Cp gdementiafor kelantan2012
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This document provides an outline for a clinical practice guideline on the approach to diagnosis and management of dementia. It covers definitions of dementia, epidemiology data on the burden of dementia, the brain regions involved in dementia, how to recognize different types of dementia, common causes of dementia including Alzheimer's disease and vascular dementia, comorbid conditions like depression and delirium, and investigations and fundamentals of management. The goal is to provide guidance to healthcare professionals on best practices for diagnosing and treating patients with dementia.
Cp gdementiafor kelantan2012
- 1. CPG ON DEMENTIA (2nd edition): APPROACH TO DIAGNOSIS AND MANAGEMENT DR NORAZAM BIN HARUN CONSULTANT PSYCHIATRIST, KOTA BHARU
- 2. OUTLINE 1. DEFINITION 2. EPIDEMIOLOGY DATA 3. DEMENTIA AND THE BRAIN 4. HOW TO RECOGNISE DEMENTIAs 5. CAUSES OF DEMENTIAs 6. TYPES OF DEMENTIAs 7. COMORBID CONDITIONS 8. INVESTIGATIONS 9. FUNDAMENTALS OF MANAGEMENT
- 3. 1. DEFINITION WHAT IS DEMENTIA?
- 4. DEMENTIA: DEFINITION (ICD10) • Dementia – is a syndrome due to disease of the brain, usually of a chronic or progressive nature, in which there is disturbance of multiple higher cortical functions, including memory, thinking, orientation, comprehension, calculation, learning capacity, language and judgement. Consciousness is not clouded. Impairments of cognitive function are commonly accompanied and occasionally preceded, by deterioration in emotional control, social behaviour or motivation. – This syndrome occurs in Alzheimer’s disease, in cerebrovascular disease and in other conditions primarily or secondarily affecting the brain.
- 5. ALZHEIMER’S DISEASE: DSM IV • Multiple cognitive deficits (‘4As’) – memory impairment (Amnesia) – impaired ability to learn new in or to recall previously learned info – Aphasia (language disturbance) – Apraxia (impaired ability to carry out motor activities) – Agnosia (failure to recognise objects) – disturbance in executive function (planning, organising, sequencing, abstracting) • These lead significant impairment in social, occupational functioning
- 6. ALZHEIMER’S DISEASE: NINCDS-ADRDA POSSIBLE: PROBABLE: • Established by clinical examination and documented by neuropsy tests, • Deficits in 2 or more areas of cognition i.e. aphasia, apraxia, agnosia, • Progressive worsening • No disturbance in conciousness • Absence of systemic or brain d/s • Absence of neuro, psych or systemic d/o to cause dementia • DEFINITE: • Evidence obtained from histopathology biopsy and/or autopsy
- 7. 2. EPIDEMIOLOGY WHAT IS THE BURDEN?
- 8. ELDERLY IN MALAYSIA (>60) (Statistik Malaysia 1990) YEAR NUMBERS % 1990 1 047 000 5.7 2010 2 094 000 7.5 2020 3 261 000 9.8 2035 3 261 000 9.8
- 9. PREVALENCE OF AD: INCREASING WITH AGE Age Prevalence 65-74 3% 75-84 18.7% >85 47.2% 5x
- 10. AD: EPIDEMIOLOGY (ADI report 2006) Region Preval ence (60+, %) Inciden ce (mil per annum, 2001) 2001 (million) 2020 (million) 2040 (million) Proporti onate increas e in number s (20012020) Proporti onate increas e in number s (20012040) WPRO B (incl China, Malaysia) 4.0 1.21 6.0 11.7 26.1 96 336 Indonesia Thailand, Sri Lanka 2.7 0.14 0.6 1.3 7 100 325
- 11. DEMENTIA BURDEN ADI report 2006, Wimo et.al. Alz Dis Asso Dis 2003;17(2):63-7, Ferri CP Lancet 2005;366:2112-7 Grey hair population Dementia • 10% total population >65 yo • 6.1% popn >65 suffers from AD (0.5% total population) • 635mil people in 2002 • 24.3 million worldwide • Expected to increase 30% in 2050 • Double every 20 years • Care of an AD person: USD 18400-36000 p.a. • Total care USD 1 bilion p.a. • 47% male Malaysian pilgrim has cognitive impairment (Harun N 2003) • Mostly in developing countries
- 12. 3. DEMENTIA AND THE BRAIN WHERE IS IT?
