BRAIN DAMAGE (CASE STUDY)

AIM: To understand brain damage using a case study (secondary data).

BASIC CONCEPTS
Brain Damage
The basic definition of brain damage is an injury to the brain caused by various conditions
such as head trauma, inadequate oxygen supply, infections, or intracranial hemorrhage. This
damage may be associated with a behavioral or functional abnormality. The brain can be
damaged in many ways and severity. Depending upon the type, location, and severity of any
damage to the brain, the outcome can range from a complete recovery to some amount of
disability or even death.
All traumatic brain injuries are head injuries. But head injury is not necessarily brain injury.
There are two types of brain injury: traumatic brain injury and acquired brain injury. Both
disrupt the brain’s normal functioning.

 Traumatic Brain Injury (TBI) is caused by an external force - such as a blow to the
head that causes the brain to move inside the skull or damages the skull. This in turn
damages the brain.
 Acquired Brain Injury (ABI) occurs at the cellular level. It is most often associated
with pressure on the brain. This could come from a tumor. Or it could result from
neurological illness, as in the case of a stroke.

Causes Of Brain Damage

Six causes of brain damage - brain tumors, cerebrovascular disorders, closed-head injuries,
infections of the brain, neurotoxins, and genetic factors.

1. Brain Tumors. A tumor, or neoplasm (literally, “new growth”), is a mass of cells that
grows independently of the rest of the body. They are almost always benign tumors—
tumors that are surgically removable with little risk of further growth in the body.
Most brain tumors are also infiltrating. Infiltrating tumors are those that grow
diffusely through surrounding tissue. As a result, they are usually malignant tumors;
that is, it is difficult to remove or destroy them completely, and any cancerous tissue
that remains after surgery continues to grow.
2. Cerebrovascular Disorders: Strokes. Strokes are sudden-onset cerebrovascular
disorders that cause brain damage. The symptoms of a stroke depend on the area of
the brain affected, but common consequences of stroke are amnesia, aphasia
(language difficulties), paralysis, and coma.
3. Closed-head Injuries. For the brain to be seriously damaged, it is not necessary for
the skull to be penetrated. In fact, any blow to the head should be treated with extreme
caution, particularly when confusion, sensorimotor disturbances, or loss of
consciousness ensues. Brain injuries produced by blows that do not penetrate the skull
are called closed-head injuries. Contusions are closed-head injuries that involve
damage to the cerebral circulatory system. Such damage produces internal
 hemorrhaging, which results in a hematoma. A hematoma is a localized collection of
clotted blood in an organ or tissue—in other words, a bruise.
4. Infections of the Brain. An invasion of the brain by microorganisms is a brain
infection, and the resulting inflammation is called encephalitis (Bentivoglio, Mariotti,
& Bertini, 2011; Kristensson, 2011).
5. Neurotoxins. The nervous system can be damaged by exposure to any one of a
variety of toxic chemicals, which can enter general circulation from the
gastrointestinal tract, from the lungs, or through the skin (Block & Calderón-
Garcidueñas, 2009). For example, heavy metals such as mercury and lead can
accumulate in the brain and permanently damage it, producing a toxic psychosis
(chronic insanity produced by a neurotoxin).
6. Genetic Factors. Some neuropsychological diseases of genetic origin are caused by
abnormal recessive genes that are passed from parent to offspring. (phenylketonuria,
or PKU.) Inherited neuropsychological disorders are rarely associated with dominant
genes because dominant genes that disturb neuropsychological function tend to be
eliminated from the gene pool—individuals who carry one usually have major
survival and reproductive disadvantages. In contrast, individuals who inherit one
abnormal recessive gene do not develop the disorder, and the gene is passed on to
future generations. Genetic accident is another major cause of neuropsychological
disorders of genetic origin. Down syndrome, which occurs in about 0.15% of births, is
such a disorder.

