CURRENT PERSPECTIVES

Behavioural Disturbances in the Demented Elderly: Phenomenology, Pharmacotherapy and Behavioural Management* MORTON

S. RApp, M.D.!, ALASTAIR J. FLINT, M.B. 2, NATHAN HERRMANN, M.D. 3 AND

Behavioural disturbances in the demented elderly cause a significant amount of distress both to the patients and their caregivers. This article first summarizes the phenomenology associated with these disturbances. It then deals with the pharmacological methods of reducing these disturbances. Finally, it deals with some of the more recent advances in combining the insights of behavioural modification with those of neuropsychology in finding non pharmacological methods of reducing problematic behaviours. It is stressed that a combination ofthe two approaches is most likely to be required, and most likely to be successful, in the individual case.

GUY-BERNARD PROULX, Ph.D. 4

explosive emotional response to stress or the possibility of task failure (4). This reaction, common in demented people who are easily frustrated by everyday tasks, may become predictable. For example, it may occur whenever the patient is placed in an unfamiliar environment, or when bathed, dressed or toiletted. Its prevalence may reach 85% in demented patients (5). Agitation may also show itself as "sundowning". This is a tendency for demented patients to become more agitated and to wander as night approaches (6). It may be that when darkness and lack of visual cues induce spatial disorientation, the demented person more readily responds with anxiety and confusion.

T

he diagnosis of dementia relies mainly on the presence of intellectual impairment, not behavioural change (l,2). Yet it is often behavioural disturbances which so deleteriously affect the quality of life for both patients and caregivers. And it is the behavioural disturbances which are the targets of both pharmacological and behavioural treatments. Even modest improvements in these disturbed behaviours can result in significant improvement in the quality of life of patients and caregivers.

Wandering is common in dementia, and can be both bothersome and dangerous in an ordinary household not equipped to deal with it. Its prevalence has been variously cited as being between three percent (7) and 59% (5), and the prevalence increases with the severity of the dementia (8,9). Wandering has been conceptualized in two ways. It may be seen as a reaction to specific brain dysfunction, such as parietal lobe damage. Or it may be seen as a functional response which relieves anxiety and tension in individuals who were formerly active or action-oriented.

Phenomenology

Screaming, or repetitive inappropriate vocalization can be a most bothersome form of agitation to the caregivers. It is common. One survey (10) found that 25% of patients surveyed screamed at least four times a week. Screaming was associated with increasing cognitive impairment, a "poor social network," and greater impairment in performing the activities of daily living.

Table I lists the more common behavioural disturbances associated with dementia. The next few paragraphs describe some of these in detail. Agitation is often a significant problem, occurring in 48% of Reisberg's patients (3). But agitation can present in many ways. One of the most dramatic is the so-called "catastrophic reaction" - an intense, sometimes

However troublesome agitation is, caregivers identify aggression and violence as the most difficult problems they encounter (5). Violence, of course, can be the end stage of different processes. It may terminate a catastrophic reaction, or follow confusion, disinhibition and/or frustration. Alternatively, it may be a response to persecutory delusions and/or frightening hallucinations. It occurs in about 20% of patients with Alzheimer's disease, and the prevalence varies directly with the severity of the dementia (8). Like agitation, it is sometimes predictable during bathing, feeding or other perceived interferences (11). Indeed, noting the circumstances

*Manuscript received August 1991, revised January 1992. IDirector of Medical Education, Whitby Psychiatric Hospital, Whitby, Ontario. 2Division of Psycho geriatrics, Toronto Hospital, Toronto, Ontario. 3Division ofPsychogeriatiics, Sunnybrook Health Sciences Centre, Toronto, Ontario. 4Baycrest Centre for Geriatric Care, Toronto, Ontario. Addressreprintrequeststo: Dr. Morton S. Rapp, Director, Medical Education and Research, Whitby Psychiatric Hospital, P.O. Box 613, 700 Gordon Street, Whitby, Ontario L1N 5S9

