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Pharmacological Interventions for the Cognitively Impaired Geriatric Patient

Pharmacological Interventions for the Cognitively Impaired Geriatric Patient. Indiana Osteopathic Association 117 th Annual Convention May 2 – 4, 2014 French Lick Resort John J. Wernert, M.D., MHA Professional Development Associates. Faculty Disclosure John J. Wernert, M.D, MHA.

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Pharmacological Interventions for the Cognitively Impaired Geriatric Patient

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  1. Pharmacological Interventions for the Cognitively Impaired Geriatric Patient Indiana Osteopathic Association 117th Annual Convention May 2 – 4, 2014 French Lick Resort John J. Wernert, M.D., MHA Professional Development Associates

  2. Faculty DisclosureJohn J. Wernert, M.D, MHA • Consultant: • Eskenazi Health • Franciscan Alliance • Federally Qualified Health Centers • Archdiocese of Indianapolis • Extended Care Facilities

  3. LEARNING OBJECTIVES • Discuss new discoveries and theories about brain deterioration and memory decline. • Explore genetic and environmental risk factors for development of cognitive disorders.                    • Differentiate Delirium, Depression and Dementia in Geriatric patients. • Review Behavioral manifestations of dementing illnesses.  • Discuss how emerging targets and therapies may impact behavioral and medical recommendations relevant to treating cognitively impaired patients.

  4. “The singular benefit of old age is to see life whole and know it’s natural course”Philosopher Arthur Schopenhauer

  5. Most common reasons for referral to Geriatric Psychiatrist: • Memory Impairment • (AACD vs MCI vs Dementia) • Affective Problems • (Apathy vs Depression) • Behavioral Problems • (wandering vs agitation)

  6. The Cost of Brain Disorders • U.S. Society = $500 Billion annually • 19 % of the average American income is devoted to treating Brain diseases • 55 % cost is Dementias • Psychiatric Illnesses = $170 Billion • AD alone > $100 billion

  7. Prevalence of Mental Disorders Age 65+ • Mental disorders: 26.3%(including dementia) • Psychiatric disorders19.8%based on prevalence of 30-40% of dementia complicated by depression, psychosis, or agitation. Jeste, et al., 1999

  8. Brain Aging is not a sudden event, but rather a continuous process. RISK FACTORS: Decline in 20’s Medical illness Genetics Plasticity Variability Crowded desktop

  9. Crowded Mental Desktop • More time needed to learn new information • Working-memory capacity is limited • Slowed retrieval time • Too much clutter – hard to prioritize • Long-term memory becomes less reliable

  10. Sensory impairments • Auditory and visual acuity decline • Quality of sensory input blurs the sharpness of the memory • By 40’s, more distractible • By 50’s, harder to focus and stay on point. • By 60’s, difficult to filter out extraneous noise • By 70’s, memory lost due to “missed” input

  11. Brain Aging: • Caused by metabolic stress • Cell Level = transcription errors • Body Level = develop comorbidities • MCI - 15% per year convert to AD • AD develops slowly over decades • Adults who will get AD, already have it! • 30% over age 65 already have amyloid plaques

  12. Risk Factors for Brain Aging: • Confirmed • Age • Family History • APOE-4 gene (only 50 % of genetic variability) • Possible • Other genes • Head trauma • Lower educational achievement (use it or loose it vs healthy lifestyle) • Chronic stress • Depression

  13. Protective Factors for Brain Aging: • Aerobic exercise • Estrogen • Anti-inflammatory drugs • Anti-oxidants • Low-fat diet • Wine (Germans say beer)

  14. Wine and Reduced Incidence of Dementia? • Copenhagen City study • 83 pt’s, 1626 controls over age 65 • Studied over 15 years • Grouped by intake and dx • MMSE scores of 24 or up • Monthly and weekly intake of wine = decreased risk • Monthly intake beer = higher risk • Total alcohol intake had no significant effect on risk • Neurology (2002;59:1313-1319)

  15. Neurodegeneration • Usually a NORMAL Brain going through a slow, gradual deterioration • Parkinsons Disease • Dementing Illnesses • Demyelinating Disorders (MS) • Infectious (HIV, Syphilis) • Neoplastic (brain vs paraneoplastic)

