Transcript Slide 1

Vascular Dementia –
biopsychosocial aspects!
Dr Maryam Hussain
Dr Cornelia van Ineveld
March 11th, 2008
Clinical Vignette
82 year old female, widowed, referred
because of rapid decline in cognition
2 year history of gradual decline in
cognition and function
Initially difficulty with memory and higher order
tasks
1 year ago episode of sudden confusion with
slurred speech, resolved but cognition worse
6 months ago developed mild paranoia, mixing
up pills, fire on stove
6 weeks ago worsened confusion with slurred
speech, drooped face, signs resolved but
cognition worse
Past history:
Diabetes Mellitus Type II
Hypertension
Osteoarthritis (knees)
Cataracts
Meds:
Glyburide (diabetes)
Metformin (diabetes)
Enalapril (high blood pressure)
Hydrochlorthiazide (high blood pressure)
Aspirin
Cognitive testing:
MMSE 18/30 (normal ≥24), 0/3 recall
Clock: All numbers spaced on right
Verbal fluency 4 (normal 10)
Impaired naming
Difficulty following complex commands
Anxious, repetitive, notable word finding
problems
Mild paranoia
Physical Examination:
Strength equal throughout
Reflexes equal throughout
Increased motor tone bilaterally, no tremor
Difficulty with rapid alternating movements
Positive palmo-mental frontal release sign
bilaterally
Gait: slowed, decreased step height,
cautious, Romberg negative
CT
Two very small strokes deep inside the
brain
Brain is smaller than it should be given
her age
Other changes deep inside the brain that
tell us it is not getting enough oxygen
(white matter ischemic changes)
Diagnosis
Mixed dementia
Clinical features of Alzhiemer’s Disease: prominent
memory loss, language changes, behavior problems
Risk factors for stroke, two suspicious events with
possible step-wise decline, CT evidence of strokes
Rapidity of decline consistent with mixed
disease
Presence of cerebrovascular (stroke) lesions with AD
pathology = more severe disease presentation
Objectives
What is Vascular Dementia (VaD)?
Different types of VaD
Neuropsychiatric manifestations
Risk factors & common presentations
Diagnostic tests
Treatment options
Dementia
Common condition, especially in the
oldest old groups
Diagnosis
memory impairment
impairment in other cognitive domains
progressive
impairment in functional status
Associated with considerable morbidity
and mortality
Types of dementia
Alzheimer's dementia (AD): 60%
Vascular dementia (VaD): 15-20%
Lewy Body dementia 10%
Others including frontal lobe dementia,
alcohol, CBG 10%
Japan/China – VaD is the commonest
Expected that VaD will become commonest
form of dementia throughout the world
History…. (just for fun!)
17th century – Thomas Willis described postapoplectic dementia
1894 – Otto Binswanger and Alois Alzheimer
differentiated between VaD and neurosyphilis (and
sub-categorized VaD into 4 subtypes)
1910 – Kraeplin concluded that “arteriosclerotic
insanity” was the most frequent form of senile
dementia
1970s – AD identified as the most common cause
of dementia
At the same time Tomlinson, Blessed and Roth
showed that loss of more than 50-100mL of brain
tissue from strokes caused cognitive impairment
and the term “multi-infarct dementia” was coined
Language, language, language
Vascular Dementia
Cognitive deficits meet clinical criteria for
dementia
Also has been called: multi-infarct dementia,
ischemic vascular dementia, arteriosclerotic
dementia, cerebrovascular dementia, ischemicvascular dementia
4 sets of diagnostic criteria: all give you slightly
different results
You can see why this is a difficult area!
Vascular Dementia
Generally clinicians look for
Stepwise progression, prolonged plateaus or
fluctuating course
Focal cognitive deficits but not necessarily
memory impairment
Impaired executive function (difficulty problem
solving, difficulty with judgement)
Diagnosis strengthened by
Focal neurological signs (weakness on one
side, difficulty with speech)
Neuroimaging (CT or MRI) consistent with
ischemia
CV risk factors, concurrent peripheral vascular
disease, coronary artery disease etc
Objectives
What is Vascular Dementia (VaD)?
