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DEMENTIA

DEMENTIA. Prof. Abdulkader Daif Consultant Neurologist 2011. Cognitive Disorders (DSM-IV). 1. Dementia 2. Delirium 3. Amnesic Disorder. Cognition. Brain functions including: Attention Initiation Memory Language Calculation Praxis Executive functions

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DEMENTIA

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  1. DEMENTIA Prof. Abdulkader Daif Consultant Neurologist 2011

  2. Cognitive Disorders (DSM-IV) 1. Dementia 2. Delirium 3. Amnesic Disorder

  3. Cognition • Brain functions including: Attention Initiation Memory Language Calculation Praxis Executive functions Visuospatial capacity Time and space orientation

  4. Common signs Cognitive Disorders: Dementia Definition of Dementia • Clinical condition/syndrome • Loss of cognitive function • Interferes with normal activities • Interferes with social relationships Dementia 1. Impairment of memory 2. Multiple disturbances of cognition 3. Impairment of executive function. 4. Disorientation. 5. Behavioral changes.

  5. Normal cognitive decline vs. Dementia • Cognitive function declines with age: • Slower learning curve • Slower reaction time • Decreased/slower working memory and frontal functions • Maintenance of vocabulary and grammatical structures When compared to younger adults

  6. Dementia is a complex syndrome Cognitive • Amnesia Apraxia Aphasia Agnosia Behavioral Behavioral disturbances • Psychological / psychiatric symptoms Functional Personal ADL Instrumental ADL

  7. Delirium ? Depression ? Reversible causes ? Dementia ? MCI ? CIND ? Acute onset Stepwise Risk factors Gait Neurological Gradual onset Memory loss Normal examination Hallucinations Fluctuations Visuospatial Parkinsonism Behavioural Language Family hx Young onset Vascular Dementia Alzheimer’s Disease Lewy Body Dementia Frontotemporal Dementia

  8. Dementia: Causes 1. Reversible 2. Irreversible

  9. Reversible Dementia (some causes) Dementia due to treatable condition: • infections • toxic effects of drugs (polypharmacy) • normal pressure hydrocephalus • head injury • nutritional deficiencies • Korsakoff’s syndrome (vitamin B1) Wernicke’s disease • metabolic problems (e.g., hypothyroidism) • mental and sensory deprivation • Depression (pseudodementia)* • Delirium* Important to treat early Can become irreversible

  10. WISCONSIN ALZHEIMER’S INSTITUTE Causes of Dementia 14

  11. Prevalence of dementia in Canada: Canadian Study of Health and Aging (1991-1992) • Female to male ratio is 2:1 • 2.4 % for 65-74 years • 34.5% for those aged 85+

  12. Prevalence of Alzheimer’s Disease and Vascular Dementia in Canada • Alzheimer’s 5.1% for 65+ • 1.0% for 65-74 years • 26% for 85+ years • Vascular dementia 1.5% for 65+ • 0.6 % for 65-74 years • 4.8 % for 85+ years

  13. Vascular Dementia: Diagnosis • Diagnostic criteria of memory decline, loss of functioning similar to AD, but: • Requires presence of focal neurologic deficits reflecting a CVA or multiple cerebrovascular risk factors • Hypertension • Coronary artery disease • Hypercholesterolemia • Obesity • Type II diabetes • Epidemiology • Second most common cause of dementia next to AD.

  14. Vascular Dementia • Symptoms • Mood lability • Stepwise course of illness • May plateau • Course is more variable than the progression of AD • Multiple medications and comorbid illnesses associated with the vascular risk factors increase vulnerability to delirium (confusion).

