DEMENTIA

Dementia is a complex and devastating problem that is a major cause of disability in the older adult population. Although the actual prevalence of dementia is unknown, estimates range from 2.5% to 24.6% of those older than 65 years of age, with the number increasing with advanced age. In long-term care facilities, up to 70% of residents have cognitive impairments.^63,64

Although there can be a decline in intellectual function with aging, dementia, sometimes called senility, is not a normal aging process. Dementia is a syndrome of acquired,

persistent impairment in several domains of intellectual function, including memory, language, visuospatial abil­ity, and cognition (i.e., abstraction, calculation, judgment, and problem solving). Mood disturbances and changes in personality and behavior often accompany the intellectual deterioration.⁵⁷

Dementia can result from a wide variety of conditions, including degenerative, vascular, neoplastic, demyelinat-ing, infectious, inflammatory, toxic, metabolic, and psy­chiatric disorders. Up to 70% of older adults with dementia (5 million Americans) are thought to have Alzheimer's dis­ease, a chronic, progressive neurologic disorder of un­known cause.⁶³ Multi-infarct dementia is the second most common disorder, with 10% to 20% of dementias attrib­uted to this vascular disorder in which multiple emboli dis­seminate throughout the brain, causing infarctions.^57,65,⁶⁷

Much work is being done in the diagnosis and treat­ment of dementia, in particular of Alzheimer's disease. Amyloid plaques and neurofibrillary tangles are the hall­marks of the disease pathology. Recent research has iden­tified enzymes called secretases, which are believed to play a role in the formation of the amyloid plaques. Studies are also investigating abnormal tau proteins that form the tan­gles involved in Alzheimer's disease. One of the more re­cent genetic findings was the discovery of apolipoprotein E alleles (apoE2, apoE3, and apoE4) on chromosome 19. Apolipoprotein E is a normal protein that helps transport blood cholesterol. It is thought that apoE2 is protective against Alzheimer's disease, apoE3 (the most common apoE allele found in the general population) plays a neu­tral role, and apoE4 increases the risk for developing late-onset Alzheimer's disease. The precise mechanism in not yet known.^65,66,⁶⁸ Although advancements in research con­tinue, as yet there are no specific diagnostic tests to deter­mine the presence of Alzheimer's disease, and the diagnosis is made by excluding other possible causes of the demen­tia symptoms.

A commonly used measure of cognitive function is the Mini-Mental State Examination (MMSE) developed by Folstein and colleagues in 1975.⁶⁹ This tool provides a brief, objective measure of cognitive functioning and has been widely used. The MMSE, which can be administered in 5 to 10 minutes, consists of a variety of questions that cover memory, orientation, attention, and constructional abilities. The test has been studied and found to fulfill its original goal of providing a brief screening tool that quan­tifies cognitive impairments and documents cognitive changes over time. However, it has been cautioned that this examination should not be used by itself as a diag­nostic tool to identify dementia.

Several medications have become available over the past decade to help halt further cognitive decline in Alzheimer's disease. Emphasis has been on increasing cholinergic synaptic transmission in areas of the brain that are concerned with memory and cognition. Drugs that in­hibit the breakdown of acetylcholine at the synaptic cleft have been developed and have been shown to be effective in slowing the progression of the disease in some persons. At present, four drugs—tacrine, donepezil, rivastigmine, and galantamine—are available in the therapeutic cate-

gory of cognitive-enhancing agents, although tacrine is no longer marketed in the United States. All four medications are acetylcholinesterase inhibitors whose action elevates acetylcholine concentrations in the cerebral cortex by slow­ing degradation of acetylcholine released by still-intact neurons. The magnitude of the cognitive-enhancing effects of tacrine, the first-released drug in this category, have been modest and associated with significant side effects that gen­erally preclude its use. Donepezil has been shown to be a more potent, specific inhibitor of acetylcholinesterase with minimal side effects.⁷⁰ The newer agents, rivastigmine and galantamine, are thought to be more selective in the bind­ing and inactivation of acetylcholinesterase; however, ad­verse reactions, especially gastrointestinal symptoms, can impede therapeutic dosing. Although there still is no cure for dementia, cholinesterase inhibitors are considered ef­ficacious as antidementia drugs on the basis of improve­ments seen on standardized cognitive tests, as well as slower decline in loss of function due to the disease process. Evi­dence suggest that the cognitive-enhancing drugs are also beneficial in individuals with vascular dementia.⁷¹ Anti-glutamatergic treatment is currently under investigation for use in moderate-to-severe Alzheimer's disease. This novel neurochemical approach assumes that overstimulation of the N-methyl-D-aspartate (NMDA) receptor by glutamate is implicated in neurodegenerative disorders. Memantine, an NMDA antagonist, shows promising results—subjects showed less decline in both cognitive and functional abil­ities while on the drug. Memantine has recently been ap­proved by the U.S. Food and Drug Administration (FDA) for general use.⁷²

