7 - The Role of Physical Exercise as a Rehabilitative Aid for Cognitive Loss in Healthy and Chronically III Older Adults

Editors: Backman, Lars; Hill, Robert D.; Neely, Anna Stigsdotter

Title: Cognitive Rehabilitation in Old Age, 1st Edition

> Table of Contents > Part IV - Rehabilitation Strategies for Cognitive Loss in Age-Related Disease > 11 - Issues in the Clinical Evaluation of Suspected Dementia: Implications for Intervention

Issues in the Clinical Evaluation of Suspected Dementia: Implications for Intervention

Thomas Schenkenberg

Patrick J. Miller

Part IV of this volume addresses rehabilitation strategies for dealing with cognitive loss in age-related disease. In keeping with the long-held tradition of diagnosing before proceeding with treatment, this chapter will focus on the clinical issues involved in the assessment of possible cognitive decline in the elderly patient. For the practicing clinician, the assessment questions are straightforward:

Is this patient experiencing a clinically significant impairment in cognitive functioning?
If so, what is causing this impairment?
What can be done about the cause?

While these clinical questions can be posed in this rather straightforward manner, the process for answering these questions is complicated at every turn. For example, a 75-year-old man who has become somewhat forgetful over the preceding year might be experiencing only a mild decline in memory function that is within expected limits for a person his age. Conversely, his forgetfulness might reflect the presence of a clinical entity such as a meningioma that has a potential for curative surgical intervention or a dementing disorder such as Dementia of the Alzheimer's Type (DAT), which is inevitably progressive despite new medications that have become available in recent years. The practicing clinician must address the range of possibilities in each older adult who presents with possible cognitive decline.

Is This Patient Experiencing a Clinically Significant Cognitive Impairment?

One of the most common issues confronting the clinician is whether the performance seen on examination represents a level of performance that is to be expected for this

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patient at this age. Thus, the clinician must understand the individual patient's cognitive background, the expected changes with increasing age, and the way those changes would present in this patient. It is only by subtracting out the expected changes that occur with increasing age that one can interpret the clinical significance of the examination findings.

Normal Aging and Cognitive Functioning

Older adults are at increased risk of central nervous system (CNS) dysfunction and frequently present in clinical settings with cognitive complaints. Additionally, chronic medical illness and the extensive medication regimens of elderly individuals can compromise their mental status. Since normal age-associated cognitive declines must often be distinguished from changes resulting from pathological causes, an understanding of the changes that can be expected in the brain and in cognitive functioning with advancing age is essential.

Physiological Changes in Brain Structure and Function

With increasing age, deterioration occurs across the various organ systems, including the central nervous system. Neurobiological findings in normal aging clearly indicate anatomical, neurochemical, and electrical changes in the brain and other nervous system structures. Brain weight declines with age in both men and women, averaging losses in peak weight of 7 8% (Kemper, 1984). Cortical atrophy is a frequent finding and tends to be maximal in frontal and temporal association cortex. Specific subcortical areas also show reduction in volume on MRI scans (Scheibel, 1992). This shrinkage in size and weight appears to be due primarily to reduction in neuronal size, rather than to significant decrease in the number of neurons (Terry, DeTeresa, & Hansen, 1987). Decreased interconnections within the older brain are reflected in the reduction of dendritic branching and declines in the neurotransmitter substances acetylcholine, dopamine, and norepinephrine (Scheibel, 1992). Mild decline in brain metabolism is suggested by evidence of reduced regional cerebral blood flow and slowed glucose metabolism in older adults as compared to younger controls (Metter, 1988). Age-related changes in brain wave frequencies and amplitudes have also been consistently reported (Dustman, Shearer, & Emmerson, 1991).

Cognitive Changes Associated with Normal Aging

Given the occurrence of neurobiological changes in the central nervous system with aging, it is not surprising that cognitive changes are frequently observed in neuropsychological studies of normal older adults. The research in this area suggests that there is increase in both interindividual and intraindividual variability with age (Albert, 1994). The intraindividual variability is a reflection of the fact that within a single individual, some functions may change, while others do not. Perhaps more striking is the interindividual variability observed among people as they age. Gerontological research has consistently demonstrated that some older persons show little cognitive, physiological, or functional loss when compared with their younger counterparts, even though the mean level of performance for their age group may have declined. It has

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also been reported that lifestyle factors (e.g., nutrition and exercise) may exaggerate or ameliorate so-called age-related changes (Rosenberg & Miller, 1992; Dustman, Emmerson, & Shearer, 1990). The terms successful and usual aging have been suggested (Rowe & Kahn, 1987) to differentiate persons who demonstrate little or no loss in function ( uccessful aging ) from those with clinically manifest age-related changes ( usual aging )

The study of effects of aging on cognitive abilities is further complicated by methodological difficulties, one of the most important of which concerns subject sampling and generational differences (Albert, 1994). Cross-sectional testing tends to maximize differences between age groups because of factors that confound comparisons of older and younger age groups, such as improved nutrition or increased level of education over successive generations. On the other hand, longitudinal studies may minimize differences due to the loss of at-risk individuals over time. Decreased survival of persons with poor cognitive performance (due to other factors that are correlated with both level of cognitive abilities and longevity) may skew the study toward the remaining subjects, who were supernormal at entry (Morris & McManus, 1991). Yet another potential confound in aging research is the possibility that normal control groups of apparently healthy and intact elderly persons include at least a few subjects who have undetected early or subtle brain disease.

Despite these difficulties, which complicate the interpretation of cognitive test results for the individual elderly person, it is clear from a growing body of research that normal aging is associated with somewhat predictable declines in cognitive function and test performance and that various abilities differ in their stability or rate of decline (Benton & Sivan, 1984). The nature of this aging pattern remains a cause of considerable debate. Some researchers have invoked the concepts of crystallized and fluid intelligence (Horn & Cattell, 1967) to account for the fact that some abilities (primarily verbal skills) hold up with advancing age, while others do not.According to this model, overlearned, well-practiced, and familiar skills, abilities, and knowledge (i.e., crystallized ) are affected little by advancing age. Conversely, activities requiring fluid intelligence (reasoning and problem solving for which familiar solutions are not available) follow a typical pattern of relatively slow decline until the late 50s or early 60s, after which decline proceeds at an increasingly rapid pace. This explanation has been posited by some (e.g., Kaufman, Reynolds, & McLean, 1989) for the finding of greater declines in Performance IQ than Verbal IQ across the life span on the Wechsler Adult Intelligence Scales. Critics of the model have suggested that Verbal-Performance differences are artifactual, reflecting practice effects of different skills or psychomotor slowing rather than neuropsychological declines (Mittenberg, Seidenberg, O'Leary, & DiGiulio, 1989; Storandt, 1990).

