Excess disability was examined in 17 nursing home residents with dementia by comparing their performance of morning care tasks under two activities of daily living (ADL) caregiving approaches—a dependence-supportive one under usual care and an independence-supportive one under functional rehabilitation. The results suggest that excess disability in severely cognitively impaired and functionally disabled residents can be reduced by increasing opportunities for independent activity, and substituting nondirective and directive verbal assists for physical assists. Further, the findings indicate that increased independence in ADL can be achieved without increasing disruptive behaviors and can foster appropriate requests for task-related help during caregiving. Functional rehabilitation, however, requires more time than usual care.

Few studies have examined the relationship between behavioral and psychological symptoms of dementia (BPSD) and neuropathology. Bondareff (1996), who summarized recent work on the subject, concluded that there is no known persecutory, erotomanic, or other specific delusional, illusionary, or hallucinatory center in the brain. Thus, cliniconeuropathologic correlations to BPSD cannot be assumed, because this would require linking complex symptoms to a single, circumscribed alteration of one neuroanatomic area, or one neurotransmitter system, or even one type of histopathologic alteration, regardless of its location. Traditionally, BPSD have been investigated as if they were psychopathologically and neuropsychologically independent of the patient's cognitive disturbances. This may have led to the modest results of some studies. Interestingly, several early studies postulated innovative hypotheses on the neuropathology of BPSD, and sought to verify those hypotheses.

The biologic mechanism by which behavioral and psychological symptoms of dementia (BPSD) occur in some patients with Alzheimer's disease (AD) is not understood, but it may be related to the selected loss of different neuronal populations or specific neurotransmitters. In many patients, these neuronal and neurotransmitter losses are likely to be the end result of the inheritance of a number of genetic risk factors for AD. Thus BPSD may arise indirectly as a result of genetic risk factors for AD. However, an alternative, or possibly complementary, hypothesis is that genetic risk factors for neuropsychiatric phenomena may, in normal circumstances, be clinically silent until neurodegeneration occurs from whatever cause.

Psychotic symptoms in Alzheimer's disease (AD) have been associated with increased rates of cognitive impairment and functional decline. Prior studies have been conflicting with regard to whether AD patients with psychosis (AD+P) have evidence of more severe neuropathologic findings at postmortem exam. We examined the severity of neuritic plaques and neurofibrillary tangles in six brain regions—middle frontal cortex, hippocampus, inferior parietal cortex, superior temporal cortex, occipital cortex, and transentorhinal cortex—in 24 AD+P subjects and 25 matched AD subjects without psychosis (AD-P). All analyses controlled for the presence of cortical Lewy bodies, and corrected for multiple comparisons. We found no significant associations between neuritic plaque and neurofibrillary tangle severity and AD+P, and no significant associations with any individual psychotic symptom. The association of AD+P with a more rapidly progressive course of AD appears to be mediated by a neuropathologic process other than increased severity of plaque and tangle formation.

The underlying causes of behavioral and psychological symptoms of dementia (BPSD) can be related to biologic factors, such as changes in brain morphology and neurotransmitter functions, and to personal factors, such as previous personality, psychological defenses, and coping strategies. We must also consider the extent to which environmental factors contribute to the etiology of BPSD.

The term behavioral and psychological symptoms of dementia (BPSD) encompasses a diverse cluster of behavioral disturbances, such as restlessness (Hope et al., 1994), aggression (Patel & Hope, 1992), and shouting (Cohen-Mansfield & Werner, 1997), and a variety of psychiatric symptoms, including delusions (Burns et al., 1990), hallucinations (Holroyd & Sheldon-Keller, 1995), depression (Greenwald et al., 1989), and anxiety (Ballard et al., 1996a). Such symptoms are extremely common in patients with dementia and have important associations with burden and depression in caregivers.

Compared with the rather uniform cognitive syndrome in Alzheimer's disease (AD), behavioral and psychological symptoms of dementia (BPSD) are considerably more heterogeneous in terms of incidence, prevalence, and association with disease duration and severity of dementia (Hope et al., 1999). The neurobiologic basis of AD is obviously less of a determinant of noncognitive symptoms than of cognitive symptoms. Therefore, the possible psychological and social causes of BPSD, such as premorbid personality, should be considered. Underlying personality traits not only shape a person's response to normal aging, but also set the stage for a range of responses to age-related stress and brain disease (Agronin, 1998).

Clinical observations leave little doubt that environment has a considerable effect on behavioral and psychological symptoms of dementia (BPSD), and many environmental interventions have been proposed and implemented in an attempt to manage behavioral problems in patients with Alzheimer's disease (AD). However, as Dr. Mintzer commented, there is no theoretical construct for validating environmental interventions. He pointed out the need for consensus on a hypothesis to be tested so that the value of environmental interventions can be proven.

Hallucinations and delusions have been described in all types of dementia, including vascular dementia, Lewy body dementia, and dementia associated with Parkinson's disease. They have been recognized in Alzheimer's disease (AD) since the illness was first described (Alzheimer, 1957).