Alzheimer's and Dementia | Copyright © 2010 CEUFast.com

Course Contents

	Purpose/Goals    Objectives    Introduction    Pathophysiology    Types of Dementia    Risk Factors    Signs and Symptoms    Diagnosis    Evaluation of Dementia    Treatment    Behavior Analysis    Drug Treatment    Other treatments    Behavior Problems    Advanced Care Planning    Prevention    Complications of Dementia    Conclusion    References    Click any section in the index above to browse to the corresponding course section

Purpose/Goals

The purpose of this course is to provide an overview of dementia with a special emphasis on the management of the disease.

Objectives

After completing this course the learner will be able to:

Introduction

Dementia prevalence increases with aging and it currently affects 2.4 to 4.5 million people. The prevalence doubles every five years after the age of 65. It affects up to 50% of people over the age of 85. It is estimated that that the number of Americans with Alzheimer's could increase to 16 million by 2050 (Alzheimer's Foundation of America, 2009). On average, it costs almost 25,000 dollars to care for each patient with dementia annually (Anderson, 2009). Although dementia is more common as one ages, it is not synonymous with aging.

Dementia is not a single disease but a condition characterized by a permanent decrease in intellectual functioning. It is not only a decrease in memory but problems with language, judgment, problem solving, and comprehension. Many conditions lead to dementia, but the most common cause of dementia in the United States is Alzheimer's disease. Dementia has no cure and is progressive; it eventually leads to total dependence and death.

Pathophysiology

Dementia is caused by an alternation in the brain's structure including a decrease in the chemicals in the brain and a destruction of nerves vital to cognitive function. Amyloid, a starch like product, is deposited abnormally in the brain in Alzheimer's disease and is responsible for many of the signs and symptoms. Amyloid plaques develop in areas of the brain used for memory and other cognitive functions.

Acetylcholine, a chemical produced by the nerves in the brain, is associated with transmission of impulses between nerve cells and allows proper brain functioning. Dementia is associated with a decline in the amount of acetylcholine, which results in a decreased ability of the body to transmit impulses between brain cells.

Another characteristic change is neurofibrillary tangles. Neurofibrillary tangles are abnormal growth of nerves that kill the normal function of cells and results in malfunction of the brain. Neurofibrillary tangles lead to the death of nerve cells and synaptic failure. Neurofibrillary tangles, amyloid plaques, chemical imbalance, inflammation and other cellular changes all contribute to the process of dementia.

Types of Dementia

Dementia comes in many forms and the exact type cannot be definitely diagnosed without a brain biopsy, but typically the disease can be determined on clinically grounds by exploring the history of the dementia and physical exam. The following Table lists common types/causes of dementias.

Alzheimer's disease (AD), the most common type of dementia, has a gradual onset, begins slowly and initially impacts the ability to think, memory and language. Short-term memory is initially affected and overtime symptoms progress. Those with AD have on average a decline in the MMSE of 3-4 points per year if they go untreated (Rabins, Lyketsos & Steele, 2006).

Vascular dementia often occurs after a stroke and affects the part of the brain that was damaged. The part of the brain that was not damaged by the stroke often remains unaffected. While Alzheimer's disease presents with a more global decline, vascular dementia affects the area of the brain that was damaged. Vascular dementia affects 15-20% of patients with dementia and often co-exists with Alzheimer's disease. Like Alzheimer's disease, vascular dementia is progressive but the symptoms typically begin more abruptly.

Dementia with Lewy bodies is slowly progressive, and appears to overlap considerably with both Alzheimer's and Parkinson's disease. The severity of this type of dementia fluctuates in severity from day-to-day and is associated with variable levels of alertness.

Risk Factors

Many risk factors are associated with dementia; age is the most dramatic. While age is not synonymous with dementia the incidence of dementia is significantly higher as one ages. The disease typically starts between ages 40 and 90, but usually after age 65. Females are at greater risk than males. Another risk factor is having a family history of dementia in a parent or sibling. History of head injury puts one at risk for dementia. Poor control of many chronic diseases, including congestive heart failure and lung disease, can make dementia worse. Risk factors typically associated with vascular disease, high blood pressure, diabetes, and high cholesterol, are associated with an increased risk of vascular dementia and Alzheimer's disease.

Signs and Symptoms

Depending on the exact cause of the dementia the presenting signs and symptoms may vary. Short-term memory loss is common as evidence by forgetting recent events. The early stages of dementia are characterized by forgetting where items were placed, asking questions repeatedly, and having difficulty learning new information.

It is at times difficult to differentiate between normal aging and dementia. Normal aging is characterized by slowness in the retrieval of information. Those with dementia have a hard time recording new information. For example, the aged individual may have a hard time recalling the name of a friend they have not seen in a long-time. Those with dementia can be told something and not recall it. A husband may tell his wife (who has dementia) that friends are coming over for dinner and the wife will not remember this fact when the friends arrive.

Using words incorrectly, difficulty finding the right word or using general words to describe a specific item is a trait of dementia. A demented person uses the word "thing" to describe many items. Personality changes, making poor decisions, and mood swings are common symptoms of early dementia. Increased confusion at night, also known as sundowning, is a common feature of early dementia.

Patients with early dementia are able to compensate well when they are in familiar environments. Problems are often first noticed when one gets out of his or her routine such as going on vacation or entering the hospital. Patients often become very anxious, depressed, scared, or have emotionally liable moods. These moods are often the direct results of the patient being aware of the progressive dementia.

As the disease progresses the patient has difficulty carrying out tasks of daily living such as bathing, handling finances, grooming, dressing, and preparing meals. This is the point at which independence is significantly impaired and a patient will need to adjust their living environment.