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Table I The More Common Behavioural Disturbances in Dementia Agitation

Abnormal eating behaviours

Affective disorders/ mood disturbances

Incontinence

Delusions

Kluver-Bucy syndrome

Hallucinations

Anxiety/phobias/fears

Illusions

Shouting/screaming

Restlessness

Demanding/critical behaviour

Wandering

Personality change

Rage/violence

Disinhibition

Sleep/wake disturbances

Sexual behaviours

Sundowning

Compulsive/ritualistic behaviours

under which aggression occurs can lead to an understanding of the etiology in specific cases (12). Violence is a concern, of course, because it can result in injury, distresses the caregivers, and may totally prevent the giving of care. Depression in dementia has recently been recognized as a common cause of excess morbidity, yet it is relatively easy to treat once diagnosed. The prevalence rates of depression in dementia cited have varied wildly (13) but a recent study of 178 patients with Alzheimer's disease found that 24% of them were considered depressed by diagnosticians, and 43% were considered depressed by family members. A full 63% of the sample had at least one symptom consistent with depression (8). Because depression has been studied most often in patients with Alzheimer's disease, it is not known if other types of dementia are associated with more or less depression (13). One study showed that both the prevalence and severity of depression were higher in patients with multi-infarct dementia than in patients with Alzheimer's disease (14). However another study showed no difference in prevalence (15). Elevated mood or mania may occur in dementia, but are less common. The frequency is probably around three percent (8). "Pseudobulbar affect" encompasses abnormal displays of emotion that can occur in many different kinds of neuropsychiatric conditions. It may be called "pathological laughing or crying." There is an exaggerated emotional response which may be incongruous with mood or out of proportion with the intensity of mood. It appears to the observer that it is turned on and off abruptly, but it can be quite prolonged. Underlying it is an upper motor neuron lesion in the cortico-bulbar tracts, with dysphagia, dysarthria a brisk jaw jerk and exaggerated gag reflex as other signs (16). The full syndrome is seen in multi -infarct dementia (17) but the display of inappropriate affect may occur in other types of dementia as well. Psychotic symptoms of dementia include hallucinations, delusions and misidentification syndromes. Hallucinations occur in about 30% of patients with dementia (13). Visual

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hallucinations are the most frequent, followed by auditory hallucinations. Olfactory hallucinations are uncommon (8,14). The majority of delusions in dementia are simple, fleeting, loosely held, and persecutory in content (18). About one-third of demented patients will express delusions during their illness (13). The delusions of dementia may be fantastic, bizarre, well systematized or held for long periods of time, but such delusions are less common. Allied with delusions are misidentification syndromes, possibly related to prosopagnosia. Affected patients incorrectly identify people (or places) that are familiar to them. This may occur in 30% of patients (19).andare more prevalent than delusions or hallucinations. Patients may misidentify relatives (Capgras syndrome), or their own mirror reflection. They may claim an absent person is actually in the house, or mislabel people on television as existing in three-dimensional space. Sexuality is often omitted from dementia studies. But inappropriate displays of sexual behaviour are not uncommon, such as disrobing, nudity or masturbation (20). One study found that 6.9% of patients engaged in these activities (8).

The Kluver-Bucy syndrome may give rise to hypersexuality. The full-blown syndrome includes hyperorality or hyperphagia, emotional blunting, a tendency to explore environmental stimuli as soon as they are noticed (hypermetamorphosis), sensory agnosia and hypersexuality (21). It occurs early in Pick's disease, and later in Alzheimer's disease. Usually only partial syndromes are found. For example, Bums (8) found binge eating in ten percent, sexual disinhibition in seven percent and wandering in 19%. Pharmacotherapy