Research regarding changes in cognitive abilities with normal aging has produced some general conclusions (American Psychological Association [APA], 1997). There appear to be age-related declines in information-processing speed, several aspects of attention (e.g., vigilance or sustained attention, divided attention, selective attention, ability to switch attention rapidly among stimuli), some aspects of language (especially word finding/naming and rapid generation of word lists), visuospatial abilities, abstraction, and mental flexibility. Memory problems constitute one of the most common complaints of elderly persons (Bolla, Lindgren, Bonaccorsy, & Bleecker, 1991). As in other areas of cognitive activity, different aspects of memory and learning differ

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in how they hold up with advancing age (Cullum & Rosenberg, 1998). Remote memory tends to be stable, as does short-term memory for small amounts of information that are passively retained and reproduced in an untransformed fashion. Similarly, gist memory, or ability to recall the general idea, is relatively unaffected by aging. On the other hand, working memory, which involves simultaneous processing and storing of information, shows steady decline beginning at about age 50 (Albert, 1994). Long-term memory also shows substantial age changes, although the decline is greater for recall than for recognition, and performance generally benefits from cuing.

It is important to note that in general, the cognitive decline associated with normal aging is modest, and changes in mental ability are not invariably present in all older persons across all domains of function. Some elderly individuals may, in fact, perform as well on some measures as individuals several decades younger. For those functions that do decline, the change is generally not severe enough to cause significant impairment in daily occupational or social functioning, as occurs with dementing disorders.

Assessment of Suspected Pathological Cognitive Decline

It is clear from the preceding discussion that results from examinations of intellectual, memory, and other abilities must be interpreted in light of characteristic changes with normal aging, in order to decide whether performance represents the effects of a pathological process. Several additional considerations are also of importance in the clinical evaluation of suspected disease-related decline: (a) determining whether current performance represents a significant change for the individual patient, compared to some previous level of functioning; (b) choosing the most useful and appropriate measures for assessment of current performance and having an awareness of the patient' s strengths and weaknesses; and (c) deciding whether current findings are indicative of clinically significant decline.

Estimating Premorbid Functioning

An estimation of expected or premorbid level of functioning is essential in determining whether performance on current measures for an individual represents a decrement or impairment. For example, a finding of a WAIS-R Full Scale IQ of 100 may suggest differing conclusions in regard to the possibility of acquired brain impairment, depending on whether the patient in question was previously intellectually gifted or average. Various methods for estimating premorbid level have been proposed: (a) historical achievement-based estimates (previous standardized testing, educational/vocational achievement, military service rank, occupation, etc.); (b) estimates based on current ability, as reflected in performance on so-called hold tests, typically tasks involving verbal skills (Blair & Spreen, 1989; McFie, 1975); (c) regression formulas based on demographics (e.g., Barona, Reynolds, & Chastain, 1984) or on combinations of demographic and current performance data (Vanderploeg & Schinka, 1995); and (d) estimates based on best performance or highest level of functioning, whether derived from test scores, other observations, or historical achievement (Lezak, 1995).

There are inherent limitations in each approach. Past indications of level of ability would provide the best and most reliable estimate of premorbid functioning. Unfortunately, in the clinical situation, these data (e.g., previously administered standardized

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tests, placement or aptitude tests, grade point average, relative class placement) are not always readily available, if they exist at all. Even educational and vocational attainment may provide spuriously low premorbid ability estimates, especially among older adults, whose educational and career opportunities may have been limited due to social, financial, or historical factors.

Current ability approaches depend on a measure or measures of cognitive ability that are thought to be relatively resistant to the effects of increasing age and therefore may provide a more valid estimate of previous level of cognitive functioning. Traditionally, these measures have involved vocabulary or other verbal skills and more recently the use of measures, such as the North American Adult Reading Test (Blair & Spreen, 1989), that assess a person's ability to pronounce phonetically irregular words, a skill that implies previous familiarity with the words. These approaches have been criticized as underestimating the premorbid ability of many patients, including those with some types of brain dysfunction, including dementing illnesses (Larrabee, Largen, & Levin, 1985; Stebbins, Wilson, Gilley, Bernard, & Fox, 1990).

Demographic regression approaches involve the use of differentially weighted variables (such as age, sex, race, education, occupation, and geographic region) in estimation formulas. This type of approach has been found to suffer from significant prediction errors, performing essentially at chance levels, due to a tendency to predict scores toward the population mean (Sweet, Moberg, & Tovian, 1990). Approaches that combine demographic data with current ability measures (e.g., Vanderploeg & Schinka, 1995) perform much better.

The best performance approach suffers from a tendency to overestimate premorbid abilities and therefore to overestimate decline, due to its underlying assumption that premorbid performance across multiple premorbid measures is comparable to the best performance on any one current measure (Mortensen, Gade, & Reinisch, 1991). The value of this method also depends on the appropriateness of the data on which estimates of premorbid ability are based and on the skill of the examiner at making what often must be subjective judgments regarding the relative weighting of different pieces of data.

Once the examiner has chosen a comparison standard, the presence or absence of deficit may be assessed by comparing the level of the patient's present cognitive performances with the expected level. A significant discrepancy between expected and observed performance levels suggests a true cognitive deficit. Obtaining significant discrepancies for multiple performance measures may reveal a pattern of deficits.

