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Dementia

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Dementia

  1. 1. 1 DEMENTIA AN APPROACH TO MANAGEMENT AND PREVENTION DR. HASANAH CHE ISMAIL PSYCHIATRISTSCHOOL OF MEDICAL SCIENCES UNIVERSITI SAINS MALAYSIA
  2. 2. 2 Definition of the dementia syndrome DEMENTIA• Multiple cognitive deficits – memory loss – aphasia – apraxia – agnosia – disturbance in executive function• These lead to functional decline
  3. 3. 3 Causes of dementiaReversible dementias Irreversible dementias• Common causes: • Common causes: – Depression – Alzheimers disease – Drug toxicity – Vascular dementia • Other causes – Lewy body disease – Picks disease (dementia of the frontal lobe type) – Parkinsons disease with dementia
  4. 4. 4Differentiating AD from other dementias dementias Cognitive impairment Exclude other causes (e.g. delirium and depression, etc) Dementia Exclude other dementias Alzheimers disease
  5. 5. 5 DEMENTIA• AD represents over 50% of all dementia cases• AD prevalence doubles every 5 years after 60 years of age• AD affects 15 million people worldwide
  6. 6. Short history 1907 Alzheimer reports the first case of August D 1960s Re-emergence of interest in dementia 1970s Cholinergic deficits in AD identified 1980s First trials of cholinergic enhancing therapies 1994 First cholinesterase inhibitor licensed Present First launches of Reminyl, a cholinesterase inhibitor and nicotinic modulatorAlois Alzheimer
  7. 7. 7Prevalence of Alzheimer’s disease 60 50% 50 Prevalence (%) 40 30% 30 20 16% 10 8% 2% 4% 1% 0 60-64 65-69 70-74 75-79 80-84 85+ 95+ Age (years) Kurz A. Eur J Neurol 1998; 5(Suppl 4): S1-8 Wimo A et al. Int J Geriatr Psychiatry 1997; 12: 841-56
  8. 8. 8 Clinical features of AD• Loss of cognition – short-term memory – language – visuospatial functions• Loss of daily function – instrumental activities of daily living (ADL) – self-maintenance skills• Abnormal behaviour
  9. 9. 9 ‘Normal’ ageing vs. dementia• Multiple cognitive domains affected• Decline of language and orientation• Deterioration in common activities of daily living
  10. 10. 10 Clinical features of AD Insidious onset Cognitive decline Functional * Memory loss impairment * Aphasia * IADL * Apraxia * ADL * Agnosia AD * Executive functionBehavioral signs difficulties* Mood swings* Agitation Age over 60 years* Wandering No gait difficulties IPA AD Conference, 1996
  11. 11. 11 Natural history of Alzheimer’s disease Early diagnosis Mild-to-moderate SevereMini-Mental State Examination (MMSE) 30 Symptoms 25 Diagnosis 20 Loss of functional independence 15 Behavioural problems 10 Nursing home placement 5 0 Death 1 2 3 4 5 6 7 8 9 Time (years) Feldman and Gracon. The Natural History of Alzheimer’s Disease. London: Martin Dunitz, 1996
  12. 12. 12 Anatomical features of AD• Gross atrophy Normal brain – shrinkage of brain – thinning of gyri – widened sulci Alzheimer brain
  13. 13. The pathological cascade of AD Clinical symptoms Cholinergic dysfunction NeurodegenerationNeurofibrillarytangles GeneticTAU hypophosphorylation β-amyloid Apo-E risk factors PS1,2Environmental APP Pathogeneticrisk factors mutations
  14. 14. 14 The cholinergic system AChE = acetylcholinesterase Presynaptic Acetyl CoA ChAT = choline nerve terminal + acetyltransferase Choline = acetylcholine ChAT Acetylcholine N = nicotinic M = muscarinic M receptor N receptor Important in: Memory and learningPostsynaptic Sensory andnerve terminal M receptor N receptor attentional functions
  15. 15. 15Cholinergic dysfunction in AD∀ ↓ Cholinergic neurons∀ ↓ Choline uptake∀ ↓ Acetylcholine release∀ ↓ Choline acetyltransferase∀ ↓ Nicotinic receptors= progressively impaired memory and cognition
  16. 16. 16NEUROTRANSMITTERACETYLCHOLINENucleus basalis ofMeynert
  17. 17. 17 Making a diagnosis of ADNeed for early Consistent onset, clinical diagnosis presentation and disease progression Practical assessment methods New symptomatic Patient and treatments caregiver support IPA AD Conference, 1996
  18. 18. 18PERUBAHANKOGNITIF:INGATANBAHASAPERTIMBANGAN
  19. 19. 19PERUBAHANPADAPERSONALITI,KELAKUAN:JUGA GEJALAPSIKIATRISEPERTIDELUSI &HALUSINASI
  20. 20. 20PERUBAHANMOTOR =>TERBARINGDI ATAS KATIL=>MENELANTERGANGGU=>MAUT