Different types of VaD
Neuropsychiatric manifestations
Risk factors & common presentations
Diagnostic tests
Treatment options
Clinical Categories
Large Vessel Vascular Dementia
Small Vessel Vascular Dementia
Ischemic-Hypoxic Vascular Dementia
Hemorrhagic dementia
Large Vessel
Post-stroke dementia/ Multi-infarct
dementia
Dementia developing after multiple completed
infarcts
Significant proportion of post-stroke dementia
remains undiagnosed
Strategic stroke
Dementia developing after occlusion of a single
large - sized vessel in a functionally critical area
Easiest to recognize, temporal relationship
of event and cognitive loss usually evident
Incidence estimates (3 months
post CVA) vary: 25-41%
Clinical features will depend largely on
what part of the brain was damaged
Depression common
Location of vascular lesion is likely
more important than how much tissue
died
Why do some patients with stroke have
cognitive impairment and others don’t?
Risk factors for post-stroke VaD:
Older age
Lower education
Recurrent stroke
Left hemisphere stroke
Trouble swallowing, gait changes and
urinary incontinence
Acute complications of stroke (seizures,
cardiac arrhythmias, aspiration pneumonia
etc)
Small Vessel Disease
Frontal lobe deficits
Executive dysfunction
Inattention
Depressive mood changes
Changes in gait
Parkinsonism
Memory impairment is less pronounced
More sub-acute course
Magnetic
resonance image
of the brain, T2
axial view without
contrast
enhancement.
Note the areas of
increased signal
bilaterally, known
as periventricular
hyperintensity
(arrows).
Mixed dementia
Vascular lesions may have synergistic
effect with AD pathology
If evidence of cerebrovascular
disease present, the density of
plaques and tangles needed to cause
dementia is lower than that needed
for “pure AD”
AD combined with lacunes
Data from Nun Study
Objectives
What is Vascular Dementia (VaD)?
Different types of VaD
Neuropsychiatric manifestations
Risk factors & common presentations
Diagnostic tests
Treatment options
Neuropsychiatric Symptoms
The neuropsychiatric symptoms of
VaD can be very different qualitatively,
as those in AD
Patients with VaD have a higher risk
for institutionalization than those with
AD, partly because of the BPSD
Frontal Sub-cortical symptoms
Area of the brain
responsible for
making us “human”
Complex social
behaviour
Initiative
Forethought
Behavioural
adaptability
Executive dysfunction – poor planning and
judgement, no anticipation of the consequences
of actions
Not thinking things through!
Difficulties with finances, financial vulnerability
Increasingly simple and automatic behaviour as
disease progresses (switching lights on and off just
because they can!)
Abulia – pervasive lack of initiative or drive
Disinhibition
Depression
AD doesn’t normally have above features until
late in the course
What is executive function?
“those processes that orchestrate
relatively simple ideas, movements,
actions into complex goal oriented
behavior” (Royall D)
“frontal executive cognitive functions
control volition, planning,
programming, anticipation, inhibition
of inappropriate behaviors and
monitoring of goal-directed,
purposeful activities” (Roman G)
Depression & VaD
Common, especially with large vessel disease
In up to 40% of VaD patients
Associated with a higher incidence of functional
impairment, failure of rehabilitation, admission to
PCH and death
More common in left hemisphere strokes; however
can be hard to diagnose in patients with right
hemisphere strokes because they have difficulty
with emotional tone of speech and awareness of
symptoms!
Most cases are undiagnosed!
Often tearfulness and sadness are absent
Will have neurovegetative symptoms (sleep
disturbances, changes in appetite, loss of
energy)
Guilt, pessimism, anhedonia are more sensitive
Atypical presentations like somatic complaints,
irritability, unexplained screaming and pathologic
laughing and crying can be seen
Responds well to pharmacotherapy
Cognitive Behavioural Therapy (CBT) less likely
to work secondary to cognitive impairment
Objectives
What is Vascular Dementia (VaD)?
