Personal Reflections on the Design and Delivery of Services to Those with Cognitive Disorders
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1 Personal Reflections on the Design and Delivery of Services to Those with Cognitive Disorders Dr. David B. Hogan Brenda Strafford Foundation Chair in Geriatric Medicine University of Calgary
2 None to declare Conflicts of Interest
3 Objectives Review evidence-based approaches to the design and delivery of services for those with cognitive disorders Reflect on the current structure of services in our own jurisdiction Identify key barriers to restructuring services and approaches to dealing with them
4 Few Things First
5 Effects of Medical Research on Treatment Cost & Disease Duration
6 Polio
7 Dementia Doesn t = Alzheimer Multiple potential causes of dementia that are present alone or in combination Commonest (older adults) Alzheimer s disease Combination (e.g., AD with cerebrovascular or Lewy body disease) Common (older adults) Dementia with Lewy Bodies, Vascular Dementia (Mixed Dementia), Frontotemporal Dementia Rarer causes Alcohol-Related, Associated with Parkinson s Disease, Huntington s Chorea, Prion Disease (CJD), AIDS-Related, Neurosyphilis, etc
8 Autopsy Studies -Mixed Disease Common in Old Patients Camberwell Dementia Case Register (avg. age 82) Mixed pathology in 34% - Br J Psychiatry 1999, 174:45-50 State of Florida Brain Bank (average age of death 79) 40% had more than 1 relevant CNS post-mortem diagnosis - Alz Dis Related Disord 2002, 16: Rush Memory and Aging Project (avg. age 88) 70% without dementia had brain pathology (e.g., AD, infarcts, Lewy bodies) All with dementia had pathological changes with over 50% having multiple diseases, which increased by 3-fold risk of dementia - Neurology 2007, 69:
9 Alzheimer Disease Most common cause (alone or in combination) in older adults 60% of all cases NINCDS-ADRDA (1984) Clinical-pathological entity - dementia and AD changes in brain coupled
10 Diseases Despite the efforts of purists, academics and dictionaries, definitions must evolve along with knowledge and concepts. The logic of words must always yield to the logic of facts they symbolize - René Dubos (White Plague)
11 Changes in How AD Viewed AD pathological changes and cognitive deficits develop over many years Dementia is the end stage (dementia and AD decoupled) Initial event felt to be disordered beta amyloid Initial event felt to be disordered beta amyloid metabolism (but still hypothesis)
12 Genetics Causative mutations (< 5%; suggested by early onset, autosomal dominant pattern) APP (chromosome 21) Presenilin 1 or PS1 (chromosome 14) Presenilin 2 or PS2 (chromosome 1) Latter two both part of gamma secretase complex Down Syndrome (trisomy 21) Three copies of the gene for APP Risk factor for late onset (65+) AD Apolipoprotein E4 allele (chromosome 19) - dose dependent relationship (homozygous > heterozygous) for risk at certain ages & earlier age of onset but not necessary or sufficient
13 Biomarkers Biomarkers major ones Beta amyloid pathology Amyloid PET imaging and low levels of beta amyloid 1-42 in CSF Neuronal injury High levels of tau and phospho-tau in CSF High levels of tau and phospho-tau in CSF Neuronal dysfunction Decreased metabolism in parietal-temporal lobes on FDG PET Neurodegeneration Temporal, parietal, and/or hippocampal atrophy on MRI
14 NIA-AA Criteria for Diagnosis of AD Three separate work groups appointed by NIA and AA ( balanced expertise & international representation from academia and industry ) Met during early-mid 2010 & came up with recommendations Presented at the 2010 International Conference on Alzheimer s disease then posted on AA webpage for public comments Revisions and harmonization in fall of 2010 Final version in early 2011 (published that year by Alzheimer s & Dementia)
15 New Criteria -Dementia Due to AD No major change in how dementia defined Probable AD dementia Dementia + insidious onset, clear history of worsening, amnestic (most common) or nonamnestic (language, visuospatial, executive) presentation No substantial cerebrovascular disease, dementia with Lewy body, frontotemporal degeneration, or other neurological or non-neurological condition (co-morbidity or medication) that could have substantial effects on cognition More certain if documented decline or carry causative gene (carriage of E4 not sufficiently specific) 15
16 Possible AD dementia Dementia Due to AD Either atypical course (e.g., abrupt onset or insufficient data on decline) or have mixed causation Probable or Possible AD dementia with evidence of the AD pathophysiological process Biomarkers of amyloid deposition or downstream neuronal degeneration but not recommended for routine use 16