  21. 21. 21 Dementia or deliriumDementia Delirium* Insidious onset with unknown date * Abrupt, precise onset, known date* Slow, gradual, progressive decline * Acute illness, lasting days or* Generally irreversible weeks* Disorientation late in illness * Usually reversible* Slight day-to-day variation * Disorientation early in illness* Less prominent physiological OR * Variable, hour by hour changes * Prominent physiological changes* Consciousness clouded * Fluctuating levels of consciousness only in late stage * Short attention span* Normal attention span * Disturbed sleep-wake cycle;* Disturbed sleep-wake cycle; hour-to-hour variation day-night * Marked early psychomotor* Psychomotor changes late in illness changes Ham, 1997
  22. 22. 22 Dementia or depressionDementia Depression* Insidious onset * Abrupt onset* No psychiatric history * History of depression* Conceals disability * Highlights disabilities* Near-miss answers * ’Dont know answers* Mood fluctuation day to day * Diurnal variation in mood* Stable cognitive loss OR * Fluctuating cognitive loss* Tries hard to perform but is * Tries less hard to perform unconcerned by losses and gets distressed by losses* Short-term memory loss * Short- and long-term memory* Memory loss occurs first loss* Associated with a decline in * Depressed mood coincides with social function memory loss * Associated with anxiety Ham, 1997, modified from Wells CE, 1979
  23. 23. 23 Diagnosing AD in primary care clinical history, questioningAsk the following questions: * How did it start? Was it sudden or gradual? * How long has it been going on? * Is the situation progressing? If so, how rapidly? * Is it step-wise or continuous? * Is it worsening, fluctuating or improving? * What changes have you noticed? * Has there been a change in personality? * Has the patient suffered any delusions or hallucinations? * Does the patient become agitated or wander?Clinical History
  24. 24. 24 Diagnosing AD in primary care functional assessment Score Score Maximum ActualFunctional Activities Questionnaire (FAQ)1. Dealing with financial matters, paying bills, writing checks 32. Keeping records of taxes, business affairs 33. Shopping for everyday necessities: groceries, clothes, etc 34. Hobbies or playing games 35. Making tea, turning the kettle on and off 36. Cooking a balanced meal 37. Perception of current events 38. Level of attention and understanding: books, television 39. Memory: remembering appointments and medications 310. Getting about: driving or taking public transport 3 Total 30Functional Assessment Pfeffer et al 1982
  25. 25. 25 Diagnosing AD in primary care physical examination* Life-threatening conditions, e.g. mass lesions, vascular lesions and infections* Blood pressure and pulse* Vision and hearing assessments* Cardiac and respiratory function* Mobility and balance* Sensory and motor system examination (tone, reflexes, gait and coordination) and depressive symptoms (sleep and weight)Physical examination
  26. 26. 26 Diagnosing AD in primary care laboratory tests All patients Most patients * Complete blood count * ECG * Thyroid function * Chest X-ray * Vitamin B12 and folate * Syphilis serology * BUN and creatinine * Calcium * Glucose * Electrolytes * Urinalysis * Liver function testsLaboratory tests
  27. 27. 27 Diagnosing AD in primary care neuroimaging, computed (axial) tomography (CT) Various CT scan reports in AD * Normal examination for the patients age * Generalized cerebral atrophy * Small vessel changes, areas of leucoencephalopathy * No signs of subdural hematoma (if head trauma suspected) * Absence of specific areas of cerebral infarctions or evidence of strokeNeuroimaging
  28. 28. 28 Diagnosing AD in primary care cognitive assessments, MMSE Score Score Maximum ActualCognitive areaMini Mental State Examination: test outline and scoringOrientation*What is the (date, day, month, year, season)? 5* Where are you (clinic, town, country)? 5Memory*Name three objects. Ask the patient to repeat them 3Attention*Serial sevens. Alternatively ask the patient to spell world 5 backwards (dlrow)Cognitive Assessment Folstein et al 1975