- 13. THE BRAIN • Average adult brain size is about medium sized cabbage • Weight: 1-1.5kg • Number of neurons: 100 000 000 000 (100billion) • Number of synapse: 100 000 000 000 000 (100trilion)
- 14. PARTS OF BRAIN INVOLVED AND MANIFESTATION AD pathology starts at Nucleus Basalis of Meynert at temporal region then expands to parietal, frontal & whole brain including subcortical structures.
- 15. 4. HOW TO RECOGNISE DEMENTIA? DIAGNOSIS SUBTYPES AND THE DIFFERENTIALS
- 16. ASSESSMENT • Standard interview and clinical data collection • History of presenting illness, current problems, why now. A – ADL B – behaviour problems C – cognitive problems • Investigate physical status • CVS, CNS, MS, endocrine problems, DM, thyroid, infections, nutrition, elimination.
- 18. Algorithm for diagnosis of dementia: 2nd CPG of Management of Dementia (2010)
- 20. CAUSES REVERSIBLE • Depression • Delirium • Drug toxicity incl alcohol • Metabolic d/o e.g. hypoNa • Hypothyroidism • Vit B12/folate def • Normal pressure hydrocephalus • Infection e.g. HIV, CJD • Hypoxia: sleep apnoea IRREVERSIBLE • Alzheimer’s d/s • Vascular dementia • Lewy body dementia • FrontoTemporal Lobe dementia • Parkinson’s d/s dementia • Huntington’s d/s dementia
- 21. RISK FACTORS NON-MODIFIABLE • 1. AGE MODIFIABLE • • Increase 5x >85yo • <0.1% in <65yo, 1-5% >65yo, 2530% in >85 • • • • • • • 2. GENDER • F>M • Female higher risk of AD • Male higher risk of VaD 3. GENETIC • Genetic loading in young onset – APOE4, chromosome 1, 14, 21 as in Down syndrome 1. CARDIOVASCULAR RISK FACTORS: • Hypertension DM CVA Hyperlipidaemia Homocysteine 2. LIFESTYLE FACTORS: • • • • • • Low education Smoking Alcohol Obesity Exercise Social network
- 22. CHOLINERGIC THEORY: DEPLETION OF ACETHYLCHOLINE • Neurons communicate with each other by neurotransmitter to activate the receiving neurons • AD causes depletion of neurotransmitters particularly acetylcholine (Ach) which a/w memory.
- 23. TAU THEORY: ABNORMAL DEPOSITION OF TAU PROTEINS • Tau protein is to maintain the structure of the axon of neurons • Intraneuronal NFT containing excessive tau protein • Distruption of Tau proteins via abnormal hyper-phosphorylation which leads to deposition of neurofibrillary tangle (NFT) eventually death of neurons
- 24. AMYLOID THEORY: EXCESSIVE DEPOSITION OF AMYLOID PLAQUE • Extracellular amyloid plaques containing Aβ amyloid • Plaque formed by abnormal degradation of a large protein (Amyloid Precursor Protein APP) into insoluble protein AB42 • Genetic factor APOE4 may contribute • Neuronal cell death
- 25. MACROSCOPIC CHANGES IN AD • Loss of overall volume of the brain • Marked atrophic changes, widening of sulci, prominent gyri, enlargement of ventricles
- 26. BRAIN PATHOLOGY IN VaD • Infarction or death of brain tissue from blockage of cerebral arteries by thrombosis or embolism • Ischaemic or hemorrage • Large or small vessels • Strategically located vessels involved
- 27. 6. DEMENTIA TYPES WHY IS IT IMPORTANT TO DETERMINE SUBTYPES? To determine treatment modalities
- 28. TYPES OF DEMENTIAS • Most common types: • Alzheimer’s disease • Vascular dementia (Mixed AD/VaD) • Dementia Lewy Body • Frontotemporal lobe dementia • Others: PDD, CJD, Huntington 50% 25% 15% 5% 1%
- 29. SPECIAL FEATURES OF DEMENTIA TYPES • ALZHEIMER’S DISEASE DEMENTIA – 4As: Amnesia, Aphasia, Apraxia, Agnosia and poor executive function • VASCULAR DEMENTIA – Step-wise deterioration, emotional lability, evidence of vascular disease • FRONTOTEMPORAL LOBE DEMENTIA – Behaviour, personality and language problems are predominant features (Disinhibition, Apathetic, Stereotypic type) • DEMENTIA OF LEWY BODY – Fluctuation of cognitive decline, visual hallucination, sensitive to neuroleptics, unsteady gait • HUNTINGTON’S DISEASE DEMENTIA and PARKINSON DISEASE DEMENTIA – Specific Movement d/o