  15. Dementia: Vascular Dementia Features • Associated with damage to the cerebral blood vessels • through arteriosclerosis • found in middle and later life (age of onset between 50-70) • accumulated effect of multiple cortical and subcortical infarcts • lead to clinical presentation • incidence higher in men • first sign delirium or small stroke

  16. Vascular Dementia MRI Imaging: Periventricular hyperintensities Ventricular capping “Small vessel ischemia”

  17. Dementia: Vascular Dementia Clinical Presentation • Abrupt onset • step-wise deterioration • somatic complaints • emotional incontinence • history of hypertension • history of cebrovascular accidents • focal neurological symptoms • focal neurological signs

  18. Management of vascular dementia • Risk assessment • Age, hypertension, smoking, diabetes, history of stroke/TIA • Reduction of risk of further damage • Management of stroke and risk factors • Treatment of secondary conditions1 • Depression, anxiety, agitation • Treatment of dementia symptoms • Cognition, global function, activities of daily living 1Gupta A, et al. Int J Clin Pract. 2002;56:531-537.

  19. Dementia:Alzheimer’s Disease History Alois Alzheimer (1864-1915) • Patient Auguste D. had dementia symptoms • Brain studies after her death revealed microscopic changes • Symptoms due to neuronal changes

  20. Dementia and Related Neurological Disorders: Alzheimer’s Disease Criteria for probable Alzheimer’s diagnosis= • Dementia • Significant cognitive deficiencies • Progressive deterioration • No loss of consciousness • 40-90 years of age • No other diseases • Medical tests • Family history • Brain scans • Other symptoms Also includes

  21. Alzheimer’s Disease: “Stages” of Progression Psychological Symptoms Early Memory loss for familiar objects and events Regular progression of loss Middle Personality changes Behavior changes Late Loss of ability to perform simple everyday functions People do not die of Alzheimer’s per se.

  22. Clinical Presentation: • Memory loss • Aphasia • Apraxia • Agnosia • Disturbance in executive functioning Diagnosis done by exclusion Autopsy is only reliable method

  23. Pathologic Hallmarks of AD • Neurofibrillary Tangles (NFT) • Cytoskeletal protein • Hyperphosphorylated Tau protein • Neuritic Plaques • Extracellular compacted insoluble amyloid protein • Aß42 peptide – abnormal secretase cleavage • Neurotoxic properties

  24. CSF Amyloid and Tau • CSF • Aß42 levels (not total Aß) are reduced in CSF in AD compared to other dementias or control subjects. • Reduction due to insolubility of Aß42 in plaques • CSF Tau • Elevated in AD relative to controls • BUT also elevated in patients with other neurologic diseases • Current Consenus • Combination of Aß and Tau better than either alone • Knopman D, Arch. Neurol, 58; 2001.

  25. AD Etiology – microscopic

  26. Amyloid plaque Alzheimer’s Disease Amyloid Plaques • Collection of waste products of dead neurons around a core of amyloid. • Formation occurs long before symptoms are evident • Amyloid-42 most common form found in plaques

  27. Tangles and Plaques http://www.ahaf.org/alzdis/about/AmyloidPlaques.htm

  28. Alzheimer’s Disease Neurofibrillary Tangles Neurofibrillary tangle • Made up of tau protein • Tau maintains microtubules within axons • Tangles form when tau changes chemically and can no longer support the microtubules • Leads to collapse of transport system within neuron

  29. Alzheimer’s Disease Neurofibrillary Tangles http://www.alzheimers.org/tangle.html

  30. Alzheimer’s Disease Causes of Alzheimer’s Disease Environmental Life style Head injury • Twin data • Japanese men who moved to Hawaii • Nun Study on mental activity • Severe injuries involving loss of consciousness • Causes damage to neurons

  31. Gene Chromosome ApoE gene 19 APP gene 21 Presenilin1 14 Presenilin 2 1 Alzheimer’s Disease Causes of Alzheimer’s Disease Familial Alzheimer’s Disease supports Genetic theory • Early onset • Late onset Majority of early-onset cases