Measurement of Suspected Clinically Signficant Cognitive Decline

A number of measures are available for the clinical evaluation of suspected cognitive decline. Generally, these can be divided into two assessment domains: neuropsychological measures and measures of functional ability (Kaszniak, 1990). Both provide unique contributions to the evaluation of the older adult. A comprehensive review of the numerous instruments available to the clinician is beyond the scope of this chapter (see Lezak, 1995). Rather, the following section offers a brief description of (a) neuropsychological assessment, (b) assessment of functional abilities, and (c) issues in the assessment of older adults.

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Neuropsychological Assessment

Neuropsychological assessment is frequently employed in clinical settings with older adults for a variety of purposes, including differentiating between age-associated cognitive declines and those related to degenerative neurological disorders, distinguishing between neurological and psychiatric disorders (e.g., dementia vs. depression), and addressing questions about legal or financial competency or ability to live independently.

Approaches to neuropsychological assessment have been divided into two major traditions, one of which relies upon a fixed battery of standard tests and the other of which employs a more flexible, individualized approach. The most popular of the neuropsychological test batteries is the Halstead-Reitan Neuropsychological Battery (HRNB; Reitan & Wolfson, 1985). The HRNB is composed of numerous tests of ability and problem solving that measure psychomotor, visuospatial, and abstract reasoning abilities. Also included in the battery are brief tests of language, motor, and sensory functions. Additionally, the Wechsler Adult Intelligence Scale and the Minnesota Multiphasic Personality Inventory are often included to assess intellectual and personality factors. Five of the tests in the battery (the Category Test, Tactual Performance, Rhythm, Speech Sounds Perception, and Finger Tapping), thought to be most sensitive to central nervous system dysfunction, yield scores that can be compared to cutoff scores to calculate an impairment index that is thought to reflect the severity of brain dysfunction.

Numerous studies have shown strong age effects on tests in the HRNB, with large percentages of normal older adults being classified as brain-damaged (Heaton, Grant, & Matthews, 1986; Schear, 1988). Refined normative data are available for interpreting results for older adults (Heaton, Grant, & Matthews, 1991). A significant practical drawback of the HRNB is that the length of administration (typically 5 hours) and the difficulty level of some of the subtests may make it inappropriate for older adults (Kaszniak, 1990).

Within flexible, individualized approaches to neuropsychological assessment, the choice of particular tests is dependent upon the nature of the assessment questions to be answered, as well as patient factors such as age and physical status (Bigler, 1988; Lezak, 1995). A basic or core battery that assesses the major functions of the individual is administered initially, and decisions regarding further testing are based on these results. Bigler (1988) proposed that, at a minimum, a core battery should include measures of intelligence, motor function, language, visuospatial skills, memory, and sensory abilities. Obviously, a thorough knowledge of neuropsychological assessment devices, relevant research literature, and test result patterns associated with different diagnoses is essential when utilizing a flexible battery. Nevertheless, the flexible approach may be quite suited to the assessment of older adults because of its emphasis on adaptation to the needs of the individual patient.

Assessment of Functional Abilities

Optimal functioning from day to day requires a host of skills or behaviors of varying complexity. Older persons are at risk for functional impairment and associated dependency in activities of daily living (ADLs) and instrumental activities of daily living (IADLs). ADLs include such basic self-care abilities as grooming, dressing, toileting, feeding, and transferring (i.e., moving in and out of bed). IADLs involve activities beyond simple self-care, such as using the telephone, shopping, preparing meals, using transportation, and managing

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personal finances. Impairment in functional abilities frequently results in inability to live independently in the community and in a lower quality of life for older persons and their caregivers.

Many instruments and approaches are available for assessing functional abilities. This process is an essential part of the evaluation of suspected decline in an elderly person. While functional ability level is correlated with cognitive status, extrapolation from findings on cognitive tests to disturbances in activities of daily living should be done with caution. Methods for assessing functional abilities include self-report measures, observational measures, and questionnaires designed to be administered to a caregiver of the patient. Some instruments assess a single area of functional ability (e.g., the Katz ADL Scale; Katz, Ford, & Moskowitz, 1963), while others (e.g., the Multidimensional Functional Assessment Questionnaire; Pfeifer, 1975) assess functional status across a number of categories, such as physical health, mental health, ADLs and IADLs, social functioning, and economic/financial status.

While, for the most part, no one instrument has been shown to be better than others that assess the same domain, there are potential methodological problems associated with the various approaches. For example, accuracy of self-reported estimates of functional ability has been questioned by some researchers. It has been noted that geriatric patients in a medical setting often overestimate their functional ability (Rubenstein, Schairer, Wieland, & Kane, 1984), while affectively impaired older adults may underestimate their own abilities (Kuriansky, Gurland, & Fleiss, 1976). Other research indicates that individual older adults may both under- and overestimate their ability to complete activities of daily living compared to performance-based measures (Sager et al., 1992). Cognitively impaired elderly pose a special challenge to clinicians, since it appears that as levels of cognitive impairment increase, validity of self-report decreases (Sager et al., 1992).

The report-by-other methodology is typically used to supplement and/or verify information obtained via self-report. External validation with other sources of information can be particularly important in the case of cognitively impaired elderly. However, when multiple reports are involved, there is always the issue of whose report is the most accurate. Rubenstein et al. (1984), for example, found that the discrepancy between the functional status of the subject and the rater's report was greater when a spouse responded rather than a child, another relative, or a friend. They also found that nurses and community proxies tended to rate patients as more dysfunctional than more objective indices suggested.

Direct observation of specific behaviors and activities of daily living frequently provides data that are more reliable and valid than those obtained from self-report or other-report approaches. Older adults may be observed in natural settings or in similar, contrived situations. While there are obvious advantages of using direct observations, there are also limitations. Direct observations of ADLs such as bathing and toileting may be intrusive and aversive for many older adults. Furthermore, functional assessment of a patient in an acute state (e.g., a patient transferred from a natural environment to the alien world of the hospital) is often invalid. It is also critical to be aware of which functions are actually required of the patient in daily life. For example, deficits in ability to manage one's finances take on a different meaning depending upon whether the person is in an assisted-living situation or attempting to live independently in the community.

