- Causes and symptoms
- Health care team roles
Dementia is a syndrome (collection of signs and symptoms) characterized by a progressive and irreversible decline in mental ability, accompanied by changes in behavior and personality. It is a condition rather than a disease in its own right. Patients with dementia commonly experience a loss of memory and other cognitive skills required to carry out activities of daily living (ADLs).
The definition of dementia has become more inclusive over the past several decades. Whereas earlier descriptions of dementia emphasized memory loss, the last three editions of the health professional's diagnostic handbook, Diagnostic and Statistical Manual of Mental Disorders (also known as the DSM) define dementia as an overall decline in intellectual function, including difficulties with language, simple calculations, planning and judgment, and motor (muscular movement) skills, as well as loss of memory. The fifth edition (DSM-5), due for publication in 2013, proposes to replace the term Page 967 | Top of Articledementia with major neurocognitive disorder, and to define it as “a disorder with greater cognitive deficits in at least one (typically two or more) of the following domains”:
- Attention (including the ability to sustain attention, divide one's attention, and speed of processing)
- Executive ability (including working memory, decision making, planning, responding to feedback, mental flexibility)
- Learning and memory
- Language skills (expressive and receptive language)
- Visual perception
- Social cognition (includes the ability to regulate one's emotions and control one's behavior).
The proposed changes in DSM-5 reflect recent research findings about dementias other than Alzheimer disease (AD). Whereas older editions of DSM used AD as the basic model of dementia and emphasized memory loss as the earliest symptom, newer studies of such disorders as cerebrovascular disease, frontotemporal degeneration, traumatic brain injury, and HIV-related dementia indicate that memory loss is often not the first or the most noticeable deficit in patients with these neurocognitive disorders. In addition, the editors of DSM-5 note that while the term dementia remains applicable to older adults, it is less appropriate for younger adults with neurocognitive deficits related to head trauma or HIV infection .
Dementia is a group of symptoms caused by the gradual death of brain cells. The loss of cognitive abilities that occurs with dementia leads to impairments in memory, reasoning, planning, language skills, emotional self-control, and personality.
While the overwhelming majority of people with dementia are elderly, neurocognitive disorders are not an inevitable part of aging . One of the challenges for health care professionals is to differentiate the early-stage cognitive deficits of dementia from normal age-related memory impairment. Persons with age-related memory impairment may tend to learn new information more slowly; but if they are given additional time, their cognitive performance is usually adequate. Other problems that may be mistakenly labeled dementia include delirium , psychosis , depression, and the side effects of various medications.
Dementia can occur at any age and may affect younger people as the result of such diseases as HIV infection, hypoxia (a deficiency of oxygen reaching the tissues of the body), or injury. However, it is primarily a disorder of the elderly. The prevalence of dementia increases rapidly with age; it doubles every five years after age 60. Dementia affects only 1% of people aged 60 to 64 but 30% to 50% of those older than 85. About 6 million persons in the United States are affected by dementia as of 2012, with the number estimated to rise to 7.9 million by 2030 and 12–16 million by 2050. AD had become the sixth leading cause of death in the United States by 2007; in addition, AD as an underlying cause of death is frequently underreported. Surveys have indicated that dementia is the condition most feared by older adults in the United States. The condition is somewhat more common among women than men. Some studies indicate that the risk for dementia is higher for African Americans and Hispanic Americans than it is for Caucasians. More than half of all nursing home admissions occur because of dementia.
Dementia presents a major health problem for the United States because of its huge impact on individuals and their families, the health care system, and society overall. The costs of dementia are considerable; $183 billion per year as of 2011, the most recent year for which data are available. The estimated cost for 2012 is $200 billion. While most people with dementia are retired and do not suffer income losses, the cost of their care is often enormous. Financial burdens include lost wages for family caregivers, medical supplies and drugs, and home modifications to ensure safety. Nursing home care may cost several thousand dollars a month or more. The psychological costs are not as easily quantifiable, but can be even more profound. The person with dementia loses control of many of the essential features of life and personality, and loved ones lose a family member even as they continue to cope with the burdens of increasing dependence and unpredictability.
The demographic distribution of dementia varies somewhat according to its cause. Moreover, recent research indicates that dementia in many patients has overlapping causes, so that it is not always easy to assess the true rates of occurrence of the different types. For example, Alzheimer's disease (AD) and multi-infarct dementia (MID) are found together in about 15% to 20% of cases; this condition is called mixed dementia. None of the known types of dementia offers protection against or lowers the risk of developing any of the others.
