2. Vascular Dementia is acquired
cognitive and behavioral dysfunction due to brain
damage caused by cerebrovascular disease.
•Two basic categories, cortical vs. subcortical, with several subtypes
•Must involve tissue damage not just insufficiency
3. Who does VaD strike ?
Dementia affects 10% of people over 65
and 20% of people over 80
Second most common form of dementia
10% to 40% of dementia patients
Mixed with DAT in 10% to 25% of patients
Onset most often in the 7th decade
Men more than woman
Blacks and Asians more than whites
4. What happens after VaD strikes?
Survival lower than other dementias, 3 to 6
years
Death usually from cardiovascular disease or
stroke
Comorbid depression in 25% to 50% of patients
Delusional thinking in 50% of patients
Anxiety in 70% of patients
5. Signs and Symptoms
a “patchy” pattern of intellectual impairment and “stuttering
course”.
memory impairment, poor judgment, dilapidation of cognitive
functioning perseveration
psychomotor slowing, lack of initiative, spontaneity and
perseverance, fatigue, loss of vigor, apathy.
irritability, paranoia, disinhibition
gait problems and falls, weakness, ataxia, rigidity, dysarthria,
parkinsonism, urinary incontinence.
nocturnal confusion, fluctuating mental status, vulnerability to
delirium and “delirium-like” episodes
6. VaD Risk factors
Uncontrolled hypertension 80%
Diabetes Mellitus 20%
Cardiac disease and heart surgery
Hx of stroke or TIA
Hyperlipidemia
Smoking
Substance abuse
Obstructive sleep apnea
Family history
Pulmonary disease
See attached comprehensive list of VaD causes.
7. VaD Subtype:
20% of VaD cases
Patchy pattern of impairment
Apraxia, agnosia, aphasia, agraphia,
inattention
Often in the distributions of the anterior,
middle, or posterior cerebral artery
circulations.
Mostly large, cortical, bilateral infarcts.
Cumulative effect of multiple cerebral embolic strokes
10. VaD Subtype:
Anomia,apraxia,dyscalcuia,agraphia,dyslexia
One large infarct in an area critical to cognitive functioning
• Cerebral artery area
• Thalamus, basal ganglia, angular
gyrus and basal forebrain
• Well-recognized syndrome with
specific neuropsychological features
11. VaD Subtype:
Psychomotor slowing, memory impairment, frontal dysfunction
Parkinsonism, ataxia, and urinary incontinence
Occlusion of small vessels causing subcortical lesions in the basal ganglia,
thalamus, internal capsule and subhemispheric white matter.
13. VaD Subtype:
Memory loss, perseveration, slowing, apathy, dysarthria,
Pseudobulbar palsy, reduced verbal fluency
Caused by uncontrolled hypertension and atherosclerosis
Widespread degeneration of cerebral white matter
14. VaD Subtype:
Pseudobulbar palsy, gaze abnormalities,
arousal problems and psychomotor slowing.
Pyramidal and extrapyramidal disorders.
Prominent frontal systems dysfunction
Pattern of infarction producing multiple small lesions in the basal
ganglia, thalamus, and internal capsule.
15. VaD Subtype:
Most vulnerable zone between middle & posterior arteries.
Aphasia, apraxia, visuospatial and memory deficits.
Reduced cerebral perfusion resulting from cardiac arrest, severe
hypotension, or loss of blood volume causing damage in border
areas between the territories of the major cerebral arteries
16. VaD Subtype:
22% of VaD patients have both large and
small vessel strokes
Next most frequent mixture is lacunar
state and Binswanger’s disease, 20%
Prevalence of mixed forms increases
with age
17. Differential Diagnosis
Vascular Dementia Alzheimer's Disease
Onset &Course Abrupt & stepwise Insidious & gradual
Risk factors HTN, DM, CVD, CVA, TIA Family history of DAT
Early memory impairment
Mental Status Fluctuating Greater intellectual loss
Personality Preserved Not preserved
Language Better fluency Worse fluency
Behavior Apathy & lability Loss of insight
Neuro exam Focal findings Non-focal findings
Neuroimaging CVA, white matter loss Generalized atrophy
Hallucinations “Delirium-like” episodes Late & vague
Neurological Ataxia, weakness Late rigidity
