THE NEUROCOGNITIVE

DISORDERS

DR. S.O. OSASONA

 NEUROCOGNITIVE DISORDERS
 Neurocognitive disorders are a group of disorders
characterized by an impairment in cognition (memory,
attention, language etc.)
 Cognitive impairment is the cardinal symptom in these
conditions.
 (Although other psychiatric disorders can exhibit a
degree of cognitive impairment as a symptom, it does
not represent a cardinal symptom in them).
 The three major neurocognitive disorders are: delirium,
dementia and amnestic disorders).
 Usually, there is a clinically significant deficit in
cognition that represents a significant change from a
previous level of functioning.
 DELIRIUM
 Delirium is an acute generalized cognitive
impairment in the setting of altered
consciousness.

 The impairment of consciousness (clouding of

consciousness) results in reduced levels of
alertness, attention and perception of the
environment (also referred to as confusional state
or acute organic syndrome; but delirium is the
preferred term).

 Classically, delirium has a sudden onset (hours or

days).
 CLINICAL FEATURES OF DELIRIUM

 The cardinal feature is impaired consciousness

occurring in association with global impairment
of cognitive functions.

 Impaired consciousness is manifested as

drowsiness, decreased awareness of
surroundings. In its most severe, the patient may
be unresponsive (stuporos). It is often subtle.

 Symptoms and signs of delirium vary widely

between patients and in the same patient at
different times of the day. Typically, symptoms
are worse at night.
 CLINICAL FEATURES OF DELIRIUM

Cognitive impairment
 Orientation to time is commonly lost even in mild cases

of delirium. In severe cases, patient may lose orientation

to place and the ability to recognize others.
NB: A delirious patient rarely loses orientation to self.
 Attention- is decreased as patient is usually highly

distractible.
 Language – Language abnormalities often include
rambling, irrelevant or incoherent speech and an impaired
ability to comprehend speech.
 Memory- The ability to register, retain and recall

memories may be impaired but recall of remote memories

may be preserved.
 Other cognitive impairments- include impaired
problem solving ability; amnesia for the period of delirium.
 CLINICAL FEATURES OF DELIRIUM CONT’D

Abnormality of Behavior
 Hyperactivity or hypo activity, restlessness,

repeatitive, purposeless movements etc. are common.

Abnormality of Mood
 Depression, emotional liability and irreliability. These

emotions may rapidly alternate with the course of a

day.

Abnormality of Perception
 Visual hallucinations, illusions, tactile and auditory

hallucinations.

Neurological Abnormalities
 Tremor, asterixis, nystagmus, incoordination and

urinary incontinence.
 CLINICAL FEATURES OF DELIRIUM CONT’D

Sleep-wake disturbance
 The sleep of a delirious patient is often disturbed, almost always

short and fragmented.

 Patients are often drowsy and nap during the day.

 Patient may have an exacerbation of delirious symptoms at

night (or bed time), a clinical situation known as ‘sundowning’.

EPIDEMIOLOGY OF DELIRIUM
 Delirium is a common disorder.

 Approximately 10-15 percent of patients on general surgical

ward and 15-25 percent of patients on general medical wards
experience delirium during their stays in the hospital.

 About 30 percent of patients in surgical intensive care units and

cardiac intensive care units have an episode of delirium.

 It is common in the extremes of life- children and the elderly.

 AETIOLOGY OF DELIRIUM
1) Toxic agents
Carbon monoxide poison, heavy metals etc.

2) Intracranial causes
 Brain trauma
 brain tumor
 infections (encephalitus and menigtis) etc.

3) Neoplasm

4) C

5) A
 AETIOLOGY OF DELIRIUM

6) Medical conditions
 Systemic infections with fever
 Septicaemia
 Organic failure (cardiac, renal and hepatic)
 Hypo-or hyperglycaemia
 Deficiency diseases (thiamie, nicotinic acid, B12 and folic acid).

7) Blood dyscriasis

8) Electrolyte imbalance of any cause

9) Drugs
 Opiates
 Phenytoin
 Salicylates
 Sedatives
 Alcohol (Alcohol withdrawal- delirium tremors)

NB: Acronym – TINCAMBED

 INVESTIGATIONS IN DELIRIUM

 FBG with differential

 Urinalysis

 Blood, urine and CSF culture

 B12, folic acid concentrations

 Thyroid function test

 Serological tests for syphilis, HIV antibody

 EEG, ECG, chest x-ray, CT brain bean, MRI of

the brain.
 Lumbar puncture & CSF examination.

