Diagnosis & Management of Dementia
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Transcript Diagnosis & Management of Dementia
Michael Mistric, PhD, RN, FNP, BC
Nurse Practitioner
Michael E. DeBakey VA Medical Center
Describe the demographics associated with
Alzheimer’s dementia
Describe the clinical features of Alzheimer’s
dementia
Describe the medical management of Alzheimer’s
dementia
Describe caregiver support services for individuals
with Alzheimer’s dementia
Describe caregiver’s basic social process of
formulating expectations of dementia care
A syndrome that has multiple reversible and
irreversible causes and requires systematic
evaluation of the patient presenting with a
cognitive complaint
An acquired, persistent decline (not secondary
to delirium) involving at least three of the
following five domains: language, memory,
visiospatial skills, executive function, and
personality and mood
Cummings, Benson, LoVerme (1980) Reversible dementia. JAMA, 243(23)
Approximately 5 million Americans have Alzheimer’s
disease (AD). Unless a cure or prevention is found,
that number will increase to 14 million by 2050.
An estimated 280,000 Texas have Alzheimer’s disease.
One in eight persons over 65 and nearly half of those
over 85 have AD. A small percentage of people as
young as their 30s and 40s get the disease.
AD is degenerative disease of the brain from which
there is no recovery.
AD is now the seventh leading cause of death in
adults.
2010 Alzheimer's Disease Facts and Figures (alz.org)
Direct and indirect costs of AD and other dementia’s
amount to more than $148 billion annually.
Almost 10 million Americans are caring for a person with
AD or another dementia; approximately one out of three
of these caregivers is 60 years or older.
In 2005, it was estimated that unpaid caregivers of people
with AD and other dementias provided 8.5 billion hours of
care valued at almost $83 billion dollars.
More than half the states in the United States provide
more than a billion dollars in unpaid care each year – Texas
$5.8 billion.
2010 Alzheimer's Disease Facts and Figures (alz.org)
The primary pathologic features of AD
are amyloid deposition, neurofibrillary
tangle formation, and neuronal loss
AD and the Brain
Plaques and Tangles: The Hallmarks of AD
The brains of people with AD have an abundance of two
abnormal structures:
• beta-amyloid plaques, which are dense deposits of protein and
cellular material that accumulate outside and around nerve
cells
• neurofibrillary tangles, which are twisted fibers that build up
inside the nerve cell
An actual AD plaque
An actual AD tangle
AD and the Brain
Beta-amyloid Plaques
1.
Amyloid precursor protein (APP) is the
precursor to amyloid plaque.
1. APP sticks through the neuron
membrane.
2.
3.
2. Enzymes cut the APP into fragments
of protein, including beta-amyloid.
3. Beta-amyloid fragments come together
in clumps to form plaques.
In AD, many of these clumps form,
disrupting the work of neurons. This
affects the hippocampus and other areas
of the cerebral cortex.
AD and the Brain
Neurofibrillary
Tangles
Neurons have an internal support structure partly made up of
microtubules. A protein called tau helps stabilize microtubules. In AD,
tau changes, causing microtubules to collapse, and tau proteins clump
together to form neurofibrillary tangles.
Memory loss
Difficulty with familiar
tasks
Trouble with abstract
thinking
Misplacing things
Problems with
language
Changes in mood or
behavior
Disorientation to time
and place
Poor or decreased
judgment
Changes in
personality
Loss of initiative
Memory impairment and 1 or more:
Aphasia (language disturbance)
Apraxia (inability to carry out motor activities
Agnosia (failure to recognize objects)
Disturbed executive function (planning, organizing)
Cognitive deficits
Gradual onset, continued decline
Deficits not due to another condition
Deficits not exclusive to delirium
AD and the Brain
The Changing Brain in
Alzheimer’s Disease
No one knows what causes AD to begin,
but we do know a lot about what happens
in the brain once AD takes hold.
