InterMtwMlPsychogeriElrrics,Vol.4, Supp. I , 1992 0 1992 Springer Publishing Company
Psychiatric Phenomena in Dementia of the Alzheimer Type Alistair Burns, M.D., M. Phil., M.R.C.P., M.R.C.Psych. Section on Old Age Psychiatry Institute of Psychiatry London, England ABSTRACT. Psychiatricsymptomsand behavioraldisturbancesare of importance in dementia of the Alzheimer type (DAT) but have been relatively neglected by researchers. The main psychiatric symptoms are disorders of thought content (delusions and paranoid ideation), disorders of perception (hallucinationsand misidentifications)and disorders of affect (depressed and elevated mood). They occur commonly in DAT, and there is evidence that they may indicate subtypesof the disorder in view of their demographic,structural, and prognosticcorrelates.Personalitychangesare very common,and thesemay be the earliest manifestation of dementia. Behavioral disturbances tend to be associated with advanced dementia and are particularly disruptive to caregivers. Structuralcorrelatessuggest that somebehaviorsare a direct result of brain damage.Psychiatricand behavioralfeaturesin DAT are important,as they may serve as a model for symptomatology in functionalpsychiatric disorders.
INTRODUCTION Psychiatric phenomena in dementia have been a hitherto neglected area of research, possibly because they were traditionally regarded as secondary to the cognitive deficits, and therefore of secondary importance. Four reasons such phenomena may occur in conjunction with a dementia syndrome have been detailed by Berrios (1989). One, they may be part of an intercurrent confusional state. Two, they may be due to disinhibition of cortical functions, resulting in "released" symptomatology. Three, they may be due to a pathoplastic effect of personality in the clinical expression of the disorder. Finally, and four, two separate mental disorders may coexist, although conventional psychiatric practice rather frowns on such a formulation. The importance of psychiatric symptomatology in dementia of the Alzheimer type (DAT) has been discussed elsewhere (Bums et al., 1990b). These phenomena can be divided into two main groups. The first group comprises 43
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psychiatric symptoms which are generally mentioned in the patient’s complaints and are detected either at mental state testing or obtained through a caregiver’s account of the patient’s speech (e.g., delusions, hallucinations, misidentifications, and depression).The second group includes behavioral disturbances which consist of outward manifestations observable by others (e.g., aggression, wandering, or disinhibition). This division, although convenient in terms of nosology, is not absolute. For example, a hallucinatory experience may be manifest as an aggressive outburst. This paper is an attempt to review psychiatric symptoms, behavioral disturbances, and changes in personality in patients with DAT and to outline some scales which may be of use in their assessment. For further information, the reader is referred to two recent excellent reviews on the subject: Wragg and Jeste (1989) and Cummings and Victoroff (1990).
DELUSIONS Alzheimer’s first case (Alzheimer, 1907)exhibited delusional thinking-jealousy toward her husband, paranoid ideas directed against her doctor, and a belief that she was about to be murdered. Reports of the proportionof DAT patients with delusions vary between 10% (Birkett, 1972) and 73% (Leuchter & Spar, 1985). Studies inevitably vary because of differences in the way in which the delusions and dementia are diagnosed and in the population under study. For example, choosing to study patients referred to a general hospital service may bias the sample toward these symptoms, thus giving a falsely high rate, whereas confining investigations to autopsy-proven cases may provide an unrepresentative sample. A recent study in which this author was involved (Bums et al., 1990b) showed that 16% of patients from a defined catchment area had delusions. The method by which delusions are diagnosed is also of importance-some studies depend on direct interviews with the patients (Cummingset al., 1987)while others depend on reports given by caregivers, either face to face (Burns et al., 1990b) or on the telephone (Kumar et al., 1988). The difficulties of assessing such phenomenology in an illness which is often of several years’ duration and requires retrospective analysis by untrained staff (for example, spouses) have not yet been fully evaluated. However, to confine the gathering of information to an interview with the patient will mean missing a significant proportion of the great array of phenomenology which may be of a transitory nature. Delusions have been associated with early disease (Goodman, 1953), late disease (Sim & Sussman, 1962), and with the middle stage (Drevet & Rubin, 1989). Several different types of delusions have been described. Cummings (1985) suggested four types: simple, complex persecutory, grandiose, and those associated with neuropsychologicaldeficits. Cutting (1987) described simple and grandiose delusions in 17 of 35 patients with acute organic psychoses but could not
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classify the others according to Cummings’s(1985) categories.Burns et al. (1990b) described delusions of theft and suspicion (equivalent to simple persecutory delusions) but also a category of systematized delusions (broadly similar to those patients that Cutting was unable to classify). Patients with systematized delusions had smaller lateral ventricles, and a higher proportion had basal ganglia calcification than patients without such delusions. Other delusions, such as Capgras’ syndrome and the phantom boarder syndrome (Merriam et al., 1988), have also been described. Cummings and Victoroff (1990) outlined four possible explanations for the presence of delusions in DAT: as a logical attempt by patients to understand their environment; as secondary to mood changes; as a coincidental diagnosis; and as secondary to the underlying disease. This last mechanism seems the most tenable, especially as delusions have been described particularly in patients with limbic dysfunction and temporal lobe pathology, both of which are affected in DAT. Some authors have described disorders of thought content which consist of paranoid ideation not held with delusional intensity (Bums et al., 1990b; Reisberg et al., 1987). It is possible that some other authors include these patients as having delusional ideas, even though their phenomenology does not satisfy traditional definitions (Fish, 1985).The exact status of this form of abnormal thinking requires further evaluation.
HALLUCINATIONS Alzheimer’s first case (Alzheimer, 1907) experienced auditory hallucinations as part of her dementia syndrome.Hallucinationshave been described less commonly than delusions in DAT and some authors do not make the fundamentaldistinction between auditory and visual hallucinosis. Early studies vaned widely in their reporting of prevalence rates-Goodman (1953) described visual hallucinationsas occurring in “the majority” of patients, while Sjogren, Sjogren, and Lindgren (1952) found 15% of their patients to be affected. Merriam et al. (1988) found 20% to have experienced hallucinations, but their study did not differentiate between patients in the auditory or visual modalities. The highest rate of hallucinations experienced was reported by Rabins et al. (1982), who found, in interviewing caregivers, that 49% of patients were affected. They did not give separate figures for visual and auditory hallucinosis. Hallucinations in other modalities have been described, including olfactory hallucinations. The obviously confounding variable in the assessment of these phenomena is that the presence of a confusional state can give rise to visual hallucinations, and that these patients will obviously be overrepresentedin samples drawn from acute care settings. By excludingpatients with confusionalepisodes, Burns et al. (1990b) found that visual and auditory hallucinations occurred in 13% and lo%, respectively, of a representative population of patients with DAT. Another significant factor affectingprevalencerates is the method by which the symptoms are assessed.