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Issues in the Assessment of Older Adults

Assessment devices designed specifically for older adults are limited, so it is often difficult to find age-appropriate measures for the variables of interest. The literature suggests, however, that the differences between older adults and other age groups are significant enough to require the use of instruments that have been normed or validated with older persons. Issues involving reliability and validity of assessment results obtained with older adults have been thoroughly discussed elsewhere (e.g., Edelstein, Staats, Kalish, & Northrop, 1996; Kaszniak, 1990). It is well known, across all age groups, that failure to consider the psychometric properties of assessment instruments and methods can lead to inaccurate assessment results. Thus, when tests are used with older adult patients that have not been studied in terms of reliability, validity, and normative data for older subjects, the possibility of measurement errors and interpretation errors should be mentioned in reports on results of these tests.

Often the most important factor in examining older persons is their cooperation. Older adults, especially those with limited formal education, are often less familiar with testing than younger adults and may be more cautious in responding or may view testing as a nuisance or invasion of privacy. The testing situation may be particularly aversive to a patient who is not feeling well or is already concerned about diminishing cognitive ability. Familiarizing the older adult with the purpose and procedures of testing is essential to obtaining optimal performance and may require more time than with younger people. Since older adults fatigue more easily, it may be necessary to adjust testing time with frequent breaks and/or multiple testing sessions. In the case of a patient who is ill or convalescing, the examiner needs to be especially alert to signs of fatigue and sensitive to effects of pain, discomfort, or current medications on performance.

Determining Clinical Significance of Decline

After the clinician has selected measures appropriate to the assessment question, determined a reasonable comparison standard, and obtained performance results suggestive of deficit(s), the question of whether the findings are clinically meaningful in regard to this individual must be considered. This question is complicated by evidence of a significant rate of false positive neuropsychological results among even healthy, well-screened older adults when cutoff scores are used to identify a performance as impaired. Palmer, Boone, Lesser, and Wohl (1998), for example, administering a flexible battery of tests to a group of neurologically healthy older subjects, found that 37% earned at least one impaired-range score (at least 2.0 standard deviations below the mean) and 20% earned at least two impaired-range scores on separate tests. Such findings illustrate the problems in interpreting isolated abnormal scores and underline the importance of gathering additional data regarding an individual's level of functioning.

Even clear evidence of decrease in cognitive function may not be indicative of functional impairment. In a study of a large, community-based, representative sample of nondemented elderly (Corey-Bloom et al., 1996), subjects 85 years of age and older were compared with others aged 65 84 on measures of cognitive and functional status. The individuals older than 84 performed significantly worse on 13 of 27 cognitive measures than the subjects 84 and younger. Poorer performance of the oldest of the

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older subjects was observed predominantly on verbal and nonverbal memory, psycho-motor/executive tasks, and category verbal fluency. However, while cognitive decline appeared to be associated with advancing age, there were no differences in functional ability between the two groups.

Clearly, the judgment regarding the presence of significant decline in the individual elderly patient can be a complicated one for the clinician. Growing numbers of patients who have cognitive changes but who are not demented are presenting for clinical evaluation (Devanand, Folz, Gorlyn, Moeller, & Stern, 1997; Graham et al., 1997). In this context, it has become increasingly apparent that the thorough assessment of the older adult requires consideration of the intimate interplay of physical, psychological, and environmental variables.

If This Patient Is Displaying a Clinically Significant Cognitive Impairment, What Is Causing This Impairment?

As noted above, many factors can contribute to impaired efficiency in cognitive tasks both in day-to-day life and in terms of formal test performance. It is the clinician's responsibility to sort through these possibilities in a systematic fashion with the initial, primary objective being to identify, if possible, the underlying cause or causes of this inefficiency.

The standard definitions of dementia according to such formulations as the International Classification of Disease (World Health Organization, 1992) and the Diagnostic and Statistical Manual (DSM) (APA, 1994) reinforce the necessity of pursuing various possible causes of the cognitive impairment. The process is one of systematically ruling in or ruling out various possibilities on the basis of the history, the nature, and the progression of the impairment and the results of various examinations and special diagnostic procedures. Several authors have provided algorithms reflecting the logical process by which the clinician sorts through the differential possibilities (Corey-Bloom et al., 1995; Geldmacher & Whitehouse, 1996; U.S. Department of Veterans Affairs [VA], 1997).

The underlying clinical purpose of this differential diagnostic process is, when possible, to isolate an etiology that would lead to a specific treatment regimen. While some individuals seem to assume that the underlying causes of cognitive inefficiencies in older adults are always permanent, progressive dementing disorders such as DAT, this is certainly not the case, and this notion represents a dangerous assumption. Indeed, some of the etiologies for cognitive impairment actually constitute disorders that are not truly dementing disorders at all but represent other important causes that must be addressed in lieu of such disorders. Some of the etiologies in both categories (i.e., true dementing disorders and other types of causes) are not only directly treatable, but are also reversible (e.g., Corey-Bloom et al., 1995; Devinsky, 1992). Clarfield (1988) reviewed a series of studies dealing with causes of dementia and concluded that 13.2% of 2,889 patients were determined to have potentially reversible causes of apparent dementia. It is also important to point out, of course, that combinations of etiological factors must always be considered.

Before addressing what could be considered true dementing disorders, we will briefly discuss some of the other etiologies for cognitive inefficiencies in older adults

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that can give a false impression that the individual is suffering from an actual dementia.

Sensory Changes and General Physical Health

Declines in visual and auditory acuity in the elderly are well-known phenomena (Storandt & VandenBos, 1994). Such changes can result in apparent, but not actual, cognitive impairment both in daily life and on formal testing. For example, hearing impairment is estimated to be present in 32% of individuals over 65 (Adams & Benson, 1992). A variety of changes in the visual system have been noted (Storandt & VandenBos, 1994). Such potentially confounding sensory variables must be considered when assessing the cognitive status of the elderly patient.

Further, decline in general physical health may contribute to poor cognitive test performance without a true underlying dementing disorder being present (Storandt & VandenBos, 1994). More than 80% of people over age 65 have at least one chronic condition, and many have more than one (Adams & Benson, 1992); arthritis, for example, being present in 48% of the sample of individuals 65 and older. Limitations in motor speed, increased fatigue, and discomfort can all play a part in poor test performance without the presence of a true underlying dementing disorder.