Pet Scan of
Normal Brain
Pet Scan of Alzheimer’s
Disease Brain
Treat a reversible
condition
AD no longer a
diagnosis of exclusion
Treat co-morbid
conditions
Drugs & programming
depend on staging
Avoid exacerbation
Limit complications
Caregivers can be
secondary victims:
provide for them as well
Relieve symptoms
AD Research: Diagnosing AD
Providers today use a number of
tools to diagnose AD:
• a detailed patient history
• information from family
and friends
• physical and neurological exams and lab tests
• neuropsychological tests (MMSE, GDS, Global
Deterioration Scale, Affect Balance, BEHAVE-D
• imaging tools such as CT scan, or magnetic
resonance imaging (MRI), PET scans
Complete PE & History
Mini-Mental State Exam (MMSE) or Physical SelfMaintenance Scale (PSMS) to establish baseline
cognition and functional ability
Global Deterioration Scale – useful for staging
Affect Balance or Geriatric Depression Scale
Katz ADLs – IADLs
BEHAVE-AD
Members of various ethnic groups, cultures,
and races manifest and cope differently
with the disease, care-giving, and related
stresses
Some Asian/Pacific Islanders view AD as a normal part of
aging
Some Hispanics view AD as a spiritual test or punishment
for a past deed.
Some African Americans rely on their spiritual faith to
deal with the illness and care-giving.
1st degree African American relatives have
higher risk than Caucasians.
African Americans are 4 times more likely
to develop AD by age 90
African Americans and Hispanics may be at
higher genetic risk based on APOE-4 allele
aberration
Hypertension and hypercholesterolemia
each place African American at a 4 times
risk for AD
http://www.ethniceldercare.net
African American family members & caregivers
may not consider dementia an illness, but rather an
expected consequence of aging
Some believe it is a form of mental illness
May be believed to be the result of “worriation”
and behaviors may be interpreted as “spells”
First cue may be in the failure to carry out role and
social functions (later than desired recognition per
professional assessment)
http://www.ethniceldercare.net
Hispanics may be 2 times more likely
than Caucasians to develop AD by age 90
Vascular dementia has higher prevalence
than AD
http://www.ethniceldercare.net
Female family members are the designated
caregivers
Dementia may be viewed as some form of
mental illness
Dementia is a source of shame,
embarrassment, stigma; and, therefore
may be a barrier to getting help
Problem not typically shared in the cultural
network
http://www.ethniceldercare.net
Dementia is a form of normal aging
Dementia is a form of mental illness
Dementia is a source of shame
Dementia is a family secret that should not
be shared
Dementia is a result of fate
http://www.ethniceldercare.net
Early Dementia
“All dressed up and no where to go”
Middle Dementia
“I want to go with you”
Late Dementia
“In his own little world”
Physical Appearance
Awareness
May still dress self appropriately
“Lost in Time”
Behaviors
Wandering
Anxious
Resistance to ADLs
Sleep disturbance
AD and the Brain
Preclinical AD
• Signs of AD are first noticed in
the entorhinal cortex, then
proceed to the hippocampus.
• Affected regions begin to shrink
as nerve cells die.
• Changes can begin 10-20 years
before symptoms appear.
• Memory loss is the first sign of
AD.
Slide 20
Eating
Eats independently
May need cueing
Remove stimulants from diet
Toileting
Needs supervision locating bathroom and reminders to go
Usually continent
Hydration
Needs supervision
Provide favorite beverages frequently
Dressing
Needs help locating and choosing clothing
Coaxing--resistance
Personal Hygiene
Needs supervision-is relatively independent
Bathing
Needs supervision
Awareness of need to bathe is variable
Physical Appearance
▪ Looks unfinished; does not want to change clothes
▪ Change in posture
Awareness
▪ May be awareness of past versus present
▪ Unable to think in the abstract
Behaviors
▪ Wanders, is suspicious, resistant to caregivers,
social butterfly
AD and the Brain
Mild to Moderate AD
• AD spreads through the brain. The
cerebral cortex begins to shrink as
more and more neurons stop
working and die.