Neurological Diseases
Five diseases associated with brain damage: epilepsy, Parkinson’s disease, Huntington’s
disease, multiple sclerosis, and Alzheimer’s disease.
1. Epilepsy. The primary symptom of epilepsy is the epileptic seizure, but not all
persons who suffer seizures are considered to have epilepsy. Sometimes, an otherwise
healthy person may have one seizure and never have another (Haut & Shinnar, 2008)
—such a one-time convulsion could be triggered by exposure to a convulsive toxin or
by a high fever.
2. Parkinson’s Disease. Parkinson’s disease is a movement disorder of middle and old
age that affects 1–2% of the elderly population (Venda et al., 2010). It is about 2.5
times more prevalent in males than in females (Lorincz, 2006). The initial symptoms
of Parkinson’s disease are mild—perhaps no more than a slight stiffness or tremor of
the fingers—but they inevitably increase in severity with advancing years. The most
common symptoms of the full-blown disorder are a tremor that is pronounced during
inactivity but not during voluntary movement or sleep, muscular rigidity, difficulty
initiating movement, slowness of movement, and a masklike face. Pain and
depression often develop before the motor symptoms become severe. Parkinson’s
disease seems to have no single cause; faulty DNA, brain infections, strokes, tumors,
traumatic brain injury, and neurotoxins have all been implicated in specific cases
(Pan-Montojo et al., 2010). However, in the majority of cases, no cause is obvious,
and there is no family history of the disorder (Calne et al., 1987). Numerous genes
have been linked to it (Kumar, Djarmati-Westenburger, & Grünewald, 2011).
3. Huntington’s Disease. Huntington’s disease is a progressive motor disorder; but,
unlike Parkinson’s disease, it is rare (1 in 10,000), it has a simple genetic basis, and it
is always associated with severe dementia. The first clinical sign of Huntington’s
 disease is often increased fidgetiness. As the disorder develops, rapid, complex, jerky
movements of entire limbs (rather than individual muscles) begin to predominate.
Eventually, motor and intellectual deterioration become so severe that sufferers are
incapable of feeding themselves, controlling their bowels, or recognizing their own
children. There is no cure; death typically occurs about 15 years after the appearance
of the first symptoms. Huntington’s disease is passed from generation to generation
by a single mutated dominant gene, called huntingtin (Milnerwood & Raymond,
2010). The protein it codes for is known as the huntingtin protein. Because the gene is
dominant, all individuals carrying the gene develop the disorder, as do about half their
offspring.
4. Multiple Sclerosis (MS). Multiple sclerosis (MS) is a progressive disease that attacks
the myelin of axons in the CNS. It is particularly disturbing because it typically
attacks young people just as they are beginning their adult life. First, there are
microscopic areas of degeneration on myelin sheaths (Lucchinetti et al., 2011); but
eventually damage to the myelin is so severe that the associated axons become
dysfunctional and degenerate (Nave, 2010; Siffrin et al., 2010). Multiple sclerosis is
an autoimmune disorder—a disorder in which the body’s immune system attacks part
of the body, as if it were a foreign substance. In multiple sclerosis, myelin is the focus
of the faulty immune reaction.
5. Alzheimer’s Disease. Alzheimer’s disease is the most common cause of dementia
(Matthew et al., 2011). It sometimes appears in individuals as young as 40, but the
likelihood of its development becomes greater with advancing years. About 10% of
people over the age of 65 suffer from the disease (Turner, 2006). Alzheimer’s disease
is progressive. Its early stages are often characterized by a selective decline in
memory, deficits in attention, and personality changes; its intermediate stages are
marked by confusion, irritability, anxiety, and deterioration of speech; and in its
advanced stages, the patient deteriorates to the point that even simple responses such
as swallowing and controlling the bladder are difficult. Alzheimer’s disease is
terminal.

Neuroplasticity
Neuroplasticity is the capacity of local neuronal networks and neural systems to change their
topography and local architecture in response to new information, sensory stimulation,
development, damage, or dysfunction.
Although neural networks also exhibit modularity and carry out specific functions, they retain
the capacity to deviate from their usual functions and to reorganize themselves.
In fact, for many years, it was considered dogma in the neurosciences that certain functions
were hard-wired in specific, localized regions of the brain that any incidents of brain damage
or recovery were mere exceptions of the rule. However, since the 1970s and 1980s,
neuroplasticity has gained wide acceptance throughout the scientific community as a
complex, multifaceted, fundamental property of the brain.

