vascular dementia – biopsychosocial aspects! dr maryam hussain dr cornelia van ineveld march 11...

Vascular Dementia – Vascular Dementia – biopsychosocial aspects!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 cognition2 year history of gradual decline in cognition and function

Initially difficulty with memory and higher order tasks1 year ago episode of sudden confusion with slurred speech, resolved but cognition worse6 months ago developed mild paranoia, mixing up pills, fire on stove6 weeks ago worsened confusion with slurred speech, drooped face, signs resolved but cognition worse

Past history: Diabetes Mellitus Type II HypertensionOsteoarthritis (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 recallClock: All numbers spaced on rightVerbal fluency 4 (normal 10)Impaired namingDifficulty following complex commandsAnxious, repetitive, notable word finding problemsMild 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

CTTwo 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 dementiaClinical 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 groupsDiagnosis

memory impairmentimpairment in other cognitive domainsprogressiveimpairment 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 commonestExpected that VaD will become commonest form of dementia throughout the world

History…. (just for fun!)

17th century – Thomas Willis described post-apoplectic dementia1894 – 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 dementia1970s – AD identified as the most common cause of dementiaAt 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 DementiaCognitive 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!

Vascular DementiaGenerally clinicians look for

Stepwise progression, prolonged plateaus or fluctuating courseFocal cognitive deficits but not necessarily memory impairmentImpaired executive function (difficulty problem solving, difficulty with judgement)

Diagnosis strengthened byFocal neurological signs (weakness on one side, difficulty with speech)Neuroimaging (CT or MRI) consistent with ischemiaCV risk factors, concurrent peripheral vascular disease, coronary artery disease etc

Objectives





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 strokeDementia 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 commonLocation 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 ageLower educationRecurrent strokeLeft hemisphere strokeTrouble swallowing, gait changes and urinary incontinenceAcute complications of stroke (seizures, cardiac arrhythmias, aspiration pneumonia etc)

Small Vessel Disease

Frontal lobe deficitsExecutive dysfunctionInattentionDepressive mood changesChanges in gaitParkinsonismMemory 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





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 vulnerabilityIncreasingly simple and automatic behaviour as disease progresses (switching lights on and off just because they can!)

Abulia – pervasive lack of initiative or driveDisinhibitionDepressionAD 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





Diagnostic tests

Treatment options

Risk factors

HypertensionDiabetesHyperlipidemiaAge GenderRaceHyper-homocysteinuria

Clinical examination

Clinician assessmentDemographics, 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 AssessmentsBloodwork: C-reactive protein, lipids, homocysteine, glucose, HbA1C, insulin, clotting factors

Objectives





Diagnostic tests

Treatment options

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/

Cognitive Tests

www.mocatest.org

Objectives





Diagnostic tests

Treatment options

Enduring POA, health care proxy, will etc.

Distraction techniquesProviding “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)

Treatment

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 drugMemantine – may be useful as an adjunct to AChEI in patients with moderate to severe dementia, not covered by PharmacareAnti depressants (specifically SSRIs)Atypical antipsychotics

Take Home Messages

VaD is a common cause of dementiaLook for risk factors of VaD and focal neurological signsSignificant memory impairment is not always presentClassic step wise progression not always presentBPSD 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

vascular dementia – biopsychosocial aspects! dr maryam hussain dr cornelia van ineveld march 11...

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