17 MCI Due to AD Core clinical criteria Concern about a change in cognition (patient, informant, or clinician), impairment in 1+ domains (typically includes memory), independence in functional abilities, and not demented To determine if etiology consistent with AD R/O other causes, look for longitudinal decline, and see if carry genetic risk factor (a causative mutation or E4) 17
18 Preclinical Stage Solely intended for research purposes and do not have any clinical implications at this time Three stages Asymptomatic cerebral amyloidosis (beta amyloid in CSF, PET amyloid imaging) Amyloid positivity + evidence of neuronal injury (tau, FDG- PET, MRI) Amyloid + neuronal injury + subtle cognitive changes Note: International Working Group suggested the term Presymptomatic AD for those carrying causative mutation - Lancet Neurology 2010, 9:
19 Fig.3 Hypothetical Model 19 Source: Alzheimer's & Dementia: The Journal of the Alzheimer's Association 2011; 7: (DOI: /j.jalz ) Copyright 2011 Terms and Conditions
20 Advantages Dementia and AD decoupled By time dementia present, pathological changes have been occurring for 25 years (N Engl J Med 2012, 367: ) with many neurons lost; the hope is earlier diagnosis might enable effective treatment before they are lost Might lead to more accurate diagnosis Might help with research? Biomarkers surrogate outcome in prevention studies? Enrollment of those with more certain diagnosis 20
21 Alzheimer Disease Pathology without a Dementia Older individuals at autopsy can have high density of AD lesions but no dementia? Plaques and tangles are epiphenomena (a secondary phenomenon occurring alongside/ in parallel to primary process)? Slow accumulation of plaques and tangles easier to deal with than rapid (i.e., cell repair mechanisms, compensation, presence of factors slowing down cascade of events)? Predisposing - need precipitant/ 2nd disease? Cerebral/ cognitive reserve 21
22 Concerns - Pre-Clinical Stage Suggested as research criteria but fear will start (& has started) to be used more widely MRIs, amyloid/ FDG-PET scanning & spinal taps available now Uncertainty re cut-points and need standardization Uncertainty re actual risk of dementia (+ for MCI) Cost Of the investigations (+ if used for MCI and dementia work-up) Cost (and harm) of further tests and therapies Opportunity costs Labeling if have a + biomarker CSF AD pattern found in more than 1/3 of cognitively normal 75 year olds Arch Neurol 2010, 67: For what purpose? No disease modifying therapy available 22
23 DSM-5 Change because Believed dementia stigmatizing and not well accepted Should focus on decline from a previous level of functioning as opposed to a deficit Memory impairment not first domain affected in all neurocognitive disorders To align better with neurological practice
24 Approach Suggested in DSM-5 First establish the presence of a neurocognitive disorder base on assessing cognitive domains Complex attention, executive function, learning & memory, language, perceptual motor, social cognition Then classify as Delirium, Mild Neurocognitive Disorder (mild cognitive impairment) and Major Neurocognitive Disorder (formerly dementia) Then specify whether Alzheimer, frontotemporal, Lewy body, vascular, traumatic brain injury, substance/ medication, HIV, prion, Parkinson, Huntington, another medical, multiple, unspecified
25 Major Neurocognitive Disorder Evidence of significant cognitive decline in 1+ cognitive domain based on Concern of person, knowledgeable informant, or clinician that there has been significant decline Substantial impairment in cognitive performance Cognitive deficits interfere with independence in everyday activities Do not occur exclusively in the context of delirium Not better explained by another mental disorder (e.g. major depression)
26 Similar except Minor Neurocognitive Disorder First point: modest decline mild decline modest impairment Second point: don t interfere with capacity for independence in everyday activities complex ones are preserved but greater effort, compensatory strategies, or accommodation may be required
27 Push to Screen for Pre-dementia Feed into belief there is value in identifying milder forms of cognitive impairment Stems from conviction that dementia is an illness that progresses through a mildly symptomatic stage where interventions are more effective Concerns that much that can be done is simply good practice, unproven benefits of many interventions, nothing conclusively shown to prevent progression, costs, and diversion of resources BMJ 2013, 347:f25 doi:10:
28 28 Lancet Neurology 2010, 9:702-16
29 Why Do So Many Alzheimer s Drugs Fail in Clinical Trials? (Time, August 26/10) Of 13 Phase 3 drugs in previous slide, 12 have failed to date (Fall 2013) Some recent high profile amyloid-based failures Semagacestat - gamma secretase R-flurbiprofen - gamma secretase Tramiprosate - prevent aggregation Solanezumab/ bapineuzumab monoclonal antibodies to beta amyloid 29
30 30 What Works?
