Clinical and Biological Interactions in Affective and Cognitive Geriatric Syndromes

Abstract

Clinical and biological complexity is the rule rather than the exception in geriatric psychiatric syndromes. Typically, geriatric psychopathology develops in the context of medical and neurological disorders. Under these circumstances, ascertainment of symptoms and signs is difficult. Moreover, behavioral abnormalities, cognitive deficits, and physical symptoms and signs are often contributed by more than one psychiatric, neurological, or medical condition. Finally, symptoms change over time as various coexisting disease processes progress or subside, further complicating clinical assessment and diagnosis. Complexity has been viewed as an obstacle to medical research, which by necessity depends on reduction. Biological and psychosocial hypotheses are nothing but logical reductions, designed to permit understanding of a small part of a larger problem. Experimental design is an operational reduction intended at giving the best chance for hypothesis testing. Such reduction processes become complicated by the clinical intricacies of geriatric psychiatry syndromes. Despite the logical and experimental challenges posed by geriatric syndromes, their complexity has begun to provide meaningful clinical and biological information. Studying depression in Alzheimer’s disease patients exemplifies how comorbid geriatric syndromes can help address clinical and biological questions. In the study by Zubenko et al. in this issue [May 2003], the high prevalence of depression in patients with probable Alzheimer’s disease was confirmed. The study also observed that the depressive syndrome of Alzheimer’s patients is of mild severity and characterized by indecisiveness and diminished ability to concentrate but with limited depressive ideation and sleep disturbances. This symptom profile is difficult to distinguish from an uncomplicated dementia syndrome, thereby contributing to the underrecognition of depression. The increased frequency of psychotic symptoms in depressed Alzheimer’s disease patients further complicates ascertainment of depression. The difficulty in diagnosing depression is evidenced by the wide differences in depression prevalence estimates among patients with Alzheimer’s disease. Improving the methods of ascertainment (1) and treatment of depression in Alzheimer’s patients is critical, since depression contributes to excess disability, personal suffering, family disruption, and premature institutionalization. In addition to highlighting an important clinical problem, the comorbidity of depression and dementia has served as the stimulus for answering both clinical and biological questions. The early concept of “pseudodementia” was based on the assumption that the biological abnormalities of depression were the unitary cause of reversible Clinical and Biological Interactions in Affective and Cognitive Geriatric Syndromes George S. Alexopoulos, M.D.