Different types of VaD
Neuropsychiatric manifestations
Risk factors & common presentations
Diagnostic tests
Treatment options
Risk factors
Hypertension
Diabetes
Hyperlipidemia
Age
Gender
Race
Hyper-homocysteinuria
Clinical examination
Clinician assessment
Demographics, family history, cardiac
risk factors, medical history, medications
Height/weight/waist circumference/
BP/timed up and go
Exact circumstances surrounding the
cognitive and functional impairment
Textbook abrupt onset/stepwise decline
often not found
On Examination
Looking for signs of neurological deficits,
parkinsonism, asymmetry, gait changes
Laboratory Assessments
Bloodwork: C-reactive protein, lipids,
homocysteine, glucose, HbA1C, insulin,
clotting factors
Objectives
What is Vascular Dementia (VaD)?
Different types of VaD
Neuropsychiatric manifestations
Risk factors & common presentations
Diagnostic tests
Treatment options
Cognitive Tests
MMSE not adequate because of lack
sensitivity in VCI, as it isn’t a sensitive test
for executive function, inattention, mood or
personality changes
Montreal Cognitive Assessment (MoCA)
Increasingly popular
Designed for vascular dementia
http://mocatest.org/
www.mocatest.org
Objectives
What is Vascular Dementia (VaD)?
Different types of VaD
Neuropsychiatric manifestations
Risk factors & common presentations
Diagnostic tests
Treatment options
Treatment
Enduring POA, health care proxy, will etc.
Distraction techniques
Providing “jobs” e.g.: folding towels, wiping off dishes
Caregiver education – patients with abulia are
not “lazy”, need to limit expectations
If resistive to personal care, limit the amount and
frequency; establish a routine
Rule out depression and treat if needed (most
commonly use serotonin selective reuptake
inhibitors)
Disinhibition – lose manners, become vulgar, are
socially inappropriate, sexually inappropriate,
shop lifting, vagrancy, irritability, combativeness
Educate caregivers: not doing things on purpose,
remove the stimulus or take the patient out of the
situation
If one has to use medication for aggression; use one
medication at a time, lowest possible dose, monitor
closely for side effects
Atypical antipsychotics [risperidone, olanzapine, seroquel],
anticonvulsants [valproic acid and carbamezipine] and
nonselective Beta Blockers [propranalol or pindolol])
In men, may consider hormonal agents that decrease
testosterone levels (medroxyprogesterone and
leuprolide)
“THE BEST NUMBER OF
MEDICATIONS TO USE IS ZERO (or
sometimes one)”
Jonathan T Stewart MD
WHEN IN DOUBT, GET RID OF
MEDICATIONS!
Pharmacologic and medical
treatment of VaD
Primary prevention:
Treatment of HTN, DM, hypercholestrolemia
Secondary prevention:
More aggressive control of HTN, DM and
hypercholestrolemia
Anti-platelet agents like Aspirin and Plavix
Warfarin in patients with Atrial fibrillation
Possible surgery in patients with documented
carotid artery stenosis
STOP SMOKING!!!
Avoid orthostatic hypotension
Good control of congestive heart
failure and obstructive sleep apnea
Once VaD is present,
Acetyl cholinesterase inhibitors (AChEI) –
may have mild - moderate benefit, patients
with VaD are more likely to experience side
effects with AChEI than AD patients and so
may be more likely to discontinue the drug
Memantine – may be useful as an adjunct
to AChEI in patients with moderate to
severe dementia, not covered by
Pharmacare
Anti depressants (specifically SSRIs)
Atypical antipsychotics
Take Home Messages
VaD is a common cause of dementia
Look for risk factors of VaD and focal
neurological signs
Significant memory impairment is not
always present
Classic step wise progression not always
present
BPSD more common and can occur at
earlier stage than AD – behavioral
strategies are helpful
References
Roma, Erkinjutti et al, Lancet Neurology 2002;1: 426-36
Stewart JT, The American Journal of Geriatric Cardiology
2007;16(3):165-70
Roman GC, Med Clin N Am 86 (2002) 477–499
The frontal/subcortical dementias: Common dementing
illnesses associated with prominent and disturbing
behavioral changes. Geriatrics August 2006
www.mocatest.org