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For example, Rabins et al. (1982) interviewed relatives about troublesome behaviors, whereas Cummings et al. (1987) confined their definition to patients actively hallucinating during an interview. They found only one patient with auditory hallucinations and none with visual hallucinations was encountered. Relatively little work has been performed in examining the relationship between hallucinations and other features of dementia. There appears to be no difference in cognitive function between patients with and without hallucinations (Berrios & Brook, 1984; Teri et al., 1988; Burns et al. 1990b), but there is evidence that hallucinated patients deteriorate more quickly (Bums et al., 1990b). The etiology of hallucinations in dementia is obscure, and it is impossible to invoke similar mechanisms for their occurrence (unlike for delusions, in which mood congruence or an understandable response to the environment can trigger occurrence). However, the hallucinations may well indicate a concomitant illness (such as acute confusion) or they may be related to underlying neuropathology. Sensory deficits are known to promote hallucinosis in the elderly, and an association was found between these phenomena and eye pathology in the study by Berrios and Brook (1984).
MISIDENTIFICATIONS These have been recently described (Rubin et al., 1988). These authors outlined three types of misidentification: the idea that other people are in the patient’s home; misidentification of the patient’s own mirror image; and misidentification of television (originally described by Berrios & Brook, 1984). Burns et al. (1990b) added a fourth misidentification-that of other people. The exact status of these phenomena is open to debate. For example, the idea that someone else is in the house (phantom boarder syndrome) could equally be classified as a delusion and may, of course, be based on a hallucinatory experience. Misidentifications, in general, may be delusions “based on a specific neurological deficit” (Cummings, 1985). However, their unique character and failure to satisfy other definitions suggest that they deserve a separate category. Rubin et al. (1988) described them in 23% of their sample: an equal proportion (12%) misidentified television images and believed others were in the house, and 7%misidentified their own mirror image. Merriam et al. (1988) found very high rates of these perceptual disturbances (up to 50%) and described 17% as having the Capgras syndrome (which may be based on misidentification of a familiar person). As these phenomena have only recently been described there is comparatively little research regarding their possible etiology. What evidence there is, however, is intriguing. Merriam et al. (1988) reported an association between degree of dementia and the presence of these phenomena. Drevets and Rubin (1989) found that patients with misidentifications have a decreased mortality compared to those without. Other studies (Mayeux et al., 1985) emphasize the increased cognitive decline in patients with psychosis. The diminished mortality in patients with
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misidentification syndromes was replicated by Bums et al. (1990b) who also found that their pmence was associated with a younger age and younger age of onset of disease, possibly indicating some parietal lobe involvement. These findings may suggest a possible subtype of DAT based on the presence or absence of misidentifications.
DEPRESSION Depressive symptomatology in DAT is a common accompaniment to the clinical syndrome, but its presence is harder to assess due to the difficulty of definition. There is no evidence to suggest that depression leads to an increased incidence of primary dementia later in life, although some work has suggested that depression occurring in the ten years before the onset of dementia may be a significant risk factor for dementia (Henderson et al. 1989).This is of importance, as it raises the possibility of noncognitive symptoms as prodromata of dementia. Also, 10% of patients with primary dementia have a past history of depression, which is more than in a control group (Agbayewa, 1986). Depressive symptomatologyin patients with DAT has been well documented by some 20 studies (Bums, 1991).The reported proportion with depressive symptoms varies between 0% and 86% (Knesevich et al., 1983; Memam et al., 1988.) Generally, depressive syndromes are less common than depressive symptoms (Wragg & Jeste, 1989). Patients who complain of depressive symptoms tend to be less cognitively impaired and have less atrophy on CT scans than patients without symptoms (Bums, 1990b). This, however, may be an artifact based on the observation that patients who are able to complete the questionnaires regarding depression are less demented than those unable to cooperate. Some studies have specifically assessed depression as reported by patients compared to that observed by others (MacKenzie et al., 1989; Rubin & Kinscherf, 1989) and found the former to be less prevalent. Bums et al. (1990b) reported the reverse finding, but this may be due to the definition of depression which included “any” depressive symptoms. Definitions of depression in dementia pose a particular problem in relation to standardized criteria. DSM-111-R (APA, 1987) recognizes four subcategories of dementia, one of which is “with depression.” As diagnoses of dementia and depression appear at first sight to be mutually exclusive, one has to diagnose depression, in conjunction with dementia, under the heading of “major depressive syndrome”-a category based purely on phenomenological grounds. This is not stated clearly in the manual, and it is therefore open to wrong interpretation. There is also a problem with regard to which instruments are suitable for the assessment of depression in dementia. Traditionally, instruments used for the assessment of depression in noncognitively impaired patients are used. However, many of the symptoms of dementia are similar to those of depression (e.g., retardation, insomnia, lack of interest, and loss of insight), so that clinical features of the
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dementia itself may produce a high score on the depression scale in the absence of a disorder of mood. Cummings and Victoroff (1990) suggest that a diagnosis of depression in dementia should include feelings of hopelessness, sadness, worthlessness, and suicidal ideation. The possibility of biological subtypes of dementia based on the presence or absenceof depression is raised by two studieswhich have assessedneuropathological differences in DAT patients with and without depression. Zubenko and Moossy ( 1988) found that demented patients with depression had more neuropathological features in the substantia nigra and locus coeruleus, while Zweig and colleagues (Zweig et al. 1988) found that affective disturbances were associated with greater neuronal loss at the midlevel of the locus coeruleus. Neurochemical abnormalities may be implicated in the genesis of depression (in the form of dysfunction of ascending noradrenergic and serotonergic systems), and it has been suggested that the abnormality in the cholinergic system in Alzheimer’s disease may be protective for major depression; anticholinergic agents produce elevated mood and cholinergic agents may cause depression.