AD is by far the most common cause of dementia in the elderly, accounting for 60% to 80% of cases. At least 360,000 Americans are diagnosed with AD each year and about 50,000 are reported to die from it. The disease strikes women more often than men, but researchers do not know yet whether the sex ratio simply reflects the fact Page 968 | Top of Articlethat women in developed countries tend to live longer than men, or whether female sex is itself a risk factor for AD. One well-known long-term study of Alzheimer disease in women is the Nun Study, begun in 1986 and presently conducted at the University of Kentucky. The researchers have identified numerous relationships between factors from early, middle, and late life and the risk of AD.
Multi-infarct dementia (MID), also called vascular dementia, is responsible for between 15% and 20% of cases of dementia (not counting cases in which it coexists with AD). Unlike AD, MID is more common in men than in women. Diabetes, high blood pressure , a history of smoking , and heart disease are all risk factors for MID. Researchers in Sweden have suggested that MID is underdiagnosed, and may coexist with other dementias more frequently than is presently recognized.
Dementia with Lewy bodies is now thought to be the second most common form of dementia after AD. But because researchers do not completely understand the relationship between Lewy bodies, AD, and Parkinson's disease , the demographic distribution of this type of dementia is also unclear.
Frontal lobe dementias (FLDs), Pick's disease, Huntington's disease, Parkinson's disease, HIV infection, alcoholism , and head trauma among other factors account for about 10% of all cases of dementia. In FLD and Pick's dementia, women appear to be affected slightly more often than men.
Dementia in children is rare; however, there are several hereditary disorders that can cause dementia in children. They include Batten disease, a fatal disorder of the central nervous system ; Lafora body disease, also a fatal disease in which children develop tiny structures called Lafora bodies in the brain, skin, liver , and muscles; and Niemann-Pick disease, a metabolic disorder in which the body cannot metabolize cholesterol properly. High levels of fatty substances accumulate in the brain as well as in other organs, leading to confusion and dementia.
There are two risk factors for dementia that people cannot change: age and heredity. Risk factors that people can change or modify include:
- Heavy drinking. Moderate use of alcohol (one drink per day for women and two for men) does not increase a person's risk of dementia, but abuse of alcohol does.
- Smoking. Smoking is a risk factor for dementia because it increases the risk of vascular disease.
- Depression. Depression in later life, particularly in men, appears to increase the risk of dementia although the reasons for the association are not known as of 2012.
- Atherosclerosis. Fatty deposits along the walls of the arteries increases the risk of Alzheimer's disease as well as MID.
- Type 2 diabetes.
- High cholesterol levels.
- High levels of total estrogen (in women).
- Abnormally high or abnormally low blood pressure.
- Obesity. Obesity is associated with an increased risk of AD and MID, although the reasons for this association are unclear as of 2012.
- High levels of homocysteine in the blood. Homocysteine is an amino acid produced in the body that is normally broken down by the B vitamins and folic acid.
Causes and symptoms
Dementia is usually caused by degeneration in the cerebral cortex, the part of the brain responsible for thoughts, memories, actions, and personality traits. The death of brain cells in this region leads to the cognitive impairment that characterizes dementia. Dementia may be caused by a variety of illnesses.
The most common cause of dementia in North America is Alzheimer's disease (AD), accounting for half to three-quarters of all cases.
Vascular dementia accounts for 5% to 30% of all dementias in the United States and Europe; however, it is the most common form of dementia in some parts of Asia. It occurs from a decrease in blood flow to the brain, most commonly due to a series of small strokes (multi-infarct dementia or MID). Other cerebrovascular causes include vasculitis from syphilis , Lyme disease, or systemic lupus erythematosus; subdural hematoma ; and subarachnoid hemorrhage. Because of the usually sudden nature of its cause, the symptoms of vascular dementia tend to appear more abruptly than those of Alzheimer dementia. Symptoms may progress with the occurrence of new strokes. Unlike AD, the incidence of vascular dementia decreases after the age of 75.
Other conditions that may cause dementia include:
- Parkinson's disease
- Lewy body disease
- Pick's disease
- Huntington's disease
- Creutzfeldt-Jakob disease (CJD)Page 969 | Top of Article
- brain tumors
- head trauma
- prolonged abuse of alcohol or other drugs
- Vitamin B12 deficiency
Genetic factors in dementia
Genetic factors play a role in several types of dementia, but the importance of these factors in the development of the dementia varies considerably. AD is known, for example, to have an autosomal (non-sex-related) dominant pattern in most early-onset cases as well as in some late-onset cases, and to show different degrees of penetrance (frequency of expression) in late-life cases. Recently, two forms of a gene responsible for recycling the proteins thought to be involved in forming the neuron-destroying amyloid plaques of AD were identified and associated with late-onset disease. Researchers have not yet discovered, however, how the genes associated with dementia interact with other risk factors to produce or trigger the dementia. One non-genetic risk factor presently being investigated is toxic substances in the environment.
