DEMENTIA and

DELIRIUM
(Clinical Science Session)
INTRODUCTION
 Delirium is defined as a transient,
usually reversible, cause of cerebral
dysfunction and manifests clinically with
a wide range of neuropsychiatric
abnormalities.
The clinical hallmarks are decreased
attention span and a waxing and
waning type of confusion.
Pathophysiology
Based on the state of arousal, 3 types of
delirium are described:
1. Hyperactive delirium is observed in patients
in a state of alcohol withdrawal or
intoxication with to phencyclidine (PCP),
amphetamine, and lysergic acid
diethylamide (LSD).
2. Hypoactive delirium is observed in patients
in states of hepatic encephalopathy and
hypercapnia.
3. In mixed delirium, individuals display
daytime sedation with nocturnal agitation
and behavioral problems.
 Delirium results from a wide variety of
structural or physiological insults.
The neuropathogenesis of delirium has been
studied in patients with hepatic
encephalopathy and alcohol withdrawal.
The main hypothesis is reversible impairment
of cerebral oxidative metabolism and multiple
neurotransmitter abnormalities.
The following observations support the
hypothesis of multiple neurotransmitter
abnormalities.
 Acetylcholine
Anticholinergic medications are a well-
known cause of acute confusional states,
and patients with impaired cholinergic
transmission, such those with Alzheimer
disease, are particularly susceptible.
In patients with postoperative delirium,
serum anticholinergic activity is increased.
 Dopamine
In the brain, a reciprocal relationship exists
between cholinergic and dopaminergic
activities.
In delirium, an excess of dopaminergic
activity occurs.
Symptomatic relief occurs with
antipsychotic medications such as
haloperidol and other neuroleptic
dopamine blockers.
Other neurotransmitters
Serotonin:
Gamma-aminobutyric acid (GABA):
Cortisol and beta-endorphins:
 Inflammatory mechanism
Recent studies have suggested a role for
cytokines, such as interleukin-1 and
interleukin-6, in the pathogenesis of delirium.
Following a wide range of infectious,
inflammatory, and toxic insults, endogenous
pyrogen, such as interleukin-1, is released
from the cells.
Head trauma and ischemia interleukin-1
and interleukin-6.
 Stress reaction mechanism
Studies indicate psychosocial stress and
sleep deprivation facilitate the onset of
delirium.
Structural mechanism
Imaging studies of metabolic (eg, hepatic
encephalopathy) and structural (eg, traumatic brain
injury, stroke) factors support the hypothesis that
certain anatomical pathways may play a more
important role than others.
The reticular formation and its connections are the
main sites of arousal and attention.
The dorsal tegmental pathway projecting from the
mesencephalic reticular formation to the tectum and
the thalamus is involved in delirium.
 Frequency:

In the US:
Delirium is common in the United States.
It has been found in 14-56% of elderly patients who are
hospitalized.
Delirium is present in 10-22% of elderly patients at the time of
admission, with an additional 10-30% of cases developing after
admission.
Delirium has been found in 40% of patients admitted to
intensive care units.
Prevalence of postoperative delirium following general surgery is
5-10% and as high as 42% following orthopedic surgery.
As many as 80% of patients develop delirium near death.
Delirium is extremely common among nursing home residents.
 Mortality/Morbidity:
In patients who are admitted with delirium,
mortality rates are 10-26%.
Patients who develop delirium during
hospitalization have a mortality rate of 22-
76% and a high rate of death during the
months following discharge.
In patients who are elderly and patients in
the postoperative period, delirium may result
in a prolonged hospital stay, increased
complications, increased cost, and long-term
disability.
 Age:
Delirium can occur at any age, but it
occurs more commonly in patients who
are elderly and have compromised
mental status.
CLINICAL
 History:
The diagnosis of delirium is clinical.
Because delirious patients often are confused and
unable to provide accurate information, getting a
detailed history from family, caregivers, and nursing
staff is particularly important.
Nursing notes can be very helpful for documentation
of episodes of disorientation, abnormal behavior, and
hallucinations.
Learning to record accurate and specific findings in
mental status as well as the particular time the
finding was observed is imperative for the staff.
Staff should not just report he was confused.
 Delirium always should be suspected when an
acute or subacute deterioration in behavior,
cognition, or function occurs, especially in
patients who are elderly, demented, or
depressed.
Patients may have visual hallucinations or
persecutory delusions as well as grandiose
delusions.
Some patients with delirium also may become
suicidal or homicidal. Therefore, they should
not be left unattended or alone.
 Delirium is mistaken for dementia or
depression, especially when patients
are quiet or withdrawn.
However, by Diagnostic and Statistical
Manual of Mental Disorders, Fourth
Edition (DSM-IV) criteria, dementia
cannot be diagnosed with certainty
when delirium is present.
 Main symptoms
Clouding of consciousness
Difficulty maintaining or shifting attention
Disorientation
Illusions
Hallucinations
Fluctuating levels of consciousness
Symptoms tend to fluctuate over the course
of the day, with some improvement in the
daytime and maximum disturbance at night.
 Reversal of the sleep-wake cycle is
common.
Neurological symptoms
Dysphasia
Dysarthria
Tremor
Asterixis in hepatic encephalopathy and
uremia
Motor abnormalities
 Patients with delirium who are hyperactive
have an increased state of arousal,
psychomotor abnormalities, and
hypervigilance.
In contrast, patients with delirium who are
hypoactive are withdrawn, less active, and
sleepy.
Hypoactive delirium sometimes is
misdiagnosed as dementia or depression.
Mixed states also occur.
In patients who are elderly, delirium often is
the presenting symptom of an underlying
illness.
 Physical:
A careful and complete physical
examination including a mental status
examination is necessary.
Testing vital signs such as temperature,
pulse, blood pressure, and respiration is
mandatory.
 Patients have difficulty sustaining
attention, problems in orientation and
short-term memory, poor insight, and
impaired judgment. Key elements here are
fluctuating levels of consciousness.
Impaired attention can be assessed with
bedside tests that require sustained
attention to a task that has not been
memorized, such as reciting the days of
the week or months of the year
backwards, counting backwards from 20,
or doing serial subtraction.
 DSM-IV diagnostic criteria for delirium
Disturbance of consciousness (ie, reduced
clarity of awareness of the environment)
occurs, with reduced ability to focus,
sustain, or shift attention.
Change in cognition (eg, memory deficit,
disorientation, language disturbance,
perceptual disturbance) occurs that is not
better accounted for by a preexisting,
established, or evolving dementia.
 The disturbance develops over a short
period (usually hours to days) and tends to
fluctuate during the course of the day.
Evidence from the history, physical
examination, or laboratory findings is
present that indicates the disturbance is
caused by a direct physiologic consequence
of a general medical condition, an
intoxicating substance, medication use, or
more than one cause.
 Other diagnostic instruments are the
Delirium Symptom Interview (DSI) and
the Confusion Assessment Method
(CAM).
Delirium symptom severity can be
assessed by the Delirium Rating Scale
(DRS) and the Memorial Delirium
Assessment Scale (MDAS).
Table 1. Differentiating Features of Delirium and