MANIA Manic symptomatology in DAT is rare compared to the proportion of patients exhibiting depressive features. Prevalence rates vary from between 3% to 15% (Rothschild, 1941; Bucht & Adolfsson, 1983).Bumset al. (1990b) found that 3.5% of patients with DAT appear manic to a skilled interviewer, and only one patient (out of a total of 110) reported subjective symptoms of mania. In this study mania did not appear to be related to cognitive function. However, manic features were associated with widening of the interhemispheric fissure on CT scan, in contrast to depression which was associated with relative preservation of the same region. Therefore, manic symptomatology may be related to frontal lobe disinhibition. The association of mania and dementia is embodied in the concept of presbyophrenia, as outlined by Berrios (1985). Elated mood, confabulation, and hyperactivity were described in a subgroup of patients with dementia in the early part of this century, but the concept fell into disrepute when dementia was redefined purely in cognitive terms. Such patients were often then diagnosed as delirious. Possible reasons for this subtype of dementia (which is also found in patients with vascular dementia) include the following: the effect of premorbid illness (bipolar affective disorder); neurochemical changes (depletion of noradrenaline); and vascular disease (Berrios, 1985). Elucidation of this concept may be helped by thorough assessment of manic symptoms in demented patients.
PERSONALITY CHANGES Changes in personality appear to be very common in DAT. They tend to be early signs and consist of coarsening of affect, disinhibition, apathy, and egocentricity
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(Petry et al., 1988).Despitetheircommonoccurrence,littlesystematic research has been done on their presence. Petry et al. (1988) found such changes to be universal, but they did not occur in a control group of subjects examined pre- and postretirement. Patients became more passive, less spontaneous,more coarse, and more immature than before the onset of dementia. Generally, measures of personality do not correlate with dementia (Petry et al., 1988), suggesting that they are relatively independent of the biological process of the disease.
BEHAVIORS Behavioral disturbances have, like psychiatric symptoms, received scant attention from researchers (Fairbum & Hope, 1988). Behavioral problems impose a particular burden on caregivers (Rabins et al., 1982) and may directly result in patients being admitted to long-term care (Sanford, 1975). Among the most common behaviors giving rise to problems are incontinence,physical violence, and wandering. Recently, some studies have begun to enumerate the problem. Swearer et al. (1988) detailed angry outbursts in 50% and “dietary change” in 21% of patients. Teri et al. (1988) reported wandering behavior in a quarter of patients, and in a later paper found one-fifth to have increased appetite (Teri et al., 1989). Aggression has also been documented in a significant proportion of patients (Ryden, 1988). Behavioral disturbancestend to be associated with increased severityof dementia. Swearer et al. (1988) reported that both violence and incontinence became progressively more severe with increasing degree of dementia. Ten et al. (1988) found wandering to be twice as common in patients with severe dementia, and Bums et al. (1990b) found incontinence to be related both to severity of dementia and subsequent mortality. A behavioral syndrome of particular interest is the Kluver-Bucy syndrome. This was originally described in monkeys following bitemporal lobectomy and consists of the following behavioral changes: visual agnosia; strong oral tendencies with hyperphagia; hypermetamorphosis(an excessive tendency to attend and to react to every visual stimulus); increased sexual behavior and emotional changes (both withdrawal and apathy, but also loss of fear and “rage” reactions). The syndrome has been described in humans following removal of the temporal lobes, but also in DAT and Pick’s disease (Sourander & Sjogren, 1970; Cummings & Duchen, 1981). Sourander and Sjogren (1970) described individual elements of the syndrome in over70% of DAT cases confirmed as Alzheimer’s disease at postmortem. Sexual disinhibition was the least frequent sign, found in 17% of cases. Bums et al. (1990b) reported a detailed analysis of the Kluver-Bucy syndrome in 178 patients with DAT diagnosed according to NINCDWADRDA criteria (McKhannet al., 1984). A new scale waspresented which purported to measure the seven behaviors traditionally associated with the syndrome. Although individual behaviors were relatively common (for example, going into rages, 36%; hypermetamorphosis, 31%; withdrawal,41%), all seven were seen in only one
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patient. AII the behaviors (except binge eating) became more common as severity of dementia increased (both measured by specific cognitive tests and global ratings of dementia). Aggression was more common in men. A factor analysis suggested three factors: one consisting of sexual disinhibition, visual agnosia, hyperorality, and withdrawal/apathy; another of rage behavior and hypermetamorphosis; and a third of binge eating. Structural correlates of behavioral disturbances have been examined. Swigar et al. (1985) found that temporal lobe atrophy was associated with aggression. Bums et al. (1990b) confirmed that finding and also found associations between wandering and Sylvian fissure enlargement, and among frontal-occipital atrophy, third ventricular enlargement, and hyperorality. Patients with at least one feature of the Kluver-Bucy syndrome were more likely to have temporal lobe atrophy. Cummings and Victoroff (1990) divided behavioral disturbances into disorders of sleep, appetite, and sexual activity, and into disturbances of psychomotor activity (restlessness, wandering, fidgeting, and agitation). They presented compelling evidence that these behaviors may be due to abnormalities in a variety of neurochemical and neuropathological processes. For example, frontal lobe release may cause increased sexual activity, serotonergic dysfunction might be implicated in regulation of feeding, and an adrenergicmediated effect may occur inpsychomotor disturbances.
SCALES USED IN THE ASSESSMENT OF PSYCHIATRIC PHENOMENA Clinical scales described in this section will assess a variety of psychiatric symptoms and behavioral disturbances in dementia.The list (in no particular order) is by no means exhaustive and does not include widely known scales in which some questions are used to assess noncognitive symptoms. The Geriatric Depression Scale (Yesavage et al., 1983). A 30-item scale with a yes/no format which excludes somatic symptoms. Of limited use in dementia as it loses its validity (Burke et al., 1989). Cornell Scalefor Depression in Dementia (Alexopouloset al., 1988). A useful scale for the assessment of depression in dementia. The Alzheimer’s Disease Assessment Scale (Rosen et al., 1984). A 21-item scale which includes a section on noncognitive behavior (with subscales assessing depression, delusions, hallucinations, pacing, and appetite disturbance). Zrritabilify and Apathy (Bums et al., 1990a). A short 10-item scale, based on information from informants, assessing irritability and apathy. Psychosis in Alzheimer’s Disease (Reisberg & Ferris, 1985). A short scale with useful questions on psychosis. Stockton Geriatric Rating Scale (Meer & Baker, 1966). A 33-item scale with four subscales of physical disability, apathy, communication failure, and socially irritating behavior. Useful for the assessment of advanced dementia.