  29. 29. 29 Diagnosing AD in primary care cognitive assessments, MMSE (continued) Score Score Maximum ActualCognitive areaMini Mental State Examination: test outline and scoringRecall*Ask for the three objects mentioned above to be repeated 3Language*Name a pencil and watch 2*Repeat, No ifs, ands or buts’ 1*A three stage command 3*Read and obey - CLOSE YOUR EYES 1*Write a sentence 1*Copy a double pentagon 1 Total 30Cognitive Assessment Folstein et al 1975
  30. 30. 30 Clinical features of AD Mild stage of AD (MMSE 21-30) IMPAIRMENTCognition Function Behavior* Recall/learning * Work * Apathy* Word finding * Money/shopping * Withdrawal* Problem * Cooking * Depression solving * Housekeeping * Irritability* Judgement * Reading* Calculation * Writing * Hobbies Adapted from Galasko, 1997
  31. 31. 31 Clinical features of AD Moderate stage of AD (MMSE 10-20) IMPAIRMENTCognition Function Behavior* Recent memory * IADL loss * Delusions (remote memory * Misplacing * Depression unaffected) objects * Wandering* Language (names, * Getting lost * Insomnia paraphasias) * Difficulty * Agitation* Insight dressing * Social skills* Orientation (sequence and unaffected* Visuospatial ability selection) Adapted from Galasko, 1997
  32. 32. 32 Clinical features of AD Severe stage of AD (MMSE <10) IMPAIRMENTCognition Function Behavior* Attention * Basic ADLs * Agitation* Difficulty -Dressing - Verbal performing -Grooming - Physical familiar activities -Bathing * Insomnia (apraxis) -Eating* Language -Continence (phrases, mutism) -Walking -Motor slowing Adapted from Galasko, 1997
  33. 33. 33 Diagnosing AD in primary care cognitive assessment The Clock Draw Test Time: 5.00 Time: .10.30 Score: 7 (normal) Score: 3 (demented) Time: no real time Time: 1/4 past 25 Score: 2 (demented) Score: 3 (demented)Cognitive Assessment Thalmann et al 1996.
  34. 34. 34 AD prognosis Optimal caseMini Mental State Examination score 25 ---------------------| Symptoms 20 |----------------------| Diagnosis 15 |-----------------------| Loss of functional independence 10 |--------------------------------| Behavioral problems Nursing home placement 5 |-------------------------------------------| 0 Death |------------------------------------------ 1 2 3 4 5 6 7 8 9 Years Feidman and Gracon, 1996
  35. 35. 35 NEUROPSYCHIATRIC SYMPTOMS @ BPSDAPATHY 72% AGITATION 60%IRRITABILITY 42% PACING ETC 38%DEPRESSION 38% ANXIETY 40%DELUSION 22% HALLUCINATION 10%EUPHORIA 8% DISINHIBITION 38%
  36. 36. 36 BPSD DELUSION :CROSS SECTIONAL STUDIES 20-50%LONGITUDINAL STUDIES 50-70% • THEFT • INFIDELITY • CAPGRAS • PHANTOM BOARDERS • PICTURE SIGN
  37. 37. 37 Neuropsychiatric disturbances in AD 80 70 60Patients (%) 50 40 30 20 10 0 ll in x B el it a it ep Ha An Irr Ag Ap AM is D D D Mega MS et al. Neurology 1996; 46: 130–5
  38. 38. 38BEHAVIOURAL CORRELATES •AGGRESSIVE •ACTIVITY DISTURBANCESCOGNITIVE CORRELATES •DEMENTIA SEVERITY •LANGUAGE, MEMORY & EXECUTIVE FUNCTION
  39. 39. 39Successful cholinergic enhancing strategies in AD Reduced breakdown of acetylcholine + Increased release of ACh into synapse = Increased availability of ACh at synapse
  40. 40. 40 Patient flow• AD is prevalent among primary care patients• However, patients and general practitioners (GPs) are often not aware of this• The diagnosis of AD comes too late• 30 memory clinics in Germany• Patients are normally followed up by GPs
  41. 41. 41 Reasons for delayed diagnosis• Cognitive decline seen as age-related• GPs feel unsure about diagnosis of AD• Lack of practical diagnostic tools• Expected benefits of treatment are low
  42. 42. 42Diagnostic problems and pitfalls• Inadequate diagnostic tools• ‘Normal’ ageing vs. dementia• Interpretation of cerebrovascular findings• Problems of mixed pathologies
  43. 43. 43Diagnostic problems and pitfalls• Inadequate diagnostic tools• ‘Normal’ ageing vs. dementia• Interpretation of cerebrovascular findings• Problems of mixed pathologies
  44. 44. 44Problems of mixed pathologies• Stroke superimposed on AD• Alzheimer’s plus Parkinson’s disease• Dementia with Lewy bodies
  45. 45. 45 ANTIPSYCHOTICS• RISPERIDONE: 1-2 mg• OLANZEPINE: 5-10 mg• QUETIAPINE: 25-250 mg• HALOPERIDOL: 0.5-3 mg
  46. 46. 46AGITATION• physical aggression• verbal aggression• active resistance to care giversRx: ANTIPSYCHOTIC ANTICONVULSANT
  47. 47. 47DEPRESSION• major depression uncommon• depressive symptoms frequent (40%)• more common with F/H• MD may precede the onset of AD
  48. 48. 48 ANTIDEPRESSANTS• SSRI = FLUVOXAMINE (LUVOX)• SNRI = VENLAFAXIN (EFFEXOR)• OTHER NEW ANTIDEPRESSANTS
