
personal responsibility for health, role of family, and Treatment Procedures
many other facets of psychological and behavioral
functioning relevant to recovery and participation in CR Examples of domains that have been a focus of CR
(Sohlberg & Mateer, 2001). include: attention, memory, language, visuoperceptual
difficulties, executive functions, and socioemotional
and behavioral disturbances. CR encompasses a range
Injury Related Variables of interventions. These can be broadly divided into
two types of techniques. The first are those that aim to
Time since Injury: Spontaneous recovery typically occurs restore or enhance function, by targeting the underlying
at a faster rate immediately following brain injury, partic- impairment (Glisky & Glisky, 2002; Sohlberg & Mateer,
ularly within the first 6 months, with significant recovery 2001). For example, Attention Process Training (APT) is a
also occurring up to 2 years following injury (Sohlberg & theoretically-driven program that contends that attention
Mateer, 2001). However, it is important to note that can be improved through repeated activation of atten-
compensatory techniques can be implemented and tional systems (Sohlberg & Mateer, 1987, 2001). APT
underlying motor and cognitive skills improved years consists of a group of hierarchically organized tasks
after injury (e.g., Shaw et al., 2005). that exercise different components of attention (e.g.,
Extent and Severity of Injury: Relatively mild injuries sustained, selective, alternating, divided attention). In
are associated with faster recovery rate and better CR of memory deficits, restorative/generalized memory
outcomes. Focal injuries are often associated with more approaches aim to improve specific memory systems
630 C Cognitive Rehabilitation

across tasks and contexts (e.g., prospective memory train- compared to a number of alternate treatment conditions,
ing, Raskin & Sohlberg, 1996 as cited by Sohlberg & with no comparison demonstrating a benefit for an
Mateer, 2001). Various approaches to executive function alternate treatment condition.
rehabilitation provide practice in executive skills (e.g., Although implementation of CR programs results in
planning) and guiding behavior through self-talk positive change, a number of methodological problems
(e.g., self instructional training, Cicerone & Giacino, 1992). have been identified in the CR literature, including but
The second category of CR interventions is compen- not limited to:
satory techniques, which aim to compensate for, or bypass
1. Variability in client characteristics and treatment
deficits (Sohlberg & Mateer, 2001; Wilson & Zangwill,
settings
2003). These include environmental supports (e.g.,
2. Insufficient description of samples
organization of physical space, manipulation of physio-
3. Small sample sizes
logical factors such as sleep, nutrition etc.) and external aids
4. Inadequate description of interventions
(e.g., calendars, pagers, checklists, etc.; Manly, Ward, &
5. A lack of standardized treatment protocols and
Robertson, 2002; Wilson & Zangwill, 2003). Compen-
treatment approaches (including type of intervention,
satory techniques can be helpful in managing diverse
length, and intensity)
types of cognitive difficulties (Sohlberg & Mateer, 2001).
6. Lack of appropriate control conditions (e.g., no
A third approach involves the use of specialized
treatment or alternate treatment)
approaches to teaching and stabilizing new behaviors
7. Lack of uniform outcome measures
and knowledge in people with memory difficulties.
These include instructional techniques such as errorless Evidence-based standards of CR are frequently
learning, in which mistakes are minimized (Wilson, identified as important in advancing the field of CR, both
Baddeley, Evans, & Shiel, 1994), the method of vanishing in terms of quality of treatment and for fiscal support at
cues (Glisky & Glisky, 2002) and traditional behavioral an organizational level (e.g., Sohlberg & Mateer, 2001).
shaping and training techniques. Cicerone et al. (2005) reviewed evidence for CR inter-
Psychosocial support or psychotherapy (e.g., sup- ventions used with TBI and stroke populations. A number
ported listening, brain injury education, relaxation training) of interventions with strong empirical support were
can also be an integral part of a rehabilitation program, identified. Strategy training (e.g., APT or Time Pressure
depending on the needs of the client (Sohlberg & Mateer, Management) was effective during postacute rehabilita-
2001). Computer programs can be used as an adjunct tion for TBI. A number of visuospatial rehabilitation
to CR, but should not be the sole form of CR (Cicerone techniques were empirically supported for improving ne-
et al., 2005). It has been recommended that computer glect following right hemisphere stroke (e.g., visuospatial
CR programs be focused, structured, monitored, and rehabilitation, scanning training). Specific gestural or
ecologically valid. A successful rehabilitation program strategy training was found to be effective in the treatment
typically involves a combination of interventions, speci- of apraxia following left hemisphere stroke. A number of
fically tailored to the individual’s level of disability language interventions were shown to have empirical
and personal goals (Manly et al., 2002; Solhberg & support, including cognitive linguistic therapies,
Mateer, 2001). pragmatic conversational skills, interventions for specific
The duration and frequency of CR varies widely (e.g., language impairments (e.g., reading comprehension), and
Geusgens, Winken, van Heugten, Jolles, & van den adjunctive computer-based interventions. Strong empiri-
Heuvel, 2007; Kurtz & Nichols, 2007). CR has been cal support was shown for memory strategy training (e.g.,
delivered both on an individual and on a group basis. visual imagery and external aids, such as memory
Significant others (e.g., family) are viewed as an integral notebooks). Some empirical support was found for self-
part of treatment (Sohlberg & Mateer, 2001). instruction and self-monitoring interventions for
executive functions. Empirical support was found for
comprehensive-holistic CR programs, which address
Efficacy Information multiple aspects of impairment.
Interventions that meet criteria for inclusion as an
Cicerone et al. (2005) examined differential treatment empirically supported treatment do not represent an
effects of CR compared to alternate treatment conditions exhaustive list of CR interventions that may be effective,
in 46 class I studies with TBI and stroke populations. but reflect the empirical status of the field of CR research
Their review suggested a clear differential benefit of CR and practice. A successful rehabilitation program typically
 Cognitive Rehabilitation C 631

involves a combination of interventions, specifically standardized observations of simulated performance of

tailored to the individual’s level of disability and personal daily tasks in a laboratory environment, and standardized
goals (Manly et al., 2002; Solhberg & Mateer, 2001). and nonstandardized reports of transfer to daily function-
Therefore, clinical considerations may demand CR inter- ing (Geusgens et al., 2007). There is a need for further
ventions with strong empirical support, as well as those development of standardized measure of transfer with C
that have less empirical support but may be beneficial to good psychometric properties (Geusgens et al., 2007). It
the client. A discussion of limitations and strengths of has been recommended that generalization should not be
empirically supported and empirically validated inter- ‘‘expected,’’ but should be ‘‘programed’’ throughout the
ventions can be found elsewhere (e.g., Chambless & CR program (Sohlberg & Mateer, 2001).
Ollendick, 2001).
There is less empirical study of CR with populations
beside TBI and stroke. A review of CR with children who Qualifications of Treatment Providers
have sustained ABI concluded that there is a sufficient
amount of evidence to recommend attention remedia- CR is typically provided by registered psychologists, and
tion, involvement of family members in the treatment occupational therapists. Speech and language therapists
plan, and provision of psychoeducation to guardians typically provide rehabilitation for language and
(Laatsch et al., 2007). A review of studies of CR with communication deficits.
people with early stage Alzheimer’s disease suggested CR
could be beneficial, particularly when flexible to the needs
of clients, of sufficient duration, and involving caregivers Cross References
(Clare, 2003). A review of studies of CR with people
with schizophrenia has suggested improvements on ▶ Assistive Technology
memory and executive functions, although it should be ▶ Attention Training
noted that this is an emerging field so is based on a ▶ Behavioral Memory Aids
small number of studies (Kurtz & Nichols, 2007). ▶ Brain Plasticity
A review of CR for people with multiple sclerosis sug- ▶ Compensatory Strategies
gested empirically based support for verbal learning and ▶ Environmental Modifications
memory intervention, and suggested additional research ▶ Errorless Learning
support is needed (O’Brien, Chiaravalloti, Govereover, & ▶ Head Injury
DeLuca, 2008). ▶ Insight, Effects on Rehabilitation
▶ Interdisciplinary Team Rehabilitation
▶ Memory
Outcome Measurement ▶ Neglect and Heminattention
▶ Neuropsychological Rehabilitation
Levine and Downey-Lamb (2002) recommend inclusion ▶ Prosthetic Memory Aids
of both specific outcome measures that relate closely to ▶ Rehabilitation Psychology
the construct addressed by the intervention, and well as ▶ Traumatic Brain Injury
general measures of functional outcomes, such as return
to work/school, interpersonal relationships, and leisure
activities. When possible, measures should have known References and Readings
psychometric properties, and be completed by both the
client and significant others. Allen, C. C., & Ruff, R. M. (1990). Self-rating vs. neuropsychological
performance of moderate vs. severe head-injured patients. Brain
Neuropsychological assessment can be a valuable tool
Injury, 4, 7–17.
at various points to: predict outcome, guide appropriate Anson, K., & Ponsford, J. (2006). Coping and emotional adjustment
rehabilitation strategies, guide vocational and educational following traumatic brain injury. The Journal of Head Trauma
planning, explain behavior, and help evaluate the extent Rehabilitation, 21, 248–259.
of injury in conjunction with other information Barrett, A. M., & Gonzalez-Rothi, L. J. (2002). Theoretical bases
for neuropsychological interventions. In P. J. Eslinger (Ed.),
(Bergquist & Malec, 2002).
Neuropsychological interventions: Clinical research and practice
Measurement of transfer of training to everyday life (pp. 16–37). London: The Guilford Press.
has been measured through assessment of performance Bergquist, T. F., & Malec, J. F. (2002). Neuropsychological assessment
on tasks similar to tasks used during training, for treatment planning and research. In P. J. Eslinger (Ed.),
632 C Cognitive Remediation

Neuropsychological interventions: Clinical research and practice (pp. Sohlberg, M. M., & Mateer, C. A. (1987). Effectiveness of an attention
38–58). London: The Guilford Press. training program. Journal of Clinical and Experimental Neuropsy-
Chambless, D. L., & Ollendick, T. H. (2001). Empirically supported chology, 19, 117–130.
psychological interventions: Controversies and evidence. Annual Sohlberg, M. M., & Mateer, C. A. (2001). Cognitive rehabilitation: An
Review of Psychology, 52, 685–716. integrated neuropsychological approach. New York: Guilford Press.
Cicerone, K. D., Dahlberg, C., Malec, J. F., Langenbahn, D. M., Wilson, B. A., Baddeley, A. D., Evans, J. J., & Shiel, A. (1994). Errorless
Felicetti, T., Kneipp, S., et al. (2005). Evidence-based cognitive learning in the rehabilitation of memory impaired people.
rehabilitation: Updated review of the literature from 1998 through Neuropsychological Rehabilitation, 4, 307–326.
2002. Archives of Physical Medicine Rehabilitation, 86, 1681–1692. Wilson, B. A., & Zangwill, O. (Eds.). (2003). Neuropsychological rehabili-
Cicerone, K. D., & Giacino, J. T. (1992). Remediation of executive tation: Theory and practice. Exton, PA: Psychology Press.
function deficits after traumatic brain injury. Neurorehabilitation,
2, 73–83.
Clare, L. (2003). Cognitive training and cognitive rehabilitation for
people with early-stage dementia. Reviews in Clinical Gerontology,
13, 75–83. Cognitive Remediation
Geusgens, C. A. V., Winken, S. I., van Heugten, C. M., Jolles, J., & van den
Heuvel, W. J. A. (2007). Occurrence and measurement of transfer in
cognitive rehabilitation: A critical review. Journal of Rehabilitation
▶ Cognitive Rehabilitation
Medicine, 39, 425–439. ▶ Neuropsychological Rehabilitation
Glisky, E. L., & Glisky, M. L. (2002). Learning and memory impairments.
In P. J. Eslinger (Ed.), Neuropsychological interventions: Clinical
research and practice (pp. 137–162). London: The Guilford Press.
Goleburn, C. R., & Golden, C. J. (2001). Traumatic brain injury outcome
in older adults: A critical review of the literature. Journal of Clinical Cognitive Reserve
Geropsychology, 7, 161–187.
Kimura, D. (1983). Sex differences in cerebral organization for
speech and practice functions. Canadian Journal of Psychology, 37,
J ESSE C HASMAN
19–35. Brown University
Kolb, B., & Cioe, J. (2004). Neuronal organization and change after Providence, RI, USA
neuronal injury. In J. Ponsford (Ed.), Cognitive and behavioral reha-
bilitation: From neurobiology to clinical practice (pp. 7–29). London:
The Guilford Press.
Kurtz, M. M., & Nichols, M. C. (2007). Cognitive rehabilitation for
Synonyms
schizophrenia: A review of recent advances. Current Psychiatry
Reviews, 3, 213–221. Brain reserve; Neural compensation; Neural reserve
Laatsch, L., Harrington, D., Hotz, G., Marcantuoro, J., Mozzoni, M. P., &
Walsh, V., et al. (2007). An evidence-based review of cognitive and
behavioral rehabilitation treatment studies in children with ac-
quired brain injury. Journal of Head Trauma Rehabilitation, 22, Definition
248–256.
Levine, B., & Downey-Lamb, M. M. (2002). Design and evaluation of
Cognitive reserve is a concept often used to describe how
rehabilitation experiments. In P. J. Eslinger (Ed.), Neuropsychological
interventions: Clinical research and practice (pp. 80–104). London:
individual differences mediate the clinical expression of
The Guilford Press. brain damage. In this context, some individuals may cope
Manly, T., Ward, S., & Robertson, I. (2002). The rehabilitation of atten- better than others and function within relatively normal
tion. In P. J. Eslinger (Ed.), Neuropsychological interventions: Clinical limits, despite the presence of neuropathology.
research and practice (pp. 105–136). London: The Guilford Press.
O’Brien, A., Chiaravalloti, N. D., Govereover, Y., & DeLuca, J. (2008).
Evidenced based cognitive rehabilitation for persons with multiple
sclerosis: A review of the literature. Archives of Physical Medicine and Historical Background
Rehabilitation, 89, 761–769.
Ponsford, J. (2004). Introduction. In J. Ponsford (Ed.), Cognitive and
behavioral rehabilitation: From neurobiology to clinical practice
Historically, one of the earliest observations of cognitive
(pp. 1–6). London: The Guilford Press. reserve was described in a study that found characteristic
Roof, R. L., Duvdevani, R., & Stein, D. G. (1993). Gender influences senile plaques and neurofibrillary tangles commonly asso-
outcome of brain injury: Progesterone plays a protective role. Brain ciated with Alzheimer’s pathology present in healthy, cog-
Research, 607, 333–336.
nitively unimpaired elderly (Blessed, Tomlinson, & Roth,
Shaw, S. E., Morris, D. M., Uswatte, G., McKay, S., Meythaler, J. M., &
Taub, E. (2005). Constraint-induced movement therapy for recovery
1968). Similar observations between brain pathology and
of upper-limb function following traumatic brain injury. Journal of performance variability frequently have been described in
Rehabilitation Research and Development, 42, 769–778. the extant literature.
 Cognitive Stimulation C 633

Current Knowledge activities, such as education, occupation, exercise, or so-

cial involvement, may provide buffers within neural net-
While the underlying mechanisms that support cognitive works to help delay the behavioral symptoms associated
reserve remain unclear, current theories focus on how the with brain pathology.
brain may develop alternative or more efficient networks C
to compensate for pathology. One theory proposed by
Satz (1993) holds that brain mass and neuronal count – Future Directions
or brain reserve capacity (BRC) – may raise or lower the
brain’s threshold to withstand a lesion or degenerative An important implication of this concept may be the
process. In this model, lower BRC would make an indi- development of interventions that aim enhances cognitive
vidual more vulnerable to neurological insult and increase reserve. In aging research, for instance, growing interest
test sensitivity in detecting impairment. Similarly, greater has revolved around the effectiveness of brain ‘‘training’’
BRC would provide a higher threshold before the effects games, exercise, or lifestyle modifications that may
of neuropathology are observed. For instance, one study strengthen and/or expand neural networks, and improve
(Katzman et al., 1988) compared a high-functioning cognitive functioning.
group of nursing home residents with Alzheimer’s pathol-
ogy with a group of healthy nursing home controls. When
compared across several cognitive domains, the Alzhei- Cross References
mer’s group performed at or above the levels of healthy
controls. In this study, the observed cognitive deficits were ▶ Brain Plasticity
much lower than predicted, given the level of brain pa- ▶ Brain Reserve Capacity
thology in these individuals. This was explained, in part,
by the finding that those in Alzheimer’s group had larger
brains with more neurons than the control group, which
References and Readings
may have helped those individuals compensate for their
Blessed, G., Tomlinson, B. E., & Roth, M. (1968). The association between
neuropathology. Genetics may play a primary role in
quantitative measures of dementia and of senile change in the
building greater BRC by increasing overall brain mass, cerebral grey matter of elderly subjects. The British Journal of Psychi-
synaptic density, or neurogenesis, all of which could pro- atry, 114(512), 797–811.
vide greater resiliency against lesions or a degenerative Katzman, R., Terry, R., DeTeresa, R., Brown, T., Davies, P., Fuld, P., et al.
process. (1988). Clinical, pathological, and neurochemical changes in de-
mentia: A subgroup with preserved mental status and numerous
By contrast, the concept of cognitive reserve suggests
neocortical plaques. Annals of Neurology, 23(2), 138–144.
that individual differences in genetics or life experiences Satz, P. (1993). Brain reserve capacity on symptom onset after brain
provide a buffer to the effects of brain disease, including injury: A formulation and review of evidence for threshold theory.
dementia. Neural reserve or neural compensation models Neuropsychology, 7(3), 273–295.
(Stern, 2002) are proposed as potentially active processes Stern, Y. (2003). The concept of cognitive reserve: A catalyst for research.
Journal of Clinical and Experimental Neuropsychology, 25(5),
that facilitate the brain’s attempts to adapt to disease
589–593.
pathology. Various lines of animal studies have supported Stern, Y. (2006). Cognitive reserve: Theory and application (studies on
this model noting the benefits of enriched environments neuropsychology, neurology, and cognition). New York: Psychology
on neurogenesis and plasticity in the brain. In humans, Press.
years of education and occupational attainment are asso-
ciated with the preservation of cognitive functions. For
instance, individuals with lower education often demon-
strate clinical manifestations of dementia earlier in the Cognitive Robots
disease process compared to those with higher education
(Stern, 2003). ▶ Cognitive Correctors
One of the important implications of the cognitive
reserve construct is that lifetime experiences can influence
individuals’ level of functioning. It is important to high-
light that current research does not suggest that cognitive Cognitive Stimulation
reserve prevents neuropathology from developing. Rather,
it is believed that a lifetime spent engaging in stimulating ▶ Reality Orientation
634 C Cognitive Trainers

nondegenerative and degenerative neurologic diseases (in-

Cognitive Trainers cluding the dementias)’’ (ASHA, 2005).
CCDs were recognized in the early 1980s as research
▶ Cognitive Correctors mounted, illustrating the interdependency of cognition
and language, particularly with regard to the roles of
attention and memory in language processing and with
regard to the pervasive impact that cognitive impairments
Cognitive-Behavioral have on functional communication abilities (Bayles &
Modification Tomoeda, 2007; Myers & Blake, 2008; Ylvisaker, Szekeres,
& Feeney, 2008). Speech-language pathologists (SLPs)
▶ Behavior Modification now routinely assess and treat those aspects of cognition
that either support, or are influenced by, speech, lan-
guage, and communication; other clinicians such as
neuropsychologists, rehabilitation psychologists, and
cognitive remediation specialists may do so as well.
Cognitive-Communication
Disorder
Categorization
S ARAH S. C HRISTMAN B UCKINGHAM
The University of Oklahoma Health Sciences Center CCDs are differentiated from linguistic impairments
Oklahoma, OK, USA (aphasias) and from motor speech disorders (dysarthrias
and apraxia of speech) by the use of overly concrete,
poorly organized, and socially insensitive communication
Synonyms despite preserved speech and language skills. CCDs may
be caused and/or complicated by impairments of atten-
Cognitive-communication impairment; Language of con- tion, memory, executive functions, and pragmatics.
fusion; Language of generalized intellectual impairment; Symptoms will vary by etiology, patterns of brain damage,
Right hemisphere impairment/disorder and individual differences in the neural organization of
cognitive functions.

Short Description or Definition Epidemiology

The American Speech-Language-Hearing Association Approximately 1.4 million individuals will suffer stroke-
(ASHA) has defined cognitive-communication disorders related CCDs each year (CDC, 2007; Tomkins, 1995).
(CCDs) as those that, ‘‘. . .encompass difficulty with any One to two million children will acquire post-traumatic
aspect of communication that is affected by disruption of CCDs annually (Blosser & DePompei, 2003; CDC, 2001;
cognition. Communication may be verbal or nonverbal and Ylvisaker et al., 2008), whereas adult and elderly indivi-
includes listening, speaking, gesturing, reading, and writing duals will sustain head injuries at rates approximating
in all domains of language (phonologic, morphologic, syn- 100–200 per 100,000, respectively (Bruns & Hauser,
tactic, semantic, and pragmatic). Cognition includes cogni- 2003). The number of individuals expected to be living
tive processes and systems (e.g., attention, perception, with dementia of the Alzheimer’s type (DAT), and thus
memory, organization, executive function). Areas of func- living with CCDs, is expected to increase from 4 million
tion affected by cognitive impairments include behavioral (in the year 2000) to 31.2 million people by the year 2050.
self-regulation, social interaction, activities of daily living,
learning and academic performance, and vocational perfor-
mance. Cognitive-communication disorders may be con- Natural History, Prognostic Factors,
genital or acquired. Congenital etiologies include but are and Outcomes
not limited to genetic disorders and pre, peri, and postnatal
neurologic injuries and diseases. Acquired etiologies in- The natural history and prognosis for improvement of
clude but are not limited to stroke, brain tumor, traumatic cognitive-communication dysfunction are tied to many
brain injury, anoxic or toxic encephalopathy, and factors, including etiology, initial severity of disorder,
 Cognitive-Communication Disorder C 635

the presence or absence of comorbid illnesses, and of the cerebrum may cause difficulty with pragmatics,
the nature of specific individual variables such as age, context-sensitive semantics, and expressive affective pros-
gender, and psychological state. In the absence of con- ody, obscuring indications of mood and compromising
founding circumstances, improvement of CCD is antici- the ability to communicate successfully in social situa-
pated when caused by stroke, excisable tumor, remitting tions. Egocentrism may impair recognition of these pro- C
disease, or traumatic brain injury. When caused by pro- blems and reduce insight into the communication needs
gressive debilitating conditions such as non-excisable of others. Deficits in vigilance, sustained and selective
tumors or dementing diseases, CCD will worsen over attention, and/or in attention switching can cause salient
time. CCD of greater initial severity has a poorer prog- information to be missed, and reduce the sequential
nosis than CCD of mild or moderate initial severity, or simultaneous processing of information from multiple
although in the case of recovery from TBI, the degree sources. Difficulties drawing inferences, extracting themes
of functionality at hospital discharge may be more pre- and topics in discourse, interpreting nonliteral language,
dictive than the initial severity of injury (Testa, Malec, and/or reading affective and prosodic cues for mean-
Moessner, & Brown, 2005). The presence of co-occurring ing during conversational exchanges may be present
illnesses may compromise the speed and extent of recov- (Ylvisaker et al., 2008). A tangential communication
ery from CCD at any severity level; CCDs arising from style often emerges, where excessive, vaguely relevant
traumatic injuries causing diffuse brain damage, for ex- details are inserted inappropriately into narratives and
ample, are likely to be accompanied by paralysis, motor discourse (Myers & Blake, 2008).
speech disorders, and injuries to vital organs. Damage to the right parietal association cortex and to
Recovery from CCD differs by etiology. Re- the right parietal-temporal-occipital (PTO) cortex can
covery after stroke is usually most rapid in the first lead to contralateral inattention, impeding reading,
3 months post onset. Recovery from thrombo-embolic writing, and listening for stimuli in left hemispace.
stroke may continue after 6 months post onset, where- Lesions in PTO cortex can also cause visual-spatial per-
as recovery from hemorrhagic stroke may plateau at the ception and recognition deficits (including topographical
6-month point. Functional improvement in cognitive- and geographical agnosias), which can impair navigation
communication abilities after severe traumatic brain in- in familiar environments if verbal mediation strategies are
jury is generally slower at the outset when compared not used to compensate. Damage to secondary (superior
with stroke and typically proceeds in a stairstep fashion temporal) association cortex may reduce the efficiency of
over months or years. Recovery from mild stroke or auditory language processing if stimuli are complex or if
brain injury often seems rapid in comparison. Many they must be processed quickly. Damage may also impair
individuals with mild brain injuries appear to recover the interpretation of affective prosody when produced by
quickly (Ylvisaker et al., 2008), but as many as 15–20% others. Lesions to prefrontal, parietal, and temporal cor-
suffer from persistent fatigue and reduced information tex have been associated with anosognosia, the failure to
processing speed for years after injury. Frequently unrec- recognize the existence or presence of illness and a prob-
ognized and untreated, these deficits cause lifelong cogni- lem that can reduce compliance with treatment activities
tive challenges that threaten social adjustment and (Myers, 2001; Myers & Blake, 2008; Tomkins, 1995).
successful community reentry. In contrast to stroke and When damage to the cerebral cortex is bilateral, def-
TBI, recovery from dementing illness is not expected. Early icits across multiple systems may interact to impair com-
stages of cognitive decline in DAT are accompanied by munication to different degrees. Bilateral cortical
forgetfulness, word-finding difficulties, and changes in so- damage, for example, can cause impairments in the self-
cial pragmatics; mid stages are characterized by increased regulation of communicative behaviors that range from
memory loss, anomia, and social withdrawal; and late failure to organize discourse efficiently to failure to in-
stages are associated with loss of most useable cognitive hibit inappropriate utterances and actions. It can also
and physical functions (Bayles & Tomoeda, 2007). diminish the ability to focus attention and memory so
as to make them useful during conversational exchanges
(Ylvisaker et al., 2008). However, if bilateral damage
Neuropsychology and Psychology of involves subcortical hippocampal structures, then funda-
Cognitive-Communication Disorder mental disruptions of declarative (semantic, episodic, and
lexical) and explicit memory may occur. Hippocampal
Damage to the prefrontal and frontal association regions damage/deterioration is common with brain injury/
of the right (or nonlanguage-dominant) hemisphere dementing disease, and it can lead to a host of
636 C Cognitive-Communication Disorder

impairments ranging from difficulty learning new infor- 5. The ability to discriminate relevant from irrelevant
mation to the presence of a severe, unremitting amnesia. detail and integrate disparate parts into a coherent
Bilateral damage to lower brain stem reticular activat- whole can be evaluated with scene description tasks.
ing circuits can severely compromise arousal, alertness, 6. Cognitive flexibility and functional problem-solving
and awareness. This can lead to brief losses of conscious- abilities can be assessed with tasks that require the
ness or to intractable coma. When caused by dementing generation of multiple strategies for achieving a goal
disease, coma is most likely followed by death. However, and that require repairs of failed communicative inter-
recovery from traumatic coma frequently leads to return changes with others (Myers, 1999).
of function through increasing levels of responsivity,
Standardized tests used to assess cognitive-communication
communication, orientation, self-regulation, and cogni-
functions subsequent to right hemisphere impairment in-
tive integration. A common sequela of traumatic brain
clude the Mini-Inventory of Right Brain Injury (Pimental &
injury is a period of post-traumatic amnesia (PTA), that
Kingsbury, 1989), The Rehabilitation Institute of Chicago
is, inability to form new memories of events happening
Clinical Management of Right Hemisphere Dysfunction
after brain injury with disorientation to time, place, or
(Halper, Cherney, & Burns, 1996), and The Burns Brief
person. In individuals who are verbal, confabulation may
Inventory of Communication and Cognition (Burns, 1997).
be present until disorientation and confusion diminish.
While these instruments will elicit symptoms of CCD
As cognitive functioning improves, individuals with brain
associated with right hemisphere damage, findings must
injuries will benefit from environmental structure and
be interpreted with a view toward evaluating impair-
external direction to support increasingly purposive, flex-
ments of underlying neuropsychological processes, for it
ible, and goal-oriented behavior.
is here that treatment will be most profitably directed
(Myers, 1999).
Standardized tests used to assess CCD after TBI in-
Evaluation
clude the American Speech-Language-Hearing Association
Functional Assessment of Communication Skills in Adults
Evaluation of a suspected CCD requires examination of
(Frattali, Thompson, Holland, Wohl, & Ferketic, 1995),
cognition as it affects and interacts with skills of speech
the Behavioral Rating Inventory of Executive Function
planning and execution, language comprehension and
(Roth, Isquith, & Gioia, 2005), the Brief Test of Head
production, and pragmatic/discourse aspects of commu-
Injury (Helm-Estabrooks & Hotz, 1991), the Ross Infor-
nication in everyday social contexts (Turkstra, Cohelo, &
mation Processing Assessment-2 (Ross-Swain, 1996), and
Ylvisaker, 2005).
the Scales of Cognitive Ability for Traumatic Brain Injury
Tests of cognitive-communication skills are used to
(Adamonovich & Henderson, 1992). The Glasgow Coma
evaluate the effects that deficits in attention, orientation,
Scale (Jennett & Teasdale, 1981) and the Rancho Los
perception, memory, organization, and executive func-
Amigos Levels of Cognitive Function Scale (Hagen,
tions can have on communication. Examples of tasks
Malkmus, Durham, & Bowman, 1979) or its revisions,
frequently included in formal and informal assessments
including a version adapted for children under 14 years of
are provided for illustration:
age (Blosser & DePompei, 2003), are frequently used to
1. Attention to left hemispace is frequently tested with assess consciousness and track recovery of cognitive func-
line-bisection, cancellation, and drawing tasks as well tions after coma.
as with more complex reading, writing, and listening Informal situational assessments of cognition and
tasks that require individuals to process communica- communication may yield valuable information that can-
tion stimuli from both right and left sides of body not be obtained from formal standardized tests (Blosser &
midline. DePompei, 2003; Turkstra et al., 2005). This naturalistic
2. Inferencing abilities are tested by asking patients to approach to assessment has been termed, ‘‘functional,
interpret humor, to recognize indirect requests for collaborative, context-sensitive, hypothesis-testing assess-
actions, and to follow the themes of conversations. ment,’’ and it should be conducted with the purpose of
3. Orientation is assessed by asking patients to respond identifying situational variables that can be manipulated
to questions about time, place, and person. to improve the successful participation of injured indivi-
4. Memory for facts, events, and procedures is evaluated duals as they operate within their everyday environments
with yes/no questions, narratives, and performance of (Ylvisaker et al., 2008). Best-practice assessment proce-
familiar routines. dures for individuals who have suffered brain injuries
 Cognitive-Communication Disorder C 637

should, therefore, include (1) completion of formal test- functional merits’’ (p. 209), improving fundamental cog-
ing in specific skill domains and (2) completion of obser- nitive processes will have the greatest automatic generali-
vational checklists (or quality of life inventories) where zation to the many untrained tasks where those processes
children (or adults) may be evaluated in natural environ- are needed.
ments (Blosser & DePompei, 2003; Turkstra et al., 2005). Generalization may be more difficult to achieve when C
This type of assessment might include administration of CCD is associated with diffuse brain injury versus focal
the Functional Assessment of Verbal Reasoning and Execu- stroke. Rehabilitation approaches that are more contextu-
tive Strategies test (MacDonald, 2005), a tool that was alized (implemented in natural settings) and more func-
developed for evaluation of cognitive-communication tion oriented (designed to support activities of daily
skills specifically related to reading, writing, and living) than traditional methods are ideal for promoting
reasoning (Turkstra et al., 2005), and the Quality of Com- rapid skill mastery and transfer. Ylvisaker et al. (2008)
munication Life Scale (Paul et al., 2005). suggest that treatment strategies designed to compensate
Assessment of CCD in dementia employs standar- for impaired executive functions and self-regulation abil-
dized screening tests, severity staging instruments, and ities will most often lead to successful rehabilitation after
comprehensive assessment batteries (Hopper & Bayles, brain injury. They advocate practicing essential cognitive-
2008). Screening tests include the Story Retelling Subtest communication tasks (such as conversing with family
of the Arizona Battery for Communication Disorders members or taking notes during lectures) within support-
of Dementia (Bayles & Tomoeda, 1993) and the FAS ive real-world environments, where stimuli likely to trig-
Verbal Fluency Test (Borkowski, Benton, & Spreen, ger errors have been removed and where the use of
1967). Tests for estimating the severity of cognitive de- external aids is encouraged.
cline include the Mini-Mental State Examination Intervention for CCD in DAT emphasizes manage-
(Folstein, Folstein, & McHugh (1975)) and the Global ment rather than rehabilitation. Goals are designed
Deterioration Scale (Reisberg, Ferris, deLeon, & to help individuals maintain functional competence for
Crook (1982)). Comprehensive assessment batteries as long as possible. Decontextualized errorless learning
include the Arizona Battery for Communication Disorders activities that drill attention and memory can bolster the
of Dementia (Bayles & Tomoeda, 1993) and the Function- encoding and retrieval of factual information in early
al Linguistic Communication Inventory (Bayles & stages of dementia. Intervention tasks that employ exter-
Tomoeda, 1994), the latter being most useful for indivi- nal memory aids that recruit long-term (remote) mem-
duals with severe dementia (Hopper & Bayles, 2008). ory (such as reminiscing about past events) and that
Assessment findings can help families work with SLPs to draw on procedural memory for familiar routines
understand and compensate for the symptoms of cogni- (such as describing how to get home) can help promote
tive decline. social communication and safety while capitalizing
on those aspects of cognition that are available in mid-
stage dementia. Tangible sensory stimuli (including dolls
and stuffed animals) can help support communication
Treatment and reduce agitation as dementia advances (Bourgeois,
1990, 1991, 1992; Hoerster, Hickey, & Bourgeois, 2001;
Treatment for CCD has traditionally been decontextua-
Hopper & Bayles, 2008).
lized (implemented in rehabilitation settings or at
bedside) and deficit oriented (designed to improve/
support impaired cognitive-communication processes).
Conventional pencil/paper or computer tasks are used to Cross References
stimulate underlying cognitive processes (e.g., attention,
memory) with the expectation that as they improve, so ▶ Attention
will the related functional skills (e.g., readiness to listen to ▶ Brain Injury
speakers taking turns, remembering a set of instructions ▶ Cognitive Functioning
given by one’s boss). Myers (1999) advocates the use ▶ Cognitive Processing
of decontextualized treatments to facilitate cognitive- ▶ Cognitive Rehabilitation
communication skills in individuals who have acquired ▶ Dementia
CCD from right hemisphere stroke. She argues that al- ▶ Executive Functioning
though the value of any treatment approach ‘‘rests on its ▶ Functional Neuroanatomy
638 C Cognitive-Communication Impairment

▶ Memory Impairment Hoerster, L., Hickey, E. M., & Bourgeois, M. S. (2001). Effects of memory
aids on conversations between nursing home residents with demen-
▶ Mild Brain Injury
tia and nursing assistants. Neuropsychological Rehabilitation, 11(3/4),
▶ Mild Cognitive Impairment 399–427.
▶ Moderate Brain Injury Hopper, T., & Bayles, K. A. (2008). Management of neurogenic commu-
▶ Pragmatic Communication nication disorders associated with dementia. In R. Chapey (Ed.),
▶ Severe Brain Injury Language intervention strategies in aphasia and related neurogenic
communication disorders (5th ed., pp. 988–1008). Philadelphia:
Lippincott Williams & Wilkins.
Jennett, B., & Teasdale, G. (1981). Management of severe head injuries.
Philadelphia: F. A. Davis.
References and Readings MacDonald, S. (2005). Functional assessment of verbal reasoning and
executive strategies. Guelph, Ontario: CCD Publishing.
Adamonovich, B., & Henderson, J. (1992). Scales of cognitive ability for Myers, P. S. (1999). Right hemisphere damage: Disorders of communication
traumatic brain injury. Chicago, IL: Riverside. and cognition. San Diego: Singular Publishing Group.
American Speech-Language-Hearing Association. (2005). Roles of speech- Myers, P. S. (2001). Toward a definition of RHD syndrome. Aphasiology,
language pathologists in the identification, diagnosis, and treatment of 15, 913–918.
individuals with cognitive-communication disorders: Position state- Myers, P. S., & Blake, M. L. (2008). Communication disorders
ment [Position Statement]. www.asha.org/policy. associated with right-hemisphere damage. In R. Chapey (Ed.), Lan-
Bayles, K. A., & Tomoeda, C. (1993). The arizona battery for communica- guage intervention strategies in aphasia and related neurogenic com-
tion disorders of dementia. Austin, TX: Pro-Ed. munication disorders (5th ed., pp. 963–987). Philadelphia: Lippincott
Bayles, K. A., & Tomoeda, C. (1994). The functional linguistic communi- Williams & Wilkins.
cation inventory. Austin, TX: Pro-Ed. Paul, D., Frattali, C. M., Holland, A. L., Thompson, C. K., Caperton, C. J.,
Bayles, K. A., & Tomoeda, C. (2007). Cognitive-communication disorders & Slater, S. (2005). Quality of communication life scale. Rockville,
of dementia. San Diego, CA: Plural Publishing. MD: American Speech-Language-Hearing Association.
Blosser, J. L., & DePompei, R. (2003). Pediatric traumatic brain injury: Pimental, P. A., & Kingsbury, N. A. (1989). Mini inventory of right brain
Proactive intervention (2nd ed.). Clifton Park, NY: Delmar Learning. injury. Austin, TX: Pro-Ed.
Borkowski, J. G., Benton, A. L., & Spreen, O. (1967). Word fluency and Reisberg, B., Ferris, S. H., deLeon, M. J., & Crook, T. (1982). The global
brain damage. Neuropsychologia, 5, 135–140. deterioration scale (GDS): An instrument for the assessment of
Bourgeois, M. S. (1990). Enhancing conversation skills in patients primary degenerative dementia (PDD). American Journal of Psychi-
with Alzheimer’s disease using a prosthetic memory aid. Journal of atry, 139(1), 136–139.
Applied Behavior Analysis, 23(1), 29–42. Ross-Swain, D. (1996). Ross information processing assessment (RIPA-2).
Bourgeois, M. S. (1991). Communication treatment for adults with Austin, TX: Pro-Ed.
dementia. Journal of Speech and Hearing Research, 34(4), 831–844. Roth, R. M., Isquith, P. K., & Gioia, G. A. (2005). Behavior rating
Bourgeois, M. S. (1992). Evaluating memory wallets in conversations inventory of executive function- Adult Version. Lutz, FL: Psychological
with persons with dementia. Journal of Speech and Hearing Research, Assessment Resources.
35(6), 1344–1357. Testa, J. A., Malec, J. F., Moessner, A. M., & Brown, A. W. (2005).
Bruns, J. Jr., & Hauser, W. A. (2003). The epidemiology of traumatic Outcome after traumatic brain injury: Effects of aging on
brain injury: A review. Epilepsia, 44(Suppl. 10), 2–10. recovery. Archives of physical medicine and rehabilitation, 86(9),
Burns, M. (1997). The burns brief inventory of communication and cogni- 1815–1823.
tion. San Antonio: Psychological Corporation. Tomkins, C. A. (1995). Right hemisphere communication disorders: Theory
Centers for Disease Control and Prevention. (2001). Traumatic brain and management. San Diego, CA: Singular Publishing Group.
injury in the United States: A report to Congress. www.cdc.gov. Turkstra, L. S., Cohelo, C., & Ylvisaker, M. (2005). The use of standar-
Centers for Disease Control and Prevention (CDC). (2007). Prevalence of dized tests for individuals with cognitive-communication disorders.
stroke—United States, 2005. Morbidity and Mortality Weekly Report, Seminars in Speech and Language, 26(4), 215–222.
56(19), 469–474. Ylvisaker, M., Szekeres, S. F., & Feeney, T. (2008). Communication
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Chicago, IL: Riverside. ▶ Cognitive-Communication Disorder
 Cognitive-Log C 639

Reliable serial assessment is crucial to document the

Cognitive-Log rapid changes in behavior and cognition during recovery
from acquired brain disorders. Therefore, there is a need
T HOMAS A. N OVACK for a brief, bedside evaluation instrument to assess other
University of Alabama at Birmingham areas of cognition that are frequently affected by acquired
Birmingham, AL, USA
C
brain injuries. Existing scales are typically too lengthy or
involved to present as part of morning rounds. Other
scales fail to adequately capture the primary limitations
Synonyms resulting from acquired brain injury. The brief scales that
have been created for serial administration in an inpatient
C-Log; Cog-Log; Cognitive Log setting have been presented without adequate psychomet-
ric properties or scaling. The Cog-Log was created to serve
as a brief bedside measure to chart neurocognitive recov-
Description ery and assist in planning rehabilitation interventions with
a wide variety of patients.
The Cog-Log is a ten-item scale designed for serial bed-
side measurement of cognitive functions in individuals
completing inpatient rehabilitation. The scale includes Psychometric Data
items assessing orientation, immediate and delayed verbal
recall, concentration, executive function, response inhibi- The reliability and validity of the Cog-Log have been
tion, and praxis. All responses are scored according to the assessed in several ways. A sample of 150 individuals with
following criteria: 3 points = spontaneously correct re- acquired brain injury was examined with the Cog-Log.
sponse, no errors; 2 points = correct on logical cueing Most of the sample (80%) had sustained moderate to severe
(e.g., ‘‘That was yesterday, so today is?’’) or in the presence TBI, with the remainder including patients with CVA and
of 1 error; 1 point = correct on multiple-choice cueing or anoxia. Internal consistency analysis (Cronbach’s alpha) was
in the presence of 2 errors; 0 points = incorrect despite conducted for the total Cog-Log score. Inter-rater reliability
cueing, more than 2 errors, unable to complete. Points for estimates (Spearman’s rho) were calculated using a subset of
time estimation are calculated as follows: 3 points = 19 patients (75 total observations). High internal consisten-
correct within  5 s; 2 points = correct within  10 s; cy (Cronbach’s alpha = 0.778) was demonstrated with a
1 point = correct within  15 s. Incorrect/absent standard error of measurement of 0.53. Inter-rater reliabili-
responses are followed by cueing at the next level for the ty coefficients for each of the ten Cog-Log items ranged
orientation and delayed memory items. Multiple-choice from 0.749 (Go/No-go task) to 1.0 (Time Estimation).
cueing, used only with the orientation items, involves Standard errors of measurement were no more than 0.10
provision of three choices, varying the location of the for single item scores, which range from 0 to 3.
correct response. Item scores are summed to provide a Factor analysis of the Cog-Log using principal com-
total score ranging from 0 to 30. Daily scores can be ponents extraction (N = 150) revealed a unitary factor
plotted to permit quick visual analysis of recovery trends. (Eigenvalue = 3.48), with all items loading on that factor.
The following specific items are included in the Cog- The highest loadings were for delayed recall of verbal
Log: three items assessing the orientation to the date, time, information and recitation of months backwards, suggest-
and hospital name; two items assessing immediate and ing a stronger contribution of complex working memory
delayed recall for a short address; counting backwards and verbal recall to this unitary factor.
from 20; reciting the months in reverse order; and estimat- The Cog-Log exhibited a significant correlation with
ing when 30 s has passed. Two motor tasks involving hand neuropsychological assessment completed on the same day,
gestures – a movement sequence (fist-edge-palm) and a including tests such as immediate and delayed recall of the
response inhibition task (go/no-go) – are also included. Wechsler Memory Scale-III Logical Memory subtest, Rey
Auditory Verbal Learning Test, Digit Span subtest of the
Wechsler Adult Intelligence Test-III, and the Trail Making
Historical Background Test. The lowest Cog-Log score obtained during acute
rehabilitation also significantly predicted 1-year outcome
Measurement of orientation and higher neurocognitive pro- in three of six neuropsychological domains (attention,
cesses are important aspects of early neurorehabilitation. executive functioning, and visuospatial abilities) after
640 C Collaborative Care

controlling for demographics and injury severity. The Cog- Lee, D., LoGalbo, A. P., Baños, J. H., & Novack, T. A. (2004). Prediction of
cognitive abilities one year following TBI based on cognitive screen-
Log was also significantly correlated with the results of the
ing during rehabilitation. Rehabilitation Psychology, 49, 167–171.
Mini Mental State Examination, a well-known cognitive Penna, S., & Novack, T. (2007). Further validation of the orientation and
screening test (r = 0.75, P < 0.001). Cognitive Log relative to the mini mental status exam. Archives of
Physical Medicine and Rehabilitation, 88, 1360–1361.

Clinical Uses
Individuals without known neurological insult received Collaborative Care
average total Cog-Log scores of 28 ( 2), and mean
individual item scores were greater than or equal to ▶ Family-Centered Care
2.4. Age, education, and gender did not predict total or
individual item scores (p > 0.05). Stepwise discriminant
analyses on a sample of 82 persons with brain injury and
82 normal controls matched for age, education, and gen-
der revealed that a cut-off score of 25 correctly classified Collagen Vascular Disease
88.4% of individuals in their respective groups.
The Cog-Log is a companion instrument to the Ori- E LLIOT J. R OTH
entation Log (O-Log). Generally, the Cog-Log is not Northwestern University
administered until a score of at least 15 is achieved on Chicago, IL, USA
the O-Log, indicating that the person is responding and
able to respond correctly to some orientation questions.
Administering the Cog-Log prior to this point has not Synonyms
proven fruitful. The Cog-Log can be administered every
day, but typically three times a week is sufficient to moni- Connective tissue disease
tor progress or detect deterioration.
Efficiency and ease of assessment were considered
when choosing items; tasks requiring additional stimuli Definition
(e.g., block construction) or extended administration
times were not included. The Cog-Log was designed for Collagen vascular diseases are a group of conditions that are
flexible administration to patients with severe cognitive characterized by malfunction of the tendons, bones, and
and behavioral disturbances. Administration time ranges connective tissue, that are supported by collagen. Their
from 7 to 10 min for confused patients, but can be as short pathogenesis is autoimmune in nature.
as 5 min for those who perform well.

Current Knowledge
Cross References The most common collagen vascular disorders include
rheumatoid arthritis, systemic lupus erythematosus,
▶ Cognitive Functioning
scleroderma, and dermatomyositis. Others include poly-
▶ Galveston Orientation and Amnesia Test
myositis, polyarteritis nodosa, ankylosing spondylitis, and
▶ Mini Mental State Examination
a number of vasculopathies. These diseases are frequently
▶ Traumatic Brain Injury
associated with diffuse inflammatory changes, abnormal
immunity. Vascular abnormalities that result from these
conditions serve as frequent causes of various types of
References and Readings vasculitis. Common features include arthritis, skin
changes, eye changes, pericarditis, pleuritis, myocarditis,
Alderson, A. L., & Novack, T. A. (2003). Reliable serial measurement of nephritis, and vasculitis of the brain, peripheral nerves, or
cognitive processes in rehabilitation: The Cognitive-Log. Archives of
extremities. They also may have a variety of hematological
Physical Medicine and Rehabilitation, 84, 668–672.
Center on Outcome Measurement in Brain Injury (COMBI). www.tbims. changes causing clotting or bleeding, and a number of
org/combi. Accessed May 26, 2009. abnormal circulating blood proteins.
 Color Agnosia C 641

The cause of most of these diseases is unknown. color perception (i.e., retaining the ability to match
Hereditary factors and deficiencies, autoimmunity, envi- colors or to identify the numbers on the Ishihara plates).
ronmental antigens, infections, allergies, and antigen- They also have difficulty matching colors, either verbally
antibody complexes in various combinations are probably or visually, to familiar colored objects (e.g., identifying
involved. the color normally associated with cherries, lettuce, C
or bananas).
Relatively rare, pure color agnosia must be distin-
Cross References guished from other disturbances of color perception
and color naming (color anomia). In color blindness,
▶ Cerebral Angiitis the individual is unable to perceive or distinguish either
▶ Lupus Cerebritis certain colors or possibly all color. In the latter case,
▶ Vasculitis the world is seen in shades of black and white. While
color blindness is usually congenital, it can also be ac-
quired, a condition known as central achromatopsia.
References and Readings The latter is a perceptual deficit thought to result
from lesions in the visual cortices (e.g., lingual gyrus
Klippel, J. H., Stone, J. H., Crofford, L. J., & White, P. H. (Eds.). (2008).
and the occipitotemporal (fusiform) gyrus). In this dis-
Primer on the rheumatic diseases (13th ed.). New York: Springer. order, the patient may have difficulty verbally naming a
visually presented color, pointing to a color named by
the examiner, or simply matching or sorting colored
objects to others of a similar hue, yet still be able
to indicate (name) the colors normally associated with
Collapsed Lung common objects (e.g., the colors of the outside, inside,
and seeds of a watermelon). In a milder form of this
▶ Pneumothorax condition (dyschromatopsia), colors are described as
‘‘dull,’’ ‘‘washed out,’’ or ‘‘faded.’’ In color anomia, the
problem is not one of perceptions, but of language.
The patient can perceive and match colors, but has diffi-
Colliculi culty naming specific colors or pointing to colors named
by the examiner.
▶ Inferior Colliculi In the few published cases, lesions associated with
color agnosia tend to occur in the left or bilateral occipi-
totemporal area.

Color Agnosia
J OHN E. M ENDOZA Cross References
Tulane University Medical Center
New Orleans, LA, USA ▶ Achromatopsia
▶ Color Anomia

Definition
Literally, a loss of previous color knowledge. References and Readings
Bauer, R. M., & Demery, J. A. (2003). Agnosia. In K. Heilman & E.
Current Knowledge Valenstein (Eds.), Clinical neuropsychology (4th ed., pp. 236–295).
New York: Oxford University Press.
Tranel, D. (2003). Disorders of color processing. In T. E. Feinberg & M. J.
In pure color agnosia, patients have difficulty naming Farah (Eds.), Behavioral neurology and neuropsychology (pp. 243–
or pointing to named colors, despite relatively preserved 256). New York: McGraw-Hill.
642 C Color Anomia

References and Readings

Color Anomia
Bauer, R. M., & Demery, J. A. (2003). Agnosia. In K. Heilman, &
J OHN E. M ENDOZA E. Valenstein (Eds.), Clinical neuropsychology (4th ed.) (pp. 236–
Tulane University Medical Center 295). New York: Oxford University Press.
New Orleans, LA, USA Tranel, D. (2003). Disorders of color processing. In T. E. Feinberg, & M. J.
Farah (Eds.), Behavioral neurology & neuropsychology (pp. 243–256).
New York: McGraw-Hill.

Definition

Anomia is the inability to name colors in the absence

of a more global anomia associated with an aphasic Color Blindness
disorder.
▶ Achromatopsia

Current Knowledge

To be classified as a color anomia, the disorder should

Color Imagery
occur in the absence of problems with color perception
J OHN E. M ENDOZA
or recognition (i.e., the patient should be able to match
Tulane University Medical Center
or sort colors). Two subtypes of the disorder have been
New Orleans, LA, USA
identified. In one, the problem is limited to an inability
to name colors that are visually presented or to point to
colors named by the examiner. This type of color
anomia is usually associated with the syndrome of alex-
Definition
ia without agraphia and results from lesions involving
The ability to visualize a color in its absence. When
the primary visual cortex of the dominant hemisphere
asked, most individuals would be able to identify
(resulting in a right homonymous hemianopsia) and
the outer color of a watermelon as well as that of the
the splenium of the corpus callosum. Visual informa-
inside of the rind, the fleshy part of the melon, and its
tion is thus restricted to the left visual field (right
seeds. Color imagery is more than an ability to simply
hemisphere) and the color information cannot cross
recall a particular visual image; it also involves the
the involved splenium of the corpus callosum to reach
capacity to mentally conjure up and manipulate colors
the left (verbal) hemisphere. In the second subtype,
at will. For example, one may imagine a blue horse or a
specific color anomia, the patient has difficulty with purely
person wearing an article of clothing of a specific color,
verbal color naming tasks, in addition to difficulty in
never having seen either before. While disturbances of
naming visually presented colors. Thus, there would be a
color perception and color imagery are frequently
naming deficiency if the patient were asked to name the
linked, in some cases the two can be distinguished clini-
colors associated with the inside and outside of a water-
cally. Thus, while a given patient may be able to name
melon. As in the first case, color matching or sorting
or match colors presented visually, that same patient
should be intact. In specific color anomia, other aphasic
may not be able to name the color of an apple in its
(naming) deficits may be present, but color names are
absence. Similarly, while accurately identifying the color
most affected.
red from an array, the patient may not be able to match
it to a black-and-white picture of the fruit, although
the latter may be identified by its shape. While the
Cross References exact anatomical site responsible for disturbances of
color imagery has not been firmly established, the left
▶ Alexia Without Agraphia temporal-occipital cortex is believed to be involved in
▶ Color Agnosia most cases.
 Colored Progressive Matrices C 643

Cross References D, and E of the standard progressive matrices (SPM) so

that intellectual capacity can be more accurately
▶ Apperceptive Visual Agnosia assessed (the score for set Ab would be omitted to
▶ Associative Visual Agnosia determine a percentile based on SPM scoring).
▶ Color Agnosia C
▶ Color Anomia
Historical Background

For information about the historical background of the

References and Readings original test, please refer to ▶ Raven Progressive Matrices.

Farah, M. J. (2003). Disorders of visual-spatial perception and cognition.

In K. M. Heilman & E. Valenstein (Eds.), Clinical neuropsychology Psychometric Data
(4th ed., pp. 146–160). New York: Oxford University Press.
Tranel, D. (2003). Disorders of color processing. In T. E. Feinberg & M. J. Norms for ages 5.5–11.5 for North America are presented
Farah (Eds.), Behavioral neurology and neuropsychology (2nd ed.,
by Raven, Raven and Court (1998, 2000). By age 9 years, a
pp. 243–256). New York: McGraw-Hill.
nearly perfect score is obtained (35/36) by the upper 5%
of the sample. Education corrected norms are available
for an abbreviated version (sets A and B, excluding Ab
which is correlated >0.90 with the sum of A and B) for
ages 55–85. In children, split-half reliability has been
Colored Progressive Matrices shown to be high (>0.80) (Raven et al. 1998), as is
test-retest reliability following days or weeks (>0.80).
V ICTORIA M. L EAVITT Over longer intervals (6 months to 1 year) these values
Kessler Foundation Research Center decline (0.59–0.79).
West Orange, NJ, USA

Clinical Uses
Description
The CPM was designed for use with children, older
 The colored progressive matrices (CPM) are an alter- people, for anthropological studies, and for clinical
nate form of the Raven’s progressive matrices (RPM) work. Its format makes it valuable for individuals who
that was published in the 1940s. Shorter and simpler cannot understand English; people with physical disabil-
than the original, this version was designed for younger ities, aphasias, cerebral palsy, or deafness; and people with
children (ages 5–11 years), the elderly (over 65 years), below normal intelligence. The colored backgrounds were
and people with moderate or severe learning difficul- introduced to attract the patient’s attention; the test
ties. As such, it also tends to be used more frequently in can be administered in the form of illustrations in a
research protocols, although it is important to note booklet or as boards with moveable pieces. Patients with
that the CPM and the RPM are not interchangeable, left hemisphere damage perform better on the colored
nor may derived scores from the two tests be inter- matrices than on the standard form (as described in
preted the same. CPM contains 36 items, grouped into Lezak, Howieson, & Loring, 2004). This is likely attribut-
three sets (A, Ab, B) of 12 items each: A and B from the able to the fact that while only one-fifth of RPM items test
original version, with the addition of set Ab. Most visuospatial skills almost exclusively, fully one-third of
items are presented on a colored background to make items on the CPM are predominantly visuospatial, with
the test visually stimulating for participants; the bright other items involving more problem-solving. Also likely
background does not seem to detract from the clarity due to the visuospatial task demands, individuals with
of the stimuli. As the last few items in set B are exactly Lewy body dementia tend to have more difficulty on the
the same as they appear in the standard version, an CPM than Alzheimer’s patients with similar levels of
examinee who succeeds on these may go on to Sets C, dementia.
644 C Coma

Cross References rating, and include the Glasgow Coma Scale (Teasdale &
Jennett, 1976) and the FOUR Score (Wijdicks, Bamlet,
▶ Advanced Progressive Matrices Maramattom, Manno, & McClelland, 2005).
▶ Raven’s Progressive Matrices
▶ Standard Progressive Matrices
Prognosis

References and Readings Mortality rates for patients in coma vary with etiology,
but commonly reach or exceed 50%. Early prognostic
Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). Neuropsycho- variables of poorer outcome include lower Glasgow
logical assessment (4th ed.). New York: Oxford University Press. Coma Scale scores (Teasdale & Jennett, 1976), increased
Raven, J. C. (1938, 1996). Progressive Matrices: A perceptual test of
intelligence. Oxford: Oxford Psychologists Press Ltd.
age, absent pupillary responses, systolic blood pres-
Raven, J., Raven, J. C., & Court, J. H. (1998). Raven manual: Section 2. sure <90 mm Hg, and computed tomography abnormal-
Colored progressive matrices. Oxford: Oxford Psychologists Press Ltd. ities, including compression, effacement, or blood within
Raven, J., Raven, J. C., & Court, J. H. (2000). Raven manual research the basal cisterns, or extensive traumatic subarachnoid
supplement 3: American norms, neuropsychological applications. hemorrhage (Posner et al., 2007).
Oxford: Oxford Psychologists Press Ltd.
Raven, J., Raven, J. C., & Court, J. H. (2003). Manual for Raven’s
progressive matrices and vocabulary scales. Section 1: General
overview. San Antonio, TX: Harcourt Assessment. Cross References
Strauss, E., Sherman, E. M. S., & Spreen, O. (Eds.). (2006). A compendium
of neuropsychological tests (3rd ed.). New York: Oxford University ▶ Decerebrate Posturing
Press.
▶ Decorticate Posturing
▶ Glasgow Coma Scale
▶ Loss of Consciousness
▶ Minimally Conscious State
Coma ▶ Stupor
▶ Vegetative State
J ACOB K EAN
Indiana University School of Medicine
Indianapolis, Indiana, USA References and Readings

Posner, J. B., Saper, C. B., Schiff, N. D., & Plum, F. (2007). Plum and
Definition Posner’s diagnosis of stupor and coma. New York: Oxford University
Press.
Coma is a state of unconsciousness in which the patient is Teasdale, G., & Jennett, B. (1976). Assessment and prognosis of coma
incapable of being awake, and is unarousable, even with after head injury. Acta Neurochirurgica, 34, 45–55.
Wijdicks, E. F. M., Bamlet, W. R., Maramattom, B. V., Manno, E. M., &
vigorous stimulation. Coma is usually the result of dis- McClelland, R. L. (2005). Validation of a new coma scale: The FOUR
ease or injury, and rarely lasts for more than 4 weeks. score. Annals of Neurology, 58, 585–593.
While comatose, a patient may respond to painful stimuli
but lack the ability to demonstrate localized response or
defensive movements (Posner, Saper, Schiff, & Plum,
2007).
Coma Recovery Scale
Current Knowledge M ARK A. S ANDBERG
Independent Practice
Diagnosis Smithtown, NY, USA

The diagnosis of patients in coma necessarily involves

examination of physiological functions, including arous- Synonyms
al, pupillary responses, respiration, motor function, and
reflexes. Several diagnostic scales are available for severity CRS; CRS-R; JFK coma recovery scale
 Coma/Near Coma Scale C 645

Definition Kalmar, K., & Giacino, J. (2005). The JFK coma recovery scale-revised.
Neuropsychological Rehabilitation, 15(3–4), 454–460.
The CRS-R, including administration and scoring information and rating
The Coma Recovery Scale (CRS-R) is a 23-item instru- forms, is available as a PDF file at www.tbims.org/combi/crs/index.
ment used to assist with differential diagnosis, prognostic html.
assessment, and treatment planning with patients having C
disorders of consciousness.

