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Care of the Person with Alzheimer's Disease

Nancy Evans, BS

Courses are approved by CECBEMS and the California Emergency Medical Services Authority. For more information about accreditation, click here. Nurse practitioners may apply these contact hours to pharmacy continuing education and prescriptive authorization.

People with Alzheimer's are people to be loved. They are our mothers and fathers, our grandmothers and grandfathers. Lela Knox Shanks Your Name Is Hughes Hannibal Shanks, 1996

Alzheimer's disease (AD) is an age-related, irreversible brain disorder that gradually erases memory, thinking, understanding, and sense of self. Over time, as neurons die in widespread areas of the brain's cerebral cortex, mild sporadic memory loss evolves into severe cognitive dysfunction as well as behavior and personality changes and, eventually, loss of physical function.

Alzheimer's disease inflicts an enormous burden on families, on finances, and on the healthcare system. One author describes AD as "death in slow motion" (Cooney, 2003). The course of AD and the rate of decline vary from person to person. On average, clients with AD live for 8 to 10 years after diagnosis but may live as long as 20 years.

Medial view of the human brain showing major landmarks. Courtesy of Alzheimer's Disease Education and Referral Center.

Alzheimer's disease is one of a group of disorders called dementias, which are characterized by progressive cognitive and behavioral changes. Symptoms commonly appear after age 60, beginning with loss of recent memory and followed by faulty judgment and personality changes. People in the early stages of AD often think less clearly and may be easily confused.

In progressive stages of the disease, people who have AD may forget how to do simple tasks, such as how to dress themselves or eat with proper utensils. In the late stages, people with AD are unable to function on their own and become completely dependent on others for their everyday care. Finally, the disease is so debilitating that people become bedfast and succumb to other illnesses and infections. Pneumonia is the most common cause of death in AD.

Although the risk of developing AD increases with age, AD and other dementia symptoms are not a part of normal aging but the result of diseases that affect the brain. In the absence of disease, the human brain can function well into the tenth decade of life.

EPIDEMIOLOGY

First described by German psychiatrist Alois Alzheimer in 1906, AD was then a rare disease. But as life expectancy in the United States has risen to 77+, so have the number of persons with AD. More than 4 .5 million Americans have AD, 20 percent of them between the ages of 75 and 84, nearly half of them age 85 and older. The number of Americans with AD has doubled since 1980 (Hebert et al., 2003). People over 85 constitute one of the fastest growing segments of the population and, as this population continues to grow, so will the number of people with AD.

Alzheimer's disease inflicts a heavy economic burden on families and on society as a whole. According to the Alzheimer's Association, the costs of caring for individuals with AD total at least $100 billion annually (Alzheimer's Association, 2006). Alzheimer's disease costs American business $61 billion a year (Koppel, 2002). Of that amount, about 40 percent represents AD healthcare and the balance represents costs related to caregivers, including lost productivity, absenteeism, and worker replacement.

One recent study found that as the functional status of a person with AD or other dementia declines, healthcare costs increase. Each impairment in activities of daily living (ADL) increases healthcare costs nearly $2,000 per person and each impairment in independent activities of daily living (IADL) increases costs more than $500 per person (Hill et al., 2006).

The staggering cost of AD for families—home healthcare, adult daycare, caregiver respite, and long-term care—are seldom covered by medical insurance or Medicare, which is intended to cover the acute healthcare needs of people over 65 and disabled people under 65. Medicare Part A mainly covers the following services:

• Hospital care with deductible
• Skilled nursing care facility for up to 120 days after hospitalization if need exists
• Limited home healthcare if need exists; AD alone is not sufficient to justify services
• Hospice care if terminally ill; this applies both to home care and nursing home care

Medicare Part B covers 80 percent of the costs for the following services:

• Evaluation and diagnosis after deductible. This includes the use of Positron Emission Tomography (PET) scans for Medicare beneficiaries with suspected AD or other dementia if other diagnostic methods have been inconclusive.
• Physician visits for treatment of AD after deductible. It is important that the physician use code 331 when completing insurance forms; otherwise, Medicare will cover only 50 percent of the physician's bills.
• Physical therapy performed by a skilled therapist as part of a written treatment plan.

Clients who have long-term care insurance, which may cover home healthcare, or those who are eligible for state-funded Medicaid programs, have some coverage for these services, but many families must pay all or most of the cost themselves.

Seven out of 10 people with AD are cared for at home and 3 out of 4 caregivers are women—wives, daughters or other women, many of whom are juggling childcare, jobs, and other responsibilities. Caring at home for someone with AD inflicts extraordinary emotional, physical, and financial stress on families. According to the Alzheimer's Association (2006), the average annual cost of nursing home care is $42,000 but it can exceed $70,000 annually in some areas of the country.

Watching loved ones become more forgetful, frustrated, and confused can evoke sadness, grieving, and anger. Eventually the disease advances to the point where families must decide about long-term care, which frequently means placing the loved one in a nursing home.

PATHOPHYSIOLOGY

Alzheimer 's is the opposite of cancer. Cancer is runaway cell growth. Alzheimer's is runaway cell death. Sandra Steingraber Origins of Dementia, Part 2

Plaques

Three decades of research have begun to shed light on how AD steadily destroys brain function. A protein called amyloid precursor protein (APP), produced by healthy neurons, is severed by two enzymes, called beta and gamma secretase. This process creates a short, sticky protein called beta amyloid.

Instead of dissolving in the fluid that surrounds the neurons, beta amyloid protein folds into insoluble clumps called fibrils. The fibrils stick together, resulting in plaques on the surface of the neuron. Beta amyloid plaques are one of two characteristic lesions of AD.

A beta-amyloid protein in a healthy cell. Courtesy of Alzheimer's Disease Education and Referral Center.

The beta-amyloid protein being cleaved by beta and gamma secretase enzymes. Courtesy of Alzheimer's Disease Education and Referral Center.

A beta-amyloid plaque forming outside the cell. Courtesy of Alzheimer's Disease Education and Referral Center.

Tangles

The other lesion that characterizes AD is called a neurofibrillary tangle that forms inside the neuron itself. Normally, healthy neurons connect with each other through slender appendages or branches called neurites. The neurites contain microtubules that maintain the shape of the cell and serve as its life support system, carrying nutrients and neurotransmitters.

A neurofibrillary tangle, which forms inside the cell. Courtesy of Alzheimer's Disease Education and Referral Center.

The walls of the microtubules are reinforced by tau proteins, which act like the rungs on a ladder. In AD, the tau proteins loosen and form neurofibrillary tangles. Without the reinforcing effect of the tau proteins, the microtubules disintegrate, cutting off life support to the neuron, which then shrivels and dies.

Disruption of Neurotransmitters

Alzheimer's disease reduces the production of certain neurotransmitters in the brain that normally act as chemical messengers, transmitting nerve impulses. These neurotransmitters include acetylcholine, norepinephrine, serotonin, and somatostatin. Reduction of acetycholine is first apparent in the entorhinal cortex, which is adjacent to the hippocampus, an area of the brain associated with recent memory and storage of new information.

ETIOLOGY

Alzheimer's disease is a complex disease with no single, clear-cut cause, and therefore no sure means of prevention. Scientists believe that AD results from the interaction of genetic, environmental, and lifestyle factors over many years, causing changes in brain structure and function.

Alzheimer's disease is classified in two ways: by heritability and by age of onset. Familial AD (FAD) follows a certain inheritance pattern, whereas sporadic AD, according to current research, does not show an inheritance pattern.

Alzheimer's disease is also classified as either early-onset or and late-onset. Early-onset AD occurs in people younger than 65 and is called pre-senile dementia. Late-onset AD, the most common form of the disease, occurs after age 65 and is referred to as senile dementia Alzheimer's type (SDAT).

Fortunately, early-onset AD is rare (about 5% to 10% of cases) and affects people between the ages of 30 and 65. It often progresses more rapidly than late-onset AD. Some forms of early-onset AD are inherited.