Two steps should precede the drug management of dementia. The first is assessment; any coexisting and complicating factors, such as unneeded medications,' physical illness, depression or environmental conditions which may complicate the dementia and/or cause or exacerbate the problem behaviour should be looked for and treated. The second is an attempt at non pharmacological treatments for targeted symptoms. The latter is dealt with in the last part of this paper. However, significant behaviour disruption may defy even the most careful assessment and behavioural intervention. When it does, pharmacotherapy is indicated. The most common drugs used are neuroleptics, though other medications may help and are discussed later. Despite 30 years of use of antipsychotic drugs in the treatment of behavioural disturbance in dementia, relatively few well-designed treatment studies exist. We know that medication is only moderately effective, and that it does not improve cognition (22,23). A recent meta-analysis of drug studies showed that neuroleptic medications were more effective than placebo, but only moderately so, and that no one drug was better than any other (24). The doses used were the equivalents of between 66 mg and 267 mg of chlorpromazine.

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It is possible that higher doses might have produced better results. However they may also produce more side-effects. Symptom specificity does not exist, but the general impressions (25-27) are that aggression, restlessness, delusions, hallucinations and some forms of inappropriate sexual behaviour are more responsive to neuroleptic medication than are persistent wandering or inappropriate noise. Wandering responds better to environmental interventions (28). Since neuroleptics are of equal efficacy, the choice of drug depends on the side-effect profile. Low potency agents such as chlorpromazine and thioridazine are associated with anticholinergic, sedative and hypotensive effects. High potency agents, such as haloperidol, have a propensity for extrapyramidal side-effects. Hence drugs in the middle range of potency (perphenazine, loxapine) are often selected. The usual tolerated doses are between 50 and 300 chlorpromazine-milligram equivalents. There is no precise information on the most desirable duration of treatment. The clinical rule is to persist for at least a month at the highest tolerated dose before giving up on a drug. If a drug is effective, periodic drug holidays should be tried, since the target symptom may have remitted spontaneously as the dementia progresses or the environment alters. Regular review of the need for the drug is important because older people are at higher risk of developing persistent tardive dyskinesia (29). What if a demented patient, living alone, demonstrates a need for antipsychotic drugs, but is unreliable in compliance? Literature oil the use of depot neuroleptics in the elderly is limited (30) but they may be tried, albeit with close monitoring. Occasionally they may forestall the need for institutionalization. Drugs other than antipsychotics are usually tried when the antipsychotics prove ineffective or produce disabling sideeffects. Of the alternatives, only the benzodiazepines have been subject to double-blind, placebo-controlled trials in elderly demented patients, so virtually all claims to efficacy are anecdotal. Benzodiazepines themselves, despite widespread use in the elderly, have been studied much less than antipsychotic drugs (31). Where the two drugs have been compared in treatment of agitation, the antipsychotics have generally proven more effective (27). Side-effects from benzodiazepines are numerous. They include sedation, worsening cognitive impairment, ataxia, falls and paradoxical enhancement of symptoms. Furthermore, long acting benzodiazepines tend to accumulate, with increased risk of toxicity. Hence drugs which are more quickly eliminated, such as oxazepam, lorazepam and temazepam, are preferable. Both groups of drugs are equally effective in controlling agitation in the elderly (32). Despite the apparently logical use of benzodiazepines in agitation characterized by high anxiety levels, no study to date has examined this specific situation (33). Clonazepam stimulates serotonin production, and might have value in the management of aggression (34). It has been

