“Dementia and Competency in the Aging

Inmate Population”FPIC Annual Conference

and Justice Institute

“Dementia and Competency in the Aging

Inmate Population”FPIC Annual Conference

and Justice Institute

Francisco Fernandez, MD, FACP, DFAPAProfessor and Chair , Department of Psychiatry and Behavioral Neurosciences

Principal Investigator, USF Memory Disorders ClinicUniversity of South Florida Morsani College of MedicineProfessor, 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

• 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

USF Memory Disorders Clinic

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 TimelineAD—History Timeline

1992AHCPR

develops screening guidelines

for AD

~200 AD

Galen “morosis” (dementia)

with old age

700 BC

2000 AD

1980Alzheimer

’sAssociatio

nestablishe

d

Early 1960s

Awareness of AD as a single disease

1907AD first

described by Dr. Alois

Alzheimer

1978?Single entity established—

senile dementia of

the Alzheimer’s type (SDAT)

1983Cholinergi

cdeficit

identified

1991APOE

implicated

1994Brain

inflammatory response

identified as pathogenetic

Treatment Guidelines Research

into treatment

s

1993First

cholinesterase inhibitor approved

1999 MCIdescribe

d

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

AAMI / ARCD

MCI

Clinical AD

Time (Years)

Cog

nitiv

e D

eclin

e “Brain”AD

Brain Aging

Mild

Moderate

Moderately Severe

Severe

(Ferris, 4/03)

Brain Aging

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)

• < 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

PSYCHIATRIC SYMPTOMS IN ALZHEIMER'S DISEASE (N=217)

Symptom %• Dysthymia and depression 40.6• Suspiciousness and paranoia 35.5• Anxiety and fearfulness 30.9• Delusions 30.0• Hallucinations 25.4• Aggressive acts 24.9• Sleep disturbances 19.4• Wandering 18.4• Miscellaneous behaviors 18.4• 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.

Course of Aging, MCI and AD

AAMI / ARCD

MCI

Clinical AD

Time (Years)

Cog

nitiv

e D

eclin

e “Brain”AD

Brain Aging

Mild

Moderate

Moderately Severe

Severe

(Ferris, 4/03)

Brain Aging

Symptomatic Effects versus Slowing Disease Progression

Impa

irmen

t

Treatment PeriodEndBaseline

Severe

Mild

Placebo

Symptomatic

Disease modifying

(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. 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

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

Benefit of Cholinesterase Inhibitor Treatment

Stern RG et al. Am J Psychiatry.

1994;151:390-396.

–6

0

6

12

180 6 12 14 26 38 50 62 74 86 98

Mea

n c

han

ge

fro

m b

asel

ine

in

AD

AS

-co

g s

core

Decline in ADAS-cog score (9–11 pointsper 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

Benefit of Cholinesterase Inhibitors

6 months

Improved

Worse Cognition

Global change

Functioning

Behavior

AChEI

Placebo

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

Changefrom

Baseline

Memantine in Advanced AD: Cognitive Benefit on SIB

Week 4 Week 12 Week 28

Wor

seni

ng

memantineplacebo

P=0.002

Reisberg, et al. NEJM, 2003

-12

-10

-8

-6

-4

-2

0

2

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 AActivators of Aββ degrading enzymes degrading enzymes

• Anti-Anti-ββ-sheet conformational agents-sheet conformational agents

• ““Vaccination” against AVaccination” against Aββ

(Wisniewski, 8/03)

“Vaccination” with A Peptides as Treatment for Alzheimer’s Disease

Transgenic “AD” mouseover-expressing APP with FADlinked codon 717 mutation

With increasing agedevelops extensiveamyloid deposits

Age 13months,cognitivedecline,neuronalpathology

Immunized at 6 weeks with A1-42

Develops antibodiesagainst A1-42

Normalold age,no amyloiddeposits

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 A1-42 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