Genetic Factors

Research to date indicates that most familial AD has an early onset and that about half of all cases of FAD are known to be caused by mutations (defects) in three genes located on three different chromosomes:

• Mutations in the APP gene on chromosome 21.
• Mutations in the presenilin 1 gene on chromosome 14.
• Mutations in the presenilin 2 gene on chromosome 1.

Everyone inherits two copies of each of these genes—one from each parent. A parent carrying a defective version of one of these genes has a 50-50 chance of transmitting the defective gene to each of his or her children. A single defective version of any one of these three genes will cause early AD nearly 100 percent of the time.

This type of inheritance pattern is called autosomal dominant inheritance. The total known number of these cases is small—between 100 and 200 worldwide. There is no scientific evidence that links these mutations with the more common sporadic, late-onset AD.

Even though autosomal dominant inheritance of genetic mutations does not appear to cause late-onset AD, research indicates that other genetic factors may increase the risk for developing the sporadic form of the disease. Scientists at Duke University's Alzheimer's Disease Center found that inheritance of one or two copies of the apolipoprotein E epsilon 4 (APOE e4) gene version on chromosome 19 increases the risk of late-onset AD (Strittmatter et al., 1993).

In contrast, APOE e2 lowers the risk of AD, and APOE e3 has no effect. Different versions of particular genes cause variations in inherited characteristics such as eye color or blood type. Everyone inherits two gene versions of the APOE gene. For instance, one person may inherit two e4 versions, and another e2/e3. The APOE variations cause changes in the manufacture of the APOE protein, one function of which is to help distribute blood cholesterol throughout the body.

The APOE protein is found in the neurons of healthy brains, but in excess amounts in the brains of people with AD and those with trisomy-21 (Down syndrome) (Bird, 2006). Studies of large populations have shown that the number of copies of the APOE e4 allele inherited influences the age of onset of AD. For example, on average, someone with two copies of APOE e4 would tend to have an earlier age of onset of AD than someone with only a single copy.

Scientists recently reported that genetic factors accounted for 58 to 79 percent of cases of AD, based on the largest twin study to date, which employed the Swedish Twin Registry. However, the authors did not rule out the importance of environmental factors. They concluded "...we confirmed that heritability for AD is high and that the same genetic factors are influential for both men and women. However, nongenetic risk factors also play an important role and might be the focus for interventions to reduce disease risk or delay disease onset" (Gatz et al., 2006).

The presence of a genetic predisposition does not ensure that AD will develop. A person may have one or two copies of the APOE e4 gene version and never develop AD, and someone else may lack APOE e4 alleles and still develop AD. The APOE e4 gene version thus increases the risk of AD, but it does not cause the disease.

In early 2003 Swiss researchers identified a second gene called CYP46 that, when mutated, also may increase the risk of developing late-onset sporadic AD (Papassotiropoulos et al., 2003). This gene plays a key role in removing cholesterol from the brain. Mutations in this gene lead to the buildup of beta-amyloid plaques in the brain. Someone with both the CYP46 mutation and the APOE e4 mutation has more than twice the risk of developing AD as someone with only the APOE e4 mutation.

Continuing research suggests that there may be other genes that contribute to both early- and late-onset AD. For example, the gene encoding ubiquilin 1 (UBQLN1) is one of several candidate genes for AD, located on chromosome 9q22. Mutations in this gene may influence alternative splicing of this gene in the brain (Bertram et al., 2005).

Other Risk Factors and Possible Preventive Strategies

Aging itself is a major risk factor for developing AD, but aging is not the cause of the disease. Normal aging involves changes throughout the body, and the brain is not exempt. Even in normal aging some neurons die; some shrink and are less effective, especially in areas of the brain related to learning, memory, and executive function (the abilities required to plan, organize, and carry out tasks).

Tangles that develop in neurons and plaques may accumulate in particular regions of the brain. Inflammation and oxidative stress increases with age. These age-related changes in the brain vary from person to person, and a healthy individual may experience only a slight decline in memory.

A 2006 report from the National Institutes of Health's Cognitive and Emotional Health Project (CEHP) identified a number of factors that affect cognitive and emotional health (Hendrie et al., 2006). Based on an analysis of 36 large longitudinal cohort studies, this report shows that the following factors contribute to declines in cognitive function:

• Increasing age
• Hypertension
• Diabetes
• Stroke, or transient ischemic attacks (TIAs)
• Presence of infarcts or white-matter lesions
• Low mood (depression)
• Higher body mass index (BMI)

Factors that protect cognitive function include:

• Higher levels of education
• Higher socioeconomic status (SES)
• Emotional support
• Better baseline cognitive function
• Better lung capacity
• More physical exercise
• Moderate alcohol use
• Use of vitamin supplements

Traumatic brain injury is considered a risk factor for AD (Plassman et al., 2000), as is depression. In fact, head injury in early adulthood increases the lifetime risk of depression (Holsinger et al., (2002). In a study of postmortem data, the brains of patients with AD who had a history of recurrent major depressive disorder showed increased hippocampal plaques and neurofibrillary tangles compared with the brains of other patients with AD who had no history of depression (Rapp et al., 2006).

Chronic stress may also be implicated in AD because of the hormonal imbalances it creates, particularly the dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis. Stress causes the hypothalamus to release corticotrophin-releasing hormone (CRH), which triggers the pituitary to signal the adrenal glands to release cortisol, the stress hormone.

Plasma homocysteine, known to be a cardiovascular risk factor, may also increase the risk of AD. Using subjects from the Framingham Heart Study, researchers found that elevated total homocysteine was a strong independent risk factor for the development of dementia and Alzheimer's disease (Sesehadri et al., 2002). There is some evidence that a high-fat diet and high cholesterol levels also may increase the risk of AD; however, more study is needed before this link can be clearly established.

Exposures to environmental toxicants such as lead may also increase the risk of AD. Research in rodents and primates suggest that early life exposure to lead may predispose the brain to AD in later life (Bolin et al., 2006; Zawia & Basha, 2005; Basha et al., 2005). Occupational studies also indicate that exposure to lead during adult life increases the risk of dementia in later life, particularly in those who have at least one APOE e4 allele (Stewart et al., 2002; Schwartz, 2000).

Other environmental exposures possibly implicated in AD include pesticides (Baldi, 2003); metals such as aluminum, methylmercury, iron, zinc, and copper (Carpenter, 2001; Polizzi et al., 2002; Becaria et al., 2002; Grant et al., 2004; Sparks & Schreurs, 2003); and extremely low-frequency magnetic fields (ELF-MF) (Feychting et al., 2003; Hankansson et al., 2003). These findings are based primarily on epidemiologic studies of workers with chronic exposures.

POSSIBLE PREVENTIVE STRATEGIES

Preventing AD would save untold suffering of patients and families, not to mention billions of dollars. Research studies to identify factors that increase or decrease the risk of developing AD are a first step toward making primary prevention a reality. For example, lifestyle choices related to diet and exercise that reduce the risk of diabetes, hypertension, stroke, and obesity could also reduce the risk of AD.

The Alzheimer's Association has developed a ten-step program for consumers called Maintain Your Brain, which encourages people to exercise, eat a "brain-healthy" diet, stay socially engaged, and make other wise choices to protect their aging brains. More information on Maintain Your Brain is available at http://search.alz.org/maintainyourbrain/overview.asp.

In May 2005 The National Institute on Aging released a 28-page booklet explaining in clear layperson's language what people can do to reduce their risk of AD. Called Genes, Lifestyles, and Crossword Puzzles: Can Alzheimer's Disease Be Prevented?, the booklet is available online at http://www.nia.nih.gov.

Preliminary research evidence suggests that certain foods and dietary supplements may also be protective against AD. These include green tea, aged garlic, vitamins C and E, and melatonin. Investigation continues on these and other nutritional approaches to preventing AD.