  49. 49. 49PERSONALITY CHANGES • APATHY 70% • IRRITABILITY 42% • DISINHIBITION 36%
  50. 50. 50 APATHY IN AD • most common behavioural change • indifference, loss of affection, decrease motivation • independent of depression• frontal hypoperfusion (mediofrontal)=> correlates with cognitive decline
  51. 51. 51CHOLINERGIC DEFICIT IN AD • ATROPHY OF NUCLEAS BASALIS • DECREASE CAT SYNTHESIS • ACETYLCHOLINE DEFICIT • INTACT CHOLINERGIC RECEPERS
  52. 52. 52CHOLINESTERASE INHIBITOR [ChEI] • improve global function • enhance cognition • improve behaviour • delay nursing home placement
  53. 53. 53CHOLINESTERASE INHIBITORS ChEIs • TACRINE • DONEPEZIL • RIVASTIGMINE • GALANTAMINE
  54. 54. 54Potential caregiver benefits • No sleep disruption • Maintenance of ADL • Suppression of behavioural symptoms = diminished caregiver burden
  55. 55. 55 The role of the primary care physician in mild to moderate AD* Define all contributory factors and other illnesses* Discuss the diagnosis, and differentiate other types of dementia* Withdraw non-essential drugs that may interfere with cognition* Treat or manage concomitant illness (e.g. depression, hearing loss) Gauthier, Burns and Pettit, 1997
  56. 56. 56 The role of the primary carephysician in mild to moderate AD (continued)* Discuss the use of symptomatic therapies* Monitor functional ability e.g. driving, safety* Referral to specialist if appropriate* Advise on will-making and advance directives* Refer to local AD association for support* Managing caregivers Gauthier, Burns and Pettit, 1997
  57. 57. 57 The role of the primary care physician in severe AD* Help caregivers discover and optimize the patients preserved function* Monitor and treat complications* Facilitate caregiver support (respite and day care programs)* Be aware of caregiver burden and stress* Plan institutionalization, if needed* Assist with end-of-life decisions Gauthier, Burns and Pettit, 1997
  58. 58. 58 Diagnosing AD in primary care A systematic approach - summary CASE-FINDING CLINICAL ASSESSMENT Symptoms YES *Clinical history suggesting *Physical examination cognitive *Laboratory tests impairment *Functional assessment *Cognitive assessment Functional decline and cognitive impairmentDIFFERENTIAL DIAGNOSIS MANAGEMENT OF AD*Exclude *Follow-up - delirium AD diagnosis *Patient and caregiver - depression counseling - other causes of dementia *Management and symptomatic*Evaluate evidence for treatment AD (neuroimaging) *Specialist referral if indicated
  59. 59. 59A BCs of Behaviour al
  60. 60. 60Iceberg 20% 80%
  61. 61. 61 The caregiving burden in AD Hours dedicated per patient over 1 month (1 month = 720 hours, including 160 working hours)• Principal (non-professional) caregiver: 280 hours• Professional caregiver: 36 hours Rice DP et al. Health Aff (Millwood) 1993; 12: 164–76 Boada M et al. Med Clin (Barc) 1999; 113: 690–5
  62. 62. 62 Caregiver burden PsychologicalPhysical Social Financial or emotionalproblems problems problems problems Family members (including principal caregiver) caring for Alzheimer patient Multidimensional: objective/subjective burden George, Gwyther, Hoening, Montgomery, Platt
  63. 63. 63 Spanish National Plan for Patients with AD & other Dementias “Plan Nacional de Atencion a los Enfermos de Alzheimer y otras demencias”Six main areas1. Health services2. Social services3. Legal and economic protection4. Family support5. Education and training for professionals6. Research
  64. 64. 64 A growing problem Projected prevalence of dementia to 2025 35 30 25 1980Millions 20 2000 15 2025 10 5 0 1980 2000 2025 Years Alzheimer’s Disease International
  65. 65. 65Qualitative changes in the Alzheimer population in the next decade Improvement of Early Impact of care provided Medical diagnosis drugs by non- progress professionals Changes in the structure of society Health and social services
  66. 66. 66 AD risk and protective factorsRisk factors Protective factors* Age * Genetic (ApoE-2)* Family History of AD * High educational level (ApoE-4) * Long-term anti-* Head trauma inflammatory* Low educational level drug use, e.g.* Environmental factors NSAIDS* Down’s syndrome * Long-term use of estrogens (in women) IPA AD Conference, 1996

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