Current Knowledge
Coma Vigile
The Coma Recovery Scale was initially developed by
▶ Vegetative State (Persistent)
Giacino and colleagues in 1991 and thereafter was revised
in 2004 as the JFK Coma Recovery Scale-Revised (Giacino,
Kalmar, & Whyte, 2004). The scale was developed with the
goal of helping to identify the neurobehavioral character-
istics of persons diagnosed with disorders of conscious- Coma/Near Coma Scale
ness, thus allowing for increased prognostic clarity and
refinement of treatment methods. In its revised form, M ARK A. S ANDBERG
the CRS-R is composed of 23 items, which coalesce into Independent Practice
six subscales addressing auditory, visual, motor, oromo- Smithtown, NY, USA
tor, communication, and arousal functions. Each subscale
is composed of hierarchically arranged items associated
with the brain stem, subcortical, and cortical processes. Synonyms
Items receiving higher scores are more likely to reflect
cognitively mediated activity. The test syllabus offers be- C/NC; CNC
havioral criteria, which provide the user with operationa-
lized characteristics used to determine whether a specific
response to sensory stimuli has been demonstrated by the
Description
patient. A rating form is included as part of the syllabus,
which allows the user to perform serial assessments.
The Coma/Near Coma (CNC) Scale was designed to
Based on the 2004 study by Giacino, Kalmar and Whyte,
measure small changes in neurobehavioral status among
interrater and test–retest reliability were described as high
patients who have sustained severe brain injuries and
for CRS-R total scores, although some systematic scoring
whose clinical functioning is consistent with vegetative
differences between raters were found on the visual and
or near-vegetative states. The CNC Scale is useful when
oromotor/verbal subscales. The CRS-R has been translated
reliable, valid, and economical assessment of patient’s func-
into Spanish, Italian, German, French, Dutch, and Norwe-
tioning is required so as to substantiate clinical change or
gian. The CRS-R offers a reliable method for measuring the
lack thereof in patients whose functioning is at markedly
trajectory of consciousness following severe brain injury,
low levels. The CNC Scale expands the levels of the
and in assisting in the differential diagnosis of patients in a
Disability Rating Scale (DRS). It has five levels and is
minimally conscious state from those in a vegetative state.
composed of 11 items. The items assess dysfunction in
the sensory and perceptual dimensions and describe the
severity of primitive response deficits.
Cross References

▶ Coma/Near Coma Scale

Historical Background

Recognizing a need for rehabilitation professionals to

References and Readings
systematically identify and chart changes in functioning
in patients whose clinical status is best characterized as
Giacino, J. T., Kalmar, K., & Whyte, J. (2004). The JFK coma recovery
scale- revised: measurement characteristics and diagnostic utility. approximately ‘‘vegetative,’’ the CNC Scale was developed
Archives of Physical Medicine and Rehabilitation, 85(12), 2020–2029. as a supplement to the Dementia Rating Scale (DRS). Use
646 C Coma/Near Coma Scale

Coma/Near Coma Scale. Table 1 Coma/near coma scale overview

Item # Dimension assessed Stimulus used Response elicited

1 Auditory Ringing bell Eye opening/orientation
2 Command Responsivity Verbal request Response to command
3 Visual Flashing light Fixation or avoidance
4 Visual Say ‘‘Look at me’’ Fixation & Tracking
5 Threat Quick movement of hand to eyes Eye blinking
6 Olfactory Ammonia capsule Withdrawal or grimacing
7 Tactile Shoulder tap Head/eye orientation or shoulder movement
8 Tactile Swab to each nostril Withdrawal/eye blink or mouth twitch
9 Pain Firm pinch to finger tip Withdrawal or agitation
10 Pain Firm ear pinch Withdrawal or agitation
11 Vocalization None; listen for any verbalization Words or sounds

of the CNC Scale is recommended whenever the DRS accuracy. Following this training, it is noted that while
score is greater than 21 (Extremely Severe Disability). single ratings can be used, ‘‘a minimum of two indepen-
The scoring form also notes that in cases in which DRS dent ratings per patient is encouraged’’ for purposes of
scores are < 21, CRC Scale ratings should be conducted promoting reliability (Rappaport, 2000). It is also recom-
monthly in conjunction with the DRS. mended that rating be taken at approximately the same
time each day whenever possible.
The CNC Scale includes 11 items representing 8 res-
Current Knowledge ponse dimensions (see Table 1). Each item includes
3 score options (0, 2, 4); 4 referring to ‘‘no responsivity
As described by Rappaport, Dougherty, and Kelting (1992) to sensory stimulation.’’ The CNC Total Score is com-
and as detailed by the Center for Outcome Measurement puted by adding the ratings (0, 2, 4) from each of the
in Traumatic Brain Injury (COMBI; www.tbims.org/ 11 items and dividing that score by the number of items
combi/cnc/index.html), interrater reliability calculated at rated. Categorical descriptions are offered to coincide
three time periods was 0.97. The lowest interrater inter- with the Total Score attained (i.e., No Coma through
correlation of 0.86 was found to exist on item 8 (nasal Extreme Coma).
swab). The internal consistency as determined using
alpha coefficients were 0.43, 0.65, and 0.65 for CNC Scale
scores taken at 1, 8, and 16 weeks post injury, respectively Cross References
(Rappaport, Dougherty, & Kelting, 1992).
A rank order correlation between CNC Scale and DRS ▶ Coma Recovery Scale
scores was 0.69 (p < 0.02). The correlation between CNC ▶ Dementia Rating Scale
Scale ratings and the prominence of sensory (auditory,
visual, and somatosensory) abnormality as determined
through evoked potential studies was 0.52 (p < 0.05) References and Readings
(Rappaport, Dougherty, & Kelting, 1992).
Discussion regarding training in the use of the CNC Rappaport, M. (2000). The coma/near coma scale. The center for outcome
Scale is offered by COMBI (www.tbims.org/combi/cnc/ measurement in brain injury. Accessed 1/6/08 from www.tbims.org/
cnctat.html). It is recommended that proper use of combi/cnc.
the instrument follows a period during which evaluations Rappaport, M. (2005). The disability rating scale and coma/near coma
scales in evaluating severe head injury. Neuropsychological Rehabili-
are performed simultaneously with several raters indepen-
tation, 15(3/4), 442–453.
dently offering judgments for each item. Interrater com- Rappaport, M., Dougherty, A., & Kelting, D. L. (1992). Evaluation of
parisons and discussion concerning the reasons for making coma and vegetative states. Archives of Physical Medicine and Reha-
specific judgments are encouraged to refine observational bilitation, 73, 628–634.
 Commission on Accreditation of Rehabilitation Facilities (CARF) C 647

CARF is governed by its President/CEO and a

Commission on Accreditation 12-member Board of Directors. The Board of Directors
of Rehabilitation Facilities consists of individuals with expertise, experience, and per-
spective on CARF-related issues. Current CARF leadership
(CARF) includes individuals with a diverse range of expertise, in- C
cluding individuals with psychology, physical therapy, and
S ARAH K. L AGEMAN
speech-language pathology expertise, social work back-
Emory University
grounds, as well as past surveyors and individuals with
Atlanta, GA, USA
business and legal training. Other perspectives on issues
CARF International offices
related to CARF-accreditation and other matters are gained
Tucson, AZ
through individuals and organizations that are members of
CARF Canada
CARF’s International Advisory Council (IAC).
Edmonton, AB, Canada
The International Advisory Council (IAC) creates a
CARF–CCAC
partnership for CARF and IAC members to promote
Washington, DC
quality in human services and enhance the lives of per-
sons served. It also provides a forum for guidance and
input into standards development and the accreditation
Membership
process and insight on issues affecting the fields in which
CARF provides accreditation services. IAC members
Commission on Accreditation of Rehabilitation Facilities
support CARF’s mission, purposes, values, and vision.
(CARF) is an independent, nonprofit organization that is
The IAC is composed of organizational and individual
an accreditor of human service providers. It was formed
members who represent a broad spectrum of stake-
in 1966 when the Association of Rehabilitation Centers
holders, including persons served, providers, profes-
(ARC) and the National Association of Sheltered Work-
sionals in the field, and purchasers. Current members
shops and Homebound Programs (NASWHP) joined
of the IAC include American Academy of Neurology,
forces to further develop their interests in setting stan-
American Academy of Orthopedic Surgeons, American
dards. Since its inception, CARF has grown significantly
Academy of Pain Medicine, American Academy of Phys-
in size and informally adopted CARF International as its
ical Medicine and Rehabilitation, American Occupa-
registered name after accrediting programs in Canada,
tional Therapy Association, Inc., American Physical
Europe, and South America.
Therapy Association, American Psychological Associa-
CARF International currently provides accreditation
tion, American Speech-Language-Hearing Association,
services in the following areas, called customer service
American Therapeutic Recreation Association, and the
units: aging services; child and youth services; behavioral
U.S. Psychiatric Rehabilitation Association, in addition
health; durable medical equipment, prosthetics, ortho-
to many other established agencies and associations
tics, and supplies (DMEPOS); employment and com-
documented on the CARF web site, http://www.carf.
munity services; medical rehabilitation; and opioid
org/About/IAC/.
treatment programs. The CARF family of organizations
currently accredits more than 6,000 providers at more
than 20,000 locations on five continents. More than Major Areas or Mission Statement
8.3 million persons of all ages are served annually by
CARF-accredited providers. In 2002, CARF Canada was The mission of CARF is ‘‘to promote the quality, value,
developed as a private, nonprofit organization serving and optimal outcomes of services through a consultative
Canadian providers. CARF acquired the Continuing accreditation process that centers on enhancing the lives of
Care Accreditation Commission (CCAC) in 2003. The the persons served’’ (retrieved June 29, 2010, from http://
CCAC provides accreditation of continuing care retire- www.carf.org/About/Mission/). CARF has identified three
ment communities and aging services networks. Finan- core values as central to its mission, and these values are
cial support for CARF includes fees from accreditation prioritized in all CARF accreditation, research, and edu-
surveys, sales of publications, grants from public and cational activities. The following are the three CARF core
private entities, fees from seminars and conferences, values: (1) all people have the right to be treated with
and contributions from International Advisory Council dignity and respect, (2) all people should have access
(IAC) members. to needed services that achieve optimum outcomes, and
648 C Commission on Accreditation of Rehabilitation Facilities (CARF)

(3) all people should be empowered to exercise informed accreditation for rehabilitation organizations providing
choice. services to workers with occupational disabilities.
In support of its mission, CARF has identified numer- CARF has also expanded the types of services for
ous purposes that are the focus of the agency, including which it provides accreditation. In September 1997,
the following (retrieved June 29, 2010, from http://www. CARF was awarded a contract by the Department of
carf.org/About/Mission/). Health and Human Services, Substance Abuse and Mental
Health Services Administration for the development and
 To develop and maintain current, field-driven stan-
implementation of opioid treatment program accredi-
dards that improve the value and responsiveness of
tation. After successful development of the program
the programs and services delivered to people in need
accreditation, CARF was recognized in November 2001
of rehabilitation and other life enhancement services.
by the Substance Abuse and Mental Health Services
 To recognize organizations that achieve accreditation
Administration (SAMHSA)/Center for Substance Abuse
through a consultative peer-review process and dem-
Treatment (CSAT) as an approved accrediting organiza-
onstrate their commitment to the continuous improve-
tion for opioid treatment programs. As noted previously,
ment of their programs and services with a focus on the
CARF acquired the Continuing Care Accreditation
needs and outcomes of the persons served.
Commission (CCAC) in 2003. Acquisition of the CCAC
 To conduct accreditation research emphasizing out-
promoted CARF’s vision of being an independent re-
comes measurement and management, and to provide
source that identifies high-quality care providers for indi-
information on common program strengths as well as
viduals of all ages, including children and older adults.
areas needing improvement.
More recently, in February 2007, CARF began accrediting
 To provide consultation, education, training, and
suppliers of certain durable medical equipment, prosthet-
publications that support organizations in achieving
ics, orthotics, and supplies (DMEPOS) after the Centers
and maintaining accreditation of their programs and
for Medicare & Medicaid Services (CMS) approved CARF
services.
as a national authority for DMEPOS suppliers.
 To provide information and education to persons
Over the decades, CARF has steadily grown and
served and other stakeholders on the value of
expanded its accreditation services to serve individuals in
accreditation.
other countries. In 1969, CARF accredited its first program
 To seek input and to be responsive to persons served
in Canada and the first program in Europe was accredited
and other stakeholders.
in August 1996. CARF Canada was incorporated in Sep-
CARF also collaborates with partners who share CARF tember 2002 in Edmonton, Alberta. Further expansion of
vision and goals, while remaining politically neutral. CARF services included accreditation of the first program in
partners include professional associations, advocacy groups, South America in December 2005. The value of CARF
governmental agencies, or individuals who are committed accreditation is extensive and includes benefits such as
to enhancing the lives of persons who receive services. business improvement, risk management, funding access,
positive visibility, accountability, peer network, in addi-
tion to other benefits detailed on the CARF web site.
Landmark Contributions

One of the key developments in the history of CARF was Major Activities
the passing of a resolution by the Council of State Admin-
istrators of Vocational Rehabilitation in April 1970, which CARF accreditation outcomes for CARF and CARF
urged state agencies to support a CARF accreditation Canada consist of a three-year accreditation, a one-year
requirement for all organizations providing rehabilitation accreditation, provisional accreditation, nonaccreditation,
services. As CARF’s services became increasingly recog- and preliminary accreditation. CARF-CCAC accreditation
nized by organizations and agencies, additional support of outcomes include a five-year accreditation and nonaccre-
CARF accreditation services has occurred. In November ditation. CARF currently has close to 1,500 surveyors
1974, Goodwill Industries of America recognized CARF throughout the North and South America and Europe.
as the accrediting organization for all Goodwill organiza- The steps to accreditation involve a year or more of
tions. Another resolution, adopted in November 1980 by preparation prior to the site survey and ongoing quality
the Association of Trial Lawyers of America, urged state improvement following the survey. CARF designates a
workers’ compensation agencies to require CARF CARF Resource Specialist to organizations seeking
 Commission on Accreditation of Rehabilitation Facilities (CARF) C 649

accreditation to provide guidance and technical assistance its accreditation areas (Behavioral Health, Employment
regarding the accreditation process. Other resources are and Community Support, and Medical Rehabilitation).
also available to facilitate the preparation process, includ- Then in 1996, CARF published the first edition of the
ing standards manuals for the various programs and Accreditation Sourcebook. A significant contribution to
services an organization can seek accreditation for and accreditation services occurred in 1998, when CARF C
the CARF Accreditation Sourcebook, which explains the rewrote its standards to be unidimensional as part of its
accreditation process. CARF accreditation requires that an commitment to implementing the Standards Confor-
organization must implement and use the standards in its mance Rating System. Additional standards were pub-
programs for at least 6 months prior to the survey. During lished in 1999, including standard manuals for Adult
this time, an organization conducts a self-study and eval- Day Services Programs and the Veterans Health Adminis-
uation of conformance to the standards using the stan- tration Comprehensive Blind Rehabilitation Services.
dards manual in conjunction with the survey preparation Moreover, that same year, CARF extended its practice of
questions. Then the organization submits the Intent to disclosing information to the public regarding an organi-
Survey, which includes detailed information about lead- zation’s survey report from just the Medical Rehabilitation
ership, programs, and services that the organization is Standards Manual to also include the Behavioral Health
seeking to accredit and the service delivery location(s). Standards Manual and the Adult Day Services Standards
CARF selects a survey team by matching program or Manual. CARF’s public information policy was extended
administrative expertise and relevant field experience to include all areas later in 2003. Standards manuals for
with the organization’s unique requirements. During the assisted living programs were published in 2000, followed
survey, the survey team determines the organization’s by the Child and Youth Services Standards Manual in 2005,
conformance to all applicable standards on site through the Aging Services Standards Manual in 2006, and Stan-
the observation of services, interviews with persons served dards for Dementia Care in 2006. In addition to these
and other stakeholders, and review of documentation. publications, CARF has continued to implement new
The survey team shares findings related to the standards standards in many of its areas of accreditation.
with the organization at an exit conference before the CARF has implemented new electronic programs
team leaves the site and this information is also submitted designed to support and further develop its mission. In
to CARF. CARF then renders the accreditation decision 2007, CARF released the uSPEQ® (pronounced you speak;
and a written survey report approximately 6–8 weeks after http://www.uspeq.org/) Consumer Experience Survey, fol-
the survey. Organizations have 90 days after notification lowed by the uSPEQ Employee Climate Survey. Both survey
of an accreditation award to fulfill an accreditation condi- tools are designed to assist organizations with their well-
tion by submitting to CARF a Quality Improvement Plan being and performance improvement. CARF launched its
(QIP) outlining actions that have been or will be imple- extranet Customer Connect (http://customerconnect.carf.
mented in response to the recommendations made in the org) for accredited organizations and those seeking accred-
survey report. CARF maintains communication with itation to manage their individual contact information,
organizations throughout the tenure of accreditation. view up-to-date information about their organization’s
CARF has published numerous standard manuals surveys, and access information about the accreditation
which have identified program evaluation standards, result- process. Most recently in 2008, CARF’s ASPIRE to Excel-
ing in improved services and programs provided to clients lence™ quality framework has been implemented in all
receiving rehabilitation services. The first publication of a standards manuals. This framework provides a logical,
new section of standards manuals for Rehabilitation Facil- action-oriented approach to ensure that organizational
ities in November 1973 became a springboard for future purpose, planning, and activity result in desired outcomes.
CARF contributions to program evaluation. In January Each year, CARF sponsors numerous in-person and
1986, standards for two new program areas (Respite Pro- web-based seminars to help providers maintain confor-
grams and Alcoholism and Drug Abuse Treatment Pro- mance to the CARF standards. The in-person seminars are
grams) were published in the 1986 Standards Manual for held in cities across the United States, Canada, and Europe.
Organizations Serving People with Disabilities. The 1988
Standards Manual for Organizations Serving People with
Disabilities included new standards in areas of Post-Acute Cross References
Brain Injury Programs and Community Mental Health
Programs. CARF published a separate volume of its 1995 ▶ Americans with Disabilities Act of 1990
Standards Manual and Interpretive Guidelines for each of ▶ Individuals with Disabilities Education Act
650 C Commissural Fibers

▶ National Center for the Dissemination of Disability Definition

Research
▶ National Dissemination Center for Children with The right and left cerebral hemispheres are connected
Disabilities by three tracts of nerve fibers or axons, which are collec-
▶ National Institute on Disability and Rehabilitation tively referred to as commissures, cerebral. These trans-
Research verse, nerve fiber bundles connect to the homologous
▶ National Institute of Neurological Disorders and Stroke regions of each hemisphere and are known as the corpus
▶ National Rehabilitation Information Center callosum, the anterior commissure and the posterior
▶ No Child Left Behind Act of 2001 commissure. The corpus callosum, also referred to as
▶ Rehabilitation Counseling the great cerebral commissure, is the largest, and it
▶ Rehabilitation Psychology interconnects the greatest portion of the cerebral hemi-
▶ Section 504 of the Rehabilitation Act of 1973 spheres, permitting the cerebral cortex to operate as a
whole. The corpus callosum is often the site for commis-
surotomy, surgical bisection, to treat certain psychiatric
References and Readings disorders and epilepsy. The anterior commissure is a
smaller bundle of nerve fibers that interconnect parts
CARF accreditation (http://www.carf.org/Accreditation/Accreditation
of the temporal lobes. The posterior commissure is an-
Process/StepstoAccreditation/). other fiber bundle that crosses beneath the pineal gland
CARF IAC (http://www.carf.org/About/IAC/). to connect the midbrain regions of the cerebral
CARF mission (http://www.carf.org/About/Mission/). hemispheres.
CARF overview (http://www.carf.org/About/).
CARF partners (http://www.carf.org/Resources/IACResources/).
CARF structure (http://www.carf.org/About/WhoWeAre/).
Value of CARF Accreditation (http://www.carf.org/Accreditation/Valueof
Accreditation/).
Cross References
▶ Commissurotomy
▶ Corpus Callosum

Commissural Fibers
▶ Commissures, Cerebral
Commissurotomy
C HRISTINA K WASNICA
Barrow Neurological Institute
Commissural Magna Phoenix, AZ, USA

▶ Corpus Callosum
Synonyms

Split-brain
Commissures, Cerebral
M ARTIN R. G RAF Definition
Virginia Commonwealth University Medical Center
Richmond, VA, USA The term referring to the medical procedure in which
interconnecting fibers between the cerebral hemispheres
are lesioned. The anatomic location includes either
Synonyms or both anterior and posterior fibers. When posterior
fibers are resected, connections to the hippocampus may
Brain commissures; Commissural fibers also be affected.
 Community Integration Questionnaire C 651

Current Knowledge key social and interpersonal bonds (staying close and
connected with individuals who matter most in daily
The neurosurgical technique is based on the premise life). Thus, effective communication depends as much
that when stimuli enters the brain it is rapidly communi- on nonverbal behaviors such as facial expression, touch,
cated via the corpus callosum to the other hemisphere. In and vocal intonation as on the exchange of words. C
refractory epilepsy, severing the corpus callosum Acquired deficits to communication ability can occur in
may prevent the spread of electrical activity between hemi- the absence of a notable loss in intelligence or nonlinguistic
spheres and generalization of the seizure activity. This cognitive functions, as in aphasia, dysarthria, dysphonia/
procedure prevents the communication of the two hemi- aphonia, and apraxia of speech.
spheres thus resulting in a clinical scenario of a ‘‘split
brain.’’ Clinical disconnection syndromes in these patients
have been studied across a large number of neurocognitive
Cross References
tasks. These surgical lesions have allowed for the study of
▶ Language
sensory perceptual processes and lateralization. Deficits
▶ Speech
have been seen in the area of perception, attention, memo-
ry, language, and reasoning. In studies of these patients, it
has become clear that the left hemisphere has limitations in
perceptual functions while the right hemisphere has more Communication Disorders
striking limitations in cognitive functions. The split brain
studies have also led to theories of consciousness and a ▶ Speech/Communication Disabilities
neurocognitive framework for the human experience.

References and Readings Community Adjustment

▶ Community Re-entry
Bogen, J. E., Fisher, E. D., & Vogel, P. J. (1965). Cerebral commissurot-
omy: A second case report. JAMA, 194, 1328–1329.
Gazzaniga, M. S. (2000). Cerebral specialization and interhemispheric
communication: Does the corpus callosum enable the human con-
dition? Brain, 123, 1293–1313.
Community Integration
▶ Community Re-entry

Communicating Artery
Community Integration
▶ Anterior Communicating Artery
Questionnaire
M ARCEL D IJKERS
Communication Ability Mount Sinai School of Medicine
New York, NY, USA
J ON G. LYON
Mazomanie, WI, USA
Synonyms
Definition CIQ

Commonly refers to the ease, efficiency, and accuracy of

the exchange of information or content between parties Description
regardless of form, i.e., spoken, written, gestured, drawn,
or using augmentative and assistive devices (communi- The Community Integration Questionnaire (CIQ) mea-
cation boards or computers). Human communication sures what the International Classification of Disability,
relies primarily on the preservation and maintenance of Functioning and Health (ICF) currently designates as
652 C Community Integration Questionnaire

Participation. The CIQ consists of 15 items relevant to resulting instrument, sometimes designated the CIQ-R,
home integration (H) (living), social integration (S) dropped one item and reassigned two to different sub-
(loving), and productive activities (P) (working). It is scales (Sander et al., 1999). The CIQ-R has been used
scored to provide subtotals for each of these domains, as infrequently. In 2002, The TBIMS dropped the CIQ, and
well as a total community integration score. The basis for replaced it (in 2007) with the Participation Assessment
scoring is primarily frequency of performing activities or with Recombined Tools (PART).
roles, with secondary weight given to whether or not
activities are done jointly with others and the nature
of these other persons (for example, with/without dis- Psychometric Data
ability). The CIQ can be completed by either the index
person or a proxy in 10–15 min. The optimal method Psychometric information for the CIQ is spread out over
of data collection is an in-person interview, but a number of sources. In addition to the three papers by
telephone interviewing is quite common, and the Trau- Willer et al. (Willer, Linn, et al., 1994; Willer, Ottenbacher,
matic Brain Injury Model Systems (TBIMS) have also et al., 1994; Willer, Rosenthal, et al., 1993) key texts
utilized self-administered CIQs. No formal training are those by Corrigan and Deming (1995), Sander et al.
and credentialing process for the administration of the (1999); Sander et al. (1997) and Tepper, Beatty and
CIQ exists. DeJong (1996). Dijkers critically summarized psychomet-
ric information available through 1997 (Dijkers, 1997),
and some later sources are given in Reistetter and Abreu’s
Historical Background 2005 article (Reistetter and Abreu, 2005).
Reliability. Results of reliability studies have been
The CIQ was developed in the early 1990s by Barry Willer, mixed. Based on the (Pearson) correlations reported in
Ph.D. and a group of professionals and consumers to the earliest study, the interrater reliability of the CIQ
provide a measure of community integration after trau- appears to be in the ‘‘acceptable’’ range. However, the
matic brain injury (TBI) that could be used in the TBIMS intraclass correlation coefficient (ICC), a more appropri-
research program (Willer, Linn, & Allen, 1994; Willer, ate measure, resulted in much lower numbers, according
Ottenbacher, & Coad, 1994; Willer, Rosenthal, Kreutzer, to a later investigation, especially for the Home (H)
Gordon, & Rempel, 1993). They used the following design dimension. More recent research also suggests that in
criteria: brevity; suitable for use in in-person or telephone home integration there is the greatest discrepancy
interviews with the person with TBI or a proxy; focus on between reports by subjects with TBI and those by their
behaviors rather than feeling states; no biases resulting proxies. In the latter study, the person with TBI tended
from age, gender, or socioeconomic status; sensitive to a to report higher values than the proxy for all three
wide variety of living situations; and value neutral. The components. Subscale ICCs ranged from 0.43 (H) to
instrument has been translated (not always using formal 0.81 (P) – fairly low values.
backtranslation methods) into French, Spanish, Japanese, For the CIQ total score, three out of four studies have
Korean, Dutch, Swedish, and Norwegian, among others. reported internal consistency levels that exceed the
It is the most extensively used measure of community criterion of a coefficient alpha above 0.80. However, the
integration/ participation in research on TBI, but has corresponding values for the S and P dimensions
also been applied in investigations of other types of are much lower, especially for the latter – quite likely
brain injury (including stroke and brain tumors), spinal due to the fact that alpha is based on only two variables,
cord injury, burns, trauma in general, ‘‘mobility disabil- which are very dissimilar from one another: work/study/
ities’’, and post-polio syndrome. The most common appli- volunteering, and travel.
cations are in program evaluation and the study of the Distribution issues. Corrigan and Deming noted
natural history of TBI and other impairments, but the negatively skewed distributions for the premorbid data
CIQ has also been used in clinical trials of interventions to for CIQ total, positive skews for H for all four samples,
improve post-injury functioning, and in construct valida- negative skews for all samples for the S dimension, and
tion studies of newly proposed participation measures. negative skew for P for the TBI-premorbid sample, but
Because the assignment of items to subscales by Willer positive skew for the three others. Various kurtosis pro-
et al. was based on a correlation matrix calculated for a blems were also noted. They recommended that the P
small sample, Sander et al. performed a factor analysis subscale not be used independently from its contribution
involving all CIQ items for a much larger sample. The to the CIQ total score. Distribution problems were also
 Community Integration Questionnaire C 653

noted by Willer et al. and Sander et al., among others. use of the CIQ is freely given but should be requested, by
Unless these can be resolved through transformations, contacting him at the Center for Research on Community
nonparametric statistics need to be used in order to deal Integration at the Ontario Brain Injury Association,
with the nonnormal distributions. 3550 Schmon Parkway, Thorold, Ont L2V 4Y6, Canada,
Validity. No formal content or face validity studies of email: willer@vaxxine.com C
the CIQ have been done, but it was developed utilizing
a panel consisting of both consumers and professionals
with expertise in TBI outcome studies. Cross References
CIQ subscales and total score have been found to
correlate with subscales and total score on CHART ▶ CHART Short Form
(another measure of community integration), impairment ▶ Community Re-entry
and disability, time since injury, CIM (a measure of subjec- ▶ Craig Handicap Assessment and Report Technique
tive community integration), and subjective quality of life, ▶ Frenchay Activity Index
according to multiple reports. Most researchers find ▶ Glasgow Outcome Scale
negative correlations between CIQ and its subtotals (except ▶ Glasgow Outcome Scale – Extended
sometimes H) and age. Females tend to have higher CIQ ▶ Impact on Participation and Autonomy Questionnaire
scores for total, H and S than males, but lower P scores. ▶ Instrumental Activities of Daily Living (I-ADL)
Sensitivity. The available research shows that the CIQ ▶ Lawton–Brody IADL scale
can validly distinguish between persons with TBI and ▶ LIFE-H
nondisabled people. Persons with TBI are less integrated ▶ Outcome, Outcome Measurement
along all dimensions than nondisabled comparison ▶ Participation Measure for Post Acute Care (PM-PAC)
groups in most research. In one study, CIQ scores distin- ▶ Participation Objective – Participation Subjective
guished between three groups of persons with TBI living ▶ Reintegration to Normal Living Index
in settings differentiated by supervision/support level: ▶ Social and Occupational Functioning Scales (SOFAS)
independent in the community, in the community with ▶ Traumatic Brain Injury Model System
some (natural) support, and in an institution such as a
nursing home, rehabilitation facility, etc. Willer et al.
reported gain in CIQ (sub)scores for people with TBI References and Readings
receiving residential rehabilitation services between the
second and third anniversary of injury, while a control Corrigan, J. D., & Deming, R. (1995). Psychometric characteristics of the
group who received no or minimal home-based services community integration questionnaire: Replication and extension.
did not show a gain. Corrigan et al. found trends toward Journal of Head Trauma Rehabilitation, 10, 41–53.
Dijkers, M. (1997). Measuring the long-term outcomes of traumatic
improvement in all three subscales and total score in a
brain injury: A review of the community integration questionnaire.
cross-sectional study covering injury anniversaries one Journal of Head Trauma Rehabilitation, 12, 74–91.
through four. However, in another investigation, a very Reistetter, T. A., & Abreu, B. C. (2005). Appraising evidence on
small increase from the first to the second anniversary of community integration following brain injury: A systematic review.
injury was reported for a group that in large majority did Occupational Therapy International, 12, 196–217.
Sander, A. M., Seel, R. T., Kreutzer, J. S., Hall, K. M., High, W. M., Jr., &
not receive rehabilitation services any longer.
Rosenthal, M. (1997). Agreement between persons with traumatic
brain injury and their relatives regarding psychosocial outcome
using the community integration questionnaire. American Journal
Clinical Uses of Physical Medicine and Rehabilitation, 78, 353–357.
Sander, A. M., Fuchs, K. L., High, W. M., Jr., Hall, K. M., Kreutzer, J. S., &
In several TBI community integration programs, the CIQ Rosenthal, M. (1999). The community integration questionnaire
revisited: An assessment of factor structure and validity.
is used to monitor patients’ progress. However, due to the
American Journal of Physical Medicine and Rehabilitation, 80,
lack of norms and the dependence of community 1303–1308.
functioning on the environment, the clinical applicability Tepper, S., Beatty, P., & DeJong, G. (1996). Outcomes in traumatic brain
of the CIQ is very much limited. injury: Self-report versus report of significant others. Brain Injury,
10, 575–581.
Willer, B., Linn, R., & Allen, K. (1994). Community integration
Note and barriers to integration for individuals with brain injury. In
Barry Willer Ph.D., who was the principal investigator in M. A. J. Finlayson & S. H. Garner (Eds.). Brain injury rehabilitation:
developing the CIQ, holds the copyright. Permission for clinical considerations. Baltimore: Williams and Wilkins.
654 C Community Re-entry

Willer, B., Ottenbacher, K. J., & Coad, M. L. (1994). The community Cross References
integration questionnaire. A comparative examination. American
Journal of Physical Medicine and Rehabilitation, 73, 103–111.
Willer, B., Rosenthal, M., Kreutzer, J. S., Gordon, W. A., & Rempel, R.
▶ Quality of Life
(1993). Assessment of community integration following rehabili-
tation for traumatic brain injury. Journal of Head Trauma
Rehabilitation, 8, 75–87. References and Readings

Americans with Disabilities Amendments Act of 2008, Pub. L. No. 110–

325, 122 Stat. 3553 (2008).
Huey, K. (1980). Patient re-entry into the community. Hospital and
Community Re-entry Community Psychiatry, 31, 51–56.
Liberman, R. P., & Silbert, K. (2005). Community re-entry: Develop-
ment of life skills. Psychiatry: Interpersonal and Biological Processes,
A LLEN N. L EWIS J R ., PAMELA H. L EWIS 68(3), 220–229.
Virginia Commonwealth University McColl, M. A., Carlson, P., Johnston, J., Minnes, P., Shue, K., Davies, D.,
Richmond, VA, USA et al. (1998). The definition of community integration: Perspectives
of people with brain injuries. Brain Injury, 12(1), 15–30.
National Institute on Disability and Rehabilitation Research. (2006).
Long-range plan for fiscal years 2005 through 2009.
Synonyms President’s New Freedom Commission Report on Mental Health (2003).
Achieving the promise: Transforming mental health care in America.
Community adjustment; Community integration Substance abuse and mental health services administration of the
U.S. Department of Health and Human Services.

Definition

Community re-entry is the extent that an individual who

is initially unable to fully function in the community due Community-Based Rehabilitation
to disability is eventually returned to the community to
work and live independently, using natural supports and A LLEN N. L EWIS J R ., PAMELA H. L EWIS
exercising full access, choice, autonomy, and striving for Virginia Commonwealth University
actualization. Actualization is the degree to which there is Richmond, Virginia
the achievement of a respectable quality of life.
The Americans with Disabilities Act (ADA) of 1990
attempted to legislate community integration by remov- Synonyms
ing physical barriers related to access and making it illegal
to discriminate on the basis of disability. However, In vivo services; Milieu-based services; Outpatient
30 years since the ADA’s passage and after the recent rehabilitation
passage of the ADA Restoration Act in late 2008, there is
still significant concern that United States society does
not fully possess nor embrace the attitudes and values Definition
commensurate with full inclusion and community
integration for individuals with disabilities. The provision of restorative or rehabilitative services
Community re-entry programs teach skills necessary targeted toward the amelioration of a disability (disability:
along a continuum of services that afford persons the any illness, condition, or impairment [congenital or
opportunity to learn behaviors needed to live full lives acquired] that interferes with functioning in a major life
with a disability. Such programs provide services and domain) and/or the mitigation of functional limitations
supports to enable the successful transition of an individ- resultant from a disability to the maximum extent possible
ual with a disability from facility-based services to a viable in a non-acute care, non-facility-based service setting.
community placement. Community-based rehabilitation services attempt to
maximize the individual’s ability to function ‘‘in vivo’’
Note within major life pursuits such as independent daily living
The authors are not related by blood or marriage. and work.
 Compartmentalization C 655

Community-based rehabilitation attempts to en- into well-perfused organs. Muscle, fat, and bone are
hance the quality of life for individuals with disabilities saturated last. These tissues can serve as storage depots
and their families. This includes meeting basic needs, for substances, contributing to the half-life of a drug and
but also going beyond to promote inclusion and partici- potentially to interaction effects days or weeks after a drug
pation. Community-based rehabilitation typically has been discontinued. C
involves several domains of functioning such as health, The body may be inappropriately be treated as a single
education, work, socialization, and one’s sense of entity or compartment. In a single-compartment model,
empowerment. Reaching a point of social acceptance in drugs are theoretically presumed to diffuse through tis-
the 1970s and 1980s, the original mission of community- sues and the differences in absorption and retention of a
based rehabilitation was to offer individuals with dis- drug are not treated as significant. This single-compart-
abilities access to programming and supports in their ment model is sufficient in many situations, but is less
own home communities using local resources. Further, useful when drugs may be preferentially retained in one
community-based rehabilitation ostensibly attempts to type of tissue. Dosage predictions fail if they do not
optimize the provision of rehabilitative services, equal- account for the gradual ambient leaching of the drug
ize opportunity, reduce poverty, and promote full social from fat or bone into general circulation.
inclusion. The instances in which a multi-compartment model
is most relevant are for individuals who are medically ill,
have unusually high or low body fat, are pregnant, have
an abnormality in pH or illnesses which impact the liver
References and Readings or kidneys (and thus profoundly alter the pharmacoki-
netics of drug metabolism). Differences in the propor-
Church, J., Saunders, D., Wanke, M., & Pong, R. (1995). Organizational
models in community based health care: A review of the literature.
tion of fatty tissue can influence dosing decisions since
Health Promotion and Programs Branch,Ottawa: Health Canada. mg/kg may be less appropriate for drugs that are less fat-
World Health Organization, (2004). CBR: A strategy for rehabilitation, soluble. One common example of this reduced alcohol
equalization of opportunities, poverty reduction and social inclu- tolerance in women since fatty tissues do not readily
sion of people with disabilities: Joint position paper/International
absorb alcohol.
Labour Organization, United Nations Educational, Scientific and
Cultural Organization and the World Health Organization.
Another form of compartmentalization is ion
trapping, in which the pH alters the ease with which a
drug is transferred into or out of a particular tissue. For
example, neonatal blood is typically more acidic than
adult blood, making it more difficult for slightly alkaline
drugs to diffuse back into maternal circulation. Similarly,
Comorbid the GI tract is more acidic than blood plasma. Weakly
acidic drugs diffuse more readily to blood than weakly
▶ Dual Diagnosis alkaline drugs.

Cross References
▶ pH
Compartmentalization ▶ Pharmacokinetics
N ADIA W EBB
Children’s Hospital of New Orleans
New Orleans, LA, USA References and Readings
Brunton, L. B., Lazo, J. S., & Parker, K. L. (Eds.). (2005). Goodman &
Definition Gilman’s the pharmacological basis of therapeutics (11th ed.).
New York: McGraw Hill.
Stahl, S. M. (2008). Stahl’s essential psychopharmacology: Neuroscientific
Drugs do not saturate tissues within the body at the same basis and practical applications. New York: Cambridge University
rate. They are quickly absorbed into blood plasma and Press.
656 C Compensation Neurosis

Compensation Neurosis Compensatory Education

Approach
B ETH K UCZYNSKI 1, S TEPHANIE A. KOLAKOWSKY-H AYNER 2
1
University of California J ILL S NYDER
Davis, CA, USA University of Northern Colorado
2
Santa Clara Valley Medical Center, Greeley, CO, USA
Rehabilitation Research Center
San Jose, CA, USA
Definition
Synonyms Compensatory educational approaches require teachers
to present material in a different format, providing
Accident neurosis students an alternative way to master a particular concept
and demonstrate knowledge.

Definition
Current Knowledge
Compensation neurosis is a condition in which
symptoms are associated with a real or presumed dis- The goal of education is to help students acquire skills and
ability (possibly exaggerated) that may bring financial master concepts that will be useful in daily living.
compensation. This type of neurosis is believed to be Generally, two approaches are used when instruction
motivated by the desire for, and hope of, monetary or fails to help students learn. These include compensatory
interpersonal gain. Many factors are involved in com- education approaches and/or remedial education
pensation neurosis, such as the psychological factors approaches (▶ Remedial Education Approach). Compen-
before and after the presumed injury, the additional satory educational approaches require teachers to present
effects on the quality of life, and the possible influences material in a different format, providing students an
of legal or insurance processes. The term is often used alternative way to master a particular concept and dem-
in litigation and seems to be quite controversial in onstrate knowledge. They are used when students lack the
psychiatry. ability to acquire a certain skill or concept. For example, a
deaf student who is unable to speak may be taught sign
language as an alternate form of communication; or, a
student with a math calculation disability may be taught
Cross References to use a calculator. When students fail to make progress in
a certain skill area, evidence-based strategies and methods
▶ Fake Bad Scale must be employed to help the student attain expected
▶ Malingering learning outcomes. In these cases, education must be
adjusted by offering different activities that facilitate the
same results. This approach in isolation does not repre-
sent best practice, and in keeping with the educational
and neuro-developmental literature, practitioners should
References and Readings offer both remedial and compensatory approaches,
depending on students’ specific academic needs. Educa-
Brown, J. T. (October 1996). Compensation neurosis rides again: tors must be careful to distinguish between the education-
A practitioner’s guide to defending PTSD claims
al content in which a student struggles (e.g., reading or
(post traumatic stress disorder). Defense Counsel Journal, 63(4),
467–482.
math), and the method in which a particular concept may
Rogers, R. (2008). Clinical assessment of malingering and deception (3rd be successfully integrated. Offering a compensatory ap-
Ed.). New York: Guilford Press. proach should be a last resort on the educational
 Compensatory Strategies C 657

continuum, and should be supported by a comprehensive Examples of behavioral strategies would include repeating
neuro-psychological evaluation. phrases during social interactions to ensure accurate pro-
cessing of conversation, or associating words with images
to enhance recall.
Cross References C
▶ Academic Competency
Current Knowledge
▶ Academic Skills
▶ Compensatory Education Approach
Compensatory strategies have shown efficacy in rando-
▶ Remedial Education Approach
mized, controlled studies for improving the ability to
▶ Strength-Based Education Approach
remember to complete activities in the future (prospective
memory) in neurologically impaired people with cogni-
tive difficulties. For example, Wilson, Emslie, Quirk, and
References and Readings Evans (2001) used an external pager in 143 people be-
tween 8 and 83 with a range of neurological illnesses or
D’Amato, R. C., & Rothlisberg, B. A. (1996). How education should trauma. Results revealed that more than 80% of clients
respond to students with traumatic brain injury. Journal of Learning
improved in carrying out self-care activities and meeting
Disabilities, 29(6), 670–683.
D’Amato, R. C., Rothlisberg, B. A., & Work, P. L. H. (1999). Neuropsy-
appointments, as well as other life skills, relative to the
chological assessment for intervention. In C. R. Reynolds, & T. B. baseline period, and effects were maintained seven weeks
Gutkin (Eds.), The handbook of school psychology (pp. 452–475). after return of the pager. Environmental modifications,
New York: Wiley. including use of signs, removal of distracting environ-
Gaddes, W. H., & Edgell, D. (1994). Learning disabilities and brain
mental stimuli, and checklists have been used effectively
function: A neuropsychological approach (3rd ed.). New York:
Springer.
in randomized, controlled trials to enhance adaptive func-
tioning and quality of life in people with severe psychiatric
illnesses as well (Velligan, Prihoda, Ritch, Maples, Bow-
Thomas, & Dassori, 2002).

Compensatory Strategies
M ATTHEW M. K URTZ Cross References
Wesleyan University
Middletown, CT, USA ▶ Cognitive Rehabilitation
▶ Environmental Modifications
▶ Mnemonic Techniques
Definition ▶ Neuropsychological Rehabilitation
▶ Prosthetic Memory Aids
Compensatory strategies are environmental modifica-
tions or behavioral strategies designed to bypass persistent
impairment in attention, memory, executive-function,
References and Readings
and/or other cognitive skills as a means to achieve desired
rehabilitation goals. Environmental modifications could
Velligan, D. I., Prihoda, T. J., Ritch, J. L., Maples, N., Bow-Thomas, C., &
include the use of external aids or modifying the setting in Dassori, A. (2002). A randomized, single-blind pilot study of com-
which activities take place. The use of an alphanumeric pensatory strategies in schizophrenia outpatients. Schizophrenia Bul-
pager and a checklist for a person with memory and letin, 28, 283–292.
executive-function deficits to ensure completion of daily Wilson, B. A. (2008). Neuropsychological rehabilitation. Annual Review
of Clinical Psychology, 4, 141–162.
tasks at specific times would be an example of external
Wilson, B. A., Emslie, H. C., Quirk, K., & Evans, J. J. (2001). Reducing
aids. Working in a distraction-free room to enhance con- everyday memory and planning problems by means of a paging
centration skills in a person with symptoms of disinhibi- system: a randomised control crossover study. Journal of Neurology,
tion would be an example of modifying an environment. Neurosurgery and Psychiatry, 70, 477–482.
658 C Competence to Testify

financial affairs, execute a will, drive, manage medica-

Competence to Testify tions, live independently, and handle even the most
basic activities of daily life (ADLs).
▶ Jenkins v. U.S. (1962) In the criminal realm, competency relates to a defen-
dant’s current ability to understand and partake in legal
proceedings. The Dusky standard states that: ‘‘The test
must be whether he (the defendant) has sufficient present
ability to consult with his lawyer with a reasonable degree
Competency of rational understanding – and whether he has a rational
as well as factual understanding of the proceedings against
M OIRA C. D UX him.’’ (p. 402). The Dusky standard outlines the minimal
University of Maryland Medical Center/Baltimore VA level of competency necessary in accordance with the U.S.
Baltimore, MD, USA Constitution for all criminal jurisdictions. Grisso (1988)
outlined five areas of analysis suggested for psychologists/
neuropsychologists conducting competency evaluations:
Synonyms (1) functional description of specific abilities, (2) causal
explanations for deficits in competency abilities, (3) in-
Capacity teractive significance of deficits in competency ability,
(4) conclusory opinions about legal competency and
incompetency, and (5) prescriptive remediation for defi-
Definition cits in competency abilities. In an attempt to operationa-
lize the Dusky ruling, the Group for the Advancement of
Competency is a legal determination to be made by a legal Psychiatry (1974) developed a 21-point list of abilities
professional (i.e., judge). It relates to a person’s capacity derived from competency assessment instruments avail-
(a clinical status as judged by a health care professional) to able at the time and included items such as: understand
make determinations/decisions or to perform certain current legal situation, understand legal defenses available
functions. In a legal context, competency typically relates in the defendant’s behalf, tolerate stress at the trial and
to one’s understanding of issues related to involvement while awaiting trial, and protect self by using available
in a legal proceeding (Reisner & Slobogin, 1990). Such an legal safeguards. As a result of Wieter v. Settle (1961), the
understanding necessitates some degree of acknowledg- U.S. District Court outlined several minimal ability
ment regarding the nature of the procedure, the risks requirements for criminal competency including (but
involved, success estimates, possible alternative options/ not limited to): mental capacity to appreciate his or her
approaches, and the pros and cons of specific courses of presence in relation to time, place, and thing; apprehends
action. Issues related to competency can be raised at any that there is a judge on the bench; apprehends that there
time during the criminal judicial process. Specific compe- is, or will be, a jury present to pass on evidence adduced as
tencies in the criminal realm include: competence to to his or her guilt or innocence of such charge; he or she
confess (or waive rights at pretrial investigations), com- has memory sufficient to relate those things in his or her
petency to plead guilty, competency to waive right to own personal manner.
counsel, competency to stand trial, competency to be Currently, there are a number of instruments designed
sentenced, competency to waive further appeal (when to assess competency (primarily in the criminal realm),
facing capital punishment), and competency to be exe- which are referred to as competency assessment tools
cuted. Competency evaluations are the most common (CATs). Examples include: the Competency Assessment
referral of mental health professional in criminal foren- Inventory-Revised, the Fitness Interview Test-Revised, the
sics. A defendant’s competency can be questioned by Georgia Court Competency Test, the Competency Assess-
attorneys and judges. In the civil realm, impairment of ment for Standing Trial for Defendants With Mental
competency, or decision-making capacity, is often a con- Retardation, and the MacArthur Competency Assessment
sequence of various types of dementias and other organic Tool-Criminal Adjudication. It is important to note
brain syndromes. Impairments in memory, judgment, that none of the aforementioned CATs have been vali-
reasoning, and planning can affect a person’s capacity dated with brain-injured or neurological populations.
to: make medical decisions, consent to research, manage Marson and colleagues (cf. Marson & Hebert, 2005)
 Complex Partial Seizure C 659

have developed instruments to assess consent capacity in Definition

older adults.
Formerly known as ‘‘psychomotor seizures,’’ complex par-
tial seizures (CPS) are defined by the International League
Cross References Against Epilepsy as focal seizures with impaired con- C
sciousness as the central feature.
▶ Financial Capacity A CPS may begin with a simple partial seizure, also
referred to as an aura. This commonly consists of feelings
References and Readings of emotional, ideational, or sensory changes. Once con-
sciousness becomes impaired, individuals with CPS may
Denney, R. L., (2005). Criminal forensic neuropsychology and assessment experience automatisms, which are often characterized as
of competency. In G. Larrabee (Ed.), Forensic neuropsychology: repetitive, semi-purposeful involuntary movements.
A scientific approach. New York: Oxford University Press. These may be oropharyngeal (e.g., lip smacking), emo-
Dusky v. United States, 362 U.S. 402 (1960).
tional (e.g., fear), gestural (e.g., picking), ambulatory (e.
Grisso, T. (1988). Competency to stand trial evaluations: A manual for
practice. Sarasota, FL: Professional Resource Exchange.
g., walking), or verbal in nature. In some cases, focal CPS
Group for the Advancement of Psychiatry (1974). Misuse of psychiatry in secondarily progresses into a generalized event (i.e.,
the criminal courts: Competency to stand trial. New York: Commit- tonic–clonic seizure). The specific paroxysmal behavior
tee on Psychiatry and Law. changes correspond to the seizure focus and the progres-
Marson, D. C., & Hebert, K. (2005). Assessing civil competencies in older
sion represents the spread of epileptiform activity. Indi-
adults with dementia: Consent capacity, financial capacity, and tes-
tamentary capacity. In G. Larrabee (Ed.), Forensic neuropsychology: A
viduals with CPS often experience brief postictal
scientific approach. New York: Oxford University Press. confusion and are usually amnestic for their ictal
Reisner, R., & Slobogin, B. (1990). Law and the mental health system behavior.
(2nd ed.). St. Paul, MN: West.
Wieter v. Settle (1961). 193 F. Supp. 318 (W.D. Mo., 1961).

Current Knowledge

Epidemiologically, CPS comprises an estimated 42% of all

Competency to Proceed partial seizures and 20% of all epilepsies. Approximately
60–80% of CPS arise from the temporal lobe, particularly
▶ Legal Competency the neocortex and inferomedial (limbic) structures. While
commonly equated with temporal lobe seizures, it is now
known that forms of CPS can originate from other brain
regions, most notably the frontal lobes. A diagnosis of
Complex Figure Test (CFT) CPS can be identified through a neurological history and
description of the events. However, the electroencephalo-
▶ Rey Complex Figure Test
gram (EEG) remains the ‘‘gold standard’’ for diagnosis.
Patients with CPS often exhibit abnormal discharges on
interictal recordings and a characteristic pattern of onset
and spread of activity when seizures are recorded. CPS is
Complex Partial Seizure most commonly treated with antiepileptic drugs. Surgical
intervention for intractable CPS has been increasingly
W ILLIAM B. B ARR , H EIDI A. B ENDER pursued in recent years. Successful outcomes are most
NYU Comprehensive Epilepsy Center often achieved following temporal lobectomy or lesion
EPC resection in CPS patients with underlying mesial tempo-
New York, USA ral sclerosis.

Synonyms Cross References

Partial epilepsy; Psychomotor seizures; Temporal lobe ▶ Aura
seizure ▶ Generalized Tonic-Clonic Seizures
660 C Complex Partial Seizures with Automatisms

▶ Temporal Lobe
▶ Temporal Lobe Epilepsy Computed Tomography
R OBIN S EKERAK
Waikato District Health Board
References and Readings Hamilton, New Zealand

Browne, T. R., & Feldman, R. G. (Eds.). (1983). Epilepsy: Diagnosis and

management (p. 39). Boston, MA: Little, Brown, & Company. Synonyms
Kotagal, P., & Loddenkemper, T. (2005). Focal seizures with impaired
consciousness. In E. Wyllie, A. Gupta, & D. K. Lachwani (Eds.), The
treatment of epilepsy: Principles & practice (4th ed., pp. 441–442).
CAT Scan; Computerized axial tomography; CT
Philadelphia, PA. Lippincott Williams & Wilkins.
Lee, G. P., & Clason, C. L. (2008). Classification of seizure disorders
and syndromes, and neuropsychological impairment in adults
with epilepsy. In J. E. Morgan, & J. H. Ricker (Eds.), Textbook of
Definition
clinical neuropsychology (pp. 439–440). United Kingdom: Taylor &
Francis. CT is an imaging modality that generates cross-sectional
Oxbury, J. M., & Duchowny, M. (2000). Diagnosis and classification. In images of the body with very good anatomical detail.
J. Oxbury, C. Polkey, & M. Duchowny (Eds.), Intractable focal This is accomplished by an X-ray tube rotating 360
epilepsy (pp. 15–16). London: W.B. Saunders.
around the body as it moves through the CT scanner.
During rotation a collimated (focused) X-ray beam is
transmitted through the body which is attenuated by
the tissues. The attenuated X-rays are sensed by an
array of detectors on the opposite side as they leave
Complex Partial Seizures with the body. The signal from the detectors is processed by
a computer to reconstruct a cross-sectional image.
Automatisms Images in axial (dividing the body into superior and
inferior sections), cornal (dividing the body into anteri-
▶ Psychomotor Epilepsy
or and posterior sections), and sagittal (dividing
the body into left and right) planes, as well as 3D,
can be reconstructed the data accquired. Images in the
axial (dividing the body into inferior and superior seg-
ments), sogittal (dividing the body into left and right
Comprehensive Driving segments), and coronal (dividing the body into anterior
Assessment and posterior segments) planes, as well as 3D images,
can be reconstructed from the data accquired. The
▶ Driving Assessment image is stored electronically and displayed on the com-
puter screen. Hard copies of the image can be photo-
graphed onto film. The image is made up of a matrix of
2D cells called pixels, similar to a digital camera. The
pixels are 2D representations of 3D volumes of tissue
called voxels.
Comprehensive System (CS) Different scanning geometries can be obtained includ-
ing helical (or spiral) and multi-slice acquisition. In heli-
▶ Rorschach cal scanning contiguous slices are obtained with
simultaneous continuous X-ray tube rotation and patient
movement. Multiple rings of detectors can be activated by
single rotation of the X-ray tube enabling multiple slices
to be obtained. CT images are produced so that you view
Compulsory Self-Incrimination the films as if looking toward the patient’s feet with the
patient lying on their back; therefore, the right side of the
▶ Self-Incrimination body is to one’s left and vice-versa.
 Computer-Aided Assessment C 661

The density of tissues (the attenuation coefficient) is Current Knowledge

expressed in Hounsfield units. All tissues are measured
relative to the density of water which is set at 0. Less dense Advantages of CT
materials, such as air, appear black; more dense materials,
 Excellent anatomical detail
such as bone, appear white. Tissue densities in between C
 Rapid imaging time
appear as various shades of gray.
 Less expensive than MRI
 Less movement artifact than MRI
Disadvantages of CT:
CT in Identifying Neurologic Disorders
 Relatively high dose of radiation
 Bony areas can cause artifact, limiting use in the
Traumatic brain injury: CT is useful in moderate to severe
posterior fossa, spine, bone/parenchyma interface,
acute head trauma. It can accurately diagnose hemor-
and pelvis
rhage, pneumocephalus, foreign bodies, and fractures
 Metallic objects also cause artifact if not MRI
(C1-C3 should be included, as upper cervical spine frac-
compatible
ture is associated with 10% of severe head injuries). Sec-
 Not good at allowing relative dating and evolution of
ondary effects of trauma such as edema and cerebral
intraparenchymal hemorrhage
herniation are easily detected by CT. MRI may show
subtle vascular dissections, diffuse axonal injuries and
infarctions not initially evident on CT, as well as, evolu-
tion of hemorrhages that allows better dating of injuries
than CT. Cross References
Hemorrhage/stroke: Non-contrast CT is the preferred
investigative modality for presentation of acute stroke, in ▶ Angiography, Cerebral
order to rule out a bleed. CT has a higher sensitivity than ▶ Magnetic Resonance Imaging
spin-echo MRI for detecting acute hemorrhage. MRI can ▶ Neuroimaging
detect site and volume of acute infarct. Some literature
suggests that a T2-weighted MRI has the same sensitivity
References and Readings
for acute hemorrhage as CT. However, rapid imaging,
less motion artifact, availability, cost, and compatibility
Bushberg, J. T., Seibert, J. A., Leidholdt, E. M., Jr., & Boone, J. M. (2001).
with ferromagnetic metals (pacemakers, foreign bodies), The essential physics of medical imaging (2nd ed., pp. 327–372).
maintain CT as the primary imaging modality in acute Baltimore, MD: Lippincott Williams & Wilkins.
stroke. Bushong, S. (2004). Radiologic science for technologists (pp. 422–457).
Gray/White matter differentiation and subtle lesions: Philadelphia: Elsevier Mosby.
Graham, D., & Cloke, P. (2003). Principles of radiological physics
CT may not be sensitive enough to detect lesions with
(pp. 384–385). Edinburg: Churchill Livingstone.
subtle contrast. MRI has better gray/white differentiation Howlett, D., & Ayers, A. (2004). The hands-on guide to imaging
and can detect subtle lesions within white matter. There- (pp. 12–13). Oxford: Blackwell Publishing.
fore, it is preferred for subtle lesions such as encephalitis, Novelline, R. (2004). Squire’s fundamentals of roentgenology (pp. 29–34).
hippocampal sclerosis, suspected intracranial tumors, Cambridge: President and Fellows of Harvard College.
Patel, P. (2005). Lecture notes: Radiology (2nd ed., pp. 8–9). Oxford:
multiple sclerosis, and acute ischemic stroke.
Blackwell Publishing.
Bony Detail: Bony pathology such as a fracture, mas- Slone, R. (2000). CT techniques and protocols. In R. M. Slone, A. J.
toiditis, or sinusitis is better imaged with CT than an Fisher, P. J. Pickhardt, F. R. Gutierrez, & D. M.Balfe (Eds.), Body CT:
MRI. However, since X-ray photons are preferentially A practical approach. New York, NY: McGraw-Hill.
absorbed by bone this can cause streaky bone artifact Wolbarst, A. B. (2000). Physics of radiology (2nd ed., p. 95). Madison, WI:
Medical Physics Publishing.
(called ‘‘cupping’’) when trying to view brain tissue at
the skull base. MRI is the preferred modality for brain-
stem lesions as there are fewer bony artifacts.
Hydrocephalus and Cerebral Atrophy: CSF containing
spaces are clearly shown on a CT and thus ventricular/ Computer-Aided Assessment
sulcal size, shape, and proportionality are easily
evaluated. ▶ Test Interpretations: Computer Based
662 C Computer-Based Test Interpretation

Historical Background
Computer-Based Test
Interpretation CARB was designed and published by Conder, Allen, and
Cox (1992) to provide a computerized tool for adminis-
▶ Test Interpretations: Computer Based tration of the forced-choice, digit recognition tasks that
were gaining popularity in assessment of effort during
neuropsychological testing. Hiscock and Hiscock (1989)
had described the use of forced-choice methods in detect-
Computerized Assessment of ing malingering, and Binder (1990) had also studied
Response Bias this method of assessing effort. The authors of CARB
elected to name the test with the phrase ‘‘response bias’’
DAVID R. C OX (as opposed to malingering or effort) to clarify that the
Chapel Hill, NC, USA test was not ‘‘diagnosing’’ malingering, but measuring a
bias in the response.
Several versions of CARB have been published and
Synonyms studied. The original version (Conder et al., 1992) utilized
three distinct trials of 37 items each. Each item includes
CARB presentation of a five digit number that is to be remem-
bered followed by a short delay during which the examin-
ee is to count silently backward from 20. The examinee
Description then selects the presented number from two choices – the
target and a foil. The groups of trials differ from one
The Computerized Assessment of Response Bias (CARB) another in that the delay between stimulus presentation
is a computer-based tool for evaluating effort. The CARB and forced-choice presentation increases from 3 to 6 and
is one of many measures characterized as symptom valid- 9 s, respectively. Initial studies of this version of CARB
ity tests (SVT), indices of response bias used to assess determined that performance at or below 89% correct
possible malingering, poor effort, or exaggeration of defi- falls more than two standard deviations below the sample
cit. The test is a computerized version of the digit recog- of individuals with documented brain injury (Conder
nition paradigm in a forced choice format, akin to the et al., 1992); performance below 90% was therefore
procedures described by Hiscock and Hiscock (1989) and deemed to be biased.
Binder (1990). Frequently, statistical determination of Subsequent versions of CARB include CARB-97
below chance performance (based on the binomial theo- (Allen, Conder, Green, & Cox, 1997) and another revi-
rem) has been used with tests such as these to identify sion referenced in Green and Iverson (2001). CARB-97
persons showing poor effort. This method requires an added auditory feedback to the original version such that
extremely low score to reach a statistically significant correct responses are followed by a pleasant tone and
level. However, as the CARB is an easy test, it allows the incorrect responses are followed by an unpleasant tone.
clinician to detect inadequate effort using above-chance The third revision shortened the delays between stimulus
cutoff scores (Millis, 2008). The test has been studied with presentation and forced choice presentation to 1.5, 2.5,
a wide variety of populations, including persons with and 3.5 s. Each CARB version has been utilized in pub-
head injury, chronic fatigue syndrome, musculoskeletal lished studies, although the original version may continue
injuries, pain disorders, and psychiatric or emotional dis- to be the most widely used (Larrabee, 2007).
turbances such as depression. Published studies have in-
cluded both adults and children. Administration time can
vary depending on the protocol used; however, it typically Psychometric Data
can be completed in no more than 10–15 min. CARB
performance results include percent correct for each As with many, if not most, symptom validity tests the
group of trials as well as the overall percent correct. Also nature of CARB – presentation of a relatively easy task
reported are the response latency for each item, average that may be perceived to be much more difficult than it
latency per group of trials, and overall, as well as other, actually is – leads to a distribution of scores that is highly
information. An interpretive summary can also be skewed toward the upper end. Individuals who put forth
provided, if desired. effort on the test get all, or nearly all, of the items correct.
 Computerized Assessment of Response Bias C 663

This appears to be true regardless of the presence or appropriate in any clinical population. The concept of
absence of brain injury or other cognitive deficits. CARB the binomial theorem and evaluation of performance
was originally validated on a small sample (8) of indivi- against chance levels is a useful and reasonably valid
duals who had documented severe brain injury. That measure. Clearly, however, there is support for the use of
group performed at 98.6% (SD = 3.6) correct (Conder CARB with cutoff scores at above-chance levels in assess- C
et al., 1992). Internal consistency across items is therefore ment of those groups of whom scientific studies have been
also quite high among individuals putting forth adequate published.
effort; biased responding with suboptimal effort is pre-
sumed, by the nature of the construct, to be more variable.
Individuals who perform at a ‘‘passing’’ level on CARB Cross References
yielded 96.6–97.6% accuracy across the blocks of trials,
whereas those who performed at a non-passing level ▶ Dissimulation
yielded accuracy scores ranging from 62.4 to 74.6% ▶ Effort
(Allen et al., 1997; Allen, Richards, Green, Iverson, & ▶ Forensic Neuropsychologist
Conder, 1998). An accuracy difference of 10% or more ▶ Forensic Neuropsychology
between any two blocks of the test correlates highly ▶ Forensic Psychology
with poor (non-passing) scores on CARB (Allen et al., ▶ Hiscock Forced-Choice Test
1997). Test–retest reliability (1-week interval) is quite ▶ Malingering
high (r = 0.97) (de Armas, 1996). ▶ Portland Digit Recognition Test
▶ Response Bias
▶ Rey 15-Item Test
Clinical Uses ▶ Symptom Validity Assessment
▶ Word Memory Test
Clinically, CARB is used to assess response bias and level
of effort and assist in the detection of symptom exaggera-
tion and/or malingering. Published studies have primarily References and Readings
involved populations of individuals alleging brain injury
Allen, L. M., Conder, R. L., Green, P., & Cox, D. R. (1997). CARB’ 97
via closed head trauma, although other diagnostic group-
manual for the computerized assessment of response bias. Durham:
ings have also been examined. These include chronic CogniSyst.
fatigue syndrome, fibromyalgia, stroke, chronic pain, Allen, L. M., Iverson, G. L., & Green, P. (2003). Computerized assessment
multiple sclerosis, brain aneurysm, and brain tumor of response bias in forensic neuropsychology. Journal of Forensic
(Allen, Iverson, & Green, 2003). Neuropsychology, 3(2), 205–225.
Allen, L. M., Richards, P. M., Green, W. P., Iverson, G. L., & Conder, R. L.
Additional studies have used samples of persons with
(1998). Performance patterns on the computerized assessment
brain injury, alleging brain injury, or with alleging other of response bias in 1752 compensation cases (Abstract). Archives of
disorders that may affect cognition. The variable of ‘‘seek- Clinical Neuropsychology, 13, 15–16.
ing versus not seeking compensation’’ as a result of an Binder, L. M. (1990). Malingering following minor head trauma. The
injury or condition is a significant one in the realm of Clinical Neuropsychologist, 4, 25–36.
Conder, R., Allen, L., & Cox, D. (1992). Manual for the computerized
assessing effort. Lending support to the notion that sec-
assessment of response bias. Durham: CogniSyst.
ondary gain can be a major factor in these cases. Gervais, de Armas, A. (1996). Detection of malingering in forensic psychological
Green, Allen, and Iverson (2001) reported that 100% of evaluations. The Forensic Examiner, July–August, 26–28.
the individuals with fibromyalgia and rheumatoid arthri- Flaro, L., Green, P., & Allen, L. M., III. (2000). Symptom validity test
tis who were not seeking compensation performed in a results with children: CARB and WMT. Archives of Clinical Neuro-
psychology, 15(8), 840.
fashion that indicated adequate effort. Age does not ap-
Gervais, R., Green, P., Allen, L., & Iverson, G. (2001). Effects of coaching
pear to be a significant factor influencing performance on on symptom validity testing in chronic pain patients presenting for
CARB. Flaro, Green, and Allen (2000) reported on chil- disability assessments. Journal of Forensic Neuropsychology, 2(2),
dren performing at or above normal adult performance 1–19.
levels on CARB. Allen et al. (2003) summarized a number Green, P., & Iverson, G. L. (2001). Validation of the computerized assess-
ment of response bias in litigating patients with head injuries. The
of studies providing validation for the utility of CARB
Clinical Neuropsychologist, 15, 492–497.
with a variety of diagnostic groupings. Hiscock, M., & Hiscock, C. K. (1989). Refining the forced-choice method
CARB appears to be an appropriate measure of effort for the detection of malingering. Journal of Clinical and Experimental
across a very large age range, and would in theory be Neuropsychology, 11, 967–974.
664 C Computerized Axial Tomography

Larrabee, G. J. (2007). Assessment of malingered neuropsychological defi- Hypothesis testing is a person’s ability to try out several
cits. New York: Oxford University Press.
possible concepts, solutions, or rules in a systematic way
Millis, S. R. (2008). Assessment of incomplete effort and malingering in
the neuropsychological examination. In Morgan, & Ricker (Eds.),
to determine which is the most useful. Cognitive psychol-
Textbook of clinical neuropsychology. New York: Taylor & Francis. ogists define concept learning as the development of
prototypes, schemas, attributions, or exemplars (Lamberts &
Shanks, 1997). Prototypes are learned typical representa-
tions of the concept. For example, a compact car is small,
gets good gas mileage, and is a Toyota. Schemas are scripts
Computerized Axial Tomography that are learnt for behaving or for evaluating behavior.
For example, an introduction usually involves a greeting,
▶ Computed Tomography a smile, and a handshake. Attributions are collections of
behavior adjectives and adverbs that define the notion of a
person, place, or behavior. For example, Republicans are
white, rich, and drive Hummers. Exemplars are collections
Concentration of examples of concepts that are stored in memory. For
example, observing people at the mall defines the concept
▶ Attention of an everyday person. Humans use several different
strategies to form concepts. Conservative focus involves
gradual manipulation of one aspect of a complex concept
at a time until the concept clarifies. Focus gambling tests
several possible hypotheses at the same time instead of
Concept Learning one at a time. Scanning involves forming global hypoth-
eses about a concept, then modifying them in accordance
R ICK PARENTE with rewards and punishments. Trial and error is the
Towson University tendency to ‘‘just keep trying until something works.’’
Towson, MD, USA Aspects of the task that improve concept acquisition
include an orderly arrangement of the items that the
person must use to form the concept. A compact display
Synonyms in which all the aspects of the concept are present also
improves acquisition. Sequential problems that present a
Hypotheses; Rules consistent concept also improve concept acquisition. The
saliency, novelty, and complexity of the concept, and
whether feedback is provided affect how quickly a person
Definition learns it (Hunt & Ellis, 2003).