Occupational studies implicating metals, pesticides, and electromagnetic fields point to the need to reduce or eliminate worker exposure to these agents. Protecting children from early exposure to lead and other metals could also reduce the number of AD cases in the future.

CLINICAL DIAGNOSIS

Alzheimer's disease remains a diagnosis of exclusion, ruling out other conditions that may cause similar symptoms, such as stroke, hypothyroidism, depression, nutritional deficiency, brain tumor, Parkinson's disease, or inappropriate medication. Conclusive diagnosis of AD is still only possible at autopsy. However, according to the National Institute on Aging (2006), "in specialized research facilities, clinicians can now diagnose AD with up to 90 percent accuracy." Tremendous progress has been made using more accurate diagnostic tests and techniques, ranging from neuropsychological testing to state-of-the-art imaging techniques such as positive emission tomography (PET) scans and magnetic resonance imaging (MRI).

Mini-Mental Status Examination

The Mini-Mental Status Examination (see below) is a quick evaluation tool used to assess people with cognitive impairment or memory loss. It measures an individual's reality orientation, registration abilities, attention and calculation skills, recall, language, and visuoconstruction (seeing and copying designs) abilities.

The highest possible score is 30 points. Those who score less than 24 need further evaluation for possible AD or other dementia, depression, delirium, or schizophrenia. Those who score 20 or less generally have one of these disorders.

THE MINI-MENTAL STATUS EXAM
Indications Cognitive Function Assessment Documentation of subsequent cognitive function decline
Questions (Total of 30 points)
Category	Points	Questions
1. Orientation	10	Year, season, date, day of week, and month State, county, town, or city Hospital or clinic, floor
2. Registration	3	Name three objects: apple, table, penny Speak each one distinctly and with a brief pause Patient repeats all three (one point for each) Repeat process until all three objects learned Record number of trials needed to learn all three
3. Attention and Calculation	5	Spell WORLD backwards: DLROW Points given up to first misplaced letter Example: DLORW scored as 2 points only
4. Recall	3	Recite the three objects memorized in number 2 (Registration)
5. Language	9	Patient names two objects when they are displayed Example: pencil and watch (1 point each) Repeat a sentence: “No ifs, ands, or buts” Follow three-stage command: Take a paper in your right hand Fold it in half Put it on the floor Read and obey the following: Close your eyes Write a sentence Copy the design (picture of two overlapped pentagons

According to a National Institute on Aging report (NIA, 2006), "Tests that measure delayed recall, verbal fluency, and overall cognitive status are highly accurate in distinguishing between cognitively healthy individuals and people with mild AD." In a large prospective Canadian study of initially nondemented patients, neuropsychological tests accurately predicted conversion to Alzheimer's disease after 5 and 10 years (Tierney et al., 2005).

Laboratory Findings

Ruling out other physical and psychological disorders that can mimic the symptoms of AD involves a number of laboratory tests including a complete blood count (CBC) to rule out anemia. Blood glucose testing is done because AD disturbs glucose metabolism. Thyroid function tests are performed to rule out hypothyroidism. Electrolyte and vitamin B₁₂ levels should also be measured and hepatic and renal function should be assessed (Kawas, 2003).

Screening of individuals for the APOE e4 gene version is now generally held to be ineffective. A lumbar puncture may be done to measure soluble amyloid beta protein precursor (sBPP) in cerebrospinal fluid, which is decreased in those with AD. Normal sBPP levels are >450 U/L (Pagana & Pagana, 2005).

Imaging Studies

Improved imaging techniques have enabled researchers to see the effects of AD on brain structure and function. Magnetic resonance imaging (MRI) studies have shown that AD causes some brain structures, particularly the hippocampus, to shrink during the early stage of the disease (Thompson et al., 2003; Goesch et al., 2002).

Positron emission tomography (PET) and single photon emission tomography (SPECT) scanning allow scientists to visualize brain activity during cognitive operations such as memorizing, recalling, speaking, reading, and learning. These techniques can help identify persons at risk for developing AD even before symptoms appear. Although there is yet no prevention or cure for AD, early screening and diagnosis enable the patient and family to plan for future care and options while the patient can still participate in decisions.

A PET scan of a normal brain. Courtesy of Alzheimer's Disease Education and Referral Center.

A PET scan of a person with advanced AD. Note the decreased brain activity (indicated by loss of orange, yellow, and green colors). Courtesy of Alzheimer's Disease Education and Referral Center.

People with mild cognitive impairment (MCI) are an increased focus of research, including studies at the University of South Florida's new Alzheimer's Disease Center, one of two centers funded by the National Institute on Aging (NIA). Mild cognitive impairment is a transitional state between the normal cognitive changes of aging and the development of AD or other dementia. Two subtypes of MCI have been established: amnestic MCI, characterized by memory problems, and nonamnestic MCI, which affects cognitive functions other than memory, such as language, attention, critical thinking, reading, and writing. Experts estimate that MCI may affect more than 20 percent of the population over age 65. People diagnosed with MCI are at increased risk of developing AD or other dementia. Based on early research, the rate of progression from amnestic MCI to AD is estimated to be between 6 and 25 percent per year (Petersen et al., 2001).

In 2001 the American Academy of Neurology (AAN) established the following criteria for an MCI diagnosis:

• An individual's self-report of memory problems, preferably confirmed by another person
• Measurable, greater-than-normal memory impairment detected with standard memory assessment tests
• Normal general thinking and reasoning skills
• Ability to perform normal daily activities (Alzheimer's Association, 2005)

Researchers in the Alzheimer's Disease Cooperative Study compared participants with amnestic MCI to persons with AD and determined that those with amnestic MCI had impaired memory but other cognitive functions were not impaired. Cognitive and functional test scores of the people with amnestic MCI fell between the scores of healthy people and those with AD (Grundmann et al., 2004).

Ongoing research on MCI suggests that earlier treatment with drugs approved for AD may slow its progression to AD. A three-year, placebo-controlled clinical trial of more than 750 patients with amnestic MCI showed that donepezil (Aricept) reduced the risk of developing AD during the first year (Petersen et al., 2005). However, by the end of the three-year study, the risk was the same as those in the placebo group. Nevertheless, delaying the progression to AD by a year represents a significant reprieve for both patients and caregivers in terms of maintaining function and quality of life as well as reducing healthcare costs.

Functional Assessment

Caring for someone with AD should include periodic assessment of the person's ability to function as the disease progresses. Researchers at Duke University developed the Functional Dementia Scale shown below to help caregivers monitor functional abilities and plan appropriate interventions.

FUNCTIONAL DEMENTIA SCALE
Circle one rating for each item 1 = None or little of the time 2 = Some of the time 3 = Good part of the time 4 = Most or all of the time		Patient: Observer: Position or relation to patient: Facility: Date:
Question	Rating	Task
1.	1 2 3 4	Has difficulty completing simple tasks on own, eg, dressing, bathing, doing arithmetic.
2.	1 2 3 4	Spends time either sitting or in apparently purposeless activity
3.	1 2 3 4	Wanders at night or needs to be restrained to prevent wandering
4.	1 2 3 4	Hears things that are not there
5.	1 2 3 4	Requires supervision or assistance in eating
6.	1 2 3 4	Loses things
7.	1 2 3 4	Appearance is disorderly if let to own devices
8.	1 2 3 4	Moans
9.	1 2 3 4	Cannot control bowel function
10.	1 2 3 4	Threatens to harm others
11.	1 2 3 4	Cannot control bladder function
12.	1 2 3 4	Needs to be watched so doesn't injure self, eg, careless smoking, leaving the stove on, falling
13.	1 2 3 4	Destructive of materials around self, eg, breaks furniture, throws food trays, tears up magazines
14.	1 2 3 4	Shouts or yells
15.	1 2 3 4	Accuses others of doing self bodily harm or stealing possessions -(when you are sure the accusations are not true)
16.	1 2 3 4	Is unaware of limitations imposed by illness
17.	1 2 3 4	Becomes confused and is not oriented to place
18.	1 2 3 4	Has trouble remembering
19.	1 2 3 4	Has sudden changes of mood, eg, gets upset, angry, or cries easily
20.	1 2 3 4	If left alone, wanders aimlessly during the day or needs to be restrained to prevent wandering
Source: Moore JT, et al. (1983). A functional dementia scale. Journal of Family Practice 16:498.