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Clifton Assessment Proceduresfor the EIderly (CAPE) (Pattie, 198 1). A comprehensive package not designed exclusively for demented patients, with cognitive and behavioral subscales. It is a shortened version of the Stockton Rating Scale. BehaviorDisturbance of Community Patients (Greene et al., 1982).Two scales rate items of behavior (including mood) and stress in the relatives. Behavior Severity Rating Scale (Swearer et al., 1988). A brief scale assessing troublesome and disruptive behaviors with subsections on aggression, bizarre behavior, psychotic features, vegetative features, and emotional changes. BEHAV-AD (Reisberg et al., 1987). The most detailed scale available, tapping an array of behaviors and psychiatric symptoms.Has been used to assess the effect of medication. Psychogeriatric Dependency Rating Scale (Wilkinson& Graham-White, 1980). A brief scale with a short behavioral section. Personality Changes (Petry et al., 1988). The only scale specifically aimed at assessing personality changes. Kluver-Bucy Syndrome (Burns et al., 1990b). A 7-item scale assessing behaviors traditionally associated with the Kluver-Bucy syndrome, based on the format used in the Stockton Rating Scale. Psychopathology in Dementia (Bucht & Adolfsson, 1983). A short scale assessing a number of emotional changes and symptoms, devised for patients with vascular dementia and for those with DAT.
CONCLUSION In conclusion, psychiatric symptomatology is an important aspect of the clinical picture of patients with DAT (and indeed in dementias of any etiology). It is surprising that these phenomena have been neglected by researchers until recently, despite their importance. This probably represents the greatly increased general interest in DAT which has developed in the last 20 years. Problems of assessment are beginning to be tackled-early work relied on essentially anecdotal reports of the presence of particular symptom complexes, while other work depended on the application of instruments not designed for cognitively impaired populations. Currently, instruments are being developed which attempt to measure these behaviors specifically in patients with dementia. Assessment of such phenomena is important, as they are particularly distressing to relatives and are amenable to conventional psychopharmacologicalagents. Their measurement will be of prime importance in monitoring the efficacy of such drugs. Increasingly, Alzheimer’s disease is being recognized as a complicated disorder (possibly affecting body systems other than the brain), and an appreciation of its myriad manifestations is desirable. The recognition of psychiatric symptoms, behavioral disturbances, and personality changes as prodromata of cognitive impairment in dementia may help to broaden our diagnostic procedures and may shed light on the very early features of the disease. Changes in personality will be particularly important in this regard.
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One of the most exciting possibilities in relation to an assessment of psychiatric phenomena in DAT is that the assessment may lead to an understanding of the neurobiology of a variety of psychiatric symptoms and behaviors, teaching us more about the so-called functional psychoses in particular and about brain-behavior relationships in general.
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Rubin, E., Drevets, W., & Burke, W. (1988). The nature of psychotic symptoms in senile dementiaof the Alzheimertype. Journal of GeriatricPsychiatry andNeurology, 1,1620. Rubin, E., & Kinscherf, D. (1989). Psychopathology of very mild dementia of the Alzheimer type. American Journal of Psychiatry: 146, 1017-1021. Ryden, M. (1988). Aggressive behavior in persons with dementia who live in the community. Alzheimer’s Disease and Associated Disorders, 2(4), 342-55. Sanford,J. (1975). Tolerance of disability in elderly dependentsby supporters at home: Its significance for hospital practice. British Medical Journal, iii, 47 1-473. Sim, M., & Sussman I. (1962). Alzheimer’s disease: Its natural history and differential diagnosis. Journal of Nervous and Mental Disease, 135,489-99. Sjogren,P., Sjogren,H., & Lindgren, A. G. H. (1952).Morbus Alzheimer and Morbus Pick. Acta Psychiatrica and Neurologica Scandinavica (Supplement), 82. Sourander, P., & Sjogren, H. (1970). The concept of Alzheimer’s disease and its clinical implications. In G. Wolstenholme & M. O’Connor (Eds.), Alzheimer’s disease and related conditions (pp. 11-32). London: Churchill. Swearer, J., Drachman, D., O’Donnell,B., & Mitchell, A. (1988). Troublesomeand destructive behaviors in dementia. Journal of the American Geriatrics Society, 36,784-90 Swigar, M., Benes, F., & Rothman, S., Opsahl, C., & Dowds, M. (1985). Behavioral correlates of CT scan changes in older psychiatric patients. Journal of the American Geriatrics Society, 33,96103, Ten, L., Borson, S., Kiyak, A., & Yamagishi,M. (1989).Behavioral disturbance,cognitive dysfunction and functional skill: Prevalence in relationship in Alzheimer’s disease. Journal of the American Geriatrics Society, 37, 109-1 16. Teri, L., Larson, E. B., & Reifler, B.(1988). Behavioral disturbance in dementia of the Alzheimer type. Journal of the American Geriatrics Society, 36, 1-6. Wilkinson, I., & Graham-White, J. (1980). Psychogeriatric Dependency Rating Scale (PGDRS): A method of assessment for use by nurses. British Journal of Psychiatry, 137,558-565. Wragg, R., & Jeste, D. (1939). Overview of depression and psychosis in Alzheimer’s disease. American Journal of Psychiatry, 146,577-581. Yesavage, J., Brink, T., Rose, T., Lum, O., Huang, V., Adey, M., & Leirer, 0. (1933). Development and validation of a geriatric depression screening scale: A preliminary report. Journal of Psychiatric Research, 17,37. Zubenko, G., & Moossy, J. (1983). Major depression in primary dementia clinical and neuropathologic correlates. Archives of Neurology, 45, 1182-1 186. Zweig, R., Ross, C., Hedreen, J., Steele, C., Cardillo, J., Whitehouse, P., Folstein, M., & Price, D. (1988). The neuropathology of aminergic nuclei in Alzheimer’s disease. Annals of Neurology, 24,233-242.
Offprints.Requests for offprints should be sent to Alistair Bums, M.D., M. Phil, M.R.C.P., M.R.C.Psych., Senior Lecturer, Section of Old Age Psychiatry, Institute of Psychiatry, De Crespigny Park, Denmark Hill, London SE5 8AF, United Kingdom.