Dementia

Features Delirium Dementia

Onset Acute Insidious
Course Fluctuating Progressive
Duration Days to weeks Months to years
Consciousness Altered Clear
Attention Impaired Normal, except for
severe dementia
Psychomotor changes Increased or decreased Often normal
Reversibility Usually Rarely
 To make an accurate diagnosis, periodic
application of diagnostic criteria such as CAM
or DSM-IV criteria and knowledge of the
patient's baseline mental status is imperative.
Confusion Assessment Method for the
Intensive Care Unit (CAM-ICU) offers the
clinician the opportunity to identify delirium in
critical care patients, especially patients on
mechanical ventilation.
The CAM-ICU makes use of nonverbal
assessments to evaluate the important
features of delirium.
 Causes:
Almost any medical illness, intoxication, or
medication can cause delirium.
Often, delirium is multifactorial in etiology,
and the physician treating the delirium
should investigate each cause contributing
to it.
Medications are the most common
reversible cause of delirium.
 DSM-IV classification of delirium
Delirium due to general medical condition
Substance intoxication delirium
Substance withdrawal delirium
Delirium due to multiple etiologies
Delirium not otherwise specified
 Some of the other common reversible
causes include the following:
Hypoxia
Hypoglycemia
Hyperthermia
Anticholinergic delirium
Alcohol or sedative withdrawal
 Other causes of delirium include the
following:
Infections
Metabolic abnormalities
Structural lesions of the brain
Postoperative states
Miscellaneous causes, such as sensory
deprivation, sleep deprivation, fecal
impaction, urinary retention, and change of
environment
 In persons who are elderly, medications at
therapeutic doses and levels can cause
delirium.
Although numerous risk factors have been
described, a recent study identified 5
important independent risk factors.
Use of physical restraints
Malnutrition
Use of a bladder catheter
Any iatrogenic event
Use of 3 or more medications
 Structural changes
Closed head injury or cerebral hemorrhage
Cerebrovascular accidents, such as
cerebral infarction, subarachnoid
hemorrhage, and hypertensive
encephalopathy
Primary or metastatic brain tumors
Brain abscess
 Dementia is one of the strongest most
consistent risk factors.
Underlying dementia is observed in 25-
50% of patients.
The presence of dementia increases the
risk of delirium 2-3 times.
 Metabolic causes
Fluid and electrolyte abnormalities, acid-
base disturbances, and hypoxia
Hypoglycemia
Hepatic or renal failure
Vitamin deficiency states (especially
thiamine and cyanocobalamin)
Endocrinopathies associated with the
thyroid and parathyroid
 Hypoperfusion states
Shock
Congestive heart failure
Cardiac arrhythmias
Anemias
Infectious causes
CNS infections such as meningitis
Encephalitis
HIV-related brain infections
Septicemia
Pneumonia
Urinary tract infections
 Toxic causes
Substance intoxication - Alcohol, heroin, cannabis,
PCP, and LSD
Medication-induced delirium
Anticholinergics (Benadryl, tricyclic antidepressants)
Narcotics (meperidine)
Sedative hypnotics (benzodiazepines)
Histamine-2 (H2) blockers (cimetidine)
Corticosteroids
Centrally acting antihypertensives (methyldopa,
reserpine)
Anti-Parkinson drugs (levodopa)
Substance withdrawal from alcohol, opioids, and
benzodiazepines
 Other causes
Postictal state
Unfamiliar environment
Operation-related delirium
Preoperative (dementia, polypharmacy, drug
withdrawal, fluid and electrolyte imbalance)
Intraoperative (meperidine, long-acting
benzodiazepines, anticholinergics such as
atropine; however, medications such as
glycopyrrolate can be used because, in contrast to
atropine, they do not cross the blood brain
barrier)
 Postoperative (hypoxia, hypotension)
Drugs are a common risk factor for
delirium, and drug-induced delirium is
commonly seen in medical practice,
especially in hospital settings.
The risk of anticholinergic toxicity is
greater in elderly persons, and the risk of
inducing delirium by medications is high in
frail, elderly persons and in those with
dementia.
DIFFERENTIALS
 Other Problems to be Considered:
Dementia
AIDS-related complex
Psychosis
 Dementia is one of the most important risk
factors for delirium. It often coexists in
patients who are hospitalized.
Delirium may be a risk factor or marker for
the development of dementia.
The safest rule is to consider delirium when
recent changes in an elderly patient's level of
consciousness and cognition have occurred in
an acute setting.
 Patients with hypoactive withdrawn delirium may be
misdiagnosed as depressed.
Depressed patients also may have cognitive symptoms, but the
patient's level of consciousness is normal.

Delirium may have to be differentiated from psychosis because

both have psychotic features.
In delirium, the patient usually does not have a previous history
of serious psychiatric illness.
The onset of symptoms of delirium is acute or subacute, the
hallucinations predominantly are visual and fluctuate, and the
patient has impaired memory and orientation and clouding of
consciousness
WORKUP
 Lab Studies:

Complete blood cell count with differential

- Helpful to diagnose infection and anemia
Electrolytes - To diagnose low or high
levels
Glucose - To diagnose hypoglycemia,
diabetic ketoacidosis, and hyperosmolar
nonketotic states
Renal and liver function tests - To diagnose
liver and renal failure
 Thyroid function studies - To diagnose
hypothyroidism
Urine analysis - Used to diagnose urinary tract
infection
Urine and blood drug screen - Used to diagnose
toxicological causes
Thiamine and vitamin B-12 levels - Used to detect
deficiency states of these vitamins
Tests for bacteriological and viral etiologies - To
diagnose infection
Sedimentation rate
Drug screen including alcohol level
 Imaging Studies:

Neuroimaging
Perform CT scan of the head.
Magnetic resonance imaging (MRI) of the
head may be helpful in the diagnosis of
stroke, hemorrhage, and structural lesions.
 Electroencephalogram
In delirium, generally, slowing of the posterior dominant
rhythm and increased generalized slow-wave activity are
observed on electroencephalogram (EEG) recordings.
In delirium resulting from alcohol/sedative withdrawal,
increased EEG fast-wave activity occurs.
In patients with hepatic encephalopathy, diffuse EEG
slowing occurs.
The type of patterns observed includes triphasic waves in
toxicity or metabolic derangement, continuous discharges in
nonconvulsive status epilepticus, and localized delta activity
in focal lesions.
Chest x-ray is used to diagnose pneumonia or
congestive heart failure.
 Other Tests:

Lumbar puncture is indicated when CNS

infection is suspected as a cause of delirium
or when the source for the systemic infection
cannot be determined.
Pulse oximetry is used to diagnose hypoxia as
a cause of delirium.
Electrocardiogram is used to diagnose
ischemic and arrhythmic causes.
TREATMENT
Medical Care:
When delirium is diagnosed or suspected, the
underlying causes should be sought.
Despite every effort, no cause for delirium
can be found in approximately 16% of
patients.
Components of delirium management include
supportive therapy and pharmacological
management.
 Fluid and nutrition
These should be given carefully because
the patient may be unwilling or physically
unable to maintain a balanced intake.
For the patient suspected of having alcohol
toxicity or alcohol withdrawal, therapy
should include multivitamins, especially
thiamine.
 Environmental modifications
Reorientation techniques or memory cues
such as a calendar, clocks, and family
photos may be helpful.
The environment should be stable, quiet,
and well-lighted. Support from a familiar
nurse and family should be encouraged.
Family members and staff should explain
proceedings at every opportunity, reinforce
orientation, and reassure the patient.
 Sensory deficits should be corrected, if necessary,
with eyeglasses and hearing aids.
Physical restraints should be avoided. Delirious
patients may pull out intravenous lines, climb out
of bed, and may not be compliant. Perceptual
problems lead to agitation, fear, combative
behavior, and wandering.
Severely delirious patients benefit from constant
observation (sitters), which may be cost effective
for these patients and help avoid the use of
physical restraints.
These patients should never be left alone or
unattended.
Consultations:
Psychiatric consultation may be
indicated for management of behavioral
problems such as agitation or
aggressive behavior.
MEDICATION
 Delirium that causes injury to the
patient or others should be treated with
medications.
The most common medications used
are neuroleptics.
Benzodiazepines often are used for
withdrawal states.
 Drug Category: Neuroleptics
The medication of choice in the treatment of
psychotic symptoms.
Older neuroleptics such as haloperidol, a
high-potency antipsychotic, are useful but
have many adverse neurological effects.
Newer neuroleptics such as risperidone,
olanzapine, and quetiapine relieve symptoms
while minimizing adverse effects.
Initial doses may need to be higher than
maintenance doses.
 Use lower doses in patients who are elderly.
Discontinue these medications as soon as possible.
Attempt a trial of tapering the medication once
symptoms are in control.
Neuroleptics can be associated with adverse
neurological effects such as extrapyramidal
symptoms, neuroleptic malignant syndrome, and
tardive dyskinesia.
Doses should be kept as low as possible to minimize
adverse effects.
Paradoxical and hypersensitivity reactions may occur.
 Drug Category: Short-acting sedatives
Reserved for delirium resulting from seizures
or withdrawal from alcohol or sedative
hypnotics.
Coadministration with neuroleptics is
considered only in patients who tolerate
lower doses of either medication or have
prominent anxiety or agitation.
Benzodiazepines are preferred over
neuroleptics for treatment of delirium
resulting from alcohol or sedative hypnotic
withdrawal.
 They also may be used when unknown
substances may have been ingested and may
be helpful in delirium from hallucinogen,
cocaine, stimulant, or PCP toxicity.
Use special precaution when using
benzodiazepines because they may cause
respiratory depression, especially in patients
who are elderly, those with pulmonary
problems, or debilitated patients.
 Drug Category: Vitamins -- Patients
with alcoholism and patients with
malnutrition are prone to thiamine and
vitamin B-12 deficiency, which can
cause delirium.
FOLLOW-UP
Further Inpatient Care:

Carefully assess patients to determine

their level of care needs.
Assessment should include behavior (24
h), daily mental status, potential for
injury, and underlying medical and
metabolic status.
Further Outpatient Care:

Following recovery, patient's memories of

events of the delirium are variable.
Educate the patient, family, and primary
caregivers about future risk factors.
It is not unusual for patients who are elderly
to require 6-8 weeks or longer for full
recovery.
Deterrence/Prevention:

Prevention should be the goal because delirium is

associated with adverse outcomes and high health
care costs.
A multicomponent intervention study that targeted
cognitive impairment, sleep deprivation, immobility,
visual impairment, hearing impairment, and
dehydration showed significant reduction in the
number and duration of episodes of delirium in older
patients who were hospitalized.
 Patients who are at high risk for delirium
should be monitored closely as outpatients,
during hospitalization, and throughout
surgical procedures.
Physicians should become familiar with
prescribing practices for patients who are
elderly, keeping dosages low and avoiding
medications that cause delirium.
Monitoring the patient's mental status as a
vital sign helps diagnose delirium early.
 Complications:

Malnutrition, fluid and electrolyte

abnormalities
Aspiration pneumonia
Pressure ulcers
Weakness, decreased mobility, and decreased
function
Falls and combative behavior leading to
injuries and fractures
Wandering and getting lost
 Prognosis:

Resolution of symptoms may take longer in

patients with poor premorbid cognitive
function, incorrect or incomplete diagnosis of
contributing factors, and structural brain
diseases treated with large doses of
psychoactive medications prior to the onset
of acute medical illness.
For some patients, the cognitive effects of
delirium may resolve slowly or not at all.
Patient Education:

Educating families and patients regarding the

etiology and course of disease is an important
role for physicians.
Educate the patient, family, and primary
caregivers about future risk factors.
Families may worry that the patient has brain
damage or a permanent psychiatric illness.
 Providing reassurance that delirium often is
temporary and is the result of a medical
condition may be beneficial to both patients
and their families.
Suggest that family members or friends visit
the patient, usually one at a time, and
provide a calm and structured environment.
Encourage them to furnish some familiar
objects, such as photos or a favorite blanket,
to help reorient the patient and make the
patient feel more secure.
MISCELLANEOUS
Special Concerns:

Delirium may be the only presenting

symptom of an underlying medical problem,
especially in people who are elderly.
Patients with infections may present without fever,
patients with myocardial infarction may present
without chest pain, and patients with acute stroke
may present without hemiparesis.
Hypoxemia from pulmonary edema or pulmonary
embolus should be considered.
 Rare causes of delirium, such as carbon
monoxide poisoning, should be considered.
Obtaining a detailed drug history is
imperative because patients may be taking
over-the-counter cold and sleep medications,
which are frequent causes of delirium.
Clinicians should be aware of medications
with a significant anticholinergic effect.
 In patients who develop delirium, a record of all
medications and supplements given within the past
few weeks should be carefully obtained.
In some cases, the drug that is responsible for an
episode of delirium is clear because of a temporal
relationship.
If not, the clinician should carefully analyze the
patient's history and look for a characteristic
constellation of drug-related findings.
Any recent addition of a new medication or increase
in dose should be verified.
 The use of complementary medicine is increasing in North
America.
While these products are considered to be "natural," they may
contain ingredients or contaminants that can contribute to
delirium.
Some examples of herbal products that have anticholinergic
effects are henbane, jimson weed, and mandrake.
Unfortunately, research on the adverse cognitive effects of
complementary and alternative medicine products is limited, so
the clinical effects may be greater than perceived.
Both the cause and symptoms of delirium should be treated
ALZHEIMER
DISEASE
DEMENTIA
INTRODUCTION
Background
Alzheimer disease (AD) is the most common
cause of dementia
AD affects approximately 5 million people in
the United States and more than 30 million
people worldwide. Statistical projections
indicate that the number of persons affected
by the disorder in the United States will
nearly triple by the year 2050.
AD is also a major public health problem from
the economic perspective.
Pathophysiology
The anatomic pathology of AD includes
neurofibrillary tangles (NFTs); senile plaques
(SPs) at the microscopic level; and
cerebrocortical atrophy, which predominantly
involves the association regions and particularly
the medial aspect of the temporal lobe.
Although NFTs and SPs are characteristic of AD,
they are not pathognomonic. These lesions must
be present in sufficient numbers and in a
characteristic topographic distribution to fulfill
the current histopathologic criteria for AD.
 Many other lesions of AD have been recognized.
These include (1) the granulovacuolar degeneration
of Shimkowicz; (2) the neuropil threads of Braak et
al; and (3) neuronal loss and synaptic degeneration.
NFTs, when present in low densities and essentially
confined to the hippocampus, were part of normal
aging. However, an early stage in which a low
density of NFTs is present in the entorhinal and
perirhinal (ie, transentorhinal) cortices. Therefore,
even small numbers of NFTs in these areas of the
medial temporal lobe should be considered abnormal.
 The presence of even low numbers of NFTs in the
cerebral neocortex is considered abnormal and
indicates AD if associated with SPs in that location,
with a specific topographic pattern.
Granulovacuolar degeneration occurs almost
exclusively in the hippocampus and has received less
attention than neuropil threads, which are an array of
dystrophic neurites diffusely distributed in the cortical
neuropil.
This lesion suggests neuropil alterations beyond
those merely due to NFTs and SPs and indicates an
even more widespread insult to the cortical circuitry
than that visualized by studying only plaques and
tangles.
 Despite the wide distribution of these lesions in the cerebral
cortex, most patients with AD have a relatively consistent
topographic pattern.
NFTs are initially and most densely distributed in the medial
aspect and in the pole of the temporal lobe; they affect the
entorhinal cortex and the hippocampus most severely. As AD
progresses, NFTs accumulate in most other cortical regions,
beginning in high-order association regions and less frequently
in the primary motor and sensory regions.
SPs also accumulate primarily in association cortices and in the
hippocampus.
Plaques and tangles have relatively discrete and stereotypical
patterns of laminar distribution in the cerebral cortex, which
indicate predominant involvement of corticocortical connections,
as many investigators have observed.
 According to this formulation, the
pathophysiologic mechanism underlying the
clinical manifestations of AD is corticocortical
disconnection due to the loss of medium-
sized pyramidal neurons effecting such
connections.
However, multiple lines of evidence suggest
that several classes of local circuit neurons
are selectively lost throughout the cerebral
cortex as well; these data demonstrate that
the corticocortical disconnection is not the
only alteration in cortical circuitry that
mediates the symptoms of AD.
Frequency
In the US: More than 14% of
individuals older than 65 years have AD,
and the prevalence increases to at least
40% in individuals older than 80 years.
Internationally: Countries
(industrialized nations) experiencing
rapid increases in the elderly segments
of their population have rates
approaching those in the United States.
Mortality/Morbidity
Second to only certain cancers and
cardiovascular disease, AD is frequently
considered a leading cause of death in
the United States.
The primary cause of death is
intercurrent illness, such as pneumonia,
in a patient who has experienced the
debilitating effects of AD for many
years.
Race
Some claim that AD affects certain
ethnic and racial groups more severely
than others, but more study is needed
before reliable statements about racial
predilections can be made.
Sex
AD affects both men and women.
Many studies indicate that the risk of
AD is significantly higher in women than
in men.
Some authorities have postulated that
this difference is due to the loss of the
neurotrophic effect of estrogen in
postmenopausal women.
Other factors may also influence this
relative difference.
Age
The prevalence of AD increases with age.
AD is most prevalent in individuals older than 60
years. Some forms of familial early-onset AD can
appear as early as the third decade, but this
represents a subgroup of the less than 10% of all
familial cases of AD.
More than 90% of cases of AD are sporadic and
occur in individuals older than 60 years.
Of interest, results of some studies of nonagenarians
and centenarians suggest that the risk decreases in
individuals older than 80 or 90 years. If so, age is not
an unqualified risk factor for the disease, but further
study of this matter is needed.
CLINICAL
History
Patients with AD most commonly present with insidiously
progressive memory loss, to which other spheres of cognitive
impairment are added over several years.
After memory loss occurs, patients may also have language
disorders (eg, anomia, progressive aphasia) and impairment in
their visuospatial skills and executive functions.
For this, the most common pattern of AD, several clinical
guidelines have benn formulated for its diagnosis. The criteria
for the diagnosis of AD require the finding of a slowly
progressive memory loss of insidious onset in a fully conscious
patient.
AD cannot be diagnosed in patients with clouded consciousness
or delirium. Toxic metabolic conditions and brain neoplasms
must also be excluded as potential causes of the patient's
dementia.
 The main focus consists of verifying the initial finding
of mild, slowly progressive memory loss, that
additional spheres of cognition are alter
compromised, and that other possible causes for
dementia (eg, cerebrovascular disease, cobalamin
deficiency, syphilis, thyroid disease) are ruled out
with a combination of clinical examination and
ancillary radiologic and laboratory tests.
Autopsy-proven presentations include right parietal