Therapeutic Approaches To Recovery After Brain Damage

1. Rehabilitation procedures consist of a variety of experiential, behavioral, and
psychological therapies.
 2. Pharmacological therapies are intended to promote recovery in the immediate post-
surgery period.
3. Brain stimulation increases brain activity.
4. Brain-tissue transplants and stem-cell-induction techniques are being developed
in the hope of restoring healthy brain function.
5. Diet provides the building blocks for plastic changes.
Rehabilitation procedures are used widely, with mixed results; drug therapy, stimulation,
implantation techniques, and diet are moving past the animal-experimentation stage into
preliminary clinical trials.
Rehabilitation
It would seem logical that people with brain injuries should be placed in some sort of
rehabilitation program. Surprisingly, however, neuroscientists as yet have little information
concerning the value of different kinds of rehabilitation, the optimal timing for initiating a
program, or even the optimal duration of rehabilitative therapy. Although both speech and
physical therapies are often assumed to be effective, the role of any specific therapy—the
kinds of changes that it brings about and how or why they take place—is a matter of debate.
Consider, for example, that patients undergoing speech therapy not only receive speech
training but also have daily contact with a therapist. Much of this interaction is social and not
strictly related to language. The importance of such stimulation cannot be overstated. For
example, evidence is growing that patients who are placed in a dedicated stroke unit, rather
than treated as outpatients, are likely to have a better outcome. In a dedicated unit, a variety
of professional rehabilitation therapists work together and provide patients with social
stimulation for much of the waking day. Results of studies of laboratory animals consistently
show that the single most successful treatment strategy for optimizing functional recovery is
placing animals in complex, stimulating environments. But far from suggesting that
rehabilitation therapies are not useful, these results reinforce that specific type of training can
alter motor maps. Consider three more examples: movement therapy, tactile stimulation, and
cognitive rehabilitation.
 Movement Therapy: Based on the observation that after stroke, many patients have
initial hemiparesis; develop strategies to use the unimpaired opposite limb; and in so
doing, fail to attempt to use the impaired limb, Edward Taub and his colleagues
developed constraint-induced movement therapy (Unwatte & Taub, 2013). The goal
of this therapy, which is accomplished by placing the unaffected limb in a sling and
forcing the patient to perform daily activities with the impaired limb, is to induce
patients to use the affected limb for several hours a day for a period of weeks.
 Tactile Stimulation: Tactile stimulation, either as massage or lighter stimulation, has
the potential to offer patients significant benefits. Physiotherapists have long used
massage in treating brain-injured patients, but few studies have examined its efficacy.
However, laboratory studies of both adult and infant cortically injured rats record
benefits from tactile stimulation using light touch with a fine brush several times daily
for 15 minutes for 2 to 3 weeks after the brain injury. The stimulation is correlated
with changes in dendritic length or spine density in cortex adjacent to the injuries. The
mechanism is proposed to be enhanced release of neurotrophic factors, such as
fibroblast growth factor-2 (FGF-2), by the skin. Such factors pass through the blood–
brain barrier and stimulate FGF-2 receptors in the brain.
 Cognitive Rehabilitation: The most critical problems faced by many brain-injured
people are not strictly sensory or motor but rather are more-complex cognitive
problems, such as memory disturbances or spatial disorientation. These patients need
 cognitive rehabilitation, and a logical place to find it is the burgeoning field of
cognitive training in aging adults without brain injury. Nori Jacoby and Merav
Ahissar (2013) review this literature and conclude that although people improve with
training, suggesting significant plasticity in the older brain, the chronic effects are
generally mild and with limited generality to novel tasks (Merzenich, 2013).
Nonetheless, interest in improving such training programs is intense. Treating patients
in hospitals is expensive, triggering a push for outpatient programs, often called
“community neurorehabilitation” (Chard, 2006). Even though the long-term benefits
remain poorly understood, several cognitive programs are available for brain-injured
adults (Prigatano, 2001; Wilson, 2011).
A broader matter, however, is the difficulty of coping with residual cognitive deficits
outside the clinic. For example, a person with spatial disorientation might benefit
somewhat from practicing various paper-and-pencil tasks, but in the end, the patient
may continue to struggle with the real-world problem of finding his or her way home.
Thus, therapy for brain damage often requires creativity and initiative on the part of
the therapist trying to develop techniques that are relevant to an individual patient.

Pharmacological Therapies
Interest in using pharmacological therapies for ameliorating the effects of brain damage is
longstanding. The general idea is to use compounds that facilitate plastic changes in the brain.
For example, psychoactive drugs such as amphetamine, nicotine, and marijuana stimulate
changes in cortical and subcortical circuits in the healthy brain. The hope is that using such
compounds in the injured brain can stimulate synaptic changes that might facilitate functional
recovery (Feeney, 1997). Research results suggest that the rate of recovery can be increased if
pharmacological treatments and experience are combined shortly after brain damage. The
success of such treatments in the laboratory has led to clinical trials using amphetamine with
stroke patients—with mixed results. A key factor is lesion size, because stimulants are most
effective in cases of restricted injuries. Even so, many clinical trials have focused on patients
with larger lesions, but with limited success.