• Mild AD signs can include memory
loss, confusion, trouble handling
money, poor judgment, mood
changes, and increased anxiety.
• Moderate AD signs can include
increased memory loss and
confusion, problems recognizing
people, difficulty with language
and thoughts, restlessness,
agitation, wandering, and repetitive
statements.
Slide 21
Eating
Trouble using utensils, positioning, and swallowing--
precut food, use prompting/cueing
Toileting
Needs assistance with mechanics--wiping, flushing,
pulling down underwear, reminders
Hydration
Hydration is dependent on caregiver attention
Dressing
Assistance in dressing due to agnosia, apraxia
Personal Hygiene
Assistance due to agnosia, apraxia, Parkinsonian
symptoms
Needs tasks broken down
Bathing
Needs supervision
Awareness of need to bathe is dependent on caregiver
Physical Appearance
▪ Looks abnormal, undresses, looks lost,
posture/balance deficits, loses weight, loss of 3D
vision
Awareness
▪ Limited to field of vision, seeks sensory stimulation
Behaviors
▪ Hyper/hypo activity, cannot communicate needs,
does not recognize self or loved ones
AD and the Brain
Severe AD
• In severe AD, extreme shrinkage
occurs in the brain. Patients are
completely dependent on others for
care.
• Symptoms can include weight loss,
seizures, skin infections, groaning,
moaning, or grunting, increased
sleeping, loss of bladder and bowel
control.
• Death usually occurs from
aspiration pneumonia or other
infections. Caregivers can turn to a
hospice for help and palliative care.
Slide 22
Eating
Total loss in eating skills: using utensils, position,
swallowing difficulty
Toileting
Total Care
May resist
Hydration
Unable to pour water or understand need or
mechanics of drinking water
Dressing
Needs total assistance
May disrobe or fiddle with clothes
Personal Hygiene
Needs total assistance.
Able to do one step tasks – e.g. washing face
Bathing
Unable to comprehend bathing
May resist sponge or bed bath
All are focused on maximizing the
potential of the patient and
managing symptoms
▪ Support cognitive functioning
▪ Reduce and prevent functional disabilities
▪ Ameliorate and mediate behavioral
disturbances
AD Research: Managing Symptoms
Between 70 to 90% of people with AD eventually
develop behavioral symptoms, including sleeplessness,
wandering and pacing, aggression, agitation, anger,
depression, and hallucinations and delusions. Experts
suggest these general coping strategies for managing
difficult behaviors:
• Stay calm and be understanding.
• Be patient and flexible. Don’t argue or try to convince.
• Acknowledge requests and respond to them.
• Try not to take behaviors personally. Remember: it’s
the disease talking, not your loved one.
Experts encourage caregivers to try non-medical coping strategies
first. However, medical treatment is often available if the behavior
has become too difficult to handle. Researchers continue to look at
both non-medical and medical ways to help caregivers.
Still are people that accept memory loss
& confusion as a natural part of aging
Cognitive impairments of any kind are
not easy to admit, recognize, or discuss
Patients hide or compensate for early
signs
Families deny what is being seen
Requires comparison of cognitive and physical
functioning relative to a previous level of
performance
Eliminate or reverse any other (vascular,
metabolic, etc.) causes
Proceed by clinical criteria and protocols for
radiologic & laboratory studies
Refer to neurologist and Alzheimer’s Disease
Research Center
What Alzheimer symptoms are most prevalent?
What significant changes have you noticed?
Memory
Behavior
Personality
Skills
Other
How have you successfully accommodated for these
changes?
What caregiving challenges are you facing?
What activities does your loved one still enjoy?
Describe a special moment you shared with your loved
one recently.
Current treatments for Alzheimer’s are not
designed to reverse the disease process
totally, yet they can produce some
improvements in cognition.
Existing medications can be effective in
slowing the progression of the disease and
helping patients remain independent for
longer periods of time.
Treating symptoms effectively is valuable not
only to patients but also to their caregivers
and families.