lobe syndrome; progressive aphasia; spastic
paraparesis; and impaired visuospatial skills, which is
subsumed under the visual variant of AD.
Physical
The earliest evidence of AD is the onset of chronic,
insidious memory loss that is slowly progressive over
several years.
This loss can be associated with slowly progressive
behavioral changes.
Although other neurologic systems (eg,
extrapyramidal, cerebellar systems) can also be
affected, the most prominent finding as the disease
progresses to its moderate and severe stages is
progressive memory impairment.
Other common neurologic presentations include
changes in language ability (eg, anomia, progressive
aphasia), impaired visuospatial skills, and impaired
executive function.
 Less common presentations are right parietal
lobe syndrome and spastic paraparesis.
Examination in the clinic or at the patient's
bedside should include a discussion with the
patient.
Any cognitive impairment or language
dysfunction should ideally be verified and
discussed with the patient's spouse and/or
caregivers.
 Memory dysfunction and problems with
activities of daily living (eg, cooking,
cleaning, money management, getting
lost, confusion, self-care) should also be
addressed.
A screening language examination and
Mini-Mental Status Testing may be
warranted (see Table).
Causes
The cause of AD is unknown.
The prevalent notion is that most cases of AD are
caused by converging risk factors that include
advancing age, head injury, and lipoprotein E-epsilon
4 genotype.
Familial forms of AD account for less than 7% of all
cases of AD, with most cases being sporadic (ie, not
inherited).
Four major loci s have been found to be responsible
for AD: (1) that for amyloid precursor protein (APP,
on chromosome 21), (2) that for presenilin I (on
chromosome 14), (3) that for presenilin II (on
chromosome 1), and (4) those for candidate markers
(on chromosomes 12 and 19) and other proposed
markers.
 Many have postulated that mutations alter
the mechanisms by which APP is processed,
leading to the deposition and eventual fibrillar
aggregation of the 40 to 43amino acid
residue known as the beta-amyloid peptide.
This beta-pleated peptide is postulated to
have neurotoxic properties and to lead to an
incompletely understood cascade of events
resulting in neuronal death, synapse loss, and
the formation of NFTs and SPs among other
lesions.
 SPs have been known to include a starchlike (or amyloid)
substance, usually in the center of these lesions, which is
surrounded by a halo or layer of degenerating (dystrophic)
neurites and reactive glia (both astrocytes and microglia).
Mechanisms leading to the development of NFTs : the main
constituent of which is the microtubule-associated protein tau
that is hyperphosphorylated and that accumulates in the
perikarya of large and medium pyramidal neurons.
Studies have shown that both exonic and intronic mutations of
the tau gene result not in AD but in familial frontotemporal
dementia associated with parkinsonism.
So far, no tau mutations have been identified in AD. These
mutations are presumed to modify properties of the neuronal
cytoskeleton, eventually leading to neuronal dysfunction and
death.
WORKUP
Lab Studies
Laboratory tests may include the
following:
Evaluation of the complete blood cell count
and cobalamin levels.
Screening of liver enzyme levels.
Assessment of blood cortisol level.
Analysis of thyroid stimulating hormone
(TSH) levels.
Rapid plasma reagent (RPR) test.
Imaging Studies
Brain MRI or CT: In assessing AD, brain
MRIs or CT scans show diffuse cortical
and/or cerebral atrophy.
SPECT: Under most circumstances,
SPECT is an optional study and not
considered mandatory for the routine
workup of patients with typical
presentations of AD.
Other Tests
EEG: EEG can help in ruling out other
diseases that cause dementia, such as prion-
related diseases (eg, Creutzfeldt-Jakob
disease).
Tau protein test: Some advocate measuring
levels of this protein, a constituent of NFTs
and amyloid protein (found in senile plaques
among other lesions) in the CSF to diagnose
AD.
Genotyping for apolipoproteins: This test is a
research tool that is helpful in determining
the risk of AD in populations.
Procedures
Lumbar puncture: Perform lumbar
puncture in select cases to rule out
conditions such as normal-pressure
hydrocephalus, neurosyphilis,
neuroborreliosis, and cryptococcosis.
Histologic Findings
See histopathologic features of AD
(Pathophysiology)
TREATMENT
Medical Care
To date, no interventions have been shown to
convincingly prevent AD or slow its progression.
Psychotropic medications and behavioral
interventions :
- Temporarily alleviate clinical manifestations of
AD, such as anxiety, agitation, depression, and
psychotic behavior, which are best approached
symptomatically.
- Behavioral interventions range from patient-
centered approaches to caregiver training to
help manage cognitive and behavioral
manifestations of AD.
- Medications that many practitioners
prefer are haloperidol, risperidone,
olanzapine, and (more recently)
quetiapine.
- Dopamine-depleting agents to aggravate
the manifestations of dementia with
cortical Lewy bodies (DCLB).
- Anticonvulsants (eg, gabapentin) may
have a role in the treatment of behavioral
problems in patients with AD.
 Cholinesterase inhibitors :
- A strategy widely used to address the symptoms
of AD is palliating the deficiency in cholinergic
innervation to the cerebral cortex. AD has been
characterized by substantial loss of acetylcholine
(ACh) in the cerebral cortex, progressive decline
in cortical levels of choline acetyltransferase
(biosynthetic enzyme necessary for the synthesis
of ACh), and severe loss of neurons in the
subcortical cholinergic nuclei that project to the
cerebral neocortex (ie, basal nucleus of Meynert)
and hippocampus (ie, medial septal nuclei).
- This theory led to development of an increasing
number of compounds capable of palliating the
cholinergic defect by interfering with the degradation
of ACh by acetylcholinesterase (AChE). More recent
compounds include substances capable of blocking
the nonsynaptic, or nonspecific, cholinesterases;
these are frequently called butyrylcholinesterases
(BuChEs).
- An often neglected aspect of palliation of cholinergic
deficits is the avoidance of centrally acting
anticholinergic medications. Patients not
uncommonly receive both ChEIs and anticholinergic
agents, which negate or at least counteracting the
effects of the former.
 N-methyl-D-aspartate antagonists: A relatively new
category of drugs, NMDA antagonists, is based on an
entirely different mechanism of action. Memantine is the
first NMDA antagonist approved in the United States. This
agent is approved for treating the advanced stages of AD,
in contrast with ChEIs, which are approved for only the
early and intermediate stages.
Antidepressants: Depression is observed in more than
30% of patients with AD, and it frequently begins before
AD is clinically diagnosed. Therefore can considerably
improve their cognitive and noncognitive performance.
Other mood modulators, such as valproic acid, can be
helpful for the treatment of disruptive behaviors and
outbursts of anger, which patients with moderately
advanced or advanced stages of AD may have.
 Other and new therapeutic interventions :
- The proposal that oxidative stress causes AD and evidence
suggesting that estrogen has a trophic effect on certain
neuronal populations that is lost after menopause were the
bases for previous recommendations to give high doses of
tocopherol (1000 IU PO bid) to all patients and estrogen
replacement therapy to postmenopausal women with AD.
Because findings show that estrogen supplementation may
be associated with cognitive impairment and that high-
dose tocopherol may cause adverse cardiovascular events,
the entire body of evidence is being re-evaluated, and few
(if any) now recommend these treatments. Results to date
indicate that patients with clinical dementia do not benefit
from estrogen replacement therapy.
 The use of anti-inflammatory agents, is based
on the postulation that inflammation is