An abstract or general idea that is inferred or derived from

specific instances. References and Readings

Hunt, R. R., & Ellis, H. C. (2003). Fundamentals of cognitive psychology.

Current Knowledge Madison, WI: Brown & Benchmark.
Lamberts, K., & Shanks, D. (Eds.). (1997). Knowledge, concepts, and
A concept is a special combination of ideas that has a categories. Cambridge, MA: MIT Press.
Parente & Herrman (2010). Retraining conceptual skills (chap. 16). In
particular meaning. Rules are concepts that direct
Retraining cognition: Techniques and applications. Austin, TX: Pro-Ed
behavior because there are consequences attached to Publishers.
them. A hypothesis relates two or more concepts with a
prediction (Parente & Herrmann, 2010). Hypothesis test-
ing, rule learning, concept learning, and problem solving
are all interrelated skills. Concept learning is how humans
learn to divide their environment into examples and Conceptual Knowledge
nonexamples of things they understand. Rule learning is
the process of associating concepts with consequences. ▶ Semantic Memory
 Concussion C 665

post-traumatic anterograde amnesia (PTA), retrograde am-

Concordance nesia, and Glasgow Coma Scale (GCS; Teasdale & Jennett,
1974). Standard neurological examination and imaging
▶ Inter-rater Reliability studies are frequently normal following concussion (i.e.
have limited sensitivity) so should not be relied on to C
diagnose concussion. Among clinical and scientific
experts, a concussion is synonymous with mild traumatic
brain injury (MTBI). Please see MTBI for a more detailed
Concurrent Validity discussion of issues related to diagnosis, management,
recovery, and outcome post concussion.
▶ Test Validity

Current Knowledge
Concussion Epidemiology
M ATTHEW R. P OWELL , M ICHAEL A. M C C REA Current epidemiology statistics likely grossly underesti-
Neuroscience Center mate the true incidence and prevalence of concussion
Waukesha, WI, USA because of imprecise surveillance systems (e.g., many
individuals with concussive injury never seek medical
care and those who do seek care are frequently not hospi-
Synonyms talized), and because current estimates are clouded by
variable research methodologies and inconsistent defini-
Mild traumatic brain injury; Sport-related concussion tions of concussion (McCrea, 2008; National Center for
Injury Prevention and Control, 2003). As discussed in
greater detail under MTBI entry, best estimates would
Definition suggest an incidence of at least 100/100,000 and perhaps
as high as 500/100,0000 population depending on study
A concussion refers to a trauma-induced alteration in methodologies (McCrea, 2008).
neurological function. Giza and Hovda (2001) and
Hovda et al. (1990) discuss the abnormal neurometabolic
processes associated with concussion. Early clinical signs
Recovery and Outcome Post Concussion
of concussion include alteration of mental status or be-
havior, and can be accompanied by other symptoms out-
Concussions fall under the general rubric of MTBI, and are
lined below.
frequently graded by severity (e.g., grade 1–3 concussion).
More significant concussive injury is associated with great-
er length of altered consciousness, LOC, or amnesia, al-
Diagnosis though concussive injury often occurs without observed
LOC or measurable amnesia. Generally speaking, acute
Diagnosis of concussion is made based on identifying neurologic, behavioral, or cognitive symptoms begin
an event with adequate biomechanical force to cause a acutely and resolve within 7–10 days, with a small percent-
concussive injury and by examining acute injury severity age of individuals exhibiting symptoms beyond 3 months
indicators. Frequent events associated with a direct trauma (Belanger & Vanderploeg, 2005; Iverson, 2005; McCrea,
or blow to the head to cause concussion include a fall, 2008). Providers should expect a relatively rapid and full
motor vehicle accident, or sports collision. In addition to a recovery for patients following a single concussion. There
direct blow to the head, a concussion can result from rapid is no apparent difference in outcome across the various
acceleration, deceleration, rotational or percussive forces grades of concussion, though there are reports of longer
that affect brain tissue. Injury severity indicators frequent- recovery periods for ‘‘complicated’’ cases, such as those
ly used to diagnose concussion include alteration of with intracranial abnormalities identified via imaging
consciousness (confusion), loss of consciousness (LOC), (Williams, Levin & Eisenberg, 1990).
666 C Conditioned Stimulus

Evaluation and Management Post References and Readings

Concussion
Belanger, H. G., & Vanderploeg, R. D. (2005). The neuropsychological
Early evaluation of symptoms and neurological status is impact of sports-related concussion: A meta-analysis. Journal of the
International Neuropsychological Society, 11, 345–357.
essential following concussion to diagnose severity of injury
Giza, C. C., & Hovda, D. A. (2001). The neurometabolic cascade of
and to rule out complications such as intracranial abnorm- concussion. Journal of Athletic Training, 36, 228–235.
alities or other comorbid injuries. Computed tomography Hovda, D. A., Prins, M., Becker, D. P., Lee, S., Bergsneider, M., & Martin,
(CT) imaging of the brain is frequently ordered by medical N. A. (1999). Neurobiology of concussion. In J. E. Bailes, M. R.
specialists because it continues to be the most sensitive Lovell, & J. C. Maroon (Eds.), Sports-related concussion (pp. 12–51).
St. Louis, MO: Quality Medical.
procedure for detecting acute intracranial abnormalities
Iverson, G. L. (2005). Outcome from mild traumatic brain injury. Current
post injury. Opinion in Psychiatry, 18, 301–317.
While spontaneous improvement over days to weeks Kelly, J. P., & Rosenberg, J. H. (1997). Diagnosis and management of
is the hallmark of recovery following concussion, it is concussion in sports. Neurology, 48(3), 575–580.
generally accepted that behavioral management (e.g., ed- McCrea, M. (2008). Mild traumatic brain injury and postconcussion syn-
drome: The new evidence base for diagnosis and treatment. New York:
ucation about MTBI, recovery and outcome; teaching
Oxford University Press.
cognitive–behavioral strategies to manage symptoms) Mittenberg, W., Canyock, E. M., Condit, D., & Patton, C. (2001). Treat-
may minimize the likelihood of a suboptimal outcome ment of Post-concussion syndrome following mild head injury.
and may contribute to improved quality of life for Journal of Clinical & Experimental Neuropsychology, 23(6), 829–836.
patients, perhaps because of greater understanding of Mittenberg, W., Tremont, G., Zielinski, R. E., Fichera, S., & Rayls, K.
(1996). Cognitive-behavioral prevention of postconcussion syn-
one’s injury and greater appreciation for the expected
drome. Archives of Clinical Neuropsychology, 11(2), 139–145.
recovery following injury. Pharmacologic intervention National Center for Injury Prevention and Control. (2003). Report to
for certain symptoms, such as pain, sleep abnormalities, congress on mild traumatic brain injury in the United States: Steps to
or mood disturbance, may also be indicated to help with prevent a serious public health problem. Atlanta, GA: Centers for
early adjustment and quality of life issues following con- Disease Control and Prevention.
Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired
cussion. Post-acute evaluation and monitoring is crucial
consciousness: A practical scale. The Lancet, 2(7872), 81–84.
for tracking a person’s recovery following injury. This will Williams, D. H., Levin, H. S., & Eisenberg, H. M. (1990). Mild head
help providers determine when it is appropriate for injury classification. Neurosurgery, 27(3), 422–428.
patients to resume prior activities, such as collision sports,
academics, or work. Individuals recovering from concus-
sion appear to be more vulnerable for re-injury or cata-
strophic injury. See Kelly and Rosenberg (1997) for an Conditioned Stimulus
excellent discussion of issues involved in management of
sports-related concussion, principles of which can be ap- ▶ Stimulus Control
plied to management of concussions resulting from any
mechanism.
Neuropsychological consultation is particularly help-
ful in the evaluation and management of patients follow-
Conduction Aphasia
ing concussion. Neurocognitive testing is sensitive to
LYN T URKSTRA
early, post-acute, and subtle symptoms associated with
University of Wisconsin-Madison
concussion, objectively tracks cognitive recovery over
Madison, WI, USA
time, and provides valuable information to inform return
to activity decision-making. Without neuropsychological
data, medical specialists must rely solely on a person’s
subjective report about residual neurocognitive symptoms.
Synonyms
Education and cognitive behavioral therapy techniques
Associative aphasia
are important treatment tools frequently employed by
neuropsychologists or other behavioral management
specialists to help prevent or treat persisting postconcussive Short Description
symptoms (Mittenberg, Canyock, Condit, & Patton,
2001; Mittenberg, Tremont, Zielinski, Fichera, & Rayls, Conduction aphasia is a subtype of fluent aphasia that is
1996). characterized by fluent speech and relatively intact
 Conduction Aphasia C 667

language comprehension, but significantly impaired rep- utterances (stereotypies). This is consistent with the
etition. Utterance length is normal or increased, and finding that the arcuate fasciculus is spared in many
speech has normal prosody and grammar and is produced patients with conduction aphasia (Quigg et al., 2006).
with normal effort. There is a reduction in content words, By contrast to the localization or modular view of
paraphasic errors are common, and oral reading is Geschwind and others, researchers in connectionist theo- C
impaired. ry have conceptualized language as the product of a
distributed cortical network that can be disrupted in
various ways to produce similar phenotypes. The advent
of functional imaging resurrected the notion of dis-
Categorization connection syndromes and more modular notions of lan-
guage (Catani & Ffytche, 2005), and the current view is
Conduction aphasia is differentiated from other types of somewhere in between a modular and connectionist
fluent aphasia (Wernicke’s aphasia, transcortical sensory perspective.
aphasia, and anomic aphasia) by the disproportionate
impairment in repetition relative to comprehension and
spontaneous production. It is differentiated from Wer-
nicke’s aphasia in particular by the patient’s awareness of Evaluation
his or her paraphasic errors.
The signs and symptoms of conduction aphasia will
be revealed only with testing of auditory and reading
comprehension, spontaneous language (e.g., asking the
Natural History, Prognostic Factors, patient to describe a picture), and repetition, so that
Outcomes the relative performance in these modalities can be
compared.
The prognosis for recovery of functional communication
in individual with conduction aphasia depends on the
underlying cause of the aphasia as well as factors such as
the size of lesion and the patient’s age, premorbid lan- Treatment
guage skills, and comorbid health conditions. Individuals
who initially present with conduction aphasia often There is no specific treatment for conduction aphasia,
evolve to a clinical profile of anomic aphasia, with rela- beyond therapies that are appropriate for aphasia in gen-
tively good auditory and reading comprehension, and eral (▶ Aphasia).
deficits primarily in word-finding and the comprehension
and production of complex syntax.

Cross References

▶ Aphasia
Neuropsychology and Psychology of
▶ Nonfluent Aphasia
Conduction Aphasia
Conduction aphasia historically has been attributed to the
interruption of white matter pathways, notably the arcuate References and Readings
fasciculus (part of the superior longitudinal fasciculus),
that connect posterior and anterior cortical structures Catani, M, & Ffytche D. H. (2005). The rises and falls of disconnection
involved in language comprehension and production. syndromes. Brain, 128(Pt 10), 2224–2239.
Thus, conduction aphasia historically was referred to as Geschwind, N. (1965). Disconnexion syndromes in animals and man. II.
a ‘‘disconnection syndrome’’ (Geschwind, 1965). Lesion Brain 88, 585–644.
Goodglass, H. (1993). Understanding Aphasia. San Diego, CA: Academic
and imaging studies have revealed, however, that conduc-
Press.
tion aphasia may result from lesions in a variety of loca- Quigg, M., Geldmacher, D. S., & Elias, W. J. (2006). Conduction aphasia
tions, and that arcuate fasciculus lesions are instead as a function of the dominant posterior perisylvian cortex: Report of
implicated in the production of repetitive, stereotypic two cases. Journal of Neurosurgery 104, 845–848.
668 C Confabulation

described as brief, partially accurate responses often

Confabulation inaccurately localized in time (Victor & Ropper, 2001).
Fantastic or productive confabulations have been described
FARZIN I RANI 1, DAVID J. L IBON 2 as more elaborate fictitious stories (Berlyne, 1972).
1
University of Pennsylvania Further distinctions have been made between confabula-
Philadelphia, PA, USA tions that are provoked by direct questions, often in the
2
Drexel Medical College context of memory testing, or spontaneous confabulations
Philadelphia, PA, USA occurring without any external trigger (Kopelman, 1987).
The boundaries between provoked/spontaneous and
momentary/fantastic confabulations are often blurred,
Description with many authors mixing these characteristics when
describing the symptoms. Some have argued against
Korsakoff initially described ‘‘pseudo-reminiscences’’ in such categorizations and instead suggested that confabu-
alcoholic patients with amnesia who made up fictitious lation should be regarded as a continuous variable,
stories about events that did not occur. In their translation ranging from minor distortions to more dramatic
of Kosakoff ’s original work, Victor and Yakovlev note that fantasies (Metcalf et al., 2007).
Korsakoff first identified patients with a ‘‘psychic disorder
in conjunction with multiple neuritis’’ who presented
with ‘‘a derangement of memory and of the association
of ideas’’ along with other symptoms of the now well- Neuropsychology of Confabulation
known Korsakoff syndrome (Korsakoff, 1955). Later, the
term confabulation was introduced and defined as the Studies using neuropsychological test performance to
‘‘falsification of memory occurring in clear consciousness examine mechanisms of confabulation have not yielded
in association with an organically derived amnesia’’ consistent results. Observations of perseverative responses
(Berlyne, 1972). It has also been referred to as ‘‘true in individuals who confabulate have implicated frontal
memories that have been misplaced in both time and executive dysfunction (e.g., Kopelman, Stanhope, &
place’’ (Kopelman, 1987) as well as the ‘‘spontaneous Kingsley, 1997). Others have argued for more prominence
narrative reports of events that never happened.’’ More of memory impairments rather than executive dys-
recently, confabulation has been defined as ‘‘statements or function (e.g., Dalla Barba, 1993). A combination of
actions that involve distortions of memories’’ (Metcalf, executive and memory deficits may be involved. Memory
Langdon & Coltheart, 2007). impairment may explain the presence or absence of
Confabulation, as a symptom, has been described in a confabulation, but the severity of confabulation may be
number of disorders including strokes (particularly influenced by the extent of executive dysfunction (Fischer,
anterior communicating artery), traumatic brain injuries, Alexander, D’Esposito, & Otto, 1995). Clinical lesion
dementia, metabolic disorders, and psychiatric disorders. studies have implicated the medial prefrontal cortex in
Confabulations are mentioned as a probable symptom in spontaneous confabulations, particularly the orbitofrontal
most of the descriptions of Korsakoff ’s syndrome despite region (Schnider, 2003). Damage to limbic structures
ambiguous clinical diagnostic guidelines (Borsutzky, involved in memory is also likely to be required for
Fujiwara, Brand, & Markowitsch, 2008). For instance, confabulations to occur (Fischer et al., 1995). The litera-
the ICD-10 mentions confabulations as a probable but ture on anterior communicating artery aneurysms
not obligatory symptom for diagnosing an ‘‘Alcohol- (ACoA) has implicated frontal structures as a necessary
Induced Amnesic Syndrome’’ while the DSM-IV site of neuropathology in confabulation, although cases of
(American Psychiatric Association, 1994) does not nonamnestic ACoA patients with frontal lesions who do
include confabulations in its guidelines for diagnosing not confabulate have suggested that both frontal lobe and
‘‘Alcohol-Induced Amnesic Syndrome.’’ basal forebrain structures may be needed for spontaneous
confabulations (DeLuca & Diamond, 1995).
Four types of cognitive models have been proposed to
account for confabulations:
Categorization
1. Source monitoring theory. This view was initially
There are different descriptions of confabulation used by promoted by Johnson, Hashtroudi, and Lindsay
several authors. Momentary confabulations have been (1993) who argued that individuals who confabulate
 Confabulation C 669

are unable to accurately monitor the source of their 4. Three-factor cognitive-neuropsychological theory.
memories which results in errors and confusion. Metcalf et al. (2007) propose a 3-factor combined
According to this view, patients who confabulate can- model that hypothesizes interplay between an execu-
not accurately identify where or when events occur. tive control retrieval deficit, an evaluation deficit, and
They may also be unable to differentiate between a person’s individual emotional/motivational biases. C
whether a representation is ‘‘real’’ or not due to Specifically, according to this view confabulatory
impairments in being able to access qualitative symptoms and content are the result of a failure of
characteristics of the representation such as details executive control that causes an impaired search and
about perceptual, contextual, affective, and semantic selection of appropriate memories from the autobio-
information. Furthermore, secondary evaluation graphical episodic memory store. Confabulators are
deficits may also lead to the over-inclusive acceptance purportedly unable to critically evaluate material from
of memories. their autobiographical or general semantic store and
2. Temporal context theory. Dalla Barba, Mantovan, accept confabulations as real memories. Further,
Cappelletti, and Denes (1998) have suggested that the personal biases may be involved in the preferential
primary impairment in confabulation is a difficulty selection of memories that are emotionally biased.
with ‘‘temporal consciousness.’’ According to this
view, patients who confabulate are confused about the
temporal order of information retrieved from memory. Evaluation
While knowledge of time is preserved and patients are
aware of a past, present, and future, they are unable to Since Korsakoff ’s initial description in 1955 of ‘‘pseudo-
make correct temporal judgments about their mem- reminiscences’’ in alcoholic patients with amnesia who
ories, resulting in sequencing errors. Schnider (2003) made up fictitious stories about events that did not
has also argued that there is confusion between pres- occur, there has been considerable variability in how con-
ently relevant and irrelevant memories, resulting in a fabulation is defined, identified, assessed, and understood.
failure to suppress activated but presently irrelevant For instance, it remains debated whether confabulations
memory traces. Neuroanatomically, Schnider et al. are readily differentiated from delusions. Some have ar-
have linked confabulation with the posterior orbito- gued that confabulations are not different from delusions
frontal cortex and the anterior limbic structures di- since both are held firmly over time. Others have viewed
rectly connected with it. Schnider argues that the confabulations, delusions, hallucinations, and insight as
adaptation of thought and behavior to ongoing reality part of a continuum. Still others have argued that delu-
is mediated by the anterior limbic system which acts sions and confabulations differ since confabulations tend
by suppressing activated memory traces that do not to be associated with partially valid memories that can be
pertain to ongoing reality. In patients who confabu- traced to real events. Further debate ensues about whether
late, this monitoring of ongoing reality in thought confabulations are deliberate attempts to compensate for
goes awry and appears to be related to the brain’s ‘‘memory gaps’’ due to embarrassment or whether they
reward system. involve source monitoring, temporal context, or retrieval
3. Retrieval theory. This view has been primarily promoted difficulties that result in an implausible or fictional out-
by Moscovitch and Melo (1997) who argue that put. Confabulation, particularly following ACoA aneur-
deficient strategic retrieval processes and monitoring ysms has also been viewed as representing differences in
deficits influence confabulation. Specifically, confabu- degree and not kind. Other important variables identi-
lation is thought to be the result of a faulty ‘‘strategic fied in the understanding of confabulation have included
retrieval’’ search and inaccurate ordering and making the distinction between an ‘‘unaware’’ or
placement of memories in context. According to this ‘‘aware’’ process, premorbid personality factors, the
view, strategic retrieval is dependent upon executive need for coexistence of amnesia, differentiation from
processes and is self-initiated and goal-directed, while an acute confusional state, disconnection syndrome,
associative retrieval is automatic and independent of and whether indifference/apathy or deceit/lying is
executive processes. Confabulators are thought to involved (DeLuca, 2000). There has been further varia-
show deficiencies in strategic retrieval, influenced by bility in decisions on how to label an individual as a
deficiencies in the neocortical/prefrontal/hippocampal ‘‘confabulator.’’ Some have used the term based on clinical
network hypothesized to be involved in strategic observations of spontaneous or provoked production of
retrieval. fabricated stories following brain injury. Other researchers
670 C Confabulation

have labeled individuals as confabulators based on the num- Cross References

ber, or quality of intrusions/confabulations produced dur-
ing standardized neuropsychological tests or experimental ▶ Capgras Syndrome
tasks. Overall, the concept of confabulation remains elusive ▶ Delusion
and its underlying mechanisms remain an area requiring ▶ Intrusion Errors
further understanding. ▶ Reduplicative Paramnesia
▶ Wernicke–Korsakoff Syndrome

Treatment

Treatment is determined in part by etiology. Some have References and Readings

proposed that rehabilitation efforts should avoid mem-
American Psychiatric Association: Diagnostic and Statistical Manual of
ory training and repeated questions about orientation.
Mental Disorders, Fourth Edition, Text Revision. Washington, DC,
For instance, according to Schnider (2003) it may be American Psychiatric Association, 2000.
easier for a confabulating patient to ‘‘accept that her Berlyne, N. (1972). Confabulation. The British Journal of Psychiatry,
baby has already received food than to convince her that 120(554), 31–39.
her baby is over 30 years old.’’ Instead, it may be more Borsutzky, S., Fujiwara, E., Brand, M., & Markowitsch, H. J. (2008).
Confabulations in alcoholic Korsakoff patients. Neuropsychologia,
beneficial to promote the engagement of patients in com-
46(13), 3133–3143.
mon everyday activities and accept their false interpreta- Dalla Barba, G. (1993). Different patterns of confabulation. Cortex, 29(4),
tion of reality until spontaneous confabulations resolve 567–581.
(Schnider). Many spontaneous confabulations eventually Dalla Barba, G., Mantovan, M. C., Cappelletti, J. Y., &
resolve. In a study of eight spontaneous confabulators, Denes, G. (1998). Temporal gradient in confabulation. Cortex, 34
(3), 417–426.
almost all stopped confabulating 18 months later and
DeLuca, J. (1992). Rehabilitation of confabulation: The issue of unaware-
regained correct orientation in time and place, as well as ness of deficit. NeuroRehabilitation, 2(3), 23–30.
the ability to refer thinking and acting to ongoing reality DeLuca, J. (2000). A cognitive neuroscience perspective on confabulation.
(Schnider, Ptak, von Daniken, & Remonda, 2000). Specif- Neuro-Psychoanalysis, 2(2), 119–132.
ically, ‘‘temporal context confusion’’ based on an inability DeLuca, J., & Diamond, B. J. (1995). Aneurysm of the anterior
communicating artery: A review of neuroanatomical and neuropsy-
to suppress intrusions of currently irrelevant memory
chological sequelae. Journal of Clinical and Experimental Neuropsy-
traces into ongoing thinking paralleled the course of chology, 17(1), 100–121.
spontaneous confabulations in this study. Patients with DeLuca, J., & Locker, R. (1996). Cognitive rehabilitation following
isolated, less extensive, orbitofrontal lesions stopped con- anterior communicating artery aneurysm bleeding: A case report.
fabulating within a few weeks and had the best neuropsy- Disability and Rehabilitation, 18(5), 265–272.
Fischer, R. S., Alexander, M. P., D’Esposito, M., & Otto, R. (1995).
chological outcomes. Patients with additional basal
Neuropsychological and neuroanatomical correlates of confabula-
forebrain lesions continued to confabulate for several tion. Journal of Clinical and Experimental Neuropsychology, 17(1),
months and remained amnestic. One patient with exten- 20–28.
sive orbitofrontal damage and perirhinal cortex damage Johnson, M. K., Hashtroudi, S., & Lindsay, D. S. (1993). Source moni-
continued to confabulate after more than 3 years. Inter- toring. Psychological Bulletin, 114(1), 3–28.
Kopelman, M. D. (1987). Two types of confabulation. Journal of Neuro-
disciplinary approaches for the rehabilitation of confabu-
logy, Neurosurgery, and Psychiatry, 50(11), 1482–1487.
lation in the treatment of patients with ACoA aneurysms Kopelman, M. D., Stanhope, N., & Kingsley, D. (1997). Temporal
have also been suggested, including a three-tiered ap- and spatial context memory in patients with focal frontal,
proach focused on improving (1) intellectual awareness, temporal lobe, and diencephalic lesions. Neuropsychologia, 35(12),
the ability to understand that one has an impairment, (2) 1533–1545.
Korsakoff, S. S. (1955). Psychic disorder in conjunction with peripheral
emergent awareness, the ability to recognize a problem
neuritis, Neurology, 5, 394–406.
when it is occurring, and (3) the ability to anticipate that a Metcalf, K., Langdon, R., & Coltheart, M. (2007). Models of confabula-
problem (confabulation) is going to occur (DeLuca, tion: A critical review and a new framework. Cognitive Neuropsy-
1992). In one case, improvements in executive function- chology, 24(1), 23–47.
ing using this rehabilitation approach removed obstacles Moscovitch, M., & Melo, B. (1997). Strategic retrieval and the frontal
lobes: Evidence from confabulation and amnesia. Neuropsychologia,
to vocational activity and social functioning by improving
35(7), 1017–1034.
the patient’s awareness of his difficulties and enabling Schnider, A. (2003). Spontaneous confabulation and the adaptation of
utilization of compensatory strategies (DeLuca & Locker, thought to ongoing reality. Nature Reviews. Neuroscience, 4(8),
1996). 662–671.
 Conflict C 671

Schnider, A., Ptak, R., von Daniken, C., & Remonda, L. (2000). Recovery References and Readings
from spontaneous confabulations parallels recovery of temporal
confusion in memory. Neurology, 55(1), 74–83.
American Psychological Association. (2002). Ethical principles of psychol-
Victor, M., & Ropper, A. H. (Eds.). (2001). Principles of neurology
ogists and code of conduct. American Psychologist, 57, 1060–1073.
(7th ed.). New York: The McGraw-Hill Companies, Inc.
Committee on Ethical Guidelines for Forensic Psychologists (1991).
Specialty guidelines for forensic psychologists. Law and Human C
Behavior, 15, 655–665.
Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin, C. (2007).
Confidentiality Psychological evaluations for the courts (3rd ed.). New York: Guilford.

R OBERT L. H EILBRONNER
Chicago Neuropsychology Group
Chicago, IL, USA
Confirmatory Bias
M OLLY E. Z IMMERMAN
Albert Einstein College of Medicine
Definition
Bronx, NY, USA
Confidentiality has been defined as ‘‘containing informa-
tion whose unauthorized disclosure could be prejudicial to
the national interest.’’ In psychology, it is one of the most
Definition
important components of the Ethical Principles of Psychol-
Confirmatory bias occurs when a clinician preferentially
ogists and Code of Conduct (2002) and the Specialty
accepts or seeks evidence that confirms an initial hypoth-
Guidelines for Forensic Psychologists (1991). The bound-
esis at the expense of thorough consideration of emerging
aries of confidentiality vary based on the setting, that is,
contradictory evidence (Garb, 2003). For example, a cli-
whether it is in the clinical versus forensic realm and
nician may formulate an initial impression that a client
whether it is in the civil versus criminal realm. In treatment
has dementia based on a referral question. During the
settings, clinicians consider confidentiality of paramount
clinical interview, the clinician may focus on questions
importance and they are reluctant to disclose information
relating to memory and change in activities of daily living
obtained from a client even when there are explicit legal or
while failing to ask questions that specifically pertain
countervailing ethical mandates to do so (such as when a
to differential diagnoses, such as major depressive
patient may harm another). Such a position is unrealistic in
disorder. In neuropsychological settings, this generally
the forensic context because the results of forensic evalua-
unintentional bias may impair judgment, hamper
tions (be it civil or criminal) are routinely disclosed to third
decision-making, produce false reports, and negatively
parties. In both clinical and forensic contexts, psychologists
impact the assessment approach and interpretation of
provide examinees with adequate ‘‘informed consent’’
findings. To address this bias, the clinician should system-
prior to engaging in the examination. In the forensic con-
atically review all available data within a hypothesis-
text, it is the duty of forensic psychologists to inform clients
testing framework in an effort to remain as impartial as
of their legal rights regarding the purpose of an evaluation,
possible (Weiner & Greene, 2007).
the anticipated forensic service, the nature of procedures to
be utilized, the limits of confidentiality, who has retained
the examiner for the evaluation, who the report may be References and Readings
directed to, and that anything which is said during the
examination could be included in a report or come up Garb, H. N. (2003). Clinical judgment and mechanical prediction. In
during deposition or trial testimony. Some jurisdictions I. B. Weiner, D. K. Freedheim, M. Gallagher, J. A. Schinka, & R. J.
do not provide for confidentiality of mental health evalua- Nelson (Eds.), Handbook of psychology (pp. 27–42). New York: Wiley.
Weiner, I. B., & Green, R. L. (2007). Handbook of personality assessment.
tions. For example, when an evaluation is conducted as a
New York: Wiley.
result of direct court order, confidentiality is not provided.

Cross References Conflict

▶ Privilege ▶ Contraindication
672 C Conformal Techniques

Conformal Techniques Confrontation Naming

▶ Involved Field Radiotherapy A NASTASIA R AYMER
Old Dominion University
Norfolk, Virginia, USA
Confound
▶ Confounding Variables Synonyms

Word finding
Confounding Variables
J AMES H. B AÑOS
Definition
University of Alabama at Birmingham
Confrontation naming involves the selection of a specific
Birmingham, AL, USA
label corresponding to a viewed stimulus, usually a
picture, of a viewed object or action. Confrontation
naming also refers to a type of task used in assessment
Synonyms
when problems with naming are of concern.
Confound; Extraneous variable; Lurking variable

Current Knowledge
Definition
Confrontation naming tasks often are incorporated as part
A confounding variable is an extraneous variable that
of clinical language testing to detect impairments of word-
obscures the true relation between two other variables or
finding abilities in individuals with various types of neuro-
groups of interest. In experimental research designs, a con-
logic impairments typically affecting the left hemisphere of
founding variable often presents as an unintended
the brain (Spreen & Risser, 2003). Although word finding
or undesirable systematic difference between groups
takes place during the course of sentence generation in
(the independent variable) that is also systematically related
conversational speech, it is most often tested clinically in
to the outcome of interest (dependent variable). It hinders
confrontation naming tasks where the vocabulary tested is
the ability to infer a causal relation between the variables
constrained to known, identified target words. Therefore,
and can lead to misattributing a causal effect to the inde-
word-finding functions are at times referred to as naming
pendent variable (a threat to internal validity). Potential
abilities (e.g., Chialant, Costa, & Caramazza, 2002).
confounding variables are most effectively addressed during
The most common published test of confrontation
study design (e.g., via random assignment, case control
naming is the Boston Naming Test (Kaplan, Goodglass,
matching), but may be addressed to some extent during
& Weintraub, 2001); other published confrontation
statistical analysis (e.g., handled as a covariate).
naming tests also exist for use in children and adults
with word-finding difficulties (An Object and Action
Cross References Naming Battery, Druks, & Masterson, 2000; Test of
Adolescent/Adult Word Finding, German, 1990). Con-
▶ Analysis of Covariance (ANCOVA)
frontation naming tests assess the ability to retrieve
▶ Error, Sources of
different types of words, including pictures of objects to
test noun retrieval, or pictures of actions to test verb
References and Readings retrieval. Although most tests of confrontation naming
test stimuli from a variety of semantic categories, some
Kazdin, A. E. (Ed.). (2003). Methodological issues & strategies in clinical
tests can differentiate pictures according to the semantic
research (3rd ed.). Washington, DC: American Psychological
Association.
category to which they belong, including pictures from a
Pearl, J. (2009). Causality: Models, reasoning, and inference. Cambridge: variety of natural categories such as animals, fruits, and
Cambridge University Press. vegetables, and man-made categories such as furniture,
 Congestive Heart Failure C 673

clothing, tools, and transportation (e.g., Goodglass, Definition

Kaplan, & Barresi, 2001).
Congestive heart failure (CHF) or heart failure is a condi-
tion in which the heart muscle is unable to pump suffi-
Cross References
cient blood to adequately supply the body’s organs. C
▶ Anomia
▶ Anomic Aphasia
Current Knowledge

References and Readings Common causes of CHF include coronary artery disease,
myocardial infarction, hypertension, cardiac valve dis-
Chialant, D., Costa, A., & Caramazza, A. (2002). Models of naming. ease, cardiomyopathy (heart muscle disease), congenital
In A. E. Hillis (Ed.), The handbook of adult language disorders heart disease, and endocarditis (heart infection). In CHF,
(pp. 123–142). New York: Psychology Press. the heart continues to pump, but exercise and activity
Druks, J., & Masterson, J. (2000). An object and action naming battery.
cause shortness of breath (‘‘dyspnea on exertion’’ or
Hove, UK: Psychology Press.
German, D. J. (1990). Test of adolescent/adult word finding. Austin, TX: DOE), fatigue, weakness, light-headedness, or syncope.
Pro-Ed. Because the heart is not pumping the blood completely
Goodglass, H., Kaplan, E., & Barresi, B. (2001). The assessment of aphasia and effectively, the blood ‘‘backs up’’ into the heart
and related disorders (3rd ed.). Philadelphia, PA: Lippincott, chambers, and ultimately into the venous system. This
Williams & Wilkins.
causes congestion of the tissues, and edema in the legs
Kaplan, E., Goodglass, H., & Weintraub, S. (2001). The Boston naming
test. Philadelphia: Lippincott, Williams & Wilkins. and internal organs, including the lungs (‘‘pulmonary
Laine, M., & Martin, N. (2006). Anomia: Theoretical and clinical aspects. edema’’), often resulting in shortness of breath, especial-
New York: Psychology Press. ly when lying supine (‘‘orthopnea’’). Electrocardiogram
Spreen, O., & Risser, A. H. (2003). Assessment of aphasia. Oxford: Oxford and certain blood tests are usually abnormal, and chest
University Press.
x-ray shows congestion of the lungs. Echocardiography
Tranel, D., Adolphs, R., Damasio, H., & Damasio, A. R. (2001). A neural
basis for the retrieval of words for actions. Cognitive Neuropsychology, is noninvasive and highly revealing, and has the potential
18(7), 655–670. to provide a quantitative measure of severity of heart
failure as indicated by the proportion of blood in the left
ventricle that can be pumped out by the muscle (‘‘ejec-
tion fraction’’).
Congenital Defects CHF is a chronic condition with acute exacerbations
during which patients may experience moderate or signif-
▶ Anencephaly icant distress. Chronic congestive heart failure can be
managed using a combination of interventions that help
the patient to ‘‘compensate’’ for the problems caused by
CHF. Acute pulmonary edema is a medical emergency.
Congenital Hypothryroidism Treatment of acute CHF episodes usually consists of rest,
salt reduction, identification, and removal of the precipi-
▶ Hypothyroidism
tating factor (such as infection, cardiac arrhythmia, or
other cause), and the use of select medications that help
to improve the pumping ability (‘‘contractility’’) of the
Congestive Heart Failure heart muscle and the capacity of the blood vessels to
provide blood supply to other organs. These medications
E LLIOT J. R OTH include angiotensin-converting enzyme inhibitors, beta-
Northwestern University blockers, digoxin, diuretics (water pills), and vasodilators.
Chicago, IL, USA At times, valve disease warrants valve replacement sur-
gery, and extremely severe heart damage may require
cardiac transplantation to prevent death. Usually, mild
Synonyms to moderate congestive heart failure can be treated with
medications, adjustments of exercise and activity levels,
Heart failure and medical supervision.
674 C Conjugate Gaze

Cross References can result, which can then cause diplopia. The mechan-
isms for horizontal eye movements are better understood
▶ Coronary Disease than vertical eye movements. As individuals age, the abil-
▶ Echocardiogram ity to look upward tends to decline. Cerebral structures
control when and where the eyes move, and the brain
stem structures control how they move.
References and Readings The centers for lateral conjugate gaze are in the frontal
and occipital cortices. In the frontal lobe, this area is in the
Jessup, M., Abraham, W. T., Casey, D. E., Feldman, A. M., Francis, G. S., posterior aspect of the frontal lobes, referred to as the
Ganiats, T. G., et al. (2009). Focused update: ACCF/AHA guidelines frontal eye fields. This area is close to the motor strip.
for the diagnosis and management of heart failure in adults: A report The function of the frontal centers is to control voluntary
of the American College of Cardiology Foundation/American Heart
conjugate eye movements to the opposite side. The frontal
Association Task Force on Practice Guidelines, Developed in collab-
oration with the International Society for Heart and Lung Trans-
eye fields (FEF) receive inputs from peristriate, parietal
plantation. Circulation, 119, 1977–2016. and superior temporal cortex, medial pulvinar, and the
dorsomedial nucleus of the thalamus. Stimulation of FEF
results in contralateral saccades. In strokes that affect this
area, one may see an eye deviation toward the side of the
lesion and away from the paralyzed limb. This usually
Conjugate Gaze occurs only in the acute phase of an infarct. At some
point, the patient may be unable to move the eyes away
M ARY-E LLEN M EADOWS from the lesion on command. However, they may be able
Brigham and Women’s Hospital to follow an object to the opposite side if the occipital lobe
Boston, MA, USA center is not damaged. The occipital lobe centers for
lateral conjugate gaze control eye movement when an
individual is following an object to the opposite side.
Synonyms Lesions of the occipital lobe that control lateral conjugate
gaze are less common than lesions of the frontal centers.
Eye movements; Versional movements Conjugate gaze can be disrupted by stroke or trauma,
depending on the location of the damage. For instance, an
intracerebral hemorrhage in the caudate nucleus or puta-
Definition men will cause conjugate deviation of eye movements to the
side of the lesion. Pineal tumors, which can press upon the
Conjugate gaze is the ability of the eyes to work together midbrain, can cause paralysis of upward gaze. Deeper dam-
or in unison. It refers to the motion of both eyes in the age can affect downward saccades. Given the extensive
same direction at the same time. The eyes can look later- anatomy of control of the visual system, damage or dys-
ally (left/right), upward, or downward. Disorders in con- function along any of the nuclei or tracts integral to eye
jugate gaze refer to the inability to look in a certain movements can result in abnormalities. Eye movements
direction with both eyes. utilize the basal ganglia and cerebellum in their planning
and coordination. Patients with basal ganglia disorders may
have involuntary, small, or slow eye movements. Patients
Current Knowledge with parkinsonian symptoms may have a restriction of
upgaze. In patients with progressive supranuclear palsy, a
Conjugate gaze is mediated in the brain stem by the cardinal feature is the restriction of upgaze, and these
medial longitudinal fasciculus, which is a nerve tract patients initially complain of difficulties with reading. The
that connects the abducens, trochlear, and oculomotor flocculus of the cerebellum is important for suppression of
nuclei. These nuclei, in turn, are responsible for the mus- vestibular reflex and for smooth pursuit movements. Parts
cles that control eye movements. The left pontine center of the vermis help to coordinate saccades, and damage can
connects with the right frontal center for conjugate gaze result in dysmetric saccades. Patients with long-standing
to the left, and the right pontine center connects with the frontal lobe lesions cannot inhibit inappropriate saccades
left frontal center for conjugate gaze to the right. If extrao- from a fixation to a peripheral, visually attractive stimulus
cular muscles are not working properly, dysconjugate gaze that appears suddenly. Frontal seizures with a focus in or
 Conners 3rd Edition (Conners 3; Conners 2008) C 675

near one eye field may manifest by turning of the eye and from the individual. These are critical for binocular single
head away from the side of the lesion. vision and depth perception.
Evoked eye movements (doll’s eye test or oculocepha-
lic reflex) and the caloric response can be used in the
examination of an unresponsive patient. However, if a Cross References C
patient is in a comatose state due to drug intoxication
or hypothermia, these tests may show no response. The ▶ Dysconjugate Gaze
assessment is as follows: ▶ Lateral Gaze Palsy
Doll’s eye test – This test can be used in either the ▶ Saccadic Eye Movements
comatose or conscious patient. Hold the patient’s eyes
open and rapidly move/rotate the head to one side and
hold it there. If the brain stem reflexes are intact, the eyes References and Readings
will move conjugately in the direction opposite to the head
rotation. If the injury is in the brain stem, the eyes do not Lavin, P. J. M., & Weissman, B. (2000). Neuro-Opthalmology. In W. G.
Bradley, R. B. Daroff, G. M. Fenichel, & C. D. Marsden (Eds.),
move. If a patient is conscious and can follow commands,
Neurology in clinical practice: Principles of diagnosis and management.
have them fixate on an object. This test should not be used Boston, MA: Butterworth-Heinemann.
in a patient who has possible cervical injuries. Marshall, K. G. (2006). Cranial nerve III, IV and VI: Disorders of conju-
Caloric test – This test can be done in the comatose gate Gaze. Patient Care Canada, 17, 51–57.
patient. The patient’s ear canal is irrigated with 20 ml of Ross, R. T. (1999). How to examine the nervous system (3rd ed.). Stamford,
CT: Appleton and Lange.
ice-cold water. The eyes should move toward the ear that
is irrigated. If the patient’s eyes do not move, the lesion is
in the brain stem. This test should not be used in a patient
who has possible cervical injuries, or who has blood in the
ear canal or a perforated eardrum. Connectionist Model of Aphasia
Conjugate eye movements allow the eyes to get an
image onto the fovea and keep it there. Fast movements ▶ Wernicke–Lichtheim Model of Aphasia
or saccades allow images onto the fovea and slower move-
ments keep them there. Smooth pursuit movements com-
pensate for target movement. There are several ocular
motor systems: Connective Tissue Disease
Saccadic system moves the eyes rapidly (up to 800 /s)
in order to fixate on new targets in the visual fields. These ▶ Collagen Vascular Disease
can be voluntary or a response to a verbal command.
Reflex saccades can also occur to stimuli that are threat-
ening or to a sound in the periphery.
Pursuit system enables the eyes to track slowly moving
targets (approximately 70 /s) so the image is stable on the Conners 3rd Edition (Conners 3;
fovea. Conners 2008)
Vestibular eye movement subsystem maintains a stable
image on the retina during head movements. The vesti- C. K EITH C ONNERS 1, J ENNI P ITKANEN 2, S ARA R. R ZEPA 2
1
bulo ocular reflex maintains the eyes in the same direction Duke University Medical School
in space during head movements. This is controlled by the Durham, North Carolina, USA
2
semicircular canals, which respond to rotational accelera- Multi-Health Systems Inc.
tion of the head. Toronto, Ontario, Canada
Optokinetic system complements the vestibular eye
movement system. It uses reference points in the environ-
ment to maintain orientation. This system uses fixation Description
and pursuit in humans.
Vergence system enables the eyes to move dysconju- The Conners 3rd Edition (Conners 3; Conners, 2008), the
gately (converge and diverge) in the horizontal axis to latest version of the Conners Rating Scales, is a thorough
maintain fixation on a moving target toward or away assessment of attention deficit/hyperactivity disorder
676 C Conners 3rd Edition (Conners 3; Conners 2008)

(ADHD) and its most commonly associated problems (including all three ADHD subtypes: ADHD predomi-
and disorders in school-aged youth. The Conners 3 is a nantly inattentive type, ADHD predominantly hyperac-
multi-informant assessment with forms for parents, tive-impulsive type, and ADHD combined type),
teachers, and youth. Parent and teacher ratings can be disruptive behavior disorders, learning disorders, anxiety
obtained about youth aged 6–18 years, and youth aged disorders, major depressive disorder, bipolar disorder, and
8–18 years can complete the self-report. pervasive developmental disorders.
The assessment features multiple content scales that
assess ADHD-related concerns such as inattention and
hyperactivity as well as related problems in executive func- Historical Background
tioning, learning, aggression, and peer/family relations.
Symptoms of distinct diagnoses can be assessed with scales The first versions of the Conners Parent and Teacher
that link directly to the Diagnostic and Statistical Manual Rating Scales were developed at the Harriet Lane Clinic
of Mental Disorders (DSM-IV-TR; American Psychiatric of the John Hopkins Hospital in the 1960s during
Association, 2000) symptomatic criteria for ADHD, con- Dr. Leon Eisenberg’s controlled studies of psychotherapy
duct disorder (CD), and oppositional defiant disorder and medications. The purpose of the original scales was to
(ODD). Anxiety and Depression Screener items are also serve as the basis for a detailed interview about a child’s
included in order to provide coverage of two internalizing problems. The first version of the parent scale contained
problems frequently associated with ADHD. The Conners items grouped in terms of problems (e.g., sleep, eating,
3 also provides two index scores: the Conners 3 ADHD temper, friendships, school). The teacher scale included
Index and the Conners 3 Global Index. The assessment items related to functioning within the classroom setting
also includes validity scales (positive impression, negative (e.g., group participation, attitude towards authority).
impression, and inconsistency index), severe conduct crit- The earliest research studies on the scales supported the
ical items, impairment items (home, school, and social research properties of the scales. For example, the very
settings), and open-ended additional questions (addition- first study on the teacher scales (Conners, 1969) demon-
al concerns, strengths). strated adequate test-retest reliability. In addition, good
The Conners 3 offers full-length, short, and index form sensitivity to drug treatment and nondrug therapy effects
options. The full-length forms convey the most detailed were established.
information of all the forms. The short forms are useful The scales were first formally published in 1989 as the
when the administration of the full-length version is not Conners Rating Scales (CRSTM, Conners, 1989, 1990) and
possible or practical (e.g., when multiple administrations offered a standard format with normative data, detailed
over time are required). The index forms are useful in information about the psychometric properties and the
screening and treatment monitoring situations. Adminis- proper use of the scales, and the hand-scorable
tration requires approximately 20 min for the full-length ‘‘QuikScoreTM’’ form allowing for easy administration
forms, 10 min for the short forms, and approximately 5 and scoring. The CRS was later revised (CRS-R; Conners,
min for the index forms. Raw scores are converted to age- 1997) to offer a self-report component and scales
and gender-based standard scores (including T-scores and linked to the Diagnostic and Statistical Manual of Mental
percentiles). Results from the DSM-IV-TR symptom Disorders – Fourth Edition (American Psychiatric Associ-
scales are also reported in terms of symptom counts, ation, 1994) criteria for ADHD. The Conners 3, the latest
that is, whether or not the minimum symptom require- revision of the Conners Rating Scales, incorporates the
ments set by the DSM-IV-TR have been met. The Conners key features of its predecessors with updated normative
3 ADHD Index produces a probability score, which indi- data and psychometric properties, an age range specific
cates whether the youth’s scores are more like youth with to the assessment of school-aged children, and an
ADHD, or with those from the general population. increased focus on the assessment of ADHD, associated
The Conners 3 normative sample consists of 3,400 features, and the disorders most commonly comorbid
assessments (1,200 parent, 1,200 teacher, and 1,000 with ADHD.
self-report assessments) including 50 boys and 50 girls
from each age (6–18 years for the parent and teacher
report, 8–18 years for the self-report). The racial/ethnic Psychometric Data
distribution of this sample closely matches the US
population. Approximately 2,100 clinical cases were also Results of reliability analyses revealed that the Conners 3
collected from youth with following diagnoses: ADHD forms have high levels of internal consistency, with
 Conners 3rd Edition (Conners 3; Conners 2008) C 677

Cronbach’s alpha ranging from 0.77 to 0.97 (mean Clinical Uses

Cronbach’a alpha = 0.90), and excellent temporal stability,
with test-retest correlations ranging from 0.71 to 0.98 The Conners 3 can be used as an assessment tool as well as
(mean r = 0.83, all correlations, p < 0.001). There is also a in planning and monitoring treatment plans. Standar-
great deal of consistency between multiple parent and/or dized scores allow for the objective comparison of an C
teacher ratings of the same youth, with inter-rater reliabil- individual with age- and gender-based expectations.
ity coefficients ranging from 0.52 to 0.94 (mean r = 0.77, Correspondence of items with DSM-IV-TR symptomatic
all correlations, p < 0.001). criteria for ADHD, CD, and ODD in combination with
The Conners 3 Manual reports a variety of studies information about associated features and level of
demonstrating convergent/divergent validity through cor- impairment facilitates differential diagnosis decisions in
relations of Conners 3 scales scores with other related clinical practice. The Conners 3 offers a scoring feature,
measures of childhood psychopathology. Overall, scales which links the assessment results to areas of eligibility
that assess similar constructs tended to be moderately to under the Individuals with Disabilities Improvement Act
strongly intercorrelated, while scales that did not assess of 2004 (IDEA 2004) making the assessment useful for
similar constructs tended to have smaller correlations. identification of appropriate educational classification
Table 1 provides highlights from these analyses. and/or services for students in the public school system.
Results from discriminative validity analyses indicated The Conners 3 can also be used as an assessment tool in
that the Conners 3 scores accurately discriminate between screening and research contexts.
relevant groups. Results from a series of multivariate In addition to being an assessment tool, the Conners
analysis of covariance revealed that, for all scales, the 3 forms can be employed as a tool for planning, monitoring,
means for the target clinical groups were significantly and evaluating treatment plans. Elevated scores from the
higher than the means for the general population Conners 3 suggest areas to target in treatment, with individ-
and other clinical groups (e.g., youth diagnosed with ual item responses can be used to guide decisions about
ADHD, predominantly hyperactive-impulsive type scored specific behaviors requiring intervention. The assessment
significantly higher on the hyperactivity/impulsivity and can also be used in treatment monitoring situations, for
ADHD hyperactive-impulsive scales than did youth example to monitor the effectiveness of an individual’s re-
without a clinical diagnoses, as well as youth diagnosed sponse to treatment or to evaluate an intervention program.
with other disorders). The sizes of the group membership The Conners 3, at the time of writing, is too recent to
effects (as determined with partial Z2) were moderate to have generated research literature, but empirical studies
large, on average, accounting for 19.1% of the variance in with earlier versions of the forms have demonstrated
scores. In terms of the classification accuracy of the scores the utility of the assessment in treatment outcome studies,
(as determined by a series of discriminant function epidemiological and etiological studies of ADHD and other
analyses), the mean overall correct classification rate was behavior problems, construct and discriminative validity
75.6% across all forms. studies, correlational studies, and cross-cultural studies.

Conners 3rd Edition (Conners 3; Conners 2008). Table 1 Overview of Correlations between the Conners 3 and Other Measures

Conners 3 scales Other measures r (range)

Inattention, ADHD inattentive BASC-2: Attention problems 0.52–0.89
ASEBA: Attention problems 0.72–0.96
Hyperactivity/Impulsivity, ADHD BASC-2: Hyperactivity 0.41–0.91
hyperactive-impulsive BRIEF: Inhibit 0.76–0.92
Executive functioning BASC-2: Executive functioning 0.43–0.68
BRIEF: Plan/Organize 0.70–0.87
Aggression, conduct disorder, oppositional BASC-2:Aggression 0.59–0.95
defiant disorder ASEBA: Aggressive behavior 0.58–0.93
Peer relations ASEBA: Social problems 0.72–0.84
Note. All rs significant, p <.05. BASC-2 = Behavior Assessment System for Children, Second Edition; ASEBA = Achenbach System of Empirically
Based Assessment; BRIEF = Behavior Rating Inventory of Executive Function.
678 C Conners Comprehensive Behavior Rating Scale

Cross References compulsive behaviors, violence potential, and physical

symptoms. Scales are also included to assess the Diagnostic
▶ Attention Deficit Hyperactivity Disorder and Statistical Manual of Mental Disorders (DSM-IV-TR;
▶ Conners Comprehensive Behavior Rating Scales American Psychiatric Association; APA, 2000) diagnostic
▶ Conners Continuous Performance Test-II criteria for symptoms of generalized anxiety disorder, sep-
▶ Individuals with Disabilities Education Act aration anxiety disorder, social phobia, obsessive compul-
sive disorder, major depressive episode, manic episode
autistic disorder, Asperger’s Disorder, attention deficit/hy-
References and Readings peractivity disorder (ADHD), conduct disorder, and oppo-
sitional defiant disorder. Other clinical indicators are also
American Psychiatric Association. (2000). Diagnostic and statistical
included for other potential problem areas, including bul-
manual of mental disorders (4th ed., text Rev.). Washington, DC:
American Psychiatric Association. lying, enuresis/encopresis, panic attack, pervasive develop-
American Psychiatric Association. (1994). Diagnostic and statistical mental disorder, pica, post-traumatic stress disorder,
manual of mental disorders (4th ed.). Washington, DC: American specific phobia, substance use, tics, and trichotillomania.
Psychiatric Association. The assessment also includes the Conners Clinical Index
Conners, C. K. (1969). A teacher rating scale for use in drug studies with
(Conners CI), Severe Conduct and Self Harm Critical
children. American Journal of Psychiatry, 126, 884–888.
Conners, C. K. (1997). Conners rating scales-revised technical manual. items, Validity scales (Positive Impression, Negative Im-
Toronto, Ontario, Canada: Multi-Health Systems. pression, and Inconsistency Index), Impairment items
Conners, C. K. (1989, 1990). Conners rating scales technical manual. (home, school, and social settings), and open-ended Addi-
Toronto, Ontario, Canada: Multi-Health Systems. tional Questions (additional concerns, strengths).
Conners, C. K. (2008). Conners 3rd edition manual. Toronto, Ontario,
In addition to the Conners CBRS form, the assessment
Canada: Multi-Health Systems.
Individuals with Disabilities Education Improvement Act of 2004 also offers the Conners CI as a standalone form. The Con-
(IDEA), Pub. L. No. 108–446, 118 Stat. 2647 (2004). [Amending ners CBRS forms provide a comprehensive view of a youth’s
20 U.S.C. 1400 et seq.]. behavioral, social, emotional, and academic functioning.
The Conners CI is a brief 24-item index with items from
the Conners CBRS form that best differentiate youth with
a clinical diagnosis from youth in the general population.
Conners Comprehensive Administration requires approximately 25 min for the
Behavior Rating Scale Conners CBRS forms and 10 min for the Conners Clinical
Index form. Raw scores are converted to age- and gender-
C. K EITH C ONNERS 1, J ENNI P ITKANEN 2, S ARA R. R ZEPA 2 based standard scores (including T-scores and percen-
1
Duke University Medical School tiles). Results from the DSM-IV-TR symptom scales are
Durham, NC, USA also reported in terms of symptom counts, that is, whether
2
Multi Health Systems Inc. or not the minimum symptom requirements set by the
Toronto, ON, Canada DSM-IV-TR have been met. The Conners CI produces a
probability score, which indicates whether the youth’s
scores are more like youth with a clinical diagnosis
Description (disruptive behavior disorder, learning/language disorder,
mood disorder, anxiety disorder, or ADHD) or with those
The Conners Comprehensive Behavior Rating Scales from the general population.
(Conners CBRS; Conners, 2008) is a comprehensive The Conners CBRS normative sample consists of
assessment tool, which can be used to assess a wide range 3,400 assessments (1,200 parent, 1,200 teacher, and
of behavioral, emotional, social, and academic issues in 1,000 self-report assessments) including 50 boys and
school-aged youth. The Conners CBRS is a multi-infor- 50 girls from each age (6–18 years for the parent and teacher
mant assessment with forms for parents, teachers, and report, 8–18 years for the self-report). The racial/ethnic
youth. Parent and teacher ratings can be obtained about distribution of this sample closely matches the US
youth aged 6–18 years, and youth aged 8–18 years can population. Approximately 2,000 clinical cases were also
complete the self-report. The assessment features multiple collected from youth with following diagnoses: ADHD,
Content scales that assess emotional distress, aggressive disruptive behavior disorders, learning disorders, anxiety
behaviors, academic difficulties, hyperactivity/impulsivity, disorders, major depressive disorder, bipolar disorder, and
social problems, separation fears, perfectionistic and pervasive developmental disorders.
 Conners Comprehensive Behavior Rating Scale C 679

Historical Background with test-retest correlations ranging from 0.56 to 0.96

(mean r = 0.81, all correlations, p < 0.001). There is also
The Conners CBRS is a new assessment tool, which is a great deal of consistency between multiple parent and/or
built on the foundation of the Conners Rating Scales. teacher ratings of the same youth, with inter-rater reliabil-
The Conners Rating Scales are a widely used and well ity coefficients ranging from 0.53 to 0.89 (mean r = 0.74, C
validated assessment of ADHD and related issues. When all correlations, p < 0.001).
updating and revising the latest version of the scales The Conners CBRS Manual reports a variety of stud-
(Conners 3rd Edition; Conners, 2008), the need for a ies demonstrating convergent/divergent validity through
comprehensive assessment of behavioral, social, emotional, correlations of Conners CBRS scales scores with other
and academic concerns became evident. The Conners related measures of childhood psychopathology. Overall,
CBRS was therefore developed to provide clinicians with scales that assess similar constructs tended to be moder-
an assessment and treatment planning/monitoring tool, ately to strongly intercorrelated, while scales that did not
which would address a broad range of clinical issues in assess similar constructs tended to have smaller correla-
school-aged youth and which could be linked to diagnos- tions. Table 1 provides highlights from these analyses.
tic and intervention systems such as the DSM-IV-TR Results from discriminative validity analyses indicated
(APA, 2000) and Individuals with Disabilities Education that the Conners CBRS scores accurately discriminate
Improvement Act of 2004. between relevant groups. Results from a series of multi-
variate analysis of covariance revealed that, for all scales,
the means for the target clinical groups were significantly
Psychometric Data higher than the means for the general population and
other clinical groups (e.g., youth diagnosed with a disrup-
Results of reliability analyses revealed that the Conners tive behavior disorder scored significantly higher on the
CBRS assessments have high levels of internal consistency, Aggressive Behavior and Violence Potential scales than
with Cronbach’s alpha ranging from 0.69 to 0.97 (mean did youth without a clinical diagnoses, as well as youth
Cronbach’a alpha = 0.86), and excellent temporal stability, diagnosed with other disorders). The sizes of the group

Conners Comprehensive Behavior Rating Scale. Table 1 Overview of correlations between the Conners CBRS
and other measures

Conners CBRS Scale Other measures r

Conners CBRS Content Scales Emotional distress BASC-2: Anxiety 0.47–0.87
ASEBA: Anxious/Depressed 0.53–0.85
Academic difficulties BASC-2: Learning problems 0.78–0.93
Aggressive behaviors, violence potential ASEBA: Aggressive behavior 0.60–0.96
Physical symptoms BASC-2 somatization 0.59–0.78
DSM-IV-TR Symptom Scales ADHD inattentive ASEBA: Attention problems 0.72–0.91
ADHD hyperactive-impulsive BRIEF: Inhibit 0.74–0.89
Major depressive episode BASC-2: Depression 0.38–0.71
ASEBA: Anxious/Depressed 0.43–0.83
Generalized anxiety disorder BASC-2: Anxiety 0.46–0.67
ASEBA: Anxious/Depressed 0.51–0.83
Social Phobia MASC: Social anxiety 0.62–0.68
Separation anxiety disorder MASC: Separation/Panic Scale 0.42–0.53
Autistic disorder, Asperger’s disorder BASC-2: Developmental social disorders 0.43–0.69
ASEBA: Social problems 0.64–0.80
Note. All rs significant, p < .05. BASC-2 = Behavior Assessment System for Children, Second Edition; ASEBA = Achenbach System of Empirically
Based Assessment; BRIEF = Behavior Rating Inventory of Executive Function; MASC = Multidimensional Anxiety Scale for Children.
680 C Conners Rating Scales

membership effects (as determined with partial Z2) were Conners, C. K. (2008). Conners 3rd Edition manual. Toronto, Ontario,
Canada: Multi-Health Systems.
moderate to large, on average, accounting for 14.5% of
Individuals with Disabilities Education Improvement Act of 2004
the variance in scores. In terms of the classification (IDEA), Pub. L. No. 108–446, 118 Stat. 2647 (2004). [Amending
accuracy of the scores (as determined by a series of 20 U.S.C. 1400 et seq.].
discriminant function analyses), the mean overall correct
classification rate was 78% across all forms.