STAGES OF ALZHEIMER'S DISEASE

Although AD is most commonly diagnosed after age 65, the brain changes characteristic of the disease may begin 10 to 20 years before symptoms appear. Buildup of beta amyloid plaques, development of neurofibrillary tangles, and consequent death of neurons ultimately shrink the hippocampus, the critical structure in memory.

The symptoms of AD are usually described in three stages: early-stage (mild), mid-stage (moderate), and late-stage (severe). The object of treatment is to slow progression of the disease and maintain maximum physical and mental function as long as possible.

Early Stage

Early-stage (mild) AD first affects memory, language, and reasoning. This stage is typically marked by one or more of the following symptoms:

• Memory loss
• Confusion about location of familiar places (getting lost begins to occur)
• Taking longer to accomplish normal daily tasks
• Trouble handling money and paying bills
• Making bad decisions due to impaired judgment
• Loss of spontaneity and sense of initiative
• Mood and personality changes, increased anxiety

Medial view of the brain with early damage to the hippocampus and portions of the frontal lobe in blue. Courtesy of Alzheimer's Disease Education and Referral Center.

Clinical diagnosis of AD is usually made during the early stage, when the person appears to be physically healthy but is having increasing difficulty making sense of the environment. The affected person and the family may mistake early signs of AD for normal age-related changes. Deciding to seek diagnostic testing can be a major hurdle for the person and the family.

Mid-Stage

Mid-stage (moderate) AD involves areas of the cerebral cortex that control language, reasoning, sensory processing, and conscious thought. These regions continue to atrophy, resulting in more pronounced and widespread symptoms.

Behavior problems, such as wandering and agitation, require more intensive supervision and care. Symptoms of this stage usually include:

• Increasing memory loss and confusion
• Shortened attention span
• Problems recognizing friends and family members
• Difficulty with language; problems with reading, writing, numbers
• Difficulty organizing thoughts and thinking logically
• Inability to learn new things or to cope with new or unexpected situations
• Restlessness, agitation, anxiety, tearfulness, wandering, especially in the late afternoon or at night
• Loss of ability to tell time; late-day time disorientation and confusion, called "sundowning"
• Repetitive statements or movement, occasional muscle twitches
• Hallucinations, delusions, suspiciousness or paranoia, irritability
• Loss of impulse control (sloppy table manners, undressing at inappropriate times or places, vulgar language)
• Perceptual-motor problems (trouble getting out of a chair or setting the table)

Medial view of the brain with mild-to-moderate AD in blue. Note the spread of damage forward into the frontal lobe and backward into the temporal lobe. Courtesy of Alzheimer's Disease Education and Referral Center.

Late Stage

Late-stage (severe) AD involves widespread plaques and tangles throughout the brain and further atrophy in the hippocampus and other areas of the cortex. Patients cannot recognize family and loved ones or communicate in any way. Completely dependent on others for care, they seem to have lost all sense of self. Other symptoms can include:

• Weight loss
• Seizures, skin infections, difficulty swallowing
• Groaning, moaning, or grunting
• Increased sleeping
• Lack of bladder and bowel control

Medial view of the brain with severe AD indicated in blue. Note the increased damage in the hippocampus (dark blue) and the spread of the disease throughout the frontal, temporal, occipital, and parietal lobes. Courtesy of Alzheimer's Disease Education and Referral Center.

At the end of life, patients are partly or completely bedfast. Death comes most often in the form of aspiration pneumonia. Unable to swallow properly, the patient breathes food or liquids into the lungs.

MEDICAL AND PHARMACOLOGIC MANAGEMENT

Care and treatment of the person with AD will change over time as the disease progresses. Care planning should begin at the time of diagnosis and should involve the patient and the family. The plan includes:

• Cholinesterase inhibitor therapy to temporarily improve cognition or slow the rate of cognitive decline
• Management of co-morbid conditions, especially sensory deficits
• Treatment of behavioral symptoms and mood disorders
• Support and resources for patient and caregiver
• Discussion of advance directives (see Ethical Considerations below)
• Compliance with state-mandated reporting requirements for driving impairment and elder abuse (see Ethical Considerations below) (Cummings et al., 2002)

Until it becomes necessary to institutionalize the patient, the primary caregiver will most likely be the spouse (usually the wife) or a child (usually a daughter). That caregiver and other family members involved need education and support to help manage the care as the patient's symptoms and needs change.

Drug Treatment

Four drugs have been approved by the Food and Drug Administration (FDA) for treatment of mild-to-moderate AD symptoms. The current drugs of choice are donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadine). These newer drugs have replaced tacrine (Cognex), the first drug approved by FDA for AD, which can cause liver damage. All of these drugs interfere with the action of acetylcholinesterase, an enzyme that normally breaks down the neurotransmitter acetylcholine.

CHOLINESTERASE INHIBITORS FOR TREATMENT OF COGNITIVE DEFICITS IN AD
Drug	Suggested dosage	Side effects	Specific cautions
Donepezil (Aricept)	Initial dosage: 5 mg QD; if necessary, dosage can be increased to 10 mg QD after 4 to 6 weeks	Mild side effects including nausea, vomiting, and diarrhea; side effects can be reduced by taking the medication with food. Initial increase of agitation in some patients, which typically subsides after a few weeks	Conflicting evidence about possible interactions with cimetidine (Tagamet), theophylline, warfarin (Coumadin), and digoxin (Lanoxin)
Rivastigmine (Exelon)	Initial dosage: 1.5 mg BID is generally well tolerated; can be increased as tolerated but not more quickly than by 1.5 mg BID every 4 weeks to maximum of 6 mg BID. BID dosing is as efficacious as TID dosing and has comparable tolerability.	Nausea, vomiting and diarrhea, headaches, dizziness, abdominal pain, fatigue, malaise, anxiety and agitation; effects can be reduced by taking the medication with food	Weight loss Interacting drugs include aminoglycosides and procainamide (Procanbid)
Galantamine (Razadine)	Initial dosage: 4 mg BID taken with morning and evening meals for 4 weeks; dosage is then increased to 8 mg BID for at least 4 weeks. An increase to 12 mg BID should be considered on an individual basis.	Mild side effects including nausea, vomiting and diarrhea; side effects can be reduced by taking the medication with food. No apparent association with sleep disturbances, which can occur with other cholinergic medications.	Contraindicated in patients with hepatic or renal impairment
Tacrine (Cognex)	Initial dosage: 10 mg 4 times per day for 4 weeks; dosage is increased to 20 mg 4 times per day for 4 weeks, then to 30 mg 4 times per day for 4 weeks, etc., until maximum tolerated dosage is achieved. Maximum dosage is 40 mg 4 times per day	High incidence of side effects including gastrointestinal problems, which can be reduced by taking the medication with food.	Hepatotoxicity is a problem and liver tests should be performed every other week for 16 weeks and every 3 months thereafter. Interacting drugs include theophylline and procainamide
Source: Cummings et al., 2002.

These drugs may slow the progression of AD for a few months or even a few years, but they are not a cure. They may help some patients with activities of daily living (ADL) and with behavioral symptoms such as delusions and agitation, and may even improve memory and speaking skills. However, physicians need to be realistic in explaining to the patient and the family the limitations of drug therapy.

Some of the side effects of Alzheimer's drugs, such as nausea, vomiting, and diarrhea, may resolve within a few weeks. If they do not resolve, or if no significant improvement is seen with 6 to 12 months of drug therapy, the medication should be discontinued. Each patient responds differently to drug therapy. Thus, if one anti-cholinesterase drug fails to elicit a response, another may.