Psychiatric Conditions

Psychiatric disorders such as depression and anxiety are well-known causes of cognitive inefficiencies, including poor memory performance (Bajulaiye & Alexopoulous, 1994; Fleming, Adams, & Petersen, 1995; Storandt & Vandenbos, 1994). Depression was found to be the cause of intellectual dysfunction in 26% of patients suspected of having a dementing disorder in a series of studies reviewed by Clarfield (1988). Indeed, the very fear associated with the possibility of DAT has reportedly caused elderly individuals to perform poorly on standardized tests (Centofanti, 1998).

Delirium and Drug Toxicity

Delirium, also known as acute confusional state, is a common cause of cognitive impairment in the elderly (U.S. Department of Veterans Affairs, 1997). In this syndrome, the patient shows disturbance of consciousness and disturbances in cognition characterized by reduced attention and concentration, failure to register new information, and failure in tasks that require sustained attention (APA, 1994). One cannot address the question of an underlying dementia while the patient is experiencing a delirium. Further complicating matters is the fact that the patient with a true underlying dementia is also particularly vulnerable to delirium (Besidine, Dicks, & Rowe, 1992)

Delirium can be caused by a number of factors, such as febrile illness, metabolic abnormalities such as hyponatremia or hypoxemia secondary to cardiac or pulmonary disease, or medication effects. Larson, Reifler, Sumi, Canfield, and Chinn (1986) found that 5% of 200 elderly outpatients with suspected dementia had metabolic conditions that produced or contributed to their cognitive dysfunction. Metabolic conditions accounted for the cause of apparent dementia in data reviewed by Clarfield (1988)

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in a subset of 1,051 patients. In one series, drug toxicity was responsible for cognitive changes in approximately 10% of patients thought to have dementia (Larson et al., 1986), and in another series, drugs were the etiological factor in 28% of the patients (Clarfield, 1988). The fact that many elderly individuals are taking large numbers of medications that might not be coordinated through one clinician adds to the likelihood that polypharmacy plays a role in what appears to be a developing cognitive decline. Again, many of these medication-related effects are reversible.

True Dementing Disorders

Having ruled out age effect alone, sensory limitations, psychiatric disorders, delirium, and the various other factors mentioned above as being sufficient explanations for what appears to be a clinically significant cognitive decline of sufficient severity to interfere with occupational and/or social functioning, the clinician must address a very long list of possible organic/physiological causes of the dementia. The list of causal entities has well over 50 categories of diseases/conditions, and from a historical perspective, this list continues to expand. For example, AIDS-related dementia and mental status changes associated with multiple sclerosis have been added to the list in recent years.

The differential diagnostic process involved in identifying the dementing disorder is typically the domain of the neurologist, geriatrician, or other medical practitioner. However, it is essential that behaviorally oriented health care providers understand the importance of pursuing the underlying biological/physiological cause of the dementia while also developing strategies to assist the patient in achieving maximum function. It should be emphasized again that there are many treatable and some reversible causes of true dementia, and virtually all of the causes are at least partially treatable if only in a palliative or collateral manner.

This diagnostic process involves careful analysis of the history, the presentation of the course of the dementia, the examination of the patient, and the results of various tests. The range of the tests that might be ordered extends from broad surveys of underlying factors such as blood studies and urinalysis to neuroimaging techniques, to very focused, invasive procedures such as brain biopsy. Again, the clinician is pursuing the possibility of a treatable or reversible cause of the dementia, such as thyroid disease, fungal infections, vitamin deficiencies, and structural lesions such as tumors, subdural hematomas, and hydrocephalus (Corey-Bloom et al., 1995).

DAT is a diagnosis by exclusion at this point, following the determination of a generalized progressive dementia with other more specific causes of dementia having been ruled out. This diagnosis by exclusion leads to a diagnosis of DAT in approximately 50% of cases. However, it is important to point out that in studies in which neuropathological confirmation was available (demonstrating the various pathological findings in brain tissue at autopsy, such as cortical Lewy bodies, abundant plaques, and neurofibrillary tangles), the accuracy rate of the diagnosis of DAT in life is only 80 90% (Corey-Bloom et al., 1995; Galasko et al, 1994; Mendez, Mastri, Sung, Zander, & Frey, 1991). In the future, DAT might be confirmed in life through various biological markers, which might also be used to identify individuals at risk for later development of DAT (Mayeux et al., 1992; Post et al., 1997; Saunders, Strittmatter, & Schmechel, 1976).

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Vascular dementia affects about 5 10% of patients with dementia (Corey-Bloom et al., 1995). Symptoms appear as the patient has recurrent strokes in various locations throughout the brain. In this category the patient will frequently show focal or lateralizing signs on examination and on neuroimaging techniques and will also present with a stair-step progression of decline rather than the continuous decline seen in DAT. The accuracy of the diagnosis of vascular dementia in life varies considerably from 25% to 85% (Erkinjuntti, Haltia, Palo, Sulkava, & Paetau, 1988; Molsa, Paljarvi, Rinne, & Sako, 1985; Wade et al., 1987).

The coexistence of DAT and vascular dementia occurs in roughly 10% of patients, and this coexistence represents a significant challenge to the clinician as he or she attempts to determine whether one entity or both are contributing to the dementing process.

Several dementing disorders are neurological conditions in their own right, dementia being only one symptom of the disease process. Parkinson's disease represents an example of such a syndrome. Dementia is evident in approximately 50% of patients with Parkinson's (Mayeux et al., 1992).

Causes that have genetic implications, such as Huntington's disease (which typically presents in younger individuals), are important to identify not only in the process of ruling out other etiologies but also because of the implications for genetic counseling. Further, causes that are transmissible from human to human, such as Creutzfeldt-Jakob disease (CJD), must be identified to address risk to other patients and clinicians as well as the risks associated with organ donation and even the use of human brain tissue in the development of such processes as the production of human growth hormone (Fradkin et al., 1991; Geldmacher & Whitehouse, 1996; Leiderman, Decker, Borcich, & Choi, 1986; Tinter et al., 1986).