Conners Rating Scales

Clinical Uses
A LLISON S. E VANS 1, A NDREW P RESTON 2
1
The Conners CBRS can be used as an assessment tool as Pawtucket, RI, USA
2
well as in planning and monitoring treatment plans. Brown University Medical School
Standardized scores allow for the objective comparison Providence, RI, USA
of an individual with age- and gender-based expectations.
Correspondence of items with DSM-IV-TR, symptomatic
criteria for a number of disorders in combination with Synonyms
information about the youth’s level of impairment, facil-
itates differential diagnosis decisions in clinical practice. CPRS; CRS
The Conners CBRS offers a scoring feature, which links
the assessment results to areas of eligibility under the
Individuals with Disabilities Improvement Act of 2004 Description
(IDEA, 2004), making the assessment useful for identifi-
cation of appropriate educational classification and/or The Conners Rating Scales are used as a general screening
services for students in the public school system. The tool for the detection of problematic behaviors, and At-
Conners CBRS forms can also be used as an assessment tention Deficit Hyperactivity Disorder (ADHD) symp-
tool in screening and research contexts. toms in particular, in children and, more recently, in
In addition to being an assessment tool, the Conners adults.
CBRS can be employed as a tool for planning, monitoring,
and evaluating treatment plans. Elevated scores from the
Conners CBRS suggest areas to target in treatment, with Historical Background
individual item responses can be used to guide decisions
about specific behaviors requiring intervention. The assess- Rating scales and symptom checklists provide an effective,
ment can also be used in treatment monitoring situations, for quick, and standard approach to the measurement of prob-
example to monitor the effectiveness of an individual’s re- lematic behaviors observed in children. The Conners rating
sponse to treatment or to evaluate an intervention program. scales were initially developed as comprehensive checklists
of basic presenting problems of children. A re-standardiza-
tion took place in the late 1990s, which was designed to
Cross References provide a stronger empirical base and a more narrowed
focus of common behavioral problems in childhood. The
▶ Conners 3rd Edition revised scales were developed with norms derived from a
▶ Conners Continuous Performance Test large, representative sample of North American children,
▶ Differential Diagnosis using confirmatory factor analyses to develop a definitive
▶ Individuals with Disabilities Education Act factor structure. The revised scales focused on behaviors
directly related to ADHD and its associated behaviors. The
item content was updated to reflect the recent knowledge
References and Readings and developments concerning ADHD. The revised scale’s
content contained fewer items, yet the authors claimed that
American Psychiatric Association. (2000). Diagnostic and statistical
with greater focus on ADHD-related behaviors and concor-
manual of mental disorders (4th ed., Rev. Ed.). Washington, DC:
American Psychiatric Association.
dance between scale items and current conceptualizations
Conners, C. K. (2008). Conners comprehensive behavior rating scales of ADHD, the CPRS-R provided better discriminatory
manual. Toronto, Ontario, Canada: Multi-Health Systems. power for detecting ADHD children than previous versions.
 Conners’ Continuous Performance Test (CPT) C 681

Psychometric Data References and Readings

The authors report that the psychometric properties of Conners, C. K. (1989). Conners’ Rating Scale Manual. New York: Multi-
the revised scale are adequate as demonstrated by good Health Systems, Inc.
Conners, C. K., Erhardt, D., & Sparrows, E. (1999). Conners’ Adult ADHD
internal reliability coefficients, high test–retest reliability, C
Rating Scales (CAARS). North Tonawanda, NY: Multi-Health
effective discriminatory power, and predictive and struc- Systems, Inc.
tural validity. Various researchers have suggested three Conners, C., Sitarenois, G., Parker, J. D., & Epstein, J. N. (1998).
main areas for the application of Conners scales: as a The revised Conners’ Parent Rating Scale (CPRS-R): factor struc-
general screening tool for the detection of problematic ture, reliability, and criterion validity. Journal of Abnormal Child
Psychology, 26, 257–268.
behaviors in children, as a complimentary tool for clarify-
Conners, C., Sitarenois, G., Parker, J. D., & Epstein, J. N. (1998). Revision
ing a specific diagnosis, and as a measurement tool for the and restandardization of the Conners’ Teacher Rating Scale (CTRS-R):
assessment of treatment results. Factor structure, reliability, and criterion validity. Journal of Abnor-
mal Child Psychology, 26, 279–291.

Clinical Uses
The Conners scales are designed to assess symptoms as
reported by various informants (e.g., parents, teachers,
self-report for adolescents) using corresponding factor
Conners’ Continuous
structures. There are also short and long forms that vary Performance Test (CPT)
from approximately 20 to 80 items. The Conners ratings
have also been compared across cultures, including (for C. K EITH C ONNERS 1, G ILL S ITARENIOS 2
1
example) Italian, British, Chinese, Brazilian, and New Duke University Medical School
Zealand cultures and, consequently, translated into a num- Durham, NC, USA
2
ber of different languages, including Sudanese Arabic, Multi Health Systems Inc.
Turkish, and Hindi. Toronto, ON, Canada
The Conners Adult ADHD Rating Scale (CAARS) was
more recently developed to assess ADHD symptomato-
logy in adults. The rating scale was designed to be com- Description
pleted by respondents about themselves or about a
significant other. Factor analyses used to select items and The Conners Continuous Performance Test - 2 (CPT-2;
determine the structure of the CAARS scale were Conners, 2000) is a computer administered test that is
based on data from a derivation sample consisting of designed to assess problems with attention. The Con-
839 normal adults and from a clinical sample consisting ners CPT-2 presents 360 stimuli trials (i.e., individual
of 167 adult. Four major dimensions were reported: three letters) on the screen, with 1, 2, or 4 s between the
corresponded to the core features of ADHD seen in chil- presentation of letters (ISI: Inter-Stimulus Interval).
dren and the fourth, a secondary consequence of ADHD: The 360 trials are divided into 18 blocks of 20 trials
(1) Inattention/Executive Functioning, (2) Hyperactivity/ each. The ISIs are counterbalanced across these blocks.
Restlessness, (3) Impulsivity/Emotional Lability, and (4) Respondents are instructed to press the spacebar or the
Problems with Self-Concept. Internal reliability coefficients appropriate key on the mouse for any letter that
for the CAARS scales for four different age groups (18 years appears, except the letter ‘‘X.’’ The CPT takes fourteen
plus) were reported to be ‘‘excellent’’ (coefficient alphas min to administer excluding the recommended practice
ranging from 0.86 to 0.92 for males and females) and test. Over the duration of the test, 324 non-X stimuli
test–retest reliability over a month was felt to be strong (i.e., targets) appear, and the letter ‘‘X’’ (nontarget)
(0.80–0.91). appears 36 times. One of the primary advantages of
this paradigm is the high proportion of targets that
appear, yielding a larger pool of responses for generat-
Cross References ing the statistical output. Many statistics are computed
including omission errors (i.e., failing to respond to a
▶ Conners 3rd Edition (Conners 3; Conners 2008) target letter), commission errors (i.e., responding to a
▶ Conners Comprehensive Behavior Rating Scales nontarget), hit reaction time (the average speed of
682 C Conners’ Continuous Performance Test (CPT)

correct presses to target letters), hit reaction time stan- was initially released as a DOS application (Conners
dard error (which assesses the consistency of responses CPT 3.0; Conners, 1994), and later renormed and
to targets), detectability (the ability to discriminate converted into a windows application (Conners, 2000).
between targets and nontargets), response style
(assesses speed vs accuracy response tendencies), per-
severations (reaction times less than 100 ms), hit reac-
tion time by block (change in reaction time as the test Psychometric Data
progresses), standard error by block (change in re-
sponse consistency as the test progresses), reaction Reliability. Split-half reliability results were computed for
time by ISI (change in mean reaction time across the original standardization sample (Conners, 1994,
ISI), and standard error by ISI (change in response 2000). The mean split-half reliability was 0.83 (range
consistency across ISI). These statistics are converted 0.66 to 0.95). Test-retest reliability is reported in Conners
to T-scores and can be interpreted in terms of various (2000) and is based on a small sample (n = 23). Test-retest
aspects of attention including inattention, impulsivity, correlation was high for the confidence index (r = 0.89),
and vigilance. The CPT-2 also provides a confidence and moderate to high for omissions, commissions,
index probability (expressed as a percentage out of 100) Hit Reaction Time, Hit Reaction Time Standard Error,
of the results being from a clinical as opposed to a non- Variability, Detectability, and Response Style (range
clinical case. r = 0.43 to r = 0.84). The Block change and ISI change
T-scores are computed using General Population (not statistics were less consistent across test administrations
pre-identified with a clinical condition) norms (Conners, (r = 0.05 to r = 0.51).
2000) obtained for children and adults aged 6 years and Validity. Validation of the CPT-2 focused on its two
above. The test is based on a total of 1,920 normative primary clinical uses: to help identify clinical problems
cases, out of which 52.8% of the cases were female, 47.0% with attention or potential neurological impairments and
were White, 27.0% Black, and 21.4% of other ethnic to monitor treatment effects. Conners (2000) compares
origin. Demographic information for age is shown in means from the General Population normative data
Table 1. T-scores are computed based on the age and (n = 1483), and ADHD cases (n = 271) in an ANCOVA
gender of the respondent. Data was also collected for controlling for age and gender for 6–17 year olds.
378 ADHD cases, and 223 neurologically impaired cases Performance of the ADHD group was significantly worse
(e.g., post-concussive, other organic brain syndrome, on the CPT-2 for all of the measures except commissions
dementia). where no significant difference was found. Discriminant
Function Analysis was also used to examine classification
accuracy for the CPT-2. For 6–17 year olds, sensitivity is
Historical Background reported at 83% and specificity at 82%. Similar analyses
were conducted on the adult samples. In addition to
The acronym ‘‘CPT’’ was first introduced by Rosvold, General Population data (n = 437), ADHD data
Mirsky, Sarason, Bransome, and Beck (1956) who used a (n = 107), neurologically impaired data was also available
particular version to detect attention lapses in subjects (n = 223). Performance of the ADHD group and
with petit mal epilepsy. In early CPTs such as the one neurologically impaired group was significantly worse
they used, subjects were required to press a key when a than the General Population group for all of the CPT-
target letter (e.g., ‘‘X’’) appeared or when the target 2 measures. The neurologically impaired group also
letter appeared preceded by another letter (e.g., ‘‘AX’’). scored significantly worse than the ADHD group on
While the CPT was being explored in clinical settings, several measures. They made significantly more omission
Mackworth (1957) initiated basic vigilance studies. errors, had significantly slower reaction times, had more
By changing basic test parameters, different CPT variable reaction times, and their standard error was
paradigms could be constructed. The CPT-2 paradigm affected more by letter presentation speed (ISI).

Conners’ Continuous Performance Test (CPT). Table 1 Age distribution of CPT-2 Normative Sample
Age 6–7 8–9 10–11 12–13 14–15 16–17 18–34 35–54 55+
n 88 283 369 258 261 224 237 146 54
 Consciousness C 683

Discriminant Function Analyses comparing ADHD to Cross References

General Population cases yielded 87% specificity
and 88% sensitivity. When comparing neurologically ▶ Attention Deficit, Hyperactivity Disorder
impaired cases to General Population cases, specificity ▶ Conners 3rd Edition (Conners 3; Conners 2008)
was 92% and sensitivity was 85%. ▶ Conners Comprehensive Behavioral Rating Scale C
In terms of treatment sensitivity, Conners, Casat,
Gualtieri, and Weller (1996) examined the efficacy of
bupropion in the treatment of children with ADHD and References and Readings
used the Conners’ CPT as one of the efficacy assessment
tools. A double-blind procedure was used with 72 ADHD Boonstra, A. M., Kooij, J. J., Oosterlaan, J., Sergeant, J. A., &
children and 32 ADHD control children aged 6–12. Buitelaar, J. K. (2005). Does methylphenidate improve inhibition
and other cognitive abilities in adults with childhood-onset ADHD?
Subjects were randomized to receive 3–6 mg/kg of
Journal of Clinical and Experimental Neuropsychology, 27, 278–298.
buproprion per day or placebo twice daily. Significant Conners, C. K. (1994). Conners’ Continuous Performance Test computer
treatment effects were found. Epstein et al. (2006) exam- program 3.0 User’s manual. Toronto, ON: Multi Health Systems Inc.
ined mean differences between 190 children who took a Conners, C. K. (2000). Conners’ Continuous Performance Test (CPT-2)
stimulant medication on the day of neurological testing computer program for windows, technical guide, and software manual.
Toronto, ON: Multi Health Systems Inc.
and 126 children who took no stimulant medication of
Conners, C. K., Casat, C. D., Gualtieri, C. T., & Weller, E. (1996).
the day of testing. Children who were not on medication Bupropion hydrochloride in attention deficit disorder with hyperac-
made significantly more omission errors and commission tivity. Journal of the American Academy of Child and Adolescent
errors, had significantly slower reaction times, and were Psychiatry, 35, 1314–1321.
significantly more variable in their response speed. Boon- Conners, C. K., Epstein, J. N., Angold, A., & Klaric, J. (2003). Continuous
Performance Test performance in a normative epidemiological
stra, Kooij, Oosterlaan, Seargeant, and Buitelaar (2005)
sample. Journal of Abnormal Child Psychology, 31, 555.
tested 43 adults with ADHD in a double-blind, cross-over, Epstein, J. N., Conners, C. K., Hervey, A. S., Tonev, S. T., Arnold, L. E.,
and placebo controlled study. The CPT-2 was adminis- Abikoff, H., et al. (2006). Assessing medication effects in the MTA
tered during the third week of titrated treatment with study using neuropsychological outcomes. Journal of Child
methylphenidate and during the third week of treatment Psychology and Psychiatry, 47, 446–456.
Epstein, J. N., Erkanli, A., Conners, C. K., Klaric, J., Costello, J. E., &
with placebo. Large medication effects were observed for
Angold, A. (2003). Relations between Continuous Performance
commission errors, standard error of hit reaction time, Test measures and ADHD behaviors. Journal of Abnormal Child
and inattentiveness. A moderate effect was also observed Psychology, 31, 543–554.
for hit reaction time. Hervey, A. S., Epstein, J. N., Curry, J. F., Tonev, S., Arnold, L. E.,
Conners, C. K., et al. (2006). Reaction time distribution analysis of
neuropsychological performance in an ADHD sample. Child
Neuropsychology, 12, 125–140.
Clinical Uses Mackworth, N. H. (1957). Some factors affecting vigilance. Advancements
in Science, 53, 389–393.
Although the CPT-2 cannot be used alone to make a Rosvold, H. E., Mirsky, A. F., Sarason, I., Bransome, E. D., Jr., &
diagnosis, it provides performance based information Beck, L. H. (1956). A continuous performance test of brain damage.
Journal of Consulting Psychology, 20, 343–350.
that aids in the diagnostic process. The performance
based information from the CPT-2 complement infor-
mant reports commonly obtained from parents, teachers,
or by self-report. Response patterns on the CPT-2 enable
practitioners to better understand the type of deficits that Consciousness
might be present (e.g., Epstein, Erkanli, Conners, Klaric,
Costello, & Angold, 2003; Hervey et al., 2006). For R ONALD A. C OHEN
example, some response patterns might suggest inatten- Brown University
tiveness or impulsivity, while other response patterns may Providence, RI, USA
indicate activation/arousal problems or difficulties main-
taining vigilance. The CPT-2 has also commonly been
used as a way of assessing treatment effectiveness. Careful Synonyms
charting of CPT scores while testing different drug
dosages can often be helpful in determining optimal Alertness; Awareness; Mindfulness; Self-awareness;
dosage levels. Wakefulness
684 C Consciousness

Definition was a primary task for psychology. He postulated that

‘‘apperception’’ represented the core activity of the mind
Consciousness comes from the Latin word ‘‘conscientia’’ and was the interface between internal and external experi-
which means ‘‘knowledge-within’’, or knowledge that is ence. Notably, Wundt’s primary method for exploring these
shared. Today the term is used to describe the experience processes was introspection, which essentially is the process
of ‘‘self ’’ as distinct from the external environment. It is of looking inward or self-reflection. These ideas evolved
characterized by experiences of alertness, self-awareness, into structuralism, the first dominant theoretical school of
and attention of oneself relative to the environment rela- psychology.
tive to the self; i.e., identify, which in turn involves aware- A dramatic shift away from consideration of con-
ness of one’s own perceptions, associations, emotional sciousness occurred during much of the twentieth century
experience, and the cognitive interpretation of these as behaviorism became the dominant perspective, as con-
experiences. More narrowly, consciousness is often de- sciousness was viewed as metaphysical and beyond em-
fined level of arousal, wakefulness, alertness, responsive- pirical observation. Even cognitive scientists tended to
ness, and adaptability in contrast to states of coma or steer away from tackling this construct, probably because
sleep. of the difficulties associated with experimentally studying
However, consciousness has defied unitary definition, it. Yet, for clinicians working with the subjective experi-
perhaps because it is intrinsically bound to subjective ences of their neurological and psychiatric patients, con-
experience. sciousness was difficult to avoid. When the neurologist
Babinski (1914) first described patients who were unaware
of their own deficits (i.e., anosognosia) he was essentially
Historical Background addressing the issue of consciousness and self-awareness.
Initially, the problem of consciousness was handled by
The nature of human consciousness has been a primary narrowing the meaning of the term to refer to the state
topic of philosophical inquiry throughout the ages. The of being awake, alert and aware, in contrast to coma,
ancient Greek philosophers contemplated questions re- stupor, or sleep, which in turn led to the idea of level of
garding the relationship between external and objective consciousness, which remains a standard part of mental
reality. For example, Plato recognized that humans can status examinations.
think and speak, and yet not be fully aware of their larger
realm and whether their observations were valid with
respect to external reality. His cave allegory was an effort Current Neuropsychological Knowledge
to describe this problem. For medieval religious philoso-
phers (e.g., Aquinas), it referred to the act of applying Over the past 2 decades there has been a major resurgence of
moral knowledge to one’s actions. Descartes extended the interest and research effort directed at the nature of con-
concept of ‘‘conscientia’’ to include the idea that it sciousness, along with growing recognition that the con-
involves a psychological state of mind, and used separate struct is a necessary one, as consciousness describes an
terms to explain this level of experience from moral important element of human experience, the sense of self.
knowledge, though he did not formally employ the mod- A number of scientific developments set the stage for this
ern concept of consciousness in his dualism of mind– shift in zeitgeist. The evolution of the field of cognitive
body interaction. John Locke later wrote ‘‘I may be held science provided empirical methods for studying covert
morally responsible for the act of which I am conscious of ‘‘mental’’ processes. Also as cognitive processes such as
having achieved; and my personal identity; my-self goes as attention and memory were better understood, foundations
far as my consciousness extends itself ’’, its first modern were established for studying phenomena like intention and
usage associated with the idea of ‘‘self ’’ and personal self-awareness. Computational neuroscience was also influ-
identity. Interestingly, Locke still linked consciousness ential in this regard. It is quite difficult to operationalize or
to the ideas of morality and responsibility. The nature conceptualize consciousness as a single node in a top-down
of consciousness was a recurrent theme of renaissance modular cognitive framework. This is less of a problem for
philosophers. computational theories that take a bottom-up approach,
The quest to better understand the nature of conscious- such as the parallel distributed processing (PDP) models
ness dominated the new science of psychology at it evolved proposed by Rummelhart and McClelland (1986), as con-
in the late nineteenth century. Wilhelm Wundt believed sciousness can be conceptualized as an emergent byproduct
that identifying the constituents of human consciousness of associative networks acting together with feedback or
 Consciousness C 685

feed-forward organization. Another major impetus for con- In contrast to AD, patients with certain other degenera-
sciousness becoming an acceptable topic for scientific in- tive conditions often show general preservation of con-
quiry was advances in the field of neuroscience itself. sciousness despite having marked impairments of other
Functional imaging methods have made it easier to measure functions. For example, patients with severe Parkinson’s
brain responses associated with subjective cognitive states, disease typically have major motor symptoms, cognitive C
providing evidence that these states have valid neurobiolog- control problems, including executive and attention dys-
ical underpinnings. Furthermore, growing recognition function. They may also show blunting of emotional re-
of the brain’s complexity has played an important role. sponse and altered emotional functioning. Yet, they are
There is now general consensus that cognition involves often painfully aware of their deficits, and have greater
interactions among large networks of cortical neurons, preservation of sense of self than the AD patient. Similarly,
which communicate across larger functional systems in an patients with Multiple Sclerosis (MS) sometimes exhibit
integrated manner. This perspective enabled cognitive neu- pseudobulbar affect. They are affectively labile with dramat-
roscientists to shift away from having to view consciousness ic shift in the outward expression of emotion, but yet they
as a unitary process sitting on top of the pyramid of cogni- report not feeling the emotion that corresponds to this
tive functions. expression. Despite these problems with affective and be-
Several lines of research and clinical evidence have had havioral control, patients with MS typically are very aware
particular bearing on current knowledge regarding the of their deficits and may feel locked in because of their
neuropsychology of consciousness. The effect of various symptoms.
types of drugs, most notably hallucinogens, opiates, and Alterations in self-awareness and consciousness also
alcohol on conscious experience provides one of the most occur as a result of damage to specific brain regions. This
clear cut illustrations of the fact that even among healthy fact is significant since it suggests that certain functional
people consciousness is not a static phenomenon. One’s anatomic systems play an important role in the experience
sense of reality, identify and self-awareness can be dra- of consciousness, though probably not as a function of
matically altered by drugs such as LSD, presumably any one of these systems alone. Subcortical lesions affect-
by altering the flow of information processing. Case stud- ing the mid-brain, brain stem and thalamus often cause
ies have consistently shown that disruption of self-aware- dramatic alterations in level of consciousness. The reticu-
ness as a function of damage to specific brain regions. lar system which generates ascending activation to cortical
Furthermore, clinicians working with patients experien- areas plays a well established role in this phenomenon,
cing neurodegenerative dementias have long been aware with damage to this system contributing to problems with
of dramatic impoverishment in the quality of conscious arousal and alertness. Damage to these areas frequently
experience as the disease progresses, corresponding underlies coma, and the electrical activity measured by
with the extent of cortical atrophy. Among patients with EEG is amplified by generators in these systems. Persistent
Alzheimer’s disease (AD) and other neuronal dementias, a vegetative state is a clinical illustration of this, as these
loss of ‘‘self ’’ is one of the hallmark features of the end- unfortunate patients exhibit impaired higher cortical
stage condition. In fact, it is when AD patients lose their functions, have persevered circadian sleep-wake cycles
ability to respond to people who are familiar and mean- and autonomic function. Compared to healthy people
ingful to them, and when they lose awareness of their own who are awake, patients with this syndrome have im-
identify, their personal memories, and the nature of their paired connectivity between brainstem and thalamic
cognitive problems that families typically experience areas and the cortex. This results in a reduced cortical
greatest despair. In fact, it is often this change, along activation, with generalized slowing consistent with coma.
with an inability for self-care that leads to nursing home These subcortical areas are clearly essential for maintain-
placement rather than the amnestic disturbance per se. ing normal consciousness, since disconnecting them from
The loss of identity in AD patients usually corresponds cortical areas impairs alertness, attention, and other cog-
with personality changes and profound impoverishment nitive functions linked to consciousness. The activation
in abstraction and associative ability. While other cogni- and arousal associated with this functional anatomic sys-
tive functions like language are often also severely tem makes an essential contribution to is a necessary part
impaired at this point, it may be difficult to fully appreci- of the maintaining consciousness, thought this activation
ate these changes, though the quality of emptiness and is not sufficient to account for the full dynamic of con-
loss of self that may ultimately be the characteristic that sciousness (i.e., self-awareness and sense of identity).
best defines severe dementia rather than impairment in a The thalamus appears to play an important role in
particular cognitive domain. consciousness, but as a convergence site of reticular
686 C Consciousness

activation from lower brain systems and because of its There is strong evidence from studies of neglect syn-
role in integrating this activation with cortical input. drome that medial frontal and anterior cingulate cortical
Bilateral ablation of the central medial zone of the intra- areas play a major role in ‘‘intention’’ (Cohen, 1993). The
laminar nucleus of the thalamus produces coma and intent and plan for action seems to be an important
persistent vegetative states. This thalamic area is affected element of consciousness, as this capacity is linked to
by general anaesthetics and drugs that cause sedation, the experience of drive and spontaneity. An illustration
suggesting that it is necessary for anti-psychotic drugs. of this is seen in patients who undergo cingulotomy, as
This evidence suggests that a functioning thalamus is their primary long-term neurocognitive deficit involves
necessary, but not sufficient, for human consciousness, diminished performance on tests requiring intention, and
though again this area alone is not sufficient to account also reduced spontaneity, initiative, and creative impulse.
for all aspects of consciousness. Cortical and limbic func- It is also noteworthy that syndromes that result in altera-
tions are necessary elements of normal consciousness. tions of consciousness that involve delusions and a frac-
Patients with bilateral occipital damage who exhibit tured sense of reality, such as reduplicative para-amnesia
blind sight are clearly experiencing some alteration in and Capgrass syndrome, tend to occur among patients with
consciousness and self-awareness. Yet, this disturbance frontal lobe damage, often involving the non-dominant
may be relative focal and limited to vision. For these hemisphere. In cases of reduplicative paramnesia, patients
individuals, altered consciousness has not affected all may feel with certainty that while the house in which they
aspects of self-awareness and identity. Damage to other are living looks identical to their real home, that it is in fact a
cortical areas may also produce specific impairments of replica of their home. When queried these patients usually
awareness and self-consciousness. For example, the ne- acknowledge the logical implausibility of their belief, but
glect syndrome commonly associated with right inferior state that they are certain because of some feeling they have,
parietal damage often results in anosognosia and im- suggesting a relationship between emotional response and
paired awareness of what is being neglected. For some of the processing of these frontal systems. Primate studies
these patients, the alteration in awareness and conscious- support the role of the frontal cortex in this regard, and
ness extends beyond the limits of the spatial disturbance led Crick and Koch (1995) to propose that consciousness is
that is observed. Yet, typically patients with these lesions largely dependent on the resonance of thalamo-cortical
do not lose their sense of self completely. They may show systems acting in a recursive manner.
diminished ability for self-reflect, but usually show abil- The role of memory and its underlying functional
ities in this regard as long as not tied to the types of spatial neuroanatomic systems raises a number of interesting
processing that is affected. issues for consciousness. Patients like HM, who have
The frontal cortex seems to have be the cortical area suffered bilateral damage to hippocampal or paralimbic
with greatest influence on consciousness, self-regulation areas, lose their ability to form new episodic memories.
and self-referential processes. The famous case of Phineus Yet, they typically retain retrograde memory for events
Gage, the railroad worker who suffered severe frontal that happened earlier in their life, which enables them to
damage when a spike penetrated his brain provided his- retain some sense of personal identity based on these
torical illustration of this. Following his injury Gage recollections. Yet, they have lost the ability to update
became indifferent to social consequences and showed these memories or to adapt these memories to new cir-
little self-regard for his own behavior (Harlow, 1848). cumstances. Clearly this results in an alteration of con-
While it is impossible to accurately evaluate the nature sciousness, though they may still report knowing who
of change in his subjective sense of consciousness and self- they are or what they think about certain topics.
awareness based on the historical record, it seems clear In addition to the contribution of specific cortical
from clinical descriptions that his self-awareness was dra- and subcortical areas to the experience of consciousness,
matically altered. In modern case study, Eslinger and his there is a rich history of research on brain laterality,
colleagues (1986) have demonstrated impaired empathy specifically the effects of disconnection between the left
associated with frontal lobe disturbance, which affects and right hemisphere of the brain. The corpus callosum
social reasoning, judgment and perspective taking. Inter- provides the white matter linkage between the hemi-
estingly, this disorder of empathy also involves problems spheres. Roger Sperry observed remarkable alterations
with moral reasoning, a notion consistent with early phil- in consciousness and awareness among patients who
osophical ideas regarding consciousness, which as dis- underwent surgical severing of the corpus callosum
cussed earlier conceptualized consciousness as tied to (split brain) for treatment of intractable seizures. When
man’s capacity for moral knowledge. the two hemispheres are no longer able to communicate,
 Consciousness C 687

each processes and interprets information presented to it likely play a significant role, by linking emotional valence
in different ways. For example, the left hemisphere is to particular associative information. In interaction with
typically more involved in language processing, and cortical areas, these limbic areas enable amplification of
therefore tended to be aware of verbal elements of infor- affective signals, and also their regulation, providing for
mation during tasks compared to the right hemisphere. the intensity and richness of emotional affective experi- C
Because of a lack of integration between the cortical ence. (5) Some type of mechanism that enables temporal
hemispheres, it is possible to dissociate elements of con- binding of associative experiences in an integrated way
sciousness tied to each side of the brain. Yet, following likely occurs that creates the feeling of a unified conscious
this procedure, it was only under experimentally con- experience and sense of single identity, ‘‘I’’.
trolled conditions that major dissociations occurred. Some of the distinctions that exist between theories of
Post-surgically, people still experienced a single identity consciousness relate to the emphasis that is placed on
in everyday experience, suggesting that splitting the two particular cognitive functions. Some recent investigators
hemispheres does not completely disrupt the sense of a have emphasized the role of posterior brain systems
unified consciousness. involved in visual processing to a greater extent. A num-
ber of theories emphasize the role of frontal brain systems.
For example, one of the first neuroscientific models of
Neuropsychological Models of consciousness proposed by Shalice (1978) viewed con-
Consciousness sciousness as a byproduct of dominant action systems
that govern the stream of thought processes. As discussed
Consideration of the neuropsychological literature to date previously, many models have focused on frontal systems
has established the foundations for the cognitive neuro- with varying degrees of emphasis on particular processes.
science of consciousness. Over the past 15 years, theoreti- Damasio’s model of consciousness emphasizes the critical
cal models have been developed to explain how the role of emotional processing systems, as well as the so-
brain creates ‘‘mind’’ and ‘‘consciousness’’. These models matic or visceral activity of the body as a whole.
include contributions from philosophers (Dennett, 1991; Perhaps the greatest distinction between theories of
Churchland, 2005), neuropsychologists/behavioral neu- consciousness stems from the extent to which it is
rologists (Cohen, 1993; Damasio, 1995, 2000) and cogni- viewed as distinct from the physical processes that com-
tive neuroscientists (Shallice, 1978; Eccles, 1994; Crick prise, or essentially indistinguishable from these physical
and Koch, 1995; McClelland et al., 1997; Grossberg, processes, as Dennett argues. Furthermore, some of these
1999). It is beyond the current scope to review each of models take more of a top-down approach, whereas others
their models. However, there are several features common view consciousness from a bottom-up perspective, as an
to each, as well as a few fundamental distinctions between emergent byproduct of all of the more basic associative
these models, as summarized below. processes that underlie cognition. The PDP approach of
Most current models of consciousness take the per- McClelland and Rummelhart (1986, 1997), and other neu-
spective that consciousness is not localized to a single rocomputational theories (e.g., Grossberg, 1999) take a
brain region, but rather is an emergent function of multi- more bottom-up approach and tend to view conscious-
ple systems acting in an integrated fashion. (1) Almost all ness as the sum total of these distributed processes. De-
researchers and theorists agree that lower brain areas (e.g., spite these differences, there seems to be little
reticular system) that energize the brain and lead to alter- disagreement that consciousness is a complex cognitive
ing levels of activation are a necessary requirement for phenomenon that results from the interaction of multiple
consciousness, but not sufficient to explain the phenome- brain systems and processes, which in an integrated co-
non. (2) The thalamus seems to play and essential role, herent manner provides for the sense of self, universally
particularly as a nexus for this activation and for integra- experienced by healthy humans.
tion and gating of cortical information. (3) Frontal
regions appear to play several important roles, including
the generation and sustaining of intention, switching and Future Directions
gating of information, and the enabling of feedback, and
feed-forward mechanisms that enable reprocessing of cer- The cognitive and neurobiological bases of consciousness
tain associative information and feedback control for remain major frontiers in neuropsychology. Clinicians
gating of this information as it flows from posterior evaluating patients following acute brain injury routinely
cortical systems. (4) Limbic areas, such as the amygdala, assess level of impaired consciousness is (i.e., the degree of
688 C Consolidation

coma, stupor or lethargy), though this level of analysis Crick, F., & Koch, C. (1990). A framework for consciousness. Nature
Neuroscience, 6(2), 119–126.
does not fully capture the richness of normal conscious
Damasio, A. R. (1995). Consciousness. Knowing how, knowing where.
experience. None the less, clinical research is likely to yield Nature, 375, 106–107.
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perience of cognitive impairments and also cognitive and dler and Rumelhart. Scientific approaches to consciousness (pp. 499–
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Parallel distributed processing: Explorations in the miccrostructure
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be achieved from these approaches.

Cross References
Consolidation
▶ Anosognosia
▶ Attention E LIZABETH S TANNARD G ROMISCH
▶ Capgras Syndrome Trinity College
▶ Minimally Conscious State Hartford, CT, USA
▶ Parallel Distributed Processing
▶ Reduplicative Paramnesia
▶ Reticular Activating System Synonyms
▶ Split-Brain
Memory consolidation

References and Readings

Churchland, P. S. (2002). Self-representation in nervous systems. Science,

Definition
296, 308–310.
Churchland, P. S. (2005). A neurophilosophical slant on consciousness Consolidation is the process of converting short-term
research. Progress in Brain Research, 149, 285–293. memory to permanent long-term memory through the
Cohen, R. A. (1993). Neuropsychology of attention. New York: Plenum.
formation of new synapses.
 Consolidation C 689

Current Knowledge Assessment and Measurement

History Assessment of consolidation is done through testing

short-term memory with material modality tests, then
The first written evidence of consolidation was by Marcus measuring long-term memory after a delay or a distrac- C
Fabius Quintilian, who stated ‘‘curious fact, of which the tion. The participants will be given a list of words, for
reason is not obvious, that the interval of a single night example, and asked to repeat them back to the examiner.
will greatly increase the strength of the memory’’ and ‘‘the After a period of time has passed (delay), the participants
power of recollection, which is the most important ele- will be prompted to repeat the words again. The examiner
ment of memory, undergoes a process of ripening and may also measure consolidation by using a distraction to
maturing during the time which intervenes.’’ The term prevent the participants from rehearsing the information.
‘‘consolidation’’ was coined by Georg Elias Müller and To effectively measure consolidation, conditions must be
Alfons Pilzecker, whose conducted research between controlled when testing both short-term memory and
1892 and 1900 and found that memory takes time to long-term memory.
‘‘consolidirung.’’ Published in their article ‘‘Experimen-
telle Beiträge zur Lehre vom Gedächtnis,’’ Müller and
Pilzecker found that it takes time to form memories, Neuroimaging
and that these new memories can be disrupted for some
time after formation. Research by Takashima et al. tracked the brain’s activity
during the process of consolidation. As the brain conso-
Process of Consolidation lidates short-term memories into long-term memories,
the functional magnetic resonance imaging (fMRI)
The process of consolidation occurs in the neocortex of shows an increase in activity in the hippocampus. Once
the brain, with memory information sent from the hip- the brain switches from consolidation to memory retriev-
pocampus. Two specific processes are involved in consoli- al, the hippocampal activity decreases and the ventral
dation based on the period of time needed to create long- medial prefrontal region increases. Sterpenich et al. used
term memories from the short-term memories. Synaptic fMRI to examine consolidation during sleep. The activa-
consolidation occurs the quickest, consolidating mem- tion in the hippocampus decreased over time (3 days
ories within the first few hours of learning. System con- compared to 6 months), indicating that the memories
solidation, on the other hand, takes between weeks to were being stored in the neocortex and no longer depen-
years for hippocampus-dependent memories to become dent on the hippocampus. After 6 months, activity
independent of the hippocampus. Consolidation can increased in the ventral medial prefrontal region.
occur more rapidly if new information is incorporated
with an already existent schema. In addition, the largest
amount of consolidation happens during rapid eye move- Cross References
ment (REM) sleep.
▶ Memory
Long-Term Memory ▶ Short-Term Memory

Studies in anterograde amnesia, such as with Patient H.

M., have shown that lesions on the medial temporal lobe References and Readings
prevent long-term memory formation. Long-term mem-
ory is information that has been consolidated and is Dudai, Y. (2004). The neurobiology of consolidations, or, how stable is
permanently stored in the brain. While consolidation is the engram? Annual Review of Psychology, 55, 51–86.
initiated in the limbic system, specifically in the hippo- Lechner, H. A., Squire, L. R., & Byrne, J. H. (1999). 100 years of consoli-
dation—remembering Müller and Pilzecker. Learning and Memory,
campus, long-term memories are stored throughout the
6, 77–87.
cortex. When the memory is retrieved, it can be modified Riberio, S., Goyal, V., Mello, C. V., & Pavlides, C. (1999). Brain gene
with recently acquired memories, thus strengthening the expression during REM sleep depends on prior waking experience.
original memory. Learning and Memory, 6, 500–508.
690 C Consortium to Establish a Registry on Alzheimer’s Disease

Sterpenich, V. et al. (2009). Sleep promotes the neural reorganization of nition (delayed) conditions, and a constructional praxis
remote emotional memory. The Journal of Neuroscience, 29(16),
test that requires examinees to copy four line drawings of
5143–5152.
Takashima, A., et al. (2005). Declarative memory consolidation in
increasing complexity (Rosen, Mohs, & Davis, 1984).
humans: A prospective functional magnetic resonance imaging Administration time for the battery is 20–30 min for
study. Proceedings of the national academy of sciences of the United persons with AD; persons without AD may complete the
States of America, Vol. 103, no. 3, 756–761. battery in less time (Morris et al., 1989). As may be
Tronson, N. C., & Taylor, J. R. (2007). Molecular mechanisms of memory
expected given the brevity of the battery and the range
reconsolidation. Nature Reviews Neuroscience, 8, 262–275.
Weingartner, H., & Parker, E. S., (Eds.). (1984). Memory consolidation:
of cognitive ability of the target populations, floor and
psychobiology of cognition. Hillsdale, NJ: Lawrence Erlbaum ceiling effects have been noted for individuals with later
Associates. stage AD and for individuals without AD, respectively
(Morris et al., 1989). Normative data are available based
on the CERAD program control sample (Welsh et al.,
1994), as well as from studies of specific demographic
groups (see Clinical Uses).
Consortium to Establish a
Registry on Alzheimer’s Disease
Historical Background
S USAN VANDERHILL 1, E STHER S TRAUSS 1
E LISABETH M. S. S HERMAN 2
1 The Consortium to Establish a Registry for Alzheimer’s
University of Victoria
Disease (CERAD) was first funded by the National Insti-
Victoria, BC, Canada
2 tute on Aging in 1986 in response to a US Congressional
University of Calgary
mandate to collect epidemiological data concerning the
Calgary, AB, Canada
incidence of AD. A nationwide consortium of 24 univer-
sity medical centers (the CERAD program) developed,
standardized, and evaluated methods for clinical, neuro-
Synonyms psychological, neuropathologic, and neuroimaging
assessments of AD. Data from the study population, in-
CERAD
cluding 1,094 patients with AD and 463 controls evalu-
ated annually between 1987 and 1996, are available on
CD-ROM for research purposes (CERAD, Box 3203,
Description Duke University Medical Center, Durham, NC 27710).
As the bulk of the CERAD data collection took place
The Consortium to Establish a Registry for Alzheimer’s
before the widespread use of cholinesterase inhibitor
Disease (CERAD) neuropsychological battery was
treatment for AD, these data provide a rich source of
designed to provide an efficient, standardized method to
information as to the natural history of AD. A special
evaluate cognitive functioning in individuals with Alzhei-
issue of Neurology (49, suppl. 3) published in 1997 com-
mer’s disease (AD). Originally employed in a large-scale
memorated the tenth anniversary of the CERAD program
longitudinal research program, tests were selected to pro-
and reviewed study design, implementation, and key find-
vide coverage of the primary cognitive deficits associated
ings from wide-ranging investigations of AD.
with AD (e.g., memory, language, praxis, and intellectual
status) and to have a range of difficulty appropriate for
use through much of the course of the disease (Morris
et al., 1989). Individual tests within the battery include Psychometric Data
well-known, commonly used measures such as the Mini-
Mental State Exam (MMSE; Folstein, Folstein, & Psychometric data for the CERAD neuropsychological
McHugh, 1975), a 15-item modified Boston Naming battery reported for participants enrolled over the first
Test (Kaplan, Goodglass, & Weintraub, 1978), and an 19 months of the study indicated good interrater reliabil-
Animal Naming verbal fluency test (Isaacs & Kennie, ity across all tests, with intraclass correlation coefficients
1973). Also included are a ten-item word list memory ranging from 0.92 to 1.0 (Morris et al., 1989). One
test, with free recall (immediate and delayed) and recog- month test–retest data showed variable reliability
 Consortium to Establish a Registry on Alzheimer’s Disease C 691

(r’s from 0.36 to 0.90), with lower correlation coefficients impact test performance. Normative data for patients
for measures whose variance may have been constrained with AD have also been reported, in addition to annual
by ceiling effects (Morris et al., 1989). The efficacy of rates of change on CERAD test scores over a 4-year period
CERAD battery measures (individually and in combina- (Morris et al., 1993).
tion) for detecting AD and for staging dementia severity The CERAD battery has been extensively translated. C
has been evaluated using discriminant function models Normative data for the CERAD are available for a wide
(Welsh, Butters, Hughes, Mohs, & Heyman, 1991; Welsh, range of racial/cultural/demographic groups (Bertolucci
Butters, Hughes, Mohs, & Heyman, 1992). The word list et al., 2001; Fillenbaum, Heyman, Huber, Ganguli, &
delayed recall measure was shown to most effectively Unverzagt, 2001; Fillenbaum et al., 2005; Ganguli et al.,
differentiate those with AD from controls (correctly 1991; Ganguli et al., 1996; Guruje et al., 1995; Whyte et al.,
identifying 94% of controls and 86% of mild AD 2005). Beeri et al. (2006) provide normative data for
patients), although the ability of this measure to distin- individuals over the age of 85.
guish dementia severity groups was limited due to floor Methods for deriving a single summary score for the
effects. For those with impaired scores on delayed recall, CERAD battery (excluding the MMSE) and normative
performance on the naming measure was shown to mod- data for this summary score for unimpaired, mild cogni-
estly increase the discrimination of those with mild from tive impairment (MCI), and AD groups have been pub-
moderate AD (improvement in overall accuracy from lished (Chandler et al., 2005). This total score was
65 to 71%). Verbal Fluency and Constructional Praxis reportedly more consistent at differentiating these three
performances were shown to increase discrimination of groups from one another compared to the MMSE total
those with moderate from severe AD (improvement in score, which showed limited ability to distinguish patients
overall accuracy from 66 to 81%). Within a cognitively with MCI from unimpaired individuals, and the word list
impaired sample, the CERAD battery has also been found delayed recall score, which showed limited ability to dis-
to distinguish those with AD from those with schizophrenia tinguish MCI from AD.
(Davidson et al., 1996). Clinical–pathological correlations Some authors have described an overreliance of the
have shown association between CERAD neuropsycho- CERAD battery on using verbal modalities of testing, at
logical performance and AD pathology on autopsy the expense of other relevant information. To address this
(Hulette et al., 1998). Data from the CERAD program issue, a visual memory measure based on recall of the
have been used to identify predictors of time to institu- Constructional Praxis test items has been proposed. Ad-
tionalization in patients with AD, but information from ministration instructions and psychometric properties of
the CERAD neuropsychological battery (with the excep- a delayed recall and recognition condition of this measure
tion of the MMSE) was not considered in this study have been reported (Spangenberg, Henderson, & Wagner,
(Heyman, Peterson, Fillenbaum, & Pieper, 1997). 1997).
In sum, the brevity of the CERAD neuropsychological
battery, combined with the vast associated research base,
make the CERAD a useful tool for assessment of cognitive
Clinical Uses function in cases of suspected dementia where ‘‘factors
such as fatigue, motivation, or incapacity prevent a more
The chief objective of the CERAD neuropsychology task extensive neuropsychological examination of cognitive
force was ‘‘to develop a brief, reliable battery of neuropsy- capacities’’ (Welsh et al., 1994). Assessment in specialized
chological tests that would be widely used by researchers memory clinics, however, would typically employ a more
and clinicians to assess the cognitive status of patients extensive neuropsychological battery.
with AD at entry and during long-term annual follow-
up’’ (Welsh-Bohmer & Mohs, 1997). The CERAD neuro-
psychological battery has been widely used in research Cross References
studies, including those completed at many of the NIH-
sponsored Alzheimer’s Disease Centers. Normative data ▶ Alzheimer’s Disease
based on 413 CERAD control subjects aged 50–89 have ▶ Blessed Dementia Screen
been published to facilitate clinical application (Welsh ▶ Clinical Dementia Rating Scale (CDR)
et al., 1994). These data are stratified by age, education, ▶ Mattis Dementia Rating Scale (DRS)
and gender, as these factors were shown to differentially ▶ Mini-Mental State Exam (MMSE)
692 C Constraint Induced Therapy

References and Readings disease (CERAD). Part IV. Rates of cognitive change in the longitu-
dinal assessment of probable Alzheimer’s disease. Neurology, 43(12),
2457–2465.
Beeri, M. S., Schmeidler, J., Sano, M., Wang, J., Lally, R., Grossman, H.,
Morris, J. C., Heyman, A., Mohs, R. C., Hughes, J. P., van Belle, G.,
et al. (2006). Age, gender, and education norms on the CERAD
Fillenbaum, G., et al. (1989). The Consortium to Establish a Registry
neuropsychological battery in the oldest old. Neurology, 67(6),
for Alzheimer’s Disease (CERAD). Part I. Clinical and neuropsycholog-
1006–1010.
ical assessment of Alzheimer’s disease. Neurology, 39(9), 1159–1165.
Bertolucci, P. H., Okamoto, I. H., Brucki, S. M., Siviero, M. O., Toniolo
Rosen, W. G., Mohs, R. C., & Davis, K. L. (1984). A new rating scale for
Neto, J., & Ramos, L. R. (2001). Applicability of the CERAD Neuro-
Alzheimer’s disease. The American Journal of Psychiatry, 141(11),
psychological Battery to Brazilian elderly. Arquivos De Neuro-
1356–1364.
Psiquiatria, 59(3-A), 532–536.
Spangenberg, K. B., Henderson, S., & Wagner, M. T. (1997). Validity of a
Chandler, M. J., Lacritz, L. H., Hynan, L. S., Barnard, H. D., Allen, G.,
recall and recognition condition to assess visual memory in the
Deschner, M., et al. (2005). A total score for the CERAD Neuropsy-
CERAD battery. Applied Neuropsychology, 4(3), 154–159.
chological Battery. Neurology, 65(1), 102–106.
Welsh-Bohmer, K. A., & Mohs, R. C. (1997). Neuropsychological assess-
Davidson, M., Harvey, P., Welsh, K. A., Powchik, P., Putnam, K. M., &
ment of Alzheimer’s disease. Neurology, 49(Suppl 3), S11–S13.
Mohs, R. C. (1996). Cognitive functioning in late-life schizophrenia:
Welsh, K. A., Butters, N., Hughes, J., Mohs, R., & Heyman, A. (1991).
a comparison of elderly schizophrenic patients and patients with
Detection of abnormal memory decline in mild cases of Alzheimer’s
Alzheimer’s disease. The American Journal of Psychiatry, 153(10),
disease using CERAD neuropsychological measures. Archives of Neu-
1274–1279.
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Fillenbaum, G. G., Heyman, A., Huber, M. S., Ganguli, M., & Unverzagt,
Welsh, K. A., Butters, N., Hughes, J. P., Mohs, R. C., & Heyman, A.
F. W. (2001). Performance of elderly African American and
(1992). Detection and staging of dementia in Alzheimer’s disease.
White community residents on the CERAD Neuropsychological
Use of the neuropsychological measures developed for the Consor-
Battery. Journal of the International Neuropsychological Society, 7(4),
tium to Establish a Registry for Alzheimer’s Disease. Archives of
502–509.
Neurology, 49(5), 448–452.
Fillenbaum, G. G., McCurry, S. M., Kuchibhatla, M., Masaki, K. H.,
Welsh, K. A., Butters, N., Mohs, R. C., Beekly, D., Edland, S., Fillenbaum,
Borenstein, A. R., Foley, D. J., et al. (2005). Performance on the
G., et al. (1994). The Consortium to Establish a Registry for Alzhei-
CERAD Neuropsychology Battery of two samples of Japanese-
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Whyte, S. R., Cullum, C. M., Hynan, L. S., Lacritz, L. H., Rosenberg,
Folstein, M. F., Folstein, S. E., & McHugh, P. R. (1975). Mini-Mental
R. N., & Weiner, M. F. (2005). Performance of elderly Native Amer-
State: A practical method for grading the cognitive state of patients
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for the clinician. Journal of Psychiatric Research, 12(3), 189–198.
Alzheimer Disease And Associated Disorders, 19(2), 74–78.
Ganguli, M., Chandra, V., Gilby, J. E., Ratcliff, G., Sharma, S. D., Pandav,
R., et al. (1996). Cognitive test performance in a community-based
nondemented elderly sample in rural India: The Indo-U.S. Cross-
National Dementia Epidemiology Study. International Psychogeria-
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Ganguli, M., Ratcliff, G., Huff, F. J., Belle, S., Kancel, M. J., Fischer, L.,
Constraint Induced Therapy
et al. (1991). Effects of age, gender, and education on cognitive
tests in a rural elderly community sample: Norms from the Mono- M ARIANNE H RABOK , K IMBERLY A. K ERNS
ngahela Valley Independent Elders Survey. Neuroepidemiology, 10(1), University of Victoria
42–52. Victoria, BC, Canada
Guruje, O., Unverzargt, F. W., Osuntokun, B. O., Hendrie, H. C.,
Baiyewu, O., Ogunniyi, A., et al. (1995). The CERAD Neuropsycho-
logical Test Battery: Norms from a Yoruba-speaking Nigerian sam-
ple. West African Journal Of Medicine, 14(1), 29–33. Definition
Heyman, A., Peterson, B., Fillenbaum, G., & Pieper, C. (1997). Predictors
of time to institutionalization of patients with Alzheimer’s disease: Constraint induced therapy (CIT) typically refers to a
the CERAD experience, part XVII. Neurology, 48(5), 1304–1309.
therapeutic intervention involving restraint of a non-
Hulette, C. M., Welsh-Bohmer, K. A., Murray, M. G., Saunders, A. M.,
Mash, D. C., & McIntyre, L. M. (1998). Neuropathological and
affected upper extremity combined with intensive practice
neuropsychological changes in ‘‘normal’’ aging: Evidence for pre- with the affected upper extremity (e.g., Alberts, Butler, &
clinical Alzheimer disease in cognitively normal individuals. Journal Wolf, 2004; Charles & Gordon, 2005; Taub & Uswatte,
of Neuropathology and Experimental Neurology, 57(12), 1168–1174. 2005, 2006).
Isaacs, B., & Kennie, A. T. (1973). The Set test as an aid to the detection of
dementia in old people. The British Journal of Psychiatry: The Journal
of Mental Science, 123(575), 467–470.
Kaplan, E., Goodglass, H., & Weintraub, S. (1978). The Boston Naming
Historical Background
Test. Boston, MA: Veterans Administration Medical Center.
Morris, J. C., Edland, S., Clark, C., Galasko, D., Koss, E., Mohs, R., et al. CIT has its origins in primate unilateral deafferentation
(1993). The Consortium to Establish a Registry for Alzheimer’s studies, where it was observed that animals avoided use
 Constraint Induced Therapy C 693

of their deafferented limb unless the intact limb was to rehabilitation strategies that focus on developing com-
restrained (e.g., Taub & Uswatte, 2005, 2006). Concepts pensatory techniques, CIT aims to optimize and develop
from CIT were then applied to humans in single case residual functions (Lillie & Mateer, 2006). Although CIT
studies, case series, and small group studies, primarily has been shown to result in significant gains in motor
with people who had sustained hemiplegia following stroke activity, it should not be expected to restore or normalize C
(Taub et al., 1993). The Extremity Constraint Induced movements to pre-injury levels (Taub & Uswatte, 2005).
Treatment (EXCITE) study is a randomized clinical trial
involving over 200 individuals enrolled at 3–9 months
post-stroke, using uniform CIT methods and measure- Treatment Participants
ment at six testing sites in the USA (Nichols-Larsen,
Clark, Zeringue, Greenspan, & Blanton, 2005; Winstein CIT has been applied in a variety of populations, includ-
et al., 2003; Wolf et al., 2006). ing upper limb hemiparesis following stroke, traumatic
brain injury, and children with hemiplegia (Charles &
Gordon, 2005; Lillie & Mateer, 2006; Shaw et al., 2005).
Rationale or Underlying Theory Research has suggested significant improvement in a
number of populations, including those with ‘‘chronic
CITreflects the integration of a wide variety of research fields,
TBI’’ (identified as > 1 year post-TBI; Shaw et al., 2005)
including neuroplasticity, motor learning, and behavioral
and both ‘‘subacute’’ and ‘‘chronic stroke’’ (identified as <
therapy (Sterr, Szameitat, Shen, & Freivogel, 2006). Two
1 year post-stroke and > 1 year post-stroke, respectively;
mechanisms are typically proposed as the basis for
Page, Levine, & Leonard, 2005).
increased use of affected extremities in CIT: overcoming
Adherence to treatment and level of residual motor
learned nonuse, and induction of use-dependant cortical
function prior to CIT is positively related to treatment
organization (Morris & Taub, 2001).
gains (Shaw et al., 2005; Taub & Uswatte, 2005). Cognitive
Learned nonuse is said to occur following brain injury
impairment is linked to less improvement (Morris et al.,
because unsuccessful motor attempts with the affected
2006). An inherent assumption in CIT is that a residual
extremity leads to punishment (e.g., pain, incoordination,
level of motor function remains in the affected extremity,
failure to meet the goal of the movement). Compensatory
which enables a degree of positive reinforcement for its
behavior also occurs when use of the non-affected extrem-
use (Taub & Uswatte, 2006). A minimal level of residual
ity is positively reinforced.
motor function is often specified as an inclusion criterion
CIT aims to counter-condition learned nonuse. For
in research studies of CIT, as is a lack of general cognitive
example, in animals, the functional limb is restrained and
impairment (e.g., Nichols-Larsen et al., 2005).
the animals complete forced, repetitive movements with
Due to the higher degree of neural plasticity early in
the affected limb. This results in an alteration in the
development, it has been suggested that children may
contingencies of reinforcement, such that compensatory
benefit from CIT to an even greater extent than adults
use of the non-affected limb is no longer reinforced, and
(e.g., Taub & Crago, 1995 as cited by Charles & Gordon,
use of the affected limb is reinforced.
2005). Specific modifications have been made to make
Use-dependant cortical reorganization is a second
CIT more amenable to childhood populations, including
primary mechanism thought to underlie CIT. Neuroim-
conducting CIT in the home environment and practice
aging and transcranial magnetic stimulation studies of the
sessions in the context of play (DeLuca, Echols, Law, &
brain prior to and following CIT have suggested cortical
Ramey, 2005).
reorganization around the infarct site, and recruitment of
a large portion of neurons adjacent to those originally
involved in the control of the limb (Dong, Dobkin, Cen,
Wu, & Winstein, 2006; Morris & Taub, 2001; Park, Butler, Treatment Procedures
Cavalheiro, Alberts, & Wolf, 2004).
CIT is generally administered as a package treatment,
incorporating restraint of the unaffected limb, and
Goals and Objectives structured practice (e.g., shaping and repetitive practice)
with the affected limb. A ‘‘transfer package’’ involving
A major goal of CIT is to increase the use of the affected limb behavioral techniques used to promote transfer of gains
in real world environments (Sterr et al., 2006). In contrast from the laboratory to daily life is emphasized in CIT
694 C Constraint Induced Therapy

(Taub & Uswatte, 2005). Structured practice with the measured in a laboratory setting, and it is therefore
affected arm involves everyday functional tasks (Alberts recommended that these dimensions be assessed separately
et al., 2004), such as eating lunch, throwing a ball, etc. (Uswatte & Taub, 2005).
(Glover, Mateer, Yoell, & Speed, 2002). The Wolf Motor Function Test is a frequently used
Conventional CIT treatment aims for restraint of the measure of laboratory motor performance (e.g., Uswatte
unaffected limb for 90% of waking hours, and structured & Taub, 2005). Functional outcome is most often studied
practice 6–8 h per day (Kaplon, Prettyma, Kushi, & through use of Motor Activity Log (MAL), a semistruc-
Winstein, 2007). The treatment period for restraint and tured interview of extremity use in real-life settings (e.g.,
structured practice is 5 days per week, for 2–3 consecutive Winstein et al., 2003).
weeks with a 1:1 therapist–patient ratio.
The intensive nature of CIT has prompted concerns
regarding its applicability to clinical settings, due to insti-
Qualifications of Treatment Providers
tutional and clinical factors. For example, facilities may
lack the space, therapist time, and associated financial
Physiotherapists most frequently provide services. Occu-
resources to administer CIT (Levine & Page, 2004).
pational therapists have also been identified as providing
Concerns have also been raised regarding attrition rates,
services (e.g., Brogardh, 2006). Specialized training in
compliance, and health care coverage (Levine & Page,
CIT is recommended (DeLuca et al., 2005; Winstein
2004; Page & Levine, 2003).
et al., 2003).
Because these factors can impede service delivery and
the aims of CIT, modifications of treatment protocols
have been introduced. For example, group delivered CIT
(Brogardh, 2006), automatized delivery of CIT with less Cross References
therapist involvement (AutoCITE; Lum, Uswatte, Taub,
Hardin, & Mark, 2006; Taub, Lum, Hardin, Mark, & ▶ Brain Plasticity
Uswatte, 2005), and fewer hours of restraint and shorter ▶ Cognitive Rehabilitation
practice sessions over longer periods (Levine & Page, ▶ Head Injury
2004; Page & Levine, 2003; Page, Sisto, Johnston, & ▶ Hemiparesis
Levine, 2002) have all resulted in significant treatment ▶ Hemiplegia
gains, often comparable to the gains of conventional ▶ Physical Therapy
CIT (e.g., Levine & Page, 2004; Lum et al., 2006). Current ▶ Rehabilitation Psychology
research suggests that particularly important features are ▶ Traumatic Brain Injury
prolonged rehearsal on specific tasks involving the affect-
ed limb and shaping in effort to improve everyday activity
(Pomeroy & Tallis, 2002). References and Readings
Alberts, J. L., Butler, A. J., & Wolf, S. L. (2004). The effects of constraint-
induced therapy on precision grip: A preliminary study. Neuroreh-
Efficacy Information abilitation and Neural Repair, 18, 250–258.
Brogardh, C. (2006). Constraint-induced movement therapy in patients
CIT has been shown to significantly improve performance with stroke: A pilot study on effects of small group training and of
extended mitt use. Clinical Rehabilitation, 20, 218–227.
on laboratory tests of motor ability and functional out-
Charles, J., & Gordon, A. M. (2005). A critical review of constraint-
come measures. The effect sizes for functional outcome induced movement therapy and forced use in children with hemiplegia.
measures tend to be very large in magnitude (Taub & Neural Plasticity, 12, 245–261.
Uswatte, 2005). Effect sizes on laboratory tests tend to DeLuca, S. C., Echols, K., Law, C. R., & Ramey, S. L. (2005). Intensive
be more variable (as reviewed by Lillie & Mateer, 2006). pediatric constraint-induced therapy for children with cerebral
palsy: Randomized, controlled, crossover trial. Journal of Child
Neurology, 21, 931–938.
Dong, Y., Dobkin, B. H., Cen, S. Y., Wu, A. D., & Winstein, C. J. (2006).
Motor cortex activation during treatment may predict therapeutic
Outcome Measurement gains in paretic hand function after stroke. Stroke, 37, 1552–1555.
Glover, J. E., Mateer, C. A., Yoell, C., & Speed, S. (2002). The effectiveness
There can be significant discrepancies between ‘‘real of constraint induced movement therapy in two young children with
world’’ spontaneous functional use and motor ability as hemiplegia. Pediatric Rehabilitation, 5, 125–131.
 Constructional Apraxia C 695