Electrical Stimulation
One effect of brain injury is reduced activity in perilesional regions. Several strategies
pioneered in the early 2000s include increasing blood pressure (Hillis, 2007); low-level
electrical stimulation (Teskey et al., 2003); and TMS (Rauschecker et al., 2002). All these
techniques would seem to carry the risk of complications, but preliminary clinical trials have
proved very promising and without complication. Vagus nerve stimulation provides a novel
form of electrical stimulation. Low-level vagal stimulation releases acetylcholine and
norepinephrine. An advantage over direct drug administration is that vagus nerve stimulation
can be precisely temporally controlled during, for example, different forms of behavioral
therapy (Hays et al., 2013). Vagus nerve stimulation has been shown to be a safe and
approved method for managing intractable epilepsy and depression in more than 60,000
patients. Laboratory studies have shown vagal stimulation effective in enhancing memory
and in treating stroke in rats, and this success is being translated into clinical trials to treat
sensory, motor, and cognitive dysfunction in humans after brain injury.

Brain-Tissue Transplants and Stem-Cell Induction

The idea of transplanting neural tissue in mammals and the techniques for doing so date back
more than a century. Yet until recently, the possibility that neural transplantation could have
practical application was viewed as remote. In the 1980s, researchers discovered that if fetal
tissue containing immature cells was extracted from particular brain regions and then inserted
into the appropriate region of a recipient animal, the fetal tissue would grow and integrate
into the host brain. Such a procedure would be impractical for repairing damage to a complex
circuit such as the neocortex, but perhaps transplantation of specific cell types, such as
dopaminergic cells from the brainstem, could benefit patients missing those cells—Parkinson
patients.
More than 100 Parkinson patients have now received fetal stem-cell transplants.
Improvements have been reported in some cases, but a large study by Curt Freed and his
colleagues (2001) is not encouraging. By and large, the relief from symptoms has been minor
or only short-lived. Perhaps the transplants do not grow sufficiently in the large human brain,
are not adequately incorporated into brain circuitry, or are affected by the same disease
process that is causing the original loss of dopamine cells.
Another approach to transplanting fetal tissue is to stimulate stem-cell growth within the
host brain by using growth factors. Knowing that the brain is capable of making new neurons
even in adulthood, researchers hypothesize that it ought to be possible to potentiate the
production of new neurons after injury. If these new neurons can then be induced to migrate
to the site of injury and integrate into that part of the brain, they may be able restore some
level of functioning there.
Many studies have used a variety of growth factors to stimulate proliferation of neural stem
cells after injury. Many growth factors act directly on their respective receptors but may also
mediate proliferation of precursor cells, although Dibajnia and Morshead point out that they
may have indirect effects too, via modulation of the immune response, protection of neurons
in the region around an injury, and the production of blood vessels. Significant challenges
block moving to the clinic with compounds to increase the proliferation of neural precursor
cells—stem cells that are able to differentiate into neurons, astrocytes, or oligodendrocytes.
Many of these compounds are powerful mitogens (chemicals that encourage cell division),
leading to potentially harmful effects. Another challenge is the route of delivery of activation
factors. Peripheral routes (intravenous, subcutaneous, intraperitoneal) may have widespread
systemic effects, and the activation factors may not enter the brain insufficient strength to
produce the required number of neurons. Direct injection into brain tissue or ventricles is
invasive and could lead to other complications.
Additionally, there is the problem of the much greater distance that proliferating cells would
have to migrate in humans compared to rodents. Finally, older brains have fewer neural
precursor cells in the sub-ventricular zone, likely making it more difficult to stimulate enough
cells to make a difference. Clearly, transition to clinical use is some time away.

Diet
Predicting that vitamin and/or mineral supplements might facilitate recovery from brain
injury is reasonable. Dietary choline supplementation in laboratory animals during the
perinatal period leads to enhanced spatial memory in various spatial navigation tasks and
increases the levels of nerve growth factor in the hippocampus and neocortex. Evidence is
growing that vitamin/mineral supplements may improve mood and reduce aggression in
adults and adolescents with various disorders and reduce social withdrawal and anger in
children with ASD. Few studies of such supplements address recovery from brain injury,
although several reports have shown enhanced recovery from early brain injuries in lab
animals (e.g., Halliwell et al., 2009).