31 Pharmacotherapy Cochrane Database AD - ChEIs are efficacious for mild-moderate AD; despite variations in modes of action, no evidence of any differences between them with respect to efficacy; one large trial shows fewer AEs with donepezil Vs. rivastigmine - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 5, 2012 PDD/DLB - available evidence supports the use of cholinesterase inhibitors in patients with PDD; he effect in DLB remains unclear - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 3,
32 Pharmacotherapy Cochrane Database VCI: some evidence of benefit with ChEIs/ more studies needed - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews.4 & 5, 2013 MCI: little evidence that ChEIs affect progression to dementia or cognitive test scores that is overwhelmed by the increased risk of adverse events, particularly GI; ChEIs not recommended for mild cognitive impairment - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 9,
33 Pharmacological Cochrane Database Atypical antipsychotics risperidone & olanzapine reduce aggression + risperidone reduces psychosis but both associated with serious AEs; neither should be used routinely unless severe distress or risk of harm to others - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 5, 2012 Halperidol reduces aggression but associated with AEs; no evidence to support routine use for other manifestations of agitation in dementia - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 5,
34 Cochrane Database Valproate preparations are ineffective in treating agitation among demented patients & are associated with an unacceptable rate of AEs - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 12, 2010 Antidepressants for agitation/ psychosis - the SSRIs sertraline and citalopram were associated with a reduction in symptoms of agitation when compared to placebo in two studies; both SSRIs appear to be tolerated reasonably well when compared to placebo, typical antipsychotics and atypical antipsychotics - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 2,
35 Cochrane Database Insufficient evidence to recommend the use of trazodone as a treatment for behavioural and psychological manifestations of dementia - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 4, 2009 No evidence that cannabinoids are effective in the improvement of disturbed behaviour in dementia or in the treatment of other symptoms of dementia - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 4,
36 Pharmacotherapy Cochrane Database Many with AD dementia & NPS can be withdrawn from chronic antipsychotic Rx without detrimental effects on behaviours but in 2 studies where agitation/ psychosis responded well pts. were more likely to relapse after stopping + 2 studies suggest those with more severe symptoms could benefit from continued therapy; programs to could be incorporated into routine practice with above qualifications - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 4,
37 Non-pharmacological Cochrane Database Consistent evidence that cognitive stimulation programs benefit cognition in mild-moderate dementia - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 2, 2012 Functional analysis (FA) for challenging behaviours (i.e., explore meaning or purpose of a person's behaviour) - potential beneficial effects of multicomponent interventions that utilize FA but too early to draw conclusions about efficacy - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 2,
38 Non-pharmacological Cochrane Database Multi-component, tailor-made psychosocial interventions can reduce carers' psychological morbidity and delay their relatives' institutionalization - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 11, 2011 There is evidence supporting the effectiveness of psychosocial interventions for reducing antipsychotic medication in care home residents - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 12,
39 Non-pharmacological Cochrane Database Reminiscence Therapy - number of promising results in studies but in view of limited number & quality of studies, the variation in types of reminiscence work reported and the variation in results between studies, more studies needed - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 1, 2009 Insufficient evidence from RCTs allow any conclusion about the efficacy of validation therapy for people with dementia or cognitive impairment 39