Kaplon, R. T., Prettyma, M. G., Kushi, C. L., & Winstein, C. J. (2007). Six constraint-induced movement therapy. Rehabilitation Psychology,
hours in the laboratory: A quantification of practice time during 50, 34–42.
constraint-induced therapy (CIT). Clinical Rehabilitation, 21, Winstein, C. J., Miller, J. P., Blanton, S., Taub, E., Uswatte, G., Morris, D.,
950–958. et al. (2003). Methods for a multisite randomized trial to investigate
Lillie, R., & Mateer, C. A. (2006). Constraint-based therapies as a pro- the effects of constraint-induced movement therapy in improving
posed model for cognitive rehabilitation. Journal of Head Trauma
Rehabilitation, 21, 119–130.
upper extremity function among adults recovering from a
cerebrovascular stroke. Neurorehabilitation and Neural Repair, 17,
C
Levine, P., & Page, S. J. (2004). Modified constraint-induced therapy: 137–152.
A promising restorative outpatient therapy. Topics in Stroke Rehabil- Wolf, S. L., Winstein, C. J., Miller, J. P., Taub, E., Uswatte, G., Morris, D.,
itation, 11, 1–10. et al. (2006). Effects of constraint-induced movement therapy on
Lum, P. S., Uswatte, G., Taub, E., Hardin, P., & Mark, V. W. (2006). upper extremity function 3 to 9 months after stroke: The EXCITE
A telerehabilitiation approach to delivery of constraint-induced randomized clinical trial. JAMA, 296, 2095–2103.
movement therapy. Journal of Rehabilitation Research and Develop-
ment, 43, 391–400.
Morris, D. M., Shaw, S. E., Mark, V. W., Uswatte, G., Barman, J., &
Taub, E. (2006). The influence of neuropsychological characteristics
on the use of CI therapy in persons with traumatic brain injury.
Neurorehabilitation, 21, 131–137. Constructional Apraxia
Morris, D. M., & Taub, E. (2001). Constraint-induced therapy approach
to restoring function after neurological injury. Topics in Stroke A MY K. B YERLEY, A NDREW S. DAVIS
Rehabilitation, 8, 16–30. Ball State University
Nichols-Larsen, D. S., Clark, P. C., Zeringue, A., Greenspan, A., &
Muncie, Indiana, USA
Blanton, S. (2005). Factors influencing stroke survivors’ quality of
life during subacute recovery. Stroke, 36, 1480–1484.
Page, S., & Levine, P. (2003). Forced use after TBI: Promoting plasticity
and function through practice. Brain Injury, 17, 675–684. Synonyms
Page, S. J., Levine, P., & Leonard, A. C. (2005). Modified constraint-
induced therapy in acute stroke: A randomized controlled pilot
Constructional dyspraxia
study. Neurorehabilitation and Neural Repair, 19, 27.
Page, S. J., Sisto, S., Johnston, M. V., & Levine, P. (2002). Modified
constraint-induced therapy after subacute stroke: A preliminary
study. Neurorehabiliation and Neural Repair, 16, 290–295. Short Description or Definition
Park, S. W., Butler, A. J., Cavalheiro, V., Alberts, J. L., & Wolf, S. I. (2004).
Changes in serial optical topography and TMS during task perfor-
mance after constraint-induced movement therapy in stroke: A case
Constructional apraxia is an inability to reproduce pat-
study. American Society of Neurorehabiliation, 18, 95–105. terns or join component parts into a whole. This condition
Pomeroy, V., & Tallis, R. (2002). Neurological rehabilitation: A science is assessed through observation of a patient completing
struggling to come of age. Physiotherapy Research International, activities such as drawing, copying, or building three-
7, 76–89.
dimensional objects (Lezak, Howieson, & Loring, 2004).
Shaw, S. E., Morris, D. M., Uswatte, G., McKay, S., Meythaler, J. M., &
Taub, E. (2005). Constraint-induced movement therapy for recovery
Impairments in processing spatial forms observed in con-
of upper-limb function following traumatic brain injury. Journal of structional apraxia can occur in the absence of apraxia of
Rehabilitation Research and Development, 42, 769–778. singular motor movements (Benton, 1969).
Sterr, A., Szameitat, A., Shen, S., & Freivogel, S. (2006). Application of
CIT concepts in the clinical environment: Hurdles, practicalities, and
clinical benefits. Cognitive Behavioral Neurology, 19, 48–53.
Taub, E., Lum, P. S., Hardin, P., Mark, V. W., & Uswatte, G. (2005).
Categorization
AutoCITE: Automated delivery of CIT with reduced effort by
therapists. Stroke, 36, 1301–1304. Recent studies suggest qualitatively different types of con-
Taub, E., Miller, N. E., Novack, T. A., Cook, E. W. III, Fleming, W. C., structional apraxia determined by the location of brain
Nepomuceno, C. S., et al. (1993). Technique to improve chronic
insult. In general, patients with right hemisphere im-
motor deficit after stroke. Archives of Physical Medicine and Rehabil-
itation, 74, 347–354.
pairment make more coordinate type errors (e.g., distance
Taub, E., & Uswatte, G. (2005). Use of CI therapy for improving motor and angular distortions), whereas those with left hemi-
ability after chronic CNS damage: A development prefigured by Paul spheric impairment tend to commit categorical errors
Bach-Y-Rita. Journal of Integrative Neuroscience, 4, 465–477. (e.g., position exchanges and pattern reversals) (Laeng,
Taub, E., & Uswatte, G. (2006). Constraint-induced movement therapy:
2006). Patients with right hemispheric impairment gener-
Answers and questions after two decades of research. Neurorehabil-
itation, 21, 93–95.
ally experience difficulties with the overall gestalt of the
Uswatte, G., & Taub, E. (2005). Implications of the learned non-use constructional task. Their approach to the task may ap-
formulation for measuring rehabilitation outcomes: Lessons from pear to be more fragmented and disjointed, not coming
696 C Constructional Apraxia

together as a whole. Constructions created by patients treatment, while others may have symptoms spontane-
with right hemisphere impairment may make drawing ously diminish. For other patients, symptoms may be
that are sparse or may be significantly distorted with permanent. Further research for prognostic factors of
regard to perspective or proportion. Some patients with constructional apraxia is warranted.
right hemisphere injury may create overdetailed or repet-
itive drawings, while others may draw elaborate pictures
that are missing important components. Additionally, Neuropsychology and Psychology of
patients with right hemispheric lesions frequently dem- Constructional Apraxia
onstrate left-sided visual inattention and include more
details on construction tasks. Symptoms associated with constructional apraxia fre-
In contrast, those with left hemisphere impairment quently indicate deficits associated with right parietal
may be able to construct the overall concept and propor- dysfunction, or the non-dominant hemisphere and
tions accurately, and their constructions may also be global cognitive processing impairment. However, re-
symmetrical. However, they often tend to generate draw- cent research has shown involvement of both hemi-
ings with fewer details (McFie & Zangwill, 1960). Patients spheres, namely the parietal lobes, in constructional
with left hemisphere impairment may perform construc- apraxia. Furthermore, neuroimaging research has
tion tasks better when given a model rather than working implicated the ventral premotor area, posterior part
on command. They tend to focus on overall shape rather of the inferior temporal sulcus, and occipital cortex
than specific details. Overall, construction deficits tend to in constructional deficits (Makuuchi, Kaminaga, &
be more common when the lesion is located in the poste- Sugishita, 2003; Nielson, Cummings, & Cotman, 1996).
rior portion of the brain rather than the anterior areas. Constructional apraxia should not be conceptualized as a
Furthermore, while patients with cortical lesions make the unitary syndrome caused by discrete lesions (Guérin, Ska,
same types of constructional errors as patients with sub- & Belleville, 1999), but as resulting from impairment in
cortical lesions, those with subcortical impairment appear lateralized perceptual processing of spatial abilities
to have more significant impairment. (Laeng, 2006). Constructional apraxia manifests more
frequently in patients with lesions in the non-dominant
hemisphere (De Renzi, 1997). Consequently, construc-
Epidemiology tional apraxia often co-occurs with deficits in visual-spa-
tial perception (Benton, 1982), although both conditions
A review of literature revealed no known reports of preva- may exist independently. Therefore, the presentation of
lence of constructional apraxia. In fact, constructional constructional apraxia differs among patients; some
apraxia is generally included as a subcategory of apraxia, struggle with copying figures, whereas others demonstrate
which is listed as a ‘‘rare disease’’ by the office of rare difficulty constructing designs with blocks (Lezak et al.,
diseases (ORD) of the National Institutes of Health 2004).
(NIH). Therefore, apraxia is known to affect less than
200,000 people in the population of the USA. Thus, as a
subcategory of apraxia, constructional apraxia affects even Evaluation
fewer individuals. Common causes of constructional aprax-
ia include dementia (e.g., Alzheimer’s Disease) and stroke, The utility of constructional apraxia as an estimate of
which are two of the most frequent neurological diseases. global cognitive functioning has a well-established his-
tory in neurology, neuropsychology, and rehabilitative
settings. Tasks commonly utilized to assess construc-
Natural History, Prognostic Factors, and tional apraxia include copying, drawing, or construct-
Outcomes ing simple figures, such as clocks or crosses. These
efficient, brief, and easy-to-administer construction
Constructional apraxia is not in itself a disease but a tasks are attractive to clinicians for use with patients
symptom of another neurological illness. Therefore, prog- with impaired test-taking skills. The tasks used to
nosis of the condition is related to the prognosis of the assess constructional apraxia have proven to be re-
underlying neurological condition. Prognosis for indivi- markably sensitive to global neurological impairment
duals with constructional apraxia varies and has not been because of the involvement of various cognitive pro-
well studied. Some patients may improve via continued cessing domains necessary for completing construction
 Content-Referenced Testing C 697

tasks. Construction tasks can require complex cogni- Benton, A. L. (2009). Constructional apraxia: Some unanswered ques-
tions. In A. L. Benton (Ed.), Brain & behavior: Research in clinical
tive processes, including visual-spatial and visuoper-
neuropsychology (pp. 129–141). Chicago: Aldine.
ceptual abilities, receptive language skills, numerical De Renzi, E. (1997). Visuospatial and construction disorders. In T. E.
knowledge, graphomotor skills, and intact executive Feinberg, & M. J. Farah (Eds.), Behavioral neurology and neuropsy-
functioning (Freedman et al., 1994; Lezak et al., 2004; chology (pp. 297–304). New York: McGraw-Hill.
C
Shulman, 2000). The sensitivity of construction tasks to Fischer, J. S., & Loring, D. W. (2004). Construction. In M. D. Lezak,
D. B. Howieson, & D. W. Loring (Eds.), Neuropsychological assess-
global cognitive impairment renders these tasks advanta-
ment (4th ed., pp. 531–568). New York: Oxford University Press.
geous in the assessment of patients with known or Freedman, M., Leach, L., Kaplan, E., Winocur, G., Shulman, K., & Delis,
suspected neurological impairment, including those D. C. (1994). Clock drawing: A neuropsychological analysis. New York:
with Alzheimer’s Disease, Huntington’s Disease, Parkin- Oxford University Press.
son’s Disease, aphasia, seizures, CVAs, and TBIs. As an Guérin, F., Ska, B., & Belleville, S. (1999). Cognitive processing of drawing
abilities. Brain and Cognition, 40:464–478.
example, construction tasks have been shown to be useful
Laeng, B. (2006). Constructional apraxia after left or right unilateral
as screening tools and markers for disease progression stroke. Neuropsychologia, 44:1595–1606.
with Alzheimer’s patients. Furthermore, the presence of Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). Neuropsychologi-
constructional apraxia early in the course of Alzheimer’s cal Assessment (4th ed.). New York: Oxford University Press.
Disease has been shown to be a predictor of accelerated Makuuchi, M., Kaminaga, T., & Sugishita, M. (2003). Both parietal lobes
are involved in drawing: A functional MRI study and implications
cognitive decline (Smith, Esiri, Barnetson, King, & Nagy,
for constructional apraxia. Brain Research, 16:338–347.
2001). McFie, J., & Zangwill, O. L. (1960). Visual construction disabilities
associated with lesions of the left cerebral hemisphere. Brain,
83:243–260.
Treatment Nielson, K., Cummings, B., & Cotman, C. (1996). Constructional apraxia
in Alzheimer’s disease correlates with neuritic neuropathology in
occipital cortex. Brain Research, 741:284–293.
While physical and occupational therapies may modestly Shulman, K. L. (2000). Clock-drawing: Is it the ideal cognitive screening
improve the functioning of an individual with construc- test? International Journal of Geriatric Psychiatry, 15:548–561.
tional apraxia, no specific medical treatment has been Smith, M., Esiri, M., Barnetson, L., King, E., & Nagy, Z. (2001). Con-
found to be effective with significantly improving con- structional apraxia in Alzheimer’s disease: Association with occipital
lobe pathology and accelerated cognitive decline. Dementia and
structional deficits. Furthermore, medications that target
Geriatric Cognitive Disorders, 12:281–288.
the slowing of dementia do not appear to help with
constructional apraxia. The most beneficial approach for
treatment of individuals with constructional apraxia
involves ensuring their environments are safe. For exam-
ple, it is important to arrange furniture in the home in a
way that the patient can navigate safely. Constructional Dyspraxia
▶ Constructional Apraxia
Cross References

▶ Apraxia
▶ Dementia
▶ Stroke
▶ Visual-Motor Function Content Validity
▶ Test Validity
References and Readings

Benton, A. L. (1969). Constructional apraxia: Some unanswered ques-

tions. In A. L. Benton (Ed.), Contributions to clinical neuropsychology
(pp. 128–141). Chicago: Aldine.
Benton, A. L. (1982). Spatial thinking in neurological patients:
Historical aspects. In M. Potegal (Ed.), Spatial abilities: Development
Content-Referenced Testing
and physiological foundations (pp. 253–271). New York: Academic
Press. ▶ Domain Referenced Test Interpretation
698 C Contextual Memory

Contingency Table. Table 2

Contextual Memory
TBI No TBI
▶ Source Memory Test + 35 15 50
Test  5 45 50
40 60 100
Cond. = Condition

Contingency Table
C HRISTIAN S CHUTTE , B RADLEY A XELROD In this example, hit rate would be calculated by adding
John D. Dingell VA Medical Center the number of true negatives and false negatives and then
Detroit, MI, USA dividing them by the number of total decisions ((TP +
FN)/total decisions). This allows for a relatively simple
way to assess the relationships between categorical
Synonyms variables.
A concrete example would be a group of 100 patients,
2  2 Table 40 of whom have a true diagnosis of traumatic brain injury
(TBI) who are administered a brief test to diagnose the
presence of the disorder. By comparing the obtained scores
to a cutting score, 55 patients are tagged as having the
Definition disorder and 45 patients as not having the disorder. Using
this information, a contingency table to find hit rate can
A contingency table is generally a representation of cate- quickly be defined, sensitivity, and specificity, as well as
gorical data in a tabular format, such as a 2  2 table, positive and negative predictive power.
though the table can have three or more variables. One can then calculate hit rate ((TP + FN)/total
decisions) or (35 + 5)/100 = .4, sensitivity (TP/(TP +
FN)) or 35/(35 + 5) = .875, specificity (TN/(TN + FP))
Current Knowledge or 45/(45 + 15) = .75, positive predictive power (TP/(TP +
FP)) or 35/(35 + 15) = .70, and negative predictive power
There are row variables on the horizontal axis and column (TN/(TN + FN)) or 45/(45 + 5) = .90. In verbal form, hit
variables on the vertical axis. It represents mutually exclu- rate is a proportion of the number of correctly identified
sive variables. Good examples of contingency tables are TBI patients and incorrectly ruled out TBI patients divided
hit rate, sensitivity, and specificity, as well as positive and by the total number of patients (40% in this case) or
negative predictive power. In the case of hit rates to assess sensitivity is computed by the percentage of people who
the number of correct classification decisions that result actually have the disorder who were appropriately detected
from the use of a particular test or measure, one would by the test (87.5% in this case).
enter the number of true positives, true negatives, false More complex contingency tables can be used, such as
positives, and false negatives into a contingency table like 3  2, 3  3, or more, though relationships between
the one below. variables are less clear owing to difficulties with interac-
tion effects. More complex contingency tables are often
analyzed with more complex statistical procedures, such
as log-linear analysis.

Contingency Table. Table 1

Cond. + Cond.  Cross References

Test + True + (TP) False + (FP) Total + Decisions
▶ Negative Predictive Power
Test  False  (FN) True  (TN) Total  Decisions
▶ Positive Predictive Power
Base Rate Cond. Absent Total of all decisions ▶ Sensitivity
Cond. = Condition ▶ Specificity
 Continuous Performance Tests C 699

more commonly used in standard neuropsychological eva-

Continuous Performance Tests luations. In fact, the CPT was one of the first neuropsycho-
logical paradigms widely adapted for computerized
R ONALD A. C OHEN assessment. Subsequently, impairments on this paradigm
Brown University were demonstrated across various disorders, most notably
Providence, RI, USA
C
schizophrenia (Nuechterlein, 1983) and attention deficit
disorder (Epstein et al., 2003).

Synonyms
Psychometric Data
CPT
In its original form, the CPT provided measures of accu-
racy and response bias over the course of a fixed time
Description period using signal detection methodology. Although the
tests may vary in terms of length and type of stimulus
An attention paradigm that has evolved into a class used, the underlying paradigm is the same across versions
of neuropsychological tests used to assess sustained of the test. Patients are presented with series of letters
attention. There is not a single continuous performance (typically) or other stimuli on a screen, and are told to
test (CPT) test, as a number of commercially available and push a response key only when they see the ‘‘target’’
research CPT tasks exist and have been published in the stimulus. They are instructed not to respond when they
neuropsychological literature. The common characteristic see any other stimuli. The letter ‘‘x’’ has often been used
of all CPT tests is that they involve sequential presentation as the target in CPT paradigms, with the task to respond
of stimuli, usually letters or numbers, over an extended to this letter while ignoring other letters that flash before
period of time. The task demand is to attend and respond them. Several common variations of the standard CPT
to particular target stimuli, while ignoring other stimuli paradigm exist, in particular, a conditional task, in which
that serve as nontarget distractors. the patient must only respond to the target letter when
another stimulus occurs immediately before it (e.g., A-X),
which increases the difficulty of the task.
Historical Background In recent years, a variety of tests based on computer-
ized CPT paradigms have been developed, with varying
Early efforts by psychologists to assess attention in the degree of sensitivity and specificity to clinical disorders of
context of intellectual or other cognitive testing typically attention. At the present time, the most widely used
relied on tests such as digit span, which provided a commercially available CPT tests are versions by Conners,
useful measure of attentional focus and span, but did not Epstein, Angold, and Klaric (2003) and the Test of
address other important elements of attention, such as the Variables of Attention (TOVA), though a variety of others
patients’ ability to selectively attend to information or to exist, such as VIGIL (1990) and the d2 Test of Attention
sustain attention (Cohen, 1993). Sustained attention was (Brickenkamp, 1992). Typically, a CPT is included as part
particularly difficult to assess using traditional paper-and- of a more comprehensive battery of tests of attention and
pencil tests, as it required the measurement of signal detec- executive functioning.
tion performance over extended periods of time. Psycholo- Given that the CPT paradigm is based on signal detec-
gists typically relied on behavioral observation or analysis of tion theory and method, there are certain indices common
patterns of inconsistency in test performance over time to to all versions of the test; correct responses, errors of
derive evidence of sustained attention problems. The devel- omission (misses), errors of commission (false positives),
opment of the tachistoscope for rapid presentation of visual and response time (RT). Correct responses are based on the
stimuli with controlled timing provided a means of circum- sum of the number of times the patient correctly responds
venting this problem. Mirsky et al. (1956) described the to the target and correctly avoids responding to distractors.
continuous performance paradigm and provided research Omission errors (misses) are errors involving a failure to
data supporting its sensitivity in detecting brain damage. respond to the target, while commission errors (false posi-
The advent and widespread availability of computer tech- tives) are errors involving a response to nontargets. Errors
nology in the decades that followed led to more widespread of commission reflect a failure to inhibit responding. High
experimentation with this paradigm and it eventually being omission rates indicate that either the patient is not
700 C Continuous Performance Tests

focusing adequately on the stimuli or that their processing of consistency across versions of the tests, particularly
speed is slow and they are unable to respond rapidly with respect to basic parameters such as the duration of
enough. CPT tests usually also provide a measure of the interstimulus interval (ISI), the total duration of the
mean response time (RT), which reflects the processing task, and the task demand. For example, a task requiring
speed of the patient during the task. Higher rates of correct detection of a single letter is much easier than a condi-
detections indicate better attention performance. tional paradigm requiring detection of a letter sequence
From these primary measures, signal detection indices (A-X). Furthermore, the duration of a typical CPT test
are usually derived based on a comparison of error types. can range from several minutes to over 20 min. Versions
Based on the total number of errors of commission with a long ISI tend to be relatively easy to perform, but
and omission on the CPT, a discrimination index (d0 ) is are tedious, with behavioral challenge arising from the
calculated which provides a measure of accuracy based on monotony of the task, which over a long test period is
standardized scores (z-scores) from normative samples. A really a test of vigilance. In contrast, versions that have a
measure of response bias (b) is also usually derived based short ISI with conditional task demands or other char-
on the difference in standard scores for each type of error. acteristics that increase difficulty tend to be more sensi-
Response bias indices provide a better way of interpreting tive to sustained attention in the context of greater
tendencies to make one type of error or the other because information processing demand and requirement for
they account for the total number of errors of each type. focused attention. Adaptive-rate continuous perfor-
Receiver operator characteristics (ROC) metrics can also mance methods provide a means of circumventing this
be derived, which provide a way of interpreting the issue. For example, the adaptive-rate continuous perfor-
tendency to make errors of each type as a function of mance test (ARCPT; Cohen, 1993) adjusts its ISI over the
the signal detection parameters of the task, such as course of the test based on accuracy of response to
percentage of targets to nontargets. General equations compensate for the slow speed of processing. The final
for d0 and b are shown below. ISI that is maintained by the end of the test provides a
strong measure of capacity limitations related to proces-
d0 ¼ zðmissesÞ þ zðfalse positivesÞ sing speed deficits. Also the ARCPT provides separate
vigilance decrement and inconsistency indices to enable
b ¼ zðmissesÞ  zðfalse positivesÞ=z ðtotal errorsÞ assessment of the temporal dynamics of performance
over 10 blocks of time over the duration of the test.
In the past, many versions of the CPT provided only these The ARCPT measures attentional performance on a
basic indices, which limited their usefulness in rapid and challenging task which is less subject to bore-
characterizing problems with sustained attention. While dom. Therefore, the ARCPT provides enables the assess-
d0 and b provide excellent measures of detection accuracy, ment of sustained attention during a cognitively
response deposition, and overall attention performance, demanding task compared to standard CPT paradigms.
they do not directly provide measures of performance Also, because the ISI adjusts to shorter durations when a
over time. Recent versions of the Conner’s and other CPT patient is performing well, the test can typically be com-
tests tend to now include a measure of temporal variability pleted in about 10 min. The ARCPT also provides several
in performance. While there are a variety of ways that the metrics that enable assessment of temporal inconsisten-
temporal nature of performance can be determined, two cies in performance.
general types of measures exist: (1) performance decrement Despite the fact that CPT tests vary in a variety of
and (2) performance inconsistency. Performance decre- ways, many of the commonly used measures (e.g., Con-
ment provides a measure of the change in performance ner’s CPT) report good test–retest reliability in healthy
between the beginning and end of the test. In theory, if a adults. CPT performance tends to correlate well with
person is failing to sustain attention, their performance performance on other information processing-based
should worsen the longer they stay on task. However, measures and performance on speeded tests of attention
often this measure is not impaired except when there is a and executive function, such as the Stroop and trail-
severe problem with sustained attention and fatigue after making test. Validation studies conducted with the
several minutes of effort. Performance inconsistency ARCPT indicate strong reliability (r = .95) for accuracy
indices provide an alternative temporal measure based on of performance (d0 ) across samples and strong validity as
variance across time, as opposed to linear decrement. indicated by the sensitivity of CPT indices to measures of
A primary problem in interpreting the meaning and structural and functional brain and systemic physiological
clinical significance of CPT findings stems from the lack disturbances as discussed in greater detail below.
 Contraindication C 701

Clinical Uses ▶ Sustained Attention

▶ Vigilance
CPT tests should be included in all comprehensive neu-
ropsychological batteries designed to provide a thorough
References and Readings
assessment attention, executive functioning, and proces- C
sing speed. There is a well-established research and clinical
Brickenkamp, R. Z. E. (1992). The d2 test of attention. Seattle, WA:
literature demonstrating that this paradigm is highly Hogrefe & Huber.
sensitive to brain dysfunction. The fact that the CPT yields Cohen, R. A. (1993). Neuropsychology of attention. New York: Plenum.
measures of information processing characteristics based Cohen, R., Lohr, I., Paul, R., & Boland, R. (2001). Impairments of atten-
on a task with controlled timing and consistency of tion and effort among patients with major affective disorders. Journal of
Neuropsychiatry and Clinical Neurosciences, 13(3), 385–395.
stimulus presentation makes it a valuable addition to
Conners, C. K., Epstein, J. N., Angold, A., & Klaric, J. (2003). Continuous
standard paper-and-pencil tests of cognitive function. performance test performance in a normative epidemiological
Performance deficits on the CPT are evident in sample. Journal of Abnormal Child Psychology, 31(5), 555–562.
patients with various forms of brain dysfunction Epstein, J. N., Erkanli, A., Conners, C. K., Klaric, J., Costello, J. E., &
(Rosvold, Mirsky, Sarason, Bransome, & Beck, 1956). Angold, A. (2003). Relations between continuous performance test
performance measures and ADHD behaviors. Journal of Abnormal
The most obvious use for the CPT is in the assessment
Child Psychology, 31(5), 543–554.
of attention deficit disorder (ADD), for which the objec- Gunstad, J., Cohen, R. A., Paul, R. H., & Gordon, E. (2006). Dissociation
tive assessment of sustained attention is central to the of the component processes of attention in healthy adults. Archives of
diagnosis. However, there is now an extensive research Clinical Neuropsychology, 21(7), 645–650.
literature demonstrating deficits or outright impairments Jerskey, B., Cohen, R. A., Jefferson, A. L., Hoth, K. F., Haley, A. P.,
Gunstad, J. J., et al. (2009). Sustained attention is associated with left
of CPT performance among patients with a wide range of
ventricular ejection fraction in older adults with heart disease. Journal
neurological and psychiatric conditions. For this reason, of the International Neuropsychological Society, 15(1), 137–141.
impaired CPT performance should be considered a highly Leark, R. A., Greenberg, L. K., Kindschi, C. L., Dupuy, T. R., & Hughes,
sensitive measure of functional attention impairment and S. J. (2007). Test of variables of attention: Clinical manual. Los
brain dysfunction, though not necessarily specific to one Alamitos: The TOVA Company.
Nuechterlein, K. H. (1983). Signal detection in vigilance tasks and behav-
type of neurological or psychiatric condition.
ioral attributes among offspring of schizophrenic mothers and among
Impairments of CPT are evident in patients with neu- hyperactive children. Journal of Abnormal Psychology, 92(1), 4–28.
rodegenerative disorders like Alzheimer’s disease, as well Rosvold, H. E., Mirsky, A. F., Sarason, I., Bransome, E. D., Jr., & Beck,
as disorders affecting subcortical and white matter brain L. H. (1956). A continuous performance test of brain damage.
systems, such as multiple sclerosis, HIV, and Journal of Consulting Psychiatry, 20, 343–350.
VIGIL: A continuous performance test. (1990). New Hampshire:
cerebrovascular disease. In fact, patients with cardiovas-
Forethought.
cular disease show a relationship between cardiac output
and CPT performance (Jerskey et al., 2009). Among
patients with severe affective disorders, CPT performance
is often impaired and associated with problems with Contraindication
effort (Cohen, Lohr, Paul, & Boland, 2001). CPT has
been shown to be sensitive to sustained attention and M ARLA S ANZONE
information processing deficits associated with neurotox- Independent Practice
ic exposure to lead, solvents, drugs, or other substances. Annapolis, MD, USA
An important clinical determination that needs to be
made when examining performance on the CPT is whether
there is evidence of an actual problem with sustained Synonyms
performance, or whether a broader problem with focused
and selective attention exists that occurs regardless of the Conflict; Counterindicant
time spend on task.

Definition
Cross References
A contraindication is a circumstance, condition, symptom,
▶ Attention Deficit Disorder (ADD) or factor that increases the risk associated with a medical
▶ Signal Detection procedure, drug, or treatment. A contraindication refers to
702 C Contrecoup Injury

any intervention considered inappropriate or inadvisable results from acceleration–deceleration events during
based upon unique factors of the situation such as potential which the force impacting the head causes the brain to
harmful interactions between drugs or medical conditions slam into the skull on the opposite side of the blow. Motor
that renders an individual vulnerable if implemented. vehicle accidents, falls, sports injuries, and physical
A contraindication may be absolute or relative. Absolute assaults with blunt objects frequently result in contrecoup
contraindications are those which are inadvisable without injuries. Skull characteristics make the most probable
exception or qualification. They are either permanently sites of injury in the frontal and temporal lobes, as tips
recommended against, or temporarily until the disqualifying of the skull can more easily be forced into the under-
condition is remediated. The use of the atypical antipsychot- lying brain tissue in the frontal and temporal lobes.
ic medication, clozapine carries a risk of agranulocytosis, a Neuropsychological evaluation can help to identify cog-
sever low white blood cell disorder condition. Clozopine nitive impairments arising from both the primary and
would be an absolute contraindication in an individual secondary sites of injury.
with a history of bone marrow suppression
Relative contraindications refer to circumstances in
which procedures or treatments are considered in com- Cross References
parative terms. They are contingent upon a risk/benefit
analysis of the relevant factors. The proportionate value of ▶ Acceleration Injury
an intervention is compared with its potential for negative ▶ Biomechanics of Injury
consequences. An example of a relative contraindication ▶ Cortical Contusion
would be the use of an anti-convulsant/mood stabilizing ▶ Traumatic Brain Injury
medication in the ongoing treatment of a pregnant
woman with severe bipolar mania and suicidality, but
whose has been asymptomatic only while on lithium. References and Readings

Cross References Graham, D. I., Saatman, K. E., Marklund, N., Copnte, V., Morales, D.,
Royo, N., & McIntosh, T. K. (2006). The neuropathology of trauma.
In R. W. Evans (Eds.), Neurology and trauma (2nd ed., pp. 45–94).
▶ Extrapyramidal Side Effects New York: Oxford University Press.
▶ Iatrogenic
▶ Signs

References and Readings

Controlled Attention
Mosby. (2006). Contra- (definition). In T. Myers (Ed.), Mosby’s dictionary
of medicine, nursing & health professions (7th ed., pp. 453). Missouri:
A NNA M AC K AY-B RANDT
Mosby Elsevier.
Venes, D., Thomas, C., Egan, E., & Houska, A. (2001). Contraindication Brown University Medical School
(definition). In D. Venes, et al. (Eds.), Taber’s medical dictionary Providence, RI, USA
(19th ed., pp. 479). Philadelphia: FA Davis Company.

Synonyms
Contrecoup Injury
Central executive; Cognitive control; Supervisory atten-
B ETH R USH tional system
Mayo Clinic
Jacksonville, FL, USA
Definition

Definition Higher-order cognitive processes that influence the

regulation of behavioral responses and the selection of
Contrecoup injury is an injury to the brain tissue directly information to be attended to are based on task-related
beneath the skull, opposite to the point of impact. It goals.
 Controlled Oral Word Association Test C 703

Current Knowledge ▶ Frontal Lobe

▶ Vigilance
Neuroanatomical

From a neuroanatomical perspective, brain networks

References and Readings
C
other than those related to frontal lobe functions can be
Anderson, M. C., & Green, C. (2001). Suppressing unwanted memories
involved in controlled aspects of attention. For example,
by executive control. Nature, 410, 366–369.
parietal lobe structures appear to be important for Baddeley, A. D., & Hitch, G. (1974). Working memory. In G. H. Bower
response intention and sensory selective attention. How- (Ed.), The psychology of learning and motivation: advances in research
ever, control behaviors such as response planning, selec- and theory (Vol. 8, pp. 47–89.). New York: Academic Press.
tion, and execution are associated with networks of Cohen, R. (1993). The neuropsychology of attention. New York: Plenum.
Miyake, A., Friedman, N. P., Emerson, M. J., Witzki, A. H., Howerton, A.,
cortical and subcortical regions linked to the frontal
& Wager, T. D. (2000). The unity and diversity of executive functions
lobes. It is these functions that are most commonly and their contributions to complex ‘‘frontal lobe’’ tasks: A latent
refer to when discussing control functions of the brain. variable analysis. Cognitive Psychology, 41, 49–100.
Although there is not a clear anatomical mapping, studies Monsell, S., & Driver, J. (2000). Attention and performance XVIII: Control
suggest that different regions of the frontal lobe (and of cognitive processes. Cambridge, MA: MIT Press.
O’Reilly, R. C., Braver, T. S., & Cohen, J. D. (1999). A biologically-based
associated networks) relate to different aspects of control,
neural network model of working memory. In P. Shah & A. Miyake
such that there is a heterogeneity of functioning that (Eds.), Models of working memory. New York: Cambridge University
would argue against any unitary conceptualization of Press.
attentional control (Cohen, 1993). Shallice, T. (1988). Form neuropsychology to mental structure. Cambridge:
Cambridge University Press.
Shallice, T., Stuss, D. T., Picton, T. W., Alexander, M. P., & Gillingham, S.
(2008). Mapping task switching in frontal cortex through neuropsy-
Cognitive chological group studies. Frontiers in Neuroscience, 2(1), 79–85.

Similarly, cognitive researchers have made an effort to

move away from a homunculus view of control functions,
pointing out that terms such as central executive (Baddely Controlled Oral Word Association
& Hitch, 1974), supervisory attentional system (Shallice, Test
1988), and executive control (e.g., Anderson & Green,
2001) all take on the role of a poorly defined black box J ANET PATTERSON
and give the impression of a unitary concept. These terms California State University East Bay
may have been useful as placeholders, while cognitive Hayward, CA, USA
researchers worked out the details of other related systems,
such as the slave systems of Baddely and Hitch’s (1974)
model of working memory. However, with an emerging Synonyms
focus on attentional control and with new tools for the
direct study of phenomena such as task switching, re- Category fluency; CFL test; COWA; COWAT; F-A-S test;
sponse inhibition, goal formation, and planning in the Letter fluency; Phonemic fluency; Verbal fluency
form of functional neuroimaging (e.g., Shallice, Picton,
Alexander, & Gillingham, 2008), computational modeling
(O’Reilly, Braver, & Cohen, 1999), and statistical model- Description
ing techniques (Miyake et al., 2000), there is a growing
body of information that specifies the subprocesses The Controlled Oral Word Association Test (COWAT) is a
involved in these selection functions with increasing clar- measure of verbal fluency and is a subtest of the Multilin-
ity (see also Monsell & Driver, 2000 for a review). gual Aphasia Examination (MAE; Benton, Hamsher, &
Sivan, 1994). The COWAT uses the three letter set of C,
F, and L to assess phonemic fluency. Individuals are given
Cross References 1 min to name as many words as possible beginning with
one of the letters. The procedure is then repeated for the
▶ Divided Attention remaining two letters (see Strauss, Sherman, & Spreen,
▶ Focused Attention 2006 and Benton, Hamsher, Rey, & Sivan, 1994 for
704 C Controlled Oral Word Association Test

specific administration instructions). Several tests of pho- more difficult, while results for the F-A-S form appeared
nemic fluency exist, some of which are part of larger test more variable. In addition, COWAT scores have been
batteries (e.g., the MAE or the Neurosensory Center Com- correlated with neuropsychological measures such as
prehensive Examination for Aphasia; Spreen & Benton, reading tests and IQ tests.
1977) and others that can be administered independently
(e.g., the F-A-S Test).
Verbal fluency is a cognitive function that facilitates Clinical Uses
information retrieval from memory. Successful retrieval
requires executive control over cognitive process such as Scoring for the COWAT and other verbal fluency tests is
selective attention, mental set shifting, internal response straightforward. The examiner writes each word as it is
generation, and self-monitoring. Tests of verbal fluency produced by the individual. The transcript is reviewed
evaluate an individual’s ability to retrieve specific informa- and inadmissible words (i.e., repetitions, proper names,
tion within restricted search parameters (Lezak, Howieson, or slang) are eliminated. The test score is the total number
Loring, Hannay, & Fischer, 2004). The two most common of different words produced for all three letters (see
parameters are semantic fluency and phonemic fluency. Strauss et al., 2006 and Benton et al., 1994 for specific
administration instructions).
Supplementary scoring measures for the COWAT and
Historical Background other phonemic fluency tests provide additional informa-
tion in clinical diagnosis and treatment. Supplementary
Borkowski, Benton, and Spreen (1967) were early propo-
scorning measures are error analysis, and cluster and
nents of systematically examining word fluency in persons
switching analysis (see Table 1). In error analysis, the
with brain damage. They recognized that so-called word
examiner notes any observable pattern of production of
fluency tasks had been used in neuropsychological inves-
errors that suggests a loosening of executive control over
tigation of patients with brain damage and undertook two
cognitive processes that would result in errors. For exam-
studies of the task. The first established the relations
ple, a pattern of multiple repetitions of previous responses
between word fluency and various English letters; the
suggests perseveration and inefficient self-monitoring.
second examined word fluency data for persons with
Error patterns provide qualitative performance data and
brain damage and control patients. They presented nor-
may appear as common patterns such as repetition of a
mative data for the first study and comparative data for
word, or idiosyncratic patterns. Clustering and switching
the second, clearly supporting their hypotheses of the
analyses evaluate the depth of the searchable knowledge
utility of word fluency assessment.
base (clusters) and the cognitive flexibility within and
Since publication of these data, word fluency tasks,
across categories (switching) (Troyer, Moscovitcvh, &
and the COWAT in particular, have been investigated in
Winocur, 1977). An example of an efficient search strategy
detail. Spreen and Risser (2003) suggest that this assess-
would be identifying a cluster or subcategory within the
ment tool in its various forms has been one of the most
category (e.g., words that begin with ‘‘cr’’ in the COWAT
frequently and thoroughly investigated neuropsychologi-
task of naming words that begin with C) and producing as
cal assessment measures for unimpaired and neurologi-
many items in that category as possible and then switch-
cally impaired persons. A search of electronic databases
ing clusters (e.g., to words beginning with ‘‘cl’’). Clusters
confirms this suggestion.
are scored by counting the number of clusters and calcu-
lating the mean cluster size; switches are scored by count-
Psychometric Data ing the number of transitions between clusters. Rules for
scoring cluster size and number of switches appear in
Psychometric data for the COWAT and other phonemic Troyer et al. (1997) and normative data for healthy adults
fluency tests, as well as other verbal fluency tasks (e.g., appear in Troyer (2000).
semantic fluency) are readily available. Norms have been Scores from the COWAT are useful in evaluation of
published for children and adults of varying ages, levels of persons with neurogenic communication disorders, such
education, ethnic diversity, and geographical diversity as aphasia following stroke, traumatic brain injury, and
(Loonstra, Tarlow, & Sellers, 2001; Strauss et al., 2006). dementia. Studies have included COWAT in the diagnos-
Some differences have been noted between test forms, tic batteries given to several patient populations and also
most notably, between the COWAT and F-A-S Test in treatment studies as measures of behavioral change.
(Barry, Bates, & Labouvie, 2008); the CFL form appeared The utility of the COWAT in identifying the nature
 Controlled Oral Word Association Test C 705

Controlled Oral Word Association Test. Table 1 An example of F-A-S Test results and cluster and switch scoring for a person
with aphasia

Responses Clusters and Switches

FAS-Test: ‘‘F’’ fast, fun, fickle, fuschsia, finger of fate, Clusters = 8 (mean size = 1.1)
four, fifty-four, forty, fornicate fast
C
fun
Words = 9 fickle
fuchsia
finger of fate
four
fifty-four
forty, fornicate

Switches = 7
FAS-Test: ‘‘A’’ apple, aardvark, alpaca, Clusters = 5 (mean size = 1)
ammonia, arsenic apple
aardvark
Words = 5 alpaca
ammonia
arsenic

Switches = 4
FAS-Test: ‘‘S’’ substantial, sum, subtraction, Clusters = 5 (mean size = 1.8)
stuck, structure, symbol, sympathy, stroke, sixty substantial, sum, subtraction
stuck, structure
Words = 9 symbol, sympathy
stroke
sixty

Switches = 4
Total Words = 23 Clusters = 18
Mean size = 1.27
Switches = 15

and severity of performance deficits in clinical popula- ▶ Boston Diagnostic Aphasia Examination
tions has been supported; however, conflicting findings ▶ Circumlocution
have been reported. Typically, the total number of ac- ▶ Clustering
ceptable responses is the reported test result; however, ▶ Cognitive-Communication Disorder
increasingly cluster and switching scores are reported as ▶ Cognitive Functioning
well. The COWAT is valuable in detecting cognitive ▶ Cognitive Processing
dysfunction, but it requires further study before defini- ▶ Cue
tive conclusions are possible with regard to performance ▶ Cued Recall
patterns that can be linked with specific neurogenic ▶ Error Recognition and Correction
behavioral deficits. ▶ Free Recall
▶ Mayos Older American Normative Studies (MOANS)
▶ National Adult Reading Test
Cross References ▶ Phonemic Cue
▶ Semantic Cue
▶ Aphasia ▶ Semantic Fluency
▶ Aphasia Tests ▶ Verbal Mediation
▶ Benton, Arthur ▶ Western Aphasia Battery
706 C Contusion (Cerebral)

References and Readings

Convulsion
Barry, D., Bates, M. E., & Labouvie, E. (2008). FAS and CFL forms of
verbal fluency differ in difficulty: A meta-analytic study. Applied ▶ Grand Mal Seizure
Neuropsychology, 15, 161–166.
Benton, A. L., Hamsher, K., Rey, G. L., & Sivan, A. B. (1994). Multilingual
Aphasia Examination (3rd ed.). Iowa City, IA: AJA Associates.
Borkowski, J. G., Benton, A. L., & Spreen, O. (1967). Word fluency and Convulsive Disorder
brain damage. Neuropsychologia, 5, 135–140.
Goodglass, H., Kaplan, E., & Baressi, B. (2001). Boston Diagnostic Aphasia
Examination (3rd ed.). San Antonio TX: Psychological Corporation.
▶ Epilepsy
Kertesz, A. (2006). Western Aphasia Battery. New York: Grune & Stratton.
Lezak, M. D., Howieson, D. B., Loring, D. W., Hannay, H. J., & Fischer,
J. S. (2004). Neuropsychological assessment (4th ed.). New York:
Oxford University Press. COPD
Loonstra, A. S., Tarlow, A. R., & Sellers, A. H. (2001). COWAT metanorms
across age, education and gender. Applied Neuropsychology, 8, ▶ Chronic Obstructive Pulmonary Disease
161–166.
Spreen, O., & Benton, A. L. (1977). Neurosensory Center Comprehensive
Examination for Aphasia. Victoria BC: University of Victoria Neuro-
psychology Laboratory.
Spreen, O., & Risser, A. H. (2003). Assessment of aphasia. Oxford: Oxford
Coping
University Press.
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). Compendium of J OEL W. H UGHES
neuropsychological tests: Administration, norms, and commentary Kent State University
(3rd ed., p. 502). Oxford: Oxford University Press. Kent, OH, USA
Troyer, A. K. (2000). Normative data for clustering and switching on
verbal fluency tasks. Journal of Clinical and Experimental Neuropsy-
chology, 22, 370–378.
Troyer, A. K., Moscovitch, M., & Winocur, G. (1997). Clustering and Synonyms
switching as two components of verbal fluency: Evidence from
younger and healthy adults. Neuropsychology, 11, 138–146. Stress management

Definition
Contusion (Cerebral)
Coping is responding to environmental stimuli, events,
▶ Cortical Contusion and circumstances for the purpose of minimizing or
managing stress, solving problems, and modulating phys-
iological and emotional responses. Coping is often paired
with stress (as the latter elicits the former) in what has
Conventional Antipsychotics become the stress and coping literature associated with
Richard Lazarus and Susan Folkman. Stress responses
▶ Antipsychotics typically involve appraising the stimulus or event, which
begins the process of assigning value (e.g., distressing)
and determining responses (e.g., fight, flight, freeze).
Coping is a process that follows stress appraisals, and
Conversation Analysis coping responses seek to manage stress with cognitive,
physiological, and behavioral responses. Various coping
▶ Discourse Assessment strategies have been categorized, such as appraisal-
focused, problem-focused, or emotion-focused coping.

Conversion Disorder Cross References

▶ Cogniform Disorder ▶ Self-Regulation

▶ Somatization ▶ Stages of Adjustment
 Coronary Artery Bypass Graft C 707

▶ Stress Patients undergo general anesthesia and a midline

▶ Stress Management incision (median sternotomy) allows the surgeon to
visualize the heart and vessels. The artery or vein grafts
are then harvested. Frequently used vessels include the
References and Readings internal thoracic arteries, radial arteries, and saphenous C
veins. The heart is then stopped using a special mixture of
Carver, C. S., Scheier, M. F., & Weintraub, J. K. (1989). Assessing coping
chemicals and the patient is placed on cardiopulmonary
strategies: A theoretically based approach. Journal of Personality and bypass where the blood flow returning to the heart is
Social Psychology, 56, 267–283. diverted through a heart–lung machine that provides ex-
Lazarus, R. S., & Folkman, S. (1984). Stress, appraisal and coping. tracorporeal circulation and oxygenation. The graft is then
New York: Springer.
sewn into place and the heart is restarted. The sternum is
then closed with wires, and the incision is sutured.

Core Battery Current Knowledge

▶ Flexible Battery In the early years of cardiac surgery several investigators
noted transitive postoperative delirium, whereas others
reported immediate postoperative neurological abnormal-
ities, however, no well-conducted or controlled studies were
Coronary Angioplasty available. More recent studies have shown a short-term
neuropsychological decline in the 7–14 days after CABG,
▶ Angioplasty including deficits in psychomotor speed, attention, verbal
learning, and memory. Studies have reported an 11–75%
incidence of postoperative cognitive decline (POCD) after
cardiac surgery. Age is considered to be the strongest pre-
Coronary Artery Bypass Graft dictive factor of postoperative cognitive dysfunction. It is
hypothesized that ‘‘off-pump’’ surgery causes less cognitive
F LORA H AMMOND 1, LORI G RAFTON 2 decline as it avoids extracorporeal circulation, but studies
1
Indiana University have not shown this to be true. Other potential causes of
Indianapolis, IN, USA neurocognitive decline include intraoperative cerebral oxy-
2
Carolinas Rehabilitation gen desaturation or microemboli.
Charlotte, NC, USA

References and Readings

Synonyms
Eagle, K. A., Guylon, R. A., Davidoff, R., Ewy, G. A., Fonger, J.,
Gardner, T. J., et al. (1999). http://circ.ahajournals.org/cgi/content/
CABG
full/100/13/1464
Jensen, B. Ø., Rasmussenb, L. S., & Steinbrüchel, D. A. (2008). Cognitive
outcomes in elderly high-risk patients 1 year after off-pump versus
Definition on-pump coronary artery bypass grafting. A randomized trial.
European Journal of Cardio-Thoracic Surgery, 34(5), 1016–1021.
Slater, J. P., Guarino, T., Stack, J., Vinod, K., Bustami, R. T., Brown, J. M.,
Coronary artery bypass surgery (CABG) is a surgical
III, et al. (2009). Cerebral oxygen desaturation predicts cognitive
procedure for coronary artery disease in which arteries decline and longer hospital stay after cardiac surgery. Annals of
or veins from other parts of the body are grafted from the Thoracic Surgery, 87(1), 36–44, discussion 44–45
aorta to the coronary arteries in order to bypass the Tarter, R. E., Butters, M., Beers, S. R. (2001). Medical neuropsychology
blocked portions. Indications for surgery include disease (2nd ed., pp. 69–71). New York: Kluwer Academic.
http://www.nlm.nih.gov/medlineplus/ency/article/002946.htm. Accessed
of the left main coronary artery and/or disease of all three
29 August, 2007.
coronary arteries and abnormal ventricular function. It http://www.sts.org/sections/patientinformation/adultcardiacsurgery/cabg/
may be performed in patients with severe angina which is index.html?CFID=3659926&CFTOKEN=93793791. Accessed 29 Au-
unresponsive to medical management. gust, 2007.
708 C Coronary Artery Disease

cardiac stress tests, and direct visualization on coronary

Coronary Artery Disease angiography or other imaging studies. The treatment
includes the use of beta-blockers, calcium channel blockers,
▶ Coronary Disease angiotensin converting enzyme inhibitors, nitroglycerine,
aspirin, or other medications; antihypertensive and lipid-
lowering agents; diet, exercise, and lifestyle changes; throm-
bolysis; angioplasty with coronary stent placement; and
coronary bypass graft surgery.
Coronary Disease
E LLIOT J. R OTH
Northwestern University Cross References
Chicago, IL, USA
▶ Angioplasty
▶ Anticoagulation
Synonyms ▶ Antiplatelet Therapy
▶ Atherosclerosis
Atherosclerotic heart disease; Coronary artery disease; ▶ Cholesterol
Coronary heart disease; Ischemic heart disease ▶ Congestive Heart Failure
▶ Infarction
▶ Ischemia
Definition ▶ Myocardial Infarction
▶ Stent
Coronary disease, or coronary artery disease (CAD), results ▶ Thrombosis
from atherosclerosis, or narrowing of the arteries that ▶ Tissue Plasminogen Activator
provide blood supply to the heart muscle (‘‘myocardium’’). ▶ Vasospasm

Current Knowledge
References and Readings
Atherosclerosis, which is the process by which cholesterol
and fat deposits adhere to the inside walls of blood vessels, Hansson, G. K. (2005). Inflammation, atherosclerosis, and coronary
creates ‘‘plaques’’ that block the blood supply through blood artery disease. New England Journal of Medicine, 352, 1685–1695.
Virmani, R., Kolodgie, F. D., Burke, A. P., Farb, A., & Schwartz, S. T.
vessels. When this narrowing or occlusive process blocks the
(2000). Lessons from sudden coronary death: a comprehensive mor-
coronary artery, the accompanying obstruction to blood phological classification scheme for atherosclerotic lesions. Arterio-
flow reduces the supply of oxygen and nutrients to the sclerosis, Thrombosis, and Vascular Biology, 20, 1262–1275.
heart muscle, creating ischemia that causes chest pain (‘‘an-
gina pectoris’’), or death of the cells of the heart (‘‘myocar-
dial infarction’’). At times, it can cause other problems such
as arrhythmias (abnormal heart rhythm) or congestive heart
failure, in which the heart is unable to pump sufficient blood
to the remainder of the body. CAD is the most common type
Coronary Heart Disease
of heart disease and the leading cause of death in the USA.
▶ Coronary Disease
Risk factors for CAD have been well studied; these include
smoking, diabetes, hypertension, hyperlipidemia, obesity,
sedentary lifestyle, excessive alcohol intake, and family his-
tory. Although chest pain is the most common symptom,
dyspnea, palpitations, diaphoresis, nausea, radiation of the
pain to the neck and left arm, and no symptoms at all, also Corporis Callosi
are possible. The diagnosis relies on electrocardiogram,
blood levels of cardiac enzymes, echocardiography, select ▶ Corpus Callosum
 Correction Factor C 709

vary widely but are generally reported to range between

Corpus Callosum 0.3 and 0.7% in the general population and as high as 3%
in individuals with development disabilities. Agenesis of
J EFF D UPREE the corpus callosum results in symptoms ranging from
Virginia Commonwealth University asymptomatic with normal intelligence to intellectual
Richmond, VA, USA
C
retardation, seizures, hydrocephalus, and spasticity. In
individuals suffering from severe epilepsy, a surgical pro-
cedure known as corpus callostomy may be performed,
Synonyms which involves the partial or complete transaction of the
corpus callosum. This procedure is only performed in
Commissural magna; Corporis callosi; Interhemispheric patients who are at risk of accidental injury resulting
commissure from severe seizures. The layman’s term for this condition
is split brain due to the loss of interhemispheric com-
munication. Much of the original research detailing the
Definition consequence of corpus callostomy was conducted by
Dr. Roger Wolcott Sperry.
Corpus callosum is the largest axonal tract of the adult
brain that provides symmetrical connections between the
two hemispheres. Cross References

▶ Ganglion
▶ Gazzaniga, M. S. (1939– )
Current Knowledge ▶ Sperry, Roger Wolcott (1913–1994)
▶ Split-brain
The corpus callosum is the largest commissure of the
adult brain that provides a bridge for the passing of
information from one cerebral hemisphere to the other References and Readings
by 200–300 million myelinated and unmyelinated axons.
The size of the corpus callosum varies greatly but is Barr, M., & Kiernan, J. (1983). The human nervous system – An anatomical
generally larger in females than in males. In the human, viewpoint (4th ed.). Philadelphia: Harper and Row.
the corpus callosum begins development around the 11th Gazzaniga, M. S. (2005). Forty-five years of split-brain research and still
going strong. Nature Reviews Neuroscience, 6(8), 653–659.
week of gestation and continues through adolescence.
Haines, D. (2006). Fundamental neuroscience for basic and clinical appli-
Initially, the corpus callosum is composed of astrocytic cations (3rd ed.). Philadelphia: Churchill Livingstone Elsevier.
processes, which serve as conduits for growing axons Kandel, E., Schwartz, J. H., & Jessel, T. M. Principles of neural science
extending to the contralateral hemisphere. This inter- (4th ed.). New York: McGraw-Hill.
hemispheric commissure lies beneath the cortex at the Paul, L. K., Brown, W. S., Adolphs, R., Tyszka, J. M., Richards, L. J.,
Mukherjee, P., et al. (2007). Agenesis of the corpus callosum:
bottom of the cerebral longitudinal fissure. It forms
Genetic, developmental and functional aspects of connectivity.
much of the roof of the lateral ventricles and is composed Nature Reviews Neuroscience, 8(4), 287–299.
of four parts: the rostrum, the genu, the body (also known
as the trunk), and the splenium. Each portion of the
corpus callosum is responsible for connecting symmetri-
cal regions of the two hemispheres with the rostrum and
genu connecting portions of the prefrontal and premotor Corpus Mamillare
cotices, the body interconnecting the premotor, motor,
supplementary motor, and the posterior parietal cortices, ▶ Mammillary Bodies
while the splenium connects portions of the temporal,
occipital, and parietal lobes. Although being the largest
white matter tract of the brain, the corpus callosum is not
essential for life. The complete or partial absence of the Correction Factor
corpus callosum is known as agenesis of the corpus callo-
sum. This condition is rare, and estimates of incidence ▶ K Scale
710 C Correlation Coefficients

plot of the data. The values of a correlation can range

Correlation Coefficients between þ1 and 1 with these two extremes representing
perfect relationships, which rarely if ever occur in
C HRISTIAN S CHUTTE , B RAD N. A XELROD research, and a correlation coefficient of 0 would
John D. Dingell VA Medical Center represent no relationship, given certain assumptions are
Detroit, MI, USA made. A line can be drawn through data that are related
that generally approximates a regression line, which is
how Galton identified the first regression line in his
Synonyms heritability studies with peas. Correlation is a measure
of the strength of the relationship between two variables.
Pearson r, r, rho Thus, if data in a scatter plot are randomly scattered, such
as in the example below, then there is no relationship, as
no single line adequately represents the data and the
Definition correlation would be roughly 0.

A measure of the strength of the relationship between two

10
variables, x and y.
8

Historical Background 6
y

4
The correlation, or co-relation, coefficient is typically
attributed to Karl Pearson who developed the formalized
2
idea of correlation during the mid- to late 1800s. However,
the beginning of the idea of correlation may have 0
come from Sir Francis Galton, cousin of Charles Darwin.
0 2 4 6 8 10
Galton worked on genetic heritability of sweet peas. x
Through his work on heritability, he developed the
If data are positively related, such that as one variable
beginnings of regression and correlation. Pearson, who
increases in value so does the other, then one would be
worked in Galton’s lab and was later his biographer, attrib-
able to draw a line that would approximately represent
uted the development of the regression slope to Galton.
the data. The below example illustrates an ideal relation-
Pearson then generalized Galton’s work into the Pearson
ship that rarely occurs in research of a þ 1 correlation
Product Moment Correlation (PPMC), or ‘‘moment’’
such that for every one unit that x goes up, y goes up one
meaning the average of a set of products. The PPMC is
unit.
often identified as ‘‘r,’’ which Galton originally used to
denote ‘‘regression’’ and Pearson later used as notation
for correlation. In 1896, Pearson published an article in 30
which he credited Bravais for developing the rudiments of
the correlation formula. In this work published in the 25
Philosophical Transactions of the Royal Society of London,
Pearson showed that the optimum values for the regres- 20
y

sion line and correlation could be derived from the prod-

uct moment or S xy=n, where x and y are deviations from
15
their respective means, usually expressed as standard z
scores and n is the number of pairs.
10
0 5 10 15 20
Current Knowledge x

There may also be negative associations, such that

A correlation, or co-relation, of two variables can be for every unit that x goes up, y goes down, or a  1
visually scanned initially by simply looking at a scatter relationship, such as the below idealized example.
 Correlation Coefficients C 711

The correlation coefficient is therefore a measure of the

10 extent to the relation of pairs of observed data points can
be expressed as a linear function. The greater the summed
8
square of differences between the observed data and the
values described by the linear function, the lower the cor- C
6
relation coefficient. The closer the observed data points lie
y

4 to the line of best fit, the higher the correlation coefficient.