It should be noted that no matter how confident the clinician is in the diagnosis, there are demonstrable error rates in diagnosis even in carefully controlled studies (Corey-Bloom et al., 1995). Combinations of various factors must always be considered. These include multiple dementing disorders in the same patient, a dementing disorder and other chronic or acute medical problems, and a dementing disorder and another factor such as depression.

What Can Be Done About the Cause of the Cognitive Impairment?

It is clear that the clinician is confronted with a complicated task when evaluating a patient with suspected dementia. Once having ruled out age effects alone, the clinician addresses other causes of apparent dementia. If these have been ruled out, the clinician (while always being concerned about combinations of causes) addresses the etiological possibilities of a true dementing disorder.

Assuming that delirium and drug-related causes have been addressed, one is left with disorders that have as a primary element, or as one element in the syndrome, a true dementia. Having identified the cause(s), the clinician can embark on a course of intervention that is tied to the causal entity. This relationship can range from a direct treatment of the underlying cause to a palliative, indirect approach.

Treatable and reversible causes of dementia such as thyroid disease, certain infections,

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vitamin deficiencies, and certain structural lesions respond to direct medical or surgical treatment. The effect on the cognitive impairment can be total reversibility in some cases (U.S. Department of Veterans Affairs, 1997).

Medical treatments for DAT have traditionally been palliative in nature, attempting to treat anxiety and acting out. However, recent attempts have been made, with some success, to treat the condition more directly through pharmacological intervention based on the demonstrated central cholinergic hypofunction seen in DAT patients (Cummings et al., 1998; Morris et al., 1998). These efforts attempt to augment central cholinergic function through acetylcholine (ACh) precursors, ACh release facilitators, cholinergic receptor agonists, and, more recently, reversible inhibitors of the ACh degradative enzyme acetylcholinesterase. Efforts in this arena appear promising.

Vascular dementia can be addressed by attempting to decrease the likelihood of further infarction through the treatment of underlying hypertension and vascular disease through medication regimens, diet/exercise regimens, and/or surgical intervention such as carotid endarterectomy.

Conditions such as Parkinson's disease have, for several decades, had medication regimens guided by an understanding of the underlying biochemical process. These approaches, which address the underlying depletion of neurotransmitters such as dopamine, have contributed to the functional status of the patient but do not directly address the dementia per se. Various surgical techniques have also been used in an attempt to improve dopamine status or to interrupt the pathways involved in producing the motor symptoms. Again, the effect of these surgical techniques on the cognitive losses in Parkinson's disease is uncertain.

While direct treatments for such diseases as Huntington's are not yet available, the underlying genetic factors are becoming better understood with each passing decade, and this understanding has led to the possibility of earlier diagnosis and points to a possible eventual treatment that will have a direct scientific link to the underlying genetic causal element. Further, genetic counseling and early diagnosis can appreciably influence the incidence of this disease.

Research on conditions such as Creutzfeldt-Jakob disease (CJD) represent an exciting frontier in molecular biology. As viruses and prions are better understood (Glausiusz, 1998), direct treatments will emerge for what are now considered untreatable illnesses.

Nonetheless, even in conditions such as CJD one can provide comfort care and proper supervision of the declining patient, can treat the behavioral aspects of the condition, and can decrease risk of transmission to others. An accurate initial diagnosis of the cause of the dementia allows the clinician and the patient to design an appropriate response.

Conclusion

It is evident from the discussion above that regardless of the cause of the underlying dementia, there is now only a partial solution in most cases. Thus, there is essential work to be done in assisting the patient to achieve the maximal level of function possible given the patient's unique circumstance. The remaining chapters in Part IV address this aspect of patient care.

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References

Adams, P. R, & Benson, V. (1992). Current estimates from the National Health Interview Survey, 1991 (Vital and Health Statistics, Series 10, No. 184). Hyattsville, MD: National Center for Health Statistics.

Albert, M. L. (1994). Cognition and aging. In W. R. Hazzard, E. L. Bierman, J. P. Blass, W. H. Ettinger, & J. B. Halter (Eds.), Principles of geriatric medicine and gerontology (3rd ed., pp. 1013 1019). New York: McGraw-Hill.

American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.; DSM-YV). Washington, DC: Author.

American Psychological Association. (1997). What practitioners should know about working with older adults. Washington, DC: Author.

Bajulaiye, R., & Alexopoulous, G. S. (1994). Pseudodementia in geriatric depression. In E. Chiu & D. Ames (Eds.), Functional psychiatric disorders of the elderly (pp. 126 141). Melbourne: Cambridge University Press.

Barona, A., Reynolds, C. R., & Chastain, R. (1984). A demographically-based index of premorbid intelligence for the WAIS-R. Journal of Consulting and Clinical Psychology, 52, 885 887.

Benton, A. L., & Sivan, A. B. (1984). Problems and conceptual issues in neuropsychological research in aging and dementia. Journal of Clinical Neuropsychology, 6, 57 64.

Besidine, R. W., Dicks, R., & Rowe, J. W. (1992). Principles of geriatric neurology: Delirium in the elderly. Philadelphia: F. A. Davis.

Bigler, E. D. (1988). Diagnostic clinical neuropsychology. Austin: University of Texas Press.

Blair, J. R., & Spreen, O. (1989). Predicting premorbid IQ: A revision of the National Adult Reading Test. Clinical Neuropsychologist, 3, 129 136.

Bolla, K. I., Lindgren, K. N., Bonaccorsy, C, & Bleecker, M. L. (1991). Memory complaints in older adults. Archives of Neurology, 48, 61 64.

Centofanti, M. (1998, June). Fear of Alzheimer's undermines health of elderly patients. APA Monitor, pp. 1, 33.

Clarfield, A. M. (1988). The reversible dementias: Do they reverse? Annals of Internal Medicine, 109, 476 486.

Corey-Bloom, J., Thai, L. J., Galasko, D., Folstein, M., Drachman, D., & Raskind, M. (1995). Diagnosis and evaluation of dementia. Neurology, 45, 211 218.

Corey-Bloom, J., Wiederholt, W. C, Edelstein, S., Salmon, D. P., Cahn, D., & Barrett-Connor, E. (1996). Cognitive and functional status of the oldest old. Journal of the American Geriatrics Society, 44, 671 674.

