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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.

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Presentation on theme: "Dementia and Competency in the Aging Inmate Population FPIC Annual Conference and Justice Institute Francisco Fernandez, MD, FACP, DFAPA Professor and."— Presentation transcript:

1 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

2 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.

3 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 Sheriffs Office Department of Detention John Bailey, D.O., Past Chairman, Florida Correctional Medical Authority

4 Provide services to persons suspected of having Alzheimers 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 Alzheimers disease Research USF Memory Disorders Clinic

5 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

6 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.

7 Dementing Disorders Neurodegenerative Dementias –Alzheimers disease –Lewy body dementia –Frontotemporal dementias –Parkinsons disease Other Dementias –Vascular dementia –AIDS dementia –Alcohol dementia

8 ADHistory Timeline 1992 AHCPR develops screening guidelines for AD ~200 AD Galen morosis (dementia) with old age 700 BC 2000 AD 1980 Alzheimers Association established Early 1960s Awareness of AD as a single disease 1907 AD first described by Dr. Alois Alzheimer 1978 ? Single entity established senile dementia of the Alzheimers type (SDAT) 1983 Cholinergic deficit identified 1991 APOE implicated 1994 Brain inflammatory response identified as pathogenetic Treatment Guidelines Research into treatments 1993 First cholinesterase inhibitor approved 1999 MCI described



11 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 communitys standards of care are –how facilities can partner with service providers for access –what pharmaceutical purchase options are available to reduce costs

12 Is there such a thing as Successful Aging? Healthy Little if any cognitive decline Cognition preserved will into the 10 th decade

13 What is Normal Typical Aging? HPTN CAD Traumatic brain injury Addictions HIV & HCV Diabetes Renal Insufficiency

14 Course of Aging, MCI and AD AAMI / ARCD MCI Clinical AD Time (Years) Cognitive Decline BrainA D Brain Aging Mild Moderate Moderately Severe Severe (Ferris, 4/03) Brain Aging

15 Neuronal Cell Loss with AD NormalAD


17 PET scan; early Alzheimer Disease CHARACTERISTIC DECREASED 18-FDG UPTAKE


19 Early and Late-Onset AD Early Onset (EOFAD) < Age 60 - rare. 5% of all AD cases –Highly penetrant (virtually 100%) –Mostly Autosomal- dominant 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 Late Onset (LOAD) Age 60 Common 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


21 PSYCHIATRIC SYMPTOMS IN ALZHEIMER'S DISEASE (N=217) Symptom % Dysthymia and depression 40.6 Suspiciousness and paranoia35.5 Anxiety and fearfulness 30.9 Delusions 30.0 Hallucinations 25.4 Aggressive acts 24.9 Sleep disturbances 19.4 Wandering 18.4 Miscellaneous behaviors18.4 Activity disturbances 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.

22 Course of Aging, MCI and AD AAMI / ARCD MCI Clinical AD Time (Years) Cognitive Decline BrainA D Brain Aging Mild Moderate Moderately Severe Severe (Ferris, 4/03) Brain Aging

23 Symptomatic Effects versus Slowing Disease Progression Impairment Treatment Period EndBaseline Severe Mild Placebo Symptomatic Disease modifying (Ferris, 8/03)

24 Treatment Guidelines nAAN, 1 APA, 1 and ISOA* 2 guidelines recommend cholinesterase inhibitors as standard therapy for mild-to-moderate AD nAPA and ISOA recommend Memantine as standard therapy for moderate-to-severe AD nACP and AAFP make weak recommendations for any use at any stage of AD 3 1. Doody et al. Arch Neurol. 2001;58:427-433. 2. Fillit et al. Am J Geriatr Pharmacother. 2006;4(suppl A):S9-S24. 3. Qaseem et al. Ann Inter Med. 2008; 148:370-378; *ISOA = Institute for the Study of Aging 24

25 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 Parkinsons Dementia Rivastigmine (Exelon, Exelon Patch) NMDA (N-methyl-D-aspartate) Antagonists –Approved for Moderate to Severe AD Memantine (Namenda)

26 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 –N onpharmacologic –Pharmacologic Specific symptom management

27 Benefit of Cholinesterase Inhibitor Treatment Stern RG et al. Am J Psychiatry. 1994;151:390-396. –6 0 6 12 18 06121426385062748698 Mean change from baseline in ADAS-cog score Decline in ADAS-cog score (9–11 points per year) based on the natural history of untreated patients with moderate AD * Weeks * Actual decline in ADAS-cog score with time is nonlinear, in contrast to the linear approximation shown. Projected benefit of AChEI treatment

28 Benefit of Cholinesterase Inhibitors 6 months Improve d Worse Cognition Global change Functioning Behavior AChEI Placebo

29 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 Alzheimers disease –Effective in combination with Aricept

30 Change from Baseline Memantine in Advanced AD: Cognitive Benefit on SIB Week 4 Week 12Week 28 Worsening memantine placebo P=0.002 Reisberg, et al. NEJM, 2003 -12 -10 -8 -6 -4 -2 0 2

31 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)Secretase inhibitors (APP processing) Activators of Aβ degrading enzymesActivators of Aβ degrading enzymes Anti-β-sheet conformational agentsAnti-β-sheet conformational agents Vaccination against AβVaccination against Aβ (Wisniewski, 8/03)

32 Vaccination with A Peptides as Treatment for Alzheimers Disease Transgenic AD mouse over-expressing APP with FAD linked codon 717 mutation With increasing age develops extensive amyloid deposits Age 13 months, cognitive decline, neuronal pathology Immunized at 6 weeks with A 1-42 Develops antibodies against A 1-42 Normal old age, no amyloid deposits Schenk et al. Nature 400: 173-177, 1999

33 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 A 1-42 toxicity (Wisniewski, 8/03)

34 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)

35 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

36 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

37 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

38 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

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