METHOD
Case Study
The single-case approach in neuropsychology has made a significant contribution to our
understanding of the architecture of human cognition. However, as Caramazza and
McCloskey (1988) note, if advances in theory are to be sustainable, they “must be based on
unimpeachable methodological foundations”. The statistical treatment of single-case study
data is one area of methodology that has been relatively neglected. In general terms, the
motivation behind the work described below is to provide methods for single-case research
that more closely match the standards demanded in group studies.
There are three basic approaches to inference in single-case studies:

1. The patient is administered fully standardized neuropsychological tests and performance is

compared to large sample normative data
2. At the other extreme, the patient’s performance is not referenced to normative data or
control performance; i.e., analysis is limited to intra-individual comparisons
3. The patient is compared to a (modestly sized) matched control sample

(1) The fully standardized approach:

Very useful and elegant methods have been devised for drawing inferences using approach
(1). However, because new constructs are constantly emerging in neuropsychology and the
collection of large-scale normative data is a time-consuming and arduous process (Crawford,
2004) the prototypical single-case study remains one in which a patient is compared to a
modestly-sized (matched) control sample.
(2) The intra-individual approach:
There are numerous single-case studies in the literature (some of which have been very
influential) in which a patient’s performance is not referenced to a control sample; i.e.
approach (2) is employed. Typically, in these studies within-individual inferential methods
are employed to compare a patient’s performance on Task X with their performance on
Task Y. For example, chi-square tests have been used in attempts to demonstrate a
dissociation between naming of living-things and non-living things. It is clear that the chi-
square test’s assumption of independence is violated in these circumstances.
Moreover, in a recent collaboration on category specificity in Alzheimer’s disease with Keith
Laws and colleagues (Laws, Gale, Leeson & Crawford, 2005), we have demonstrated how
these intra-individual analyses can be very misleading. For example, patients can show a
significant difference between living and non-living naming on chi-square tests (i.e. they are
classified as exhibiting a dissociation) but such raw differences are not unusual when
standardized against control performance (i.e. the within-individual method yields a false
positive). Conversely, patients whose chi-square results are not significant, can show strong
evidence of a dissociation between living and non-living naming when referenced to control
performance. Laws et al even found a case in which a putative dissociation in one direction
was reversed when performance was referenced to control performance. It can be concluded
that single-case studies should never rely on within-individual analysis alone; a patient’s
performance should always be referenced to control performance.
(3) The matched control sample approach (i.e., the case-controls design):
As noted above, in the third approach to inference, a patient’s performance is referenced to a
matched control sample. This approach is very widely employed in single-case research. By
far the most common approach to the statistical analysis of such data uses z. That is, the
patient’s performance is converted to a z score based on the mean and SD of the control
sample and this z is referred to a table of areas under the normal curve. With this approach
the control sample is treated as though it were a population (i.e. the sample statistics are
treated as parameters). However, as the size of the control samples in most single-case
studies is modest (i.e. N is often < 10 and can even be < 5), this is not appropriate. The upshot
is that these methods are associated with an inflated Type I error rate and overestimate the
abnormality of the patient’s score. The following case study was taken from Nelson, C. G.,
Elta, T., Bannister, J., Dzandu, J., Mangram, A., & Zach, V. (2016, March 23). Severe
Traumatic Brain Injury: A Case Report. PubMed Central (PMC).from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4807741/.

SECONDARY DATA

Secondary data is the data that has already been collected through primary sources and made
readily available for researchers to use for their own research. It is a type of data that has
already been collected in the past.

A researcher may have collected the data for a particular project, then made it available to be
used by another researcher. The data may also have been collected for general use with no
specific research purpose like in the case of the national census.

Data classified as secondary for particular research may be said to be primary for another
research. This is the case when data is being reused, making it primary data for the first
research and secondary data for the second research it is being used for.
Sources of Secondary Data

Sources of secondary data include books, personal sources, journals, newspapers, web-sitess,
government records etc. Secondary data are known to be readily available compared to that
of primary data. It requires very little research and needs for manpower to use these sources.

With the advent of electronic media and the internet, secondary data sources have become
more easily accessible. Some of these sources are highlighted below.

 Books
 Published Sources
 Unpublished Personal Sources
 Journal
 Newspapers
 Websites
 Blogs
 Diaries
 Government Records
 Podcasts
Advantages of Secondary data

 Ease of Access: Most of the sources of secondary data are easily accessible to
researchers. Most of these sources can be accessed online through a mobile
device. People who do not have access to the internet can also access them through
print. They are usually available in libraries, book stores, and can even be borrowed
from other people.

 Inexpensive: Secondary data mostly require little to no cost for people to acquire
them. Many books, journals, and magazines can be downloaded for free
online. Books can also be borrowed for free from public libraries by people who do
not have access to the internet. Researchers do not have to spend money on
investigations, and very little is spent on acquiring books if any.

 Time-Saving: The time spent on collecting secondary data is usually very little
compared to that of primary data. The only investigation necessary for secondary data
collection is the process of sourcing for necessary data sources. Therefore, cutting the
time that would normally be spent on the investigation. This will save a significant
amount of time for the researcher.