There are several forms of correlation that need to
2 be addressed including those for continuous variables,
categorical variables, and correlations that are better
0 descriptions of nonlinear and skewed relationships. The
0 2 4
x
6 8 10 scope of this article is to cover the basic foundations of
correlation coefficients. The use of correlation ranges far
However, typically a scatter plot will not be as obvious and wide and a thorough examination of this subject is
and the data will look more like an ellipse such as in the the subject of chapters and entire texts referenced below.
example below, which still illustrates a strong correlation The object of this entry is to cover foundational
of over .8. issues related to correlation coefficients. There are more
correlation coefficients than those presented below,
though several different forms of correlation and their
properties are considered.
8
It is important to note that correlation, even a strong
correlation, does not infer causation. In other words,
6
simply because two variables are related does not mean
that one causes the other. For example, you need light to
y

read this text. Simply because the light is on while you are
4 reading does not mean that light is causing you to read,
they are certainly related, as there will always be some
light source when you read, but one does not cause the
2 other. A determination of causation requires adequate
0 2 4
x
6 8 10 experimental design.
There are certain important components that underlie
The above examples show linear relationships between
most correlations. Correlations are most meaningful
variables, which is an assumption of most correlation
when certain criteria are met, and different correlation
coefficients. An examination of scatter plots can also
coefficients are affected differently by failure to meet
show nonlinear relationships, which are not well repre-
different assumptions. The Pearson product moment
sented by standard correlation coefficients, such as the
correlation coefficient has the most stringent set of
PPMC, but can be shown with other methods, such as
assumptions. These include:
eta. The below example has a near 0 Pearson r, but the
variables are clearly related nonlinearly. 1. The data are interval: The level of measurement must
at least be interval as opposed to nominal or ordinal,
25 though this can be managed if it is violated.
2. The data must have a linear relationship: Most correla-
20 tions assume that the data are linearly related, as op-
posed to nonlinear. To the degree which the data are
15
better explained by a nonlinear relationship correlation
y

10
coefficients will underestimate the relationship. Prior to
completing a correlation analysis this can be examined
5 by looking at a scatter plot, as discussed above.
3. The variables have similar and normal underlying
0 distributions (more formally in a bivariate correlation,
0 5 10 15 20 such as the Pearson r): To the degree that the
x
712 C Correlation Coefficients

distributions of the different variables differ, the cor- also other methods that are more robust to violations of
relation will attenuate the relationship between them. the above assumptions, such as Spearman’s rho or eta in
For example, if correlating a variable that is normally the case of a nonlinear relationship. The correlation
distributed, like height, with one that is highly skewed coefficient is considered a measure of effect size, which is
like ability to walk. This is done when correlating a a measure of how different two distributions are. By
continuous variable with a dichotomous variable or convention a correlation of .1 is small, .3 moderate and
when correlating interval data with ordinal. If this .5 large (Cohen, 1988), at least in the behavioral sciences
assumption is violated to a significant degree then that can expect weaker relationships in general due to
rank order correlation may be used, such as the the complexity of the subject matter. For example, the
Spearman’s rho or other nonparametric correlations. correlation between IQ and academic achievement is
4. The data must have homoscedasticity: The error, or approximately .55 (Griffenstein & Baker, 2003), but one
random variance in X and Y, contained in the data, is would expect no effect for a correlation between IQ and
assumed to be equal along the entire distribution. If, height. The correlation coefficient can also be squared to
for example, one portion of the distribution has a give the coefficient of determination, which is the amount
much larger random variance, then the correlation of variance in one variable that is accounted for by
may overrepresent the relationship because it would another. For example, if one had a correlation of .55
underrepresent the amount of variance that is between IQ and academic achievement then the coeffi-
attributable to error. If data are heteroscedastic, then cient of determination (r 2) would be .30, which means
the distribution will not be normal and the correlation that approximately 30% of the variance in academic
may misrepresent the data. achievement is accounted for by IQ.
5. The data has no or limited outliers: Correlation is
1. PPMC or r: The PPMS is an association of two
sensitive to outliers. Some forms of correlation are
continuous variables that shows the degree of linear
more robust to a violation of this assumption than
relationship between them. It can be calculated using
others, but normally correlation is a representation of
raw scores, deviation scores, or by using a covariance
deviations of mean values. Thus, to the degree that the
formula. A common method is to calculate the
mean is affected by outliers then the correlation will be
standard score (or z score) and sum the products of
also. If there are many outliers, or few that are large,
the two variables and divide them by the degrees of
this problem can be managed through use of a
freedom (n  1) or S xy=n S 1.
Spearman rho, which ranks data.
2. Point-biserial or rpb: This is a special case of the PPMC
6. There is limited measurement error present in the
for use when there is a continuous variable, such as
sample: It is assumed that the measurement is relative-
height, and a dichotomous nominal variable, such as
ly free from or has limited error. In other words, if one
gender. The point-biserial correlation is for naturally
has an invalid test that only measures error then
dichotomous variables, such as gender, not artificially
the correlation will be near zero, as the data will be
dichotomized variables, such as taking a naturally
random and show little relationship. It is rare in
continuous distribution, such as intelligence, and
behavioral research to be free from error, but limiting
making it into high and low intelligence.
it is an important aspect of experimental control.
3. Phi: This is a special case of the PPMC for use when
7. The data have adequate variance: In order to
both variables are dichotomous and nominal. Note that
adequately assess relationships among variables there
as with rpb this is for naturally dichotomous variables,
must be variance among the variables. In general, the
such as gender, not artificially dichotomized variables.
more variance the higher the correlation will be.
4. Biserial or rb: This is for use when there is one contin-
To the extent that these criteria are violated, which they uous variable, such as height, and a dichotomized
often are, the correlation coefficient is more or less im- variable, such as high and low intelligence. So, the
pacted depending on the type of correlation. biserial correlation measures the relationship between
There are several different methods calculating basic X and Y as if Y were not artificially dichotomized. This
correlation coefficients depending on the type and char- is similar to the point-biserial, but the formula is
acteristics of the data being analyzed. There are several designed to replace some of the variance that is lost.
different types of correlation that depend on the level of One of the important components listed above is that
measurement (nominal, ordinal, interval, ratio) being the data have adequate variance. However, when a
made. Most are special cases of the Pearson r. There are variable is dichotomized much of the variance is lost.
 Cortical Blindness C 713

Thus, the biserial formula replaces some of that Cross References

variance, which always yields a higher correlation
than a point-biserial correlation. ▶ Statistical Significance
5. Tetrachoric: This is similar to the phi, except that it is ▶ z Score
assumed that there is a continuous distribution C
underlying the dichotomized variables and it thusly
replaces some of that variance, as opposed to phi References and Readings
that assumes that the two variables are naturally
dichotomous, such as gender and employment status. Chen, P., & Popovich, P. (2002). Correlation: Parametric and nonparametric
measures. Thousand Oaks, CA: Sage.
6. Spearman’s rho or rs or r: Spearman’s rho is a non-
Cohen, J. (1988). Statistical power analysis for the behavioral sciences
parametric statistic. In other words, it makes no (2nd ed.). New Jersey: Erlbaum.
assumptions about the underlying distribution of the
variables. One of the primary components of the
typical PPMC is that there is a normal or bell-shaped
distribution underlying the variable. However, in
many cases, distributions are highly skewed. For
Cortex
example, if one were to look at a distribution of people
▶ Cerebral Cortex
who live into adulthood in the USA, the distribution
would likely be very skewed to the left, meaning that
the vast majority of people live at least until they are of
adult age. Relate that distribution to the number of
people who vote, which would be positively skewed, Cortical Activation
meaning that few people of adult age vote proportion-
ally and a PPMC would not yield an inaccurate repre- ▶ Arousal
sentation, as this distribution significantly violates the
assumptions of the PPMC. Thus, one could convert
raw scores into ranks and complete the correlation.
This is more robust to violations of some of the Cortical Arousal
underlying components of correlation.
7. Measures of nonlinear relationships: Eta is a measure ▶ Arousal
of association that can be used if the data are nonline-
ar, as in the final scatter plot above. It is a measure of
the strength of the effect and is always positive. Eta is
always higher than jrj and is therefore a biased
estimate of the effect. Cortical Blindness
In practical usage, many of the different correlation coef-
S TEVEN Z. R APCSAK , G. A LEX H ISHAW
ficients are calculated using the same method, such as the
University of Arizona
PPMC and the point-biserial, given the ubiquity of com-
Tucson, Arizona, USA
puter statistical packages. What is important to note with
any correlation being used are the number and degree of
the components that are violated and what impact that
Synonyms
has on the relationship between the variables. For exam-
ple, if one is using a PPMC to assess highly skewed data
Anton’s syndrome; Blindsight
then the relationship may be very low, where actually, if a
nonparametric method is used, such as the Spearman’s
rho, then the relationship may be significant. Conversely,
if a PPMC is used on data that have many large outliers Short Description or Definition
the relationship may look strong and be significant, but in
reality it is the impact of those large outliers that are Cortical blindness refers to severe visual loss produced
falsely raising the strength of the associations. by bilateral damage to the geniculostriate visual
714 C Cortical Blindness

pathways. The underlying pathophysiological mecha- currently unclear whether recovery of visual capacity in
nism involves direct destruction and/or de-afferentation cortical blindness is mediated by spared neural tissue
of primary visual cortex (striate cortex, Brodmann area within primary visual cortex, or whether it reflects the
17, or V1). The term Anton’s syndrome is applied to strengthening and increasing utilization of alternative
patients with cortical blindness who demonstrate explic- visual pathways to extrastriate cortical regions that bypass
it denial or unawareness (anosognosia) of their visual the damaged geniculostriate system, or both. Anosogno-
impairment. sia for visual loss in patients with Anton’s syndrome also
tends to diminish over time, often parallel to the resolu-
tion of the visual impairment, but partial defects of aware-
ness are not uncommon. In cases of transient cortical
Categorization
blindness due to RPLS, full recovery of vision can occur
within a few days along with complete resolution of the
Although no universally agreed upon classification system
characteristic neuroradiological abnormalities.
exists, patients with cortical blindness differ in terms of the
severity of the visual loss, the presence/absence of spared
visual abilities (conscious or unconscious), the degree of
awareness of the deficit, and the extent of functional recov-
ery. There are also variations across cases with respect to the
Neuropsychology and Psychology of
capacity to generate internal visual representations using
Cortical Blindness
mental imagery and the susceptibility to experience abnor-
In severe cases of cortical blindness, all forms of conscious
mal visual sensations/hallucinations. The precise neurobio-
visual perception may be abolished. However, this type
logical mechanisms underlying these individual differences
of total visual loss is relatively uncommon and many
in clinical presentation remain to be determined.
patients retain at least some rudimentary visual awareness
of motion or light. Visual form discrimination is pro-
foundly impaired and objects, faces, or written words can-
Epidemiology not be identified. Visuospatial orientation is also severely
compromised and patients may repeatedly bump into
Cortical blindness is a relatively rare condition, typically objects when attempting to navigate in their environment.
caused by bilateral occipital strokes in the territory of the Although individuals with cortical blindness do not
posterior cerebral arteries. Other less common etiologies have normal conscious awareness of visual events, they
include anoxic brain damage, carbon monoxide poison- can sometimes demonstrate surprising ability to respond
ing, head trauma, and occipital lobe tumors. Transient to stimuli presented within the blind portions of their
cortical blindness can be seen in the context of the revers- visual fields. Specifically, patients may be able to detect,
ible posterior leukoencephalopathy syndrome (RPLS) locate, and discriminate visual stimuli that they claim not
related to hypertensive encephalopathy, the use of chemo- to see. Residual visual capacity within the cortically blind
therapeutic and immunosuppressant drugs, or the injec- field in the absence of conscious awareness has been
tion of radiological contrast agents during cerebral referred to as ‘‘blindsight’’ (Weiskrantz, 1986; Stoerig &
angiography. Cowey, 1997, 2007; Stoerig, 2006). The fact that blindsight
can be observed in patients with extensive destruction or
de-afferentation of primary visual cortex suggests that the
Natural History, Prognostic Factors, preserved visual abilities of these individuals are mediated
Outcomes by neural pathways from retina to extrastriate visual cor-
tex that bypass the damaged geniculostriate system. There
Although some recovery of visual function is observed in are in fact a number of alternative non-geniculostriate
most cases of cortical blindness, patients with neuroim- pathways capable of transmitting visual information to a
aging evidence of extensive structural damage to occipital variety of temporo-parietal extrastriate cortical areas via
cortex typically do not regain full normal vision. Residual subcortical relay nuclei in the midbrain and diencephalon
visual field defects are common, and cortical blindness (Weiskrantz, 1986; Stoerig & Cowey, 1997, 2007; Stoerig,
may evolve into visual agnosia characterized by a persis- 2006). The specific visual functions retained in blindsight
tent inability to recognize objects, faces, or words despite may depend on which of these multiple parallel visual
the return of more elementary visual functions. It is pathways are available to patients. For instance, the
 Cortical Blindness C 715

residual capacity to detect motion and to locate and visual imagery may provide faulty input to an otherwise
manually grasp targets presented in the blind field may intact monitor. The loss of normal visual input following
depend on projections from the retina to the superior damage to primary visual cortex may in fact give rise to
colliculus, with additional connections to the pulvinar frequent ‘‘release’’ hallucinations in patients with cortical
and to middle temporal (MT/V5) and dorsal parietal blindness due to increased cortical excitability in de-affer- C
cortex (Danckert & Rossetti, 2005). Other alternative ented extrastriate areas. Furthermore, since visual percep-
pathways from retina to ventral extrastriate cortex or tion and imagery are mutually inhibitory under normal
amygdala might be involved in mediating unconscious circumstances, the absence of bottom-up activation by
visual form discrimination (Trevethan, Sahraie, & Wei- geniculostriate afferent signals may be accompanied by a
skrantz, 2007) and implicit recognition of emotional fa- relative enhancement of visual imagery mediated by unop-
cial expressions (Morris, DeGelder, Weiskrantz, & Dolan, posed top-down activation of sensory representations in
2001; Pegna, Khateb, Lazeyras, & Seghier, 2005). Func- extrastriate cortex. Patients may deny blindness because
tional imaging studies in patients with blindsight are con- they continue to experience internally generated visual sen-
sistent with the notion that unconscious processing of sations and may mistake these for veridical perceptions
visual information depends on non-geniculostriate visual resulting from retinal stimulation by external visual events.
pathways. Specifically, these investigations have demon- To understand anosognosia for visual loss, it is useful
strated activation in midbrain/thalamic nuclei, extrastriate to briefly consider what is currently known about
cortical areas, and the amygdala in the absence of concomi- the neural correlates of normal visual awareness. In this
tant activity in the lesioned primary visual cortex during context, it is important to emphasize that conscious
visual stimulation of the blind field (Sahraie, Weiskrantz, awareness of visual events normally entails the capacity
Barbur, Simmons, Williams, & Brammer, 1997; Stoerig, to acknowledge, describe, reflect upon, and make appro-
2006; Morris et al., 2001; Pegna et al., 2005). priate cognitive judgments about ongoing visual ex-
Patients with cortical blindness may demonstrate un- periences (Weiskrantz, 1997; Block, 2005; Dehaene,
awareness of their profound visual impairment. This Changeux, Naccache, Sackur, & Sergent, 2006). Thus,
striking clinical condition is referred to as Anton’s syn- awareness and the ability to provide introspective report
drome. Anosognosia for visual loss can take several dif- or commentary about the quality, content, and veridi-
ferent forms. In extreme cases, patients emphatically deny cality of visual perceptions are closely related functions.
being blind and produce confabulatory responses when Although localized neural activity in cortical visual areas
questioned about their visual abilities. Other patients (striate and extrastriate cortex) is obviously necessary for
acknowledge a change in their vision but they typically visual information to reach this ‘‘commentary stage’’ of
offer a variety of excuses to explain the difficulty, attribut- conscious awareness, it is by itself not sufficient (Wei-
ing it to poor lighting conditions or to a problem skrantz, 1997; Rees, Kreiman, & Koch, 2002; Dehaene
with their eyeglasses. A number of theories have been et al., 2006). In particular, evidence from recent neuroim-
advanced to explain anosognosia for blindness (Bisiach aging studies suggests that conscious vision requires the
& Geminiani, 1991; Heilman, 1991; Celesia, Brigell, & additional recruitment of dorsolateral prefrontal and pa-
Vaphiades, 1997; Adair, Schwartz, & Barrett, 2003). For rietal cortical regions implicated in visual attention and
instance, it has been proposed that normal visual aware- working memory (Rees, Kreiman, & Koch, 2002; Dehaene
ness depends on a hypothetical monitor located in extra- et al., 2006). Prefrontal cortex is also involved in mediat-
striate visual association areas that receives afferent input ing strategic cognitive operations necessary for critically
from primary visual cortex (Heilman, 1991). In addition evaluating and interpreting the meaning and signific-
to evaluating activity within the visual areas of the brain, ance of visual experiences in order to determine the
the monitor also sends efferent information to cortical most appropriate behavioral response.
language areas enabling subjects to verbally comment on Activation of frontal and parietal regions by input
their visual experiences. Lesions that disrupt the input from cortical visual areas is also likely to play an essential
and/or output connections of the visual monitor, or pro- role in awareness of abnormal visual function. Specifi-
duce damage to the monitor itself, result in anosognosia cally, damage to primary visual cortex and extrastriate
for visual impairment that may include verbal denial of areas may give rise to visual field defects and/or domain-
the deficit and the production of confabulatory responses specific impairments in processing distinct visual stimu-
by the disconnected language areas. It has also been sug- lus attributes (e.g., form, color, motion). If the same lesions
gested that in cases of cortical blindness, internally gener- also interfere with the bottom-up activation of the fronto-
ated visual experiences in the form of hallucinations or parietal cortical network that normally enables conscious
716 C Cortical Blindness

awareness and introspective report about visual experi- movement, or identity of objects presented in their blind
ences, anosognosia for the visual impairment ensues. De- field using a forced-choice response method (e.g., was it a
fective awareness of visual function may also result from key or a coin?). Better than chance performance on these
direct damage to the putative fronto-parietal network that types of tasks is taken to be indicative of blindsight. Alter-
provides the critical top-down attentional amplification natively, patients can be asked to try to reach for and grasp
required for perceptual information processed within objects in their blind field. Regardless of the testing method
visual cortical modules to enter consciousness, or it may used, it is important to establish after each trial whether
be produced by lesions that disrupt feedforward/feedback the patient had any conscious awareness of the visual
connections between fronto-parietal cortex and visual stimulus. Visual imagery can be tested by asking the sub-
processing areas. In summary, conscious awareness of jects to answer questions about the visual attributes of
both normal and abnormal vision requires dynamic re- familiar objects or animals (e.g., do polar bears have long
ciprocal interactions between cortical visual areas and or short tails?). Patients should be questioned about ab-
specialized regions within frontal and parietal cortex. normal visual perceptions and hallucinations. Unaware-
Lesions that disrupt the spatial distribution, intensity, ness of deficit may be revealed by spontaneous comments
or timing of activation across the different functional or behavior, but patients should also be specifically asked
components of this large-scale neural system may give to describe the quality and content of their visual experi-
rise to a variety of clinical conditions characterized by ences. The severity of anosognosia can be quantified by
unawareness of preserved or impaired visual processing, simple rating scales (Bisiach & Geminiani, 1991; Celesia,
including blindsight, visual neglect, and anosognosia for Brigell, & Vaphiades, 1997).
blindness. Structural neuroimaging (CT/MRI) studies in
patients with cortical blindness due to stroke typically
reveal extensive bilateral infarctions involving primary
Evaluation visual cortex and underlying white matter, often with
evidence of lesion extension into adjacent extrastriate
Neuro-ophthalmological examination in cortical blind- visual association areas (Brodmann areas 18/19, 37)
ness confirms the normal fundoscopic appearance of the (Figure 1). SPECT/PET scans frequently demonstrate
retinas and optic nerves. The pupillary light response is blood flow/metabolic abnormalities that extend beyond
characteristically preserved, as the retinal fibers that me- the boundaries of the lesions seen on CT/MRI, providing
diate this reflex leave the optic tract prior to the origin of evidence that the cortical visual areas that appear spared
the geniculostriate pathways. Reflexive blinking to threat- by structural imaging studies are in fact functionally
ening visual gestures is usually absent, and in the majority compromised. In patients with transient cortical blind-
of cases optokinetic nystagmus cannot be elicited by ness due to RPLS, neuroimaging studies have demon-
moving a striped object in front of the patient’s eyes. strated reversible bilateral subcortical white matter
The dissociation between preserved pupillary light re- abnormalities in posterior occipito-temporo-parietal
sponse and absent optokinetic nystagmus can have diag- regions attributable to vasogenic edema.
nostic utility in distinguishing patients with cortical
blindness from patients with severe peripheral visual loss
due to bilateral eye or optic nerve pathology in whom
both responses are lost, and also from individuals with Treatment
psychogenic blindness in whom both responses are
retained. A number of behavioral approaches have been tried with
Clinical evaluation of visual function in patients with varying degrees of success to restore visual function in the
cortical blindness should include tests of visual acuity, cortically blind field and/or help patients learn alternative
determination of light and motion perception in different strategies to compensate for their visual impairment
sectors of the visual field, tests of spatial localization, as (Kerkhoff, 2000). Attempts to increase awareness of the
well as assessments of color perception, object and face visual deficit in patients with anosognosia constitute an
recognition, and reading ability. Studying blindsight usu- important component of the treatment program. It has
ally requires the use of specialized testing equipment in an been shown that blindsight performance can be improved
experimental laboratory environment. However, in the by training, and the use of these techniques may aid the
clinical setting blindsight can be tested by requiring recovery of vision in individuals with cortical blindness
patients to guess the presence/absence, location, (Stoerig, 2006; Sahraie et al., 2006).
 Cortical Blindness C 717

Cortical Blindness. Figure 1 Diffusion-weighted MRI scan in a patient with cortical blindness following bilateral posterior
cerebral artery strokes. Note massive destruction of primary visual cortex (Brodmann area 17), with lesion extension into ventral
extrastriate visual association areas (Brodmann areas 18,19,37). This individual demonstrated complete denial of blindness
(anosognosia), consistent with Anton’s syndrome

Cross References Kerkhoff, G. (2000). Neurovisual rehabilitation: Recent developments

and future directions. Journal of Neurology, Neurosurgery, and Psy-
chiatry, 68, 691–706.
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▶ Visual Hallucinations ential extrageniculostriate and amygdala responses to presentation
of emotional faces in a cortically blind field. Brain, 124, 1241–1252.
Pegna, A. J., Khateb, A., Lazeyras, F., & Seghier, M. L. (2005). Discrimi-
nating emotional faces without primary visual cortices involves right
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guided actions? Neuroscience and Biobehavioral Reviews, 29, 1035–1046. Stoerig, P., & Cowey, A. (2007). Blindsight. Current Biology, 17,
Dehaene, S., Changeux, J. -P., Naccache, L., Sackur, J., & Sergent, C. R822–R824.
(2006). Conscious, preconscious, and subliminal processing: A test- Trevethan, C. T., Sahraie, A., & Weiskrantz, L. (2007). Form discrimina-
able taxonomy. Trends in Cognitive Sciences, 10, 204–211. tion in a case of blindsight. Neuropsychologia, 45, 2092–2103.
Heilman, K. M. (1991). Anosognosia: Possible neuropsychological Weiskrantz, L. (1986). Blindsight: A case study and implications. Oxford:
mechanisms. In G. P. Prigatano & D. L. Schacter (Eds.), Awareness Clarendon Press.
of deficit after brain injury: Clinical and theoretical issues (pp. 53–62). Weiskrantz, L. (1997). Consciousness lost and found. Oxford: Oxford
New York: Oxford University Press. University Press.
718 C Cortical Color Blindness

Cross References
Cortical Color Blindness
▶ Contrecoup Injury
▶ Achromatopsia ▶ Edema
▶ Focal Lesion, Contusion
▶ Intracranial Pressure

Cortical Contusion References and Readings

B ETH R USH Bigler, E. D. (2001). The lesions in traumatic brain injury: Implications
Mayo Clinic for clinical neurophysiology. Archives of Clinical Neuropsychology,
16, 95–131.
Jacksonville, FL, USA
Graham, D. I., Saatman, K. E., Marklund, N., Conte, V., Morales, D.,
Royo, N., & McIntosh, T. K. (2006). The neuropathology of trauma.
In R. W. Evans (Eds.), Neurology and Trauma (2nd ed., pp. 45–94).
Synonyms New York: Oxford University Press.

Bruise; Contusion (cerebral)

Cortical Deafness
Definition
▶ Pure Word Deafness
Cortical contusions are bruises on the brain tissue that
form from the small blood vessel leaks (veins and arteries
covering the parenchymal tissue), or a series of microhe-
morrhages following trauma. Trauma is usually the result
of physical blows to the head such as those sustained in a Cortical Lewy Body Disease
motor vehicle accident, direct blow to the head from (CLBD)
assault, or significant sports-related injuries. Veins and
arteries on the surface of the brain are damaged, which ▶ Dementia with Lewy Bodies
results in bleeding and bruising. When the blood vessel is
torn, blood escapes from the vessel at a rate that is faster
than the blood that can be absorbed by the brain. Conse-
quently, cortical contusions commonly result in edema
and increased intracranial pressure.
Cortical Magnification
R ONALD A. C OHEN
Current Knowledge Brown University
Providence, RI, USA
Second to diffuse axonal injury, cortical contusion is the
most common type of intra-axial lesion following brain
trauma. By radiologic definition, a cortical contusion Definition
must involve some portion of the superficial gray matter.
Because gray matter has more vasculature than white Cortical magnification refers to the fact that the number
matter, most cortical contusions are hemorrhagic, where- of neurons in the visual cortex responsible for processing
as diffuse axonal injuries are rarely hemorrhagic. The the visual stimulus of a given size varies as a function of
frontal and temporal lobes are the most common sites the location of the stimulus in the visual field. Stimuli
of cortical contusions. When present, cortical contusions occurring in the center of the visual field that have been
are usually found bilaterally. Compared to diffuse axonal detected in the fovea of retina are processed by a very large
injury lesions, cortical contusions are much less likely to number of neurons in the primary visual cortex of
involve an initial presentation of coma or altered loss of the occipital lobe, though these neurons handle only a
consciousness. very small region of the central visual field. Conversely,
 Cortical Mapping C 719

stimuli detected in the peripheral visual field tend to be specific informational characteristics (e.g., shape, color,
processed by a much smaller number of neurons in the texture, position, movement), neurons with greatest sen-
primary visual cortex. sitivity to these dimensions vary as a function of cortical
magnification factors and a tradeoff of size of the recep-
tive field and the number of neurons dedicated to each C
Current Knowledge part of the field.

Cortical magnification reflects an important concept in

the field of cognitive neuroscience; the cortical volume,
and ultimately the number of neurons allocated to a
Cross References
particular function, typically varies as a function of the
▶ Feature Detection
significance of the function. For example, since the
▶ Magnocellular Neurons
sense of touch is particularly important for the hands,
▶ Parvocellular Neurons
there are many more nerve receptors in the finger tips
▶ Spatial Frequencies
than in the trunk of the body. Similarly, the volume of
▶ Spatial Processing
motor cortex dedicated to controlling the hands and
mouth in humans is much greater than the volume
dedicated to large muscle groups with more limited
action. Given the critical role that vision plays in References and Readings
human cognition, tremendous magnification of neu-
rons is dedicated to visual processing, with this magni- Daniel, P. M., & Whitteridge, D. (1961). The representation of the visual
fication occurring at various processing stages along the field on the cerebral cortex in monkeys. Journal of Physiology, 159,
203–221.
visual pathways beginning in the retina. The extent of
cortical magnification is often expressed as a ratio of
millimeters of cortical surface per degree of visual
angle. This ratio varies across visual areas. Among
primates, neurons devoted to processing foveal input
from the retina are about 100 times more prevalent Cortical Malformation
than neurons devoted to peripheral stimuli in the pri-
mary visual cortex (Daniel & Whitteridge, 1961). ▶ Heterotopia
The principle of cortical magnification indicates an
important relationship between the number of neurons
dedicated to big or small visual angles and the receptive
field of those neurons. When a large number of neurons
are involved in a small visual angle, there is inherently a Cortical Mapping
large processing capacity being assigned to a smaller area
of visual focus. Conversely, a smaller number of neurons M ARLA J. H AMBERGER
handling a visual angle are indicative of a larger receptive Columbia University
field, as each neuron must be sensitive to changes occur- New York, NY, USA
ring across a larger area of space. This creates an inherent
relationship between the spatial frequency of the visual
information being processed and the size of the receptive Synonyms
field that is essential for considering how neurons across
different visual cortical areas are tuned to respond to the Direct stimulation mapping; Electrical stimulation
featural and spatial characteristics of visual input. A mapping (ESM); Functional mapping
consequence of this organization for the primary visual
cortex is that visual acuity and the ability to detect small
features of stimuli are best in the center of the visual field Description
and poorest in the periphery. Yet, broad spatial changes
with movement are easily detected at the periphery. Cortical mapping is an invasive procedure in which
Since visual cortical areas differ in their emphasis on electrical stimulation is applied briefly to the cortical
720 C Cortical Mapping

surface for the purpose of identifying areas critical for is based on negative responses, thorough mapping of
sensory, motor or language function. This procedure is language cortex requires administration of tasks assessing
utilized when brain surgery involves the removal or a range of language functions.
disruption of potentially functional cortical areas. Sites Depending on the location of the area identified and
identified via cortical mapping are typically spared the nature of the response elicited by stimulation, it is
from resection, with the goal of preserving function generally held that removal of a positive sensory, motor,
postoperatively. or language site identified by stimulation will result in
Stimulation is applied using a bipolar stimulator, usu- impaired function postoperatively. Of the few clinical
ally via pairs of adjacent subdural electrodes. The procedure series published, results suggest that postoperative
can be conducted intra-operatively in a conscious patient function is best preserved when the resection margin
before resection of brain tissue, or extra-operatively, if sub- exceeds 1 cm from the functional site. On the other
dural electrodes have been implanted, most commonly in hand, there is some evidence that certain sites identified
pharmacologically resistant epilepsy patients who require by stimulation can be removed without concern of
intracranial EEG monitoring to delineate the region of postoperative decline. These include motor sites identi-
seizure onset (Fig. 1). The identification of sensory and fied in the supplementary motor area, tongue, and lower
motor sites is based on stimulation-evoked ‘‘positive’’ face areas (due to their bilateral representation), and
responses, such as a subjective sensation (e.g., tingling) possibly, language sites identified in the basal temporal
or an observable movement (e.g., muscle twitch). In con- region, although this is somewhat controversial.
trast, stimulation of language cortex elicits no experiential For motor and sensory mapping, the duration of elec-
or observable response in an inactive patient. Rather, trical stimulation is typically 2 s, whereas language
cortical language mapping relies on ‘‘negative’’ responses, mapping typically requires 4–8 s of stimulation, depending
in that the patient must be engaged in a language task on the particular task under assessment. The level of stim-
and stimulation of language cortex will disrupt task ulation administered ranges from 1 mA to a maximum of
performance. Thus, for language mapping, stimulation 17 mA, with motor and sensory cortex typically utilizing
produces a discrete, reversible lesion, theoretically en- <10 mA and language cortex typically requiring >10 mA.
abling the examiner to observe the functional conse- Under normal circumstances, cortical stimulation causes
quences of damage to the site(s) stimulated. Stimulation neither pain nor discomfort. One risk of stimulation, how-
of frontal language cortex typically produces speech ar- ever, is the evocation of a seizure, particularly in patients
rest, whereas stimulation of posterior (temporal/parietal) with epilepsy, due to a likely lower seizure threshold in
language cortex typically elicits comprehension, naming epileptogenic areas. To minimize the probability of a stim-
or reading difficulties. Because cortical language mapping ulation induced seizure, EEG is monitored on an ongoing

Cortical Mapping. Figure 1 Implanted subdural electrode grid used for EEG recording and electrical stimulation mapping
 Cortical Motor Pathways C 721

basis, and the stimulation intensity is lowered when location of posterior temporal and parietal language
abnormal discharges are associated with stimulation. Nev- sites appears to vary more among individuals, although
ertheless, benzodiazepines are typically kept close at hand this might merely reflect alterations in the distribution of
for IV administration for instances when a seizure occurs language sites in patients with epileptogenic cortex in the
and fails to resolve rapidly on its own. temporal region. C

Historical Background
Clinical Uses
Alteration of function via cortical stimulation in both
One of the main challenges with brain surgery involving
animals and humans dates back to the mid 1800s. The
cortical regions is to remove a sufficient amount of
procedure came into clinical use in the early twentieth
pathological tissue without removing areas critical for
century in association with surgical resection of epilepto-
function. Cortical mapping is used to identify cortical
genic cortex in patients with pharmacologically refractory
regions critical for function, in order to spare these areas
epilepsy. Initially used to identify sensory and motor
from resection or protect them from damage during
cortex, Wilder Penfield and colleagues pioneered the tech-
surgical procedures. Cortical mapping is typically
nique in the 1950s for use in the identification of language
performed when there is concern that resective brain
cortex. Stimulation-based language mapping was further
surgery (e.g., tumor resection, epilepsy surgery) might
refined by George Ojemann and colleagues who essential-
impinge upon, or possibly overlap with cortical regions
ly established the current clinical standards. In addition to
necessary for function.
its clinical utility, investigators have used the opportunity
provided by clinical stimulation to investigate structure-
function relations. These studies build upon the lesion
model, contributing more precise information regarding Cross References
functional localization due to both the controlled setting,
and the smaller, more discrete ‘‘lesions’’ induced ▶ Epilepsy
temporarily by stimulation than that typically found ▶ Functional Imaging
with naturally occurring lesions. ▶ Localization

Psychometric Data References and Readings

Cortical mapping procedures remain unstandardized.
Hamberger, M. (2007). Cortical language mapping in epilepsy: A critical
Due to its highly invasive nature, data from cortical review. Neuropsychology Review, 4, 477–489.
mapping are based on clinical rather than normal popu- Ojemann, G. A. (1983). Electrical stimulation and the neurobiology of
lations, and therefore, classic psychometric data are language. The Behavioral and Brain Sciences, 2, 221–230.
unavailable. It has also been difficult to assess reliability,
as cortical mapping is rarely performed more than once
in the same patient. Nevertheless, patients with indwell-
ing subdural grids who undergo mapping over 2 or more
days, and patients who require a second surgery involv- Cortical Motor Pathways
ing adjacent brain regions provide opportunities for
repeat mapping, although these circumstances are rela- C HRISTINA R. M ARMAROU
tively infrequent. In the absence of published studies Virginia Commonwealth University
addressing this issue, anecdotal reports suggest a reason- Richmond, VA, USA
able level of consistency in the location of simulation-
identified sites within individuals. Across individuals,
consistency is relatively high for the location of motor Synonyms
and sensory cortex. Frontal language cortex is slightly
more variable, with most positive sites clustered in the Corticospinal tract; Pyramidal tract; Voluntary motor
frontal opercular region, anterior to the tongue area. The tract
722 C Cortical Motor Pathways

Definition pyramidal decussation, ultimately terminating in the

ventral horn of the cervical-through-lumbar spinal
The cortical motor pathway consists of four regions of the cord. These cortical motor pathways work in tandem
cerebral cortex (primary motor cortex, posterior parietal with other cortical motor areas of the brain – notably
cortex, premotor cortex, and supplementary motor cor- the cerebellum and subcortical motor nuclei (the basal
tex) whose neuronal cell bodies are located in layer V ganglia) – to execute planning and control of voluntary
(five) and whose projections are involved with the execu- motor activity. Other projections from layer V of M-I
tion of muscle contraction largely on the contralateral side include the corticostriatal fibers to the striatum (caudate
of the body. and putamen), corticorubral fibers to the red nucleus,
and projections that terminate in the reticular forma-
tions with the medulla and pons of the brain stem. M-I
projections also modulate other motor areas within the
Current Knowledge
cortex and include reciprocal connections with the sup-
plementary motor area, the premotor and posterior
The cortical motor pathway describes a trajectory of fibers
parietal motor areas. These fibers are part of a vast
whose cells of origin are located in layer V of the cerebral
reciprocal network that cross via the corpus callosum
motor cortex. The cerebral motor cortex is a term that
and are referred to as callosal connections. The SMA
describes the four main areas of the cerebral cortex that
contributes to the corticospinal tract and has reciprocal
contribute to the planning, control, and execution of
callosal projections to contralateral areas of the motor
voluntary motor fibers; the primary motor cortex (M1),
cortex. The premotor cortex (PMC) contributes to the
secondary motor cortices, premotor cortex, and the sup-
corticospinal tract and also has extensive reciprocal con-
plementary motor area (SMA).
nections to both SMA and MI.

Cortical Location and Overall Function

Cross References
The primary motor cortex (M1) is located in the frontal
lobe of the brain and the cells of origin, in layer V, are ▶ Cerebral Cortex
found within the precentral gyrus. These cells generate ▶ Decerebrate Posturing
neural impulses that control the execution of movement ▶ Decorticate Posturing
directed to skeletal muscles on the contralateral side of the ▶ Hemiplegia
body. Other regions of the cortex that contribute to ▶ Homunculus
the cortical motor pathway – termed secondary motor ▶ Internal Capsule
cortices – include the posterior parietal area (PMA), the ▶ Periventricular White Matter
premotor cortex (PMC) and the supplementary motor ▶ Precentral Gyrus
area (SMA). The posterior parietal cortex is responsible ▶ Pyramidal System
for transforming visual information into motor com- ▶ Sensorimotor Assessment
mands relayed via the premotor and supplementary ▶ Supplementary Motor Area
motor area. The premotor cortex is involved in sensory
guidance of movement and control of proximal and trunk
muscles of the body. The supplementary motor area is
involved in the planning and coordination of complex References and Readings
movements, such as those requiring coordination of
two-handed movement. Berne, R. M., & Levy, M. N. (2000). Principles of physiology. St. Louis,
Multiple pathways arise from the efferent projections MO: Mosby.
of the motor cortices. Neuronal cell bodies located in layer Fix, J. (1995). Neuroanatomy. Baltimore, MD: Williams & Wilkins.
V of the M1, SMA, and premotor cortex send vast projec- Haines, D. E. (2000). Neuroanatomy. Philadelphia, PA: Lippincott
Williams & Wilkins.
tions that collectively give rise to the largest single path-
Haines, D. E. (2004). Neuroanatomy: An atlas of structures, sections, and
way, the pyramidal or corticospinal tract. The tract systems. Philadelphia, PA: Lippincott Williams & Wilkens.
descends through the internal capsule and forms the Kandel, E. R., Schwartz, J. H., & Jessel, T. M. (1991). Principles of
pyramids of the medulla, crossing midline at the neuroscience. Norwalk, CT: Appleton and Lange.
 Cortical–Subcortical Loop C 723

inhibition related to social context or emotional subject

Cortical–Subcortical Loop matter. In this loop, the lateral orbitofrontal cortex
(OFC) projects via the ventromedial caudate nucleus to
J ANNA L. H ARRIS VA and MD thalamic nuclei, which in turn send projec-
University of Kansas Medical Center tions back to lateral OFC.
Kansas, KS, USA
C
Affective-motivational loop. This loop is also called
the ‘‘Limbic loop.’’ This circuit plays a role in emotional
and motivational behaviors. Widespread areas of ‘‘limbic
Synonyms cortex’’ including the anterior cingulate gyrus, medial
OFC, and portions of the temporal lobe all send projec-
Basal ganglia-thalamocortical circuit; Cortico-basal tions via the nucleus accumbens to MD thalamus. The
ganglia loop circuit is completed by thalamocortical projections from
MD to the anterior cingulate and medial OFC.
Definition

The cortical–subcortical loop describes a class of distinct,

Clinical Disorders and Treatment
parallel circuits that connect specific regions of cerebral
Approaches
cortex with the basal ganglia and specific thalamic nuclei.
The thalamic nuclei complete the loop by projecting back to
An understanding of the architecture of cortical–subcortical
the same regions of cortex from which the circuits originate.
loops has given rise to a prevailing view of numerous clinical
disorders as essentially circuit disorders, arising from abnor-
Current Knowledge mal neuronal activity at some stage of the finely tuned
circuit. The best-studied examples involve the motor loop,
Several distinct, anatomically segregated cortical–subcor- where disturbances within the circuit can result in either
tical loops may be characterized based on the functional hypokinetic movement disorders (e.g., Parkinson’s disease)
role of the cortical regions involved. or hyperkinetic disorders (e.g., chorea, ballismus, and dys-
Motor loop. The motor loop plays a role in the prep- tonia). In addition, abnormal activity within the non-motor
aration and execution of movement. Primary motor cor- loops may be associated with disorders as diverse as obses-
tex and associated premotor areas project via the putamen sive–compulsive disorder, schizophrenia, and Tourette syn-
to the ventral tier nuclei of the thalamus, which then drome. Recently, interventions that surgically remove or
complete the loop with projections back to motor cortex. modify (e.g., with deep brain stimulation) the dysfunctional
Somatotopic organization is maintained through all component of the cortical–subcortical loop have met with
stages of this circuit. considerable success. These promising treatment approaches
Oculomotor loop. The oculomotor loop is involved are the subject of intensive ongoing research.
in the control of eye movements. The frontal eye fields
(FEF) and supplementary eye fields (SEF) project via the
body of the caudate nucleus to the ventral anterior (VA) Cross References
and mediodorsal (MD) thalamic nuclei, which complete
the loop by projecting back to FEF and SEF. ▶ Basal Ganglia
Prefrontal associative loops. The prefrontal associa- ▶ Deep Brain Stimulator (Parkinsons)
tive loops describe two distinct components, which sub- ▶ Parkinson’s Disease
serve different aspects of higher cognitive processing.
The ‘‘dorsolateral prefrontal loop’’ plays a role in cogni-
tive processes including spatial memory and working References and Readings
memory. In this circuit, the dorsolateral prefrontal cor-
tex (PFC) projects via the dorsolateral head of the cau- Alexander, G. E., Crutcher, M. D., & DeLong, M. R. (1990). Basal ganglia-
date to VA and MD thalamic nuclei, which then project thalamocortical circuits: Parallel substrates for motor, oculomotor,
‘‘prefrontal’’ and ‘‘limbic’’ functions. Progress in Brain Research, 85,
back to dorsolateral PFC. The ‘‘lateral orbitofrontal
119–146.
loop’’ plays a role in cognitive processes including the DeLong, M. R., & Wichmann, T. (2007). Circuits and circuit disorders of
ability to select and shift behavioral sets, and response the basal ganglia. Archives of Neurology, 64(1), 20–24.
724 C Corticobasal Degeneration

complex’’ of disorders (Kertesz, 2003). Given the clinically

Corticobasal Degeneration heterogeneous presentation of CBD, and the fact that the
core features of CBD can be produced by other condi-
A LEXANDER I. T RÖSTER tions, it has been recommended that the term corticobasal
University of North Carolina syndrome (CBS) be applied to the core clinical features of
Chapel Hill, NC, USA CBD regardless of etiology. In contrast, the term cortico-
basal degeneration (CBD) should be reserved for the
distinctive neuropathological condition of CBD, regard-
Synonyms less of its clinical presentation (Lang, 2003).
From a neuropathologic standpoint, CBD, like fron-
Corticobasal syndrome; Corticodentatonigral degenera- totemporal lobar degeneration, has been categorized as a
tion with neuronal achromasia tauopathy. Tau is a microtubule-associated protein that
promotes the polymerization of tubulin and thus, micro-
tubule assembly. The human tau gene, containing 16
Short Description or Definition exons, is located on the long arm of chromosome 17
and encodes for the six isoforms of tau found in the
First described as corticodentatonigral degeneration with central nervous system. The isoforms differ by the pres-
neuronal achromasia by Rebeiz et al. in 1968, corticobasal ence or absence of amino acid inserts encoded by exons 2,
degeneration (CBD) was long thought to be predomi- 3, and 10. Whether the transcript of exon 10 is spliced in
nantly a motor disorder. Indeed, the original description or out of the final tau protein product determines whether
of the disorder emphasized the relative preservation of the isoform has three or four repeated microtubule-bind-
mental faculties. More recently, emphasis has been placed ing domains (three isoforms have three repeats and three
on the neurobehavioral features of CBD, and the over- isoforms have four repeats). The four repeat isoforms of
lapping clinical and neuropathological features of CBD tau (4R tau) promote microtubule assembly at more than
with frontotemporal lobar degenerations continue to gen- twice the rate of the three repeat (3R tau) isoforms.
erate debate about the classification and nosology of the Although the expression of 3R and 4R tau is cell-type
disorder. specific, the 3R tau expression in normal human brain
The motor presentation of CBD most often involves is 1–1.5-fold higher than the 4R expression level. In
an asymmetric, progressive, akinetic-rigid parkinsonism spontaneous and genetic CBD, 4R tau represents the
of gradual onset that responds minimally if at all to main pathological inclusion. Recent findings that
levodopa and is sometimes accompanied by dystonia or mutations associated with parkinsonism (in LRRK2)
myoclonus. Cortical signs that are common in CBD and frontotemporal lobar degeneration (in progranulin)
include asymmetric apraxia, cortical sensory signs can be seen in some cases presenting with corticobasal
(e.g., astereognosis, graphesthesia), and alien hand sign. syndrome further highlight the heterogeneity of cortico-
The latter may involve a sense of lack of ownership of the basal syndrome (CBS).
limb in the absence of visual cues, involuntary purposeful Autopsy in CBD cases reveals asymmetric frontal and
movements, or frank interference of one limb with the parietal atrophy, depigmentation of the substantia nigra
other’s execution of purposeful movement. These motor without Lewy bodies, and often the presence of ballooned
and cortical signs are core features of CBD. cells in cortex. Tau-positive astrocytic plaques, oligoden-
droglial coiled bodies, and threadlike lesions are seen in
white and gray matter, especially the superior frontal and
Categorization parietal gyri and the pre- and post-central gyri, and in the
striatum.
The neurobehavioral expression of CBD can be quite
variable, and cases with confirmed CBD neuropathology
have presented with features suggestive of primary pro- Epidemiology
gressive aphasia and frontotemporal dementia. Coupled
with the recognition of CBD as a tauopathy, the occasion- Prevalence and incidence of CBD are unknown, and poor
al neurobehavioral resemblance of CBD to frontotem- diagnostic accuracy no doubt contributes to this. Al-
poral dementia and primary progressive aphasia has lead though the H1/H1 tau haplotype has been identified as
some to argue that CBD is a member of the ‘‘Pick heightening susceptibility to both CBD and progressive
 Corticobasal Degeneration C 725

supranuclear palsy, no clear genetic etiology has been retrieval deficits. Remote memory has been little studied
identified. Dementia and other cognitive and behavioral in CBD, but the pattern of poor recall but intact recogni-
abnormalities were thought to be rare in CBD until the tion on remote memory tasks suggests a retrieval deficit.
last decade, but it is now appreciated that the frequency of Visuospatial impairments have been observed.
neurobehavioral abnormalities observed as a presenting With respect to emotional and neuropsychiatric C
problem or during the course of the condition is quite issues, depression is common in CBD (73% of patients),
high. It might be that the inconsistent incidence and though apathy (40%), irritability (20%), and agitation
prevalence estimates of cognitive impairment in CBD (20%) also occur with frequency.
are a function of whether patients were drawn from
movement disorder, dementia, or psychiatry clinics.
Evaluation
Natural History, Prognostic Factors, The selection of specific neuropsychological tests in CBD,
Outcomes like any other condition, should be guided by the referral
questions and the patient’s ability to cooperate and meet
Disease onset is usually in the sixth decade of life, and task demands. However, tests of executive function (e.g.,
mean time to death from diagnosis is about 7 years. planning, abstraction, and cognitive flexibility), praxis,
visuospatial functions, attention, learning and memory,
and word retrieval should be employed. Symptom
Neuropsychology and Psychology of inventories relating to apathy, depression, and ‘‘frontal’’
Corticobasal Degeneration behavior syndromes, such as the Neuropsychiatric
Inventory, Hamilton depression scale, and Frontal
CBD involves an asymmetric apraxia, most often of the Systems Behavior Scale can be helpful in characterizing
ideomotor type, but ideational and limb kinetic apraxias neuropsychiatric features of CBD.
also occur. Thus, patients most often have difficulty
demonstrating the use of tools. Poor drawing (construc-
tional apraxia) is also commonly seen. Language distur- Treatment
bance occurs early or during progression of the syndrome,
and the aphasia is most often non-fluent (about 56% of Some cases may show transient improvement in parkin-
cases) or anomic (30%). The pattern of performance on sonian features with levodopa treatment; dopamine ago-
language tests in patients with the traditional CBD pre- nists are generally even less helpful than levodopa.
sentation is somewhat inconsistent across studies, but Tremor, if present, may be alleviated by benzodiazepines.
phonological impairments may be an important feature. Antidepressants with anticholinergic profiles are to be
Performance on verbal fluency tests, especially lexical or avoided given possible adverse cognitive side effects, but
phonemic fluency tests, is usually impaired either due to selective serotonin reuptake inhibitors may be helpful in
the executive demands of those tasks or aphasia. Perfor- treating depression. Speech therapy is helpful in treating
mance on semantic memory tasks such as conceptual dysphagia.
matching and visual confrontation naming and expressive
vocabulary is relatively preserved and impaired in a mi-
nority of patients, although some studies have reported Cross References
considerable impairment on semantic tasks early in the
disease. When naming is impaired, disproportionate ▶ Basal Ganglia
benefit is derived from cuing suggesting a retrieval rather ▶ Corticobasal Degeneration
than semantic memory deficit. Comprehension is typical- ▶ Frontal Lobes
ly preserved early, but comprehension of grammatically ▶ Frontal Temporal Dementia
complex material declines with disease progression. ▶ Frontotemporal Lobar Degeneration
Executive dysfunction, as indicated by poor perfor- ▶ Gait Disorders
mance on tasks such as the card sorting tasks and the ▶ Movement Disorders
Trailmaking test is common. Episodic memory impair- ▶ Parkinson Plus Syndromes
ments in CBD are relatively mild early in the course of the ▶ Parkinson’s Disease
condition and appear to involve both encoding and ▶ Parkinsonian Movement
726 C Cortico-Basal Ganglia Loop

▶ Striatum
▶ Tauopathy Corticoliberin
▶ Corticotropin-Releasing Hormone
References and Readings

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Rosen, H. J., et al. (2006). Clinical and neuropsychological features
of corticobasal degeneration. Mechanisms of Ageing and Develop-
ment, 127, 203–207.
Boeve, B. F. (2007). Parkinson-related dementias. Neurologic Clinics, 25,
Corticospinal Tract
761–781.
Geda, Y. E., Boeve, B. F., Negash, S., Graff-Radford, N. R., Knopman, ▶ Cortical Motor Pathways
D. S., Parisi, J. E., et al. (2007). Neuropsychiatric features in 36
pathologically confirmed cases of corticobasal degeneration. Journal
of Neuropsychiatry and Clinical Neurosciences, 19, 77–80.
Graham, N. L., Bak, T. H., & Hodges, J. R. (2003). Corticobasal degener-
ation as a cognitive disorder. Movement Disorders, 18, 1224–1232.
Kertesz, A. (2003). Pick complex: An integrative approach to frontotem- Corticotropin-Releasing Factor
poral dementia: Primary progressive aphasia, corticobasal degenera-
tion, and progressive supranuclear palsy. The Neurologist, 9, 311–317.
(CRF)
Lang, A. E. (2003). Corticobasal degeneration: Selected developments.
Movement Disorders, 18(Suppl. 6), S51–56. ▶ Corticotropin-Releasing Hormone
Litvan, I., Cummings, J. L., & Mega, M. (1998). Neuropsychiatric features
of corticobasal degeneration. Journal of Neurology, Neurosurgery, and
Psychiatry, 65, 717–721.
Murray, R., Neumann, M., Forman, M. S., Farmer, J., Massimo, L.,
Rice, A., et al. (2007). Cognitive and motor assessment in autopsy-
proven corticobasal degeneration. Neurology, 68, 1274–1283. Corticotropin-Releasing Hormone
Sha, S., Hou, C., Viskontas, I. V., & Miller, B. L. (2006). Are frontotem-
poral lobar degeneration, progressive supranuclear palsy and corti- B ETH K UCZYNSKI 1, S TEPHANIE A. KOLAKOWSKY-H AYNER 2
cobasal degeneration distinct diseases? Nature Clinical Practice 1
University of California
Neurology, 2, 658–665.
Davis, CA, USA
Tröster, A. I., & Fields, J. A. (2008). Parkinson’s disease, progressive 2
supranuclear palsy, corticobasal degeneration, and related disorders Santa Clara Valley Medical Center,
of the frontostriatal system. In J. E. Morgan & J. H. Ricker (Eds.), Rehabilitation Research Center
Textbook of clinical neuropsychology (pp. 536–577). New York: Psy- San Jose, CA, USA
chology Press.

Synonyms
Cortico-Basal Ganglia Loop
Corticoliberin; Corticotropin-releasing factor (CRF)
▶ Cortical–Subcortical Loop

Definition
Corticobasal Syndrome
Corticotropin-releasing hormone (CRH) is a hormone
▶ Corticobasal Degeneration that is primarily produced by the hypothalamus and is
involved in the stress response. It is released from the
paraventricular nucleus of the hypothalamus with the
Corticodentatonigral primary action within the anterior lobe of the pituitary
to initiate the release of adrenocorticotropic hormone
Degeneration with Neuronal (ACTH). CRH (41 amino acids long) is derived from a
Achromasia 191 amino acid preprohormone. Other areas of CRH
synthesis include peripheral tissues, and it is highly
▶ Corticobasal Degeneration expressed in the placenta.
 CPT C 727

Cross References
Counterindicant
▶ Hormone
▶ Contraindication
C
References and Readings

Bennett, M. (2008). Stress and anxiety in schizophrenia and depression:

Glucocorticoids, corticotropin-releasing hormone and synapse re- Couples Therapy
gression. Australian & New Zealand Journal of Psychiatry, 42(12),
995–1002. ▶ Cognitive Behavioral Couples Therapy
Fabricio, A., Tringali, G., Pozzoli, G., & Navarra, P. (2005). Mirtazapine
acutely inhibits basal and Kþ-stimulated release of corticotropin-
releasing hormone from the rat hypothalamus via a non-genomic
mechanism. Psychopharmacology, 178(1), 78–82.
Guendelman, S., Lang Kosa, J., Pearl, M., Graham, S., & Kharrazi, M.
(2008). Exploring the relationship of second-trimester corticotropin
releasing hormone, chronic stress and preterm delivery. Journal of COWA
Maternal-Fetal & Neonatal Medicine, 21(11), 788–795.
Watts, A., Kelly, A., & Sanchez-Watts, G. (1995). Neuropeptides and ▶ Controlled Oral Word Association Test
thirst: The temporal response of corticotropin-releasing hormone ▶ F-A-S Test
and neurotensin/neuromedin N gene expression in rat limbic fore-
brain neurons to drinking hypertonic saline. Behavioral Neurosci-
▶ Verbal Fluency
ence, 109(6), 1146–1157.
Weber, M., & Richardson, R. (2001). Centrally administered
corticotropin-releasing hormone and peripheral injections of strych-
nine hydrochloride potentiate the acoustic startle response in pre-
weanling rats. Behavioral Neuroscience, 115(6), 1273–1282. COWAT
▶ Controlled Oral Word Association Test
▶ F-A-S Test
▶ Verbal Fluency
Cortisteroids
▶ Steroids

CPM
Coumadin® ▶ Raven Matrices

▶ Warfarin (Coumadin)

CPRS
Counseling
▶ Conners Rating Scales
▶ Psychotherapy

Counseling Relationship CPT

▶ Therapist–Patient Relationship ▶ Continuous Performance Tests
728 C Craig Handicap Assessment and Reporting Technique

The CHART was designed to be administered by

Craig Handicap Assessment and interview, either in person or by telephone and takes
Reporting Technique approximately 15 min to administer. Participant-proxy
agreement across disability groups on the CHART has
G ALE G. W HITENECK provided evidence in support of the use of proxy data
Craig Hospital for persons with various types of disabilities (Cusick,
Englewood, CO, USA Brooks, & Whiteneck, 2001). There is no set time period
for administering the CHART; however, it is recom-
mended that multiple measurements be taken over the
Synonyms course of a person’s lifetime to assess changes with
adaptation to the disability and to gain insight into
CHART; CHART-SF changes in participation, which may occur over time.