Cholinesterase inhibitors
Receptor agonists
Estrogen
Anti-inflammatory drugs
Antioxidants
Various experimental agents
Behavioral controls
Cholinesterase Inhibitors
Donepezil (Aricept): Mild/Moderate Dementia
▪ Start with 5 mg/day; increase to 10 mg/day in 4 weeks
▪ Nausea; Diarrhea; Poor Appetite
Rivastigmine (Exelon): Mild/Moderate Dementia
▪ Start with 4.6 mg/24 hour patch daily; increase to 9.5
mg/24 hour patch daily in 4 weeks
▪ Nausea; Diarrhea; Poor Appetite
Galantamine (Reminyl): Mild/Moderate Dementia
▪ Start with 8 mg a day; increase by 8 mg every four weeks
up to 24 mg a day
▪ Nausea; Diarrhea; Poor Appetite
N-methyl-D-aspartate (NMDA)
Memantine (Namenda): Moderate/Severe
Dementia
Start with 5 mg a day; increase by 5 mg a week up to 10 mg
twice a day
Headache; Dizziness; Confusion
Tacrine (Cognex):
Not used anymore
Prototypical cholinesterase inhibitor for the treatment of
Alzheimer's disease
Muscarinic receptor agonists
M1-type muscarinic acetylcholine receptors play a role
in cognitive processing.
In Alzheimer disease (AD) amyloid formation may
decrease the ability of these receptors to transmit their
signals leading to decrease cholinergic activity.
A number of muscarinic agonists have been developed
and are under investigation to treat AD.
These agents show promise as they are neurotrophic,
decrease amyloid depositions, and improve damage
due to oxidative stress.
Nicotinic receptor agonists
Nicotine has long been known to improve cognitive
function, but its adverse effects make it problematic as
a treatment for diseases of cognitive dysfunction
Recent research has revealed that certain subtypes of
nicotinic acetylcholinesterase receptors (nAChRs) in the
brain are involved in cognitive function
Agents that target these nAChRs have shown promise
in Alzheimer’s disease
Research also suggests that these agents may not only
improve cognition but also be neuroprotective
Early studies of estrogen suggested that it might help
prevent AD in older women.
However, a clinical study of several thousand
postmenopausal women aged 65 or older found that
combination therapy with estrogen and progestin
substantially increased the risk of AD.
Estrogen alone also appeared to slightly increase the risk
of dementia in this study.
Therefore, based on epidemiological correlations, the use
of estrogen to prevent or treat dementia has not been
supported by follow-up studies and is not recommended.
http://www.medicinenet.com
Several studies have found evidence of brain inflammation in
AD and researchers have proposed that drugs that control
inflammation, such as NSAIDs, might prevent the disease or
slow its progression and early studies of these drugs in
humans have shown promising results.
However, a large NIH-funded clinical trial of two NSAIDS
(naproxen and celecoxib) to prevent AD was stopped in late
2004 because of an increase in stroke and heart attack in
people taking naproxen, and an unrelated study that linked
celecoxib to an increased risk of heart attack.
Therefore, based on epidemiological correlations, the use of
NSAIDs to prevent or treat dementia has not been supported
by follow-up studies and is not recommended.
http://www.medicinenet.com
A recent double-blind, placebo-controlled
study of Vitamin E and donepezil for the
treatment of mild cognitive impairment was
unable to demonstrate benefit form Vitamin E
and showed only modest and short-term benefit
from donepezil.
This result suggested there was no role for the
use of Vitamin E in the prevention or early
treatment of Alzheimer’s Dementia.
Petersen et al. (2005). New England Journal of Medicine (352)
Many researchers believe a vaccine that reduces the
number of amyloid plaques in the brain might ultimately
prove to be the most effective treatment for AD.
In 2001, researchers began one clinical trial of a vaccine
called AN-1792.
The study was halted after a number of people developed
inflammation of the brain and spinal cord.
Despite these problems, one patient appeared to have
reduced numbers of amyloid plaques in the brain.