 NB: Investigation are guided by clinical

picture.
 DIFFERENTIAL DIAGNOSIS OF DELIRIUM
1) Dementia
Delirium Dementia

• Acute onset Insidious onset

• Global cognitive Global cognitive impairment

impairment

• Symptoms fluctuate often Symptoms are more stable

and do not fluctuate over the
course of day.

• Impaired consciousness Patient is usually alert

• Does not run a chronic Runs a chronic course

course

• Largely are reversible Largely irreversible

 DIFFERENTIAL DIAGNOSIS OF DELIRIUM CONT’D

2) Schizophrenia
 Some patients with psychotic disorders, usually
schizophrenia or manic episodes may have
periods of extremely disorganized behaviour,
difficult to distinguish from delirium.
 Schizophrenic patients usually experience no
change in their level of consciousness or in their
orientation.
3) Depression
 Patients with hypoactive symptoms of delirium
may appear somewhat similar to severely
depressed patients but can be distinguished on
the basis of EEG.
 COURSE AND PROGNOSIS OF DELIRIUM
 Although the onset of delirium is usually sudden,
prodromal symptoms (such as restlessness and
fearfulness) may occur in the days preceding the
onset of florid symptoms.

 The symptoms of delirium usually persists as long

as the causally relevant factors are present,
although delirium generally lasts less than a week.

 After identifications and removal of the causative

factors, the symptoms of delirium usually recede
over a 3-7 day period, but some symptoms may
take up to 2 weeks to resolve completely.
 COURSE AND PROGRAMME OF DELIRIUM CONT’D

 The older a patient is the longer the delirium

takes to resolve.

NB: Recall of what transpired during a

delirium, once it is over, is characteristically
spotty; a patient may refer to the episode as a
bad dream or a nightmare only vaguely
remembered.
 TREATMENT OF DELIRIUM

Drug Treatment
 The mainstay of treatment is to identify and
treat the underlying cause of the delirium.

 Many patients require medication to control

agitation and distress and permit adequate
sleep.

 The drug of choice is usually an antipsychotic,

and Haloperidol is conventionally used in a
dose carefully titrated to achieve the desired
calming without excess sedation or side-
effects.
 TREATMENT OF DELIRIUM CONT’D

 Generally
between 2.5 and 10mg/day of
Haloperidol is adequate.

 The first dose can be given

intramuscularly.

 Antipsychoticsshould be avoided in
delirium associated with alcohol
withdrawal (delirium tremens) or with
epilepsy, because of the risk of seizures.
 TREATMENT OF DELIRIUM CONT’D
 In delirium tremens, a benzodiazepine-
chlordiazepoxide is the standard treatment.

NB: All sedative drugs should be used sparingly in

liver failure because of the danger of precipitating
hepatic coma.

GENERAL PRINCIPLES OF MANAGEMENT IN DELIRIUM

 Frequent explanation, reorientation and
reassurance.
 Unnecessary change in staff caring for the

patient should be avoided.

 The patient should ideally be nursed in a quiet

single room.
 DEMENTIA
 Dementia is a clinical syndrome
characterized by global impairment of
intellect, memory and personality, but
without impairment of consciousness

 Other cognitive functions that can be

affected in dementia include learning,
language, problem solving, orientation,
attention and concentration, judgment and
abstract thinking.

 There is also impairment of social abilities,

this is, perhaps on extension of the
impairment of personality
 CLINICAL FEATURES OF DEMENTIA

Memory
 The presenting complaint is usually of poor
memory (forgetfulness), which is usually
early and prominent

 Memory loss is more evident for recent than

for remote materials

 There is relative preservation of procedural

memory (for instance, riding a bicycle) and
general knowledge about the world at large
 CLINICAL FEATURES OF DEMENTIA CONT’D

Behaviour
 Loss of flexibility and adaptability in
new situations with the appearance
of rigid and stereotyped routines
(organic orderliness)

 When tasked beyond restricted

abilities sudden explosion of rage or
grief occurs (catastrophic
reaction).
 CLINICAL FEATURES OF DEMENTIA CONT’D
Behaviour
 Asthe illness progresses patients lose
the capacity to care for themselves
and they neglect social conventions;
the inability to perform tasks become
increasingly severe and spreads to
everyday task such as grocery
shopping as dementia progresses.