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most often used and investigated in younger patients. It is potentially useful where dementia is complicated by hyperactivity, insomnia, social intrusiveness and impulsiveness (35). There is anecdotal evidence (35) that clonazepam, in doses of 0.25 mg to 1.0 mg daily, added to an antipsychotic drug, is useful in treating agitation where either drug alone is ineffective. Clonzepam's long elimination half-life must be taken into consideration (36). Trazodone is another serotonergic drug which has been used, in doses of 200 mg to 900 mg daily, to treat dementia with aggression (37,38). Most of the use, however, has been in middle-aged patients with traumatic dementia. Thus far, there are no reports on the use of fluoxetine or fluvoxamine in this patient population. Beta-adrenergic blockers, lithium and carbamazepine have all been proposed for the treatment of agitation in dementia, based on clinical experience in younger patients (34). Propanolol may decrease aggression in various organic brain syndromes (39,40). Doses in younger patients are from 60 mg to 600 mg daily. Response time varies from one day to several months. Potential side-effects include hypotension, bradycardia, exacerbation of chronic obstructive airway disease, worsening of hypoglycemia, increasing cognitive impairment, depression and sleep disturbance. Use of propanolol in the elderly is not extensively documented (40). Demented patients with manic-like symptoms and/or a cyclical pattern to the symptoms may benefit from a trial of either lithium or carbamazepine (41). However, both drugs may cause much more neurotoxicity in the elderly, even at blood levels regarded as therapeutic (27,33). Lithium, ifused, should start at a dose of 150 mg daily and be gradually adjusted to achieve a plasma level of 004 to 0.8 millimoles per litre. Carbamazepine initial dose should be 50 mg bid, with gradual upward titration limited by side-effects. One must bear in mind carbamazepine's effect on the hepatic metabolism of other drugs, and its hamatological side-effects (27,33). Little is known about the best ways to manage inappropriate sexual behaviour occurring in dementia. Antipsychotic medications are sometimes helpful. Medroxyprogesterone acetate (42) and cyproterone acetate may be helpful. But decreased levels of testosterone are not always accompanied by alteration in sexual behaviour. Space does not permit a detailed discussion of the ethical issues involving pharmacotherapy in elderly patients, many of whom are incompetent to consent to treatment. However, these issues (43) need to be addressed before treatment is started.

Behavioural Management Successful behavioural management of some patients with dementia and behavioural disturbance results from a useful blending of the insights of neuropsychology with those of clinical psychology - an adaptation of behavioural assessment techniques to the neurologically impaired patient (44).

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Table II Baseline Observation Period Antecedent Behaviour

Date

Time

08-09

08:00

Woke up

28-09

15:30

Got up from nap

02-10

08:30

Had breakfast

Problem Behaviour Wife: B:

"Where are my pants? Did you take my stuff away?"

Wife: B: "Do we go to school today?"

Much of the recent work on the assessment and management of cognitively impaired patients comes from work on the young victims of traumatic brain damage. But this work can readily be adapted to work with the cognitively impaired elderly in selected cases. There are, however, several difficulties which hinder cognitive rehabilitation ofthe demented elderly. First, the disruptive behaviours themselves may stand in the way of accurate assessment and treatment interventions. Second, the sheer number of psychosocial problems secondary to the condition may be overwhelming. Third, the basic condition is usually accompanied by multiple medical problems and complicated by the side-effects of necessary drug treatments (for the target symptoms and/or the accompanying systemic diseases). Fourth, unlike other areas of behavioural management, the patient is generally unaware of even the surface manifestations of the problem. And finally, the relationship between the specific cognitive deficit and the environmental factors may be complex and multiform. Therefore, caregivers need practical behavioural management techniques to deal with all these problems. In behaviour management, one attempts to change the frequency, intensity, duration or location of specific problem behaviours or sets of behaviours, through systematically varying antecedent stimuli or consequential events. It has become known as the "ABC" approach to behavioural analysis. It is based on the observation that behaviour is intertwined with environmental events which precede and follow the occurrence of the behaviour (45). In this model, the "A" (antecedent) is the environmental event(s) or situation(s) occurring immediately before the targeted behaviour. The "B" is the behaviour targeted for modification. The "C" (consequence) is the observable environmental event(s) or situation(s) occurring immediately after the targeted behaviour. Typically, this might be the response of the caregiver to a specific behaviour on the part of the patient. The "ABC" model is extensively used by behavioural clinicians who work with children and younger adults. It has been applied less often to the cognitively-impaired elderly (46). For it to be effective, no fewer than seven specific steps must occur, as follows.

Wife: B: Wife:

Consequential Behaviour "What stuff?" "My money. 1 haven't a cent. You leave me broke. Come on. Give me my money. "What things?" "I don't know. There's a name for it. Come look it over. See the paper on the bed." "There isn't any paper. "Yes. Are there any kids here to go to school?" "You mean the Day Centre (at the hospital)?