Among the neuroprotective drugs that are proposed to delay the onset or progression of Alzheimer's disease are extracts of Ginkgo biloba, vitamin E, nonsteroidal anti-inflammatory drugs (NSAIDs), and calcium channel block-ers. Extracts of Ginkgo biloba, derived from the leaf of a subtropical tree, are available in health food stores. The compounds, which supposedly have antioxidant, neuro-trophic, and anti-inflammatory properties, are promoted as a remedy for memory problems in persons with Alzheimer's disease.⁷³ A metaanalysis of five studies that examined the efficacy of the compound on cognition concluded that Ginkgo biloba extract improves cognition slightly.⁷⁴ The pathology of Alzheimer's disease may involve oxidative stress and the accumulation of free radicals, leading to neu-ronal degeneration in the brain. Vitamin E, a fat-soluble vitamin, interacts with cell membranes, traps free radicals, and may interrupt chain reactions that damage cells.⁷⁵ In the past, estrogen was felt to have neuroprotective effects for postmenopausal women. More recently, however, multicenter randomized placebo-controlled trials failed to show any improvement associated with the use of estrogen in women who already have Alzheimer's disease.⁷⁶ As a re­sult, current evidence does not support the use of estrogen in the treatment of Alzheimer's disease.⁷⁷ The NSAIDs are thought to decrease the inflammatory response to inflam­matory mediators released from injured or degenerating nerve cells. Calcium channel blockers prevent calcium in­flux, which is proposed to cause neuronal death due to re­lease of intracellular enzymes. Use of Ginkgo biloba, NSAIDs,

and calcium channel blockers for Alzheimer's disease is generally not advised; however, most clinicians do advo­cate the use of vitamin E.

The term mild cognitive impairment (MCI) has been used to denote cognitive impairment with aging that does not meet criteria for dementia and that is not attributed to any known medical condition. Studies suggest, however, that most of those diagnosed with MCI will go on to de­velop Alzheimer's disease. Treatment approaches are aimed at slowing declining over time and generally include both pharmacologic and behavioral approaches.

Management of older adults with Alzheimer's disease and other dementias usually involves assuming increasing responsibility for and supplying increasing care to indi­viduals as the illness renders them incapable. Impaired judgment and cognition can prevent the older adult from making reasonable decisions and choices and eventually threatens their overall well-being. Family members often assume the monumental task of caring for older adults with dementia until the burden becomes too great, at which time many older adults may be relocated to long-term care facilities.

Some specific behavioral problems commonly are seen in older adults with dementia, including agitation, depression, hallucinations, aggressiveness, and wander­ing. It may be necessary to use low doses of pharmacologic agents such as neuroleptics, antidepressants, and anxi-olytics. Nonpharmacologic interventions can help control behavioral problems and may preclude the need for med­ications. Ensuring that the individual's physical needs, such as hygiene, bowel and bladder elimination, safety, and nutrition, are met can help prevent catastrophic reac­tions. Providing a consistent routine in familiar surround­ings also helps to alleviate stress. Matching the cognitive needs of the older adult by avoiding understimulation and overstimulation assists in preventing behavior problems.

The work of Hall has shown positive results in the care of older adults with Alzheimer's disease.⁷⁷ Hall's concep­tual model, progressively lowered stress threshold (PLST), proposes that the demented individual's ability to tolerate any type of stress progressively declines as the disease ad­vances. Interventions for the older adult with dementia therefore center on eliminating and avoiding stressors as a way to prevent dysfunctional behaviors. These stressors in­clude fatigue, change of routine, excessive demands, over­whelming stimuli, and physical stressors. Hall's work with the PLST model has shown that individuals tend to awaken less at night, use less sedatives and hypnotics, eat better, socialize more, function at a higher level, and experience fewer episodes of anxiety, agitation, and other dysfunc­tional behaviors. Further work has shown that family care-givers trained using the PLST model improved their abilities to provide care to loved ones with dementia and lowered their own stress levels.⁷⁸