VASCULAR DEMENTIA AND

ALZHEIMERS DEMENTIA

A. Laksmidewi
Department Of Neurology Faculty Of Medicine, Udayanauniversity
Sanglah Hospital Denpasar
THE NEUROBEHAVIOR

A patients performance on mental status

examination is always in part a reflection of
non disease variables :
*Age
*Level of education
*Cultural background
*Employment history
*Language
THE NEUROBEHAVIOR DOMAINS

1. Attention & concentration.

2. Language.
3. Memory.
4. Visuospatial function.
5. Emotion & Executive functions
(cognitive skills).
 What is Dementia?
Dementia is a term used to describe a
cluster of symptoms including:
Forgetfulness (progressive)
Difficulty doing familiar tasks
Confusion
Poor judgment
Decline in intellectual functioning
Dementia is not the name of an actual disease
Dementia is not a part of normal aging
 Diagnostic Criteria for Dementia (DSM-IV)

Memory impairment: Impaired ability to learn new information or to recall

old information

One or more of the following: aphasia ,apraxia; agnosia. disturbance in

executive functioning-impaired ability to plan, organize, sequence, abstract

The cognitive deficits : result in functional impairment

(social/occupational)

The cognitive deficits do not occur exclusively solely during

a delirium

NOT due to other medical or psychiatric conditions

Etiology of Dementia Frequency(%)
Alzheimer disease 50-60
Vascular dementia 10-30
Depresion 5-15
Alcoholics 1-10
Metabolic disorders 1-10
Intoxications 1-10
Hydrocephalus 1-5
Cerebral anoxia 1-2
Cerebral infections 1-2
Cerebral injuries 1-2
Subdural hematome 1-2
Others 10-20
DEMENTIA DIAGNOSTIC CRITERIA
(DSM-IV 1994)
Dementia is characterized by development of
Multiple cognitive deficits (including Memory
impairments):
1. Demonstrated by memory loss, Impaired ability to
learn new information) and impairment of
language, praxis, recognition or abstract thinking.
2. The cognitive impairment is chronic and
progressive and has resulted in functional decline.
3. Delirium has been ruled out.
 What it is?
Type ?

DEMENTIA

Diagnose? Management?
COMMON SYMPTOM OF DEMENTIA

Memory loss affecting job skills/other activities

Difficulty performing familiar tasks
Problem with language
Disorientation
Impairment judgment
Problems with abstract thinking
Continuous misplacement of personal
possessions
Changes in mood or behavior
Changes in personality
Loss of initiative
 Inside the Human
BrainMain Players
The Three

1. Cerebral Hemispheres where sensory information received from

the outside world is processed; this part of the brain controls
voluntary movement and regulates conscious thought and mental
activity:
accounts for 85% of brains weight
consists of two hemispheres connected by the corpus callosum
is covered by an outer layer called the cerebral cortex

Slide 9
 Inside the Human
BrainMain Players
The Three

2. Cerebellum in charge of balance and coordination:

takes up about 10% of brain
consists of two hemispheres
receives information from eyes, ears, and muscles and
joints about bodys movements and position

Slide 10
 Inside the Human
BrainMain Players
The Three

3. Brain Stem connects the spinal cord with the brain

relays and receives messages to and from muscles, skin,
and other organs
controls automatic functions such as heart rate, blood
pressure, and breathing

Slide 11
 Inside the Human
Brain
Other Crucial Parts

Hippocampus: where short-term memories are converted to long-term

memories
Thalamus: receives sensory and limbic information and sends to cerebral
cortex
Hypothalamus: monitors certain activities and controls bodys internal
clock
Limbic system: controls emotions and instinctive behavior (includes the
hippocampus and parts of the cortex)

