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
1.
2.
AD and the Brain
Beta-amyloid Plaques Amyloid precursor protein (APP) is the precursor to amyloid plaque. 1.
APP sticks through the neuron membrane.
2.
Enzymes cut the APP into fragments of protein, including beta-amyloid.
3.
Beta-amyloid fragments come together in clumps to form plaques.
3.
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 together to form neurofibrillary tangles.
tau
proteins clump
Memory loss Difficulty with familiar tasks Problems with language Disorientation to time and place Poor or decreased judgment
Trouble with abstract thinking Misplacing things Changes in mood or behavior 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
Treat co-morbid conditions
Avoid exacerbation
Limit complications
Relieve symptoms
AD no longer a diagnosis of exclusion
Drugs & programming depend on staging
Caregivers can be secondary victims: provide for them as well
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 Self Maintenance 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.
1 st 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
May still dress self appropriately
Awareness
“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
Sees losses
Stage 2: Takes on caregiver role
Fills gaps
Stage 3: Relinquishes caregiver role
Recognizes limits
Acknowledges need for LTC placement
Responds to relinquishment of care
Stage 4: Selects and evaluates LTC facility
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 Foru m
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