First, is an accurate neuropsychological evaluation of cognitive strengths and deficits in the patient. If these are poorly understood, one may suggest responses which exacerbate inappropriate behaviours. But where they are well understood, one can design an effective treatment program. Second, a specific and measurable observable behaviour is targeted for modification. One must not try to modify too many behaviours at once. Third, systematic observation of the targeted behaviour is made, using the"ABC" model. That is, one determines both the antecedents and the consequences of the behaviour. Fourth, one records and measures the type, frequency and duration of the targeted behaviour under "baseline" conditions ----' that is, under the conditions existing before any intervention is attempted. These data must be in a form that can be communicated to the caregiver or the patient, depending on the situation. Fifth, the treatment program is designed. Typically it is "multidimensional" - includes several approaches. It may include counseling caregivers to help bring their demands and expectations into line with the nature of the cognitive deficits. It usually includes training in the ways in which to reinforce (strengthen) or extinguish (lessen) the occurrence of specific desirable and undesirable behaviours, respectively. It may include environmental changes that help to compensate for cognitive dysfunctions which in tum are responsible for the disruptive behaviour. It may include psychotherapy to assist the caregivers. Sixth, the program is implemented. Finally, there has to be evaluation, feedback and monitoring of the program. How well is it working? Do certain measures need to be changed? Can one determine what measures will maintain the gains which have been made? These principles will be illustrated with two examples.

Case One: Mr. A

Mr. A was a 78 year old man with a four year history of memory loss and paranoia. He was afraid of things breaking, and had a fear of strangers and of fire. He would often strike himself on the head, or throw stones at passersby. There was nothing to suggest hallucinations or depression. Antipsychotic medication was minimally effective. A neurological evaluation uncovered an abnormal EEG, with bilateral focal

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temporal slow waves. The CT showed marked cerebral atrophy from multiple infarcts, especially in the left posterior temporal and right anterior and mid-temporal areas. A neuropsychological exam revealed disorientation for time. Attention was preserved, but his performance on "digits reversed" was much poorer than on "digits forward." He could not retain the task-information he had learned, for more than a few minutes. This prevailed in all tests of verbal and non verbal memory, which themselves were preserved. He had good remote memory but needed cues to help him retrieve the information. Language functions were relatively preserved. Paraphasia, problems with naming, and mild difficulties with praxis, were observed. His wife was asked to keep a daily log of events occurring before the inappropriate "paranoid" behaviours, and of her responses to them (the consequences). The first week served as a "baseline" period, and no intervention was attempted. In that first week, 30 "confused-paranoid" behaviours were recorded. It became apparent that many of the problem behaviours occurred immediately after awakening in the morning, or after a nap. Naps tended to occur in the early afternoon, after lunch. Mr. A's periods of confusion occurred at times during which such incidents are to be expected. For example, disorientation on awakening is common in the aged (47). Nocturnal confusion is a common feature of multiple infarct dementia (48). Excessive daytime sleepiness and confusion are also common in the elderly (49). Daytime sleepiness fluctuates on an approximately 90 minute cycle (50) and may well peak during the so-called "post-lunch dip." A's confusions occurred during periods of low arousal. We also learned that A's wife was inadvertently reinforcing his confused behaviour. She often queried his confused and aphasic statements, which led to its continuation as he attempted to work though his already muddled flow of logic. His wife was advised to continue monitoring, but to attend more to her own responses. She was counseled to not respond at all to his confused behaviour, where possible. She was also counseled to reduce his number of daily naps. Over a three week period, and with periodic counseling of A's wife, the number of inappropriate behaviours reduced to about ten per week, mainly in the mornings. Nocturnal confused states virtually disappeared. A's management showed that the correct targeting of the antecedent behaviour, plus counseling to reduce the inadvertent reinforcement of his bothersome "paranoid-confused" behaviour, markedly reduce the frequency of it, and simplify his management at home.

