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3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
3-A Vascular Dementia
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3-A Vascular Dementia

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

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