 Eventually patient may require

constant supervision and help to
perform even the most basic tasks of
daily living.
 CLINICAL FEATURES OF DEMENTIA CONT’D
Orientation
 Orientation to time, place and person ( in
that order) can be progressively affected
during the course of dementia illness for
example, patients may forget how to get
back to their rooms after going to the
bathroom

NB: No matter how severe the

disorientation seems, patients show no
impairment in their level of consciousness
 CLINICAL FEATURES OF DEMENTIA CONT’D

Language changes
 Dementing process that affect the cortex
e.g dementia of the Alzheimer’s type and
vascular dementia can affect patients
language abilities: nominal aphasia
(difficulty in naming objects, circumstantial
locution)

Personality change
 Patients with frontal and temporal lobe
involvement are likely to have marked
personality changes, they may become
irritable and explosive
 CLINICAL FEATURES OF DEMENTIA CONT’D

Psychotic symptoms
 About 20 to 30 percent of patients
with dementia, primarily patient with
dementia of Alzheimer’s type have
hallucination.

 About 30 to 40 percent have delusions

primarily of persecutory nature
 CLINICAL FEATURES OF DEMENTIA CONT’D

Mood changes
 Depression and anxiety are major
symptoms in about 40 to 50 percent of the
patients, although the full syndrome of
depressive disorder may be present in only
10 to 20 percent

 Patients may also exhibit pathological

laughter or crying that is, extremes of
emotions with no apparent provocation

Neurological Symptoms (in addition to aphasia)

 Seizure, primitive reflexes (grasp, suck
reflexes etc) headache, dizziness, faintness,
dysarthria etc
 DIAGNOSIS OF DEMENTIA
 Although dementia is a global or generalized
disorder, it often begins with local cognitive
or behavioral disturbances

 Impairment in two or more cardinal domains

(memory, language, abstract thinking,
judgment, personality and social conduct)
sufficient to interfere with social or
occupational functioning

 Difficulty may initially be to mild or

circumscribed to fulfill this definitions, and a
diagnosis of mild cognitive impairment is
made
 EPIDEMIOLOGY OF DEMENTIA

 Dementia is essentially a disease of older

people

 Of all patients with dementia 50 to 60 percent

have the most common type of dementia
(dementia of Alzheimer’s type). It is more
common among people who reach age 65 years,
and most common in those who reach 85 years
and above

 The concept of senile and pre-senile dementia

fading?

 Being female is a risk factor for developing

dementia (especially dementia due to
 ACTIOLOGY OF DEMENTIA

1. Primary neurodegenerative disorders

 Alzheimer’s Disease : dementia due to
Alzheimer’s disease
 Dementia due to picks disease
 Dementia due to Parkinson's disease,
 Dementia with lewy bodies
 Prion disease
 Hutington’s disease

2. Vascular dementia
 Multiple sclerosis , subdural haematoma

3. Inflammatory and autoimmune causes

 SLE with CNS Involvement, Multiple Sclerosis
 ACTIOLOGY OF DEMENTIA CONT’D

4. Traumatic Causes
 Severe head injury or repeated head injury
in boxers (dementia pugilistica)
5. Metabolic and Endocrime causes
 Sustained uraemia
 Renal dialysis
 Liver failure
 Hypothyroidism
 Hyperthyroidism
 Cushions syndrome
 Hypopituitarism
 Adrenal insufficiency
 ACTIOLOGY OF DEMENTIA CONT’D
6. Neoplastic causes

7. Post radiation

8. Post anoxic
 Severe anaemia
 Carbon monoxide poison
 Chronic respiratory failure

9. Vitamin and other nutritional deciencies

 Sustained lack of XXXXX
 Folate

Toxic causes
 Alcohol
 Organic solvents
 Organic phosphates
 ACTIOLOGY OF DEMENTIA CONT’D

11. Others
 Normal pressure hydrocephalus
 HIV related dementia
 Genetics

NB: In rare cases, it is impossible to determine

a specific cause
 INVESTIGATIONS IN DEMENTIA

 As discussed under delirium above

NEURO PATHOLOGY OF DEMENTIA

 Gross anatomical observation of a
brain from a patient with Alzeimer’s
disease will reveal:
 Diffuse atrophy
 Flattened cortical sulci
 Enlarged ventricles
 NEURO PATHOLOGY OF DEMENTIA CONT’D
Microscopic Neuropathological findings
 Neurofibrillary tangles: They are composed
phosphorylated tau protein. It is not unique to
Alzheimer’s disease- can be seen in Down’s
Syndrome, dementia pugilistica (punch-drunk
syndrome) and the brains of normal people as
they age.

 Senile (amyloid) plague are much more

indicative of Alzheimer’s disease, although
they are also seen in Down’s Syndrome and,
to some extent, in normal aging.
Microscopic Neuropathological Findings
Cont’d
Senile plaque are composed of a particular
insoluble protein” (also called A or A4),
astrocytes, degenerating neural processes and
microglia.