Description Historical Background

The Craig Handicap Assessment and Reporting Technique WHO describes a conceptual model of disablement that
(CHART) is a 32-item instrument designed to provide a includes impairment at the organ level, disability de-
simple, objective measure of the degree to which impair- scribing functional status, and ‘‘handicap,’’ or more re-
ments and disabilities result in handicaps (societal partici- cently, ‘‘participation,’’ encompassing the roles one plays
pation limitations) for adolescents and adults (15 years and in the world and society. Despite its importance as a
older) in the years after initial rehabilitation. The CHART rehabilitation goal, handicap (absence of social partici-
includes six subscales (physical independence, cognitive pation) is the least often measured of all rehabilitation
independence, mobility, occupation, social integration, outcomes. A great deal of work has been done in devel-
and economic independence), which closely reflect the oping tools to measure and document impairment and
disablement model developed by the World Health disability; however, limited attempts have focused on the
Organization (WHO, 1980, 2001). Each subscale contains measurement and assessment of long-term participation
3–7 questions, which together quantify the extent to which limitations (handicap), despite the fact that psychosocial
individuals fulfill various social roles. CHART focuses on adjustment is clearly regarded as the ultimate outcome
objective, observable criteria that are easily quantifiable and of rehabilitation. The CHART was specifically developed
unlikely to be open to subjective interpretation. Each of the to help fill this gap – to assess the WHO dimensions of
domains or subscales of the CHART has a maximum score handicap and to provide a simple, objective measure of
of 100 points, which is considered to be the level of perfor- the degree to which impairments and disabilities result
mance typical of the average nondisabled person. High in participation limitations in the years after initial
subscale scores indicate less handicap or higher social and rehabilitation.
community participation. The model of disablement suggested by the WHO
The CHART was developed in 1992 for use with provides useful conceptual distinctions for impairment,
persons with spinal cord injury (SCI) and originally did disability, and handicap (WHO, 1980). In practical terms,
not address the WHO handicap dimension described as impairment occurs at the organ level, representing any loss
‘‘orientation’’ (Whiteneck, Charlifue, Gerhart, Overhos- or abnormality of psychological, physiological, or
ler, & Richardson, 1992). The current CHART was revised anatomical structure or function. Disability occurs at the
in 1995 with the addition of a ‘‘Cognitive Independence’’ person level, demonstrated as any restriction or lack of
subscale (to assess orientation) and has proven to be an ability (resulting from impairment) to perform any
appropriate measure of societal participation that can be activity in the manner or within the range considered
used with individuals having a range of physical or cogni- normal for a human being. Handicap occurs at the societal
tive impairments (Mellick, Walker, Brooks, & Whiteneck, level. It is a disadvantage for a given individual, resulting
1999). A 19-item Short Form with subscales closely from an impairment or a disability that limits or prevents
approximating the subscale scores for the CHART long the fulfillment of a role that is normal (depending on age,
form is recommended for those applications or popula- sex, and social and cultural factors) for that individual.
tions in which time is at a minimum (Whiteneck et al., The initial disablement model, the ‘‘International Classi-
1998). fication of Impairment, Disability and Health (ICIDH)’’
 Craig Handicap Assessment and Reporting Technique C 729

(WHO, 1980), was later revised as the ‘‘International factors included in this subscale include household com-
Classification of Functioning, Disability and Health position, romantic involvement; the number of relatives,
(ICF)’’ (WHO, 2001). The domain of ‘‘handicap’’ was business associates, and friends with whom regular writ-
reconceptualized and changed to ‘‘participation.’’ The ten or oral contract is maintained, and the frequency of
migration away from the use of ‘‘handicap’’ toward the initiating conversations with strangers. C
more widespread use of ‘‘participation’’ is evident in Economic Self-Sufficiency is the individual’s ability to
literature published since 2001. According to the WHO, sustain customary socioeconomic activity and indepen-
handicap (participation) describes the total effects and dence. This dimension is defined as the remaining dispos-
interplay of all the consequences of disability: social, able household family income after nonreimbursed
economic, cultural, and environmental. medical expenses have been excluded.
Each CHART dimension of handicap is characterized
by directly observable qualities which lend themselves to
easy quantification. While an infinite number of factors Psychometric Data
might have been included, to keep the instrument to a
practical length the following dimensions have been Initial calibration of the CHART scoring system was based
operationalized based on the WHO definitions. on administration of the instrument to 88 able-bodied
Physical Independence is the individual’s ability to individuals and 100 persons with SCI. Once the norms
sustain a customarily effective independent existence. had been established, two studies were conducted to
The major component of this subscale is the number of assess the psychometric properties. CHART showed high
hours per day someone is needed to provide routine or test–retest reliability – 0.93 for the total score and from
occasional assistance (whether paid or unpaid). Indivi- 0.80 to 0.95 for the subscales. The correlation of subject‐
duals are viewed as somewhat less handicapped if they proxy scores was 0.83 for the total CHART score. Rasch
take primary responsibility for instructing and directing analysis established that CHART is a well-calibrated linear
people who are providing assistance to them. scale, with a good fit of both items and persons to its data
Cognitive Independence is the individual’s ability to (Whiteneck et al., 1992).These studies established the
sustain a customary level of independence without the CHART as a reliable and valid instrument, as well as a
need for supervision. The factors included in this subscale well-calibrated linear scale (Whiteneck et al.; Dijkers,
reflect the amount of hours that a person needs supervi- 1991). A decade later, subsequent testing on a group of
sion both inside and outside the home, as well as the 236 persons with SCI reported similar results – test–retest
amount of difficulty an individual has in remembering, correlations of 0.87 and subject‐proxy correlations of 0.85
communicating, and managing money. were reported (Whiteneck, Brooks, & Mellick, 1997).
Mobility is the individual’s ability to move about The Revised CHART which included the ‘‘Cognitive
effectively in his/her surroundings and is demonstrated Independence’’ subscale was tested on 1,110 persons in
by the hours per day out of bed, days per week out of the six impairment categories – SCI, traumatic brain injury,
house, nights per year spent away from home, accessibility stroke, multiple sclerosis, amputation, and burn
of the home, and transportation utilization. (Whiteneck , Brooks et al., 1997). Results indicated that
Occupation is the individual’s ability to occupy time in the cognitive subscale of the CHART was reliable and
the manner customary to that person’s sex, age, and enhanced the appropriateness of the CHART in assessing
culture. The time spent in various activities is used to handicap among persons having cognitive impairments
measure this dimension. The relative value society places (Mellick et al., 1999). Participant-proxy agreement across
on different activities is used to weight the time in each the six disability groups provided evidence in support of
category. Although there was a potential for subjective the inclusion of proxy data for persons with various types
bias based on value judgments in developing the scale in of disabilities (Cusick et al., 2001)
this dimension, priority has been give to gainful employ- In an effort to reduce the number of items in the
ment, schooling, and active homemaking and mainte- CHART, a short form was developed. A multidimensional
nance, and this prioritization has been supported by analysis was performed which showed that fewer variables
validity and reliability testing. Other elements documen- were needed to obtain CHART scores. Regression analyses
ted include volunteer work, recreational pursuits, and were performed on each subscale with the dependent mea-
self-improvement activities. sure being the scale score and the variables contributing to
Social Integration is the individual’s ability to partici- the subscale acting as the predictor variables. All CHART
pate in and maintain customary social relationships. The subscale scores could be reduced by fewer questions to reach
730 C Craig Handicap Assessment and Reporting Technique (CHART) Short Form

90% explained variance except Economic Self-Sufficiency, Mellick, D., Walker, N., Brooks, C. A., & Whiteneck, G. (1999). Incorpor-
ating the cognitive independence domain into CHART. Journal of
which using the main variables could only explain 45%.
Rehabilitation Outcome Measures, 3(3), 12–21.
For additional information about the development, Segal, M. E., & Schall, R. R. (1995). Assessing handicap of stroke
testing, and scoring procedures for the CHART and survivors. A validation study of the Craig handicap assessment and
CHART-SF please consult the Guide for use of the reporting technique. American Journal of Physical Medicine &
CHART: Craig Handicap Assessment and Reporting Rehabilitation, 74, 276–286.
Walker, N., Mellick, D., Brooks, C. A., Whiteneck, G. G. (2003).
Technique at www.craighospital.org/Research/CHART.
Measuring participation across impairment groups using the Craig
handicap assessment and reporting technique. American Journal of
Physical Medicine and Rehabilitation, 82(12), 936–941.
Clinical Uses Whiteneck, G., Brooks, C. A., Charlifue, S., Gerhart, K. A., Mellick, D.,
Overholser, D., et al. (1998). Guide for use of the CHART: Craig
handicap assessment and reporting technique. www.craighospital.
The CHART is a useful tool to measure handicap
org/Research/CHART December 29, 2009.
(participation limitations) in populations with injury or Whiteneck, G. G., Brooks, C. A., & Mellick, D. C. (1997). Handicap
chronic illness with or without rehabilitation interven- assessment – Final report. Rehabilitation research and training center
tion. The CHART is designed as an interview tool, on functional assessment and evaluation of rehabilitation outcomes.
which can be administered face-to-face or by telephone. Buffalo, NY: State University of New York.
Whiteneck, G. G., Charlifue, S. W., Gerhart, K. A., Overhosler, J. D., &
Each item on the instrument has been carefully and con-
Richardson, G. N. (1992). Quantifying handicap: A new measure of
cisely worded to minimize ambiguity of interpretation. It long-term rehabilitation outcomes. Archives of Physical Medicine and
is possible to use the instrument as a mailed question- Rehabilitation, 73, 519–526.
naire, although some valuable data potentially would be Whiteneck, G. G., Fougeyrolles, P., & Gerhart, K. A. (1997). Elaborating
lost in the absence of interaction with an interviewer the model of disablement. In M. Fuhrer (Ed.), Assessing medical
rehabilitation practices: The promise of outcomes research. Baltimore:
providing consistent prompts. There is no set time period
Paul H. Brooks Publishing Co.
for administering the CHART; however, it is recom- World Health Organization. (1980). International classification of impair-
mended that multiple measurements be taken over the ments, disabilities and handicaps: A manual of classification relating to
course of a person’s lifetime to assess changes with adap- the consequences of disease. Geneva: World Health Organization.
tation to the disability and to gain insight into changes in World Health Organization. (2001). International classification of func-
tioning, disability and health. Geneva: World Health Organization.
participation which may occur over time. CHART has
been demonstrated to be a reliable measure of societal
participation limitations in a variety of populations in-
cluding people with physical and/or cognitive functional
limitations.
Craig Handicap Assessment and
Reporting Technique (CHART)
Cross References Short Form
▶ CHART Short Form
▶ CHART Short Form

References and Readings

Cusick, C. P., Brooks, C. A., & Whiteneck, G. G. (2001). The use of
proxies in community integration research. Archives of Physical Cramping
Medicine and Rehabilitation, 82(8), 1018–1024. Manuscript in
development. ▶ Dystonia
Cusick, C. P., Gerhart, K. A., & Mellick, D. C. (2000). Participant-proxy
reliability in traumatic brain injury outcome research. Journal of
Head Trauma Rehabilitation, 15(1), 739–749.
Dijkers, M. (1991). Scoring CHART: Survey and sensitivity analysis.
Journal of the American Paraplegia Society, 14, 85–86.
Hall, K. M., Dijkers, M., Whiteneck, G., Brooks, C. A., & Krause, J. S.
(1998). The Craig handicap assessment and reporting technique
Cranial Aerocele
(CHART): Metric properties and scoring. Topics in Spinal Cord
Injury Rehabilitation, 4(1), 16–30. ▶ Pneumocephalus
 Cranial Nerves C 731

may be considered mixed nerves, meaning that they

Cranial Nerves carry a combination of motor and sensory fibers (CNs
V, VII, IX, and X). As a general rule, the brainstem nuclei
M ELISSA J. M C G INN associated with sensory cranial nerve fibers are located
Virginia Commonwealth University School of Medicine more laterally in the brainstem, while the motor nuclei
Richmond, VA, USA
C
are positioned more medially. The sulcus limitans is the
landmark that demarcates the boundary between these
efferent (motor) and afferent (sensory) nuclear zones in
Definition the brainstem, which are typically arranged in a longitu-
dinal columnar manner according to functional compo-
Cranial nerves serve as conduits for communication nents (see Functional Components below). Motor
between the brain and the body, providing motor and neurons that comprise these brainstem nuclei send axo-
sensory innervation to structures in the head and neck nal projections, via cranial nerves, to control glandular
as well as the thoracic and abdominal viscera. There are tissue secretions and the contraction of various types of
12 pairs of cranial nerves, each of which is designated by a muscle (skeletal, smooth, and cardiac muscle). Con-
Roman numeral and a name (see Table 1). Roman numer- versely, the sensory cranial nerve fibers typically origi-
als I–XII indicate the rostrocaudal order in which cranial nate from sensory neurons located in sensory ganglia
nerves originate from the brain, while the name desig- (collections of neurons residing outside of the brain)
nated to each pair of cranial nerves denotes either its and function to transmit sensation from various types
function or distribution. of sensory receptors (i.e., pain and temperature recep-
tors on the skin) to the brainstem.
Functional Components. In addition to the generalized
Historical Background classification of cranial nerves as sensory, motor, or mixed
nerves, the fibers that comprise each CN can be further
The enumeration of the cranial nerves can be traced back categorized according to the specific nature of the afferent
to second century Greek physician–philosopher Galen; or efferent information being transmitted and the types
whose initial description included 7 of the 12 currently of structures innervated. These fiber classifications,
accepted pairs. English physician and neuroanatomist which are often referred to as functional components
Thomas Willis’ reclassification of the cranial nerves in include somatic motor, visceral motor, branchial motor,
the seventeenth century consisted of nine pairs and super- somatic sensory, visceral sensory, and special sensory
seded Galen’s previous description. German anatomist fibers. A cranial nerve can carry one or several of these
Samuel Thomas von Soemmerring introduced the con- functional components.
temporary classification system, comprising 12 pairs of Motor Cranial Nerves. Three of the six functional
cranial nerves, in the late eighteenth century. classifications of cranial nerve fibers convey motor inner-
vation: somatic motor, branchial motor, and visceral
motor fibers. Somatic motor fibers originate in motor
nuclei located in the medial-most cell column of the
Current Knowledge brainstem and function to transmit motor impulses to
voluntary skeletal muscle (of developmental somatic
Cranial Nerve Nuclei. The majority of cranial nerves myotome origin) in the head and neck. CNs III, IV, and
(CNs) originate from collections of neurons (nuclei) VI carry somatic motor fibers that innervate the extrao-
located within the brainstem (exceptions to this rule cular muscles, CNXI provides somatic motor innervation
are CNs I and II, which are associated with the forebrain to two muscles located within the neck/shoulder region
and diencephalon, respectively). CNs III and IV emerge and CN XII conveys somatic motor information to the
from the midbrain portion of the brainstem, CNs V–VIII intrinsic muscles of the tongue.
arise from the pons, and the remaining cranial nerves Branchial motor fibers are similar to somatic motor
(CNs IX–XII) originate in the medulla. Taken together, fibers in that they provide motor innervation to voluntary
the cranial nerves convey both motor and sensory inner- striated muscles located within the head and neck region.
vation. However, individual cranial nerves may transmit However, branchial motor fibers and the muscles that
sensory information only (CNs I, II, and VIII), motor they innervate are afforded a separate classification
innervation only (CNs III, IV, VI, XI, and XII), or they based on their embryologic derivation from branchial/
732 C Cranial Nerves

Cranial Nerves. Table 1 List of cranial nerves

Functional Deficits/symptoms
Number Name componenta Function of dysfunction
I Olfactory N. Special sensory Olfaction (smell) Hyposmia and anosmia
II Optic N. Special sensory Vision Anopsia
III Oculomotor N. Somatic motor Extraocular muscles (superior, inferior, and Diplopia and ptosis
medial rectus muscles)
Visceral motor Ciliary and pupillary constrictor muscles Pupil dilation
IV Trochlear N. Somatic motor Extraocular muscle (superior oblique muscle) Diplopia
V Trigeminal N. Somatic sensory Face, mouth/jaw, teeth, sinuses, meninges, Trigeminal neuralgia
oral and nasal mucosa
Branchial motor Muscles of mastication Asymmetric chewing
VI Abducens N. Somatic motor Extraocular muscle (lateral rectus muscle) Diplopia and medial
deviation of eye
VII Facial N. Special sensory Taste (anterior 2/3 of tongue) Loss of taste
Somatic sensory Skin on ear and tympanic membrane
Branchial motor Muscles of facial expression Facial paralysis and Bell’s
palsy
Visceral motor All salivary glands (excluding the parotid
gland) and lacrimal glands
VIII Vestibulocochlear N. Special sensory Audition and balance Deafness, tinnitus, and
vertigo
IX Glossopharyngeal N. Special sensory Taste (posterior 1/3 of tongue) Loss of taste
Somatic sensory Skin on ear, tympanic membrane, posterior
1/3 of tongue, and tonsillar fossa
Branchial motor Stylopharyngeus muscle
Visceral motor Parotid gland
Visceral sensory Carotid body and carotid sinus Blood pressure
regulation deficits
X Vagus N. Special sensory Taste (epiglottis) Loss of taste
General sensory Skin on external ear
Branchial motor Muscles of the larynx and pharynx Dysphagia and
dysphonia
Visceral motor Glands, smooth and cardiac muscle in the
neck, thorax, and abdomen
Visceral sensory Pharynx, larynx, and thoracic and abdominal
viscera
XI Spinal Accessory N. Somatic motor Trapezius and sternocleidomastoid muscles Shoulder drop and
weakened neck rotation
XII Hypoglossal N. Somatic motor Muscles of the tongue Tongue deviation
a
Alternative names for the functional components include following: General somatic efferent (GSE), somatic motor; general visceral efferent
(GVE), visceral motor; special visceral efferent (SVE), branchial motor; general somatic afferent (GSA), somatic sensory; general visceral afferent
(GVA), visceral sensory; special somatic afferent (SSA) and special visceral afferent (SVA), special sensory.

pharyngeal arches and the fact that branchial motor nu- expression (innervated by CN VII), the pharyngeal and
clei are located in distinct brainstem columns (immedi- laryngeal muscles (innervated by CNs IX, X and the
ately adjacent and lateral to the somatic motor nuclei). cranial portion of CN XI), and the muscles of mastication
Muscles of branchial origin include the muscles of facial (innervated by CN V).
 Cranial Nerves C 733

Visceral motor fibers provide autonomic (parasympa- relating to olfaction (CN I), vision (CN II), audition (CN
thetic) innervation to the head, neck, thoracic, and ab- VIII), balance (CN VIII), and taste (CNs VII, IX, and X).
dominal viscera, where they control glandular secretions This special sensory designation is an all-encompassing
and smooth and cardiac muscle contraction. The motor classification in that it does not distinguish between the
neurons that regulate parasympathetic visceral motor somatic senses (vision, audition, and balance) and the C
processes are typically positioned immediately lateral to more visceral sensations (olfaction and taste).
the branchial motor nuclei column in the brainstem. Intracranial Courses. Cranial nerves must traverse
Visceral motor fibers in CN III transmit parasympathetic through foramina (small holes) within the skull in order
innervation to structures in the eye that regulate pupil to navigate the path between the brain and the various
constriction and lens accommodation. CN VII regulates structures to which they provide innervation. Often, cra-
the secretion of tears (via the lacrimal glands) and salivary nial nerves will travel through these foramina together in
gland secretions (along with CN IX). CN X conveys vis- groups as they exit the cranium. For example, CNs IX, X,
ceral motor innervation to glandular tissue, smooth and and XI pass through the jugular foramen on their descent
cardiac muscles of the gastrointestinal, pulmonary, and to structures in the neck, thoracic, and abdominal cav-
cardiovascular systems. CN X has the most extensive ities; while CNs III, IV, and VI all traverse the superior
distribution of the cranial nerves, with its innervation orbital fissure to enter into the orbit to innervate the
spanning structures within the head and neck down to extraocular muscles. Knowledge of the origins of cranial
the thoracic and abdominal regions. nerves (i.e., brain stem nuclei), their intracranial course
Sensory Cranial Nerves. The remaining three func- and the cranial foramina through which they pass is
tional classifications of cranial nerve fibers convey sensory crucial to any neurological exam, as the diagnosis of
information and include somatic sensory, visceral sen- dysfunction of specific nerves can help to pinpoint the
sory, and special sensory fibers. As previously mentioned, site of and provide valuable information about damage or
the brainstem nuclei associated with these sensory fibers injury to the brain. For example, one of the early symp-
are located more laterally in the brainstem relative to toms of a pituitary adenoma is impaired vision, which
motor nuclei and are arranged in longitudinal columns results from the close proximity between the pituitary
according to functional components (from lateral to me- gland and fibers of CN II, which can become compressed
dial: special sensory, somatic sensory, and visceral sensory as a result of the tumor bulk. Similarly, CN VI has a very
nuclei). Somatic sensory fibers carry information from long intracranial course and, due to its emergence near
exteroreceptors and proprioceptors in the skin, muscles, the bottom of the brain and its course through the cav-
tendons, and joints of the head and neck, mediating the ernous sinus, it is often the first cranial nerve to be
perception of pain, temperature, touch, and propriocep- affected in the case of elevated intracranial pressure, com-
tion. CN V is the major somatic sensory nerve of the head, mon symptoms of which include painful eye movement
mediating cutaneous and proprioceptive sensation from and blurred or double vision (diplopia). Unlike the ma-
the skin, muscles, and joints in the face, mouth, and jaw as jority of cranial nerves, which exit from the ventral surface
well as sensory innervation of the teeth, oral and nasal of the brainstem, CN IV exits the midbrain dorsally and
mucosa, sinuses, and meninges. CN IX also transmits wraps around the lateral surface of the brainstem to enter
somatic sensory information from a portion of the oral the orbit. Due to this long peripheral course around
mucosa (the posterior third of the tongue and tonsillar the brainstem, CN IV is particularly susceptible to head
fossa) and, together with CNs VII and X, mediates sensa- trauma, where damage to this nerve is manifested by
tion of the skin on the outer ear. diplopia or blurred vision. Such examples demonstrate
In contrast to somatic sensory fibers, visceral sensory the manner in which cranial nerve dysfunction can pro-
fibers receive sensory input from receptive endings in vide insight into the various pathological situations that
visceral structures, such as walls of blood vessels or of can occur in the brain.
the digestive tract. Congruent with its expansive distribu- Cranial Nerve Dysfunction. Cranial nerve dysfunction
tion, CN X mediates the majority of visceral sensation in is not uncommon and can result from a variety of under-
the pharynx, larynx, thoracic, and abdominal cavities. CN lying pathologies, ranging from brain trauma to various
IX transmits visceral sensory information from the carotid forms of neurological disease. Common cranial nerve
sinus and carotid body, important structures in the regula- dysfunctions/disorders include Trigeminal Neuralgia
tion of blood pressure and respiration. (CN V), Bell’s Palsy (CN VII), Ramsay Hunt Syndrome
The final category of sensory cranial nerve fibers is the (CN VII), acoustic neuroma (CN VIII), Glossopharyngeal
special sensory fibers, which convey sensory information Neuralgia (CN IX), eye movement-related cranial nerve
734 C Cranial Pneumocyst

palsies (CNs III, IV, and VI), hyposmia/anosmia (CN I),

and various anopsias (CN II), among others. Due to its Cranial Pneumocyst
expansive innervation, CN X damage/dysfunction can re-
sult in a variety of deficits relating to visceral processes in ▶ Pneumocephalus
the heart, lungs, and abdomen. Interestingly, CN X nerve
stimulation is an emerging adjunctive treatment for certain
types of intractable epilepsy and refractory (treatment-re- Craniectomy
sistant) depression; however, the manner in which CN X
stimulation exerts its therapeutic effects is yet to be fully J AMES F. M ALEC
established. Mayo Clinic
Indianapolis, IN, USA

Cross References
Synonyms
▶ Acoustic Neuroma
▶ Anosmia Decompressive craniectomy
▶ Auditory Pathway
▶ Auditory System
▶ Autonomic Nervous System Definition
▶ Bell’s Palsy
▶ Deaf/Hearing Impairment Craniectomy or decompressive craniectomy is a surgical
▶ Diplopia procedure in which a section of the skull is removed
▶ Dysphagia and not immediately replaced (Hutchinson, Timofeev, &
▶ Dysphonia Kirkpatrick, 2007; Aarabi, Hesdorffer, Ahn, Aresco,
▶ Medulla Scalea, & Eisenberg, 2006). This procedure is most fre-
▶ Midbrain quently used when increased intracranial pressure follow-
▶ Neurologic Examination ing traumatic brain injury does not respond to other less
▶ Olfaction aggressive interventions. Following brain trauma, the
▶ Olfactory Bulb brain may expand within the skull. The resulting
▶ Optic Nerve increased intracranial pressure can compromise brain
▶ Optic Neuropathy function, particularly in the brain stem. Compression of
▶ Pons the brain stem can compromise its basic life support
▶ Ptosis functions, that is, cardiac and respiratory regulation, cre-
▶ Pupillary Light Response ating a life-threatening situation. By removing part of the
▶ Taste skull, the swelling brain is provided room to expand,
▶ Tinnitus reducing intracranial pressure and pressure on the brain-
▶ Trochlear Nerve stem. Although the section of the skull that is removed
▶ Vestibulocochlear Nerve in a craniectomy is not immediately replaced, the bone
▶ Visual Field Deficit removed may be stored and replaced at a later date when
▶ Visual System brain swelling is reduced and stable. Artificial materials
▶ Vertigo may also be used to replace the removed skull. In a
craniotomy, a section of the skull is removed and replaced
as part of the initial surgical procedure. Craniotomy is
more frequently performed as part of surgical interven-
References and Readings tion for disorders such as brain tumor or arteriovenous
malformation. However, a craniectomy may be preferred
Kandel, E. R., Schwartz, J. H., & Jessell, T. M. (2000). Principles of neural
in such cases if the condition appears to be associated with
science (4th ed.). New York: McGraw-Hill.
Shaw, J. P. (1992). A history of the enumeration of cranial nerves by brain swelling. Craniectomy may have no advantage over
European and British Anatomists from the time of Galen to 1895, craniotomy in long-term outcome after severe brain
with comments on nomenclature. Clinical Anatomy, 5(6), 466–484. injury (Woertgen, Rothoerl, Schebesch, & Albert, 2006).
 Cranioplasty C 735

However, standard craniectomy appears to result in better

outcomes than limited craniectomy (Jiang et al., 2005).

Cross References C
▶ Brain Swelling
▶ Craniotomy

References and Readings

Aarabi, B., Hesdorffer, D., Ahn, E., Aresco, C., Scalea, T. M., &
Eisenberg, H. M. (2006). Outcome following decompressive craniect-
omy for malignant swelling due to severe head injury. Journal of
Neurosurgery, 104, 469–479.
Hutchinson, P., Timofeev, I., & Kirkpatrick, P. (2007). Surgery for brain
edema. Neurosurgical Focus, 22(5), E14.
Jiang, J. Y., Xu, W., Li, W. P., Xu, W. H., Zhang, J., Bao, Y. H., et al. (2005).
Efficacy of standard trauma craniectomy for refractory intracranial
hypertension with severe traumatic brain injury: A multicenter, Craniopharyngioma. Figure 1 Courtesy Michael Fisher, MD,
prospective, randomized controlled study. Journal of Neurotrauma, Peter C. Phillips, MD. The Children’s Hospital of Philadelphia
22(6), 623–628.
Woertgen, C., Rothoerl, R. D., Schebesch, K. M., & Albert, R. (2006).
Comparison of craniotomy and craniectomy in patients with acute References and Readings
subdural haematoma. Journal of Clinical Neuroscience, 13(7),
718–721. Fahlbusch, R., Honegger, J., Paulus, W., Huk, W., & Buchfelder, M.
(1999). Surgical treatment of craniopharyngiomas: experience with
168 patients. Journal of Neurosurgery, 90, 237–250.

Craniopharyngioma
Cranioplasty
E THAN M OITRA
Drexel University J ACINTA M C E LLIGOTT
Morgantown, WV, USA National Rehabilitation Hospital
Dun Laoghaire Co., Dublin, Ireland

Definition
Definition
Craniopharyngioma is a slow-growing, extra-axial,
epithelial-squamous, calcified cystic tumor. It occupies Cranioplasty or replacement of bone flap or prosthesis is a
the suprasellar/sellar region and shows benign histology surgical procedure usually performed to fill in, or replace
but malignant behavior, as it may invade surrounding a defect in the skull following a craniectomy or removal
areas and recur after the treatment (Fahlbusch, Honegger, of a bone flap (Fig. 1).
Paulus, Huk, & Buchfelder, 1999). Craniopharyngiomas
may develop embryogenetically, arising from remnants
of the craniopharyngeal duct and/or Rathke cleft or meta- Further Reading
plastically because of residual squamous epithelium. The
most common presenting symptoms are endocrine dys- Cranioplasty can be performed using the patients own
function, headache, and visual disturbances. Craniophar- bone flap, which has been frozen or stored in the patient’s
yngiomas are treated with surgery or surgery followed by abdomen, or multiple materials such as titanium mesh,
radiotherapy. hydoxyapatite, and polymethylmethacrylate can be used
736 C Craniospinal Irradiation

Gardner, W. J. (1945). Closure of defects of the skull with tantalum.

Surgery, Gynecology Obstetrics, 80, 303–312.
Long, D. F. (2007). Diagnosis and management of late intracranial com-
plications of TBI. In N. D. Zasler, D. L. Katz, & R. D. Zafonte (Eds.),
Brain injury medicine. Principles and practice. New York: Demos.
Winder, R. J., Cooke, R. S., Gray, J., Fannin, T., & Fegan, T. (1999).
Medical rapid prototyping and 3D CT in the manufacture of custom
made cranial titanium plates. Journal of Medical Engineering and
Technology, 23(1), 26–28.

Craniospinal Irradiation
▶ Craniospinal Radiotherapy

Cranioplasty. Figure 1 Source: Winder, Cooke, Gray, Fannin,

and Fegan (1999)

Craniospinal Radiotherapy
as alternative to create a cranioplasty flap, where necessary
computerized techniques may be used to generate a J ACQUELINE L. C UNNINGHAM
custom made cranioplasty (Long, 2007). Children’s Hospital of Philadelphia
The decision to perform and the timing of the cranio- Philadelphia, PA, USA
plasty to replace the skull defect following craniectomy
can be variable. Originally considered to be largely a
cosmetic rather than a therapeutic procedure, cranio- Synonyms
plasty may be now be performed to prevent late neuro-
logical complications associated and identified with Craniospinal irradiation; CSI
craniectomy including the so called ‘‘syndrome of
trephined’’ (Dujovny, Agner, & Aviles, 1999; Long,
2007). Characteristics of this syndrome include headache, Definition
dizziness, irritability, epilepsy, discomfort, and psychiatric
symptoms, and in addition, the skin overlying the skull Craniospinal radiotherapy is an irradiation that is
defect may become indented (Dujovny, Aviles, Fernandez, & directed at the whole brain and length of the spinal axis,
Charbel, 1997). The pathophysiology of the ‘‘the including the meninges, as part of the cancer treatment to
syndrome of the trephined’’ is unknown, however, a control malignant cells. It serves as a radical (curative)
number of factors have been implicated including antineoplastic therapy, as a prophylaxis against a neo-
atmospheric pressure, cerebral blood flow, and cerebro- plasm’s involvement with the central nervous system, or
spinal fluid changes (Dujovny et al., 1997). Neurological as a palliative recourse when cure is impossible. Craniosp-
and functional improvements have been shown to inal irradiation (CSI) is technically challenging, and is
improve following cranioplasty in this syndrome, for used with computed tomography (CT) simulation and
example, in 1945 Gardner described the improvement in multimodality MRI registration to define a large target
symptoms in some patients following cranioplasty with volume, which spares healthy tissues, and assures exact
tantalum (Dujovny et al., 1997; Gardner, 1945). reproducibility of treatment from day-to-day.
MRI evidence of the craniospinal radiation injury to
the brain has been seen in l’Hermitte’s sign (a side effect of
References and Readings
radiotherapy on the spinal cord, experienced as shock
sensations), telangiectasia (dilated capillaries), white mat-
Dujovny, M., Agner, C., & Aviles, A. (1999). Syndrome of the trephined:
Theory and facts. Critical Reviews in Neurosurgery: CR, 9(5), 271–278.
ter changes, basal ganglia change, necrosis, and cerebral
Dujovny, M., Aviles, A., Fernandez, P., & Charbel, F. T. (1997). Cranio- atrophy. Although the differential sensitivity of specific
plasty: Cosmetic or therapeutic? Surgical Neurology, 47, 238–241. brain regions to radiotherapy has not been determined,
 Craniotomy C 737

factors relating to total dose, dose per fraction, and inter- Definition
val between fractions have been identified as important
variables influencing the brain’s response to radiation. Neurosurgical procedure involving the opening of the
Present research focuses on the development of treatment skull as a means of decreasing intracranial pressure
protocols based on the efficacy in tumor control while and/or for purposes of removal of a mass lesion. C
using the least dose of craniospinal radiotherapy
(1,800 cGy), often in conjunction with chemotherapy, as
the efficacy of CSI dose reduction in ameliorating neuro- Current Knowledge
endocrine and neurocognitive sequelae remains unclear.
Today, in contrast to the much higher doses used in the Craniotomy as a treatment for increased ICP from a mass
past decades, CSI doses of 2,400 and 3,600 cGy (with daily lesion has its foundation early in the history of neurosur-
fractions of 150 or 180 cGy) are standard. Studies contin- gery. Decompressive craniotomy (DC) initially was intro-
ue to evaluate how low a dose will remain effective in a duced to lower the intracranial pressure (ICP) in patients
risk-adapted setting. Controversy also exists on the with inoperable tumors and in managing uncontrolled
expression of radiation effects on specific neurocognitive ICP after traumatic brain injury (Brit & Hamilton,
domains. Attention and memory are known to bear a 1978). In recent years, DC has been recommended as an
vulnerability to neurotoxicity, but issues of individual alternative treatment for space occupying acute hemi-
differences, including premorbid and disease-related risk spheric infarction with or without massive medically
factors, are expected to influence neuropsychological uncontrolled brain edema (Schwab, 1998). During the
outcomes. acute period following cerebral infarction, neurologic
decline is often attributed to surrounding edema. Apart
from relieving the mass effect, restoration of the micro-
Cross References circulation around the infarcted area is the target of DC.
The management of increased intracranial pressure is a
▶ Radiation Injury common clinical scenario in neurosurgery. Strategies for
▶ Radiation Oncology the management of ICP fall into two general categories:
▶ Radiotherapy to reduce the volume of the intracranial compartment
(medical management) and to remove the mechanical
constraints imposed by the cranial vault (surgical).
In patients who sustain a severe non-penetrating
References and Readings head injury, overall 25–45% require a craniotomy for
evacuation of a hemorrhagic mass lesion, including epi-
Armstrong, C. L., Gyato, K., Awadalla, A. W., Lustig, R., & Tochner, Z. A.
(2004). A critical review of the clinical effects of therapeutic irradia-
dural, subdural, and intracerebral hematomas (Miller,
tion damage to the brain: The roots of controversy. Neuropsychology 1981). There is little debate in the surgical management
Review, 14, 65–86. of a rapidly deteriorating patient with a focal neurological
Brady, L. W., Heilmann, H. P., Molls, M., & Schlegel, W. (2006). New deficit and neuroimaging findings of an expanding intra-
techniques in radiation oncology. New York: Springer.
cranial hematoma associated with significant mass effect
and midline shift. For less obvious situations controversy
remains given the lack of class I and II data to support any
treatment standard. Complete removal of a brain tumor
without inflicting neurological deficits is a desirable end
Craniotomy result in neurosurgical practice. Craniotomy was tailored
to encompass tumor plus adjacent areas presumed to
E DUARDO L OPEZ contain eloquent cortex. Magnetic brain stimulation or
Johnson Rehabilitation Institute intraoperative cortical stimulation can be used to guide
Edison, NJ, USA resection of functional cortex.
DC remains a controversial procedure in spite of a
number of studies published in the literature on its use
Synonyms in the treatment of intracranial hypertension secondary
to malignant cerebral edema, traumatic brain injury,
Craniectomy; Trephination aneurysmal subarachnoid hemorrhage, central venous
738 C Cretinism

thrombosis, encephalitis, intracerebral hematoma, and conditions are characterized pathologically by neuronal
metabolic encephalopathies. It has been shown to be loss, spongiform change, and astrocytic gliosis. Cell loss
effective in reduction of ICP refractory to medical therapy can be seen microscopically as multiple perforations to
but evidence supporting an improvement in clinical out- the brain tissue creating the characteristic ‘‘sponge-like’’
come has not been conclusive. appearance. Prion diseases are caused by infectious
agents, which are abnormal self-replicating forms of a
normal brain protein, prion protein.
Cross References
▶ Temporal Lobectomy
Categorization and Epidemiology
Creutzfeldt–Jakob Disease (CJD) may be sporadic (that is
References and Readings develop spontaneously without apparent cause), familial
(inherited), or acquired (transmitted by infection).
Brit, R., & Hamilton, R., (1978). Large decompressive craniotomy in the
treatment of acute subdural hematoma. Neurosurgery, 2(3), 195–200.
CJD occurs worldwide with a mean annual incidence
Bullock, R., Chestnut, R., Ghajar, J., Gordon, D., Hartl, R., Newell, D. W., of approximately 1–2 cases per million population
et al. (2006). Surgical management of subdural hematoma. (Ladogana et al., 2005). Except for variant and iatrogenic
Neurosurgery, 58(3), S2–16–S2–24. CJDs, which are in decline, the disease has a relatively
Chen, C., Smith, E., Ogilvy, C., Carter, B. S., (2006). Decompressive
stable incidence with no convincing evidence of geo-
craniectomy: Physiological rationale, clinical indications, and
surgical considerations. 5, 70–80.
graphical clustering (although there are regions with an
increased incidence of familial cases). The gender inci-
dence is equal.

Cretinism Natural History, Prognostic Factors,

▶ Hypothyroidism
Outcomes

Historical Background

Sporadic and familial CJDs have been recognized as prion

Creutzfeldt-Jakob Disease diseases for many years, showing wide geographical spread;
however, variant CJD has been confined largely to the
K ARI H AWKINS 1,2 , R. G. W ILL 1, N ARINDER K APUR 2 United Kingdom, with the first cases reported in 1996.
1
University of Edinburgh It is thought that meat products intended for human con-
Edinburgh, UK sumption contained contaminated brain and spinal cord
2
Addenbrooke’s Hospital from animals affected by the epidemic of a prion disease in
Cambridge, UK cattle (Bovine Spongiform Encephalopathy) in the 1980s
(Hilton, 2006). Initial fears of a catastrophic epidemic
of vCJD among humans have been partially quelled,
Synonyms with a peak in new cases during 2000 reducing steadily
to only one new case in 2007 (http://www.cjd.ed.ac.uk).
CJD; Prion disease; Transmissible spongiform encepha- However, all vCJD cases to date have shared a common
lopathy (TSE) genotype (Methionine/Methionine) raising the possibil-
ity of subsequent peaks, which occur due to lengthened
incubation times among other genotypic groups. In addi-
Short Description or Definition tion, evidence from Kuru, an acquired prion disease aris-
ing from cannibalistic funeral practices among the Fore
Creutzfeldt–Jakob Disease (CJD) is a rare, fatal neurode- people of Papua New Guinea carried out until 1950s,
generative disease, which is one of the transmissible spon- suggests that incubation times for acquired prion disease
giform encephalopathies or prion diseases. These may stretch to several decades (Collinge et al., 2006). It is
 Creutzfeldt-Jakob Disease C 739

also possible for a person-to-person spread to occur, as has Variant CJD presents with a psychiatric syndrome,
been seen in four cases of blood transfusion-associated including depression and anxiety, for about 6 months
vCJD infection (most recent incidence figures are available before there is a progressive neurological and cognitive
from http://www.cjd.ed.ac.uk). decline as in sCJD, although chorea and dystonia occur as
well as myoclonus. The mean survival is 14 months, and C
vCJD affects a younger age group, with the mean age
Natural History and Prognosis being 29 years at death.

Different CJD phenotypes develop and progress at differ-

ent rates, although all subtypes develop profound demen- Neuropsychology and Psychology of
tia and multiple neurological features progressing to loss Creutzfeldt–Jakob Disease
of awareness and death. A summary of clinical presenting
features is given in Table 1. The Presentation of the CJD Patient
sCJD presents with cumulative multifocal neurological
deficits in association with a rapidly progressive dementia. The differential diagnosis is often the question at refer-
The cardinal clinical signs are dementia and myoclonus, ral, in particular, the distinction between a psychiatric
with a significant proportion of cases exhibiting ataxia or neurological basis for the presenting symptoms or to
and paratonic rigidity of the limbs. The mean survival distinguish CJD from other neurological conditions. A
from onset to death is only 4 months, although patients in thorough history, as always, is essential in establishing
the younger age groups often survive for more than a year. both the profile of the presenting symptoms and the
sCJD affects predominantly the older age groups with the course of the illness, and care should be taken to obtain
mean age being 65 years at death. corroborative reporting from relatives given the diffi-
The clinical presentation in familial CJD is often sim- culties of accurate history taking in individuals with
ilar to sCJD, but the age of onset is about 10 years earlier, cognitive decline. Sporadic CJD can often be distin-
and in some forms, there may be early ataxia and/or slow guished from other disorders by the speed and degree
progression. of cognitive decline, the short duration of illness, and
Iatrogenic CJD may present as in sCJD, but human the associated neurological signs. Some cases of fCJD
pituitary hormone recipients typically develop progressive present very similarly to sCJD; however, in fCJD, there is
ataxia and cognitive impairment develops late, if at all. often a younger age of onset, a longer disease duration,

Creutzfeldt-Jakob Disease. Table 1 Forms, causes, and incidence of CJD

Form Phenotype Cause Incidence

Sporadic Sporadic Unknown. Approximately one case per million
Creutzfeldt– population. Accounts for around 85% of CJD
Jakob Disease cases.
(sCJD)
Familial Familial Inheritance of mutation in the PrP gene. Approximately 10–15% of CJD cases are
Creutzfeldt– familial.
Jakob Disease
(fCJD)
Acquired Iatrogenic Case-to-case transmission via contaminated Less than 1% of CJD cases arise through
neurosurgical instruments, human dura mater acquired infection.
grafts, or exposure to human pituitary
hormones. The variant form of CJD can also be
transmitted via blood transfusion.
Variant CJD Ingestion of contaminated meat products from 166 cases in total in the UK, 23 cases in
(vCJD) cattle infected with Bovine Spongiform France, and a total of 18 cases elsewhere in
Encephalopathy. the world (as of May 2008).
740 C Creutzfeldt-Jakob Disease

Creutzfeldt-Jakob Disease. Table 2 Clinical presentation of CJD

Approximate
duration of Early clinical
Form Age at onset illness features Neuropsychological findings Exceptions
Sporadic 90% of cases 4 months (65% of Neurological signs Areas of early cognitive deficit Rare cases occur
between 50 cases survive <6 including cerebellar vary in this heterogeneous younger than 50.
and 80 years, months from ataxia, cognitive group, but there is often marked Young cases may
mean 65 years symptom onset). impairment (global impairment by the time of a present with some
dementia or referral for testing. Most cases psychiatric
specific deficits in show rapid progression to a symptoms
earlier stages), wide-ranging dementia initially, similar to
followed by including verbal and nonverbal the vCJD
myoclonus, rigidity, memory, executive dysfunction, presentation, and
and rapid and nominal skills. Poor memory may have longer
deterioration to loss and/or attention are often early disease duration.
of speech, features, but there may be 19% sCJD cases
voluntary occasional cases where initial have a disease
movement, and deficits reflect dysphasia or visual duration >12
awareness. disturbance. months
Heidenhain form:
very focal visual
difficulties for
weeks/months
before other
cognitive
symptoms.
Look for: Rapid cognitive decline Brownell–
over multiple test sessions. Oppenheimer
Fluctuations in responsiveness form: pure
and distractibility. cerebellar
syndrome for
Intrusion errors.
several weeks or
Verbal and motor perseveration. months before
cognitive decline
Familial Dependent on Dependent on the Dependent on fCJD cases may demonstrate less Some cases can
the specific specific mutation, mutation, may severe/rapid cognitive decline at have an illness
mutation of but on average present in a similar the early stages of a longer duration of years.
the prion 2–5 years fashion to sCJD or disease course than sCJD or vCJD Fatal Familial
protein gene, with predominant cases. A single case in 2000 Insomnia: early
but most often sleep and showed specific isolated deficits sleep disturbance
between the autonomic in delayed verbal memory and and autonomic
ages of 30 and disturbance or word finding prior to global dysfunction is
50 years. cerebellar ataxia involvement. One study suggests prominent
(see Exceptions, that naming ability may be
Gerstmann
right). Deterioration preserved in some cases in
Straussler
is usually slower comparison to sCJD and vCJD.
syndrome:
than in vCJD or Look for: Family history of CJD or
progressive
sCJD with a longer other (possibly misclassified)
cerebellar ataxia
disease course. neurological disease
 Creutzfeldt-Jakob Disease C 741

Creutzfeldt-Jakob Disease. Table 2 (Continued)

Approximate
duration of Early clinical
Form Age at onset illness features Neuropsychological findings Exceptions
Iatrogenic Dependent on Following dura Human growth Dependent on mode of C
age at mater graft similar hormone infection: transmission; human growth
exposure. to sCJD, With progressive hormone patients present with
Incubation human pituitary cerebellar ataxia with relatively preserved
period hormones 12–18 syndrome, delayed cognitive function until later
following months onset of dementia stages, while intracerebral cases
intracerebral Human dura mater present with broad-ranging
exposure is infection: rapidly dementia with rapid
19–46 months, progressive deterioration as seen in sCJD.
extending to dementia, similar to Look for: Rapid cognitive decline
many years or sCJD over multiple test sessions for
decades with intracerebral exposure cases.
peripheral History of relevant exposure to
exposure. differentiate from sCJD.
Variant Median age 28 Median 14 Most commonly, Measurable impairments on tests In 15%,
(range 12–74) months initial presentation of both verbal and nonverbal neurological
is psychiatric memory, executive function, symptoms
disturbance speed of attention, and nominal precede
including skills have characterized psychiatric.
depression, descriptions of published cases.
agitation, and Language, verbal reasoning, and
behavioral changes, visuoperceptual skills may be less
although in some frequently impaired, although
cases cognitive this may reflect an earlier disease
changes may be stage at the time of testing. One
the first sign of study suggests possible
abnormality. preserved ability in some
A delay of months components of visuoperception
is possible before in comparison to patients
distinct suffering from sCJD or fCJD.
neurological signs, Global involvement follows with
although cognitive rapid disease progression.
changes may be Look for: Fluctuating attention
found earlier in the and effort during testing.
disease course. Cognitive impairment more
Sensory symptoms profound than expected for
such as pain or odd depression or including areas of
sensation in limbs deficit unusual for psychiatric
or face may be disorders.
reported. Ataxia, Significant cognitive decline over
myoclonus, and follow-up assessment sessions.
significant
cognitive
impairment (such
as memory)
develop as the
disease progresses
Sources of information for this table are referenced under ‘‘References and Readings’’.
742 C Creutzfeldt-Jakob Disease

Creutzfeldt-Jakob Disease. Table 3 Investigations used in the diagnosis of CJD

Phenotype MRI EEG CSF 14–3–3 Tonsil biopsy Blood test History
Sporadic Important in In 60–80% of A positive 14-3-3 Negative At codon 129
(sCJD) excluding other cases, generalized CSF immunoassay of the prion
conditions. High bi- or triphasic is strongly protein gene:
signal on FLAIR or periodic sharp supportive of a 70%
DWI sequences in wave complexes diagnosis of sCJD methionine
the caudate and at 1/s. May not in the appropriate homozygous
putamen in about appear until later clinical context
70% of cases stages of the i.e., rapidly
disease progressive
dementia. Positive
in 90% of cases of
sCJD
Familial Some cases Characteristic Positive less Negative Analysis of Positive family
(fCJD) similar to sCJD periodic pattern is frequently than the prion history of CJD in
less frequently sCJD protein gene about 30% of
seen than in sCJD. for mutations cases
Iatrogenic Similar to sporadic Characteristic Positive in a Negative Mainly Relevant
CJD periodic pattern is proportion of homozygous exposure risk
less frequently cases methionine such as
seen than in sCJD. or valine treatment with
cadaveric
derived human
growth hormone
or human dura
mater graft
Variant Characteristic Normal or Positive in 50% of As vCJD, unlike All tested
(vCJD) high signal in the nonspecifically cases, but does the other CJD cases
posterior thalamic abnormal. not distinguish phenotypes, methionine
region (the Characteristic from sCJD involves the homozygous
‘‘pulvinar sign’’) in periodic pattern lymphoreticular
over 90% of cases in two cases late system, abnormal
on FLAIR or DWI in clinical course. protein may be
sequences. found in the
biopsy of tonsil
tissue in about
90% of cases.
Adapted from The National Creutzfeldt–Jakob Disease Surveillance Unit website (http://www.cjd.ed.ac.uk/investigations.htm).

and a family history of either CJD or another neurolog- Neuropsychological Testing

ical disorder. In iatrogenic cases, there should be a clear
history of a relevant exposure. The history in vCJD cases Patients with CJD often present at too late a stage for
includes early psychiatric symptoms (including mood, formal testing with a full neuropsychological battery. This
delusion, and agitation) and may also reveal cognitive is reflected in the literature, in which reports focus on
decline in everyday activities, of the type that might small cohorts and case studies. Efforts should be made to
typically be attributed to depression. In some cases, obtain sufficient breadth across cognitive domains when
neuropsychological symptoms may precede psychiatric testing to aid diagnosis and enable repeat testing if appro-
or neurological indicators that develop as the disease priate. Observations of test behavior will also be helpful.
progresses. The early presenting features in all CJD A study is currently underway to establish whether a brief
subtypes are summarized in Table 2. bedside screening test might be sufficient to give an
 Creutzfeldt-Jakob Disease C 743

indication of whether the degree or pattern of impairment professionals in supporting individuals and their families
seen in a patient could indicate CJD. through a period of acceptance, adjustment, loss, and
ultimately grief. Provision might also be made for the
counselling of healthcare staff involved in these distressing
Evaluation cases. C
Neuropsychological testing may occur prior to, in parallel
with, or following medical investigations and may provide
support for a diagnosis of CJD or prompt the clinician to
Cross References
instigate more extensive investigation than would usually
▶ Prion Disease
be undertaken in patients presenting, for example, with
▶ Spongiform Encephalopathy
primarily psychiatric complaints as in vCJD. A number of
further investigations may be used in the diagnosis of CJD
(Table 3).
References and Readings

Treatment Clare, L. (2007). Neuropsychological rehabilitation and people with demen-

tia. Hove, England: Psychology Press.
Collinge, J., Whitfield, J., McKintosh, E., Beck, J., Mead, S., Thomas, D. J.,
CJD is fatal. There is currently no effective treatment for et al. (2006). Kuru in the 21st century – an acquired human prion
the disease itself, despite ongoing trials of Quinacrine, disease with very long incubation periods. Lancet, 367(9528),
Pentosan Polysulfate, and Flupirtine (Stewart, Rydzewska, 2068–2074.
Keogh, & Knight, 2008; see the MRC New Therapies Cordery, R. J., Alner, K., Cipolotti, L., Ron, M., Kennedy, A., Collinge, J.,
et al. (2005). The neuropsychology of variant CJD: a comparative
Scrutiny Group for Prion Disease website for up-to-date
study with inherited and sporadic forms of prion disease. Journal of
information concerning recent treatment studies). Medi- Neurology, Neurosurgery and Psychiatry, 76, 330–336.
cal management should focus on alleviating discomfort, Creutzfeldt-Jakob Disease Foundation website. http://www.cjdfoundation.
including the use of medication to manage myoclonic org
jerks or pain and, as the disease progresses, the manage- Gass, C. S., Luis, C. A., Meyers, T. L., & Kuljis, R. O. (2000). Familial
Creutzfeldt-Jakob disease: a neuropsychological case study. Archives
ment of issues such as feeding or continence. Intervention
of Clinical Neuropsychology, 15(2), 165–175.
may be needed for the management of mood or psychotic Hilton, D. A. (2006). Pathogenesis and prevalence of variant Creutzfeldt-
symptoms. Since a high level of care will inevitably be- Jakob disease. Journal of Pathology, 208(2), 134–141.
come necessary, planning for the provision of this should Kapur, N., Abbott, P., Lowman, A., & Will, R. G. (2003). The neuropsy-
begin early, in consultation with the family. In the case of chological profile associated with variant Creutzfeldt-Jakob disease.
Brain, 126, 2693–2702.
a diagnosis of familial CJD, the family will face difficult
Ladogana, A., Puopolo, M., Croes, E. A., Budka, H., Jarius, C., Collins, S.,
decisions regarding genetic screening and should be guid- et al. (2005). Mortality from Creutzfeldt-Jakob disease and related
ed through such a process by an appropriately qualified disorders in Europe, Australia, and Canada. Neurology, 64,
professional. 1586–1591.
It is often the case that the cognitive symptoms of Medical Research Council New Therapies Scrutiny Group for Prion
Disease website http://www.mrc.ac.uk/PolicyGuidance/PolicyDeve-
CJD show extremely rapid deterioration and, in view of
lopment/NewTherapiesScrutinyGroupforPrionDisease.
this, cognitive rehabilitative efforts are unlikely to pro- National Creutzfeldt-Jakob Disease Surveillance Unit (NCJDSU) website.
duce helpful returns. However, in cases with early refer- http://www.cjd.ed.ac.uk
ral or a longer disease course, supportive aids (such as a National Prion Clinic website. http://www.nationalprionclinic.org
calendar for orientation) or environmental adaptations Smith-Bathgate, B. (2005). Creutzfeldt-Jakob disease: diagnosis and
nursing care issues. Nursing Times, 101, 52–53.
may produce improvements in activities of daily living,
Snowden, J. S., Mann, D. M. A., & Neary, D. (2002). Distinct neuropsy-
self-efficacy, and mood, at least in the early days, as is the chological characteristics in Creutzfeldt-Jakob disease. Journal of
case in other dementias (Clare, 2007; Smith-Bathgate, Neurology, Neurosurgery and Psychiatry, 73, 686–694.
2005). Spencer, M. D., Knight, R. S. G., & Will, R. G. (2002). First hundred cases
While the patients themselves are likely to lose aware- of variant Creutzfeldt-Jakob disease: retrospective case note review
of early psychiatric and neurological features. British Medical Jour-
ness of their predicament as their cognitive ability
nal, 324, 1479–1482.
declines, their families observe a devastating deterioration Stewart, L. A., Rydzewska, L. H. M., Keogh, G. F., & Knight, R. S. G.
in their loved ones. There is a role for the clinical psychol- (2008). Systematic review of therapeutic interventions in human
ogist, nurse practitioner, or other qualified healthcare prion disease. Neurology, 70, 1272–1281.
744 C Criminal Forensics

Denney, R. L., & Sullivan, J. P. (2008). Clinical neuropsychology in the

Criminal Forensics criminal forensic setting. New York: Guilford.
Denney, R. L., & Wynkoop, T. F. (2000). Clinical neuropsychology in the
criminal forensic setting. Journal of Head Trauma Rehabilitation, 15,
M OIRA C. D UX
804–828.
University of Maryland Medical Center/Baltimore VA Mrad, D. (1996). Criminal responsibility evaluations. Paper presented at
Baltimore, MD, USA issues in forensic assessment symposium. Atlanta, GA: Federal Bu-
reau of Prisons.

Definition

Within the field of forensic psychology, the utilization of Criminal Litigation

clinical neuropsychological expertise for criminal forensic
cases can be considered a subspecialty of the field. Denney M OIRA C. D UX
and Wynkoop (2000) modified Mrad’s (1996) multiple University of Maryland Medical Center/Baltimore VA
data source model (MDSM) to the practice of criminal Baltimore, MD, USA
forensic neuropsychology. The purpose of the model is to
provide a framework for clinicians to evaluate all relevant
sources of information, most notably information relevant Definition
to the defendant’s mental state at the time of the offense.
The model covers three time points of analysis: present, In civil litigation, a lawsuit is filed by a private party,
time of offense, and prior history. Moreover, the model seeking damages from another party as a result of some
assesses symptoms/behaviors, explanations, etc. via the type of injury, negligence, or malpractice. In criminal
self-report of the defendant as well as via other sources of litigation, the case is filed by the government against a
data (e.g., neuropsychological tests, mental status exam, defendant whom the government believes has committed
medical/neurological exam, arrest reports, witness state- a crime. Crimes are classified into one of two categories:
ments, physical evidence, hospital/psychiatric records, misdemeanors or felonies. Punishment for misdemeanors
employment records, family/friend reports, etc.). Once involve a maximum possible sentence of less than 1 year of
all of the relevant pieces of information are gathered, incarceration; felonies carry a maximum possible sen-
spanning the three time points, it is the role of the forensic tence of more than 1 year of incarceration. The burden
neuropsychologist to consolidate the information and of proof in criminal litigation is always assumed by the
formulate opinions. Evaluators involved in criminal for- state. Thus, it is the state’s responsibility to prove that
ensics typically have very different roles compared to gen- the defendant is guilty of having committed a crime.
eral practitioners. Specifically, in forensic evaluations, the However, if a defendant claims insanity (e.g., cannot
client is typically not the person being examined, and the appreciate the wrongfulness of the act nor conform their
ultimate goal is to evaluate the facts, not to maintain an conduct to the requirements of the law), then the burden
alliance with the examinee as is the case in a clinical of proof in proving one’s insanity falls on the defendant.
context. Moreover, forensic criminal evaluations typically Under criminal litigation, the state must demonstrate that
involve much more extensive application of corroborative the accused satisfied each element of the statutory
information as well as validated assessments of negative definition of the crime and prove the defendant’s involve-
response bias, symptom validity, and malingering. ment beyond a reasonable doubt. In the context of
criminal litigation, forensic neuropsychologists often
provide determinations regarding ‘‘mens rea’’ (e.g., guilty
Cross References
mind) or not guilty by reason of insanity (NGRI),
competent waiver of Miranda rights, and/or competence
▶ Criminal Litigation
to proceed (e.g., stand trial, to be sentenced, etc.).

References and Readings

Cross References
Denney, R. L. (2005). Criminal responsibility and other criminal forensic
issues. In G. Larrabee (Ed.), Forensic neuropsychology: A scientific ▶ Actus Rea
approach. New York: Oxford University Press. ▶ Criminal Forensics
 Crisis Intervention C 745

▶ Insanity related issue. Nonetheless, neuropsychologists are

▶ Mens Rea increasingly being called upon to determine whether or
not brain pathology may contribute to criminal behavior
(Barr, 2008).
References and Readings C
Denney, R. L., & Sullivan, J. P. (2008). Clinical neuropsychology in the
criminal forensic setting. New York: Guilford. Cross References
Greiffenstein, M. F., & Cohen, L. (2005). Neuropsychology and the law:
Principles of productive attorney-neuropsychologist relations. In ▶ Actus Rea
G. Larrabee (Ed.), Forensic neuropsychology: A scientific approach. ▶ Diminished Capacity
New York: Oxford University Press.
▶ Diminished Responsibility
▶ Insanity
▶ Intent
▶ Mens Rea
Criminal Responsibility
R OBERT L. H EILBRONNER References and Readings
Chicago Neuropsychology Group
Chicago, IL, USA Barr, W. B. (2008). Neuropsychological approaches to criminality and
violence. In R. Denney, & J. Sullivan (Eds.), Clinical neuropsychology
in the criminal forensic setting. New York: Guilford.
Denney, R. L. (2005). Criminal responsibility and other criminal forensic
Definition issues. In G. Larrabee (Ed.), Forensic neuropsychology: A scientific
approach. New York: Oxford University Press.
Criminal responsibility, or the conclusion of guilt for a Heilbronner, R. L., & Waller, D. (2008). Neuropsychological consultation
in the sentencing phase of capital cases. In R. Denney, & J. Sullivan
criminal offense, centers on four elements: (1) The
(Eds.), Clinical neuropsychology in the criminal forensic setting.
defendant must have committed the act (actus reus). New York: Guilford.
(2) The defendant’s actions must have caused the crime. Shapiro, D. L. (1999). Criminal responsibility evaluations: A manual for
(3) The defendant must have committed the crime with a practice. Sarasota, FL: Professional Resource Press.
guilty state of mind (mens rea). (4) There must be no Wrightsman, L. S., Greene, E., Nietzel, M. T., & Fortune, W. H. (2002).
Psychology and the legal system (5th ed.). Belmont, CA: Wadsworth,
circumstance constituting a legal defense for the charged
Thompson Learning.
crime (e.g., self-defense). In short, there must be the Yates, K. F., & Denney, R. L. (2008). Neuropsychology in the assessment
criminal act and the criminal intent and both must be of mental state at the time of the offense. In R. Denney, & J. Sullivan
proven, beyond a reasonable doubt. Mental health profes- (Eds.), Clinical neuropsychology in the criminal forensic setting.
sionals are typically involved with establishing intent and New York: Guilford.
mens rea, which involves the assessment and professional
opinions related to a defendant’s sanity and/or dimin-
ished capacity (which includes a decreased level of intent).
Criminal responsibility evaluations are also called san-
ity evaluations or assessment of mental state at the time of Crisis Intervention
the offense evaluations. Determining whether or not a
defendant was sane at the time of the offense is one of E LISE K. H ODGES 1, J EFFREY G. K UENTZEL 2
1
the most controversial questions forensic examiners are University of Michigan Health System
asked to address given that the purpose of the exam is to Ann Arbor, MI, USA
2
identify individuals who should not be held morally Wayne State University
responsible (‘‘not guilty by reason of insanity’’) for their Detroit, MI, USA
acts (Yates & Denney, 2008). An insanity plea is pursued
in about 9 out of 1,000 cases, and it is successful approxi-
mately 25% of the time (Wrightsman, Greene, Nietzel, & Synonyms
Fortune, 2002). It is very rare when a defendant is
acquitted secondary to insanity caused by a brain-injury- Emergency mental health treatment
746 C Criterion Validity

Definition Roberts (2005) developed a seven-stage crisis inter-

vention model:
Crisis intervention techniques target the resolution of an
1. Conduct a biopsychosocial/imminent danger assessment
immediate crisis and restoration of the affected indivi-
2. Establish a collaborative relationship
dual’s previous level of functioning. Roberts (2005)
3. Identify the major problems and crisis precipitants
defines a crisis as ‘‘a period of psychological disequilibri-
4. Encourage exploration of feelings
um, experienced as a result of a hazardous event or situa-
5. Generate alternatives and new coping strategies
tion that constitutes a significant problem that cannot be
6. Restore functioning via implementation of an action
remedied by using familiar coping strategies.’’
plan
7. Plan follow-up and booster sessions
Hospitals, clinics, and schools typically have in place a set
Current Knowledge
of policies and procedures for how staff should intervene
in the crisis situations that are most likely to be encoun-
It is important to stress that most individuals who expe-
tered. Staff trainings on these protocols should be con-
rience a crisis or traumatic event tend to recover on their
ducted routinely to ensure a high level of preparedness.
own accord (i.e., crisis intervention may not be needed).

Cross References
Crisis Intervention Approaches
▶ Stress Management
Critical incident stress management (CISM; Mitchell &
Everly, 1993) is an approach to crisis intervention that has
garnered considerable attention since its initial develop- References and Readings
ment in the 1980s. A key component of CISM is the critical
incident stress debriefing (CISD), a group session held Mitchell, J. T., & Everly, G. S. (1993). Critical incident stress debriefing: An
shortly after an incident. Led by CISM-trained facilitators, operations manual for the prevention of traumatic stress among emer-
gency services and disaster workers. Ellicott City, MD: Chevron.
the CISD session allows participants to share their experi-
National Child Traumatic Stress Network and National Center for PTSD
ences of the incident, and the leaders provide psychoedu- (2006). Psychological first aid: Field operations guide, (2nd ed.). Re-
cation about stress reactions and recommended coping trieved March 5, 2010, from http://www.ncptsd.va.gov/ncmain/
strategies. In the 1990s, a controversy developed surround- ncdocs/manuals/PFA_V2.pdf.
ing CISM, as research evidence mounted that failed to National Institute of Mental Health (2002). Mental health and mass
violence: Evidence-based early psychological intervention for victims/
show its effectiveness. A National Institute of Mental
survivors of mass violence. A workshop to reach consensus on best
Health (NIMH) report (2002) suggested that stand-alone practices. NIH Publication No. 02-5138, Washington, D.C.: U.S.
CISD does not consistently prevent post-traumatic disor- Government Printing Office.
ders, and that some individuals, such as those with high Roberts, A. R. (2005). Crisis intervention handbook: Assessment, treatment,
arousal, may be put at heightened risk for adverse out- and research. (3rd. ed.). New York: Oxford University Press.
comes as a result of CISD-type interventions. Thus, man-
datory participation in group debriefing sessions is
considered very questionable.
An alternative to CISM is psychological first aid
(PFA; National Child Traumatic Stress Network and
Criterion Validity
National Center for PTSD, 2006). PFA is an evidence-
▶ Test Validity
informed, pragmatic approach that targets acute stress reac-
tions and the immediate needs of persons exposed to a
critical incident (NIMH, 2002). The goals of PFA include
enhancement of safety (both objective and subjective), re-
duction of stress-related symptoms, restoration of rest and Criterion-Referenced Testing
sleep, linkage with resources, and facilitation of social
support. ▶ Domain Referenced Test Interpretation
 Cross-Examination C 747

sinistrality. However, familial sinistrality is absent in the

Critical Periods majority (63%) of reported CA cases (Coppens, Hungerford,
Yamaguchi, & Yamadori, 2002). Further, there does not
▶ Sensitive Periods seem to be any difference in CA symptomatology when
comparing patients with and without familial sinistrality, C
and the presence of familial sinistrality does not increase
the number of anomalous cases, as could be expected if
Crossed Aphasia language laterality were weak (Coppens et al., 2002).
Individuals with CA also often display typical right-
PATRICK C OPPENS
hemisphere symptoms (e.g., left-side neglect, visuospa-
SUNY Plattsburgh
tial/visuoconstruction problems, affective dysprosody,
Plattsburgh, NY, USA
and spatial agraphia) which indicates that those skills
may lateralize independent of language. The aphasic dif-
ficulties may obscure these right-hemisphere signs, but
Definition
these represent a major difference in symptomatology
between CA and LHA.
Crossed aphasia is an acquired language impairment fol-
lowing a lesion in the right hemisphere in a right-handed
individual.
Cross References
Current Knowledge ▶ Aphasia
▶ Handedness
The term ‘‘crossed aphasia’’ (CA) was coined by Byrom
Bramwell (1899) to indicate an aphasia caused by a cere-
bral lesion ipsilateral to the dominant hand regardless of References and Readings
handedness. Currently, CA only refers to right-handed
individuals. The frequency of CA among stroke survivors Alexander, M. P., Fischette, M. R., & Fischer, R. S. (1989). Crossed
is rare (1–3%). aphasias can be mirror image or anomalous. Brain, 112, 953–973.
Although some earlier authors considered CA to Basso, A., Capitani, E., Laiacona, M., & Zanobio, M. E. (1985). Crossed
aphasia: One or more syndromes? Cortex, 21, 25–45.
be the consequence of a weaker language lateralization,
Bramwell, B. (1899). On ‘‘crossed’’ aphasia. Lancet, 1473–1479.
it appears that individuals with CA have language as Coppens, P., Hungerford, S., Yamaguchi, S., & Yamadori, A. (2002).
strongly lateralized as those with left-hemisphere aphasia Crossed aphasia: An analysis of the symptoms, their frequency, and
(LHA), mainly because both populations show a similar a comparison with left-hemisphere aphasia symptomatology. Brain
prognosis. and Language, 83, 425–463.
Fujii, T., Yamadori, A., Fukatsu, R., Ogawa, T., & Suzuki, K. (1997).
CA can be mirror image or anomalous (Alexander,
Crossed mixed transcortical aphasia with hypernomia. European
Fischette, & Fischer, 1989). Mirror-image CA denotes Neurology, 37, 193–194.
the expected correspondence between symptomatology
and lesion location within the language-dominant
hemisphere, whereas anomalous CA implies the presence
of unexpected language symptoms given the lesion loca- Cross-Examination
tion (e.g., Wernicke’s aphasia following a frontal lesion
[Basso, Capitani, Laiacona, & Zanobio, 1985], a mixed M OIRA C. D UX
transcortical aphasia with preserved naming [Fujii, University of Maryland Medical Center/Baltimore VA
Yamadori, Fukatsu, Ogawa, & Suzuki, 1997]). Close to Baltimore, MD, USA
two thirds of CA cases are mirror image. The CA language
symptomatology is virtually indistinguishable from LHA,
and all aphasia types have been reported in CA. Definition
The cause of CA is essentially unknown, but the influ-
ence of left-handedness in the family has long been consid- A deposition or actual trial testimony consists of two
ered an important causal factor, a hypothesis called familial parts: the direct examination and the cross-examination.
748 C CRS

Direct examination precedes the cross-examination and

involves testimony brought forth by the retaining attor- CRS-R
ney. Cross-examination occurs immediately after the
direct examination and is carried out by the opposing ▶ Coma Recovery Scale
attorney. The main purpose of cross-examination is to
test the ‘‘reliability, accuracy and credibility’’ of witnesses’
testimony produced during the direct examination.
Questions posed during cross-examination typically fall
into two categories: those intended to expose weaknesses Crystallized Intelligence
or errors in the expert witnesses’ data acquisition or
interpretations, and those related to expose biases in the ▶ Intelligence
testimony. During cross-examination, expert witnesses
are expected to give responsive answers. That is, they
are to provide relevant answers, but the answers need
not be those implicitly desired by the opposing attorney.
The opposing attorney may use several tactics during
cross examination including: challenging credibility,
CSI
establishing doubt, leading questions, feigned ignorance,
▶ Craniospinal Radiotherapy
the cut-off (e.g., testimony of witness terminated to stop
the witness from providing further information that
could be detrimental to the opposing attorney’s position),
intentional ambiguity, implying impropriety, rattling the
witness, and many others.
CS-PFP
▶ Physical Functional Performance
Cross References

▶ Direct Examination

CS-PFP10
References and Readings
▶ Physical Functional Performance
Brodsky, S. L. (2004). Coping with cross-examination and other pathways
to effective testimony. Washington, DC: American Psychological
Association.
(1975). Federal rules of evidence for United States courts and magistrates.
St. Paul, MN: West Publishing.
Greiffenstein, M. F., & Cohen, L. (2005). Neuropsychology and the law: CT
Principles of productive attorney neuropsychologist relations. In
G. Larrabee (Ed.), Forensic neuropsychology: A scientific approach. ▶ Category Test
New York: Oxford University Press.
▶ Computed Tomography

CRS
CT Scan
▶ Coma Recovery Scale
▶ Conners Rating Scales ▶ Computed Tomography
 Cue C 749

may appear spontaneously as a behavior is unfolding

Cue in order to effect immediate change. For example,
when one sees the cue of a deer running into the
J ANET PATTERSON road one veers away to avoid a collision, or when one
California State University is engaged in conversation and hears the cue of his or
Hayward, CA, USA
C
her sentence that does not adequately express the
intended meaning one immediately changes the sen-
tence. Cues may also appear as a learned strategy and
Synonyms be repeated in a consistent format. For example, dri-
vers know that when the yellow traffic light appears
Discriminative stimulus; Prime; Prompt they should slow the car in preparation to stop when
the red traffic light appears, or in a communication
Definition interaction when another individual offers a greeting
one should respond. Some examples of self-generated,
A cue is a verbal or nonverbal instruction to induce internal cues are reminders for future action (e.g.,
behavior change. Cues are self-generated or may come remember to walk the dog), mental sequences used in
from the environment (including an examiner). They the tip-of-the-tongue state (e.g., telling oneself that the

Present Cue # 1 Present Cue # 4

Present a picture and say, “Say the name of this,” or Say “It starts with ___” and say the first sound
“What’s this” or “Tell me the name of this”
If correct response
If correct response (a) Say “correct” or “right”
(a) Say “correct” or “right” (b) Present Cue #3
(b) Ask for five repetitions
(c) Move to next picture item If incorrect response
(a) Present Cue #5
If incorrect response
(a) Present Cue #2
Present Cue # 5
Present Cue # 2 Say “The word is ___” and say the name of the item

Say “It goes with ____” and give the semantic cue
If correct response
If correct response (a) Say “correct” or “right”
(1) Say “correct” or “right” (b) Present Cue #4
(2) Present Cue #1
If incorrect response
If incorrect response (a) Repeat cue and ask for repetition
(a) Present Cue #3 (b) If unable to repeat item name after three
consecutive presentations of Cue #5
Present Cue # 3 move to next picture item
Say “It sounds like ___” and give the rhyme cue

If correct response
(a) Say “correct” or “right”
(b) Present Cue #2

If incorrect response
(a) Present Cue #4

Cue. Figure 1 An example of a cueing hierarchy for oral naming using semantic and phonological cues
750 C Cue Dominance

name rhymes with sock), or teaching/treatment strate- Definition

gies (e.g., using an association strategy for naming,
such as reciting the alphabet to cue the name). Exam- Cue dominance refers to the tendency to perceive or
ples of external cues are environmental signs (e.g., respond to a particular stimulus or class of stimuli over
walk/do not walk signals), preprogrammed reminders others in the environment. Stimuli may either have in-
(e.g., alarm clock), or teaching/treatment techniques trinsic properties that give them strength or ‘‘dominance’’
(e.g., semantic-phonological cueing hierarchy). A cue- based on physical attributes (e.g., loudness, color), or may
ing hierarchy is a set of cues progressing from weak cues acquire dominance (i.e., propensity to elicit a response) as
providing little information about the target response, to a function of associative learning and task demands.
strong cues providing much information (Wambaugh,
Linebaugh, Doyle, Martinez, Kalinyak-Fliszar, & Spencer,
2001) (Fig. 1). Current Knowledge

Cue dominance is an important principle derived from

behavioral studies of animal conditioning and learning the-
Cross References ories. It provides a theoretical foundation for the neurosci-
ence of selective attention, linking basic behavioral and
▶ Cue Dominance
learning processes with higher order information processing.
▶ Cued Recall
In the context of behavioral conditioning, cues refer
▶ Free Recall
to stimuli that have the capacity to elicit an orienting
▶ Phonemic Cue
response, anticipation, subsequent attention, and re-
▶ Recency Effect
sponse intention and preparation. Cues lack the inherent
▶ Semantic Cue
biological salience of unconditioned stimuli, and do not
▶ Semantic Fluency
elicit unconditioned Pavlovian responses, but can become
▶ Verbal Fluency
conditioned stimuli through associative learning. Studies
of discrimination learning conducted in the middle of the
twentieth century established many of the operational
References and Readings characteristics underlying cue dominance. For example,
studies examining intrinsic cue dominance demonstrated
Patterson, J. P., & Hinnach, S. E. (2005). Word familiarity effects during that monkeys have a natural preference for response to
naming and discourse production in aphasia. Presentation to the color over other perceptual dimensions, such as size and
American Speech-Language-Hearing Association Annual Conven- shape (Draper, 1965). Experiments with human infants
tion. San Diego. demonstrated cue dominance for certain shapes over
Wambaugh, J. L., Linebaugh, C. W., Doyle, P. J., Martinez, A. L.,
others based on whether they resembled the shape of a
Kalinyak-Fliszar, M., & Spencer, K. A. (2001). Effects of two cueing
treatments on lexical retrieval in aphasic speakers with different human face (Fantz & Miranda, 1975). While certain stim-
levels of deficit. Aphasiology, 15(10/11), 933–950. ulus features have intrinsic cue dominance across many
animal species, the ability to form complex cues based on
the association of simple cues appears greatest among
humans, as is the ability to exhibit reversal learning in
order to shift response from one cue to another (Kendler &
Ward, 1972; Kendler, 1971).
Cue Dominance In neuropsychological studies and assessment meth-
ods, cues are often used to either facilitate attention to
R ONALD A. C OHEN particular spatial locations, semantic information, or re-
Brown University sponse demands. Alternatively, cues are used to create
Providence, RI, USA interference to test the effects of distraction or the redi-
rection of attention away from the primary demands of a
task. This is a fundamental element of the spatial selective
Synonyms attention paradigms that involve cueing to spatial loca-
tions (Posner, Snyder, & Davidson, 1980). Furthermore,
Cue salience; Orienting stimulus; Stimulus strength the tendency of the semantic value associated with a word
 Cued Recall C 751

to be dominant over color and to interfere with attention from free recall in that a cue or word is presented that is
to and naming of the actual color that is being presented related to the information being remembered. This aides
underlies the Stroop effect. Researchers and clinicians in the process of memory retrieval. Some examples of
studying or assessing attentional processes need to ac- cued recalls are the names of the categories in which
count for both the inherent and acquired cue dominance words were originally grouped or the presentation of C
of stimuli being used in the context of particular tasks. related words. For instance, in remembering the word
feather, the word bird may be used as a cued recall.