needed for many AD lesions, especially SPs,
to develop and progress through the
theoretical stages of increasing severity.
New drugs under development include
clioquinoline, an antibiotic that may help
reduce brain amyloid deposition in patients
with AD.
Surgical Care
No accepted surgical treatments exist for AD.
One unconfirmed postulate was that omental
transposition to the brain may be beneficial in AD,
but most experts remain highly skeptical of this
claim.
Potential surgical treatments in the future may
include the use of devices to infuse neurotrophic
factors, such as growth factors, to palliate AD.
Studies are also underway to evaluate a claim that
ventriculoperitoneal shunting of CSF may be
beneficial in AD.
Diet
No special dietary considerations exist
for AD.
Activity
Both physical and mental activities are recommended for
patients with AD. Many experts recommend mentally
challenging activities, such as doing crossword puzzles and
brainteasers, both to prevent deterioration and to slow its rate.
The mental activities should be kept within a reasonable level of
difficulty for the patient, they should preferably be interactive, and
they should be designed to allow the patient to recognize and
correct mistakes.
Most important, these activities should be administered in a
manner that does not cause excessive frustration and that ideally
motivates the patient to engage in them frequently.
Some investigators have attempted various forms of cognitive
retraining, also known as cognitive rehabilitation.
FOLLOW-UP
Patient Education
Some investigators have postulated that
education has a protective effect against AD.
They state that individuals with low levels of
education and mental and/or intellectual
activity are said to be at increased risk for AD
and to have a low functional reserve to offset
the cognitive and behavioral effect of AD.
These notions must be subjected to rigorous
scientific assessment both to assess their
validity and, if true, to design cognitive and
behavioral interventions to palliate AD.
VASCULAR
DEMENTIA
INTRODUCTION
Background
Vascular dementia is the second most
common form of dementia after
Alzheimer disease (AD).
Vascular dementia is preventable;
therefore, early detection and an
accurate diagnosis are important.
Patients who have had a stroke are at
increased risk for vascular dementia.
Pathophysiology
Many subtypes of vascular dementia have been
described to date.
The spectrum includes (1) mild vascular cognitive
impairment, (2) multi-infarct dementia, (3) vascular
dementia due to a strategic single infarct, (4)
vascular dementia due to lacunar lesions, (5)
vascular dementia due to hemorrhagic lesions, (6)
Binswanger disease, and (7) mixed dementia
(combination of AD and vascular dementia).
Vascular dementia is sometimes further classified as
cortical or subcortical dementia.
 Vascular disease produces either focal or diffuse effects
on the brain and causes cognitive decline.
Focal cerebrovascular disease occurs secondary to
thrombotic or embolic vascular occlusions.
Common areas of the brain associated with cognitive
decline are the white matter of the cerebral hemispheres
and the deep gray nuclei, especially the striatum and the
thalamus.
Hypertension is the major cause of diffuse disease, and in
many patients, both focal and diffuse disease are
observed together.
The 3 most common mechanisms of vascular dementia
are multiple cortical infarcts, a strategic single infarct, and
small vessel disease.
 Mild vascular cognitive impairment can occur in elderly
persons.
It is associated with cognitive decline that is worse than
expected for age and educational level, but the effects do
not meet the criteria for dementia and are not associated
with vascular risk factors or evidence of silent strokes or
extensive white matter infarcts on CT scanning.
These people have subjective and objective evidence of
memory problems, but their daily functional living skills
are within normal limits.
In multi-infarct dementia, the combined effects of
different infarcts produce cognitive decline by affecting
the neural nets.
 In single-infarct dementia, different areas in the brain
can be affected, which may result in significant
impairment in cognition.
This may be observed in cases of anterior cerebral
artery infarct, parietal lobe infarcts, thalamic
infarction, and singular gyrus infarction.
Small vessel disease affects all the small vessels of
the brain and produces 2 major syndromes,
Binswanger disease and lacunar state.
Small vessel disease results in arterial wall changes,
expansion of the Virchow-Robin spaces, and
perivascular parenchymal rarefaction and gliosis.
 Lacunar disease is due to small vessel occlusions and
produces small cavitary lesions within the brain
parenchyma secondary to occlusion of small penetrating
arterial branches.
These lacunae are found more typically in the internal
capsule, deep gray nuclei, and white matter.
Lacunar state is a condition in which numerous lacunae,
which indicate widespread severe small vessel disease,
are present.
Binswanger disease (also known as subcortical
leukoencephalopathy) is due to diffuse white matter
disease.
In Binswanger disease, vascular changes observed are
fibrohyalinosis of the small arteries and fibrinoid necrosis
of the larger vessels inside the brain.
 In cerebral amyloid angiopathyassociated vasculopathy,
aneurysm formation and stenosis in the leptomeningeal
and cortical vessels cause damage to the subcortical white
matter.
In hereditary cystatin-C amyloid angiopathy, patients have
recurrent cerebral hemorrhages before age 40 years that
can lead to dementia.
Cerebral autosomal dominant arteriopathy with subcortical
infarcts and leukoencephalopathy is a rare autosomal
dominant condition localized to chromosome arm 19q12
that affects small vessels supplying the deep white
matter.
Pathologically, multiple small infarcts are observed in the
white matter, thalamus, basal ganglia, and pons.
 Rare arteriopathies such as inflammatory arteriopathy (eg,
polyarteritis nodosa, temporal arteritis) and
noninflammatory arteriopathy (eg, moyamoya disease,
fibromuscular dysplasia) can cause multiple infarcts and
can lead to vascular dementia.
Hypoperfusion due to large vessel or cardiac disease can
affect the watershed areas of the brain and lead to
vascular dementia.
Mixed dementia is diagnosed when patients have evidence
of Alzheimer dementia and cerebrovascular disease, either
clinically or based on neuroimaging evidence of ischemic
lesions.
Growing evidence indicates that vascular dementia and
Alzheimer dementia often coexist, especially in older
patients with dementia.
 Autopsy studies have shown the association between AD and
vascular lesions.
Several recent studies also suggest that the risk of developing AD
is increased when a patient is exposed to vascular risk factors such
as hypertension, diabetes mellitus, peripheral arterial disease, and
smoking, which usually are associated with cerebrovascular disease
and vascular dementia.
Recent evidence suggests that the vascular processes in both
disorders may mutually induce each other.
Apolipoprotein E may play a role in AD and vascular dementia.
Apolipoprotein E-IV also increases the risk of dementia in stroke
survivors and is a strong risk factor for the development of cerebral
amyloid angiopathy in patients with AD.
In elderly individuals, many cases of dementia may be caused by
the cumulative effect of cerebrovascular and Alzheimer pathology.
Frequency
Vascular dementia is the second most common
cause of dementia in the United States and
Europe, but it is the most common form in some
parts of Asia.
The prevalence rate of vascular dementia is
1.5% in Western countries and approximately
2.2% in Japan.
In Japan, it accounts for 50% of all dementias
that occur in individuals older than 65 years.
In Europe, vascular dementia and mixed
dementia account for approximately 20% and
40% of cases, respectively.
In Latin America, 15% of all dementias are
vascular.
 In community-based studies in Australia, the
prevalence rate for vascular and mixed