In moderate-to-severe AD, physicians commonly prescribe a drug called memantine (Namenda). Approved by FDA in 2003, memantine is an N-methyl-D-aspartate (NMDA) antagonist, which reduces overstimulation of the NMDA receptor by glutamate. Trials of memantine in patients taking one of the anticholinesterase drugs showed modest improvements in cognitive function, ability to perform activities of daily living, and reduced frequency of new behavioral symptoms (Tariot et al., 2004).

A number of older drugs have shown some promise in slowing the progression of AD. One study showed that daily intake of 2,000 IU of vitamin E or 10 mg of selegiline (Eldepryl) slowed the progression of symptoms in patients with AD. Based on this study, some physicians now recommend high-dose vitamin E supplements (2000 IU daily) as part of the standard treatment regimen for AD. Some studies suggest that Vitamin C may also help delay the progression to AD.

At one time, hormone replacement therapy (HRT) in women was believed to delay the onset of AD. However, the Women's Health Initiative Study showed that HRT actually increased the risk of dementia among postmenopausal women (Shumaker et al., 2003). Thus HRT is not recommended for treatment or prevention of AD. Ginkgo biloba is widely touted by manufacturers in the popular media as improving memory; however, research to date does not support that claim.

Scientists continue to search for new and better treatments for AD. A small study in Australia showed that patients given a metal-binding compound called iodochlorhydroxyquin (Clioquinol) showed significant improvement in cognitive function among the most severely affected patients. The drug prevents zinc and copper ions from binding to beta amyloid, reducing the buildup of plaques (Ritchie et al., 2003). Clinical trials also are underway on vitamins B₆ and B₁₂, anti-inflammatory drugs such as Celebrex, and the cholesterol-lowering drugs known as statins. In addition, three large biotechnology companies have launched large trials on new drugs for AD (Elias, 2006).

Patients who are not helped by currently available drugs may want to consider clinical trials. More information is available on the website of National Institute on Aging's Alzheimer's Disease Education and Referral (ADEAR) Center. You can reach its Clinical Trials Database at http://www.nia.nih.gov/Alzheimers/ResearchInformation/ClinicalTrials.

Co-Existing Health Problems

People with AD often have other health problems common to older adults, such as impaired hearing and vision, dental problems, hypertension, congestive heart failure, diabetes, hypothyroidism, genitourinary conditions, and arthritis. Any of these conditions, alone or in combination, can further diminish the patient's ability to function in the world.

For example, people who do not see or hear well may be easily confused in unfamiliar situations. Couple those limitations with AD, and the confusion intensifies. Recognition and treatment of any and all co-existing conditions can help improve the patient's ability to function and quality of life.

Many older adults suffer from depression, and patients with AD are no exception. Unless treated, depression can further impair function. Antidepressants with limited anticholinergic side effects such as citalopram (Celexa) and sertraline (Zoloft) have been shown to be effective in treating depression in patients with dementia (Lyketsos et al., 2003). Effective treatment of the patient's depression has a secondary benefit of reducing caregiver stress.

Patients with AD and depression may benefit from regular exercise. Researchers compared the effects of an exercise-behavior intervention with routine care in 153 patients with AD between the ages of 55 and 93 years who were living at home. Over a three-month period, one group of patients and their caregivers attended 12 one-hour sessions. The other group received routine care. In the intervention group, caregivers learned behavior management techniques, including identification of activities that patients enjoyed.

The goal of the intervention was for patients to engage in moderate-intensity exercise for a minimum of 30 minutes daily. After three months, patients in the intervention group had reduced rates of depression and improved physical health and function. Those in the routine care group declined on both function and depression. A 24-month followup found that significant functional improvement persisted in the treatment group, while behavioral problems in the routine-care group had led to increased institutionalization (Teri et al., 2003).

NURSING MANAGEMENT

We do not know to what degree the patient is able to understand at any stage of this illness, but who is to say that the inability to communicate represents the real person who may still be struggling inside (Wolanin-Phillips, 1981). Care of the patient with AD demands ongoing assessment, planning, intervention, and evaluation throughout the course of the disease.

Fundamental to all care is the creation of a supportive environment (Box 1). Whether at home or in an institution, the goals are the same: to maximize the person's functional abilities and quality of life and to provide competent, compassionate care that acknowledges and respects the patient and family. Ideally, that care would be multidisciplinary, including medicine, nursing, and social work. Nurses contribute a wealth of expertise in Alzheimer's care as caregivers, counselors, and case managers.

Case managers are particularly important for patients with AD who live alone or with a spouse who is unable to act as caregiver. These patients are at high risk for injury or self-neglect. The case manager can serve as an advocate and primary support person, accompanying the patient to medical appointments and coordinating community services. If a person has advanced AD, the case manager can apply for a court-appointed conservator to establish guardianship and surrogate decision-making authority.

The challenges of caring for someone with AD include communicating effectively with the person; managing behavior problems such as agitation, wandering, and sleep disturbance; assisting with ADLs while helping maintain the person's independence; and planning activities that will help maintain well-being and prevent boredom. Meeting these challenges may become more difficult as the disease progresses.

COMMUNICATION ISSUES

Give us time to speak, wait for us to search around that untidy heap on the floor of the brain for the word we want to use. Try not to finish our sentences. Just listen, and don't let us feel embarrassed if we lose the thread of what we say. Christine Bryden, Diagnosed with Alzheimer's at age 46

Communicating with the person who has AD begins with patience, respect, and understanding. Remember that the patient is not deliberately being difficult. Face the patient, make eye contact, and speak directly in a calm, even tone. If patients have hearing problems, be sure they are wearing a hearing aid. Keep sentences simple; focus on one idea at a time.

Minimize questions because they may make the patient feel anxious or threatened. If the patient doesn't understand, offer nonverbal cues, such as pointing, demonstrating the desired action (eating, drinking), or nodding. Even though patients may be unable to speak, they may still understand—so do not talk about the patient to others in the patient's presence.

Nonverbal communication, especially touch, between caregiver and patient is also important. Patients who may be unable to respond verbally will respond to a smile, kind gesture, and caring touch. Some patients may need reminders during a meal to begin or continue eating, for example, by placing the spoon in the patient's hand.

Careful observation of the patient's facial expressions, eye contact or lack of eye contact, and body language can help the caregiver assess comfort or pain, anger, hostility, and misunderstanding. For example, increased motor activity and shaking fists suggest frustration or anger. Experience and patience over time helps caregivers gain skill interpreting these nonverbal signals.

Patients with AD may ask the same question repeatedly because they do not remember the answer given. Respond to the question, then try to distract the patient with an activity or a change of topic or a change of scene. Activities or events should not be discussed with the patient until they are about to happen; otherwise, the patient may retain the idea that something is going to happen but forget the details, triggering more questions.

BEHAVIOR MANAGEMENT

At one time, the recommendation was to bring patients back to reality by correcting their misconceptions. Now the rule is the opposite. As one staff member put it: If you can't bring them back to a better reality than they are experiencing in their heads, let them be. Pipher, 1999

Behavioral symptoms of Alzheimer's disease include agitation, vocal outbursts, wandering, and sleep disturbance. Although medications are available to treat these disorders—antidepressants, antipsychotic drugs, and sedatives—all have side effects and may interact with other medications, and most show limited efficacy. In 2005 the U.S. Food and Drug Administration (FDA) issued a public health advisory because use of "atypical" antipsychotic drugs (eg, olanzapine, risperidone, quetiapine) in people with dementia were associated with a slightly increased risk of death (FDA, 2005).

A meta-analysis of 15 trials of atypical antipsychotics found other adverse events, including urinary tract infection, incontinence, worsened cognitive test scores, and an increased risk of cerebrovascular events including stroke, especially with risperidone (Schneider et al., 2006). In view of these findings, nondrug approaches should be attempted before resorting to medications.