EARLY-ONSET ALZHEIMER'S DISEASE. In early-onset AD (also called young-onset AD), which accounts for 2% to 7% of cases of AD, the symptoms develop before age 60. It is usually caused by an inherited genetic mutation. Early-onset AD is also associated with Down syndrome (trisomy 21), in that persons with trisomy 21 (three forms of human chromosome 21 instead of a pair) often develop early-onset AD.
LATE-ONSET ALZHEIMER'S DISEASE. Recent research indicates that late-onset AD is a polygenic disorder; that is, its development is influenced by more than one gene. It has been known since 1993 that a specific form of a gene (the APOE gene) on human chromosome 19 is a genetic risk factor for late-onset AD. In 1998 researchers at the University of Pittsburgh reported on another gene that controls the production of bleomycin hydrolase (BH) as a second genetic risk factor that acts independently of the APOE gene. In December 2000, three separate research studies reported that a gene on chromosome 10 that may affect the processing of a protein (called amyloid-beta protein) is also involved in the development of late-onset AD. When this protein is not properly broken down, a starchy substance builds up in the brains of people with AD to form the plaques that are characteristic of the disease. The most recent development is the confirmation of the involvement of variant forms of a gene called SORL1. The proteins controlled by this gene are related to the production of amyloid-beta protein. Low levels of the protein encoded by the SORL1 gene cause amyloid–beta levels near cells to rise.
MULTI-INFARCT DEMENTIA (MID). While the chief risk factors for MID are high blood pressure, advanced age, and male sex, there is an inherited form of MID called CADASIL, which stands for cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. CADASIL can cause psychiatric disturbances and severe headaches as well as dementia.
FRONTAL LOBE DEMENTIAS (FLDS). Researchers think that between 25% and 50% of cases of frontal lobe dementia involve genetic factors. Pick's dementia appears to have a much smaller genetic component than FLD. It is not yet known what other risk factors combine with inherited traits to influence the development of frontal lobe dementias.
FAMILIAL BRITISH DEMENTIA (FBD). FBD is a rare autosomal dominant disorder that was first reported in the 1940s in a large British family extending over nine generations. FBD resembles AD in that the patient develops a progressive dementia related to amyloid deposits in the brain. In 1999, a mutated gene that produces the amyloid responsible for FBD was discovered on human chromosome 13. Studies of this mutation may yield further clues to the development of AD as well as FBD itself.
CREUTZFELDT-JAKOB DISEASE (CJD). Although Creutzfeldt-Jakob disease is caused by a prion (a proteinaceous infectious particle consisting only of protein, as opposed to a virus, which consists of protein and nucleic acid, or a virion, which consists of nucleic acid), researchers think that 5% to 15% of cases may have a genetic component.
DSM-IV-TR identifies certain symptoms as criteria that must be met for a patient to be diagnosed with dementia. One criterion is significant weakening of the patient's memory with regard to learning new information as well as recalling previously learned information. In addition, the patient must be found to have one or more of the following disturbances:
- Aphasia. Aphasia refers to loss of language function. A person with dementia may use vague words like “it” or “thing,” often because he or she cannot recall the exact name of an object; the affected person may echo what other people say, or repeat a word or phrase over and over. People in the later stages of dementia may stop speaking at all.Page 970 | Top of Article
- Apraxia. Apraxia refers to loss of the ability to perform intentional movements even though the person is not paralyzed, has not lost the sense of touch, and knows what he or she is trying to do. For example, a patient with apraxia may stop brushing his teeth or have trouble tying his shoelaces.
- Agnosia. Agnosia refers to loss of the ability to recognize objects even though the person's sight and sense of touch are normal. People with severe agnosia may fail to recognize family members or even their own face reflected in a mirror.
- Problems with abstract thinking and complex behavior. This criterion refers to the loss of the ability to make plans, carry out the steps of a task in the proper order, make appropriate decisions, evaluate situations, and show good judgment. For example, a patient might light a stove burner under a saucepan before putting food or water in the pan, or be unable to record checks and balance a checkbook.
DSM-IV-TR also specifies that these disturbances must be severe enough to cause problems in the person's daily life, and that they must represent a decline from a previously higher level of functioning. As noted above, DSM-5 proposes six domains of functioning; a patient must show a measurable decline in two or more, and the “cognitive deficits must be sufficient to interfere with functional independence.”
In addition to the changes in cognitive functioning, the symptoms of dementia may also include personality changes and emotional instability. Patients with dementia sometimes become mildly paranoid because their loss of short-term memory leads them to think that mislaid items have been stolen. About 25% of patients with dementia develop a significant degree of paranoia; that is, generalized suspiciousness or specific delusions of persecution. Mood swings, anxiety , and irritability or anger are also frequent occurrences, particularly when patients with dementia are in situations that force them to recognize the extent of their impairment.
