3-A Vascular Dementia

1. Vascular Dementia biopsychosocial aspects! Dr Maryam Hussain Dr Cornelia van Ineveld March 11 th , 2008

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

6months 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

Glyburide (diabetes)

Metformin (diabetes)

Enalapril (high blood pressure)

Hydrochlorthiazide (high blood pressure)

Aspirin

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

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

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)

Mixed dementia

Clinical features of Alzhiemers 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

What is Vascular Dementia (VaD)?

Different types of VaD

Neuropsychiatric manifestations

Risk factors & common presentations

Diagnostic tests

Treatment options

Common condition , especiallyin the oldest old groups

Diagnosis

memory impairment

impairment in other cognitive domains

progressive

impairment in functional status

Associated with considerable morbidity and mortality

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

17 thcentury Thomas Willis described post-apoplectic 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

Vascular Dementia

Cognitive deficits meet clinical criteria for dementia

Also has been called: multi-infarct dementia, ischemic vascular dementia, arteriosclerotic dementia, cerebrovascular dementia, ischemic-vascular dementia

4 sets of diagnostic criteria: all give you slightly different results

You can see why this is a difficult area!

Generally clinicians look for

Stepwise progression, prolonged plateaus or fluctuating course

Focal cognitive deficitsbut 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

Diagnostic tests

Treatment options

Large Vessel Vascular Dementia

Small Vessel Vascular Dementia

Ischemic-Hypoxic Vascular Dementia

Hemorrhagic dementia

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 monthspost CVA) vary: 25-41%

Clinical features will depend largely on what part of the brain was damaged

Depression common

Location of vascular lesion is likelymore important than how much tissuedied

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)

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).

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

Diagnostic tests

Treatment options

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

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 doesnt normally have above features until late in the course

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)

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

Diagnostic tests

Treatment options

Hypertension

Diabetes

Hyperlipidemia

Gender

Hyper-homocysteinuria

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

Diagnostic tests

Treatment options

MMSE not adequate because of lack sensitivity in VCI, as it isnt 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

Diagnostic tests

Treatment options

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!

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

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

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

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) 477499

The frontal/subcortical dementias: Common dementing illnesses associated with prominent and disturbing behavioral changes. Geriatrics August 2006

www.mocatest.org

3-A Vascular Dementia

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