 Longitudinal and Comparative Studies: Secondary data makes it easy to carry out
longitudinal studies without having to wait for a couple of years to draw conclusions.
For example, you may want to compare the country’s population according to census
5 years ago, and now. Rather than waiting for 5 years, the comparison can easily be
made by collecting the census 5 years ago and now.

 Generating new insights: When re-evaluating data, especially through another

person’s lens or point of view, new things are uncovered. There might be a thing that
wasn’t discovered in the past by the primary data collector, that secondary data
collection may reveal. For example, when customers complain about difficulty using
an app to the customer service team, they may decide to create a user guide teaching
customers how to use it.
Disadvantages of secondary data

 Data Quality: The data collected through secondary sources may not be as authentic
as when collected directly from the source. This is a very common disadvantage with
online sources due to a lack of regulatory bodies to monitor the kind of content that is
being shared. Therefore, working with this kind of data may have negative effects on
the research being carried out.

 Irrelevant Data: Researchers spend so much time surfing through a pool of irrelevant
data before finally getting the one they need. This is because the data was not
collected mainly for the researcher. In some cases, a researcher may not even find the
exact data he or she needs, but have to settle for the next best alternative.

 Exaggerated Data: Some data sources are known to exaggerate the information that
is being shared. This bias may be some to maintain a good public image or due to a
paid advert. This is very common with many online blogs that even go a bead to share
 false information just to gain web traffic. For example, a FinTech startup may
exaggerate the amount of money it has processed just to attract more customers. A
researcher gathering this data to investigate the total amount of money processed by
FinTech startups in the US for the quarter may have to use this exaggerated data.

 Outdated Information
Some of the data sources are outdated and there are no new available data to replace
the old ones. For example, the national census is not usually updated yearly.
Therefore, there have been changes in the country’s population since the last census.
However, someone working with the country’s population will have to settle for the
previously recorded figure even though it is outdated.

EVALUATION
SEVERE TRAUMATIC BRAIN INJURY: A CASE REPORT
By: Clinton G. Nelson and Tara Elta

Case report
In this case report, we demonstrate the unanticipated recovery of a 28-year-old male patient
who presented with a severe traumatic brain injury after being in a motorcycle accident
without wearing a helmet. He presented with several exam and imaging findings that are
statistically associated with increased mortality and morbidity.
Bystanders found a 28-year-old, unhelmeted, white male prone and unconscious after he had
lost control of his motor- cycle and went off the road. He was brought to the Emergency
Department via ambulance intubated as a Level 1 Trauma activation.

Physical examination results

The physical examination revealed a GCS of 3. 4 mm bilaterally fixed pupils (bilateral

mydriasis), negative corneal response, right parietal cephalohematoma, and cerebral spinal
fluid (CSF) otorrhea on the right.
The Glasgow Coma Scale (GCS) uses exam findings to quantify level of consciousness
following TBI, with 3 being the worst, defined as deep coma or death, and 15 being the best,
a fully awake person. In a study by Fearnside et al., out of 315 patients with severe TBI, 65%
with initial GCS of 3 died. In a larger study by Marshall et al., out of 746 patients, 78.4%
with initial GCS 3 died and 7.2% had mild to moderate disability

cerebral spinal fluid (CSF) otorrhea on the right- otorrhea means Discharge of fluid from an
external ear.CSF otorrhea occurs on the basis of skull fracture, tumor, infections, congenital
anomalies, and operative trauma.

corneal reflex a reflex action of the eye resulting in automatic closing of the eyelid when the
cornea is stimulated. The corneal reflex can be elicited in a normal person by gently touching
the cornea with a wisp of cotton. Absence of the corneal reflex(negative corneal
response) indicates deep coma or injury of one of the nerves carrying the reflex arc.
A cephalhaematoma is a hemorrhage of blood between the skull and the periosteum of any
age human, including a newborn baby secondary to rupture of blood vessels crossing the
periosteum. The periosteum is the medical definition for the membrane of blood vessels and
nerves that wraps around most of your bones.

Mydriasis is the medical term for an unusual dilation or widening of the pupils.
Normally, a person’s pupils dilate when the light is dim so that more light can enter the eye.
Mydriasis describes a condition where the pupils dilate without a change in the levels of light.
When someone’s pupils dilate in an unusual way, it is called mydriasis. This may be caused
by an injury, psychological factors, or when someone takes certain drugs or medications.
According to the guideline Early Indicators of Prognosis in Severe Traumatic Brain Injury,
on average, 88% of patients who presented with bilaterally unreactive pupils became
vegetative or died, and 4% had good recovery or moderate disability.