Slide 12
VASCULAR DEMENTIA(VaD)
VaD is probably the second most common form of
dementia
Dementias presenting with prominent motor features
VaD is a heterogenous syndrome
Pathophysiological classification of VaD are due to:
-Vessel size, Haemodynamic factors,
Venous occlusion,Hemorrhagic factors
-Mixed type dementia
NT. deficit occurred in VaD especially in the
cholinergic system
Clinical sign ,relevant with location, volume &
pathophysiologies.
The DSM-IV definition for VaD

Focal Neurologic signs and symptoms or laboratory

evidence of focal neurologic damage.
The cognitive deficits cause a significant impairment
in social or occupational functioning
> 1 are judge to be etiologically related to the
disturbance
The deficits do not occur exclusively during the
course of delirium
Course characterized by sustained periods of
clinical stability punctuated by sudden significant
cognitive and functional losses
THE KEY ELEMENTS FOR
DIAGNOSING VAD

Clinical diagnosis of VaD ideally includes :

I. Evidence for a dementia syndrome including :
*Memory dysfunction
*Evidence for other cognitive or
behavioral deficits,which may include
1. Executive dysfunction
2. Focal cortical sign (eg. aphasia,apraxia or
agnosia)
3. Personality changes (eg.apathy or irritability)
4. Affective changes (eg depression or anxiety)
The key.

II. Evidence for cerebrovascular disease, supported by at least one of

the following:
*History of clear-cut cerebrovascular event (eg. acute
hemiparesis)
*Physical findings consistent with cerebrovascular events
*Imaging findings consistent with clinically relevant CVD

III Evidence that I and II are temporally linked , e.g one of the following
*No evidence for cognitive decline prior to stroke episode
*Abrupt onset of dementia with focal neurologic features
*Step wise decline in cognition
VaD, Criteria NINDS-AIREN
I.Probable VaD:
a. Deficits in multiple domains of cognitive functions, confirmed
clinically and neuropsychologically
and interfering with every day life.
b. CVD: Focal neuro signs & evidence of VD on CT or MRI.
c. Temporal relationship between I a & I b.
Features consistent include: early gait disturbance, unsteadiness .
Urinary symptoms,pseudobulbar palsy, personality and mood
changes.
Features that make diagnosis unlikely include: early memory
deficit/progressive without focal lesions on neuroimaging ,
absence of focal neuro signs, absence of vascular lesions on CT
or MRI.

CONTINUE.
II.Possible VaD:
a. Features of section I a with focal neuro signs but
CT/MRI has not been performed to confirm vascular
lesion
b. Absence of a temporal relationship between I a & I
b.

III Definite VaD

a. Clinical criteria for probable VaD
b. Histopathological evidence from biopsy or autopsy
c. Absence of neuropathological features of AD
d. Absence of other clinical or pathological cause for
the disease.
PATHOLOGICAL LESIONS CAPABLE
OF PRODUCING VAD AS FOLLOW

1. Multi-infarct dementia.
2. Strategic single infarct dementia.
3. Small vessel disease with dementia.
4. Ischemic-hypoxic dementia.
5. Hemorrhagic dementia.
RISK FACTORS FOR VAD:

1. Hypertension.
2. Alcohol use.
3. Smoking.
4. Dietary factors.
5. D.M.
6. Hematologic factors.
Assessment
Cognition

Dementia
Function Behavior
Ass.

Careful history from family members

Physical /Neurological exam.
Evaluation of behavior & mood
ALZHEIMERS DEMENTIA (AD)

AD is the most common form of dementia

This Dementia usually presenting without motor sign.