Dementia is marked by a gradual decline of thought and other mental activities. The onset may be slow, occurring over months or years. The slow progression of dementia is in contrast with delirium, which involves some of the same symptoms, but has a very rapid onset and fluctuating course with alteration in the level of consciousness. However, delirium may occur along with dementia, especially since the person with dementia is more susceptible to the delirium-inducing effects of many types of drugs.
The following signs and symptoms are used to differentiate among the various types of dementia during a diagnostic evaluation:
- Alzheimer's disease: Dementia related to AD often progresses slowly; it may be accompanied by irritability, wide mood swings, and personality changes in the early stage. Many patients, however, retain their normal degree of sociability in the early stages of AD. In second-stage AD, the patient typically gets lost easily, is completely disoriented with regard to time and space, and may become angry, uncooperative, or aggressive. Patients in second-stage AD are at high risk for falls and other accidents. In final-stage AD, the patient is completely bedridden, has lost control over bowel and bladder functions, and may be unable to swallow or eat. The risk of seizures increases as the patient progresses from early to end-stage AD. Death usually results from an infection or from malnutrition.
- Multi-infarct dementia. In MID, the symptoms are more likely to occur after age 70. In the early stages, the patient retains his or her personality more fully than a patient with AD. Another distinctive feature of this type of dementia is that it often progresses in a stepwise fashion; that is, the patient shows rapid changes in functioning, then remains at a plateau for a while rather than showing a continuous decline. The symptoms of MID may also have a “patchy” quality; that is, some of the patient's mental functions may be severely affected while others are relatively undamaged. Other symptoms of MID include exaggerated reflexes, an abnormal gait (manner of walking), loss of bladder or bowel control, and inappropriate laughing or crying.
- Dementia with Lewy bodies. This type of dementia may combine some features of AD, such as severe memory loss and confusion, with certain symptoms associated with Parkinson's disease, including stiff muscles, a shuffling gait, and trembling or shaking of the hands. Visual hallucinations may be one of the first symptoms of dementia with Lewy bodies.
- Frontal lobe dementias. The frontal lobe dementias are gradual in onset. Pick's dementia is most likely to develop in persons between 40 and 60, while FLD typically begins before the age of 65. The first symptoms of the frontal lobe dementias often include socially inappropriate behavior (rude remarks, sexual acting-out, disregard of personal hygiene, etc.). Patients are also often obsessed with eating and may put non-food items in their mouths or make frequent sucking or smacking noises. In the later stages of frontal lobe dementia or Pick's disease, the patient may develop muscle weakness, twitching, and delusions or hallucinations.
- Creutzfeldt-Jakob disease. The dementia associated with Creutzfeldt-Jakob disease occurs most often in persons between 40 and 60. It is typically preceded by a period of several weeks in which the patient complains Page 971 | Top of Articleof unusual fatigue, anxiety, loss of appetite, or difficulty concentrating. This type of dementia also usually progresses much more rapidly than other dementias, resulting in the death of the affected person within a few months to one year.
In some cases, a patient's primary physician may be able to make a clinical diagnosis of the dementia; in many instances, however, the patient will be referred to a neurologist or a gerontologist (specialist in medical care of the elderly). The differential diagnosis of dementia is complicated because of the number of possible causes; because more than one cause may be present at the same time; and because dementia can coexist with such other conditions as depression and delirium. As of 2012, an autopsy or postmortem brain biopsy is the only way to make a definitive diagnosis of AD.
Delirium is a temporary disturbance of consciousness marked by confusion, restlessness, inability to focus one's attention, hallucinations, or delusions. In elderly people, delirium is frequently a side effect of surgery, medications, infectious illnesses, or dehydration . Delirium can be distinguished from dementia by the fact that delirium usually comes on fairly suddenly (in a few hours or days) and may vary in severity; it is often worse at night. Dementia develops much more slowly, over a period of months or years, and the patient's symptoms are relatively stable. It is possible for a person to have delirium and dementia at the same time.
Dementia may be suspected by the health care professional if memory deficits are exhibited during an examination or assessment. Information from the family members, friends, and caregivers may point to dementia as well. Diagnosis begins with a thorough physical exam and complete medical history, including the length of time the patient has been having the symptoms; six months is the usual length of time required for a tentative diagnosis of dementia.
A family history of either Alzheimer's disease or cerebrovascular disease may provide clues to the cause of the patient's symptoms. If dementia is suspected, a complete review of medications and an assessment for chronic disease processes are indicated. If the patient shows no improvement after eliminating unnecessary medications and treating the chronic disease, then other tests are warranted.
