“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