Those with advanced dementia are dependent on others for care. They have a very limited memory and usually are not oriented to place, time, and often name. Patients with advanced dementia may not know the name of his or her spouse or children.

Loss of the swallowing reflex is a common complication of advanced dementia, which leads to medical complications such as malnutrition and aspiration pneumonia. Malnutrition decreases the ability to fight off infection and increases the risk of death from infection. Loss of the swallowing reflex increases the risk of dehydration. Patients with advanced dementia have more seizures.

Behavioral changes are more common as dementia advances. Mood swings, with the patient going from calm and pleasant to completely out of control within minutes can occur. Personality changes are seen in dementia with the demented patient showing an increased incidence of irritability, suspiciousness, and fearfulness. Hallucinations and delusions are hallmarks of advancing dementia. Hallucinations are misinterpretation of sensory stimulus. They can include seeing things that are not there such as dead relatives or hearing voices when there are none. Delusions are fixed, false beliefs. Common delusions include thinking people are out to get them, thinking that someone is trying to poison them, or believing they are God.

Clinical history and exam can help differentiate between some of the different types of dementia. Alzheimer's disease is the most common dementia and therefore the most likely diagnosis when a dementia presents. Some salient features of Alzheimer's disease include: early memory loss with cognitive impairment and at least one other area deficit such as language dysfunction, agnosis, apraxia, visuospatial disorder, and executive dysfunction. It typically has an insidious onset and a progressive course. Memory impairment is highlighted by a storage deficit; patients are not able to recall something with a cue. For example, if you are performing the mini-mental status exam (MMSE) and the patient is asked to recall three items after five minutes, the patient will not be able to recall them even after you give them a clue. As the disease progresses long-term memory becomes impaired. Later changes also include seizures, apathy, aggression, wandering, agitation, depression, and anxiety.

Vascular dementia can have either an abrupt or insidious onset and the progression can be stepwise, fluctuating, or a continuous decline. Patients with vascular dementia typically have cardiovascular risk factors such as hypertension, hyperlipidemia, and diabetes. Focal neurological deficits are common in those with vascular dementia. Memory impairment is not as pronounced in the early stage, whereas executive function (concentration, decision making, and higher-order problem solving) is impaired early.

Dementia with Lewy bodies (DLB) accounts for 10-15% of cases. DLB typically presents with memory loss. It is difficult to differentiate between DLB and Parkinson's disease with dementia. If the onset of dementia is within one year of Parkinson's disease than the most likely diagnosis is DLB. If the onset of dementia is greater than one year from the onset of Parkinson's disease, than the likely diagnosis is Parkinson's disease with dementia. DLB is more associated with the Parkinson's symptoms of masked facies and postural instability as opposed to tremor. Other features noticed with DLB are a fluctuating cognitive course, early impairment of executive function, more problems in attention, visuospatial function and constructional abilities when compared to AD and more autonomic involvement. Patients typically have recurrent visual hallucinations. There is often repeated falls and occasional syncope.

Frontotemporal dementia (FTD), characterized by a shrinking of the frontal and temporal anterior lobes of the brain, often presents with personality and behavioral changes over memory loss, at least early on. This disease runs in families. Symptoms of FTD fall into two clinical patterns that involve either changes in behavior or problems with language. Patients are typically impulsive, act socially unacceptable, disinhibited, lack insight, and are agitated or socially withdrawn. Those with language disturbance have difficulty speaking or understanding speech. Frontotemporal dementia occurs at a younger age than does Alzheimer's disease, typically between the ages of 40 and 70.

Diagnosis

Dementia is not diagnosed with fancy, expensive tests; but, by a history and physical examination. The work up involves performing a mental status examination. Standardized tests can be used to document mental decline, monitor decline and help make the diagnosis. Mental status examinations test the patient's memory and intellectual function. These tests look for memory impairment, language disturbance, ability to carry out purposeful movements, and ability to recognize objects. Mental status exams ask the patient to report the date and location, recall lists of items, write sentences, follow written commands, name objects, and copy diagrams. The American Academy of Neurology recommends the use of the mini-mental state exam (MMSE) or the memory impairment screen as tools to screen for dementia (American Academy of Neurology, 2004). It is important to note that one needs an IQ of about 90 to get a normal score on the MMSE.

Other testing is often employed. Early changes in mental decline are often not picked up on the MMSE. If the spouse or caregiver notices changes and the MMSE is normal, more sensitive testing may need to be employed. If the diagnosis is in doubt then more extensive testing, known as neuropsychological testing, typically done by a specialist, is performed.

Neuropsychological testing is a more comprehensive method for the evaluation of mental status. Testing is done by a neurologist, psychiatrist, or psychologist. It looks at higher cognitive functions including but not limited to abstract, logical, and conceptual reasoning, visuospatial orientation, memory, verbal fluency and reasoning. The test identifies cognitive impairment in patients with higher baseline cognitive abilities and determines if dementia is present in its more mild stages. It is more sensitive than other types of testing and can differentiate between mild cognitive impairment and dementia. The test is helpful for those who do not speak English as their native language and those with limited education. It also can help pick up anxiety and depression.

The work up of dementia rules out other causes of mental decline and consists of imaging and laboratory evaluation. The two most highly recommended tests include a vitamin 12 level and a thyroid test. Other testing is up to the individual health care provider and may include a complete blood count, glucose, kidney function test, electrolyte tests, and liver function tests (American Academy of Neurology, 2004). Other tests can be performed if the patient is deemed at high risk and the clinician has reason to suspect a more rare cause of dementia including: serology for syphilis, HIV testing, genetic testing, Lyme disease titers, testing for heavy metals, urinalysis, erythrocyte sedimentation rate, and serum folic acid. A lumbar puncture is sometimes performed if cerebral Lyme disease, cerebral vasculitis, neurosyphilis, or HIV is suspected as a cause of the dementia.