40 Cochrane Database Music Therapy - methodological quality too poor to draw useful conclusions - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 3, 2011 Aroma therapy RCTs needed before conclusions can be made - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 4, 2009 No convincing evidence supporting efficacy of snoezelen (multi-sensory stimulation) for dementia - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 4, 2009 Insufficient evidence to assess value of light therapy for dementia - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 4,
41 Non-pharmacological Cochrane Database Available evidence regarding cognitive training for mild/ moderate dementia remains limited & of poor quality; no indication of any significant benefit - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 6, 2013 Available literature fails to demonstrate the benefit of driver assessment for either preserving transport mobility or reducing motor vehicle accidents - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 8,
42 Cochrane Database Insufficient evidence to be able to say whether or not physical activity programs are beneficial for people with dementia - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 4, 2009 Current evidence does not demonstrate benefits or AEs from the use of respite care for people with dementia or their caregivers; these results should be treated with caution as they may reflect the lack of high quality research in this area rather than an actual lack of benefit - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 4,
43 Cochrane Database Insufficient evidence to suggest that enteral tube feeding is beneficial in patients with advanced dementia - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 4, 2009 Special Care Units (SCUs) no RCTs on the effects of SCUs on behavioural symptoms in dementia & no strong evidence of benefit from available non-rcts; probably more important to implement best practices than to provide a specialized care environment - Cochrane Dementia and Cognitive Improvement Group Cochrane Database of Systematic Reviews. 5,
44 Cost-effectiveness of Prevention, Care and Treatment Strategies for Dementia Pharmacological interventions Cholinesterase inhibitors, memantine Non-pharmacological Cognitive stimulation, exercise, occupational therapy, caregiver interventions, care management Barriers Limited research base, difficulty generalizing from available studies, narrow perspective when measuring cost, reluctance to act on data, fragmented care Int J Geriatr Psychiatry
45 Common Elements Diagnosis primary & secondary Advance care planning Support to patient & family Develop & implement treatment plan Referrals as needed Continuity of care Monitoring over time Case (or care) management Mobilize dementia friendly community- and facility-based services as needed CMAJ :
46 2009 Action Plan -Meeting the Challenge of Alzheimer s Disease and Related Disorders Increase knowledge & adopting different attitudes Provide access to co-ordinated, personalized services Enhance quality of life and care In alternative living facilities At the end of life For family/informal caregivers Professional & support staff training Research 46
47 Barriers To implement recommendations need to: Ensure clinicians are adequately trained & motivated Required resources and services are available Explore different models of care 47
48 Training Many health care providers are uninformed Educational needs among primary care physicians Knowledge about local diagnostic & support services Assessment & communication skills Management of behavioral problems Coordination of support services Skeptical about the effectiveness of available interventions 48
49 Guideline Adherence Poor by physicians without interventions Common obstacles identified by Canadian physicians Inadequate time Inadequate remuneration Lack of accessible community resources 49
50 Potential Solutions Every community should examine the services locally available, assess their adequacy, and implement plans to deal with identified deficiencies Coordination and competition Models of care Modified (i.e., less reliance on promotion of patient selfmanagement coupled with greater caregiver involvement) chronic disease management Shared care models should be developed and evaluated Dementia care must be adequately funded (globally) and reimbursed (at the level of the practitioner) 50
51 Up-front Costs Could be Revenue Neutral if Effective Over Time UK nationwide memory services for early diagnosis and intervention for dementia Modeling indicates that if the service can achieve modest increase in average quality of life of people with dementia and divert 10% from residential to community care it would be cost-effective but would take 4-10 years to see Int J Geriatr Psychiatry
52 52 Merci/ Thank You
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