Agitation

Agitation is always related to fear or lack of control (Wolanin-Phillips, 1981). Caregivers need education and training to respond effectively to the agitated patient without becoming agitated themselves.

Speaking softly and calmly, the caregiver can gently and quietly take control of the situation. Ask the patient if he or she needs to use the bathroom. If not, try to determine what the patient needs: an extra blanket, a drink of water, food, or a warm hug.

Another approach to the problem of agitation is the three Rs: repeat, reassure, and redirect (Sultzer & Cummings, 1993). Using this approach, the caregiver repeats an instruction or answer to a question, reassures the patient, and redirects the patient to a different activity to divert attention from the problem.

Aromatherapy is emerging as a potential treatment for agitation. Three recent placebo-controlled trials have reported significant benefits on agitation, with almost total compliance and no side effects. Two essential oils were used: lemon balm (Melissa officinalis) or lavender oil (Lavendula officinalis), administered either by inhalation or skin application (Ballard et al., 2002; Holmes et al., 2002; Smallwood et al., 2001). Because no extended period of massage was used, it appears that the oils had a direct chemical effect. Many essential oils have shown cholinergic activity.

Vocal Outbursts

Disruptive vocal outbursts—screaming, swearing, crying, shouting, negative comments to staff and/or other patients, self-talk—become increasingly common as AD progresses. Men generally display more aggressive vocalizations, such as swearing, while women typically exhibit more agitated vocalizations, such as crying or complaining. Until these behaviors diminish in the final stages of the disease, they present an ongoing challenge to caregivers.

Managing vocal outbursts effectively demands special intervention training and education for staff. Inadequate behavior management training for staff can result in overmedication of the patient, inappropriate use of restraints, physically combative behavior, or isolation of the patient. The staff may suffer stress and burnout, leading to high turnover. Learning to manage these disruptive outbursts successfully respects the patient's human dignity and builds confidence, improved morale, and job satisfaction in the staff.

Staff need to remember that the patient is not deliberately misbehaving; these are not temper tantrums. Staff should not take remarks or attacks personally, nor should they try to reason with the patient. Instead of focusing on the problem, staff need to acknowledge that the dementia is causing the problems.

Behavior problems such as vocal outbursts and wandering are major reasons why family caregivers decide to seek long-term care for their loved one. Staff can gain valuable insights from the family into the patient's behavioral history, which will aid in planning effective interventions. Together with psychological and medical evaluations, this behavioral history can alert staff to important triggers for behavioral problems.

Experienced staff often can anticipate outbursts and intervene to prevent them. Signs of an impending outburst vary from person to person, but these events are often preceded by restlessness, refusals, and blushing. Emotional triggers can include fear, anger, depression, grief, confusion, helplessness, loneliness, sadness, impatience, and frustration. Environmental factors such as poor lighting, seasonal changes, over-stimulation or lack of stimulation, loud noises, or excessive heat, can also trigger outbursts.

Outbursts may also signal physical illness or discomfort, including pain, hunger, thirst, incontinence, constipation, infection, or fatigue. Once the outburst has subsided, a thorough physical assessment may reveal the underlying physical problem, which can then be remedied.

Managing outbursts triggered by environmental or physical factors is simpler than dealing with outbursts that stem from an unknown emotional or psychological cause. With training and experience, however, staff can better manage and even prevent vocal outbursts. Interventions begin with distracting and diverting the patient, taking him or her to a quiet room, or taking a walk. This disconnects the patient from the problem and makes possible other interventions such as:

• Prompting the patient to reminisce.
• Engaging the patient in group activities such as games, singing, or listening to music.
• Touching the patient, hugging or holding hands.
• Giving the patient something to hold, a soft doll or a stuffed animal.
• Showing movies or interactive videos such as sing-alongs.
• Using headphones to listen to soothing sounds such as mountain brooks or the ocean.
• Playing audiotapes of the spouse or other family members recalling happy times together.

The techniques listed above are most effective as prevention measures. Once an outburst occurs, distraction is necessary to disconnect the patient from the problem. Otherwise, there is a risk of reinforcing inappropriate behaviors, which may result in more frequent outbursts.

Wandering

Wandering is a major behavior problem in patients with AD, more so than in patients with other types of dementias. For that reason, all persons diagnosed with AD should be registered in the Alzheimer's Association nationwide Safe Return Program (Alzheimer's Association, 2006). Registration includes an identification bracelet that should be worn at all times.

Agitation, restlessness, and sleep disturbances all lead to wandering, particularly at night, increasing the risk of injury to the patient and others. Wandering is generally one of two types: goal-directed, in which the patient attempts to reach an impossible goal such as going home or going to the store, and non-goal-directed, in which the patient wanders aimlessly. Wandering patterns include:

• Moving to a specific location
• Lapping or circling alone a path or track
• Pacing back and forth
• Wandering at random

Confusion and failing memory can lead to wandering because the patient is unable to keep a clear destination in mind. Wandering may also represent a search for social interaction when the patient can no longer communicate verbally. Unable to sleep, the patient walks to keep busy, or to find a loved one. Wandering in the late afternoon or early evening may be triggered by a fading memory of leaving work to go home.

Wandering may also be caused by a physical need, such as toileting. Staff can use large-print signs to mark destinations with a drawing of the activity. Placing a photo of the patient as a younger adult on the room door may help a wanderer find "home."

Wanderers are more likely to have delusions, hallucinations, and severe depressions. Long-term use of neuroleptics, such as haloperidol (Haldol), chlorpromazine (Thorazine), or thioridazine (Mellaril) can induce aimless wandering. Men are more likely to wander than women are, and wandering often increases as AD progresses.

The family can help staff identify and anticipate wandering in the newly admitted resident. Staff needs to learn as much as possible about the resident's lifestyle prior to diagnosis with AD, what kind of work the person did, previous patterns of exercise, stress, and response to touch. Once a wanderer is identified, the facility can have photographs made and distributed to other units, and assign special clothing or identification bands.

To prevent wandering outside the facility, staff can conceal or camouflage doors by:

• Placing a Velcro cloth strip or panel across doors
• Painting doorknobs the same color as doors
• Installing grid patterns on floors in front of doors

Safety locks, alarm systems, and personal monitoring devices can also help control persistent wanderers. Staff should use the least-restrictive methods possible to reduce, redirect, or prevent wandering. Interventions for goal-directed wandering involve distracting the person. A calm, gentle, and respectful approach helps to establish trust.

Approach the person from the front and use simple commands to change direction if necessary and guide the wanderer away from the exit. Diversions such as listening to music, looking at pictures, or exercising may be effective. Staff should avoid negative or harsh commands such as "Don't go out there!" and should not argue with the person.

Wandering in a safe area can be good exercise for the person with AD and helps manage non-goal-directed wandering. Many facilities are designed with these safe areas in the form of sheltered courts, gardens, lounges, or pathways.

Education and training for staff can help them identify and anticipate problem behaviors and learn diversionary strategies to manage these behaviors. Gaining competence builds confidence in staff and enhances the quality of life for residents with AD.

Sleep Disturbance

Patients with AD often have disturbed sleep patterns due to medications, sleep apnea, and disruption in their biorhythms. New research shows that exposing patients to a few hours of bright light each day, both morning and evening, helps them sleep longer at night and maintain a more normal sleeping schedule. Light therapy can include natural light outdoors or in a sunny room, or artificial light that is brighter than ordinary indoor light.

Exercise and physical activity, such as walking during the day, also helps patients sleep better at night. The activities should be as vigorous as possible within the limitations of the client. Those who are bedfast can still benefit from passive exercise.

Daytime napping can interfere with sleep at night. Napping may signal boredom or depression and the need for more stimulating daytime activity. Limiting fluid intake during the evening will reduce the need to urinate at night.

