“Dementia and Competency in the Aging Inmate Population” FPIC Annual Conference and Justice Institute Francisco Fernandez, MD, FACP, DFAPA Professor and Chair , Department of Psychiatry.
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“Dementia and Competency in the Aging Inmate Population” FPIC Annual Conference and Justice Institute Francisco Fernandez, MD, FACP, DFAPA Professor and Chair , Department of Psychiatry and Behavioral Neurosciences Principal Investigator, USF Memory Disorders Clinic University of South Florida Morsani College of Medicine Professor, Department of Community and Family Health Tampa, FL http://health.usf.edu/medicine/psychiatry/p_memory_disorders_clinic.htm Abstract • The average age of inmates is growing rapidly. • Physically, inmates are thought to age an average of 10 years faster than the community population. • Dementia, which involves loss of memory, language, recognition, planning and purposeful behavior, is progressive and ultimately fatal. – There are no known cures. – Chronic illnesses, brain trauma and substance abuse also “age the brain” and raise the risk of dementia. • According to mental health experts all demographics and early reports indicate that there will soon be an exponential growth of dementia in our aging inmate population. Dementia and Competency in the Aging Inmate Population • Judge Mark Speiser, 17th Judicial Circuit • Francisco Fernandez, M.D., Chair, Dept. of Psychiatry, USF Health • Timothy Ludwig, Ph.D., Broward County Sheriff’s Office Department of Detention • John Bailey, D.O., Past Chairman, Florida Correctional Medical Authority USF Memory Disorders Clinic • • • Provide services to persons suspected of having Alzheimer’s disease and other related dementias Evaluate and identify needs of people undergoing medical evaluation and family members to provide appropriate referrals for services Identify and disseminate information on community resources for assistance with Alzheimer’s disease Research Top 10 Challenges 1. Difficulties in recruitment, retention, succession planning and staff training 2. Providing adequate medical care and mental health services 3. Technology/management systems 4. Funding – insufficient + burden of “unfunded” mandates 5. Administrative issues 6. Facilities and physical plant 7. Immigration and illegals 8. Public education 9. Re-entry initiatives, security threat groups 10. Special needs groups Definition • Dementia is a clinical state characterized by a significant loss of function in multiple cognitive domains, that is not due to an impaired level of arousal. – The presence of dementia does not necessarily imply irreversibility, a progressive course, or any specific cause. – Exclude delirium or impaired consciousness. Dementing Disorders • Neurodegenerative Dementias – Alzheimer’s disease – Lewy body dementia – Frontotemporal dementias – Parkinson’s disease • Other Dementias – Vascular dementia – AIDS dementia – Alcohol dementia AD—History Timeline 1907 AD first described by Dr. Alois Alzheimer Early 1960s Awareness of AD as a single disease 1991 APOE implicated 1980 Alzheimer’s Association established 1993 First cholinesterase 1999 MCI inhibitor described approved Treatment Guidelines Research into treatments 700 BC 2000 AD ~200 AD Galen “morosis” (dementia) with old age 1978? Single entity established— senile dementia of the Alzheimer’s type (SDAT) 1983 Cholinergic deficit identified 1992 AHCPR develops screening guidelines for AD 1994 Brain inflammatory response identified as pathogenetic Why Is This Of Any Importance? • Life expectancy is increasing • As we age, there is an increase – In concurrent medical disorders – In cognitive disorders – Risk for AD • Behavioral complications • Need to establish the “big picture” – Identifying what types of cognitive health inmates are experiencing – what services are available – what the community’s standards of care are – how facilities can partner with service providers for access – what pharmaceutical purchase options are available to reduce costs Is there such a thing as Successful Aging? • Healthy • Little if any cognitive decline • Cognition preserved will into the 10th decade What is “Normal” Typical Aging? • HPTN • CAD • Traumatic brain injury • Addictions • HIV & HCV • Diabetes • Renal Insufficiency Course of Aging, MCI and AD Brain Aging Cognitive Decline AAMI / ARCD Brain Aging “Brain”A D MCI Mild Moderate Clinical AD Moderately Severe Severe Time (Years) (Ferris, 4/03) Neuronal Cell Loss with AD Normal AD BILATERAL SEVERE ATROPHY PET scan; early Alzheimer Disease CHARACTERISTIC DECREASED 18-FDG UPTAKE Early and Late-Onset AD Early Onset (EOFAD) Late Onset (LOAD) • < Age 60 - rare. ≈ 5% • ≥ Age 60 • Common of all AD cases – Highly penetrant (virtually 100%) – Mostly Autosomaldominant • Mutations in three genes that cause early-onset AD – Alzheimer Disease Type 1 (AD1) mutations in APP (15%) – Chromosome 21 – Alzheimer Disease Type 3 (AD3) mutations of PSEN1 (70%) Chromosome 14 – Alzheimer Disease Type 4 (AD4) mutations in PSEN2 (5%) Chromosome 1 polymorphisms – Chromosome 19 - gene that produces a protein called apolipoprotein E (ApoE). • e4: involved in the formation of beta-amyloid plaques. • e2: protectective • Relatively low penetrance - high prevalence PSYCHIATRIC SYMPTOMS IN ALZHEIMER'S DISEASE (N=217) Symptom % • • • • • • • • • • Dysthymia and depression Suspiciousness and paranoia Anxiety and fearfulness Delusions Hallucinations Aggressive acts Sleep disturbances