He was bradycardic (Bradycardia is a slow heart rate), with his lowest heart rate recorded at
28 bpm, and hypertensive with an initial blood pressure of 172/118 mmHg and markedly
elevated blood pressure of 221/105 mm Hg 30 min after his arrival at our facility.

CT scan results
CT of the head showed subarachnoid hemorrhage with left frontal and temporal subdural
hemorrhage, effacement of the suprasellar cistern, and effacement of the 3rd and 4th
ventricles. In addition, CT studies showed a left frontal/temporal and parietal hematoma (An
intracranial hematoma is a collection of blood within the skull. It's usually caused by a blood
vessel that bursts in the brain) with mass effect and cerebral edema (cerebral edema
is swelling of the brain. Midline shift refers to the shift of the brain past its center line)
causing a 5.38-mm left to right midline shift, a frontal skull base fracture, and a complex non-
displaced comminuted fracture of the right temporal bone.

Subarachnoid hemorrhage (SAH) is a life-threatening type of stroke caused by bleeding into

the space surrounding the brain. The subarachnoid space is the area between the brain and the
skull. It is filled with cerebrospinal fluid (CSF), which acts as a floating cushion to protect the
brain. When blood is released into the subarachnoid space, it irritates the lining of the brain,
increases pressure on the brain, and damages brain cells. At the same time, the area of brain
that previously received oxygen-rich blood from the affected artery is now deprived of blood,
resulting in a stroke.

The subarachnoid cisterns, or basal cisterns, are compartments within the subarachnoid
space where the pia mater and arachnoid membrane are not in close approximation and
cerebrospinal fluid (CSF) forms pools or cisterns. The suprasellar cistern (also known
as the chiasmatic cistern or pentagon of basal cisterns) is one of the cerebrospinal fluid-
filled subarachnoid cisterns.
Progression of cerebral edema after hemispheric stroke will result in midline shift when this
capacity for compensation is exhausted and compartmental pressure rises.
a frontal skull base fracture, a complex non-displaced comminuted fracture of the right
temporal bone. If the bone is in many pieces, it is called a comminuted fracture. In a non-
displaced fracture, the bone cracks either part or all of the way through, but does move and
maintains its proper alignment.

Radiographic findings can also be used be used to predict morbidity and mortality, and can be
used to guide surgical intervention. A review of 753 computed tomography (CT) studies that
revealed abnormal mesencephalic cisterns, midline shift, and subarachnoid hemorrhage were
associated with an increased risk of elevated intracranial pressure (ICP) and death.

Treatment and observation

On hospital day 1, an arterial line and central venous catheters were placed for fluid and
medication administration. Postoperatively, an external ventricular drain (EVD) was placed;
the initial intracranial pressure (ICP) was 14 mmHg. The patient was examined
postoperatively and also after EVD placement. His GCS was 5T, with bilaterally reactive
pupils, and positive corneal reflex in the left eye.

On hospital day (HD) 2 the patient’s ICP was elevated in the upper 20s in the setting of
shivering, hypertension, and fever, which were controlled with increased sedation,
nicardipine infusion, and targeted temperature management, respectively.

On HD 3 his GCS improved from 6T to 8T, with intact brain stem reflexes.

he next day, HD 4, the patient’s oxygen saturation dropped from 96% to 87% requiring an
increase in fraction of inspired oxygen (FIO2) from 50% to 80% and positive end-expiratory
pressure (PEEP).

On HD 5, The patient’s GCS deteriorated from 8T to 3T in the setting of elevated ICP.

During bronchoscopy, his ICP was noted to be markedly elevated at 46; therefore, 23% NaCl
was administered intravenously over a period of 10 min.

Respiratory cultures on HD 6 revealed methicillin-sensitive staphylococcus aureus (>10 000

cfu/ml) and pseudomo nas aeruginosa (>10 000cfu)

Examination on HD 8 revealed an improved GCS of 6T. His ICP was controlled during an
EVD clamp trial, and the EVD was then removed. The patient was started on IV Zosyn and
cefepime was discontinued. ICP was controlled by administering 23% NaCl. During a
sedation vacation, his oxygen saturation decreased from 95% to 70% and the ventilator
settings were therefore changed to airway pressure release ventilation (APRV) mode.
On HD 14, his oxygenation was improving and remained stable at 97%. The ventilator mode
was weaned from APRV to continuous mandatory ventilation (CMV).