Psychiatric Phenomena in Dementia of the Alzheimer Type Alistair Burns, M.D., M. Phil., M.R.C.P., M.R.C.Psych. Section on Old Age Psychiatry Institute of Psychiatry London, England ABSTRACT. Psychiatricsymptomsand behavioraldisturbancesare of importance in dementia of the Alzheimer type (DAT) but have been relatively neglected by researchers. The main psychiatric symptoms are disorders of thought content (delusions and paranoid ideation), disorders of perception (hallucinationsand misidentifications)and disorders of affect (depressed and elevated mood). They occur commonly in DAT, and there is evidence that they may indicate subtypesof the disorder in view of their demographic,structural, and prognosticcorrelates.Personalitychangesare very common,and thesemay be the earliest manifestation of dementia. Behavioral disturbances tend to be associated with advanced dementia and are particularly disruptive to caregivers. Structuralcorrelatessuggest that somebehaviorsare a direct result of brain damage.Psychiatricand behavioralfeaturesin DAT are important,as they may serve as a model for symptomatology in functionalpsychiatric disorders.
INTRODUCTION Psychiatric phenomena in dementia have been a hitherto neglected area of research, possibly because they were traditionally regarded as secondary to the cognitive deficits, and therefore of secondary importance. Four reasons such phenomena may occur in conjunction with a dementia syndrome have been detailed by Berrios (1989). One, they may be part of an intercurrent confusional state. Two, they may be due to disinhibition of cortical functions, resulting in "released" symptomatology. Three, they may be due to a pathoplastic effect of personality in the clinical expression of the disorder. Finally, and four, two separate mental disorders may coexist, although conventional psychiatric practice rather frowns on such a formulation. The importance of psychiatric symptomatology in dementia of the Alzheimer type (DAT) has been discussed elsewhere (Bums et al., 1990b). These phenomena can be divided into two main groups. The first group comprises 43
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psychiatric symptoms which are generally mentioned in the patient’s complaints and are detected either at mental state testing or obtained through a caregiver’s account of the patient’s speech (e.g., delusions, hallucinations, misidentifications, and depression).The second group includes behavioral disturbances which consist of outward manifestations observable by others (e.g., aggression, wandering, or disinhibition). This division, although convenient in terms of nosology, is not absolute. For example, a hallucinatory experience may be manifest as an aggressive outburst. This paper is an attempt to review psychiatric symptoms, behavioral disturbances, and changes in personality in patients with DAT and to outline some scales which may be of use in their assessment. For further information, the reader is referred to two recent excellent reviews on the subject: Wragg and Jeste (1989) and Cummings and Victoroff (1990).
DELUSIONS Alzheimer’s first case (Alzheimer, 1907)exhibited delusional thinking-jealousy toward her husband, paranoid ideas directed against her doctor, and a belief that she was about to be murdered. Reports of the proportionof DAT patients with delusions vary between 10% (Birkett, 1972) and 73% (Leuchter & Spar, 1985). Studies inevitably vary because of differences in the way in which the delusions and dementia are diagnosed and in the population under study. For example, choosing to study patients referred to a general hospital service may bias the sample toward these symptoms, thus giving a falsely high rate, whereas confining investigations to autopsy-proven cases may provide an unrepresentative sample. A recent study in which this author was involved (Bums et al., 1990b) showed that 16% of patients from a defined catchment area had delusions. The method by which delusions are diagnosed is also of importance-some studies depend on direct interviews with the patients (Cummingset al., 1987)while others depend on reports given by caregivers, either face to face (Burns et al., 1990b) or on the telephone (Kumar et al., 1988). The difficulties of assessing such phenomenology in an illness which is often of several years’ duration and requires retrospective analysis by untrained staff (for example, spouses) have not yet been fully evaluated. However, to confine the gathering of information to an interview with the patient will mean missing a significant proportion of the great array of phenomenology which may be of a transitory nature. Delusions have been associated with early disease (Goodman, 1953), late disease (Sim & Sussman, 1962), and with the middle stage (Drevet & Rubin, 1989). Several different types of delusions have been described. Cummings (1985) suggested four types: simple, complex persecutory, grandiose, and those associated with neuropsychologicaldeficits. Cutting (1987) described simple and grandiose delusions in 17 of 35 patients with acute organic psychoses but could not
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classify the others according to Cummings’s(1985) categories.Burns et al. (1990b) described delusions of theft and suspicion (equivalent to simple persecutory delusions) but also a category of systematized delusions (broadly similar to those patients that Cutting was unable to classify). Patients with systematized delusions had smaller lateral ventricles, and a higher proportion had basal ganglia calcification than patients without such delusions. Other delusions, such as Capgras’ syndrome and the phantom boarder syndrome (Merriam et al., 1988), have also been described. Cummings and Victoroff (1990) outlined four possible explanations for the presence of delusions in DAT: as a logical attempt by patients to understand their environment; as secondary to mood changes; as a coincidental diagnosis; and as secondary to the underlying disease. This last mechanism seems the most tenable, especially as delusions have been described particularly in patients with limbic dysfunction and temporal lobe pathology, both of which are affected in DAT. Some authors have described disorders of thought content which consist of paranoid ideation not held with delusional intensity (Bums et al., 1990b; Reisberg et al., 1987). It is possible that some other authors include these patients as having delusional ideas, even though their phenomenology does not satisfy traditional definitions (Fish, 1985).The exact status of this form of abnormal thinking requires further evaluation.
HALLUCINATIONS Alzheimer’s first case (Alzheimer, 1907) experienced auditory hallucinations as part of her dementia syndrome.Hallucinationshave been described less commonly than delusions in DAT and some authors do not make the fundamentaldistinction between auditory and visual hallucinosis. Early studies vaned widely in their reporting of prevalence rates-Goodman (1953) described visual hallucinationsas occurring in “the majority” of patients, while Sjogren, Sjogren, and Lindgren (1952) found 15% of their patients to be affected. Merriam et al. (1988) found 20% to have experienced hallucinations, but their study did not differentiate between patients in the auditory or visual modalities. The highest rate of hallucinations experienced was reported by Rabins et al. (1982), who found, in interviewing caregivers, that 49% of patients were affected. They did not give separate figures for visual and auditory hallucinosis. Hallucinations in other modalities have been described, including olfactory hallucinations. The obviously confounding variable in the assessment of these phenomena is that the presence of a confusional state can give rise to visual hallucinations, and that these patients will obviously be overrepresentedin samples drawn from acute care settings. By excludingpatients with confusionalepisodes, Burns et al. (1990b) found that visual and auditory hallucinations occurred in 13% and lo%, respectively, of a representative population of patients with DAT. Another significant factor affectingprevalencerates is the method by which the symptoms are assessed.