Testing for depression is critical as memory loss can be one of the manifestations of depression. Depression can present with memory loss and memory loss can reverse with treatment of depression. In addition, depression complicates the course of dementia if they both exist.

Many patients with dementia undergo an imaging examination to rule out other causes of disease. Its ability to identify a reversible cause of dementia is low but noncontrast computed tomography or magnetic resonance imaging is recommended as part of the initial evaluation of a patient with dementia (American Academy of Neurology, 2004). Those who are younger than 60, had recent head trauma, a history of cancer, gait disturbance, urinary incontinence, localized neurologic signs or symptoms, or those with a rapid or atypical course of dementia have the greatest chance of having a diagnostic yield from imaging studies. Imaging can rule out brain tumors, subdural hematomas, stroke, or normal-pressure hydrocephalus. The only way to confirm the diagnosis is to perform a brain biopsy, which is rarely done or necessary.

More advanced testing includes photon emission tomography (PET) scans or single photon emission computed tomography (SPECT) scans. These tests are not routinely done but are often done in research settings to help distinguish between different types of dementia. Current guidelines do not recommend their routine use.

Evaluation of Dementia

The need to evaluate for dementia can be picked up during a routine examination, from patient or family concern or from routine screening. The first step after performing a history and physical exam is to administer the MMSE. If the score is greater than 24/30 and dementia is highly suspected than referral for neuropsychological testing is appropriate. If the number is less than 24, than the first step is to evaluate for depression and treat if appropriate. After three months of depression treatment, mental status should be reevaluated.

If the number is less than 24 and there is no depression, or neuropsychological testing determines dementia is present then a work up for reversible causes of dementia should ensue. This work up should include the laboratory evaluation outlined above and neuro-imaging. Any reversible causes of dementia that are found should be treated and then mental status should be reevaluated. If there is improvement then routine reevaluations are appropriate. If there is no change then dementia is likely.

If the work up for reversible causes of dementia is negative, then dementia is probable. Based on the clinical findings on history and physical exam determining the type of dementia is possible.

Questions to consider when assessing a demented patient

What type of dementia is present? Although the current state of medical science is often unable to accurately diagnosis the specific type of dementia, it is helpful to know what type of dementia is present to help educate the patient and their family.

How was the diagnosis made? A doctor bases diagnosis on an examination, but laboratory evaluation and neuro-imaging should have been done to rule out other diseases.

Is there a reversible cause of dementia? Has it been looked for it? Some conditions – such as infections, depression or hormonal disturbances – can lead to a state of temporary confusion that, if treated, can result in a reversal of the confusion.

How severe is the dementia? Dementia is often broken down into mild, moderate and severe, which is typically based on functional ability and MMSE score.

Are there any medicines that may prolong cognitive function? Certain individuals respond to medicines that may help slow down the disease process.

What interventions may help control behaviors? Interventions listed below are effective at controlling symptoms. After utilizing the behavior analysis (discussed later), determine which interventions would be helpful. If non-drug treatments do not work, than the addition of pharmacological options may be necessary.

Are medicines needed to control behavior? Patients with dementia often have sleep disturbances, problems with hallucinations, delusions and aggressive behaviors that may respond to medications.

Is the patient safe to live independently? As the disease progresses and memory fails demented patients lose the ability to function independently. At some point during the disease it becomes necessary for the patient to have some assistance. The assistance may start in the form of home health aids or moving in with a loved one and lead to 24-hour care. Many patients with dementia progress to a point where they need nursing home placement.

What community services would be helpful? Are there any support groups in the area that may help? Dementia is a very stressful disease and it is often more stressful on the family as the disease progresses. Support groups can provide a lot of help for family members including, not only medical resources, but also psychological help.

Should a psychiatrist and/or neurologist see the patient? These specialists are not necessary for every patient with dementia, but in cases where the diagnosis is unclear or treatments are not effective or behavior problems are severe, specialty help is warranted.

Is depression present? Depression is a condition that is very commonly associated with dementia. It often makes the disease worse. There are many treatments that can help patients with dementia and co-existing depression.

Treatment

Currently, no treatment stops or restores mental decline that accompanies dementia, but some treatments and interventions may slow down the disease process and improve quality of life.

One of the most important steps in the treatment of dementia is to identify and treat reversible causes including vitamin B12 deficiency, subdural hematomas, normal pressure hydrocephalus and hypothyroidism.

Providing support for the patient and the family is an important job of the health care system. Support groups help the patient and family cope with this progressive and disabling disease. It is important that the health care system gives guidance about what is to be expected for the disease.

Demented patients need a peaceful and calm surrounding to minimize behavior problems that are common with dementia. Non-drug treatments can significant support the patient with dementia (see table 3).

Table 3: Non-Drug Interventions to Reduce Behavior Problems in Dementia

Frequently orienting the patient to their surroundings including time and place aides the demented individual with confusion.       Helping the patient remember the past with reminiscing and pictures.       Providing sensory stimulation including tough/massage and aromatherapy.       Maintaining an active social life.       Scheduled toileting and prompted voiding helps patients suffering with urinary incontinence maintain their continence.       Regular exercise

Demented patients thrive in familiar environments. Providing consistency and structure is an important step in managing dementia. Maintaining a routine schedule preserves orientation and allows him or her to function on a higher level. Keeping all of the items such as clothes, shoes, medications, and furniture in the same place is one suggestion. Keep a large calendar in the home with important dates such as birthdays and doctor appointments visible. Keep important phone numbers in plain view so they can be easily found reduces frustration. Labeling drawers and cabinets helps with orientation.