Case Two: Mr. B Mr. B is a 67 year old resident of a continuing care unit, who was referred for disruptive behaviour. He was demanding, noisy, agitated and uncooperative. He had had an intracerebral hemorrhage from a right middle cerebral artery aneurysm four years ago, leaving him

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with dense left hemiplegia, left hemianopsia and multi-sensory neglect. In the institution, most ofthe troublesome behaviours were assumed to be due to a personality change resulting from his stroke. However, a neuropsychological examination had not been requested because his verbal skills were intact. Since right-hemisphere cognitive defects are less apparent to caregivers, the possibility that his "personality change" was due to neurological deficits had been under-appreciated. He presented as restless and excitable, but with a flat affect. He could not estimate time and did not know his age. He was articulate, but his thinking style caused him to jump rapidly from topic to topic, haphazardly. His voice was raspy and choppy, and his speech had poor prosody. The volume of his speech would increase as he spoke, and his modulation was poor. Testing showed marked impairment of both perceptual and constructional abilities related to right hemispheric function. Drawings were fragmented, spatial relations and organization were poor, and when writing, he consistently wrote to the right side. He neglected the left side when copying designs, and ignored the left side when reading. He had associated impaired memory of location and of visual information. He performed normally on most tests of verbal functioning. He could register, retain and recall presented verbally. The most impaired functions were poor modulation of affect, left unilateral multi-sensory neglect, perceptual and constructional deficits, and consequent poor memory for non verbal tasks. It could then be seen why his abilities had been so grossly over-estimated. To assess his aggression, staff completed "ABC" charts showing the events which preceded and followed the undesirable behaviour. In the first week, 12 aggressive outbursts were recorded. It also became apparent that these were related to his hemi-inattention. For example, when he was being returned to his room, he would become agitated and insist he was on the wrong floor. We determined that when he was taken from his room, he neglected the left side of the hall. But when he was returned to his room, he would neglect the opposite side of the hall- and thus was perceiving a totally different world during the two trips. Similarly, wheel-chair collisions with other patients, .and resulting aggression, stemmed from his hemi-inattention on the left. Again, his room was laid out so that when he was in bed, staff approached from his left, making him feel vulnerable, and resulting in defensive aggression. Once this was understood, family and staff were educated about his deficits and how they effected him, and ways of getting around his difficulties were sought. Environmental changes in his room helped him to compensate for his visuoperceptual problem. All this resulted in a marked decrease in aggressive outbursts. Once that was achieved, caregivers were taught how to use more frequent and consistent verbal cuing when communicating with him. It was also possible to teach him a compensatory method of reading for the first time since his stroke.

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It can be seen from these two cases that a proper behavioural analysis combined with a good understanding of the patient's neuropsychological status, can often lead to useful strategies for reducing or eliminating problem behaviours.