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For example, Rabins et al. (1982) interviewed relatives about troublesome behaviors, whereas Cummings et al. (1987) confined their definition to patients actively hallucinating during an interview. They found only one patient with auditory hallucinations and none with visual hallucinations was encountered. Relatively little work has been performed in examining the relationship between hallucinations and other features of dementia. There appears to be no difference in cognitive function between patients with and without hallucinations (Berrios & Brook, 1984; Teri et al., 1988; Burns et al. 1990b), but there is evidence that hallucinated patients deteriorate more quickly (Bums et al., 1990b). The etiology of hallucinations in dementia is obscure, and it is impossible to invoke similar mechanisms for their occurrence (unlike for delusions, in which mood congruence or an understandable response to the environment can trigger occurrence). However, the hallucinations may well indicate a concomitant illness (such as acute confusion) or they may be related to underlying neuropathology. Sensory deficits are known to promote hallucinosis in the elderly, and an association was found between these phenomena and eye pathology in the study by Berrios and Brook (1984).
MISIDENTIFICATIONS These have been recently described (Rubin et al., 1988). These authors outlined three types of misidentification: the idea that other people are in the patient’s home; misidentification of the patient’s own mirror image; and misidentification of television (originally described by Berrios & Brook, 1984). Burns et al. (1990b) added a fourth misidentification-that of other people. The exact status of these phenomena is open to debate. For example, the idea that someone else is in the house (phantom boarder syndrome) could equally be classified as a delusion and may, of course, be based on a hallucinatory experience. Misidentifications, in general, may be delusions “based on a specific neurological deficit” (Cummings, 1985). However, their unique character and failure to satisfy other definitions suggest that they deserve a separate category. Rubin et al. (1988) described them in 23% of their sample: an equal proportion (12%) misidentified television images and believed others were in the house, and 7%misidentified their own mirror image. Merriam et al. (1988) found very high rates of these perceptual disturbances (up to 50%) and described 17% as having the Capgras syndrome (which may be based on misidentification of a familiar person). As these phenomena have only recently been described there is comparatively little research regarding their possible etiology. What evidence there is, however, is intriguing. Merriam et al. (1988) reported an association between degree of dementia and the presence of these phenomena. Drevets and Rubin (1989) found that patients with misidentifications have a decreased mortality compared to those without. Other studies (Mayeux et al., 1985) emphasize the increased cognitive decline in patients with psychosis. The diminished mortality in patients with
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misidentification syndromes was replicated by Bums et al. (1990b) who also found that their pmence was associated with a younger age and younger age of onset of disease, possibly indicating some parietal lobe involvement. These findings may suggest a possible subtype of DAT based on the presence or absence of misidentifications.
DEPRESSION Depressive symptomatology in DAT is a common accompaniment to the clinical syndrome, but its presence is harder to assess due to the difficulty of definition. There is no evidence to suggest that depression leads to an increased incidence of primary dementia later in life, although some work has suggested that depression occurring in the ten years before the onset of dementia may be a significant risk factor for dementia (Henderson et al. 1989).This is of importance, as it raises the possibility of noncognitive symptoms as prodromata of dementia. Also, 10% of patients with primary dementia have a past history of depression, which is more than in a control group (Agbayewa, 1986). Depressive symptomatologyin patients with DAT has been well documented by some 20 studies (Bums, 1991).The reported proportion with depressive symptoms varies between 0% and 86% (Knesevich et al., 1983; Memam et al., 1988.) Generally, depressive syndromes are less common than depressive symptoms (Wragg & Jeste, 1989). Patients who complain of depressive symptoms tend to be less cognitively impaired and have less atrophy on CT scans than patients without symptoms (Bums, 1990b). This, however, may be an artifact based on the observation that patients who are able to complete the questionnaires regarding depression are less demented than those unable to cooperate. Some studies have specifically assessed depression as reported by patients compared to that observed by others (MacKenzie et al., 1989; Rubin & Kinscherf, 1989) and found the former to be less prevalent. Bums et al. (1990b) reported the reverse finding, but this may be due to the definition of depression which included “any” depressive symptoms. Definitions of depression in dementia pose a particular problem in relation to standardized criteria. DSM-111-R (APA, 1987) recognizes four subcategories of dementia, one of which is “with depression.” As diagnoses of dementia and depression appear at first sight to be mutually exclusive, one has to diagnose depression, in conjunction with dementia, under the heading of “major depressive syndrome”-a category based purely on phenomenological grounds. This is not stated clearly in the manual, and it is therefore open to wrong interpretation. There is also a problem with regard to which instruments are suitable for the assessment of depression in dementia. Traditionally, instruments used for the assessment of depression in noncognitively impaired patients are used. However, many of the symptoms of dementia are similar to those of depression (e.g., retardation, insomnia, lack of interest, and loss of insight), so that clinical features of the
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dementia itself may produce a high score on the depression scale in the absence of a disorder of mood. Cummings and Victoroff (1990) suggest that a diagnosis of depression in dementia should include feelings of hopelessness, sadness, worthlessness, and suicidal ideation. The possibility of biological subtypes of dementia based on the presence or absenceof depression is raised by two studieswhich have assessedneuropathological differences in DAT patients with and without depression. Zubenko and Moossy ( 1988) found that demented patients with depression had more neuropathological features in the substantia nigra and locus coeruleus, while Zweig and colleagues (Zweig et al. 1988) found that affective disturbances were associated with greater neuronal loss at the midlevel of the locus coeruleus. Neurochemical abnormalities may be implicated in the genesis of depression (in the form of dysfunction of ascending noradrenergic and serotonergic systems), and it has been suggested that the abnormality in the cholinergic system in Alzheimer’s disease may be protective for major depression; anticholinergic agents produce elevated mood and cholinergic agents may cause depression.
MANIA Manic symptomatology in DAT is rare compared to the proportion of patients exhibiting depressive features. Prevalence rates vary from between 3% to 15% (Rothschild, 1941; Bucht & Adolfsson, 1983).Bumset al. (1990b) found that 3.5% of patients with DAT appear manic to a skilled interviewer, and only one patient (out of a total of 110) reported subjective symptoms of mania. In this study mania did not appear to be related to cognitive function. However, manic features were associated with widening of the interhemispheric fissure on CT scan, in contrast to depression which was associated with relative preservation of the same region. Therefore, manic symptomatology may be related to frontal lobe disinhibition. The association of mania and dementia is embodied in the concept of presbyophrenia, as outlined by Berrios (1985). Elated mood, confabulation, and hyperactivity were described in a subgroup of patients with dementia in the early part of this century, but the concept fell into disrepute when dementia was redefined purely in cognitive terms. Such patients were often then diagnosed as delirious. Possible reasons for this subtype of dementia (which is also found in patients with vascular dementia) include the following: the effect of premorbid illness (bipolar affective disorder); neurochemical changes (depletion of noradrenaline); and vascular disease (Berrios, 1985). Elucidation of this concept may be helped by thorough assessment of manic symptoms in demented patients.