dementia is 13% and 28%, respectively.
The prevalence rate of dementia is 9 times
higher in patients who have had a stroke
than in controls.
One year after a stroke, 25% of patients
develop new-onset dementia.
Within 4 years following a stroke, the relative
risk of incident dementia is 5.5%.
Mortality/Morbidity
In patients with dementia who have had a
stroke, the increase in mortality is significant.
The 5-year survival rate is 39% for patients
with vascular dementia compared with 75%
for age-matched controls.
Vascular dementia is associated with a higher
mortality rate than AD, presumably because
of the coexistence of other atherosclerotic
diseases.
Sex
The prevalence of vascular dementia is
higher in men than in women.
Age
Incidence increases with age.
CLINICAL
History
Cognitive impairment, acutely or
subacutely, after an acute neurologic
event with a stepwise progression is a
typical history suggestive of vascular
dementia.
However, this classic history is usually
observed with multi-infarct dementia
and may not be observed with lacunar
state.
 Binswanger disease
The average age of onset is between the fourth and seventh
decades of life, and 80% of patients have a history of
hypertension.
Patients also show progressive motor, cognitive, mood, and
behavioral changes over a period of 5-10 years. Mood and
behavioral changes are observed early and, in some
patients, may be the presenting feature.
Patients may be apathetic or abulic.
Intellectual deficits are also observed early in the disease,
and patients are frequently described as disoriented, having
memory deficits, inattentive, and vague.
Patients with Binswanger dementia often have early-onset
urinary incontinence and gait disturbances.
 Cerebral autosomal dominant arteriopathy with subcortical
infarcts and leukoencephalopathy
The onset of the disease occurs between the third and
fourth decades of life.
The clinical picture is similar to Binswanger disease but
without a history of hypertension and risk factors for
cerebrovascular disease.
Vascular dementia in general
Patients with vascular dementia commonly have mood
and behavioral changes.
Severe depression is more common in persons with
vascular dementia than in those with AD.
In some patients with lacunar state and Binswanger
disease, such problems may be more prominent than
intellectual deficits.
Even psychotic symptoms, particularly delusions, have
been described in patients with vascular dementia.
Physical
A commonly used cognitive screening
tool is the Folstein Mini-Mental State
Examination.
Patchy defects are present in persons
with vascular dementia.
The deficits are global in persons with
Alzheimer dementia.
 The DSM-IV criteria have good sensitivity but low specificity. A
summary of the DSM-IV diagnostic criteria is as follows:
The patient has developed multiple cognitive deficits
manifesting as both (1) memory impairment and (2) one or
more of the following cognitive disturbances: aphasia, apraxia,
agnosia, and disturbance in executive functioning.
The cognitive deficits in the above criteria cause significant
impairment in social or occupational functioning and represent
a significant decline from the previous level of functioning.
Focal neurologic signs and symptoms or radiologic evidence
indicative of cerebrovascular disease are present that are
judged to be etiologically related to the dementia.
The deficits do not occur exclusively during the course of
delirium.
 The NINDS-AIREN criteria are the most
specific of all available criteria and are used
most commonly in research.
They provide 3 levels of certainty: definite,
probable, and possible.
Lateralizing signs such as hemiparesis,
bradykinesia, hyperreflexia, extensor plantar
reflexes, ataxia, pseudobulbar palsy, and gait
and swallowing difficulties may be observed.
 Neuropsychological testing is as follows:
Patients with vascular dementia have patchy
neuropsychological deficits. With vascular dementia,
patients have better free recall and fewer recall intrusions
compared with patients with AD. Apathy early in the
disease is more suggestive of vascular dementia because
it usually occurs in the later stages of AD.
Patients with vascular dementia have poor verbal fluency
and more perseverative behavior compared with patients
with AD. They may even have other signs of executive
dysfunction such as cognitive slowing, difficulty in shifting
sets, and problems with abstraction. Commonly used
mental status tests include the Folstein Mini-Mental State
Examination and the Cognitive Abilities Screening
Instrument.
 Neuropsychological findings vary with the site and
severity of cerebrovascular disease.
For patients with single or multiple large infarcts,
deficits correlate with the site and extent of the
infarct.
In patients with extensive deep white matter
disease, impairments may be observed in tests of
psychomotor speed, dexterity, executive function,
and motor aspects of speech (eg, dysarthria,
reduced verbal output).
DIFFERENTIALS
Other Problems to be
Considered
Patients with AD have early language and
visuospatial deficits. The deficits in short-term
memory are severe, and clues do not help in
retrieving information. The onset of the disease is
gradual, with a slow progression. Usually, no motor
findings are present until the middle or late stages of
the disease.
Patients with vascular dementia have patchy
cognitive impairment, often with focal neurologic
signs and symptoms. Onset may be abrupt, with a
stepwise decline.
Patients with Parkinson dementia have cognitive
slowing with extrapyramidal signs such as rigidity,
bradykinesia, tremor, and gait disturbances. Usually,
dementia is seen in later stages of the disease.
 Patients with dementia due to head trauma have memory
impairment, and other cognitive deficits associated with a
history of head trauma occur. The physical findings depend
on the location of injury. Usually, it is not progressive unless
the person has a history of repeated head trauma (eg,
dementia pugilistica).
Patients with HIV dementia have cognitive changes with
neurologic signs and a positive result from an HIV test.
Patients with Pick disease have memory problems,
personality changes, and deterioration of social skills. Onset
is usually between the fifth and sixth decades of life. Upon
physical examination, the patient has frontal release signs
such as snout and grasp reflex.
 Huntington disease is an autosomal dominant disease with an
onset of cognitive changes as early as the third decade of life,
with physical signs of choreoathetosis.
In Creutzfeldt-Jakob disease, onset is between the fourth and
sixth decades of life and is associated with signs such as
myoclonus, seizures, and ataxia. A rapid progression is typical.
Patients with Lewy body dementia have recurrent visual
hallucinations, fluctuating cognitive impairment, and
parkinsonism features. Also, the frequency of adverse reactions
to antipsychotic medications is high.
 In the case of cognitive symptoms secondary to
depression, the onset is acute compared with the insidious
onset in most types of dementia.
The term pseudodementia has been used to describe the
condition when cognitive symptoms are prominent.
The current and more accurate name for this state is
dementia of depression.
Patients with depression usually report their cognitive
difficulties, which is unusual for patients with dementia.
Patients with depression tend to state that they do not
know the answers to questions, and they appear to not
try very hard during neuropsychological evaluations.
Mood symptoms are prominent in patients with dementia
of depression.
WORKUP
Lab Studies
Laboratory tests should be performed to rule out
other causes of dementia. These tests should
routinely include a CBC count, erythrocyte
sedimentation rate, glucose level, renal and liver
function tests, serologic tests for syphilis, vitamin B-
12 and red blood cell folate levels, and thyroid
function tests.
In selected patients, optional tests include HIV
serology testing, lupus anticoagulant testing,
antiphospholipid antibody testing, antinuclear