The holidays are a particularly challenging time for demented patients because parties, interrupted time schedules, and decorating leads to significant confusion. Decorating just one room of the house with holiday decorations and not allowing anyone with dementia to go in the room may help.

Keeping the patient with dementia safe becomes more important as the disease progresses. Keep instructions simple; minimize instructions to less than five words. Setting up a safe and pleasant environment is essential. Lighting needs to be bright to prevent falls; night-lights are helpful. Remove sharp objects from the home or put them in a locked area to prevent the demented patient from harm. Occupational therapists provide home evaluations to assure safety measures are in place to keep the demented patient safe. Cleaning services reduce clutter in the home, which reduces falls. Place identification tags, carried in many pharmacies, on the patient in case he or she gets lost. Alarms can be placed at the exits of the home to prevent the patient from wandering off.

Simplifying task, developing routines and providing proper rest reduces the incidence of behavior problems. Structured games and activities reduce behavior problems. Re-assuring an upset patient, repeating instructions as needed and redirecting the agitated persons reduces agitation. Sensory deprivation exacerbates the disease process and assuring that they can see (glasses on) and hear (hearing aids in) helps in reducing behavioral problems.

Problem behaviors can trouble not only patients, but caregivers. Paranoia, aggressiveness, and anxiety are more commonly a problem that leads to nursing home placement than memory loss. Analysis of behavior is another strategy that may be helpful for problem behaviors.

Behavior Analysis

Behavior analysis is helpful to determine triggers that agitate the person or make them more confused. It should be the first step employed when behavior problems are encountered. Controlling situations that agitate the patient or increase confusion can go a long way into making the disease more manageable. The behavior chart below (Table 4) can be used by loved ones of patients with dementia to help understand what triggers behavior problems. Recording activities, medications, the people present, and the corresponding behaviors identifies patterns to help loved ones understand what agitates the patient. The behavior chart does not need to be filled out everyday but it should be filled out if there is a change in behavior, a few days before a doctor's appointment, or after a medication change.

The behavior chart has six columns. The first column is where the time is recorded. The next column is where the activity that the patient is doing at that given time is recorded. Examples of activities include: sleeping, talking on the phone (and with whom), interacting with people, watching television (be specific about which show), eating, or shopping. The next column is to record the people who are around. Certain people can make patients much more irritable and filling out this column may reveal specific people that increase agitation. The next column is a place to record when medications for dementia are taken. This may demonstrate a pattern such as behaviors are much worse 6 hours after taking the medication prescribed for behaviors control. These patterns are important to recognize as they can affect the way doctors prescribe medications. The last column is a place for any miscellaneous comments.

Drug Treatment

Advances in pharmacology may prolong cognitive function in patients with dementia. One change prominent in dementia is loss of the cholinergic neurons in the basal forebrain. Cholinesterase inhibitors improve this deficient state. They increase the concentration of acetylcholine and the duration of its action in synapses by slowing down the enzyme, acetylcholinesterase. This is an enzyme that metabolizes acetylcholine.

The first drug developed, tacrine (Cognex), is rarely used today. Its dosing schedule is inconvenient (four times a day) and it has an adverse side effect profile including hepatotoxicity, nausea, and diarrhea.

Donepezil (Aricept), a drug dosed once a day, has been shown to decrease memory loss and functional decline. It is indicated for mild, moderate and severe dementia. Side effects include nausea, nightmares, headache, dizziness, vomiting, and diarrhea. Less commonly bradycardia and syncope can occur. Side effects are more common when this drug is started and dissipate as the body gets used to the medication.

Rivastigmine (Exelon), another medicine in the same class, may improve memory, functional impairment and behaviors. It is approved for mild to moderate dementia as well as Parkinson's disease dementia. Rivastigmine acts on slightly different chemical compounds in the brain but most studies suggest it is no more beneficial than any other cholinesterase inhibitor. It acts on both acetyl and butyryl cholinesterase and has a short half-life. The dose needs to be titrated to reach maximal effect.

Rivastigmine is beneficial for those with mild to moderate dementia. It slows down the decline of cognitive function and reduces the rate of decline in the ability to perform activities of daily living (Birks, Grimley, Evans, Iakovidou, Tsolaki & Holt, 2009).

Rivastigmine has more GI side effects than donepezil with weight loss being one significant problem. Other side effects include nausea, vomiting, diarrhea, not wanting to eat, dizziness, and headache. Interestingly the addition of memantine (Namenda) to rivastigmine significantly lowered the incidence of nausea and vomiting. None-the-less the rates of nausea and vomiting were high even with both medications (Olin, Bhatnagar, Reyes, Koumaras, Meng & Brannan, 2009).

Rivastigmine is now available as a transdermal patch. The low dose patch is associated with fewer side effects than the oral form or the high dose patch.

Galantamine (Razadyne) is another drug in this class with similar efficacy and benefits. It also acts on acetylcholinesterase and butyryl cholinesterase. In addition, it acts on the nicotinic receptor sites. This medication also needs to be titrated and is associated with gastrointestinal side effects such as GI upset, weight loss, and anorexia.

These are not miracle drugs and are not effective for all individuals. Many experts feel that these drugs are not beneficial except in a small subgroup of patients. All three of these medications are approved for Alzheimer's disease and rivastigmine is also approved for dementia associated with Parkinson's disease. Donepezil is approved for mild, moderate and severe dementia while rivastigmine and galantamine are approved for mild-moderate dementia.