- 30. VASCULAR DEMENTIA • Sudden onset (<3 months post stroke) • Step-wise deterioration • Specific neurological signs: physical and/or neuroimaging evidence • SUBTYPES: – Large or small vessels: Post-stroke or Multi-infarct dementia (MID) – Cortical or Subcortical Ischemic VaD (SIVD) – Ischaemic or hemorrhagic – Single specific infarct dementia may manifest s/s depending on location e.g. • cortical or subcortical (BG, Thalamus, Basal forebrain)
- 31. LEWY BODY DEMENTIA • LBD is a clinically defined syndrome and consists of a primary dementia characterised by visuoperceptual and executive dysfx. Lewy bodies (deposits of synuclein protein) in the brain. • Presence of 2 out 3 core clinical features (McKeith IG et.al. Neurology 2005;65(12):1863-72): • Prominent visual hallucination • Fluctuating attention • Parkinsonism • ‘One year rule’ to differentiate with Parkinson d/s dementia • Increased sensitivity to neuroleptics (suggestive feature) • Risk of fall(supportive feature)
- 32. FRONTOTEMPORAL LOBE DEMENTIA (Lund-Manchester criteria, Neurology 1998;51: 1546-54) • Characterised by frontal signs • Personality changes (Disinhibited type) • Behaviour problems prominent (Stereotypic type) • Characterised by temporal signs • Language problems (Apathetic type) • Memory problems may present late
- 33. 7. COMORBID CONDITIONS IN DEMENTIA HOW TO DIFFERENTIATE THEM
- 34. DEMENTIA Vs DELIRIUM Vs DEPRESSION DEMENTIA DELIRIUM DEPRESSION ONSET Insidious Acute Gradual DURATION Years Hours/days Weeks/months COURSE Progressive (stepwise for VaD) Fluctuates, sundowning Worse in morning ALERTNESS Normal Fluctuates Normal ORIENTATION May be normal Always impaired Normal MEMORY Impaired recent, maybe intact remote Impaired Recent maybe impaired but remote good THOUGHTS Delusion common in late stage Paranoid, bizarre, disjointed, occur early Slow response, negative thoughts PERCEPTIONS Hallucination occur late Illusions, hallucination Mood congruent psychosis EMOTIONS Shallow, apathetic Irritable, fearful Sad, may be agitated SLEEP Disturbed diurnal rhythm Nocturnal confusion Early morning awakening Organic cause Past h/o mood do OTHER FEATURES
- 35. BEHAVIOURAL AND PSYCHOLOGICAL SYMPTOMS OF DEMENTIA (BPSD) Medical Research Council Aging Study, 2008 Symptoms Without dementia (%) With dementia (%) P value Apathy 12.1 50.3 <0.001 Sleep problems 43.8 42 0.574 Irritability 12.8 28.8 <0.001 Persecution 8.1 25.4 <0.001 Depression 8.6 20.5 <0.001 Misidentification 3.0 20.3 <0.001 Hallucination 3.7 15.1 <0.001 Wandering 0.3 12.8 <0.001 Elation 3.2 9.5 <0.001 Agitation 3.6 9.0 <0.001 Anxiety 6.3 8.9 <0.001
- 36. BEHAVIOURAL AND PSYCHOLOGICAL SYMPTOMS OF DEMENTIA (BPSD) • Behavioural disturbance is the most significant factor for institutionalisation: • • • • • • Psychosis Wandering Aggression/agitation sleep disturbance Anxiety Depression 79% 73% 68% 73% 47% 42% • St Louis Uni BPSD study 1996
- 37. BPSD SYMPTOMS THAT CAUSED DISTRESS TO CARERS (Norazam H 2006)
- 38. COMORBID CONDITIONS: DELUSION • Occur in cognitive disorders but not all impaired patients have delusions • In A.D. 40-75% patients have some kind of delusional ideas • Types of delusions: - stealing - jealousy - mis-identification (house, spouse, impostors) - secondary delusions • More common in cortical dementias • Usually later in course of disease • Associated with increasing cognitive decline and aggressive behaviour • Mis-identification relate to lesions of right frontal lobe in A.D. • Delusions may be related to right temporal lobe lesions