The number and density of senile plagues

present in postmortem brains have been
correlated with the severity of the disease that
affected the person
 NEUROTRANSMITTERS INVOLVED IN
DEMENTIA
 Some neurotransmitters are implicated in the
pathophysiology of Alzheimer’s disease:
acetylcholine and noradrenaline.
 Both neurotransmitters are hypothesized to be
hypoactive in Alzheimer’s disease.
 This is sequel to specific degeneration of
cholinergic neurons in the brain (especially in
the nucleus basalis of Meynert) in people with
Alzheimer’s disease.

 The consistent findings of decrease in

acetylcholine and choline acetyl transferase
concentration in the brain support cholinergic
deficit hypothesis.
 THE COURSE OF DEMENTIA

 Dementia may be progressive or static,

permanent or reversible.
 The potential reversibility of dementia is
related to the underlying pathological
condition and the availability and
application of effective treatment.
 Approximately 15 percent of people with
dementia have reversible illnesses if
treatment is initiated before irreversible
damage takes place.
 DIFFERENTIA DIAGNOSIS OF DEMENTIA
1. Delirium – as discussed under delirium

2. Depression: Some patients with depression

have symptoms of cognitive impairment
difficult to distinguish from symptoms of
dementia. This clinical picture is
sometimes referred to as pseudo
dementia; although the term depression-
related cognitive dysfunction is preferable
and more descriptive. They have more
insight into their symptoms than do
demented patients, and often have a past
history of depressive episodes.

3. Schizophrenia
 DIFFERENTIA DIAGNOSIS OF DEMENTIA CONT’D

4. Normal aging (benign senescent

forgetfulness or age associated
memory impairment). This is of a
minor severity and does not
significantly interfere with a person’s
social or occupational behavior.

5. Factitious disorders: Persons who

attempt to simulate memory loss they
do so in an erratic and inconsistent
manner.
 PHARMACOTHERAPY OF
DEMENTIA
Drug therapy for Insomnia and Anxiety
 Short acting benzodiazepine; please take
cognizance of possible idiosyncratic drug
effects in older people (Paradoxical
excitement, confusion and increased
sedation), also falls (Sundowner
syndrome).
 PHARMACOTHERAPY OF DEMENTIA CONT’D

Drug therapy for cognitive deficits:

1) Cholinesterase Inhibitors
a) Tacrine – 120mg/day and above is effective in decreasing
cognitive deficits
Risk of liver damage is high
b) Donepexil (Aricept): 5-10mg/day
Effective in increasing cognitive performance
Less severe side effects than tacrine

2) Vit. E – 200 – 2,000iu/day decreasing rate of

functional decline
3) Selegiline
 A MAO inhibitor that delays cognitive deterioration 5-
10mg/day
 Major side effect is orthostatic hypotension
 PHARMACOTHERAPY OF DEMENTIA CONT’D

Drug therapy for psychosis and agitation

 Antipsychotic Medication (no evidence
that one is superior to another)
 a) Risperichone (less EPS)

Use low dose – 0.5 – 2.0mg/day

 b) Clozapine – regular WBC because of

risk of agranulocytosis

Drug therapy for depression

SSRI preferable
 PHARMACOTHERAPY OF DEMENTIA CONT’D

Other Drugs
 Anticonvulsant agents

 Hormones: antiandrogens (medroxy

progesterone) may be useful to treat

disinhibited sexual behavior

Psychosocial Treatment in Dementia

1. Stimulation – oriented therapy e.g.
recreational activity, art therapy, dance
therapy, pet therapy.
2. Reminiscence therapy – talking about past
can improve mood.
 GENERAL PRINCIPLES IN DEMENTIA TREATMENT

 Identify and treat general medical

conditions
 See patient on regular basis once a week
when starting therapy, once a month
thereafter.
 Evaluate for suicidal potential or self
harm
 Restrict driving
 Educate family about disease, financial
decisions, living will, support groups,
community organizations.
 AMNESTIC DISORDERS (SYNDROME)
 Amnesia is loss of memory

 Amnestic disorder is characterized by a specific and

permanent memory impairment in the absence of
other significant cognitive impairments or impaired
consciousness.

 It may manifest as inability to learn new information

(anterograde amnesia) and to recall past events
(retrograde amnesia).

 The symptom of memory impairment is

accompanied by significant impairment in social and
occupational functioning.
 AMNESTIC DISORDERS (SYNDROME) CONT’D

 Alsoaccompanied by evidence of a
general medical condition
aetiologically related to the memory
impairment.

 Noevidence of generalized intellectual

dysfunction.
EPIDEMIOLOGY OF AMNESTIC DISORDERS

 Studies of prevalence or incidence are scanty.