  16. Neurodegeneration predisposes to the “Three D’s”: • Delirium ↓↓ ↑↑ • Dementia ↕↕ • Depression

  17. Neurodegenerative Conditions lead to all three “D’s” • High risk of polypharmacy • Despondency of chronic illness • Weakened resistance • Fragile brain = iatrogenic illnesses • Sensitive to drug side effects

  18. Delirium vs Dementia • Delirium • Acute • Fluctuating course • Dementia • Insidious Onset • Chronic memory Disturbances • Persistent Sxs • Dementia pt’s 3x more likely to get delirious • Delirious elderly patients are 4X more likely to have dementia

  19. Delirium; • Under-recognized (missed 50%) • Reversible (if cause correctible) • Present in 30 % of hospitalized elderly • Delays discharge • Increases need for ECF placement • Higher mortality (6 mo mortality>50%)

  20. Depression Associated with Worse Health Outcomes • Worse outcomes • Hip fractures • Myocardial infarction • Cancer(Mossey 1990; Penninx et al. 2001; Evans 1999) • Increased mortality rates • Myocardial Infarction(Frasure-Smith 1993, 1995) • Long term Care Residents(Katz 1989, Rovner 1991, Parmelee 1992; Ashby1991; Shah 1993, Samuels 1997)

  21. Depression in Older Adults and Health Care Costs Unutzer, et al., 1997; JAMA

  22. Suicide in Older Adults • 65+: highest suicide rate of any age group • 85+: 2X the national average (CDC 1999) • Peak suicide rates: • Suicide rate goes up continuously for men • Peaks at midlife for women, then declines • 1/3 of older men saw their primary care physician in the week before completing suicide; 70% within the prior month

  23. Summary of Findings • Dementia and Delirium strongly linked • Depression is common in medical disorders among older patients • All three “D’s”; • Associated with worse health outcomes • Greater use and costs of medications • Greater incidence of iatrogenic illness • ↑ medical outpatient visits, emergency visits, and hospitalizations

  24. Example of Neurodegenerative Condition prone to the three “D’s”:Parkinson’s Disease • Imbalance of ACH – Dopamine • Not enough Dop = Parkinsons • Too much Dop = psychosis • 20-30 % will develop Dementia • Increasing Dop doesn’t prevent dementia • 50 % will become depressed sometime during illness • Drug-induced delirium and hallucinations common cause of psychiatric symptoms

  25. Dementia • Acquired persistent decline in several realms of intellectual ability • Demence described in Paris Assylums (1820’s) • Frequent alteration in behavior and mood • Alzheimer’s Dz most common, but not all dementia is AD • Constitutes the greatest health challenge for the Baby Boom generation – will be the #1 reason why you need an ECF

  26. Course of Age-Related Changes in Dementia Age-Associated Memory Impairment C O G N I T I O N Assymptomatic MCI AD Age 30 40 50 60 70 80

  27. SDAT • 39 % go undiagnosed • Early onset of Memory Deficits • Absense of Neurologic Deficits • No CVA or injury on CT • Makes up 70 % of Dementia Pt’s • >5.5 million Americans currently Dx • Already 4th leading cause of death • Live 7 – 10 years after DX

  28. International Working Group for New Research Criteria for the DX of Alzheimer’s Disease • Current dx dependent upon documenting mental decline • New Proposed Diagnostic Criteria for SDAT • MCI and evidence of AD from biomarkers ( eg, + amyloid scan, CSF markers of amyloid or tau) • AD = Dementia + biomarkers

  29. Three of the new guidelines focus on three stages of Alzheimer's disease: • (1) dementia due to Alzheimer's • (2) mild cognitive impairment (MCI) due to Alzheimer's • (3) preclinical (presymptomatic) Alzheimer's.

  30. “Pre-clinical Alzheimer’s” • 5 year study of monoclonal antibodies + screening tests • Looking for specific biomarkers • 30% over 65 have amyloid plaques • Brain changes caused by the disease may begin decades before symptoms such as memory loss and confusion occur.