ACTIVITIES OF DAILY LIVING

Although senile dementia, like the dying process, may be irreversible and progressive, the living involved during the process can still be hopeful, filled with good feelings and moments of satisfaction. Wolanin-Phillips, 1981

Habit memory outlives all other types of memory in AD because it is stored in an area of the brain unaffected until the late stage. One woman recalled her mother's deterioration from AD: "She finally quit smoking because she forgot to smoke, but she would pat her breast pocket (where she carried her cigarettes) and then go through the motions of smoking, holding up two fingers, putting them to her mouth, inhaling, and then blowing out, but without any cigarette." Habit memory enables patients in the early and mid-stages of AD to remain physically able to manage ADL, but they may need reminders about hygiene and grooming.

Establishing and maintaining a routine in ADL helps the patient retain learned habits longer, and therefore the patient needs less assistance. Once the routine becomes automatic, the patient no longer needs to stop and think what to do next. A fixed routine for eating and toileting also reduces the incidence of incontinence.

Bathing can be a challenge because patients with AD may be frightened by showers. If it is not possible to offer a bath instead, using a shower bench with a hand-held shower may be less threatening. The bathroom should be prepared in advance, with water at the correct temperature.

Dressing can be simplified by offering one or two choices, or just laying out the garments to be worn. If the patient wants to wear the same clothes every day, make duplicates available so that favorite clothes can be laundered. Many older patients, with or without AD, feel embarrassed when completely undressed, so removing and replacing one article of clothing at a time may work better.

As the disease progresses, however, patients forget about hygiene and grooming and may even forget to eat. Sleep patterns are disrupted; day and night are confused. Caregivers need to monitor nutrition and fluid intake as well as elimination because the patient no longer responds to thirst, hunger, and signals to defecate. Incontinence increases as health deteriorates. In moderate and late-stage AD, the patient needs someone to plan and provide personal care.

Eating habits and behaviors change during the course of AD, and may be caused by physiologic or psychological factors. In early-stage AD, depression related to the diagnosis may result in anorexia and weight loss. Patients may forget to eat or refuse to eat. Confusion and agitation may lead to extreme eating behaviors such as gorging.

Physiologic factors affecting eating behaviors may include dental problems such as uncomfortable dentures, missing teeth, and/or periodontal (gum) disease. Neurofibrillary tangles and plaques can affect the function of the hypothalamus, which regulates appetite and hunger signals. Many persons with AD lose their sense of smell, which affects taste and appetite. Some medications can also affect appetite.

In addition to depression, other psychological factors that affect eating behaviors include new and unfamiliar environments, which create confusion and agitation, distractions such as loud noises, unappealing food, and unusual odors such as urine.

Weight loss is common among patients with AD, regardless of quality of care. Wandering, restlessness, and agitation expend energy and interfere with food intake. In mid- and late-stage AD, patients are unable to feed themselves or to chew and swallow the food when placed in their mouths. Patients who are unable to swallow properly can be come dehydrated and can aspirate food, leading to aspiration pneumonia.

It is essential to maintain the nutritional well-being of the patient with AD (Box 2). Monitoring the patient's nutritional status for weight loss and possible nutritional deficiencies should include:

• Oral assessment to check for denture problems, missing teeth, and gum problems, with referral for any treatment needed.
• Review of medications to check for drugs such as Digoxin that may affect appetite
• Vision problems that could cause confusion at mealtime
• Assessment for depression

PHYSICAL AND SOCIAL ACTIVITIES

As horizons of experience narrow, small pleasures in life become more and more important. In dementia care, those pleasures and gratifications that are small loom large. Stephen G. Post, 2000

Physical activity plus social and cognitive stimulation help maintain general well-being and prevent boredom and agitation in people with AD—especially in the early stage of the disease. Walking in safe areas also helps people sleep better at night. Someone who enjoyed dancing may still find pleasure in that activity.

Those living at home can help with household tasks appropriate to their abilities and interests. For example, a woman who is no longer able to cook a meal may be able to peel the potatoes, shell the peas, or set the table. Gardening or other hobbies, arts and crafts, or pets can all be enjoyable sources of stimulation.

Activities should be tailored to the individual's personality. Shy, introverted people should not be required to participate in group activities, whereas more outgoing individuals may be happiest in a group. Those who enjoy music, either as listeners or performers, can find pleasure in listening to the radio or to recorded music. Group sing-a-longs may awaken pleasant memories of familiar songs.

People with AD who formerly liked to read may still like to leaf through magazines or books, especially those with interesting pictures. Television can be entertaining for some; for others, it can be frustrating and upsetting when they are no longer able to understand the story.

Simple games can provide enjoyment for people with AD. One Japanese study found that the cognitive and daily performance abilities of patients with Alzheimer's disease regress to the level of a child between 4 and 5 years old (Shoji et al., 2002). Although the person with AD should not be treated as a child, keeping this developmental level in mind when planning recreational activities can be helpful.

A limited activities budget does not have to limit creativity when planning entertaining and stimulating activities for people with AD. (See Activities on a Shoestring: http://www.angelfire.com/in/shoestring2.)

FAMILY AND CAREGIVER STRESS MANAGEMENT

Alzheimer's disease exacts a heavy toll on the emotional, physical, and financial resources of the family, especially the primary caregiver, usually a spouse or a daughter. Even though the family member willingly assumes the role of caregiver, the physical and emotional energy required can exhaust the most devoted individual. Multiple losses—loss of the companion and the relationship, even though the person with AD is still physically alive, and loss of plans for the future together—evoke grief and sadness. As one author wrote:

...it's like being dropped into the Everglades on a cloudy night without flashlight or compass. The darkness smothers and the imagination breeds terror. You know you must keep moving but have no idea which direction is least dangerous. (Wheeler, 2002)

The time commitment required to care for a person with AD is daunting. An Alzheimer's Association survey showed that caregivers who live with a relative with AD spend about one hundred hours weekly providing care. Caregivers who are employed outside the home devote an average of 40 hours weekly to providing care—equivalent to a second full-time job. Half of all caregivers reported not having enough time for themselves. The caregiver is always on call; theirs is a 36-hour day (Mace & Rabins, 2001).

As AD progresses, the physical energy required to care for the increasingly dependent patient may deplete the caregiver's capacity. By mid-stage AD, the patient needs help with bathing, dressing, and a host of other activities. According to the Alzheimer's Association, 45 percent of caregivers report not getting enough sleep.

Role changes and new responsibilities can also prove stressful. Spouses must accept responsibilities formerly shouldered by or shared with the patient. If an adult daughter or son is the caregiver, he or she joins the "sandwich generation," caught between the parent's needs and the demands of career and family at home.

The lives of the caregiver and the patient are inextricably linked in a long, painful dance toward death. When the caregiver's quality of life suffers, it affects the quality of care for the person with AD. Without help and support from family, friends, health professionals, and community resources, caregivers are at great risk for:

• Emotional distress, such as depression and anxiety
• Fatigue and sleep deprivation
• Social isolation, when relatives and friends stop calling or visiting
• Family conflict
• Substance abuse

Just as education and training for staff can improve care and quality of life for patients, educational interventions for family members can make a positive difference in the caregivers' ability to cope with their difficult task. Caregivers' guides also are available from many hospitals and government agencies including the National Institute on Aging: http://www.nia.nih.gov/Alzheimers/Publications/caregiverguide.htm.

Better understanding of the dementia and techniques to cope with it can reduce caregivers' burdens and the negative reactions to disruptive behaviors common to AD. Reducing the burdens of caregiving can delay the need for nursing home care.

ETHICAL CONSIDERATIONS

Alzheimer's disease raises a host of ethical issues that, ideally, the physician discusses with the patient and the family at the time of diagnosis. These issues include:

• Driving
• Advance directives
• CPR vs. DNR
• Nutrition and hydration
• Hospice care

That the patient or the family may suspect Alzheimer's disease does not lessen the impact of the diagnosis, so it is up to the physician or other healthcare professional to raise these issues and help prepare families to discuss them while the patient can still share in the process.

