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“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