Cross References Current Knowledge

▶ Enhancement
Tests of Cued Recall
▶ Selective Attention
▶ Visual Discrimination
There are many tests of cued recall. One of the most
commonly used tests of cued recall is the California Verbal
Learning Test (CVLT) developed by Delis et al. This se-
References and Readings mantic test, like many other tests of memory, utilizes both
free and cued recall.
Draper, W. A. (1965). Cue dominance in oddity discriminations by
rhesus monkeys. Journal of Comparative and Physiological Psychology,
60(1), 140–141. Clinical Uses of Cued Recall Testing
Fantz, R. L., & Miranda, S. B. (1975). Newborn infant attention to form
of contour. Child Development, 46(1), 224–228.
Kendler, T. S. (1971). Continuity theory and cue-dominance. In H. H.
In addition to the use of free recall tests, tests of cued
Kendler & J. T. Spence (Eds.), Essays in neobehaviorism: A memorial recall may be used in identifying memory impairments in
volume to Kenneth W. Spence. East Norwalk: Appleton-Century- a wide array of disorders including mild cognitive im-
Crofts. pairment and Alzheimer’s disease. In some instances, tests
Kendler, H. H., & Ward, J. W. (1972). Reversal learning: The effects of
of cued recall may be more accurate than free recall tests
conceptual and perceptual training in the absence of differential
observing responses. Psychonomic Science, 28(6), 346–348.
in detecting cognitive changes. For example, Ivanoiu et al.
Posner, M. I., Snyder, C. R., & Davidson, B. J. (1980). Attention and the (2005) found that a cued recall test is more reliable in
detection of signals. Journal of Experimental Psychology: General, testing memory impairment in Alzheimer’s disease than
109(2), 160–174. free recall testing. While both tests of memory are im-
paired in such individuals, cued recall may be a more
accurate measure of cognitive decline. This is because
deficits other than pure memory deficits, such as impaired
Cue Salience attention or depression, may account for a decreased
performance in free recall. Conversely, cued recall tests
▶ Cue Dominance may be used to more directly measure the encoding and
retrieval that takes place in memory tasks.

Cross References
Cued Recall
▶ California Verbal Learning Test (California Verbal
M ARGARET M OULT Learning Test-II)
Institute of Living Hartford ▶ Cue
CT, USA ▶ Free Recall

References and Readings

Definition
Carpenter, S. K., Pashler, H., & Vul, E. (2006). What types of learning are
Cued recall is the retrieval of memory with the help of enhanced by a cued recall test? Psychonomic Bulletin & Review, 13,
cues. Such cues are often semantic. Cued recall differs 826–830.
752 C Cultural Diversity in Neuropsychology

Ivanoiu, A., Adam, S., Van der Linden, M., Salmon, E., Juillerat, A. C., Recent studies emphasize that the deconstruction of
Mulligan, et al. (2005). Memory evaluation with a new cued recall
race is critical for improved clinical care of ethnically di-
test in patients with mild cognitive impairment and Alzheimer’s
disease. Journal of Neurology, 252, 47–55.
verse populations. The construct has been identified as a
Vogel, A., Morentsen, L., Gade, A., & Waldemar, G. (2007). The category ‘‘proxy for more meaningful but complex variables’’ such as
cued recall tests in very mild Alzheimer’s disease: Discriminative acculturation and indicators of quality of education, which
validity and correlation with semantic memory functions. European account for significant proportions of racial and ethnic
Journal of Neurology, 14, 102–108.
differences in neuropsychological test scores (Romero
et al., 2009, p. 765). However, increasing emphasis has
been placed on the importance of the clinician knowing
when to apply race- and ethnic-based norms, as their use
can actually reduce detection of neuropsychological im-
Cultural Diversity in pairment. The complexity of this issue was demonstrated
Neuropsychology in one of the Mayo’s Older African American Normative
Studies (MOAANS) project studies. In this study, adjust-
S ARAH K. L AGEMAN ment of test scores for reading level surprisingly reduced
Emory University detection of cognitive impairment in African Americans.
Atlanta, GA, USA Lucas and colleagues (2005) suggest that their findings
indicate that cohort differences in reading level may be
more reflective of individual differences in cognitive abil-
Definition ity rather than contextual differences such as educational
backgrounds. While race may be a very efficient and
The term ‘‘cultural diversity’’ generally refers to the differ- parsimonious variable for clinicians to use at times, the
ences in defining cultural features that exist between confounding of causes and effects of these variables pre-
people (or within a given population), such as language, sents a significant challenge. The Diversity Summit parti-
dress, and traditions, as well as more abstract concepts cipants unanimously agreed that guidelines for
involving significant variations in societal organization neuropsychological practice among ethic and racial mino-
and interaction styles between individuals and environ- rities are needed to further improve clinical service for
ments. With respect to neuropsychology, the term ethic and racial minorities.
encompasses the racial and ethnic diversity among neu- In an effort to initiate the development of practical
ropsychologists themselves and the populations they in- guidelines regarding the use of demographic corrections,
teract with, as well as issues related to the influences of clinical criteria have been developed. As detailed in the
race and ethnicity on neuropsychological evaluations and Diversity Summit proceedings, demographic corrections
treatments. are useful to identify and characterize acquired neurocog-
nitive impairments in adults who (1) are natives of the
country of assessment, (2) developed normally, (3) received
Current Knowledge mainstream education, and (4) speak English as their first
language (for the U.S. norms). Demographic corrections
Multicultural competency is a developing area of focus are sometimes useful to identify and characterize acquired
within the field of neuropsychology. As the ethnic and neurocognitive impairments in (1) teenagers or young
racial diversity of the United States increases, so do efforts adults who have not completed their education, (2) adults
to provide neuropsychological services to ethnic minori- who may have had a mild developmental disorder, or (3)
ties. Thus, clinical and research studies have begun to anyone with a linguistic, cultural, or educational back-
examine how cultural variables influence performance ground not well represented in the normative subject
on neuropsychological measures. While the past decade sample. Demographic corrections are not recommended
has witnessed some publications providing test norms for when the clinician is asked (1) to characterize ‘‘absolute’’
specific racial and ethnic groups, the use of racial and levels of functioning, (2) to identify or characterize possi-
ethnic norms for neuropsychological measures remains a ble acquired impairment in capital punishment cases or
contentious issue. Readers are encouraged to examine the when determining qualifications for special services,
summary of the 2008 Diversity Summit for additional or (3) in cases of possible acquired impairment in indivi-
details (Romero et al., 2009). Highlights of the summit duals who have developmental disability, (4) to character-
and recent literature are provided below. ize acquired cognitive impairment in individuals who
 Cultural Diversity in Neuropsychology C 753

have major background differences from the normative importance of training in cross-cultural neuropsychology
sample, (5) to predict future performance in employment will become increasingly important as the Spanish-
or academic settings, and (6) for employment selection speaking Latino population in the United States grows.
decisions. In addition to these clinical guidelines, empha- In keeping with the demographic changes in the
sis is being increasingly placed on correctly using proba- United States, training programs and national organiza- C
bilistic statistics to predict group membership (i.e., tions are brainstorming ways to promote recruitment and
diagnosis) for individuals. Readers are encouraged to retention of students with diverse racial and ethnic back-
review recent publications regarding likelihood ratios, grounds in the study of neuropsychology. Emphasis has
which express the risk associated with certain test scores been placed on student exposure to neuropsychology
(Smith, Ivnik, & Lucas, 2008). earlier in academic careers, mentoring with minority
While additional study of the deconstruction of race is and nonminority faculty who are sensitive to diversity
needed, development of ethnic group norms itself is a issues and financial support of minority students. The
challenging and complex task. Test publishers are increas- study of cultural diversity itself has gained support and
ingly making efforts to include important background many licensing bureaus require documentation of diver-
variables in normative samples. However, the cost of sity training in graduate school for licensure. Numerous
recruiting and assessing large cohorts is prohibitive for organizations, including the American Psychological
individual centers and researchers and is often even a Association (APA) Division 40, the International Neuro-
challenge for larger test publishing companies. While psychological Society (INS), and the National Academy of
inclusion of demographic variables in research articles is Neuropsychology (NAN), promote awareness of diversity
an important piece to further develop this area, federal issues and foster collaborations among clinicians and
and foundation-funded grants may be necessary to sup- researchers interested in diversity issues. Readers are
port multicenter partnerships, ideally suited to study encouraged to review current guidelines, including the
large, diverse cohorts. APA Ethical Principles (2002) and the APA Multicultural
Despite the development of racially and ethnically Guidelines (2002) for further details.
diverse norms, including the widely used Heaton norms Diversity in neuropsychology has become of increasing
for African American and Caucasian adults, the almost interest and importance; however, measures to improve
endless variety possible with regard to individuals’ language, diagnostic assessment of ethnic minorities may not fully
culture, and education backgrounds limits the application address the issue of improving clinical care of ethnic mino-
of demographically corrected norms for every possible clin- rities, given limited health care access of non-English-
ical situation (Heaton, Miller, Taylor, & Grant, 2004). Local speaking patients. Access to care and other factors affecting
norms may be helpful for clinicians working with popu- ethnic minority patient outcomes have increasingly been
lation groups with less common background variables; examined in the field of neuropsychology. Readers are
however, integration of test scores with a person’s individ- encouraged to review two issues of the Journal of Head
ual context is ultimately critical for formulation of an Trauma Rehabilitation, dedicated to U.S. and international
accurate diagnosis. In clinical practice, other issues re- cultural issues in the rehabilitation of survivors of traumatic
garding assessment of ethnic, linguistic, and cultural head injury (‘‘Cultural Issues,’’ 2007 and ‘‘International
minorities are also present. The use of translated tests, Programs and Perspectives,’’ 2007). Articles in these issues
interpreters, and bilingual psychometrists are all current highlight complex relationships between functional out-
methods for evaluating non-English-speaking patients. comes, disability severity, return to work, and utilization
However, the shear complexity of language fluency is of professional psychological services in ethnic minority
important to consider. Language fluency of an individual groups. The international issue describes models of care
can vary widely with regard to (1) age of acquisition, (2) used in the context of various health care systems as well
proficiency, (3) manner of learning, (4) amount of lan- as international perspectives on research and develop-
guage exposure, (5) predominant mode of bilingual inter- ment in the field of traumatic brain injury rehabilitation.
action, and (6) language structure variables (i.e., alphabetic The study of health disparities among ethnic minority
versus logographic languages and phonemic versus non- populations is a complex, but critical field of research.
phonemic status). Currently, the use of translated tests and Multiple dimensions of disparity exist, including many of
official interpreters or bilingual psychometrists are pre- the variables discussed regarding the deconstruction of
ferred over using family members as interpreters and site race such as ethnicity, education, income, occupation,
translation, which refers to the practice of quickly translat- and geography. Continuous study of these variables is
ing a test with no standardization procedures. The critical to improve clinical care for ethnic minorities.
754 C Cultural Sensitivity

Cross References ethnic minorities: Summit proceedings. The Clinical Neuropsycholo-

gist, 23, 761–779.
Smith, G. E., Ivnik, R. J., & Lucas, J. (2008). Assessment techniques:
▶ AACN Practice Guidelines Tests, test batteries, norms, and methodological approaches. In
▶ Clinical Practice Guidelines J. E. Morgan & J. H. Ricker (Eds.), Textbook of clinical neuropsychol-
▶ Cultural Sensitivity ogy (pp. 38–57). New York: Taylor & Francis.
▶ Culture Fair Tests Uzzell, B. P., Pontón, M., & Ardila, A. (Eds.). (2007). International
handbook of cross-cultural neuropsychology. Mahwah, NJ: Lawrence
▶ Ethics in the Practice of Neuropsychology
Erlbaum Associates, Inc.

References and Readings

Cultural Sensitivity
American Academy of Clinical Neuropsychology (AACN). Multicultural
references. Retrieved March 16, 2010, from the AACN Web site:
http://www.theaacn.org/position_papers/AACN_multicultural_ref
C HRISTIAN S CHUTTE , B RADLEY A XELROD
erences.pdf John D. Dingell VA Medical Center
American Psychological Association’s Ethical Principles of Psychologists Detroit, Michigan, USA
and Code of Conduct with the 2010 Amendments (http://www.apa.
org/ethics/code/index.aspx)
American Psychological Association’s Ethnic Minority Affairs Office
(http://www.apa.org/pi/oema/index.aspx)
Synonyms
American Psychological Association’s Minority Fellowship Program
(http://www.apa.org/pi/mfp/) Multicultural
American Psychological Association’s Division 45, Society for the Psy-
chological Study of Ethnic Minority Issues (http://www.apa.org/
divisions/div45/) Definition
American Psychological Association. (2002). Guidelines on multicultural
education, training, research, practice, and organizational change for Awareness of how a patient’s background, including eth-
psychologists. Retrieved June 30, 2010, from http://www.apa.org/
nicity and demographic factors, affects treatment, assess-
practice/guidelines/multicultural.pdf
Arango-Lasprilla, J. C., & Niemeier, J. (Eds.). (2007). Cultural issues in
ment, and research.
the rehabilitation of TBI survivors: Recent research and new fron-
tiers. Journal of Head Trauma Rehabilitation, 22(2), 73–139.
Ardila, A., Rosselli, M., & Puente, A. (1994). Neuropsychological evalua-
Current Knowledge
tion of the Spanish speaker. New York: Plenum Press.
Board of Directors (2007). American Academy of Clinical Neuropsychol- There are a couple of pertinent definitions, or applications,
ogy (AACN) Practice Guidelines for Neuropsychological Assessment of cultural sensitivity to the field of neuropsychology.
and Consultation. The Clinical Neuropsychologist, 21, 209–231. Re-
The position of the American Psychological Associa-
trieved March 16, 2010, from http://www.theaacn.org/position_
papers/AACNPractice_Guidelines.pdf
tion (APA), which is reflected in the 2002 APA ethical
Ferraro, F. R. (Ed.). (2002). Minority and cross-cultural aspects of neuro- principles of psychologists and code of conduct, state
psychological assessment. Lisse, Netherlands: Swets & Zeitlinger. ‘‘Psychologists are aware of and respect cultural, individ-
Fletcher-Janzen, E., Strickland, T. L., & Reynolds, C. R. (Eds.). (2000). ual, and role differences, including those based on age,
Handbook of cross-cultural neuropsychology. New York: Kluwer
gender, gender identity, race, ethnicity, culture, national
Academic/Plenum Publishers.
Heaton, R. K., Miller, S. W., Taylor, M. J., & Grant, I. (2004). Revised
origin, religion, sexual orientation, disability, language,
comprehensive norms for an expanded Halstead-Reitan battery: demo- and socioeconomic status and consider these factors
graphically adjusted neuropsychological norms for African American and when working with members of such groups. Psycholo-
Caucasian adults. Lutz, FL: Psychological Assessment Resources, Inc. gists try to eliminate the effect on their work of biases
International Programs and Perspectives on Traumatic Brain Injury Re-
based on those factors, and they do not knowingly partic-
habilitation. (2007). Journal of Head Trauma Rehabilitation, 22(4),
209–256.
ipate in or condone activities of others based upon such
Lucas, J. A., Ivnik, R., Willis, F., Ferman, T., Smith, G., Parfitt, F., et al. prejudices.’’
(2005). Mayo’s Older African American Normative Studies: Norma- Cultural sensitivity is also reflected in the 2002 APA
tive data for commonly used clinical neuropsychological measures. Guidelines on multicultural education, training, research,
The Clinical Neuropsychologist, 19, 162–183.
practice, and organizational change for psychologists.
Nell, V. (1999). Cross-cultural neuropsychological assessment: Theory and
practice. Mahwah, NJ: Lawrence Erlbaum Associates, Inc.
The APA defines ‘‘multicultural’’ specifically as referring
Romero, H. R., Lageman, S. K., Kamath, V., Irani, F., Sim, A., Suarez, P., to interactions with ‘‘individuals from minority ethnic
et al. (2009). Challenges in the neuropsychological assessment of and racial groups in the United States and the dominant
 Culture Fair Test C 755

European-American culture.’’ This document states that Heaton, R. K., Miller, S. W., Taylor, M. J., & Grant, I. (2004). Revised
comprehensive norms for an expanded Halstead-Reitan Battery: demo-
all individuals are in a social, political, and economic
graphically adjusted neuropsychological norms for African American and
context. Therefore, it is increasingly important for psy- Caucasian Adults. Lutz, FL: Psychological Assessment Resources Inc.
chologists to be aware of the specific needs of individuals Nagra, A., Skeel, R. L., & Sbrage, T. P. (2007). A pilot investigation on the
based on their ethnic/racial heritage and social group effects of stress on neuropsychological performance in Asian-Indians
C
identity. Guidelines relating to research direct psycho- in the United States. Cultural Diversity & Ethnic Minority Issues, 13,
54–63.
logists to ‘‘recognize the importance of conducting cul-
Smith, G. E., Ivnik, R. J., & Jucan, J. (2008). Assessment techniques:
ture-centered and ethical psychological research among tests, test batteries, norms and methodological approaches. In
persons from ethnic, linguistic, and racial minority J. E. Morgan, & J. H. Ricker (Eds.), Textbook of clinical neuropsycho-
backgrounds.’’ logy (pp. 38–57). New York: Taylor & Francis.
A second area of cultural sensitivity that directly
relates to neuropsychology is the impact of culture on
testing and on normative data. It is important that an
individual examinee’s test performance be related to indi-
viduals of similar backgrounds. For example, the norma- Culturally Reduced Test
tive group of an elderly, well-educated African American
man should closely match his background. Without close ▶ Culture Fair Test
matching of cultural, demographic, and educational
background, unacceptable problems with misclassifica-
tion of normal test results as abnormal can result in
misdiagnosis of the patient. There is evidence that exam-
iners belonging to a culture different from that of the
examinee can elicit some anxiety, which may have a dele-
Culture Fair Test
terious effect on test scores on more demanding cognitive
G LEN E. G ETZ
tasks (Nagra, Skeel, & Sbrage, 2007). Additionally, cultural
Allegheny General Hospital
background, demographics and educational history, can
Pittsburgh, PA, USA
have a sizeable impact on normative data. Smith, Ivnik
and Jucan (2008) discuss the development of norms spe-
cifically for older adults on commonly used neuropsy-
Synonyms
chological tests. They subsequently developed more
specific norms for older African Americans, as it was
Culture free test; Culturally reduced test
found that culture had a significant impact on normative
data. Heaton, Miller, Taylor and Grant (2004) have pub-
lished norms that take into account age, education, and
cultural background. This area of cultural sensitivity plays Definition
an important role in neuropsychology in terms of diag-
nosis and test evaluation. Culture fair test is a test that is equally fair to all cultural
groups. Fairness is related to a lack of bias in the inter-
pretation or use of a test to classify or diagnose. In a
Cross References culture fair test, the validity of the interpretation is
similar across different cultural groups. It is unlikely
▶ Cultural Diversity that any test can entirely eliminate the influence of
▶ Normative Data learning and cultural experience, given that the test con-
tent, language, directions, and validity criteria are cul-
turally bound. However, avoiding culturally loaded
References and Readings items, items that are found to be unfair to certain groups
of people, increases the likelihood of it being a culturally
American Psychological Association. (2002). Ethical principals of psychol-
fair test. Culturally loaded items, such as those that
ogists and code of conduct.
American Psychological Association. (2002). Guidelines on multicultural
utilize pictures or general information that are differen-
education, training, research, practice and organizational change for tially prevalent for certain cultures, decrease the likeli-
psychologists. hood of a culturally fair test.
756 C Culture Free Test

Cross References is part of the occipital lobe, corresponding to Broadmann

area 17. Pyramidal cells in the cuneus (striate cortex)
▶ Cultural Sensitivity project to extrastriate cortices (Broadmann areas 18
▶ Raven’s Progressive Matrices and 19). The cuneus consists of both striatal and extra-
striatal visual cortex consisting of five layers. The striatal
areas are largely posterior and are idiotypic homomodal
(Mesulam’s classification), while the extrastriatal areas
References and Readings
contain heterotypic cell types that respond to more com-
plex visual information. The cuneus receives input from
Jensen, A. R. (1974). How biased are culture-loaded tests? Genetic
Psychology Monographs, 90, 185–244.
the contralateral superior retina corresponding to the
Scarr, S. (1994). Culture fair and culture free test. In R. J. Sternberg (Ed.), lower visual field. From the extrastrial areas of cuneus,
Encyclopedia of human intelligence. New York: Macmillan. information is processed through both ventral and dorsal
pathways. The dorsal pathway is particularly important
for higher spatial analysis and visual integration.

Culture Free Test Function

The cuneus plays as essential role in primary visual proces-

▶ Culture Fair Test
sing. The striatal regions that contain primary visual pro-
cessing areas contain neurons with small receptive fields
that are sensitive to very basic visual frequency information
related to position, local orientation, spatial-frequency, and
color (Beason-Held et al., 1998; Jeannerod, 2004; Ulbert,
Cuneate Nucleus Karmos, Heit, & Halgren, 2001; Ungerleider & Pribram,
1977). However, more anterior to the primary visual areas
▶ Nucleus Cuneatus are neurons that respond to more complex information
contained in the visual information processed by the
primary receptors (Ungerleider & Haxby, 1994). Accord-
ingly, the cuneus plays a role in both primary and second-
ary visual processing. Extrastriatal areas of the cuneus are
known to respond to reward, anticipatory, attention, and
Cuneus working memory manipulations, and there is even evi-
dence that posterior striatal areas respond to attentional
R ONALD A. C OHEN
signals, providing evidence that this cortical plays some
Brown University
role in higher cognitive function involving basic visual
Providence, RI, USA
information.

Synonyms
Illness
Broadmann area 17
Damage to the cuneus would typically occur among
patients experiencing focal brain lesions. Most often
such lesions occur secondary to cerebral infarction
Structure (stroke) typically involving the posterior cerebral circula-
tion, though neurosurgery to remove neoplasm may re-
The term cuneus comes from the Latin term for wedge, sult in focal damage to the cuneus as well. Some atypical
which reflects the shape of this occipital brain area. The neurodegenerative diseases are also known to cause tissue
cuneus is a wedge-shaped cortical area located in the loss in this occipital area. The effects of focal damage to
medial occipital gyri, superior to the calcarine fissure the cuneus are known primarily from experimental abla-
and posterior to the parietal–occipital fissure. The cuneus tion in primate studies and to some extent from single-
 Cuneus C 757

tral
Cen
us
sulc Paracentr
al

eu
s lobule Su
n p fr
cu ont
ae al g
Pr Cing
ulate yru
s
C
Pa Cingulate gyrus sul
cus
r ie
to-
oc m
callosu
Cuneus Corpus
c ip.

nix
For
Fi

Fissure
ss
ur
e

y
tor
r in

Isthmus fac
rol
lca

Lingual gyrus Pa ea
Ca

Hippo Uncus a r
camp
al gyr
Fusif us
Infr orm
Inf. T temp. gyrus
emp.
Gyru
s sulcus

Cuneus. Figure 1 Sagital illutration showing the cuneus in the posterior cortex

case studies of stroke. Posterior cuneus lesions tend to ▶ ‘What System’

disrupt primary visual perception, particularly response ▶ ‘Where System’
to stimuli occurring in the lower visual fields. Damage to
more anterior areas of the cuneus also affects visual func-
tions (e.g., movement perception), though often for
higher level operations involved in object perception and References and Readings
spatial analysis, including attention (De Weerd, Peralta,
Desimone, & Ungerleider, 1999). Beason-Held, L. L., Purpura, K. P., Krasuski, J. S., Maisog, J. M., Daly,
Interestingly, there is also evidence that cuneus vol- E. M., Mangot, D. J., et al. (1998). Cortical regions involved in visual
texture perception: A fMRI study. Brain Research Cognitive Brain
ume is related to other behavioral processes not obviously
Research, 7(2), 111–118.
tied in a direct way to visual processing. For example, one Crockford, D. N., Goodyear, B., Edwards, J., Quickfall, J., & el-Guebaly, N.
recent study found greater cuneus volume to be associated (2005). Cue-induced brain activity in pathological gamblers.
with greater inhibitory control among patients with bipo- Biological Psychiatry, 58(10), 787–795.
lar disorder affective disorder (Haldane, Cunningham, De Weerd, P., Peralta, M. R., III, Desimone, R., & Ungerleider, L. G.
(1999). Loss of attentional stimulus selection after extrastriate corti-
Androutsos, & Frangou, 2008). Another study found
cal lesions in macaques. Nature Neuroscience, 2(8), 753–758.
that compulsive gamblers had increased activity in dorsal Haldane, M., Cunningham, G., Androutsos, C., & Frangou, S. (2008).
visual processing pathways, including the cuneus when Structural brain correlates of response inhibition in Bipolar Disorder I.
compared with controls (Crockford, Goodyear, Edwards, Journal of Psychopharmacology, 22(2), 138–143.
Quickfall, & el-Guebaly, 2005). Whether such findings Jeannerod, M. (2004). Visual and action cues contribute to the self-other
distinction. Nature Neuroscience, 7(5), 422–423.
reflect a specific role of the cuneus in these psychiatric
Ulbert, I., Karmos, G., Heit, G., & Halgren, E. (2001). Early discrimina-
disorders versus more incidental findings needs to be tion of coherent versus incoherent motion by multiunit and synaptic
determined in future investigations. activity in human putative MT + . Human Brain Mapping, 13(4),
226–238.
Ungerleider, L. G., & Haxby, J. V. (1994). ‘‘What’’ and ‘‘where’’ in the
human brain. Current Opinion in Neurobiology, 4(2), 157–165.
Cross References
Ungerleider, L. G., & Pribram, K. H. (1977). Inferotemporal versus
combined pulvinar-prestriate lesions in the rhesus monkey: Effects
▶ Feature Detection on color, object and pattern discrimination. Neuropsychologia,
▶ Spatial Frequency Analysis 15(4–5), 481–498.
758 C Cushing’s Syndrome

peripheral circulation and reaches cells in the cortex of the

Cushing’s Syndrome adrenal gland where cortisol biosynthesis is initiated. Cor-
tisol itself exerts negative feedback control on ACTH and
I SABELLE B OURDEAU 1, H ÉLÈNE F ORGET 2 CRH secretion, maintaining a normal secretion rate in case
1
CHUM-Hôtel-Dieu of HPA activation, in stress for example (Fig. 1). ACTH is
Montréal, QC, Canada released physiologically in a series of secretory episodes,
2
Université du Québec en Outaouais followed by an equal number of cortisol bursts in plasma.
Gatineau, QC, Canada Thus, plasma cortisol levels are maximum in the early
morning hours around awakening, gradually decline
throughout the morning, and reach nadir values late in
Short Description or Definition the evening. Midnight serum cortisol >200 nmol/L strong-
ly suggests the diagnosis of CS (Stewart, 2008). Variations
Endogenous Cushing’s syndrome (CS) is a rare disorder of ACTH and cortisol values constitute the normal cir-
occurring in about 0.7–2.4 per million population per cadian rhythm. CS is caused by pituitary or adrenal
year (Newell-Price, Bertagna, Grossman, & Nieman, abnormalities or may be secondary to ectopic ACTH or
2006). CS includes symptoms and signs resulting from CRH secretion by various nonpituitary tumors, such as
chronic supraphysiological exposure to glucocorticoids lung carcinoma. CS is classified into ACTH-dependent
(GC). The classical clinical features of CS are centripetal and -independent causes which are described in Table 1.
obesity with abnormal fat distribution, mainly affecting Cushing’s disease refers to CS due to excessive pituitary
the face, neck, trunk, and abdomen, and sparing the ACTH secretion from pituitary tumors.
extremities. Other findings are facial plethora, easy
bruisability, purple abdominal striae, hirsutism, muscle
weakness, hypertension, and glucose intolerance (Stewart, Evaluation or Diagnosis
2008). In addition, mood alterations and psychiatric
diseases – mainly depressive and anxiety disorders – as The diagnosis of endogenous CS may be challenging and
well as cognitive impairment are highly prevalent in CS require the expertise of an endocrinologist. Authors will
patients (Bourdeau et al., 2005). briefly discuss the evaluation and various tests used to
The principal aim of this chapter is to present diagnose CS. The first step is to confirm CS by biochemi-
psychiatric and cognitive data on adult patients with CS. cal investigation. Then, the cause of the disease should be
The recognition of psychoneurological abnormalities
associated with hypercortisolism is of clinical importance
in the management of patients affected by CS.
Hypothalamus

Etiology
CRH
Exogenous CS refers to iatrogenic CS resulting from chron-
ic GC therapy. GC, which have potent anti-inflammatory Pituitary
and immunologic actions, are widely used for the treat-
ment of various diseases such as inflammatory bowel
disease, asthma, rheumatoid arthritis, and organ transplan- ACTH
tation. Thus, exogenous CS is the most common form of
CS. Endogenous CS may be caused by dysregulation at
Adrenal gland
various levels of the hypothalamic–pituitary–adrenal axis
(HPA), resulting in cortisol overproduction. The regulation
of cortisol synthesis and secretion is mediated by the hypo- Cortisol
thalamus, the pituitary, and the adrenal glands. Corticotro-
pin (ACTH) is synthesized and secreted by corticotrophs of Cushing’s Syndrome. Figure 1 Schematic representation of
the pituitary which are mainly regulated by two hypotha- the hypothalamus–pituitary axis. Normally cortisol negatively
lamic hormones, corticotropin-releasing hormone (CRH), regulates corticotropin-releasing hormone (CRH) and ACTH
and arginine-vasopressin. Pituitary ACTH is secreted in the secretion
 Cushing’s Syndrome C 759

Cushing’s Syndrome. Table 1 Classification of the etiologies and cognition, has increased considerably in the recent
of endogenous Cushing’s syndrome (CS) years. McEwen, Weiss, and Schwartz (1968) demonstrated
the presence of glucocorticoid receptors (GR) in the rat
ACTH-dependent CS (80% of cases)
brain. Loss of brain volume was documented in patients
Pituitary adenoma (Cushing’s disease) (80%)
with endogenous and exogenous CS (Bourdeau et al., C
Ectopic ACTH or corticotropin-releasing hormone (CRH)
2002). In addition, cerebral magnetic resonance spectros-
secretion from nonpituitary neoplasms (20%)
copy revealed abnormalities of cerebral metabolism in
ACTH-independent CS (20% of cases) patients with CS (Khiat et al., 1999).
Adrenal adenoma (60%) Psychiatric disturbances occur in patients with both
Adrenal carcinoma (40%) exogenous and endogenous CS. Interestingly, patients
Bilateral ACTH-independent macronodular adrenal with endogenous depression frequently have high corti-
hyperplasia (rare) sol levels, and present HPA axis dysregulation, disclosed
Bilateral micronodular adrenal hyperplasia (primary by abnormal suppression on the dexamethasone test.
pigmented nodular adrenocortical disease and However, diurnal rhythm is usually maintained in de-
nonpigmented adrenal hyperplasia) (rare) pressed patients, and they do not develop physical signs
of CS. CS is also associated with an increased prevalence
of cognitive impairments, particularly of attention,
learning, and memory. Patients with CS represent a
identified. During the investigation, it is important to natural model that illustrates the interactions between
evaluate patients for other illnesses, drugs, alcohol, or hypercortisolism and brain function. The following sec-
depression. All these conditions may lead to misinterpre- tion focuses on the psychiatric and neuropsychological
tation of the endocrine test results. The overnight 1-mg anomalies in CS.
dexamethasone suppression test, a screening tool for the
diagnosis of CS, consists of administering 1 mg of dexa-
methasone at bedtime (23:00 h) with measurement of Psychiatric Disorders Associated with CS
plasma cortisol the following morning (08:00–09:00 h).
Normal subjects should suppress plasma cortisol to less Depression is a frequent feature of CS. In fact, several
than 50 nmol/L. Measurement of free cortisol in 24- reports indicate that more than 50% of CS patients pres-
h urine collection is useful to confirm the diagnosis; ent severe depressive symptoms that reach the threshold
values fourfold greater than the upper limit of normal of a major depressive disorder. Haskett (1985) observed a
are highly suggestive of CS. More recently, late-night lifetime history of psychiatric symptoms and signs in
salivary cortisol has proven useful in the diagnosis of CS patients with proven CS. He found that the majority of
(Nieman et al., 2008). Once a diagnosis of CS is con- them experienced psychiatric disturbances that closely
firmed, the next step is to establish the etiology. Plasma resembled typical syndromes, with episodes of major
ACTH will distinguish between ACTH-dependent and - affective disorder (endogenous depression, mania, or
independent CS. ACTH values lower than 1.1 pmol/L hypomania). Moreover, Haskett (1985) noted that there
indicate ACTH-independent CS, and CT imaging of the were no significant differences between pituitary-
adrenal glands should be performed (Newell-Price et al., dependent and -independent forms of CS in the occur-
2006). ACTH values above 3.3 pmol/L suggest ACTH- rence of major depression. His observations were later
dependent CS, and further endocrine investigations confirmed by independent investigations (Kelly, 1996;
should be undertaken, including magnetic resonance im- Sonino, Fava, Belluardo, Girelli, & Boscaro, 1993). Using
aging of the pituitary glands and other tests that are DSM-III criteria (American Psychiatric Association,
beyond the scope of this chapter. 1980), Hudson, Hudson, Griffing, Melby, and Pope
(1987) reported a high lifetime diagnosis of mood
disorders in CS patients, of whom 14% were assessed to
Psychiatric Diseases and have major affective disorder. Loosen, Chambliss, DeBold,
Neuropsychological Disturbances Shelton, and Orth (1992) recognized major depressive
Associated with CS disorder in 68% of adult patients with CS. In addition,
this disorder was frequently associated with anxiety
Understanding the importance and complexity of adrenal disorder (generalized anxiety disorder and/or panic dis-
hormones impacting cerebral function, particularly affect order), indicating a syndrome of anxious depression in
760 C Cushing’s Syndrome

patients with active CS (Loosen et al., 1992). Focusing on reported generalized impairment of cognitive functions
Cushing’s disease, Sonino, Fava, Raffi, Boscaro, and Fallo (decreased concentration and memory, perceptual distor-
(1998) found major depression in more than half of their tions). More recently, Starkman, Gebarski, Berent, and
patients studied. Moreover, major depression was signifi- Schteingart (1992) observed moderate-to-severe deficits
cantly correlated with older age, female gender, higher in a wide variety of language and nonverbal subtests
pretreatment urinary cortisol levels, and more severe among more than two-thirds of their CS patients.
clinical conditions. Kelly, Kelly, and Faragher (1996) Difficulties with reasoning ability, comprehension, and
reported that some patients with CS were diagnosed to processing of new information also were found. Deficits
have depression and were more depressed than patients in these areas of cognition were confirmed in a recent
with other pituitary tumors. Concentrating on the controlled study of 19 CS patients (Forget, Lacroix,
question of whether depression in CS more consistently Somma, & Cohen, 2000). In fact, memory was the most
resembles any of the clinical subcategories, Dorn et al. studied function in CS because the emphasis was on the
(1995) established that patients with active endogenous hippocampus which is rich in GR. However, the distribu-
CS exhibited significant psychopathology, expressed pri- tion of GR in many areas of the cerebral cortex suggests
marily by ‘‘atypical’’ depression. This concept of atypical that extrahippocampic sites could also be the target of
depression refers to the presence of weight gain or cortisol, and generalized impairment of cognitive func-
increased appetite, fatigue, hypersomnia, leaden paralysis, tions after chronic hypercortisolism may be related to this
and longstanding interpersonal rejection sensitivity wide dispersion of GR.
(American Psychiatric Association, 1994).
In summary:
Treatment
1. More than 50% of patients with CS report severe
depressive symptoms
The goal of CS treatment is to correct the hypersecretion
2. There are no significant differences between ACTH-
of adrenal hormones. In most cases, tumor-specific
dependent and -independent forms of CS in the
surgery will be performed. In Cushing’s disease, pituitary
occurrence of major depression
tumors should be resected, and in adrenal CS adrenalec-
3. Major depressive disorders are commonly associated
tomy performed. In cases of ectopic ACTH secretion
with anxiety disorders
secondary to benign tumors, the latter should be
4. Major depression is significantly correlated with
removed; but in most cases, there are metastatic malig-
older age, female gender, higher pretreatment urinary
nant tumors. If surgery is unsuccessful, drugs that block
cortisol levels, and more severe clinical conditions
steroid synthesis may be administrated to achieve
5. A high prevalence of atypical depression features is
eucortisolism (Biller et al., 2008; Stewart, 2008).
seen in CS

Neuropsychological Disorders Associated Natural History, Prognostic Factors,

with CS Outcomes

Neuropsychological disorders have been detected in about The reversibility of brain volume loss after the correction
two-thirds of patients with CS. The first such investiga- of hypercortisolism in patients affected by CS was previ-
tion evaluated unselected CS patients on the Michigan ously demonstrated (Bourdeau et al., 2002). Similarly,
Neuropsychological Test Battery (Whelan Schteingart, treatment of hypercortisolism is often efficacious in
Starkman, & Smith, 1980). This test battery included decreasing the depressive components of illness. Signifi-
standardized and objective measures with a broad range cant improvement in depressive symptoms was observed
of discrete language, verbal and nonverbal reasoning, when patients with CS were assessed by psychometric
auditory and visual memory, and sensory and motor methods before and after the treatment of their endo-
functions. The study revealed diffuse bilateral cerebral crine condition, (Dorn et al., 1997; Forget, Lacroix, &
dysfunction in CS with impairment in nonverbal, visual– Cohen, 2002; Kelly et al., 1996; Starkman, Giordani,
ideational, visual-memory, and spatial–constructional Gebarski, & Schteingart, 2006; Starkman, Schteingart, &
abilities. Starkman, Schteingart, and Schork (1981) Schork, 1986). In a longitudinal study of depressive and
 Cushing’s Syndrome C 761

neuropsychological symptoms in CS, Forget et al. (2002) References and Readings

reported a significant improvement in Beck Depression
Inventory scores 1 year after the correction of hypercorti- van Aken, M. O., Pereira, A. M., Biermasz, N. R., van Thiel, S. W.,
solism. More recently, Starkman et al. (2006) showed Hoftijzer, H. C., Smit, J. W. A., et al. (2005). Quality of life in patients
after long-term biochemical cure of Cushing’s disease. The Journal of
significant changes in depression and anxiety subscales C
Clinical Endocrinology and Metabolism, 90, 3279–3286.
on SCL-90-R after the successful treatment of hypercor- American Psychiatric Association. (1980). Diagnostic and statistical
tisolism in CS. However, psychological distress does not manual of mental disorders (3rd ed.). Washington, DC: American
always disappear upon proper treatment. For example, Psychiatric Association.
Dorn et al. (1997) disclosed that the incidence of atypical American Psychiatric Association. (1994). Diagnostic and statistical
manual of mental disorders (4th ed.). Washington, DC: American
depression progressively decreased after the correction of
Psychiatric Association.
hypercortisolism – this disorder, however, continued to be Biller, B. M., Grossman, A. B., Stewart, P. M., et al. (2008). Treatment of
the prevailing psychiatric diagnosis after the successful adrenocorticotropin-dependent Cushing’s syndrome: A consensus
cure of CS. It is likely that the psychopathology symptoms statement. The Journal of Clinical Endocrinology and Metabolism,
still seen after the correction of CS may be related to the as 93, 2454–2462.
Bourdeau, I., Bard, C., Forget, H., Boulanger, Y., & Cohen, H., Lacroix, A.
yet unexplored interaction between endocrine and
(2005). Cognitive function and cerebral assessment in patients with
psychosocial factors. Indeed, despite the correction of Cushing’s syndrome. In J. W. Findling & H. Raff (Eds.), Cushing’s
hypercortisolism, patients with CS experience a consider- Syndrome. Endocrinology and Metabolism Clinics of North America,
able decrease in quality of life, even after long-term cure 32(2), 441–458.
(Lindsay, Nansel, Baid, Gumowski, & Nieman, 2006; van Bourdeau, I., Bard, C., Noel, B., Leclerc, I., Cordeau, M. P., Bélair, M.,
et al. (2002). Loss of brain volume in endogenous Cushing’s
Aken et al., 2005). The authors postulated that there
syndrome and its reversibility after correction of hypercortisolism.
might be irreversible changes in central neural function The Journal of Clinical Endocrinology and Metabolism, 87,
in these patients (Heald et al., 2004). 1949–1954.
Few studies have objectively examined the reversibility Dorn, L. D., Burgess, E. S., Dubbert, B., Simpson, S. E., Friedman, T.,
of cognitive disorders after successful treatment. Mauri Kling, M., et al. (1995). Psychopathology in patients with endoge-
nous Cushing’s syndrome: ‘Atypical’ or melancholic features.
et al. (1993) demonstrated significant amelioration in
Clinical Endocrinology, 43, 433–442.
verbal memory performance and attentive and visuomo- Dorn, L. D., Burgess, E. S., Friedman, T. C., Dubbert, B., Gold, P. W., &
tor functions 6 months after surgery. No changes in other Chrousos, G. P. (1997). The longitudinal course of psychopathology
cognitive functions could be detected. On the other hand, in Cushing’s syndrome after correction of hypercortisolism. The
no differences between Cushing’s patients and their Journal of Clinical Endocrinology and Metabolism, 82, 912–919.
Dorn, L. D., & Cerrone, P. (2000). Cognitive function in patients with
controls were found in cognitive function 12 months
Cushing syndrome. Clinical Nursing Research, 9, 420–440.
post-treatment (Dorn & Cerrone, 2000). Forget et al. Forget, H., Lacroix, A., & Cohen, H. (2002). Persistent cognitive im-
(2002) evaluated subjects who presented with CS on a pairment following surgical treatment of Cushing’s syndrome. Psy-
battery of tests, including attention, visuospatial proces- choneuroendocrinology, 27, 367–383.
sing, memory, reasoning, and verbal fluency. Except for Forget, H., Lacroix, A., Somma, M., & Cohen, H. (2000). Cognitive
decline in patients with Cushing’s syndrome. Journal of the Interna-
one task of visual organization, the results showed little
tional Neuropsychological Society, 6, 20–29.
change in performance, suggesting that prolonged Haskett, R. F. (1985). Diagnostic categorization of psychiatric disturbance
exposure to high cortisol levels can cause long-lasting in Cushing’s syndrome. The American Journal of Psychiatry, 142,
deleterious effects on cognitive function. The data indi- 911–916.
cate that correction of hypercortisolism is not necessarily Heald, A. H., Ghosh, S., Bray, S., Gibson, C., Anderson, S. G., Buckler, H.,
et al. (2004). Long-term negative impact on quality of life in patients
correlated with short-term improvement in cognitive
with successfully treated Cushing’s disease. Clinical Endocrinology,
function. More recently, Hook et al. (2007) postulated 61, 458–465.
that the age of Cushing’s patients appeared to be a signifi- Hook, J. N., Giordani, B., Schteingart, D. E., Guire, K., Giles, J., Ryan, K.,
cant factor determining when and how cognitive function et al. (2007). Patterns of cognitive change over time and relationship
manifested signs of recovery. to age following successful treatment of Cushing’s disease. Journal of
International Neuropsychological Society, 13, 21–29.
In conclusion, the psychiatric and neuropsychological
Hudson, J. I., Hudson, M. S., Griffing, G. T., Melby, J. C., & Pope, H. G.,
disturbances associated with CS may compromise quality Jr. (1987). Phenomenology and family history of affective disorder
of life and produce a broad array of handicaps and in Cushing’s disease. The American Journal of Psychiatry, 144,
disabilities. Moreover, these functional impairments may 951–953.
persist long after successful treatment and in clinical Kelly, W. F. (1996). Psychiatric aspects of Cushing’s syndrome. QJM:
Monthly Journal of the Association of Physicians, 89, 543–551.
remission. Thus, such symptoms warrant clinical attention.
762 C Customized Employment

Kelly, W. F., Kelly, M. J., & Faragher, C. (1996). A prospective study

of psychiatric and psychological aspects of Cushing’s syndrome. Customized Job Retention
Clinical Endocrinology, 45, 715–720.
Khiat, A., Bard, C., Lacroix, A., et al. (1999). Brain metabolic alterations Services
in Cushing’s syndrome as monitored by proton magnetic resonance
spectroscopy. NMR in Biomedicine, 12, 357–363. A MY J. A RMSTRONG
Lindsay, J. R., Nansel, T., Baid, S., Gumowski, J., & Nieman, L. K. (2006). Virginia Commonwealth University
Long-term impaired quality of life in Cushing’s syndrome despite
Richmond, VA, USA
initial improvement after surgical remission. The Journal of Clinical
Endocrinology and Metabolism, 91, 447–453.
Loosen, P. T., Chambliss, B., DeBold, C. R., Shelton, R., & Orth, D. N.
(1992). Psychiatric phenomenology in Cushing’s disease. Pharma- Definition
copsychiatry, 25, 192–198.
Mauri, M., Sinforiani, E., Bono, G., Vignati, F., Berselli, M. E.,
Job retention is the process of facilitating the tenure of an
Attanasio, R., et al. (1993). Memory impairment in Cushing’s
disease. Acta Neurologica Scandinavica, 87, 52–55. individual in a particular employment setting. Customized
McEwen, B. S., Weiss, J. M., & Schwartz, L. S. (1968). Selective retention job retention services begin with the completion of a thor-
of corticosterone by limbic structures in rat brain. Nature, 220, ough assessment to determine the individual’s strengths,
911–912. interests and preferences, and support needs. The results of
Newell-Price, J., Bertagna, X., Grossman, A. B., & Nieman, L. K. (2006).
the assessment will inform the job development and selec-
Cushing’s syndrome. Lancet, 367, 1605–1617.
Nieman, L. K., Biller, B. M., Findling, J. W., et al. (2008). The diagnosis tion process. Placement and retention plans are individua-
of Cushing’s syndrome: An endocrine society clinical practice lized; however, general guidelines insure job retention
guideline. The Journal of Clinical Endocrinology and Metabolism, including promoting consumer choice and involvement,
93, 1526–1540. identifying jobs that are meaningful in terms of wages
Sonino, N., Fava, G. A., Belluardo, P., Girelli, M. E., & Boscaro, M. (1993).
earned, benefits, inclusion, and opportunities for career
Course of depression in Cushing’s syndrome: Response to treatment
and comparison with Graves’ disease. Hormone Research, 39, growth, and the provision of long-term supports. Research
202–206. indicates that the provision of ongoing supports increases
Sonino, N., Fava, G. A., Raffi, A. R., Boscaro, M., & Fallo, F. (1998). the employment retention rate of individuals with signifi-
Clinical correlates of major depression in Cushing’s disease. Psycho- cant disabilities. Retention services may also include sup-
pathology, 31, 302–306.
ports addressing skill acquisition, production demands, the
Starkman, M. N., Gebarski, S. S., Berent, S., & Schteingart, D. E. (1992).
Hippocampal formation volume, memory dysfunction, and cortisol development of soft skills such as interpersonal communi-
levels in patients with Cushing’s syndrome. Biological Psychiatry, 32, cation, problem-solving skills and responding to the daily
756–765. expectations and stressors associated with the respective
Starkman, M. N., Giordani, B., Gebarski, S. S., & Schteingart, D. E. position. Retention services must also ensure that the
(2006). Improvement in mood and ideation associated with increase
needs of the employer are understood and met.
in right caudate volume. Journal of Affective Disorders, 101, 139–147.
Starkman, M. N., Schteingart, D. E., & Schork, M. A. (1981). Depressed Job retention is directly related to quality of life, as
mood and other psychiatric manifestations of Cushing’s syndrome: reported by individuals with disabilities. Employment
Relationship to hormone levels. Psychosomatic Medicine, 43, 3–18. statistics (i.e., employment rate, ability to stay in a job
Starkman, M. N., Schteingart, D. E., & Schork, M. A. (1986). Cushing’s overtime) document the need for the provision of custo-
syndrome after treatment: Changes in cortisol and ACTH levels, and
mized job retention services. Improved job tenure rates
amelioration of the depression syndrome. Psychiatry Research, 19,
177–188. for individuals with disabilities are a primary objective for
Stewart, P. M. (2008). The adrenal cortex. In P. R. Larsen, H. M. Kronen- rehabilitation services.
berg, S. Melmed, & K. S. Polonsky (Eds.), Williams textbook of
endocrinology, pp. 445–503.
Whelan, T. B., Schteingart, D. E., Starkman, M. N., & Smith, A. (1980). Cross References
Neuropsychological deficits in Cushing’s syndrome. The Journal of
Nervous and Mental Disease, 168, 753–757.
▶ Customized Employment
▶ Supported Employment

References and Readings

Customized Employment Griffin, C., Hammis, D., & Geary T. (2007). The job developer’s handbook:
Practical tactics for customized employment. Baltimore, MD: Paul
▶ Supported Employment H. Brookes.
 CVLT-C C 763

Rubin, S., & Roessler, R. (2008). Foundations of the vocational rehabilita- to assess the disorder must be reliably able to measure the
tion process. Austin, TX: Pro-Ed.
particular abilities, taking into consideration the span
Szymanski, E. M., & Parker, R. M. (2003). Work and disability: Issues and
strategies in career development and job placement (2nd ed.). Austin,
of the standard error, to place an education-altering
TX: Pro-Ed. label on that child. If such standards are not followed,
Wagner, C. C., Armstrong, A. J., Fraser, R. T., Vandergoot, D., & Thomas, then clinicians run the risk of basing a decision on a C
D. F. (2006). Evidence-based employment practices in vocational ‘‘false-positive’’ (the discovery of a limitation when none
rehabilitation. In K. J. Hagglund & A. W. Heinemann (Eds.), Applied
exists in actuality) or a ‘‘false-negative’’ (the missing of
disability and rehabilitation research. New York: Springer.
Wehman, P., Inge, K. J., Revell, G., & Brooke, V. (2007). Real work for real
a limitation when one truly exists).
pay: Inclusive employment for people with disabilities. Baltimore, MD: To consider an example, a cutoff score may be the
Paul H. Brookes. score differentiating between intact performance and im-
pairment on a particular test. To speak in terms of diag-
nosing cognitive impairment, in a normal distribution of
scores, a cutoff score would be any score below 95% which
is obtained by the intact group within a particular stan-
Cut Scores dardization sample.
Clinicians may adjust cutoff scores because of individ-
▶ Cut Off Scores, Cutting Scores ual or cultural variables that render the reliability of a
test nonapplicable to the individual or sample being
assessed. Otherwise, the clinician could run the risk of
pathologizing an individual who does not truly exhibit
the pathology.

Cut Off Scores, Cutting Scores

S ANDRA B ANKS References and Readings
Allegheny General Hospital
Pittsburgh, PA, USA Nunnally, J. C., & Bernstein, I. H. (1994). Psychometric theory (3rd ed.).
New York: McGraw-Hill.

Synonyms

Cut scores
CVA

Definition ▶ Stroke

Cutoff scores, also referred to as cutting scores, are scores

that differentiate the levels of performance.

CVLT

Current Knowledge ▶ California Verbal Learning Test (California Verbal

Learning Test-II)
The reliability of a measure is an essential factor to con-
sider when using cutoff scores. Nunnally and Bernstein
(1994) suggest that a test must have an internal consis-
tency coefficient of at least 0.90, and ideally above 0.95, to
designate a particular score as a diagnostic cutoff point, CVLT-C
although this might be a high standard. For instance, if a
child is demonstrating a learning disorder, the tests used ▶ California Verbal Learning Test – Children’s Version
764 C Cyst

major role in drug metabolism and is the cause for some

Cyst adverse drug reactions. Metabolism and clearance of a
drug are presumed to be stable, allowing for basic predic-
E THAN M OITRA tions about a drug’s dose, blood levels, and pharmacolog-
Drexel University ical effects. Drugs are typically metabolized by a limited
Philadelphia, PA, USA number of mechanisms, some of these include the P450
enzyme pathways. Drugs, foods, or herbal preparations
that alter the efficiency of those pathways may also alter
Synonyms the plasma concentration of some drugs by inhibiting
or inducing (increasing) the efficiency of a particular
Nodule; Polyp enzymatic pathway. There are drugs/herbs that can simul-
taneously induce and inhibit different isoenzymes
(St. John’s Wort), or simply induce their own metabolism
Definition (carbamazepine).
Although over the counter preparations are less likely
Cyst refers to an abnormal growth of benign cells, typically to be mentioned, some effect P450 enzyme pathways (e.g.,
containing normal cerebrospinal fluid. Central nervous cigarettes or the topical antifungal ketoconazole). Smo-
system cysts may occur as neoplasms or subsequent to kers, for example, may require increased doses of drugs
leptomeningitis, hemorrhage, or surgery. Most patients because cigarette smoking has the ability to induce an
presenting with cyst are asymptomatic, though headache; enzyme that deactivates some medication. As a corollary,
calvarial bulging; intracranial hypertension; craniome- an abrupt cessation of smoking would then increase the
galy; developmental delay; visual loss; precocious puberty; plasma level of these drugs unless and until the dose is
and seizures, with focal neurologic signs can occur. Addi- modified.
tional cognitive consequences may include symptoms of P450 isoenzymes are widely distributed, but often
dementia and inattention. Arachnoid cysts represent the thought of as liver enzymes because the liver metabolizes
most common form of benign cyst and occur in the drugs through oxidation as well as reduction and hydro-
cerebrospinal axis. Size of arachnoid cysts is not directly lysis. The p450 cytochrome system is critical to a number
affected by changes in the ventricular system. of oxidative reactions (the addition of an oxygen molecule
or the removal of hydrogen from a molecule). The P450
Cross References isoenzymes share a heme (iron) cofactor, although they
may use a number of different molecules as a basis for
▶ Neoplasm enzyme reactions. The term cytochrome arose because the
isoenzymes were differentiated by their cellular (cyto)
location and their color (chrome) or wavelength during
spectrophotometric studies. P450 enzymes absorb light at
Cytochrome P450 450 nm. Specific CYP enzyme pathways are noted in
shorthand (e.g., CYP3A4 or CYP 2D6). Typically, authors
N ADIA W EBB include the prefix CYP before a three character alphanu-
Children’s Hospital of New Orleans meric 3A4, but it may be abandoned if the author is
New Orleans, LA, USA writing casually or for an audience familiar with the
terms. The alphanumeric denotes the gene family, sub-
family, and individual gene. The three most common
Synonyms isoenzymes involved in human drug metabolism are
CYP3A4, CYP2D6, and CYP2C9.
P450 isoforms; P450 isoenzymes; P450 system

Definition Cross References

The liver-mediated cytochrome P450 isoenzymes (abbre- ▶ Cmax

viated as CYP) constitute an enzyme family that plays a ▶ p450 Cytochrome System
 Cytotoxic Edema C 765

▶ Pharmacokinetics Stahl, S. M. (2008). Stahl’s essential psychopharmacology: Neuroscientific

basis and practical applications. New York: Cambridge University
▶ Side Effects
Press.

References and Readings C

Brunton, L. B., Lazo, J. S., & Parker, K. L. (Eds.). (2005). Goodman &
Cytotoxic Edema
Gilman’s the pharmacological basis of therapeutics (11th ed.).
New York: McGraw Hill. ▶ Cerebral Edema