antibody testing, and antineutrophil cytoplasmic
antibody testing.
Imaging Studies
Neuroimaging studies may include CT brain
scanning and MRI of the brain.
The absence of cerebrovascular lesions on CT
scanning or MRI is evidence against vascular
etiology.
The features on CT scanning or MRI that are
suggestive of vascular dementia are bilateral
multiple infarcts located in the dominant
hemisphere and limbic structures, multiple lacunar
strokes, or periventricular white matter lesions
extending into the deep white matter.
 Functional imaging studies include the following:
According to a 2000 study by Nagata et al, positron
emission tomography may be useful for differentiating
vascular dementia from AD. Hypoperfusion and
hypometabolism can be observed in the frontal lobe,
including the cingulate and superior frontal gyri, in
patients with vascular dementia; a parietotemporal
pattern is observed in patients with AD.
Starkstein et al in 1996 and other authors have
demonstrated that single-photon emission CT scanning
produce similar findings.
 Cerebral angiography is not performed
routinely during the evaluation of
vascular dementia, but it is performed
before carotid artery surgery. It also is
useful in cases of possible cerebral
vasculitis; cerebral vessels can
demonstrate beading.
Other Tests
Tests that may be useful for evaluation
of stroke and in certain cases of
vascular dementia include the following:
Echocardiography
Holter monitoring
Carotid duplex Doppler scanning
TREATMENT
Medical Care
The mainstay of management of vascular dementia is
the prevention of new strokes.
This includes administering antiplatelet drugs and
controlling major vascular risk factors.
Aspirin has also been found to slow the progression
of vascular dementia.
Recent guidelines from the American Psychiatric
Association provide both treatment principles and
possible specific therapies.
Drug treatment is primarily used to prevent further
worsening of vascular dementia by treating the underlying
disease such as hypertension and diabetes mellitus.
Antiplatelet agents are indicated.
 Pentoxifylline and, to a more limited extent, ergoloid
mesylates (Hydergine), may be useful for increasing
cerebral blood flow. In the European Pentoxifylline Multi-
Infarct Dementia Study, which is a double-blinded,
placebo-controlled, multicenter study, treatment with
pentoxifylline was found to be beneficial for patients with
multi-infarct dementia. Significant improvement was
observed in the scales used for assessing intellectual and
cognitive function.
Neuroprotective drugs such as nimodipine,
propentofylline, and posatirelin are currently under study
and may be useful for vascular dementia.
Increasing evidence supports the involvement of the
cholinergic system in vascular dementia, similar to that
seen in Alzheimer dementia. However, no cholinesterase
inhibitors have been approved to date for the treatment
of vascular dementia, despite positive results in clinical
trials with this medication.
 The general management of dementia
includes appropriate referral to
community services, judgment and
decision-making regarding legal and
ethical issues (eg, driving, competency,
advance directives), and consideration
of caregiver stress.
Diet
In the Rotterdam study, an increased
risk of vascular dementia was
associated with total fat intake,
whereas fish consumption was inversely
related to dementia.
Low levels of folate, vitamin B-6, and
vitamin B-12 are associated with
increased homocysteine levels, a risk
factor for stroke.
FOLLOW-UP
Further Inpatient Care
If depressed patients do not respond to medical
management or if the depression is severe (ie, with life-
threatening behavior such as suicide attempts),
electroconvulsive therapy is indicated and patients should
be hospitalized.
As dementia progresses, more troubling behaviors such as
agitation, aggression, wandering, sleep disorders, and
inappropriate sexual behavior are observed. The decision
for placement in institutions is usually made when
problem behaviors become unmanageable, when more
assistance is necessary in performing activities of daily
living, when caring duties exceed the capacity of the
caregiver, or when a breakdown in the family caregiver's
health occurs.
Further Outpatient Care
Regular follow-up every 4-6 months is
recommended to assess the patient's general
condition and cognitive and noncognitive
symptoms.
Frequent visits may be needed for patients
with behavioral problems and patients who
are on specific therapies such as
neuroprotective agents.
Treatment of risk factors such as
hypertension, hypercholesterolemia, and
diabetes mellitus require special attention.
Deterrence/Prevention
Vascular cognitive impairment is modifiable and preventable.
Modifying vascular risk factors (eg, hypertension, diabetes
mellitus, smoking, hyperhomocystinemia) and dietary factors
(eg, hypercholesterolemia) in midlife may help to prevent
stroke and vascular dementia. The single most important
risk factor is hypertension. Epidemiologic cohort studies and
intervention trials with antihypertensive medications
demonstrated the usefulness of antihypertensive drugs in
the prevention of vascular dementia.
Appropriate treatment for atrial fibrillation, coronary artery
disease, congestive heart failure, and stroke is also
recommended.
Adequate management of vascular risk factors, stroke, and
heart disease in middle age may be the most effective way
to prevent vascular dementia later in life. The distinction
between vascular dementia and Alzheimer dementia is
becoming increasingly blurred because vascular risk factors
play a role in both diseases.
 In patients with early cognitive
impairment or with neuroimaging
findings that demonstrate leukoaraiosis
or stroke, secondary prevention can be
facilitated by applying standard stroke-
preventive therapies such as
antiplatelet agents, warfarin, or carotid
endarterectomy according to accepted
guidelines.
Complications
Behavioral problems, including wandering, delusions,
hallucinations, and poor judgment
Depression
Falls and gait abnormality
Aspiration pneumonia
Decubitus ulcers
Caregiver burden and stress: This should be
considered a complication of any dementia, including
vascular dementia. This can lead to increased
psychiatric and medical morbidity in the caregiver.
Prognosis
According to some studies, vascular dementia
shortens life expectancy by approximately
50% in men, in persons with lower education,
and in persons who perform worse on
neuropsychological tests.
The causes of death are due to complications
of dementia, cardiovascular disease, and
miscellaneous factors, including malignancy.
Patient Education
Caregiver education is important to dementia
management.
Structured, respectful, and friendly caregiving is best, and it
forms the most important aspect of behavioral care for
patients with vascular dementia.
Educating the caregiver on how to take care of these
patients, how to react to certain behaviors and agitation,
and how to reorient the patient improves the quality of care
and treatment in these patients.
Well-informed caregivers are best equipped to address the
problems that vascular dementia presents.
 Guidelines for caregiver education are as follows:
Use short simple sentences when communicating
with patients with dementia.
Simplify and create a routine for all self-care tasks
such as bathing and dressing.
Establish a daily routine for all activities such as
meals, medication administration, recreation,
exercise, and sleep.
To reorient the patient, use signs and pictures,
clocks and calendars, family photos, and a list of
daily activities.
Use distraction, not confrontation, to control
irritable or socially inappropriate behaviors.
 Initiate discussion about long-term care
planning, including nursing home placement
and issues regarding caregiver stress and
respite care. Respite care is a community
resource that gives the caregiver relief for a
short period.
Day programs can also provide relief for
families, particularly working families, and
can provide structure and activities for
patients with dementia.
Thank You