A physical examination and a variety of laboratory tests may rule out potentially treatable causes of dementia. These may include hearing or visual deficits, hypothyroidism, vitamin B 12 deficiency, and depression.
A neurological examination includes an evaluation of the patient's cranial nerves and reflexes . The cranial nerves govern the ability to speak as well as sight, hearing, taste , and smell . The patient will be asked to stick out her tongue, follow the examiner's finger with her eyes, raise her eyebrows, etc. The patient is also asked to perform certain actions (e.g., touching the nose with the eyes closed) that test coordination and spatial orientation. The doctor will usually touch or tap certain areas of the body, such as the knee or the sole of the foot, to test the patient's reflexes. Failure to respond to the touch or tap may indicate damage to certain parts of the brain.
A mental status examination (MSE) evaluates the patient's ability to communicate, follow instructions, recall information, and perform simple tasks involving movement and coordination. The MSE also gives information about the patient's emotional state and general sense of space and time. The MSE includes the doctor's informal evaluation of the patient's appearance, vocal tone, facial expressions, posture, and gait as well as formal questions or instructions. A common form that has been used since 1975 is the so-called Folstein Mini-Mental Status Examination, or MMSE. Questions that are relevant to diagnosing dementia include asking the patient to count backward from 100 by 7s, to make change, to name the current president of the United States (in Canada, the current prime minister), to repeat a short phrase after the examiner (e.g., “no ifs, ands, or buts”); to draw a clock face or geometric figure, and to follow a set of instructions involving movement (e.g., “Show me how to throw a ball” or “Fold this piece of paper and place it under the lamp on the bookshelf.”) The examiner may test the patient's abstract reasoning ability by asking him or her to explain a familiar proverb (e.g., “People who live in glass houses shouldn't throw stones”) or test the patient's judgment by asking about a problem with a commonsense solution, such as what one does when a prescription runs out.
Some of the laboratory tests that might be performed include a complete blood cell count and urinalysis to rule out infection; serum electrolytes, glucose and calcium levels; and kidney and liver function tests . A lumbar puncture (spinal tap) may be done to rule out neurosyphilis.
The use of computed tomography (CT) or magnetic resonance imaging (MRI) to rule out vascular disease is somewhat controversial, since even if a cause is discovered, less than 11% of patients with cognitive decline can partially or fully reverse the effects of the disease. As of 2012, however, both single-photon emission computed tomography (SPECT) and positron emission tomography (PET) Page 972 | Top of Articleare being used to assist in the differential diagnosis of dementia.
The primary goals of treatment for progressive dementia are to preserve as much functioning and independence as possible, and to maintain quality of life as long as possible. It is important that the patient and caregivers are aware that caring for a person with dementia can be difficult, complex, and often last for years. The patient must learn to cope with functional and cognitive limitations, while family members or other caregivers may need to assume increasing responsibility for the person's physical needs. The patient and family should be educated early on in the disease progression to help them anticipate and plan for inevitable changes.
Treatment of dementia starts with treatment of the underlying disease, where possible.
Reversible and responsive dementias
Some types of dementia are reversible, and a few types respond to specific treatments related to their causes. Dementia related to dietary deficiencies or metabolic disorders is treated with the appropriate vitamins or thyroid medication. Dementia related to HIV infection often responds well to zidovudine (Retrovir), a drug given to prevent the AIDS virus from replicating. Multi-infarct dementia is usually treated by controlling the patient's blood pressure and/or diabetes; while treatments for these disorders cannot undo damage already caused to brain tissue, they can slow the progress of the dementia. Such neuroprotective drugs as nimodipine, propentofylline, and posatirelin are currently under study as possible treatments for vascular dementia. Patients with alcohol-related dementia often improve over the long term if they are able to stop drinking. Dementias related to head injuries, hydrocephalus , and tumors are treated by surgery.
As of 2012, there are no medications or surgical techniques that can cure AD, the frontal lobe dementias, MID, or dementia with Lewy bodies. There are also no “magic bullets” that can slow or stop the progression of these dementias. Early intervention may allow the patient to compensate for the alterations in functioning, help to minimize complications, and have an improved quality of life. It may also allow the patient and family to plan for the future and to identify resources for the patient's care.
Behavioral approaches may be used to reduce the frequency or severity of problem behaviors such as aggression or socially inappropriate conduct. Problem behavior may be a reaction to frustration or over-stimulation. Understanding and modifying the situations that trigger it can be effective; strategies may include breaking down such complex tasks as dressing or feeding into simpler steps, or reducing the amount of activity in the environment to avoid confusion and agitation. Such pleasurable activities as crafts, games, and music can provide therapeutic stimulation and improve mood.