Limited data is available on the efficacy of these medications on other types of dementia such as vascular dementia or dementia with Lewy bodies. Since there are no other medications approved for these conditions, and considering some similar pathology they are often used off label in an attempt to improve cognition.

Recent analysis of cholinesterase inhibitors in the treatment of Alzheimer's disease suggested that there is small clinical benefit and the studies used to prove their efficacy used flawed methods (Kaduszkiewicz, Zommermann, Beck-Bornholdt, & van den Bussche, 2005). Because of flawed methods and small clinical benefits, the scientific basis for recommending cholinesterase inhibitors for the treatment of Alzheimer's disease is questionable.

A Cochrane review (Birks, 2006) reports that the three cholinesterase inhibitors are effective in mild-to-moderate Alzheimer's disease. While all three have a slightly different mode of action there is no evidence any one is better than another. Not everyone responds to these treatments and there is no reliable method to determine which patients will respond favorably. Studies suggest that cholinesterase inhibitors are not cost effective.

Not everyone agrees with this opinion. The National Institute of Clinical Excellence (NICE) (Mayor, 2006) said that this class of medication would be considered in those with moderately-severe Alzheimer's disease with MMSE scores between 10-20. The NICE committee concluded that cholinesterase inhibitors were clinically and cost effective in patients with moderate Alzheimer's disease.

There still may be hope for acetylcholinesterase inhibitors. A small recent study showed that patients with dementia taking acetylcholinesterase inhibitors have MMSE scores that decline at a slower rate than patients not taking the drug (Nelson, Kryscio, Abner, Schmitt, Jicha, Mendiondo, Cooper, Smith & Markesbery, 2009).

A recent analysis suggested the cholinesterase inhibitors might have disease-modifying effects. The use of drugs that modify the butyryl cholinesterase system may have the most disease modifying effect. It was shown that there was some benefit, albeit not a dramatic one, over 3-4 years (Shanks, 2009).

The use of cholinesterase inhibitors in mild cognitive impairment shows questionable effect. There is no convincing positive effect in delaying the progression to dementia. These studies may have been flawed and further investigation is needed before a definitive answer is given (Farlow, 2009).

The newest medicine, approved in October of 2003, in the treatment of dementia is memantine HCl (Namenda). This drug is approved for moderate-severe Alzheimer's dementia and is sometimes combined with cholinesterase inhibitors. Side effects include dizziness, confusion, headache, and constipation. NICE (Mayor, 2006) did not recommend the use of memantine, because there was insufficient evidence of its clinical benefit for patients with moderately-severe or severe Alzheimer's.

While there is some evidence that these medications work, the evidence is not overwhelming. Given that fact there are few other options they are often used. When used, patients must be given reasonable advice on what to expect.

Other treatments

Treatment of depression is an important step in treating dementia. Treating depression improves mental function, lessens confusion, and improves dementia.

Other medicines that have been suggested for the treatment of dementia include non-steroidal anti-inflammatory medications, vitamin E, estrogen, and ginkgo biloba. Caution must be exercised with these medications as they have not been rigorously studied and not approved for dementia.

Non-steroidal anti-inflammatory medications include ibuprofen (Advil, Motrin), celecoxib (Celebrex) and naproxen (Aleve). They are postulated to benefit patients with Alzheimer's disease but research does not convincingly back-up that claim. Theoretically they slow down neurodegeneration as they reduce inflammation in the brain, which is associated with the development of the neuritic plaques. Some data shows these medications reduce the incidence of dementia, but there is some question of bias in these studies and therefore it is not recommended as an agent to prevent dementia. Due to its theoretical benefit, scientists are still holding out hope that further research will prove it is a therapeutic strategy for Alzheimer's disease.

Free radicals can damage nerves in the brain. They are the by-products of oxidative metabolism and some evidence suggests that vitamin E, selegiline, and ginkgo biloba may be protective against this process. Vitamin E, at doses of 1000 IU two times a day, may be slightly beneficial in patients with Alzheimer's disease as it may delay the need for patients with Alzheimer's disease to need placement in long-term care (Sano, Ernesto, Thomas, Klauber, Schafer, Grundman, Woodbury, Growdon, Cotman, Pfeiffer, Schneider, & Thal, 1997). Caution must be used with Vitamin E because it increases the risk for bleeding which is especially concerning if on blood thinners.

Recent studies do not support the benefit of vitamin E in Alzheimer's disease. A small study suggested that vitamin E may help maintain cognition is some people with Alzheimer's disease. In others, vitamin E actually has a negative effect on cognition. Based on current medical science it is not possible to determine who will be responders and who will be non-responders. Therefore, vitamin E is not recommended (Lloret A, Badia MC, Mora NJ, Pallardo FV, Alonso MD vina J, 2009).

Over all the jury is still out on Vitamin E. If you want to take vitamin E remember that there is a risk that it will speed up cognitive decline. A Cochrane review recommended that evidence is insufficient to say that vitamin E can prevent or treat people with Alzheimer's disease. More research is needed (Isaac MG, Quinn R & Tabet N, 2008).

Ginkgo biloba is an herbal product that has multiple uses including depression, anxiety, ringing in the ears, confusion, headache and memory problems. One of its biggest uses is for memory conditions. Ginkgo biloba, an herbal preparation, showed mild effectiveness on cognitive deficit in Alzheimer's disease (Luiz dos Santos-Neto L, de Vilhena Toledo MA & Medeiros-Souza P, 2006). A recent Cochran review suggest that gingko is safe to use, but likely not terribly effective (Birks J & Grimley-Evans J, 2009). More studies are needed to prove its effectiveness in the prevention and treatment of dementia. Risks associated with gingko include bleeding and seizures. Use caution with simultaneous use of any blood thinners.