Other patients showed little or no cognitive decline during
the course of the study, suggesting that the vaccine may
slow or halt the disease.
Researchers are now trying to find safer and more effective
vaccines for AD.
http://www.medicinenet.com
Look for concurrent illness/problems
Look at medications
Try non-pharmocologic alternatives
Target the dominant symptom
Start drugs low and go slow
Look at drug with best side effect profile
Review compliance
Simplify
Give clear and written instructions
Respiridone (Resperdal)
0.5 - 2 mg/day in two divided doses
Sedation; Parkinson's Disease symptoms
Haloperidol (Haldol)
0.25 - 2 mg/day. Gradually increase this dose. Use sparingly only for
severe agitation
Parkinson's Disease symptoms; Sedation; Falling; Abnormal
Movements
Quetiapine (Seroquel)
12.5 - 200 mg/day in two divided doses
Sedation; Light headedness
Olanzapine (Zyprexia)
2.5 - 10 mg/day
Sedation; Light headedness; Confusion; Dry Mouth; Constipation
Citalopram (Celexa)
10 - 60 mg/day
Nausea; Dry Mouth; Sedation
Mirtazepine (Remeron)
15 - 30 mg at night
Sedation; Weight Gain; Dry Mouth
Sertraline (Zoloft)
50 - 200 mg/day
Insomnia; Diarrhea; Tremor
People with AD usually die from complications
Without an advance directive executed while the
individual was competent, a substitute decision maker
makes difficult life and death decisions
End-of-life choices may include the use, limitation,
withdrawal or refusal of:
procedures, treatments or technology such as tube
feeding
mechanical respirators or ventilators
cardiopulmonary resuscitation (CPR)
surgery
the use of antibiotics
A hospice program offers a more humane and
compassionate option than the nursing home or
hospital during the final months
Simplify - Simplify - Simplify
Medications: Start Slow
Look for concurrent illness/problems
Remember your goal:
To improve quality of life
Do no harm!
Consider the caregiver and family
The specific aims were to:
Elicit subjective perspectives of family members about
what constitutes quality LTC for loved-ones with
dementia, and
Develop a grounded theory of shared meanings about
quality dementia care that reflects the expectations of
family members in various stages of giving care and
relinquishing care for a loved-one with dementia
Research Question:
How do family members describe their expectations of
dementia care in the LTC setting?
Stage 1: Transitions to caregiver role
Stage 2: Takes on caregiver role
Recognizes limits
Acknowledges need for LTC placement
Responds to relinquishment of care
Stage 4: Selects and evaluates LTC facility
Fills gaps
Stage 3: Relinquishes caregiver role
Sees losses
Makes selection
Evaluates care
Stage 5: Accepts LTC resident status
Accepts LTC status
Justifies LTC placement
Patient Care
Nutrition, hygiene,
toileting, medications,
and activities
Pleasant Surroundings
Resident’s room and
facility common areas
Competent Staff
Ability to provide
dementia care and care of
individuals in LTC
Caring Staff
Treat with dignity and
respect; free from neglect
and abuse
Communication
What is communicated &
when communication
should occur
Institutional
Responsiveness
Staff response to
questions and concerns
The Alzheimer’s Association
http://www.alz.org
Family Caregiver Alliance
http://www.caregiver.org
AgeNet; follow the "Geriatric Health" link
http://www.agenet.com/early_alz_guide.html
Mayo Clinic Health Oasis
http://www.mayohealth.org/
Alzheimer's Disease Education and Referral Center
(ADEAR Center)
http://www.alzheimers.org
Alzheimer's Research Forum
http://www.alzforum.org
American Academy of Neurology
http://www.aan.com
National Institute of Neurological Disorders and Stroke
http://www.ninds.nih.gov
Medic Alert
http://www.medicalert.org
National Institute on Aging and Eldercare Locator
http://www.eldercare.gov
American Health Assistance Foundation (AHAF)
http://www.ahaf.org
Ethnicity and Dementia
http://www.ethnicelderscare.net
Summary