Modifying the environment can increase safety and comfort while decreasing agitation. Home modifications for safety include removal or lock-up of hazards such as sharp knives, dangerous chemicals, and tools. Childproof latches may be used to limit access as well. Bed rails and bathroom safety rails can be important safety measures. Confusion may be reduced with the use of simpler decorative schemes and the presence of familiar objects. Covering or disguising doors may reduce the tendency to wander. Positioning the bed in view of the bathroom can decrease incontinence.
Long-term institutional care may be required for the person with dementia, as profound cognitive losses often precede death by a number of years. Early planning for the financial burden of nursing home care is critical. Useful information about financial planning for long-term care is available through the Alzheimer's Association.
Periodically, new drugs are studied for the treatment of dementia. There are five medications approved by the Food and Drug Administration (FDA) as of 2012 to slow cognitive deterioration in AD. Four of these medications—donepezil (Aricept), galantamine (Razadyne), tacrine (Cognex), and rivastigmine (Exelon)—are cholinesterase inhibitors, which increase levels of acetylcholine in the brain, and these medications are effective in some people who have mild or moderate AD. Acetylcholine is a neurotransmitter (nerve signaling molecule) that facilitates communication among neurons . These drugs may provide temporary improvement in cognitive functioning for about 40% of patients with mild-to-moderate AD. Another type of drug is the NMDA receptor antagonist memantine (Axura, Namenda), which may help stabilize memory in people with moderate to severe AD.
Drug therapy for dementia can be complicated by the patient's forgetfulness, especially if the drug must be taken several times a day. Guidelines published in 2008 by the American College of Physicians and the American Academy of Family Practice indicate that there is no evidence at present to recommend one of the drugs listed Page 973 | Top of Articleabove over the others in treating dementia. In general, medications should be administered very cautiously to demented patients in the lowest possible effective doses to minimize side effects. Supervision of the patient taking medications is generally required.
Although a few studies have suggested that estrogen replacement therapy may lower the risk of dementia in women, other studies have found that estrogen treatments do not either prevent dementia or improve cognitive function in women over 65.
Psychotic symptoms, including paranoia, delusions, and hallucinations, may be treated with such antipsychotic drugs as haloperidol, chlorpromazine, risperidone, and clozapine. The side effects of these drugs can be significant, however. Such antianxiety drugs as Valium may improve behavioral symptoms, especially agitation and anxiety, although BuSpar has fewer side effects. The anticonvulsant carbamazepine is also sometimes prescribed for agitation.
It is important to evaluate and treat elderly patients for depression, because the symptoms of depression in older people often mimic dementia. This condition is sometimes called pseudodementia. In addition, patients who have both depression and dementia often show some improvement in intellectual functioning when the depression is treated. The medications most often used for depression related to dementia are the selective serotonin reuptake inhibitors (SSRIs) paroxetine and sertraline. The patient's mental status examination should be repeated after 6 to 12 weeks of antidepressant medication.
There are a number of different alternative and complementary approaches to the treatment of dementia.
NUTRITIONAL SUPPLEMENTS. Some nutritional supplements may be helpful, especially if the dementia is caused by deficiency of these essential nutrients:
- Acetyl-L-carnitine: improves brain function and increases attention span, enhances ability to concentrate and increases energy in patients with Alzheimer's disease.
- Antioxidants (vitamin E, vitamin C, beta-carotene, or selenium): may slow disease progression by preventing the damaging effects of free radicals. An 18-year-long study of more than 4,000 persons reported in 2007 that people who take 50 mg a day of beta-carotene for at least 15 years are less likely to develop dementia than those who do not take the dietary supplement.
- B-complex vitamins and vitamin B12: may significantly improve mental function in patients who have low levels of these essential nutrients.
- Coenzyme Q10: helps deliver more oxygen to the brain.
- DHEA: may increase brain function in the elderly.
- Magnesium: may be helpful if the dementia is caused by magnesium deficiency and/or accumulation of aluminum in the brain.
- Phosphotidylserine: deficiency may decrease mental function and cause depression.
- Zinc: may boost short-term memory and increase attention span.
HERBAL TREATMENTS. Herbal remedies that may be helpful in treating dementia include Chinese or Korean ginseng, Siberian ginseng, gotu kola, and ginkgo biloba. Of these, ginkgo biloba is the best-known and most widely accepted by Western medicine. Ginkgo extract, derived from the leaves of the Ginkgo biloba tree, interferes with a circulatory protein called platelet-activating factor. It also increases circulation and oxygenation to the brain. Ginkgo extract has been used for many years in China and is widely prescribed in Europe for treatment of circulatory problems. Some scientists believe that, taken early enough in the process, Ginkgo biloba can delay the onset of Alzheimer's, but this claim is still under investigation as of 2012. A traditional Chinese herb, ba wei di huang wan, is useful in helping slow cognitive and physical decline in people with dementia, according to the American Geriatrics Society.