Estrogen has antioxidant and anti-inflammatory properties that are likely associated with their benefit in dementia. It also has positive effects on nerves in the brain and acetylcholine concentrations. Science does not have enough clinical data to make conclusions about the efficacy of estrogen in the treatment and prevention of dementia and Alzheimer's disease. Given the current data and the risks of side effects (increased cardiovascular risk, blood clot formation and death rates) estrogen is not recommended as a treatment modality to improve cognitive function or prevent cognitive decline in women older than 65.

Behavior Problems

Behavior problems are a concern with dementia as the disease progresses. Psychosis, depression, and anxiety are three common problems. These symptoms are difficult for those with Alzheimer's disease and can be associated with risk for others as there is at times physical aggression. Non-drug interventions, listed above, are the first interventions to treat behavioral problems. Keeping a behavioral chart defines the problem and facilitates in the treatment of the undesirable behaviors.

When non-drug interventions fail there are medicines to treat behavior problems. Anti-anxiety medicines, such as lorazepam (Ativan) or alprazolam (Xanax), reduce anxiety and related behavior problems. Caution must be used with benzodiazepines as they can cause excessive sedation and potentially paradoxical agitation. Buspirone (Buspar) can be tried, but its effectiveness is variable. Its dose needs to be titrated. The addition of trazodone at bedtime can aid with anxiety, depression, and insomnia.

Some evidence exists for the use of cholinesterase inhibitors in the management of agitation. But data does not prove its effectiveness (Howard, Juszczak, Ballard, et al. 2007). While this class of drug is not the ideal solution for the treatment of behavior problems, it may delay the emergence of behavior problems. Future studies will define the role these agents have in the treatment of behavior problems with dementia.

The use of memantine or memantine with donepezil may help reduce behavior problems in those with Alzheimer's disease. In addition, cholinesterase inhibitors may reduce psychosis and behavioral problem in those with dementia with Lewy bodies. Symptoms that are most likely to benefit include apathy, agitation, aggression, delusions and hallucinations (Daiello, 2007).

Visual hallucinations and paranoid delusions are two of the most common psychotic features in dementia. Psychotic symptoms are often treated with antipsychotics with varied success. While no medication is approved for behavior disturbances in dementia, they are often used. In addition to their use in psychosis, neuroleptics are used with variable success in the treatment of behavioral disturbances in dementia such as agitation, aggressiveness, and wandering.

Aggression and agitation are commonly treated with antipsychotic medications. They are helpful in managing these symptoms in the short-term for less than 3 months, but they are associated with some risk.

Antipsychotic can be broken down into typical and atypical medications. Typical agents are more commonly associated with extrapyramidal effects such as slowed movement, rigidity, and tremor. Atypical agents are less likely to have extrapyramidal effects but are less predictable in their efficacy. These medicines are not approved by the food and drug administration for use in dementia but are used extensively. Risperidone (Risperdal), quetiapine (Seroquel) and olanzapine (Zyprexa) are atypical drugs in this class. The most common typical medication prescribed is haloperidol (Haldol). Most patients can tolerate a low maintenance dose without extrapyramidal effects. Patients with DLB are more prone to neuroleptic sensitivity and extreme caution must be used when using these medications in DLB.

Acute psychotic crises can arise and may require hospitalization. Intramuscular antipsychotic medication such as haloperidol in a dose of 5-10 mg often calms an acute psychosis. After the acute episode and lower maintenance dose may be needed to prevent another crisis.

While these medications are widely used for those with dementia and behavioral disturbances they need to be used with extreme caution. They are not approved for psychosis in dementia. Evidence is not convincing that these agents are effective. In respect to reduction of agitation and psychosis atypical agents show approximately 20 percent greater response rate than placebo (McKeith and Cummings, 2005). One study showed that dementia patients treated with quetiapine had an accelerated cognitive decline over placebo (Ballard, Margallo-Lana, Juszczak, Douglas, Swann, Thomas, O'Brien, Everratt, Sadler, Maddison, Lee, Bannister, Elvish, & Jacoby, 2005).

Increased death rates and rates of stroke are a major concern with the use of atypical antipsychotics in the demented population. Stroke rates were shown to be 2-3 times higher and mortality showed a 1.6-1.7 fold increase (Smith, & Beier, 2004). While other studies raise questions to such high numbers, significant caution should be used with these medications. Completely avoiding these medications is not appropriate as some patient see significant improvement in quality of life with their use.

The degree of symptoms may predict on how well antipsychotic medications work. In nursing home residents, those with more severe behavioral disturbances have a better response to antipsychotic medications. The response to medications may be most effective in those who are most profoundly affected by agitation and aggression without psychosis (Daiello, 2007).

As dementia progresses there is often a decrease in the severity and frequency of behavior disturbances. It is therefore a wise practice to try to taper or discontinue antipsychotic medications after 2-8 months of treatment (Daiello, 2007).

Selective Serotonin Reuptake Inhibitors (SSRI) may be effective for the treatment of psychotic symptoms in dementia. A small study suggested that the antidepressant citalopram (Celexa) is as effective as risperidone in reducing psychotic symptoms such as hallucinations, delusions, and suspicious thoughts (Pollock, Mulsant, Rosen, Maxumdar, Blakesley, Houck, & Huber, 2007), with fewer side effects. This was a small study and it warrants further investigation before SSRIs can be recommended to treat psychosis in dementia.