On HD 15, he began blinking to threat, with a GCS of 10T. A CT of his head showed
improvement in diffuse cerebral edema and effacement of basal cisterns.. He underwent a
percutaneous tracheostomy with video-assisted bronchoscopy, and open gastrostomy tube
placement by trauma surgery.

The patient remained neurologically unchanged on HD 16, but repeat chest x-ray revealed an
interval increase in right-sided infiltrates with resolution of left lung opacity.

On HD 17, he continued to maintain adequate oxygen saturation at 97% and was started on
continuous positive airway pressure (CPAP).

On HD 18 the patient developed tachypnea and he was placed back on CMV. The antibiotics
were changed from Zosyn to levofloxacin and nebulized tobramycin.

On HD 19 his neurologic status was unchanged and he was started on Provigil. He was also
given a protective helmet.

Two days later, on HD 21, the patient’s neurologic status remained unchanged and he was
discharged to a long-term care facility.

Recovery
 A follow-up visit three months later revealed the patient was living at home with his
mother.
 In the interim his tracheostomy and gastrostomy tube had been removed
 His major neurologic sequelae were transcortical motor aphasia and mood disorder.

 His GCS was 13

 His GOS, on a 5-point scale, was 3, with severe injury and permanent need for help
with daily living. (The Glasgow Outcome Score (GOS) is a scale of patients with
brain injuries, such as cerebral traumas that groups victims by the objective degree of
recovery.)
 His Modified Rankin Scale was 3 with moderate disability, requiring some help, but
able to walk without assistance. (The modified Rankin Scale (mRS) is a commonly
used scale for measuring the degree of disability or dependence in the daily
activities of people who have suffered a stroke or other causes
of neurological disability.)
 His Lawton instrumrntal activites of daily living scale was 4/8 (The Lawton
Instrumental Activities of Daily Living Scale (IADL) is an appropriate instrument to
assess independent living skills).
  Barthal index was 95/100 (The Barthel index is an ordinal scale that measures
functional independence in the domains of personal care and mobility in patients with
chronic, disabling conditions.)
 His speech was markedly improved with speech therapy
 Speech therapy is the assessment and treatment of communication problems and
speech disorders. It is performed by speech-language pathologists (SLPs), which are
often referred to as speech therapists. Speech therapy techniques are used to improve
communication. These include articulation therapy, language intervention activities,
and others depending on the type of speech or language disorder.Speech therapy may
be needed for speech disorders that develop in childhood or speech impairments in
adults caused by an injury or illness, such as stroke or brain injury.
 Eleven months after the accident he had similar outcome scores and had developed a
seizure disorder.
 typically, a person is diagnosed with a seizure disorder once you’ve had two or more
“unprovoked” seizures. Unprovoked seizures have what are considered natural
causes, such as genetic factors or metabolic imbalances in your body.“Provoked”
seizures are triggered by a specific event like a brain injury or stroke. To be diagnosed
with epilepsy or a seizure disorder, you need to have at least two unprovoked seizures.

Discussion
When predicting mortality and unfavorable outcome following TBI, exam, laboratory, and
imaging findings can be used together by utilizing the CRASH and IMPACT calculators.
Unfavorable outcome is described as death, vegetative state, or severe disability. This is case
of a patient who presented with a GCS of 3, bilaterally fixed pupils, and CT findings of
subarachnoid bleeding, midline shift, subdural hematoma, effaced 3rd ventricle, effaced 4th
ventricle, and effaced basal cisterns.
The patient left the facility bedbound, ventilator- and tube feed-dependent, and in a
minimally conscious state with a GCS 10T.
Yet despite all this, he had a favorable recovery. Within 1 year of discharge he was able to
live at home, interact, and go shopping with his mother, walk, feed himself, and perform
simple chores and ADLs.
This is a poignant reminder that variability between individual patients makes
prognosticating after traumatic brain injury difficult and uncertain.

Conclusion
Our case shows that severe caution should be taken when using prior studies to make medical
decisions about individual patients. Treatment of traumatic brain injuries is complex, and
should continue to evolve with evidence-based medicine. Improvement in outcome is not
based on 1 intervention; rather, it is the additive effect of multiple interventions. In addition,
daily multidisciplinary rounds with Neurocritical Care, Trauma Critical Care, Infectious
Disease, Pharmacy, Respiratory Therapy, Physical Therapy, Occupational Therapy, Social
Services, and Dietary Services provided optimal medical management in a team-based
approach. Further studies need to be conducted to explore the effect that daily
multidisciplinary rounds have on the outcome of severe TBIs.
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