Criteria For Clinical Diagnosis of AD :

Probable AD
Possible AD
Definite AD
ALZHEIMER DEMENTIA (AD)
Probable AD
Dementia established,deficits in 2/ more areas of
cognition
Progressive worsening of memory etc
Onset between ages 40 and 90
Absence of systemic or other brain diseases
Possible AD
Atypical onset
Presence of a second systemic or brain disorder
sufficient to produce dementia but not considered to
be the cause of dementia
Definite AD
Criteria for probable AD
Histopathologic evidence obtained from a biopsy or
autopsy
ALZEIMERS DISEASE: CLINICAL
Lost of interest
Inability to think clearly
Substandard performance
Wide variation in mood
Loss of recent memory
Diorientasion
Lack of insight
Loss of all intellects
Slurred speech, aphasia
Vegetative
Death by pneumonia, ect.
AD and the
Brain
Preclinical AD
Signs of AD are first noticed in
the entorhinal cortex, then
proceed to the hippocampus.
Affected regions begin to shrink
as nerve cells die.
Changes can begin 10-20 years
before symptoms appear.
Memory loss is the first sign of
AD.

Slide 20
 AD and the
Brain
Mild to Moderate AD
AD spreads through the brain.
The cerebral cortex begins to
shrink as more and more neurons
stop working and die.
Mild AD signs can include
memory loss, confusion, trouble
handling money, poor judgment,
mood changes, and increased
anxiety.
Moderate AD signs can include
increased memory loss and
confusion, problems recognizing
people, difficulty with language
and thoughts, restlessness,
agitation, wandering, and
repetitive statements. Slide 21
AD and the
Brain
Severe AD
In severe AD, extreme shrinkage
occurs in the brain. Patients are
completely dependent on others
for care.
Symptoms can include weight
loss, seizures, skin infections,
groaning, moaning, or grunting,
increased sleeping, loss of
bladder and bowel control.
Death usually occurs from
aspiration pneumonia or other
infections. Caregivers can turn to
a hospice for help and palliative
care.
Slide 22
Alzheimer's Disease: Genetics and Biochemistry

1. Chromosomes 21(APP), 19 (apo-E)

14 (Presenilin 1), 1 (presenilin 2).

2. Expression of 4 of apo-E (dose dependent)

3. Decreased acetylcholine in neocortical

cholinergic terminals
 AD and the Brain
Beta-amyloid Plaques
1. Amyloid precursor protein (APP) is the
precursor to amyloid plaque.
1. APP sticks through the neuron
membrane.
2. Enzymes cut the APP into fragments
of protein, including beta-amyloid.
2.
3. Beta-amyloid fragments come
together in clumps to form plaques.

In AD, many of these clumps form,

disrupting the work of neurons. This
3. affects the hippocampus and other
areas of the cerebral cortex.
Slide 17
AD

Gross Pathology:
Diffuse cerebral atrophy
Dilatation of ventricles
Microscopic :
Neurofibrillary tangles (NFT)
Senile plaques (SP)
Targets in particular :
-cortex,hippocampus,amygdala
-cholinergic basal forebrain
Massive loss of synapses that correlates with
cognitive decline.
 AD and the
Brain
Neurofibrillary
Tangles

Neurons have an internal support structure partly made up of

microtubules. A protein called tau helps stabilize microtubules. In AD,
tau changes, causing microtubules to collapse, and tau proteins
clump together to form neurofibrillary tangles. Slide 18
AD, Atrophy of cerebral cortex
HOW TO DIAGNOSE ALZHEIMER?

How to differentiated AD with other

dementias?
How to make staging in AD ?
What test should be used ?
MMSE , CDT.
CERAD(The Consortium to Established a
Registry for AD)
Table : Comparison of
VaD & AD
Vascular Dementia Alzheimers Dementia
(VaD) (AD)
Gender Males more commonly Females commonly
Genetic Not clear Suspected
Onset Relatively sudden Insidious
Course Stepwise progression Gradual & progress
Somatic Complaints Common Rare
Hypertension More common Less common
Focal Neuro sign Present Unusual
Personality Well preserved Disintegration
Insight Preserved Lost early
Affect Depression, Anxiety, Affect blunted
Lability
MANAGEMENT OF
DEMENTIA
NONPHARMACOLOGICAL THERAPY
Neurocognitive Therapy
(Reminiscent, Reality, Behavior,
Recreation-Music Therapy)