Depression can be a vexing problem that is difficult to uncover in dementia. SSRI [sertraline (Zoloft), fluoxetine (Prozac), paroxetine (Paxil)] are first line agents in the treatment of depression. Tricyclic antidepressants are not recommended in this population as there is the potential for increased confusion, urinary retention, constipation, blurred vision, sedation, and increased agitation.

Another question that has recently been looked at is the use of antidepressants in the prevention of dementia. A recent study suggested that the continued long-term use of antidepressants (it did not matter which antidepressant or antidepressant class was chosen) lowered the rates of dementia. This study evaluated those with depression and dementia. For those with both conditions there is most likely a benefit of treating depression in regard to lowering the rates of dementia (Kessing, Sondergard, Forman, Anderson, 2009).

Behavioral interventions may be used in the management of behavioral problems in place of medications. There is some evidence that aromatherapy may be effective for agitation (Ballard, Gauthier, Cummings et al, 2009).

Sleep problems are a common complication of dementia. First line interventions include non-drug interventions such as: reducing caffeine/nicotine/alcohol, regular exercise, discouraging long day-time naps, instituting soothing bedtime rituals and maintaining a consistent bed-time routine. If this fails than the addition of short-acting sedative-hypnotic medications are one solution to restoring sleep. Agents to be considered include zolpidem (Ambien), eszopiclone (Lunesta) and remelteon (Rozerem). Zolpidem is approved for short-term use and comes in an extended release form. Eszopiclone helps in the initiation of sleep and maintenance. Ramelteon, which acts on different receptors, is another option when other medications fail. Ramelteon and eszopiclone are approved for long-term use.

Advanced Care Planning

Dementia is a progressive disease that eventually robs one of their memories. Before memory fails it is paramount to make medical wishes known. This is done with advanced care planning. Making life and death decisions can be uncomfortable but making these wishes known will assure advance directives are carried out.

The advanced directive should include a durable power of attorney for health care and a living will. The durable power of attorney for health care is naming a person to make health care decisions for the patient when he or she cannot. It is often a relative or close friend. Ideally this person will know what type of medical wishes the patient wants. A living will discusses the patient's medical wishes in advance. This helps guide the health care team and the durable power of attorney in making decisions when the patient is unable to do so.

Prevention

Research in preventing dementia is sparse but does provide some suggestions. Stimulating the mind through playing chess, reading or playing a musical instrument is the most important thing one can do to keep the mind sharp and decrease the risk of getting dementia. While drugs and supplements have hinted at their ability to prevent dementing illness, there is limited data to suggest effectiveness. Cholinesterase inhibitors do not reduce the rates of progression from memory impairment to dementia (Raschetti R, Albanese E, Vanacore N, & Maggini M, 2007).

Complications of Dementia

Dementia is a progressive disease that has the potential to cause many problems as it advances. Dysphagia is typically a later disease concern. Aspiration is a major problem in those who develop dysphagia. A speech therapist can perform a swallowing study and make recommendations to decrease the risk of aspiration. Some possible interventions include:

	Altering the consistency of the food
	Cutting food into smaller pieces
	Changing the position of the patient when he or she swallows
	Encouraging the patient to tuck the chin while swallowing
	Eating with someone who can monitor for any aspiration or provide cues to safe eating

Some patients with dementia will hold food in their mouth, not swallow it and spit it out. This is common with frontotemporal dementia and is best treated with behavioral interventions.

The use of feeding tubes has fallen out of favor over the last number of years as they have not proven to extend life expectancy or improve quality of life. They can be utilized if aspiration is severe or the patient does not eat enough to maintain nutrition and it is wanted by patient and durable power of attorney of health care. Feeding tubes do not prevent malnutrition, reduce incidence of aspiration pneumonia, improve function, or extend life (Li, 2002). If permanent feeding tube replacement is desired than percutaneous gastrostomy is better than a nasogastric tube. Consideration must be given to quality of life and complications when deciding on the use of a feeding tube. Hand feeding is an alternative to feeding tubes and it may provide more comfort to the patient.

Those with dementia are typically older; older age comes with a greater risk of many chronic diseases. Having dementia makes it more likely that proper treatment will not ensue. For example, those with a heart attack may not be able to communicate the pain that they are feeling due to the dementia, which will result in delayed care and worse outcomes.

Poor nutrition is another common complication of dementia. Poor nutrition increases the risk of infection and poor body healing. The combination of older age, poor communication and a compromised immune system make the demented individual at high risk for poor outcomes.

Conclusion

As the population ages dementia will become a more prevalent disease. It is a devastating disease that affects not only the mind but the body. Current medical science does not have a cure for the disease, but there are many treatment options. Treatment should always focus on non-pharmacological interventions with sparing use of medications to improve quality of life. Nurses need to have an understanding of the disease and how to help patients and families cope with dementia.

References

American Academy of Neurology. (2004). AAN Guideline Summary for clinicians. Detection, Diagnosis and Management of Dementia. Retrieved September 1, 2009 from http://www.aan.com/professionals/practice/pdfs/dementia_guideline.pdf

Alzheimer's Foundation of American. About Alzheimer's. Statistics. Retrieved August 31, 2009 from http://www.alzfdn.org/alzheimers/statistics.shtml

Anderson HS. Alzheimer's Disease. Retrieved September 1, 2009 from http://emedicine.medscape.com/article/1134817-print

Ballard CG, Gauthier S, Cummings JL, et al. (2009). Management of agitationand aggression associated with Alzheimer disease. Nature Reviews Neurology; 5(5): 245-55.

