Dementia

Dementia, also referred to as major neurocognitive disorder in DSM-5, is

marked by severe impairment in memory, judgment, orientation, and
cognition. The subcategories are
(1) dementia of the Alzheimer’s type, which usually occurs in persons older than 65
years of age and is manifested by progressive intellectual disorientation and dementia,
delusions, or depression.
 (2) vascular dementia, caused by vessel thrombosis or hemorrhage.
 (3) human immunodeficiency virus (HIV) disease.
 (4) head trauma; (5) Pick’s disease or frontotemporal lobar degeneration. (6) Prion
disease such as Creutzfeldt–Jakob disease, which is caused by a slow-growing
transmittable virus).
 (7) substance induced, caused by toxin or medication (e.g., gasoline fumes, atropine).
 (8) multiple etiologies.
(9) not specified (if cause is unknown).
Epidemiology
The prevalence of dementia is rising. The prevalence of moderate to
severe dementia in different population groups is approximately 5% in the
general population older than 65 years of age, 20% to 40% in the general
population older than 85 years of age, 15% to 20% in outpatient general
medical practices, and 50% in chronic care facilities.
 Of all patients with dementia, 50% to 60% have the most common type
of dementia, dementia of the Alzheimer’s type (Alzheimer’s disease).
The second most common type of dementia is vascular dementia, which
is causally related to cerebrovascular diseases.
Other common causes of dementia, each representing 1% to 5% of all
cases, include head trauma, alcohol-related dementias, and various
movement disorder–related dementias, such as Huntington’s disease and
Parkinson’s disease.
Etiology
The most common causes of dementia in individuals older
than 65 years of age are
 (1) Alzheimer’s disease
 (2) vascular dementia,
 (3) mixed vascular and Alzheimer’s dementia.
 Other illnesses that account for approximately 10% include:
 Lewy body dementia.
 Pick’s disease.
 frontotemporal dementias.
 normal-pressure hydrocephalus (NPH).
 alcoholic dementia.
 infectious dementia, such as that due to infection with HIV or syphilis.
 Parkinson’s disease.
Diagnosis, signs, and symptoms
The major defects in dementia involve orientation,
memory, perception, intellectual functioning, and
reasoning. Marked changes in personality, affect, and
behavior can occur.
 Dementias are commonly accompanied by hallucinations
(20% to 30% of patients) and delusions (30% to 40%).
Symptoms of depression and anxiety are present in 40%
to 50% of patients with dementia.
Dementia is diagnosed according to etiology
Laboratory tests
First, identify a potentially reversible cause for the dementia, and
then identify other treatable medical conditions that may otherwise
worsen the dementia (cognitive decline is often precipitated by
other medical illness).
The workup should include vital signs, complete blood cell count
with differential sedimentation rate (ESR), complete blood
chemistries, serum B12 and folate levels, liver and renal function
tests, thyroid function tests, urinalysis, urine toxicology, ECG, chest
roentgenography, computed tomography (CT) or magnetic
resonance imaging (MRI) of the head, and lumbar puncture.
Singlephoton emission computed tomography (SPECT) can be used
to detect patterns of brain metabolism in certain types of dementia.
Differential diagnosis
1. Age-associated memory impairment (normal aging).
There is a
decreased ability to learn new material and a slowing of
thought
processes as a consequence of normal aging. In addition,
there is a
syndrome of benign senescent forgetfulness, which does
not show a
progressively deteriorating course.
 2. Depression. Depression in the elderly may present as
symptoms of cognitive impairment, which has led to the term
pseudodementia.
The apparently demented patient is really depressed and
responds well to antidepressant drugs or electroconvulsive
therapy (ECT).
Many demented patients also become depressed as they
begin to comprehend their progressive cognitive impairment.
 In patients with both dementia and depression, a treatment
trial with antidepressants is often warranted. ECT may be of
help in refractory cases.
3. Delirium. Also characterized by global cognitive
impairment.
Demented patients often have a superimposed delirium.
Dementia tends to be chronic and lacks the prominent
features of rapid fluctuations, sudden onset, impaired
attention, changing level of consciousness, psychomotor
disturbance, acutely disturbed sleep– wake cycle, and
prominent hallucinations or delusions that characterize
delirium.
Course and prognosis
Dementia may be progressive, remitting, or stable. Because about
15% of dementias are reversible (e.g., hypothyroidism, CNS syphilis,
subdural hematoma, vitamin B12 deficiency, uremia, hypoxia), the
course in these cases depends on how quickly the cause is reversed.
 If the cause is reversed too late, the patient may have residual
deficits with a subsequently stable course if extensive brain damage
has not occurred.
 For dementia with no identifiable cause (e.g., dementia of the
Alzheimer’s type), the course is likely to be one of slow deterioration.
The patient may become lost in familiar places, lose the ability to
handle money, later fail to recognize family members, and eventually
become incontinent of stool and urine.
Treatment
Treatment is generally supportive. Ensure proper treatment
of any concurrent medical problems. Maintain proper nutrition, exercise,
and activities. Provide an environment with frequent cues for orientation
to day, date, place, and time. As functioning decreases, nursing home
placement may be necessary. Often, cognitive impairment may become
worse at night (sundowning). Some nursing homes have successfully
developed a schedule of nighttime activities to help manage this
problem.
 1. Psychological. Supportive therapy, group therapy, and referral to
organizations for families of demented patients can help them to cope
and feel less frustrated and helpless.
2. Pharmacologic.
 In general, barbiturates and benzodiazepines should be avoided because they can
worsen cognition.
 For agitation, low doses of an antipsychotic may be effective (e.g., 2 mg of