PERSONALITY CHANGES Changes in personality appear to be very common in DAT. They tend to be early signs and consist of coarsening of affect, disinhibition, apathy, and egocentricity
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(Petry et al., 1988).Despitetheircommonoccurrence,littlesystematic research has been done on their presence. Petry et al. (1988) found such changes to be universal, but they did not occur in a control group of subjects examined pre- and postretirement. Patients became more passive, less spontaneous,more coarse, and more immature than before the onset of dementia. Generally, measures of personality do not correlate with dementia (Petry et al., 1988), suggesting that they are relatively independent of the biological process of the disease.
BEHAVIORS Behavioral disturbances have, like psychiatric symptoms, received scant attention from researchers (Fairbum & Hope, 1988). Behavioral problems impose a particular burden on caregivers (Rabins et al., 1982) and may directly result in patients being admitted to long-term care (Sanford, 1975). Among the most common behaviors giving rise to problems are incontinence,physical violence, and wandering. Recently, some studies have begun to enumerate the problem. Swearer et al. (1988) detailed angry outbursts in 50% and “dietary change” in 21% of patients. Teri et al. (1988) reported wandering behavior in a quarter of patients, and in a later paper found one-fifth to have increased appetite (Teri et al., 1989). Aggression has also been documented in a significant proportion of patients (Ryden, 1988). Behavioral disturbancestend to be associated with increased severityof dementia. Swearer et al. (1988) reported that both violence and incontinence became progressively more severe with increasing degree of dementia. Ten et al. (1988) found wandering to be twice as common in patients with severe dementia, and Bums et al. (1990b) found incontinence to be related both to severity of dementia and subsequent mortality. A behavioral syndrome of particular interest is the Kluver-Bucy syndrome. This was originally described in monkeys following bitemporal lobectomy and consists of the following behavioral changes: visual agnosia; strong oral tendencies with hyperphagia; hypermetamorphosis(an excessive tendency to attend and to react to every visual stimulus); increased sexual behavior and emotional changes (both withdrawal and apathy, but also loss of fear and “rage” reactions). The syndrome has been described in humans following removal of the temporal lobes, but also in DAT and Pick’s disease (Sourander & Sjogren, 1970; Cummings & Duchen, 1981). Sourander and Sjogren (1970) described individual elements of the syndrome in over70% of DAT cases confirmed as Alzheimer’s disease at postmortem. Sexual disinhibition was the least frequent sign, found in 17% of cases. Bums et al. (1990b) reported a detailed analysis of the Kluver-Bucy syndrome in 178 patients with DAT diagnosed according to NINCDWADRDA criteria (McKhannet al., 1984). A new scale waspresented which purported to measure the seven behaviors traditionally associated with the syndrome. Although individual behaviors were relatively common (for example, going into rages, 36%; hypermetamorphosis, 31%; withdrawal,41%), all seven were seen in only one
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patient. AII the behaviors (except binge eating) became more common as severity of dementia increased (both measured by specific cognitive tests and global ratings of dementia). Aggression was more common in men. A factor analysis suggested three factors: one consisting of sexual disinhibition, visual agnosia, hyperorality, and withdrawal/apathy; another of rage behavior and hypermetamorphosis; and a third of binge eating. Structural correlates of behavioral disturbances have been examined. Swigar et al. (1985) found that temporal lobe atrophy was associated with aggression. Bums et al. (1990b) confirmed that finding and also found associations between wandering and Sylvian fissure enlargement, and among frontal-occipital atrophy, third ventricular enlargement, and hyperorality. Patients with at least one feature of the Kluver-Bucy syndrome were more likely to have temporal lobe atrophy. Cummings and Victoroff (1990) divided behavioral disturbances into disorders of sleep, appetite, and sexual activity, and into disturbances of psychomotor activity (restlessness, wandering, fidgeting, and agitation). They presented compelling evidence that these behaviors may be due to abnormalities in a variety of neurochemical and neuropathological processes. For example, frontal lobe release may cause increased sexual activity, serotonergic dysfunction might be implicated in regulation of feeding, and an adrenergicmediated effect may occur inpsychomotor disturbances.
SCALES USED IN THE ASSESSMENT OF PSYCHIATRIC PHENOMENA Clinical scales described in this section will assess a variety of psychiatric symptoms and behavioral disturbances in dementia.The list (in no particular order) is by no means exhaustive and does not include widely known scales in which some questions are used to assess noncognitive symptoms. The Geriatric Depression Scale (Yesavage et al., 1983). A 30-item scale with a yes/no format which excludes somatic symptoms. Of limited use in dementia as it loses its validity (Burke et al., 1989). Cornell Scalefor Depression in Dementia (Alexopouloset al., 1988). A useful scale for the assessment of depression in dementia. The Alzheimer’s Disease Assessment Scale (Rosen et al., 1984). A 21-item scale which includes a section on noncognitive behavior (with subscales assessing depression, delusions, hallucinations, pacing, and appetite disturbance). Zrritabilify and Apathy (Bums et al., 1990a). A short 10-item scale, based on information from informants, assessing irritability and apathy. Psychosis in Alzheimer’s Disease (Reisberg & Ferris, 1985). A short scale with useful questions on psychosis. Stockton Geriatric Rating Scale (Meer & Baker, 1966). A 33-item scale with four subscales of physical disability, apathy, communication failure, and socially irritating behavior. Useful for the assessment of advanced dementia.