  32. Genes and Alzheimer’s disease(60% - 80 % of causation)(all known genes relate to bamyloid) • Familial AD (onset < 60 y/o) (<5%) • Presenilin I, II (ch 14, 1) • APP (ch 21) • Non-familial (late onset) • APOE • Clinical studies suggest 40 – 50% due to e4 • If e2 is considered, may be 95% of causation • Population studies suggest 10 – 20% cause • Evolution over last 300,000 to 200,000 years • At least 20 other genes

  33. Risk Factors • Advanced age • 4-allele of apolipoprotein E-Gene (ApoE) • Female gender?

  34. Focal neurodegenerative dementias: Frontotemporal Lobar Degeneration (FTLD) Focal neurodegenerative diseases, affecting primarily temporal and frontal lobes: 1. Fronto-temporal dementia 2. Primary progressive aphasia 3. Semantic dementia

  35. Pick’s Disease -1892 Arnold Pick Frontotemporal dementia • Frontal lobar atrophy • Pick’s bodies – tau protein • Chr 17 abnormality

  36. FTLD - General Features • 1. Pre-senile dementias (<65 years of age) • 2. SPECT Scan: Anterior (frontotemporal defects) • 3. Normal EEG • 4. Memory and visuospatial functions are normal until the disease is advanced

  37. FTD: Pathological Types • Pick’s disease • Non-specific frontal degeneration • Frontal degeneration with anterior spinal neuron loss

  38. FTD: Clinical Features (I) • Behavioral abnormalities. • Inertia, loss of volition, decreased initiative. • Social disinhibition, loss of insight. • Impulsivity, overactivity. • Emotional blunting. • Stereotyped and perseverative behavior.

  39. FTD: Clinical Features (II) • Mean age of presentation: 53 years • Predominantly males • High familial aggregation • Cognitive impairment mostly in areas of executive function (planning, judgement, problem-solving) and attention • Memory, visuospatial and calculation might be relatively preserved at the beginning • Speech might be either economical leading to mutism, or increased / pressed in disinhibited patients

  40. Frontotemporal Dementia The brain of a person with frontotemporal dementia shows a shrunken and sometimes asymmetric frontal lobe and a normal parietal lobe.

  41. May appear similar to Alzheimer’s….. Early treatment may reverse cognitive changes before they become permanent Triad of symptoms: gait instability, urinary incontinence and dementia Wide-based, shuffling gait with poor coordination Incontinence follows gait change, includes urgency Slow thinking/response, decreased spontaneity Enlarged ventricles on MRI But no evidence of atrophy: Alzheimer’s shows large ventricles due to brain atrophy Normal-Pressure Hydrocephalus 42

  42. Dementia with Lewy Bodies • Cortical Lewy Bodies on path • Overlap with AD and PD • Fluctuations in mental status (may appear delirious) • Early delusions and hallucinations • Mild extrapyramidal signs • Neuroleptic hypersensitivity!!! • Unexplained falls or transient changes in consciousness

  43. Dementia with Lewy Bodies (DLB) • Etiology • Lewy bodies – protein deposits containing damaged neurons • Symptoms: decline in • memory • language • Judgment & reasoning

  44. Lewy Bodies

  45. AIDS dementia complex Approximately two-thirds of persons with AIDS develop dementia, mostly due to AIDS dementia complex. In some patients HIV is found in the CNS at postmortem. In others an immune mechanism or an unidentified pathogen is blamed. Dementia is initially of a "subcortical " type. CT - atrophy; MRI - increased T2 signal from white matter. Treatment with Zidovudine (AZT) halts and partially revers neuropsychological deficit.

  46. Rapid onset marked attentional disturbance confusion prominent/clouding of consciousness fluctuating clinical course agitation and behavioral symptoms potentially reversible Usually insidious onset memory systems impaired consciousness intact slower, progressive course subtle behavioral symptoms can be irreversible Differential DiagnosisDelirium Dementia

  47. MANAGEMENT………. 49

  48. SYMPTOM MANAGEMENT Psychoses (delusions, hallucinations) Sleep disturbances Aggression, agitation 50

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