HOMEOPATHY. A homeopathic practitioner may prescribe patient-specific homeopathic remedies to alleviate symptoms of dementia.
AROMATHERAPY. Aromatherapists use essential oils as inhalants or in baths to improve mental performance and to calm the nerves.
CHELATION THERAPY. This controversial treatment may provide symptomatic improvement in some patients. However, its effectiveness has not been supported by clinical studies. In addition, this form of therapy may cause kidney damage. Therefore, it should only be given under the watchful eyes of a qualified physician.
OTHER ALTERNATIVE THERAPIES. A Canadian study reported in 2008 that such relaxation techniques as music and massage therapy can decrease agitation and improve the quality of life in persons with dementia. The study showed that playing favorite music to patients and giving them a massage by hand, used individually or together, significantly reduced agitation in people with mild to moderate dementia in a nursing home setting.
The prognosis for dementia depends on the underlying disease. The prognosis for reversible dementia related to nutritional or thyroid problems is usually good once the cause has been identified and treated. The prognoses for dementias related to alcoholism or HIV infection depend on the patient's age and the severity of the underlying disorder.
The prognosis for the irreversible dementias is gradual deterioration of the patient's functioning ending in death. The length of time varies somewhat. Patients with AD may live from two to 20 years with the disease, Page 975 | Top of Articlewith an average of seven years of life after diagnosis. The five-year survival rate for patients with vascular dementia is 39%. Patients with frontal lobe dementia or Pick's disease live on average between five and 10 years after diagnosis. The course of Creutzfeldt-Jakob disease is much more rapid, with patients living between five and 12 months after diagnosis.
Health care team roles
Any member of the health care team may work with patients with dementia. A neurologist or gerontologist normally makes the diagnosis. Laboratory technicians may obtain laboratory tests, and radiology technicians may perform imaging studies, if ordered. Nurses assess patients and how dementia affects their functioning. Patient education is very important in managing dementia and is a nursing responsibility.
Members of the health care team may also be consulted by the patient's caregivers about referrals to social service agencies or support groups. Family members or others caring for a person with dementia are often subject to extreme emotional and physical stress , and may develop feelings of anger, resentment, guilt, and hopelessness, in addition to the sorrow they feel for their loved one and for themselves. Depression is an extremely common consequence of being a full-time caregiver for a person with dementia.
There is no known way to completely prevent AD, although several drugs under investigation may reduce its risk or slow its progression. According to the National Institute of Neurological Disorders and Stroke (NINDS), people with type 2 diabetes who maintain good control over their blood sugar tend to retain their cognitive abilities better than those with poorly controlled diabetes. In addition, some studies indicate that people who engage in such intellectually stimulating activities as chess, crossword puzzles, interacting socially, and playing a musical instrument significantly lower their risk of developing AD and other forms of dementia. There is also evidence that people with higher levels of education are less likely to develop dementia; the researchers think that education may cause the brain to develop stronger nerve cell networks that can help compensate for the cell damage caused by AD.
Some possible preventive measures under investigation as of 2012 include lowering blood pressure, lowering blood cholesterol and homocysteine levels, getting regular exercise , taking regular doses of ibuprofen, naproxen or other NSAIDs, and controlling inflammation in the body. So far, however, none of these approaches have been definitively proven to lower a person's risk of dementia.
The risk of developing multi-infarct dementia may be lowered by reducing the overall risk for strokes.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th edition, text revision. Washington, DC: American Psychiatric Association, 2000.
Larner, A.J. Dementia in Clinical Practice. New York: Springer, 2012.
Mace, Nancy L., and Peter V. Rabins. The 36-Hour Day: A Family Guide to Caring for People with Alzheimer Disease, Other Dementias, and Memory Loss in Later Life, 4th ed. Baltimore, MD: Johns Hopkins University Press, 2006.
Miller, Mark D., and LalithKumar K. Solai, eds. Geriatric Psychiatry. New York: Oxford University Press, 2013.
Weiner, Myron F., and Anne M. Lipton, eds. Clinical Manual of Alzheimer Disease and Other Dementias. Washington, DC: American Psychiatric Publishing, 2012.
Ballard, C., et al. “Treatment of Dementia with Lewy Bodies and Parkinson's Disease Dementia.” Drugs and Aging 28 (October 1, 2011): 769–777.
Chaston, D. “Between a Rock and a Hard Place: Exploring the Service Needs of Younger People with Dementia.” Contemporary Nurse 38 (October 2011): 130–139.