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Clifton Assessment Proceduresfor the EIderly (CAPE) (Pattie, 198 1). A comprehensive package not designed exclusively for demented patients, with cognitive and behavioral subscales. It is a shortened version of the Stockton Rating Scale. BehaviorDisturbance of Community Patients (Greene et al., 1982).Two scales rate items of behavior (including mood) and stress in the relatives. Behavior Severity Rating Scale (Swearer et al., 1988). A brief scale assessing troublesome and disruptive behaviors with subsections on aggression, bizarre behavior, psychotic features, vegetative features, and emotional changes. BEHAV-AD (Reisberg et al., 1987). The most detailed scale available, tapping an array of behaviors and psychiatric symptoms.Has been used to assess the effect of medication. Psychogeriatric Dependency Rating Scale (Wilkinson& Graham-White, 1980). A brief scale with a short behavioral section. Personality Changes (Petry et al., 1988). The only scale specifically aimed at assessing personality changes. Kluver-Bucy Syndrome (Burns et al., 1990b). A 7-item scale assessing behaviors traditionally associated with the Kluver-Bucy syndrome, based on the format used in the Stockton Rating Scale. Psychopathology in Dementia (Bucht & Adolfsson, 1983). A short scale assessing a number of emotional changes and symptoms, devised for patients with vascular dementia and for those with DAT.
CONCLUSION In conclusion, psychiatric symptomatology is an important aspect of the clinical picture of patients with DAT (and indeed in dementias of any etiology). It is surprising that these phenomena have been neglected by researchers until recently, despite their importance. This probably represents the greatly increased general interest in DAT which has developed in the last 20 years. Problems of assessment are beginning to be tackled-early work relied on essentially anecdotal reports of the presence of particular symptom complexes, while other work depended on the application of instruments not designed for cognitively impaired populations. Currently, instruments are being developed which attempt to measure these behaviors specifically in patients with dementia. Assessment of such phenomena is important, as they are particularly distressing to relatives and are amenable to conventional psychopharmacologicalagents. Their measurement will be of prime importance in monitoring the efficacy of such drugs. Increasingly, Alzheimer’s disease is being recognized as a complicated disorder (possibly affecting body systems other than the brain), and an appreciation of its myriad manifestations is desirable. The recognition of psychiatric symptoms, behavioral disturbances, and personality changes as prodromata of cognitive impairment in dementia may help to broaden our diagnostic procedures and may shed light on the very early features of the disease. Changes in personality will be particularly important in this regard.
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One of the most exciting possibilities in relation to an assessment of psychiatric phenomena in DAT is that the assessment may lead to an understanding of the neurobiology of a variety of psychiatric symptoms and behaviors, teaching us more about the so-called functional psychoses in particular and about brain-behavior relationships in general.
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Fairbum C, & Hope, R. (1933). Changes in behavior in dementia: A neglected research area. British Journal of Psychiatry, 152,406407. Fish, F., (1985). In M. Hamilton (Ed.), Fish’s clinical psychopathology (pp. 16-36) (2nd ed.). Bristol: John Wright and Sons. Goodman, L. (1953). Alzheimer’sdisease: A clinical pathologic analysis of 23 cases with a theory on pathogeneses. Journal of Nervous and Mental Disease, I 1 7(2), 97-130. Greene, J., Smith, R., Gardener, M., & Timbury, G. (1982). Measuring behavioral disturbanceof elderly demented patients in the community and its effects on relatives. Age and Ageing, 11,121-126. Henderson, A., Broe, G., & Creasey, H., McCuster, E., Korten, A., Jorm, A., Langley, W., & Anthony,J. (1989). In Psychiatry today-accomplishments andprom-ses.Abstracts of VIII World Congress of Psychiatry, Athens. Netherlands: Elsevier Scientific Publishers. (International Congress Series No. 899) 200. Knesevich, J., Martin, R., Berg, L., & Danziger,W. (1983). Preliminary reporton affective symptoms in the early stages of senile dementia of the Alzheimer type. American Journal of Psychiatry, 140,233-235. Kumar, A., Koss, E., Metzler, D., Moore, A., & Friedland, R. (1988). Behavioral symptomatology in dementia of the Alzheimer type. Alzheimer’sDisease and Associated Disorders, 2(4), 363-65. Leuchter,A., & Spar, J. (1985). The late onset psychoses: Clinical and diagnostic features. Journal of Nervous and Mental Disease, 173,488-494. Mayeux, R., Stem, Y.,& Sano, N. (1985). Psychosis in patients with dementia of the Alzheimer type. Annals of Neurology, 18, 144. McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadlan, E. (1984). Clinical diagnosis of Alzheimer’s Disease: Report on the NINCDS-ADRDA work group under the auspices of the Dept. of Health and Human Services Task Force on Alzheimer’s Disease. Neurology, 34,939-44. MacKenzie, T., Robiner, W., & Knopman, D. (1989). Differences between patient and family assessments of depression in Alzheimer’s disease. American Journal of Psychiatry, 146, 1174-1 178. Meer, B., & Baker, J. (1966). Stockton Geriatric Rating Scale.Journal of Gerontology,21, 372403. Merriam, A., Aronson, N., Gaston, P., Wey, S., & Katz, R. (1988). The Psychiatric Symptoms of Alzheimer’s Disease. Journal of the American GeriatricsSociety,36,7-12. Pattie, A. (198 1). A survey version of the CAPE. British Journal of Clinical Psychology, 20, 173-178. Petry, S.,Cummings,J.,Hill, M.,& Shapira,J. (1988). Personalityalternationsindementia of the Alzheimer type. Archives of Neurology, 45, 1187-1 190. Rabins, P., Mace, M., & Lucas, M. (1982). The impact of dementia on the family. Journal of the American Medical Association, 248, 333-5, Reisberg, B., Borenstein, J., Salob, S., Ferris, S., Franssen, E., & Georgotas, A. (1987). Behavioral Symptoms in Alzheimer’s Disease: Phenomenology and Treatment. Journal of Clinical Psychiatry, 48(5) (Supplement), 9-15. Reisberg, B., & Ferris, S. (1985). A clinical rating scale for symptoms of psychosis in Alzheimer’s disease. PsychopharmacofogyBulletin, 2 1 , 1014. Rosen, W., Mohs, R., & Davis, K. (1984). A new rating scale for Alzheimer’s disease. American Journal of Psychiatry, 141, 1356-1 364. Rothschild,A. (194 1). The clinical differentiation of senileand arterioscleroticpsychoses. American Journal of Psychiatry, 98,324-333.
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Offprints.Requests for offprints should be sent to Alistair Bums, M.D., M. Phil, M.R.C.P., M.R.C.Psych., Senior Lecturer, Section of Old Age Psychiatry, Institute of Psychiatry, De Crespigny Park, Denmark Hill, London SE5 8AF, United Kingdom.