Summary

This paper has described many of the forms of disturbed behaviour which occurs in the dementias of the elderly. It goes on to describe the strengths and limitations of current psychopharmacological management of disturbed behaviours. It then describes how a blending of neuropsychology with behavioural analysis can lead to reduction of many problem behaviours in this patient group. As with other psychiatric problems, it is important to adhere to classical biopsychosocial principles. Excellent management of behavioural problems in the demented elderly will usually involve a skilled blending of pharmacological, behavioural and environmental approaches. References 1. Diagnostic and statistical manual of mental disorders, third edition, revised. Washington DC: American Psychiatric Press, Inc., 1987. 2. NINCDS-ADRDA Work Group: Criteria for the clinical diagnosis of Alzheimer's disease. J Am Geriatr Soc 1985; 33(1): 2-3. 3. Reisberg B, Borenstein J, Salob S, et al. Behavioural symptoms in Alzheimer's disease: phenomenology and treatment. J Clin Psychiatry 1987; 48: 5(Suppl): 9-15. 4. Goldstein K. The after-effects of brain injuries in war: their evaluation and treatment. New York: Grone and Stratton, 1942. 5. Rabins PV, Mace NL, Lucas MJ. The impact of dementia on the family. JAMA 1982; 248: 333-335. 6. Cameron DE. Studies in senile nocturnal delirium. Psychiatr Q 1841; 15: 47-55. 7. Steele C, Rovner B, Chase GA, et al. Psychiatric symptoms and nursing home placement of patients with Alzheimer's disease. Am J Psychiatry 1990; 147: 1049-1051. 8. Burns A, Jacoby R, Levy R. Psychiatric phenomena in Alzheimer's disease. IY. Disorders of behaviour. Br J Psychiatry 1990; 157: 86-94. 9. Teri L, Larson EB, Reifler BY. Behavioral disturbance in dementia of the Alzheimer type. J Am Geriatr Soc 1988; 36: 1-6. 10. Cohen-Mansfield J, Werner P, Marx MS. Screaming in nursing home residents. J Am Geriatr Soc 1990; 38: 785-792. 11. Jones MK. Patient violence. J Psychosoc Nurs Ment Health Serv 1985; 23(6): 12-17. 12. Ware CJC, Fairburn CG, Hope RA. A community-based study of aggressive behaviour in dementia. International Journal of Geriatric Psychiatry 1990; 5: 337-342. 13. Wragg, RE, Jeste DY. Overview of depression and psychosis in Alzheimer's disease. Am J Psychiatry 1989; 146: 577-587. 14. Cummings JL, Miller B, Hill MA, et al. Neuropsychiatric aspects of multi-infarct dementia and dementia of the Alzheimer's type. Arch Neurol 1987; 44: 389-393. 15. Fischer P, Simanyi M, Danielczyk W. Depression in dementia of the Alzheimer type and in multi-infarct dementia. Am J Psychiatry 1990; 147: 1484-1487. 16. Cummings JL. Clinical neuropsychiatry. Orlando FL: Grone & Stratton, 1985.

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17. Cummings JL. Multi-infarct dementia: diagnosis and management. Psychosomatics 1987; 28: 117-126. 18. Cummings JL. Organic delusions: phenomenology, anatomical correlations and review. Br J Psychiatry 1985; 146: 184-197. 19. Burns A, Jacoby R, Levy R. Psychiatric phenomena in Alzheimer's disease. II. Disorders of perception. Br J Psychiatry 1990; 157: 76-81. 20. Burnside I: Nursing care. In: Garwick LF, Winograd CH, eds. Treatments for the Alzheimer's patient. New York: Springer, 1988. 21. Cummings JL, DuchenLW. Kluver-Bucy syndrome in Pick's disease: clinical and pathologic correlations. Neurology 1981; 31: 1415-1422. 22. Salzman C. Treatment of agitation in the elderly. In: Melzer HY, ed. Psychopharmacology, a generation of progress. New York: Raven Press, 1989: 1167-1176. 23. Sunderland T, Silver MA. Neuroleptics in the treatment of dementia. International Journal of Geriatric Psychiatry 1988; 3: 784-790. 24. Schneider LS, Pollock VE, Lyness SA. A metaanalysis of controlled trials of neuroleptic treatment in dementia. J Am Geriatr Soc 1990; 38: 553-563. 25. Flint AI. Delusions in dementia: a review. Joumal of Neuropsychiatry and Clinical Neurosciences 1991; 3: 121-130. 26. Flint AJ. Delusion, hallucinations and depression in Alzheimer's disease: a biological perspective. American Journal of Alzheimer's Care and Related Disorders and Research 1991; 6(3): 21-28. 27. Risse SC, Bames R. Pharmacological treatment of agitation associated with dementia. J Am Geriatr Soc 1986; 34: 368-376. 28. Cohen-Mansfield J, Billig N. Agitated behaviours in the elderly. I. A conceptual review. J Am Geriatr Soc 1986; 34: 711-721. 29. Jenike MA. Tardive dyskinesia: special risk in the elderly. J Am Geriatr Soc 1983; 32: 71-73. 30. Gottlieb GL, McAllisterTW, Gur RC. Depot neuroleptics in the treatment of behavioural disorders in patients with Alzheimer's disease. JAm Geriatr Soc 1988; 36: 619-621. 31. De Leo D, Stella AG, Spagnoli A. Prescription of psychotropic drugs in geriatric institutions. International Journal of Geriatric Psychiatry 1989; 4: 11-16. 32. Salzman C. Treatment of the elderly agitated patient. J Clin Psychiatry 1987; 48(5 Supp\): 19-22. . 33. Liebovici A, Tariot PN. Agitation associated with dementia: a systematic approach to treatment. Psychopharrnacol Bull 1988; 24(1): 49-53. 34. Sheard MH. Clinical pharmacology of aggressive behaviour. Clin Neuropharrnacol 1988; II (6): 483-492. 35. Smeroski PJ. Clonazepam treatment of multi-infarct dementia. J Geriatr Psychiatry Neurol 1988; 1: 47-48. 36. Rosenbaum JE New uses for clonazepam in psychiatry: introduction and overview. J Clin Psychiatry 1987; 48(10 Suppl): 3-9. 37. Pinner E, Rich CL. Effects of trazodone on aggressive behaviour in seven patients with organic mental disorders. Am J Psychiatry 1988; 145(10): 1295-1296. 38. Simpson DM, Foster D. Improvement in organically disturbed behaviour with trazodone treatment. J Clin Psychiatry 1986; 47(4): 191-193. 39. Greendyke RM, Schuster DB, Wooton JA. Propanolol in the treatment of assaultive patients with organic brain disease. J Clin Psychopharmacol 1984; 4(5): 282-285. 40. Weller PG, Mungus D, Bernick C. Popanolol for the control of disruptive behaviour in senile dementia. J Geriatr Psychiatry Neurol 1988; 1: 226-230.