Hogan, C., and E. Wilkins. “Neurological Complications in HIV.” Clinical Medicine 11 (December 2011): 571–575.
Keating, B., and N. Gaudet. “Quality of Life of Persons with Dementia.” Journal of Nutrition, Health and Aging 16 (May 2012): 454–456.
Kerchner, G.A., et al. “Abhorring the Vacuum: Use of Alzheimer's Disease Medications in Frontotemporal Dementia.” Expert Review of Neurotherapeutics 11 (May 2011): 709–717.
Lyketsos, C.G., et al. “Neuropsychiatric Symptoms in Alzheimer's Disease.” Alzheimer's and Dementia 7 (September 2011): 532–539.
Perry, E., and M.J. Howes. “Medicinal Plants and Dementia Therapy: Herbal Hopes for Brain Aging?” CNS Neuroscience and Therapeutics 17 (December 2011): 683–698.
Sahathevan, R., et al. “Dementia, Stroke, and Vascular Risk Factors; A Review.” International Journal of Stroke 7 (January 2012): 61–73.
Takeda, N., et al. “Pick's Disease.” Advances in Experimental Medicine and Biology 724 (2012): 300–316.
Toney, L.K., et al. “Nuclear Medicine Imaging in Dementia: A Practical Overview for Hospitalists.” Hospital Practice (Minneapolis) 39 (August 2011): 149–160.
Alzheimer's Association. “Key Types of Dementia.” http://www.alz.org/alzheimers_disease_related_diseases.asp (accessed May 5, 2012).
Alzheimer's Association. “What Is Dementia?” http://www.alz.org/alzheimers_disease_what_is_dementia.asp (accessed May 5, 2012).
American Psychiatric Association (APA) DSM-5 Development. “S 04 Major Neurocognitive Disorder.” http://www.dsm5.org/proposedrevision/pages/proposedrevision.aspx?rid=419# (accessed May 6, 2012).
Medscape. “Alzheimer Disease.” http://emedicine.medscape.com/article/1134817-overview (accessed May 6, 2012).
Medscape. “Pick Disease.” http://emedicine.medscape.com/article/1135504-overview (accessed May 6, 2012).
Medscape. “Vascular Dementia.” http://emedicine.medscape.com/article/292105-overview (accessed May 6, 2012).
Merck Manual for Health Care Professionals. “Dementia.” http://www.merckmanuals.com/professional/neurologic_disorders/delirium_and_dementia/dementia.html (accessed May 6, 2012).
National Institute of Neurological Disorders and Stroke (NINDS). “Dementia: Hope through Research.” http://www.ninds.nih.gov/disorders/dementias/detail_dementia.htm (accessed May 5, 2012).
National Institute on Aging (NIA) Alzheimer's Disease and Education Center (ADEAR). “About Alzheimer's Disease: Alzheimer's Basics.” http://www.nia.nih.gov/alzheimers/topics/alzheimers-basics (accessed May 6, 2012).
National Stroke Association. “Vascular Dementia and Stroke.” http://www.stroke.org/site/PageServer?pagename=VA-DEM (accessed May 6, 2012).
Alzheimer's Association, 225 N. Michigan Ave., Fl. 17, Chicago, IL United States 60601-7633, (312) 335-8700, Fax: (866) 699-1246, (800) 272–3900, firstname.lastname@example.org, http://www.alz.org/index.asp
American Academy of Neurology (AAN), 1080 Montreal Avenue, Saint Paul, MN United States 55116, (651) 695-2717, Fax: (651) 695-2791, (800) 879-1960, http://www.aan.com/go/home
American Psychiatric Association (APA), 1000 Wilson Boulevard, Suite 1825, Arlington, VA United States 22209-3901, (703) 907-7300, email@example.com, http://www.psychiatry.org/
National Institute of Neurological Disorders and Stroke (NINDS), P.O. Box 5801, Bethesda, MD United States 20824, (301) 496-5751, (800) 352-9424, http://www.ninds.nih.gov/index.htm
National Institute on Aging (NIA) Alzheimer's Disease and Education Center (ADEAR), Building 31, Room 5C27, 31 Center Drive, MSC 2292, Bethesda, MD United States 20892, (800) 438-4380, firstname.lastname@example.org, http://www.nia.nih.gov/alzheimers
National Stroke Association, 9707 E. Easter Lane, Suite B, Centennial, CO United States 80112, Fax: (303) 649-1328, (800) STROKES (787-6537), Info@stroke.org, http://www.stroke.org/site/PageNavigator/HOME
Deanna M. Swartout-Corbeil, R.N.
Rebecca J. Frey, Ph.D.
Gale Document Number: GALE|CX2760400298