- 39. COMORBID CONDITIONS: DEPRESSION Alzheimer’s Disease - 10-20% Parkinson’s Disease - 47% Huntington’s Disease - 38% Stroke - 20-40% • Depression is more prevalent in subcortical diseases and where major pathology is in the striatum and frontal lobes, particularly the left • Depression occur early in dementias, often before onset of defining cognitive or motor features and argues for a neuropathological relationship, rather than a psychological reaction to the disease
- 40. COMORBID CONDITIONS: WANDERING • MILD DEMENTIA • SEVERE DEMENTIA • PROBLEM TO CARERS POSSIBLE CAUSES - being lost - catastrophic reaction - relocation anxiety - boredom - psychosis - agitated depression - medication side-effects - dementia pathology 18% 50% 40%
- 42. INVESTIGATIONS All patients Most patients • Full blood count • ECG • Thyroid function • Chest X-ray • Vitamin B12 and folate • Neuroimaging • BUN and creatinine • Syphilis serology • Calcium • Glucose • Electrolytes • Urinalysis • Liver function tests • Lipid profile
- 43. PSYCHOLOGICAL AND FUNCTIONAL INVESTIGATIONS COGNITIVE NON-COGNITIVE • Elderly Cognitive Assessment Qs (Kua et.al) • Geriatric Depression Scale (Yesavage) • MMSE (Folstein et.al.) • Cornell Depression scale • Symptoms of Dementia Screener (for carer) • Neuropsychiatric Inventories (NPI) - Cummings • Clock Drawing Test • Zarit Burden Scale (carer) • Abbreviated Mental Test • • Clinical Dementia Rating (Morris) Activity of Daily Living (ADL) – Barthel, Katz • CIBIC • Instrumental ADL – Barthel, Lawton • ADAS-COG • Hatchinski Scale (Vascular) • CAMCOG
- 44. 9. FUNDAMENTALS OF MANAGEMENT WHAT TO DO AND HOW TO DO IT
- 45. MANAGEMENT 1. Drugs to palliate primary cognitive symptoms of dementias 2. Treatment of non-cognitive symptoms (BPSD) – depression, delirium, BPSD, psychosis 3. Psychosocial and environmental strategies 4. Preventions 5. Care for carers
- 46. MANAGEMENT • Assess the patient • Assess family/caregivers • Identify target symptoms • Utilise evidence • Weigh risks and benefits • Avoid polypharmacy • Psychosocial and pharmacological treatments can be used together • Review!
- 47. COGNITIVE ENHANCERS FOR DEMENTIAs (CPG on the Mx of Dementias 2nd Ed) • CHOLINESTERASE INHIBITORS (for mildmoderate AD) • Tacrine THA(Cognex) – withdrawn because of s/e • Donepezil (Aricept) • 5-10mg OD • Rivastigmine (Exelon) • 1.5-6mg BiD • 4.6mg-9.5mg patch/24hrs • Galantamine (Reminyl) • 4-8mg BiD • N-METHYL D-ASPARTATE ANTAGONIST (for severe AD) • Memantine (Ebixa) • 5-20mg OD
- 48. RIVASTIGMINE AND IMPROVEMENT IN ADAS-COG (Emre et.al. NEJM 2004;351;2509-18) * Change from baseline, ADAS-cog –2.5 Rivastigmine (n = 329) –2.0 ** Placebo (n = 161) Improvement –1.5 –1.0 –0.5 Baseline 0 0.5 Deterioration 1.0 Week: 0 16 24
- 49. ARICEPT IN MILD – MODERATE AD (Winblad et.al. 2006)
- 50. MANAGEMENT FOR BPSD Non pharmacology management should be institute first before pharmacology Mx • Activity programmes appear successful, but interventions vary in style and content • Music appears most promising when personalised to individual taste and background • Bright light exposure decreases daytime sleep and sundowning
- 51. NON – PHARMACOLOGY MANAGEMENT FOR BPSD • Reality orientation therapy • Reminiscence therapy • Validation therapy • Behavioural modification – stimulus control • Sensory stimulation - aromatherapy • Motor activity – OT, PT, podiatrist, massage • Snoezelen room • Therapeutic buildings includes wandering path