  31. “Pre-clinical Alzheimer’s” • The new guidelines are not an immediate call for diagnosis of this preclinical stage and do not include specific diagnostic criteria. They rather propose a research agenda to identify biomarkers that may signal when these presymptomatic brain changes begin.

  32. Reliable predictors don’t exist • There are currently no validated biomarkers for Alzheimer's disease, but researchers are investigating several promising candidates • We now know that Alzheimer's has already caused severe brain damage in individuals who meet the criteria for mental decline.

  33. Neuroimaging

  34. Neuroimaging and Dementia • AAN Guidelines = MRI / CT • Medicare reimbursement – FDG-PET to differentiate AD from FTD • Developing PET technologies – amyloid plaque and tau tangle imaging • Neurology 2004; www.cms.gov

  35. Amyloid Scans

  36. Pre-senile Alzheimer’s Disease • Rare • Prior to age 60 • Autosomal dominant inheritance due to mutations presenelin I (chrom 14), presenelin II (chrom 1) and APOE (chrom 19). • Earlier symptom onset (personality sx) • Abnormal / high amyloid deposition

  37. SDAT: Making the Diagnosis Earlier (risk factors) • Early warning signs • Progressive and insidious • Functional • Behavioral • “Red Flags” (Natural Brain Stress tests) • Delirium (especially recurrent) • Depression (or AD apathy) • Catastophic Rxn (too much input) • Concurrent Medical Illnesses • Why is this pt doing poorly NOW • Listen to the Family (“He’s just not right”) • See them separately • They will tell you the diagnosis

  38. Genetic Considerations • Should NOT be used solely as predictive test – helpful in research and validation • Rare autosomal dominant families with early onset (age 50 – 60) dementia • Mutations cause the disease • Presenilin genes (chromosomes 1 and 14) • APP gene (Chromosome 21) • Apolipoprotein E (APOE) • Gene on chrom 19; 3 alleles, 5 common genotypes (3/3, 3/4, 2/3, 2/4, 4/4) • APOE-4 in 20% US population • APOE-4 increases risk, lowers age onset • APOE alone not considered useful predictive test

  39. Genetic Risk factors; Early onset of mutations in chromosome 1, 14, and 21 Late onset of mutations in chromosome 19     -apolipoprotein E gen (APOE 2, 3, and 4)     4/4 greatest risk (3% of population)     3/4 next risk (20% of population)     2 may be protective  APOE 4 neither necessary nor sufficient to cause dementia

  40. Why Diagnose AD Early? • Safety Issues (driving, compliance) • Advanced Planning while Pt competent (POA, HCR, Guardian) • Family Stress and Misunderstanding • Early Education of Caregivers • Specific, stabilizing Tx Available

  41. Approved AD/Cognitive Treatments • Aricept (Donepezil) • Exelon (Rivastigmine) AChE + BuChE • Reminyl (Galantamine) • Namenda (Memantine) • Vitamin E (a-tocopherol) 1200 IU/d

  42. Possibly beneficial: • Estrogen (HRT) • Selegiline • Ginko biloba • Cholesterol lowering agents • Reality Therapy • Music Therapy

  43. …and the Pipeline is dry… • NMDA receptor antagonists. Limits excitotoxicity caused by excessive pre-synaptic glutamate release. Mixed results • Alzhemed – organic molecule to prevent formation & deposition of beta amyloid fibrils in the brain. (withdrawn 2007) • Preventive Therapies – “Alzheimer’s vaccine” (Lilly's Alzheimer's drug solanezumab flunks out 2012)

  44. Vascular Dementia • 20% of Dementias • Not always clear findings on CT/MRI • Early Gait Disturbance • Frequent falls • Early incontinence • Usually prominent personality and mood changes

  45. 4 Sub-types of Vascular Dementia • Single infarct Dementia (behavior worse with frontal involvement) • MID • Small vessel disease (must be more than mild) • Watershed injury (hypoperfusion) • Males vs Female considerations

  46. The remaining 10 % • Frontal Lobe Dementias (Picks) • Lewy Body Dementia • Parkinson’s Dz • Other Neurodegenerative conditions

  47. Bottom Line - Diagnose early, Treat early, So patients can Stay Home Longer! (on average, 18 – 24 months)

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