Cognitive impairment in depression is well recognized but poorly understood. A subset of depressed patients exhibit a syndrome of severe neuropsychological deficits which may be partially reversible upon episode resolution. This has been called depressive pseudodementia, the dementia syndrome of depression and depression induced cognitive impairment. The epidemiology, clinical features, natural history and prognosis of this condition support the notion of an underlying organic aetiology. The most plausible neurobiological candidate involved in the pathogenesis is hyperactivity of the hypothalamo-pituitary-adrenal (HPA) axis. The homeostatic regulation of the HPA axis becomes increasingly vulnerable to disruption in geriatric depression and perhaps particularly in depressive dementia. Hypercortisolaemia has been correlated with cognitive impairment in depression as well as in other related psychiatric conditions. The mechanism of this abnormality may involve hippocampal dysfunction. Further longitudinal studies are needed to clarify the role of the HPA axis in the cognitive decline of depressive illness.
KEY WORDS-HPA axis; cognition; geriatric depression; hippocampus; pseudodementia Major depressive disorder is almost invariably associated with some degree of impairment on neuropsychological testing (Cassens et al., 1990). Until recently it was assumed that these deficits were minor and related to the poor concentration and cooperation of the depressed patients. It is now clear that a significant proportion of sufferers from affective disorder develop cognitive abnormalities which are quantitatively (and perhaps qualitatively) indistinguishable from patients with primary degenerative dementia (Lamberty and Bieliauskas, 1993;Rabins and Pearlson, 1994). The aetiology of the dementia syndrome of depression is poorly understood (Emery and Oxman, 1992). Classically it was thought to be both functional and completely reversible, distinct from the primary degenerative dementias. These assumptions have recently been called into question as the clinical and prognostic separation of these syndromes is unclear (Desrosiers, 1992).
The possible organic basis to depression induced cognitive impairment has been a neglected topic of