PHARMACOLOGICAL THERAPY
-Cholinesterase Inhibitors
SKOR ISKEMIK HACHINSKI

RIWAYAT DAN GEJALA YA TIDAK

1. AWITAN (ONSET) MENDADAK 2 0
2. DETERIORASI BERTAHAP 1 0
3. PERJALANAN KLINIS BERVARIASI 2 0
4. KEBINGUNGAN MALAM HARI 1 0
5. KEPRIBADIAN RELATIF TIDAK TGG 1 0
6. DEPRESI 1 0
7. KELUHAN SOMATIK 1 0
8. EMOSI TIDAK STABIL 1 0
9. RIWAYAT HIPERTENSI 1 0
10. RIWAYAT PENY SEREBROVASKULER 2 0
11. ARTERIOSKLEROSIS PENYERTA 1 0
12. KELUHAN NEUROLOGI FOKAL 2 0
13. GEJALA NEUROLOGI FOKAL 2 0

< 7 DEMENSIA DEGENERATIF

7 DEMENSIA VASKULAR (VaD)
AKTIVITAS HIDUP SEHARI-HARI:
ADL DAN IADL
ADL (ACTIVITIES OF DAILY LIVING)
NILAI KETERGANTUNGAN PADA BANTUAN:
0 : TIDAK PERLU / MANDIRI
1 : SEDIKIT MEMBUTUHKAN BANTUAN
2 : BANYAK BUTUH BANTUAN/KETERGANTUNGAN PENUH

NO AKTIVITAS 1 2 3
1 MAKAN
2 MENGENAKAN&MELEPASKAN PAKAIAN
3 MENYISIR RAMBUT & BERCUKUR
4 BERJALAN
5 TURUN & NAIK KE TEMPAT TIDUR
6 MANDI
7 KE KAMAR MANDI(TOILETING)
8 BUTUH BANTUAN UNT BELANJA,MANDI DLL
9 INKONTINENSIA(TIDAK; 1-2X/mgg ; 3 mgg )
IADL

IADL (INSTRUMENTAL ACTIVITIES OF DAILY LIVING)

NILAI KETERGANTUNGAN PADA BANTUAN:
0 : TIDAK PERLU / MANDIRI
1 : SEDIKIT MEMBUTUHKAN BANTUAN
2 : BANYAK BUTUH BANTUAN/KETERGANTUNGAN PENUH

NO AKTIVITAS 1 2 3
1. MENGGUNAKAN TELEPON
2. BEPERGIAN DGN KENDARAAN/ BIS/ TAKSI
3. BELANJA BAHAN MAKANAN & PAKAIAN
4. MENYEDIAKAN MAKANAN/TATA MEJA
5. MELAKUKAN PEKERJAAN RUMAH
6. MINUM OBAT SENDIRI
7. MENGATUR KEUANGAN SENDIRI
SKOR ISKEMIK HACHINSKI

RIWAYAT DAN GEJALA YA TIDAK

1. AWITAN (ONSET) MENDADAK 2 0
2. DETERIORASI BERTAHAP 1 0
3. PERJALANAN KLINIS BERVARIASI 2 0
4. KEBINGUNGAN MALAM HARI 1 0
5. KEPRIBADIAN RELATIF TIDAK TGG 1 0
6. DEPRESI 1 0
7. KELUHAN SOMATIK 1 0
8. EMOSI TIDAK STABIL 1 0
9. RIWAYAT HIPERTENSI 1 0
10. RIWAYAT PENY SEREBROVASKULER 2 0
11. ARTERIOSKLEROSIS PENYERTA 1 0
12. KELUHAN NEUROLOGI FOKAL 2 0
13. GEJALA NEUROLOGI FOKAL 2 0

< 7 DEMENSIA DEGENERATIF

7 DEMENSIA VASKULAR (VaD)