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Residual neuropsychological impairments in euthymia




Kraepelin (1921) distinguished manic depression from schizophrenia on the basis of its relapsing and remitting course. Patients with affective illness, unlike those with dementia praecox, were thought to experience remission without cognitive impairment. Recent investigations of patients in the euthymic phase of bipolar disorder, however, have challenged this view. Many patients continue to experience psychological and social difficulties, and while the extent to which neuropsychological impairment remains is less clear, most studies report at least some degree of residual cognitive dysfunction in one or more tasks administered.

Asarnow & MacCrimmon (1981) used a test of attention and visual information processing to compare the performance of out-patients with manic depression or schizophrenia — both groups judged by their attending psychiatrists to be free from major symptoms — with that of healthy controls. Performance of the manic depression group was midway between that of the schizophrenia and control groups, suggesting that people with bipolar disorder demonstrate cognitive impairments that are probably not entirely due to residual psychotic symptoms. Similarly, Tham et al (1997) administered an extensive range of neuropsychological tasks to patients with recurrent mood disorder (10 unipolar and 16 bipolar) who were euthymic at the time of neuropsychological assessment. Cognitive functioning was markedly impaired in a substantial number of these patients. More recently, Ferrier et al (1999) reported residual impairment of executive function in people with euthymic bipolar disorder after controlling for age, premorbid intelligence and depressive symptomatology. Rubinsztein et al (2000) found asymptomatic patients with bipolar disorder (in remission for at least 4 months) to show deficits on tests of visuospatial recognition memory; response latency, but not accuracy, on four distinct tests of executive function, was also impaired. Other investigators have reported evidence of residual impairment as well (Jones et al, 1994; McKay et al, 1995; Kessing, 1998 — but see Kerry et al, 1983).

While the jury is still out on the precise neuropsychological profile found in euthymic bipolar disorder, the balance of evidence from such studies supports a hypothesis of residual cognitive impairment. It is important to note that the bulk of these studies employ cross-sectional, between-subject designs that compare euthymic patients with bipolar disorder with healthy controls. As mentioned above, longitudinal, within-subject designs are more effective in assessing how cognitive performance changes with symptomatic recovery. Clearly, both types of study are necessary if we are to address whether performance of euthymic patients with bipolar disorder is inferior to that of healthy controls, and to demonstrate deterioration or improvement of cognitive functioning within a single subject group. One final note of caution is that some studies do not measure manic or depressive symptomatology during the euthymic phase under study (see Rubinsztein et al, 2000, for a notable exception). It is therefore possible that subclinical psychopathology may at least partially account for the residual deficits observed.

Thus, while recent experiments have established the range and depth of cognitive impairments associated with depression, mania is clearly suffering from a lack of attention. Preliminary results suggest wide-ranging deficits in patients with mania; but a comprehensive investigation of cognitive functioning across a full spectrum of tasks should still be undertaken. Comparisons of unipolar and bipolar forms of depression have revealed interesting findings; they suggest that studies presupposing the essential similarity of unipolar illness with bipolar illness may be too simplistic. Likewise, the presumption that (bipolar) mania and unipolar depression represent opposite emotional pales in a cognitive—affective continuum may also be an over-simplified model. It is also possible that the cognitive deficits observed in bipolar disorder (depressed phase) could stem from a source unrelated to that of similar impairments in unipolar depression, and that the relationship of affect to all these impairments might be more complicated.

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