 Amnesia is most commonly found in alcohol use

disorders and in head injury.

CLINICAL FEATURES OF AMNESTIC DISORDER

 The central symptom of amnestic disorders is the
development of a memory disorder characterized by
impairment in ability to learn new information and to
recall previously remembered knowledge.
 Impaired social and occupational functioning.

 Short term memory and memory for events in the

last decade is usually impaired.

 Memory for overlearned information or events from

the remote past, such as childhood experience is

good.
CLINICAL FEATURES OF AMNESTIC DISORDER CONT’D

 The onset of symptoms may be sudden, as in

trauma, cerebrovascular events and neurotoxic
chemical assaults, or gradual as in nutritional
deficiency and cerebral tumors.

 Amnesia can be transient (usually lasting 1 month

or less) or persistent (lasting more than 1 month).

 Both subtle and gross changes in personality

accompany the symptoms of memory impairment
in amnestic disorder. e.g. patient may be
apathetic, lack initiative, have unprovoked
episodes of agitation, or appear to be overly
friendly or agreeable.
CLINICAL FEATURES OF AMNESTIC DISORDER CONT’D

 Confublation: Patients attempt to cover

gaps or deficits in memory by filling them
with detailed but wholly fictitious account
or events which the patient believes was
true.

 Insight is lacking.
 AMNESTIC DISORDERS (SYNDROME)
 Amnesia is loss of memory
 Amnestic disorder is characterized by a specific

and permanent memory impairment in the

absence of other significant memory impairments
or impaired consciousness.
 It may manifest as inability to learn new

information (antero grade amnesia) and to recall

past events (retrograde amnesia).
 AMNESTIC DISORDERS (SYNDROME)
 The symptom of memory impairment is
accompanied by significant impairment in
social and occupational functioning.
 Also accompanied by evidence of a general

medical condition aetiologically related to the

memory impairment.
 No evidence of generalized intellectual

dysfunction.
EPIDEMIOLOGY OF AMNESTIC DISORDERS
 Studies or prevalence or incidence are scanty.
 Amnesia is most common, found in alcohol use

disorders and in head injury.

CLINICAL FEATURES OF AMNESIA SYNDROME

 The central symptom of amnestic disorders is the
development of a memory disorder characterized
by impairment in ability to learn new information
and to recall previously remembered knowledge.
 CLINICAL FEATURES OF AMNESIA SYNDROME CONT’D

 Impaired social and occupational functioning.

 Short term memory and memory for events

in the last decade is usually impaired.

 Memory for overlearned information or

events from the remote past, such as
childhood experience is good.
 The onset of symptoms may be sudden, as in
trauma, cerebrovascular events and neurotoxic
chemical assaults, or gradual as in nutritional
deficiency and cerebral tumors.

 Amnesia can be transient (usually lasting 1 month

or less) or persistent (lasting more than 1 month).

 Both subtle and gross changes in personality

accompany.

The symptoms in memory impairment in amnestic

disorder. e.g. patient may be apathetic lack
initiative, have unprovoked episodes of agitation, or
appear to be overly friendly or agreeable.
 Confublation: Patients attempt to cover gaps or
deficits in memory by filling them with detailed
but wholly fictitious account or events which the
patient believes was true.
 Insight is lacking.

AETIOLOGY OF AMNESTIC DISORDERS

 Head injury
 Epilepsy (transient epileptic amnesia)

 Alcohol (alcoholic blackouts)

 Post-ECT

 Encephalites

 Cerebral tumour

 Nutritional deficiency etc.

 TREATMENT OF AMNESTIC DISORDERS
 The primary approach is to treat the underlying
cause.

 Supportive prompts about the date, the time and

the patients location can be helpful and can reduce
the patient’s anxiety.

 After resolution of the amnestic episode,

psychotherapy of some type (cognitive,
psychodynamic, or supportive) may help patients.
 SUBTYPES OF AMNESTIC DISORDER

Korsakov (Korsakoff) syndrome

 Name after the Russian neuropsychiatrist
who described it in 1889.

 Korsakov syndrome usually follows an acute

neurological syndrome called Wernicke
encephalopathy which is characterized by
delirium, truncal ataxia, pupillary
abnormalities, ophthalmoplegia, nystagmus
and peripheral neuropathy.
 SUBTYPES OF AMNESTIC DISORDER CONT’D

Korsakov (Korsakoff) syndrome

 The primary aetiological factor is thiamine

deficiency.

 Thiamine deficiency →Wernicke’s encephalopathy

→Kosarkov Syndrome.

 Korsakov syndrome is sometimes referred to as

Wernicke-Korsakov Syndrome.
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