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Vascular Dementia – biopsychosocial aspects!

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

  2. 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

  3. Past history: • Diabetes Mellitus Type II • Hypertension • Osteoarthritis (knees) • Cataracts • Meds: • Glyburide (diabetes) • Metformin (diabetes) • Enalapril (high blood pressure) • Hydrochlorthiazide (high blood pressure) • Aspirin

  4. 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

  5. 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

  6. 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)

  7. 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

  8. Objectives • What is Vascular Dementia (VaD)? • Different types of VaD • Neuropsychiatric manifestations • Risk factors & common presentations • Diagnostic tests • Treatment options

  9. 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

  10. 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

  11. History…. (just for fun!) • 17th century – 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

  12. 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, ischemic-vascular dementia • 4 sets of diagnostic criteria: all give you slightly different results • You can see why this is a difficult area!

  13. 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

  14. Objectives • What is Vascular Dementia (VaD)? • Different types of VaD • Neuropsychiatric manifestations • Risk factors & common presentations • Diagnostic tests • Treatment options

  15. Clinical Categories • Large Vessel Vascular Dementia • Small Vessel Vascular Dementia • Ischemic-Hypoxic Vascular Dementia • Hemorrhagic dementia

  16. 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

  17. 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

  18. 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)

  19. 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

  20. Magnetic resonance image of the brain, T2 axial view without contrast enhancement. Note the areas of increased signal bilaterally, known as periventricular hyperintensity (arrows).

  21. 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”

  22. AD combined with lacunes Data from Nun Study

  23. Objectives • What is Vascular Dementia (VaD)? • Different types of VaD • Neuropsychiatric manifestations • Risk factors & common presentations • Diagnostic tests • Treatment options

  24. 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

  25. Frontal Sub-cortical symptoms • Area of the brain responsible for making us “human” • Complex social behaviour • Initiative • Forethought • Behavioural adaptability

  26. 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

  27. 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)

  28. 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!

  29. 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

  30. Objectives • What is Vascular Dementia (VaD)? • Different types of VaD • Neuropsychiatric manifestations • Risk factors & common presentations • Diagnostic tests • Treatment options

  31. Risk factors • Hypertension • Diabetes • Hyperlipidemia • Age • Gender • Race • Hyper-homocysteinuria

  32. 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

  33. 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

  34. Objectives • What is Vascular Dementia (VaD)? • Different types of VaD • Neuropsychiatric manifestations • Risk factors & common presentations • Diagnostic tests • Treatment options

  35. 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 •


  37. Objectives • What is Vascular Dementia (VaD)? • Different types of VaD • Neuropsychiatric manifestations • Risk factors & common presentations • Diagnostic tests • Treatment options

  38. 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)

  39. 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)


  41. 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