Ballard C, Margallo-Lana M, Juszczak E, Douglas S, Swann A, Thomas A, O'Brien J, Everratt A, Sadler S, Maddison C, Lee L, Bannister C, Elvish R, & Jacoby R. (2005). Quetiapine and rivastigmine and cognitive decline in Alzheimer's disease: randomized double blind placebo controlled trial. British Medical Journal. 330, 874-877.

Birks J, Grimley, Evans J, Iakovidou V, Tsolaki M & Holt FE. (2009). Rivastigmine for Alzheimer's disease. Cochrane Database Systematic Reviews. 15;(2):CD001191.

Birks J, Grimley & Evans J. (2009). Ginkgo biloba for cognitive impairment and dementia Cochrane Database Systematic Reviews. 21;(1):CD003120.

Birks S. (2006). Cholinesterase inhibitors for Alzheimer's disease. Cochrane Database Systematic Reviews. 25; (1): Article CD005593.

Daiello LA. (2007) Atypical antipsychotics for the treatment of dementia-related behaviors: an update. Medicine and Health, Rhode Island; 90(6): 191-4.

Farlow MR. (2009). Treatment of mild cognitive impairment (MCI). Current Alzheimer's Research; 6(4): 362-7.

Howard RJ, Juszczak E, Ballard CG, Bentham P, Brown RG, Bullock R, Burns AS, Holmes C, Jacoby R, Johnson T, Knapp M, Lindesay J, O'Brien JT, Wilcock G, Katona C, Jones RW, DeCesare J, Rodger M, & CALM-AD Trial Group. (2007). Donepezil for the Treatment of Agitation in Alzheimer's Disease. New England Journal of Medicine. 357, 1382-1392.

Isaac MG, Quinn R & Tabet N. (2008). Vitamin E for Alzheimer's disease and mild cognitive impairment. Cochrane Database Systematic Reviews 16;(3): CD002854.

Kaduszkiewicz H, Zimmermann T, Beck-Bornholdt HP & van den Bussche H. (2005). Cholinesterase inhibitors for patients with Alzheimer's disease: systematic review of randomized clinical trials. British Medical Journal. 331(7512), 321-7.

Kessing LV, Sondergard L, Forman, JL & Andersen PK. (2009). Antidepressants and dementia. Journal of Affective Disorders. 117(1-2): 24-9.

Li I. (2002). Feeding Tubes in Patients with Severe Dementia. American Family Physician. 65(8), 1605-1610

Lloret A, Badia MC, Mora NJ, Pallardo FV, Alonso M & Vina J. (2009). Vitamin E paradox in Alzheimer's disease: it does not prevent loss of cognition and may even be detrimental. Journal of Alzheimer's Disease; 17(1):143-9.

Luiz dos Santos-Neto L, de Vilhena Toledo MA, Medeiros-Souza P. (2006). The Use of Herbal Medicine in Alzheimer's disease—A Systematic Review. Evidence Based Complement Alternative Medicine. 3(4), 441–445.

Mayor S. (2006). NICE recommends drugs for moderate Alzheimer's disease. British Medical Journal. 332, 115

McKeith I & Cummings J. (2005). Behavioral changes and psychological symptoms in dementia disorders. Lancet Neurology. 4, 735-742.

Nelson PT, Kryscio RJ, Abner EL, Schmitt FA , Jicha GA, Mendiondo MS, Greg Cooper G, Smith CB, & Markesbery WR. (2009). Acetylcholinesterase Inhibitor Treatment is Associated with Relatively Slow Cognitive Decline in Patients with Alzheimer's Disease and AD + DLB. Journal of Alzheimer's Disease. 16(1): 29-34.

Olin JT, Bhatnagar V, Reyes P, Koumaras B, Meng X & Brannan S. (2009). Safety and tolerability of rivastigmine capsule with memantine in patients with probable Alzheimer's disease: a 26-week, open-label, prospective trial. International Journal of Geriatric Psychiatry. Abstract. Retrieved October 1, 2009 from: http://www.ncbi.nlm.nih.gov/pubmed/19670390

Pollock BG, Mulsant BH, Rosen J, Maxumdar S, Blakesley RE, Houck PR, & Huber KA. (2007). A Double-Blind Comparison of Citalopram and Risperidone for the Treatment of Behavioral and Psychotic Symptoms Associated With Dementia. American Journal of Psychiatry. 15(11), 942-952.

Rabins PV, Lyketsos CG & Steele CD. (2006). Practical Dementia Care, Second Edition, Oxford University Press: New York.

Raschetti R, Albanese E, Vanacore N, Maggini M. (2007). Cholinesterase Inhibitors in Mild Cognitive Impairment: A Systematic Review ofRandomized Trials. PLoS Med. 4(11), e338.

Sano M, Ernesto C, Thomas RG, Klauber MR, Schafer K, Grundman M, Woodbury P, Growdon J, Cotman CW, Pfeiffer E, Schneider LS, & Thal LJ. (1997). A controlled trial of selegiline, alpha-tocopherol, or both as treatment of Alzheimer's disease. The Alzheimer's disease Cooperative Study. New England Journal of Medicine. 336, 1216-1222.

Smith D. & Beier M. (2004). Association between risperidone treatment and cerebrovascular adverse events: examining the evidence and postulation hypotheses for an underlying mechanism. JAMA. 5, 129-132.

Shanks M, Kivipelto M, Bullock R & Lane R. (2009). Cholinesterase inhibition: is there evidence for disease-modifying effects? Current Medical Research Opinions. 25(10): 2439-2449.