haloperidol orally or intramuscularly or 0.25 to 1.0 mg of risperidone per day
orally).
 However, black-box warnings have been issued for conventional and atypical
antipsychotics alerting clinicians to reports of elevated mortality in demented,
agitated elderly patients treated with these agents. Some studies also question
their efficacy.
 When using antipsychotics, use the lowest effective dose and review progress
frequently.
 Some clinicians suggest a short-acting benzodiazepine for sleep (e.g., 0.25 mg of
triazolam [Halcion] orally), but this may cause further memory deficits the next day.
Dementia of the Alzheimer’s Type (DAT)
Definition progressive dementia in which all known reversible causes
have been ruled out. Two types—with late onset (onset after age 65)
and with early onset (onset before or at age 65).
Diagnosis, signs, and symptoms. Multiple cognitive deficits with
behavioral disturbances.
 Epidemiology. Most common cause of dementia.
DAT accounts for 50% to 60% of all dementias. May affect as many as
5% of persons over age 65 and 15% to 20% of persons age 85 or older.
Risk factors include female sex, history of head injury, and having a first-
degree relative with the disorder.
Incidence increases with age.
Patients with DAT occupy more than 50% of nursing home beds
Etiology
Genetic factors play a role; up to 40% of patients have a
family history of DAT. Concordance rate for monozygotic twins is 43%,
versus 8% for dizygotic twins. Several cases have documented
autosomal dominant transmission. Down syndrome is associated with
DAT. The gene for amyloid precursor protein on chromosome 21 may be
involved. The neurotransmitters most often implicated are acetylcholine
and norepinephrine. Both are believed to be hypoactive. Degeneration of
cholinergic neurons in the nucleus basalis of Meynert in addition to
decreased brain concentrations of acetylcholine and its key synthetic
enzyme choline acetyltransferase have been noted. Further evidence for
a cholinergic hypothesis includes the beneficial effects of cholinesterase
inhibitors and the further impairment of cognition associated with
anticholinergics. Some evidence has been found of a decrease in
norepinephrine-containing neurons in the locus ceruleus. Decreased
levels of corticotropin and somatostatin may also be involved. Other
proposed causes include abnormal regulation of cell membrane
phospholipid metabolism, aluminum toxicity, and abnormal brain
glutamate metabolism.
Neuropathology.
The characteristic neuropathologic changes, first
described by Alois Alzheimer, are neurofibrillary tangles, senile plaques,
and granulovacuolar degenerations. These changes can also appear with
normal aging, but they are always present in the brains of DAT patients.
They are most prominent in the amygdala, hippocampus, cortex, and
basal forebrain. A definitive diagnosis of Alzheimer’s disease can be
made only by histopathology. The aluminum toxicity etiologic theory is
based on the fact that these pathologic structures in the brain contain
high amounts of aluminum. The clinical diagnosis of DAT should be
considered only either possible or probable in Alzheimer’s diseaseOther abnormalities that have
been found in DAT patients include
diffuse cortical atrophy on CT or MRI, enlarged ventricles, and
decreased brain acetylcholine metabolism. The finding of low levels of
acetylcholine explains why these patients are highly susceptible to the
effects of anticholinergic medication and has led to development of
choline-replacement strategies for treatment.
Course and prognosis
1. Onset usually insidious in a person’s 50s or 60s; slowly progressive.
2. Aphasia, apraxia, and agnosia often present after several years.
3. Motor and gait disturbances may develop later; patient may become
bedridden.
4. Mean survival is 8 years; ranges from 1 to 20 years.
Treatment.
 Donepezil (Aricept), rivastigmine (Exelon), galatamine (Remynal), and tacrine (Cognex)
are cholinesterase inhibitors.
 These drugs can enhance cognition and slow the cognitive decline in some patients with
mild to moderate Alzheimer’s disease.
 The most recentlyintroduced drug, mementine (Namenda), acts on glutamate receptors.
None of these alters the underlying disease process. Tacrine is rarely
used because of liver toxicity.
Vascular Dementia
 Vascular dementia of acute onset
 Multi-infarct dementia
 Subcortical vascular dementia
 Mixed cortical and subcortical vascular dementia
 Other vascular dementia
 Vascular dementia, unspecified
Diagnostic guidelines:
a) Presence of a dementia
b) Uneven impairment of cognitive function + focal
neurological signs
c) Insight and judgement relatively well preserved
d) An abrupt onset or a stepwise deterioration
Associated features:
a) Hypertension
b) Emotional lability, weeping or explosive laughter
c) Transient episodes of clouded consciousness
d) Personality relatively well preserved, accentuation of
previous traits (egocentrism, paranoid attitudes, irritability).
Epilepsy

1. Ictal and postictal confusional syndromes.

2. Prevalence of psychosis in epilepsy is 7%.
3. Epilepsy is three to seven times more common in
psychotic patients.
4. Lifetime prevalence of psychosis in patients with
epilepsy is 10%.
5. Seizures versus pseudoseizures
TLE
 a. TLE is the most likely type to produce psychiatric symptoms.
 b. Often involves schizophrenia like psychosis.
 c. Often difficult to distinguish from schizophrenia with aggressiveness.
 d. Varied and complex auras that may masquerade as functional illness (e.g.,
hallucinations, depersonalization, derealization).
 e. Automatisms, autonomic effects, and visceral sensations (e.g., epigastric aura,
stomach churning, salivation, flushing, tachycardia, dizziness).
 f. Altered perceptual experiences (e.g., distortions, hallucinations,
 depersonalization, feeling remote, feeling something has a peculiar significance
[déjà vu, jamais vu]).
 g. Hallucinations of taste and smell are common and may be
 accompanied by lip smacking or pursing, chewing, or tasting and swallowing
movements.
 h. Subjective disorders of thinking and memory.
 i. Strong affective experiences, most commonly fear and anxiety.