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41. Patterson JF. A preliminary study of carbamazepine in the treatment of assaultive patients with dementia. J Geriatr Psychiatry Neuro11988; I: 21-23. 42. Cooper AJ. Medroxyprogesterone acetate treatment of sexual acting out in men suffering from dementia. J Clin Psychiatry 1987; 48(9): 368-370. 43. Halleck SL. The ethics of antiandrogen therapy. Am J Psychiatry 1981; 138: 642-643. 44. Wilson B. Rehabilitation of memory. New York: The Guilford Press, 1987. 45. Hussain RA, Davis RL. Responsive care: behavioural intervention with elderly patients. Champaign IL: Research Press, 1985 46. Patterson R. Family management of the elderly. In: Carstensen LL, Edelstein BA, eds. Handbook of clinical gerontology. New York: Pergamon Press, 1987. 47. Prinz P, Raskind M. Aging and sleep disorders. In: Williams R, Karacan I, eds. Sleep disorders: diagnosis and treatment. New York: Wiley, 1978: 303-321. 48. Hachinski YC, Lassen NA, Marshall J. Multi-infarct dementia: a cause of mental deterioration in the elderly. Lancet 1974; 2: 207-210. 49. Miles L, Dement W. Sleep and aging. Sleep 1985; 3: 119-120.

50. Broughton R. Biorhythmic variations in consciousness and psychological functions. Canadian Psychological Review 1975; 16: 217-239.

Resume

Les perturbations du comportement de la personne agee atteinte de demence provoquent une detresse considerable tant chez Ie malade que chez les prestateurs de soins. Les auteurs commencent par resumer les phenomenes associes a ces perturbations. Puis, its examinent les methodes pharmacologiques permettant d' attenuer ces dernieres. Finalement, its abordent certains progres recents accomplis en conjugant les enseignements de la modification du comportement et de la neuropsychologie pour decouvrir des methodes non pharmacologiques limitant les comportements problematiques. Selon eux, dans Ie traitement de cas individuels, la combinaison des deux approches est souvent necessaire et ofire Ie plus de chance de reussite.