Cullum, C. M., & Rosenberg, R. N. (1998). Memory loss When is it Alzheimer's disease? Journal of the American Medical Association, 279(21), 1689 1690.

Cummings, J. L., Cyrus, P. A., Bieber, F., Mas, J., Orazam, J., Gulanski, B., & the Metrifonate Study Group. (1998). Metrifonate treatment of the cognitive deficits of Alzheimer's disease. Neurology, 50, 1214 1221.

Devanand, D. P., Folz, M., Gorlyn, M., Moeller, J. R., & Stern, Y. (1997). Questionable dementia: Clinical course and predictors of outcome. Journal of the American Geriatrics Society, 45, 321 328.

Devinsky, O. (1992). Behavioral neurology. St. Louis: Mosby Year Book.

Dustman, R. E., Emmerson, R. Y., & Shearer, D. E. (1990). Electrophysiology and aging: Slowing, inhibition, and aerobic fitness. In M. L. Howe, M. J. Stones, & C. J. Brainerd (Eds.), Cognitive and behavioral performance factors in atypical aging. New York: Springer-Verlag.

P.221

Dustman, R. E., Shearer, D. E., & Emmerson, R. Y. (1991). Evoked potentials and EEG suggest CNS inhibitory deficits in aging. In D. A. Armstrong (Ed.), The effects of aging and environment on vision. New York: Plenum Press.

Edelstein, B., Staats, N., Kalish, K. D., & Northrop, L. E. (1996). Assessment of older adults. In M. Hersen & V. B. Hasselt (Eds.), Psychological treatment of older adults: An introductory text (pp. 35 68). New York: Plenum Press.

Erkinjuntti, T., Haltia, M., Palo, J., Sulkava, R., & Paetau, A. (1988). Accuracy of the clinical diagnosis of vascular dementia: A prospective clinical and post-mortem pathological study. Journal of Neurology, Neurosurgery and Psychiatry, 51, 1037 1044.

Fleming, D. C, Adams, A. C, & Petersen, R. C. (1995). Dementia: Diagnosis and evaluation. Mayo Clinic Proceedings, 70, 1093 1107.

Fradkin, J. E., Schonberger, L. B., Mills, J. L., Gunn, W. J., Piper, J. M., & Wysowski, D. K. (1991). Creutzfeldt-Jakob disease in pituitary growth hormone recipients in the United States. Journal of the American Medical Association, 265, 880 884.

Galasko, D., Hansen, L. A., Katzman, R., Wiederholt, W., Masliah, E., & Terry, R. (1994). Clinical-neuropathological correlations in Alzheimer's disease and related dementias. Archives of Neurology, 51, 888 895.

Geldmacher, D. S., & Whitehouse, P. J. (1996). Evaluation of dementia. New England Journal of Medicine, 335, 330 336.

Glausiusz, J. (1998, January). Medicine 1997: Case closed. Discovery, pp. 56 57.

Graham, J. E., Rockwood, K., Beattie, B. L., Eastwood, R., Gauthier, S., & Tuokko, H. (1997). Prevalence and severity of cognitive impairment with and without dementia in an elderly population. Lancet, 349, 1793 1796.

Heaton, R. K., Grant, I., & Matthews, C. G. (1986). Differences in neuropsychological test performance associated with age, education, and sex. In I. Grant & K. M. Adams (Eds.), Neuropsychological assessment of neuropsychiatric disorders (pp. 100 120). New York: Oxford University Press.

Heaton, R. K., Grant, L, & Matthews, C. G. (1991). Comprehensive norms for an expanded Halstead-Reitan battery: Demographic corrections, research findings, and clinical applications. Odessa, FL: Psychological Assessment Resources.

Horn, J. L., & Cattell, R. B. (1967). Age differences in fluid and crystallized intelligence. Acta Psychologica, 26, 107 129.

Kaszniak, A. W. (1990). Psychological assessment of the aging individual. In J. E. Birren & K. W. Schaie (Eds.), Handbook of the psychology of aging (pp. 427 445). New York: Academic Press.

Katz, S., Ford, A., & Moskowitz, R. (1963). The index of ADL: A standardized measure of biological and psychosocial function. Journal of the American Medical Association, 185, 914 919.

Kaufman, A. S., Reynolds, C. R., & McLean, J. E. (1989). Age and WAIS-R intelligence in a national sample of adults in the 20 74 age range: A cross-sectional analysis with educational level controlled. Intelligence, 13, 235 253.

Kemper, T. (1984). Neuroanatomical and neuropathological changes in normal aging and in dementia. In M. L. Albert (Ed.), Clinical neurology of aging (pp. 9 52). New York: Oxford University Press.

Kuriansky, J. B., Gurland, B. J., & Fleiss, J. L. (1976). The assessment of self-care capacity in geriatric psychiatric patients by objective and subjective methods. Journal of Clinical Psychology, 32(1), 95 102.

Larrabee, G. J., Largen, J. W., & Levin, H. S. (1985). Sensitivity of age decline resistant ( Hold ) WAIS subtests to Alzheimer's disease. Journal of Clinical and Experimental Neuropsychology, 7, 497 504.

P.222

Larson, E. B., Reifler, B. V., Sumi, S. M., Canfield, C. G., & Chinn, N. M. (1986). Diagnostic tests in the evaluation of dementia: A prospective study of 200 elderly outpatients. Archives of Internal Medicine, 146, 1917 1922.

Leiderman, D. B., Decker, K. P., Borcich, J., & Choi, D. W. (1986). Sporadic Creutzfeldt-Jakob disease in two coworkers. Neurology, 36, 835 837.

Lezak, M. D. (1995). Neuropsychological assessment (3rd ed.). New York: Oxford University Press.

Mayeux, R., Denaro, J., Hemenegildo, N., Marder, K., Tang, M., & Cote, L. J. (1992). A population-based investigation of Parkinson's disease with and without dementia: Relationship to age and gender. Archives of Neurology, 49, 492 497.

Mayeux, R., Stern, Y., & Ottman, R. (1993). The apolipoprotein epsilon4 allelle in patients with Alzheimer's disease. Annals of Neurology, 34, 752 754.

