Depressive pseudodementia in the elderly

It was noted over 100 years ago that severe affective disorder could lead to cognitive dysfunction. Patients with depressive illness have been misdiagnosed as having dementia and conversely patients with dementia have been misdiagnosed as depressed. The former error is especially unfortunate since available treatment may be withheld. The apparent similarity of the cognitive deficits at clinical presentation, particularly in the elderly, is responsible, in part, for the difficulty of differential diagnosis. This article addresses two main questions: (a) is the cognitive dysfunction associated with depression actually distinguishable from that of the dementias, either cortical or subcortical? ; (2) does normalization of cognition occur on recovery from depression? As Berrios (1985) has pointed out, it was realized as early as 1883 that severe affective disorder could lead to cognitive impairment. The term ‘pseudodementia’ was first used in 1952 by Madden et al. to describe cases in which the clinical presentation had led to a diagnosis of dementia subsequently to be changed because of remission of symptoms. In a study of 300 patients over the age of 45 years, Madden et al. found that pseudodementia presented as disorientation, defects in recent memory, retention, calculation, and judgement, being particularly common in involutional psychoses and in psychoses associated with cerebrovascular disease and depression. Since then, pseudodementia has been associated with many additional psychiatric and medical conditions (Kloh, 1961; Marsden and Harrison, 1972; Nott and Fleminger, 1975; Wells, 1979; Smith and Kiloh, 1981). McAllister (1 983) reported that patients with depressive pseudodementia were significantly older than patients with other psychiatric illness. Thus, it is not surprising that the term pseudodementia is often used in clinical practice synonymously with depressive pseudodementia in the elderly, nor that it poses severe problems of differential diagnosis with dementia. For example, a substantial proportion (8-lOY0) of patients initially diagnosed as demented were later considered to be suffering from depression or affective disorders (Marsden and Harrison, 1972; Ron et al., 1979). Furthermore, in a recent study, the corollary form of misdiagnosis has been demonstrated. Sachdev et al. (1990) reported a follow-up study of 19 patients diagnosed as having pseudodementia over 10 years earlier (Smith and Kiloh, 1981) in which two cases were possibly misdiagnosed; one was a case of definite dementia and in the other dementia could not be excluded. At clinical presentation, the cognitive deficits appear so similar that a difficulty of differential diagnosis arises, and the true diagnosis becomes clear only during the course of the illness. At least until recently, dementia has been defined as an acquired, global condition of cognitive impairment which is progressive and irreversible (Trethowan, 1979; Lishman, 1987). In marked contrast, the hallmarks of pseudodementia are regarded as reversibility and lack of progression, since it is induced by a ‘functional’ illness and therefore symptomatology clears on recovery (Madden et al., 1952; Kiloh, 1961; Wells, 1979). Despite the lack of diagnostic specificity of the term pseudodementia, Sachdev et al. (1 990) have argued that nevertheless it has descriptive value for clinicians, who find it useful to indicate one or more of the following: (1) impairments in memory, learning, and related cognitive functions caused by psychiatric illness; (2) when the impairment is likely to be non-progressive and is potentially reversible if the primary illness is treated; and (3) either no neuropathological process can be identified, or if