Wandering Miscellaneous behaviors Activity disturbances 40.6 35.5 30.9 30.0 25.4 24.9 19.4 18.4 18.4 9.2 Mendez, M.F, et al., (1990). Psychiatric symptoms associated with Alzheimer's disease. The Journal of Clinical Neuropsychiatry and Clinical Neurosciences, 2, 28-33. Course of Aging, MCI and AD Brain Aging Cognitive Decline AAMI / ARCD Brain Aging “Brain”A D MCI Mild Moderate Clinical AD Moderately Severe Severe Time (Years) (Ferris, 4/03) Symptomatic Effects versus Slowing Disease Progression Impairment Mild Placebo Symptomatic Disease modifying Severe Baseline Treatment Period End (Ferris, 8/03) Treatment Guidelines AAN,1 APA,1 and ISOA*2 guidelines recommend cholinesterase inhibitors as standard therapy for mild-to-moderate AD APA and ISOA recommend Memantine as standard therapy for moderate-to-severe AD ACP and AAFP make weak recommendations for any use at any stage of AD3 1. Doody et al. Arch Neurol. 2001;58:427-433. 2. Fillit et al. Am J Geriatr Pharmacother. 24 2006;4(suppl A):S9-S24. 3. Qaseem et al. Ann Inter Med. 2008; 148:370-378; *ISOA = Institute for the Study of Aging FDA Approved Treatments for Dementia • Acetylcholinesterase Inhibitors – Approved for Mild to Moderate AD • • • • Tacrine (Cognex) Donepezil (Aricept) Galantamine (Reminyl, Razadyne) Rivastigmine (Exelon, Exelon Patch) – Approved for Severe AD • Donepezil (Aricept) – Approved for Parkinson’s Dementia • Rivastigmine (Exelon, Exelon Patch) • NMDA (N-methyl-D-aspartate) Antagonists – Approved for Moderate to Severe AD • Memantine (Namenda) TREATMENT & MANAGEMENT • Primary therapy – To enhance quality of life & maximize functional performance by improving cognition, mood, and behavior – Based on central defect • Secondary therapy – Similar goal based on associated pathogenesis • Palliative therapy – Nonpharmacologic – Pharmacologic • Specific symptom management Mean change from baseline in ADAS-cog score Benefit of Cholinesterase Inhibitor Treatment –6 0 6 Projected benefit of AChEI treatment Decline in ADAS-cog score (9–11 points per year) based on the natural history of untreated patients with moderate AD* 12 18 0 6 12 14 26 38 50 Weeks 62 74 86 98 * Actual decline in ADAS-cog score with time is nonlinear, Stern RG et al. Am J Psychiatry. in contrast to the linear approximation shown. 1994;151:390-396. Benefit of Cholinesterase Inhibitors AChEI Improve d Worse Cognition Global change Placebo Functioning Behavior 6 months Memantine • A different mechanism: inhibits glutamate neurotransmitter system (NMDA receptor) – Large positive U.S. trial coordinated by NYU ADRC – Approved in Europe for moderate to severe Alzheimer’s disease – Effective in combination with Aricept Memantine in Advanced AD: Cognitive Benefit on SIB 2 Change from Baseline Worsening 0 -2 -4 -6 P=0.002 -8 -10 memantine placebo -12 Week 4 Week 12 Week 28 Reisberg, et al. NEJM, 2003 Potential Anti–Amyloid Therapies (Thomas Wisniewski, MD) • Cholinergic therapies (phenserine, etc.) • Cholesterol lowering drugs (statins) • Anti-inflammatory drugs (NSAIDs, COX-II inhibitors) • Anti-oxidants (Ginkgo, etc.) • Secretase inhibitors (APP processing) • Activators of Aβ degrading enzymes • Anti-β-sheet conformational agents • “Vaccination” against Aβ (Wisniewski, 8/03) “Vaccination” with Ab Peptides as Treatment for Alzheimer’s Disease Age 13 months, cognitive decline, neuronal pathology With increasing age develops extensive amyloid deposits Transgenic “AD” mouse over-expressing APP with FAD linked codon 717 mutation Develops antibodies against Ab1-42 Immunized at 6 weeks with Ab1-42 Normal old age, no amyloid deposits Schenk et al. Nature 400: 173-177, 1999 Elan AD Vaccine Clinical Trial • Trial was suspended • As some predicted, a major problem was vaccine toxicity • 15 patients out of about 300 developed “cerebral inflammation” • These complications were likely related to direct or indirect Ab1-42 toxicity (Wisniewski, 8/03) Nonpharmacologic Treatment • Evaluation of Patient – MMSE or other cognitive tool helpful to follow – Functional assessment every 6-12 months – Behavioral interview with each visit (sleep, wandering, eating, hallucinations, agitation) Nonpharmacologic Treatment • Advance directives (for health care and finances) early • Not all gloom and doom – Quality of life may be quite good during much of course – Every patient does not develop every problem associated with dementia – Some problems get better with time SUMMARY • Dementia is common in older adults but is NOT an inherent part of aging • AD is the most common type of dementia, followed by vascular dementia and dementia with Lewy bodies • MCI is a precursor of AD • Evaluation includes history with informant, physical & functional assessment, focused labs, & possibly brain imaging SUMMARY • Primary treatment goals: enhance quality of life, maximize function by improving cognition, mood, behavior • Treatment may use both medications and nonpharmacologic interventions • Community resources should be used to support patient, family, caregivers ACKNOWLEDGMENTS • USF Memory Disorders Clinic: – Yvonne Bannon, RN – Ryan Estevez, M.D., MPH, PhD – Jean Fils, MD – Ofie Grenadillo, MSW – Michelle Mattingly, PhD – Thea Moore, Pharm.D. – Eric Rinehardt, PhD, Coordinator – Michael Schoenberg, PhD • Division of Neuroimmunology: – Brian Giunta, MD – Jamie W. Fernandez, MD • Neuropharmacology Laboratory – Lynn Wecker, PhD • Roskamp Laboratory: – Gabriel de Erausquin, MD, PhD • Silver Child Development Center: – Jun Tan, MD, PhD