The patient who lives alone but has intact relationships with geographically distant family members may consent to have the diagnosis shared with those relatives. If the patient is alone or has no local family member, friend, or significant other, a case manager can fill that role and can apply for a court-appointed conservator to establish guardianship and surrogate decision-making authority (Snyder, 2001).

Driving

Safe driving requires mental alertness, quick reflexes, and good judgment, all of which are eroded by AD, often before the patient or the family is aware of the problem. One recent study found that persons mildly impaired with AD and their caregivers underestimated their difficulties with driving, both on a questionnaire and on a standardized road test judged by an independent evaluator (Wild & Cotrell, 2003). The drivers with AD also rated significantly worse than healthy elders on 9 out of 10 driving behaviors.

Families are usually the first to notice unsafe driving behaviors in the person with AD but often find it difficult to convince the person that he or she should stop driving. Helpful information is available from the following websites: http://www.theribbon.com/articles/brakes.asp? and http://www.thehartford.com/alzheimers/warning_signs_form.html.

Once the diagnosis of AD is established, the physician needs to encourage the patient to stop driving. Some patients do this willingly; others are reluctant to give up the independence that driving represents, thereby creating a significant threat to personal and public safety. Those who refuse to quit driving even though they pose a hazard must be prevented from driving by other means, either by hiding the car keys or disabling the car.

Although many states encourage physicians and other health professionals to report people with conditions that may affect their ability to drive safely, only California has a public policy specifically requiring the reporting of individuals who have Alzheimer's disease. In Florida, any physician, person, or agency knowing of a licensed driver's (or applicant's) mental or physical disability to drive is authorized to report this to the department of highway safety and motor vehicles.

PREVENTION OF ELDER ABUSE

Abuse of older adults is a well-kept secret in America. According to the National Administration on Aging, hundreds of thousands of elders are abused, neglected, and exploited by family members and others. Many cases go unreported. People with Alzheimer's disease or other cognitive impairment are at higher risk than other older adults. Most known perpetrators of abuse and neglect are family members, usually an adult child or a spouse.

The burden of caring for a person with AD can lead to stress, depression, feelings of isolation, financial worries, and substance abuse, any or all of which can contribute to elder abuse. Violent behavior by the patient may also lead to physical abuse by the caregiver.

Respite care for the patient and support group and counseling for the caregiver can help to prevent elder abuse. In severe cases of abuse, it is usually necessary to separate the patient from the caregiver, initiate legal action, and find a safe facility for the patient.

Signs of abuse include bruises, skin wounds, burns or fractures, and lack of explanation for falls and injuries. Physical signs of neglect include severe weight loss, dehydration, poor personal hygiene, and pressure ulcers (bedsores).

LEGAL CONSIDERATIONS

Getting legal affairs in order—drawing up advance directives, powers of attorney, wills, or trusts should be done as soon as possible after diagnosis, while the patient is able to express personal wishes and participate in decisions. Referral to the local chapter of the Alzheimer's Association can help families find attorneys who specialize in elder law or estate planning.

This referral should not be made abruptly but as a suggestion, emphasizing that every adult, regardless of health status, should make such a plan. This helps ensure that one's wishes are respected in end-of-life care and disposition of property after death. Otherwise, families will need to make difficult decisions without knowing the patient's wishes.

Advance Directives

An advance directive specifies a person's preferences for care in the event that he or she is unable to communicate those wishes—for example, in the advanced stages of AD. A living will is one type of advance directive. In an advance directive, the person can also name a representative to see that his or her wishes concerning care are carried out. This is sometimes called a durable power of attorney for healthcare.

Physicians should have copies of advance directives available or be able to refer families to a source for the appropriate forms. Federal law requires hospitals to inform patients that they have a right to complete an advance directive (the Patient Self-Determination Act), but advance directives are regulated by state law and may differ from state to state.

Family Caregiver Alliance (http://www.caregiver.org) can provide state-specific information and appropriate forms for advance directives. Advance directives are used by almost half (46.6%) of all Floridians with severe cognitive impairment, compared with 37.6 percent of their counterparts nationwide (Brown University, 2004).

CPR vs. DNR Orders

One type of advance directive is a do-not-resuscitate order (DNRO), which informs medical personnel that a patient does not want to have cardiopulmonary resuscitation (CPR) performed in the event of cardiac or respiratory arrest. These DNROs are also regulated by state law.

A DNRO order should be posted prominently, either on the head or foot of the bed, or, if the patient is at home, on the refrigerator, and also be included in the patient's chart. The DNRO should be readily available in the event of an emergency to ensure that the patient's wishes will be honored. Some patients prefer the additional safeguard of wearing a bracelet or necklace to alert care providers that a DNRO is in force.

Nutrition and Hydration

In the late stages of AD, patients may become unable to consume sufficient oral feedings to prevent weight loss. If the patient's advance directive indicates that he or she does not want artificial nutrition and hydration (ANH), caregivers must respect that decision. However, if the decision was not made earlier, this is the time when the patient's surrogate (also called a proxy) decision maker, together with the physician and other members of the health team, must decide together whether to initiate tube feedings.

Deciding whether to have ANH means weighing the potential benefit and the burden to the patient. The physician and care providers need to help families understand that forgoing ANH is not "killing" or "starving" the patient.

The Ethics Advisory Panel of the Alzheimer's Association (2000) recommends assisted oral feeding coupled with hospice care, when needed, as the compassionate alternative to tube feeding. This recommendation is based on several studies that point out tube feeding:

• Is associated with in creased diarrhea and related discomforts
• Results in increased use of physical restraints to prevent patients from pulling tubes out of their abdomens
• Does not usually improve nutritional status
• Does not lower the incidence of aspiration pneumonia or skin breakdown
• Does not improve longevity
• Denies the patient the gratification of tasting preferred foods

The Alzheimer's Association emphasizes that "assisted oral feeding should be available to all persons with advanced Alzheimer's as needed. Neglect in this area should not be tolerated, and concerted efforts are called for to educate and support professional and family caregivers in techniques of assisted oral feeding."

Eventually, the ability to swallow is lost, at which time the patient is considered terminal. This is a normal part of the final stage of AD, and research suggests that those patients who forgo ANH do not seem to feel thirsty or hungry. Without ANH, patients have less trouble with fluid in the lungs, which causes shortness of breath, or fluid in the throat, which means less need for suctioning.

Research also indicates that forgoing ANH actually increases the body's natural pain-relieving hormones, called endorphins, making the patient more comfortable and less likely to experience pain (Lynn & Harrold, 1999). The only side effect of dehydration at the end of life is dry mouth, which can be relieved by good mouth care, ice chips, or moistened sponge swabs.

Hospice Care

Hospice is a philosophy of care that emphasizes physical comfort, pain and symptom management, and death with dignity. It encompasses the spiritual and psychosocial aspects of care, both for the patient and the family, and includes bereavement support for the surviving family members.

During the terminal stages of AD , hospice care can be particularly beneficial to patients and families. Each year, more than half a million terminally ill people enter hospice programs for end-of-life care. Most of them are people with cancer. Unfortunately, few clients with AD receive hospice care, accounting for only about 7 percent of the annual hospice census.

Physicians and other health professionals need to educate families about the benefits of hospice care for their loved one with AD and for themselves. Ideally, this education would begin at the time of diagnosis, when the patient is still capable of expressing preferences about end-of-life care.

Hospice care involves a team of health professionals, including doctors, nurses, social workers, clergy, therapists, and trained volunteers. Hospice care is most often given in a patient's own home, but it can also be given in nursing homes or hospitals. A few communities may have separate facilities designated for hospice care.

To qualify for insurance reimbursement (including Medicare) for hospice services, a physician must certify that the patient has less than six months to live. Medicare covers the cost of hospice care in every state, as does most private long-term care insurance.

Posted April 3, 2006

Expires June 2, 2008

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