- 52. PHARMACOTHERAPEUTIC APPROACH FOR BPSD • Cholinergic therapies • NMDA antagonist therapy • Antipsychotics • Off-label use of antipsychotics however use with caution because of the cerebrovascular risk (RR: 1.4-3.5 Douglas IJ et.al BMJ 2008;337;1227) • Recommended for aggression, agitation and psychosis • Benzodiazepines: use cautiously and for short term • Antidepressants: SSRI is recommended for depression • Anti-epileptics: Valproate and Carbamazepine for impulsivity • Beta adrenergic receptor blockers: propranolol for agitation • Hormonal therapy: antiandrogen for sexually disinhibited
- 53. RECOMMENDED DOSE OF ANTIPSYCHOTICS (CPG ON MX OF DEMENTIA 2nd Edition) NAME STARTING DOSE MAXIMUM DOSE ADVERSE EFFECTS RISPERIDONE 0.5mg OD 2mg OD EPS, hyper prolactinaemia OLANZAPINE 2.5mg OD 10mg OD EPS, weight gain, hyper lipidaemia/ glycaemia QUETIAPINE 12.5-50mg OD 200-300mg OD EPS, somnolence, orthostatic hypotension 15mg OD EPS, weight gain, anxiety ARIPIPRAZOLE 5mg OD
- 54. PREVENTION • Prevent modifiable CVS risk factors: • Hypertension Rx of mid-life HTN reduce 60% risk of AD Syst-Euro study:– Lancet 1998; 352: 1847-51 • However other studies –ve (PROGRESS, SCOPE, HOPE, SHEP, MRC) • DM: controlled DM – less risk of VaD only with other risk factors Lu FP Plos One 2009;4(1);4144 • Lipid control – midlife TC may have higher risk BUT statins were not beneficial Szwart et.al Neurology 2007: 69:187380 • Homocysteinanemia: inconclusive results (Cochrane review 2008 October 8)
- 55. PREVENTION • GINKGO-BILOBA EGB 761: • Cochrane Review 2007(2) and NICE did not recommend as adverse events outweigh benefits • ANTIOXIDANT: • Vitamin E: not significant findings (Petersen et.al NEJM 2005;352:2379-88) • NICE guidelines did not recommend • NSAIDS: • ADAPT trial 2006 did not support use • OESTROGEN: • HRT has no benefit (Cochrane Review 2004)
- 56. PREVENTION • DIET: • Mediterranean diet may be beneficial (Sofi F et.al BMJ 2008;337;1344) • EXERCISE: • ADAS-COG improved among healthy elderly Lautenschlager et.al. JAMA 2008;300:1027-37 • SMOKING: • Increased risk of AD in elderly smokers (Rotterdam study, Neurology 2007;69:998-1005) • ALCOHOL: • Moderate red wine (resveratol) may benefit (Gottenburg Study Am J Epid 2008; 167: 684-91)
- 57. PREVENTION • EDUCATION AND MENTAL STIMULATION: • Higher education may prevent AD (NUN study JAMA 1997;277:813-7) – ‘brain reserve’ • Cognitive stimulation may benefit by 1.2-2.6 points in MMSE on healthy adults (Valenzuela et.al. Am J Geri 2009;17(3):179-87 • SOCIAL NETWORK: • Live alone and reduce social may increase risk (HonoluluAsia Aging Study, Am J Epid 2006;163:433-40)
- 58. HEALTHY LIFE STYLE PREVENT DEMENTIA BY: • Control vascular risk factors: HTN, DM, hyperlipidaemia • Healthy Mediterranean diet: fresh vegies, fruits, olive oil, fish, legumes (e.g. Sardinian people, Okinawan) • Stop smoking • Reduce weight (within Normal BMI) • Regular aerobic exercise (150min/week) • Cognitive stimulation • Education • Active socialisation
- 59. WHAT PATIENT AND FAMILY/CARER SHOULD KNOW? • Education in Dementia and Care • Knowledge, understanding, Rx available and course of disease (mildmoderate-severe phase) • Attitude Change – valuing the person • Sensitive to persons problems and disabilities • Not blaming the victim – attribute to disease • Optimism replacing pessimism • Refute ‘ageism’ via education to person, family, public, health professional • Environmental Change • Orientation – familiar place, familiar faces, familiar routines • Dealing with Psychological and Physiological Issues • Support groups available in the community
- 60. THANK YOU