McFie, J. (1975). Assessment of organic intellectual impairment. London: Academic Press.

Mendez, M. F., Mastri, A. R., Sung, J. H., Zander, B. A., & Frey, W. H. (1991). Neuropatho-logically confirmed Alzheimer's disease: Clinical diagnoses in 394 cases. Journal of Geriatric Psychiatry and Neurology, 4, 26 29.

Metter, E. J. (1988). Positron tomography and cerebral blood flow studies. In M. S. Albert & M. B. Moss (Eds.), Geriatric neuropsychology (pp. 228 261). New York: Guilford Press.

Mittenberg, W., Seidenberg, M., O'Leary, D. S., & DiGiulio, D. V. (1989). Changes in cerebral functioning associated with normal aging. Journal of Clinical and Experimental Neuropsychology, 11, 918 932.

Molsa, P. K., Paljarvi, L., Rinne, J. O., Rinne, U. K., & Sako, E. (1985). Validity of clinical diagnosis in dementia: A prospective clinico-pathological study. Journal of Neurology, Neurosurgery and Psychiatry, 48, 1085 1090.

Morris, J. C, Cyrus, P. A., Orazam, J., Mas, J., Bieber, F., & Ruzicka, B. B. (1998). Metrifonate benefits cognitive, behavioral, and global function in patients with Alzheimer's disease. Neurology, 50, 1222 1230.

Morris, J. C, & McManus, D. Q. (1991). The neurology of aging: Normal versus pathologic change. Geriatrics, 46(8), 47 54.

Mortensen, E. L., Gade, A., & Reinisch, J. M. (1991). A critical note on Lezak's best performance method in clinical neuropsychology. Journal of Clinical and Experimental Neuropsychology, 13, 361 371.

Palmer, B. W., Boone, K. B., Lesser, I. M., & Wohl, M. A. (1998). Base rates of impaired neuropsychological test performance among healthy older adults. Archives of Clinical Neuropsychology, 13(6), 503 511.

Pfeifer, E. (Ed.). (1975). Multidimensional functional assessment: The OARS Methodology. Durham, NC: Duke University Center for the Study of Aging and Human Development.

Post, S. G., Whitehouse, P. J., Binstock, R. H., Bird, T. D., Eckert, S. K., & Farrer, L. A. (1997). The clinical introduction of genetic testing for Alzheimer disease: An ethical perspective. Journal of the American Medical Association, 277(10), 832 836.

Reitan, R. M., & Wolfson, D. (1985). The Halstead-Reitan Neuropsychological Test Battery: Theory and clinical interpretation. Tucson, AZ: Neuropsychology Press.

Rosenberg, I. H., & Miller, J. W. (1992). Nutritional factors in physical and cognitive functions of elderly people. American Journal of Clinical Nutrition, 55, 1237 1243

Rowe, J. W., & Kahn, R. (1987). Human aging: Usual versus successful. Science, 237, 143 149.

Rubenstein, L. Z., Schairer, C, Wieland, G. D., & Kane, R. (1984). Systematic biases in functional status assessment of elderly adults: Effects of different data sources. Journal of Gerontology, 39(6), 686 691.

P.223

Sager, M. A., Dunham, N. C, Schwantes, A., Mecum, L., Halverson, K., & Harlowe, D. (1992). Measurement of activities of daily living in hospitalized elderly: A comparison of selfreport and performance-based methods. Journal of the American Geriatrics Society, 40, 457 462.

Saunders, A. A., Strittmatter, W. J., & Schmechel, D. (1976). Association of apolipoprotein E allelle epsilon4 with late-onset familian and sporadic Alzheimer's disease. Neurology, 76, 1467 1472.

Schear, J. M. (1988). Attempt to cross-validate norm-based dysfunction scores in young and older neuropsychiatric patients. Clinical Neuropsychologist, 2, 57 66.

Scheibel, A. B. (1992). Structural changes in the aging brain. In J. E. Birren, R. B. Sloane, & G. Cohen (Eds.), Handbook of mental health and aging (pp. 147 173). New York: Academic Press.

Stebbins, G. T., Wilson, R. S., Gilley, D. W., Bernard, B. A., & Fox, J. H. (1990). Use of the National Adult Reading Test to estimate premorbid IQ in dementia. Clinical Neuropsychologist, 4, 18 24.

Storandt, M. (1990). Longitudinal studies of aging and age-associated dementias. In F. Boiler & J. Grafman (Eds.), Handbook of neuropsychology (Vol. 4). Amsterdam: Elsevier.

Storandt, M., & VandenBos, G. R. (1994). Dementia and depression in older adults. Washington, DC: American Psychological Association.

Sweet, J. J., Moberg, P. J., & Tovian, S. M. (1990). Evaluation of the WAIS-R premorbid IQ formulas in clinical populations. Psychological Assessment, 2, 41 44.

Terry, R. D., DeTeresa, R., & Hansen, L. A. (1987). Neocortical cell counts in normal human adult aging. Annals of Neurology, 21, 530 539.

Tinter, R., Brown, P., Hedley-Whyte, E. T., Rappaport, E. B., Piccardo, C. P., & Gajdusek, D. C. (1986). Neuropathologic verification of Creutzfeldt-Jakob disease in the exhumed American recipient of human pituitary growth hormone: Epidemiologic and pathogenic implications. Neurology, 36, 932 936.

U.S. Department of Veterans Affairs. (1997). Dementia identification and assessment: Guidelines for primary care practitioners (U.S. Department of Veterans Affairs). Washington, DC: U.S. Government Printing Office.

Vanderploeg, R. D., & Schinka, J. A. (1995). Predicting WAIS-R IQ premorbid ability: Combining subtest performance and demographic variable predictors. Archives of Clinical Neuropsychology, 10, 225 239.

Wade, J. P. H., Mirsen, T. R., Hachinski, V. C, Fishman, M., Lau, C, & Merskey, H. (1987). The clinical diagnosis of Alzheimer's disease. Archives of Neurology, 44, 24 29.

World Health Organization (WHO). (1992). The ICD-10 classification of mental and behavioral disorders. Clinical descriptions and diagnostic guidelines. Geneva: World Health Organization.