The vulnerability of remitted depressed patients for illness relapse may be related to the (re)activation of depressive thinking styles triggered by temporary dysphoric states. This is the first study to link such differences to prognosis following successful treatment for depression. Further understanding of factors predisposing to relapse/recurrence in recovered patients may help to shorten the potentially lifelong course of depression.

This study examined the nature of cognitive reactivity to mood changes in formerly depressed patients. Patients who recovered either through cognitive-behavior therapy (CBT; N = 25) or through pharmacotherapy (PT; N = 29) completed self-reported ratings of dysfunctional attitudes before and after a negative mood induction procedure. In response to similar levels of induced sad mood, PT patients showed a significant increase in dysfunctional cognitions compared with patients in the CBT group. To evaluate the effects of such cognitive reactivity on the subsequent course of depression, follow-up analyses reassessed 30 patients several years after initial testing. Results indicated that patients' reactions to the mood induction procedure were predictive of depressive relapse. These findings argue for differential effects of treatment on cognitive reactivity to mood induction and for the link between such reactivity and risk for later depressive relapse.

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A mood induction paradigm was used to examine dysphoria-related changes in two types of cognitive processing in individuals who had previously experienced depression. Formerly depressed patients (n = 23) and never-depressed controls (n = 27) completed the Dysfunctional Attitudes Scale, a self-report measure of effortful processing, and performed the Implicit Association Test, an automatic-reaction time task that measures evaluative bias, before and after a negative-mood induction. The formerly depressed group showed both an increase in endorsement of dysfunctional attitudes and a more negative evaluative bias for self-relevant information after the induction, relative to controls--however, there was no association between the mood-linked changes observed on these two measures. The shift in evaluative bias shown by the formerly depressed group was similar to that seen in a group of 32 currently depressed individuals. These findings suggest that even a mild negative mood in formerly depressed individuals can reinstate some of the cognitive features observed in depression itself.

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SynopsisA cognitive science analysis of the interaction between psychosocial stress and the neurobiology of affective illness highlights a number of mechanisms relevant to the study of recurrence in major depressive disorder. It builds on observations previously offered by Post (1992) regarding the importance of kindling and sensitization effects in determining activation of neural structures, and proposes a model of knowledge structure activation that follows similar parameters. Vulnerability to depressive relapse/recurrence is determined by the increased risk of particular negative patterns of information processing being activated in depressed states. As is found in studies of kindling and behavioural sensitization, the likelihood of cognitive patterns being activated is dependent on the frequency of past usage, and increased reliance on these patterns of processing makes it easier for their future activation to be achieved on the basis of increasingly minimal cues. This model suggests that the processes related to relapse/recurrence and episode onset may not be isomorphic and, as such, treatments that emphasize relapse prevention strategies should take this distinction into account.

The authors investigated processing of self-descriptive emotional information in depression using a modified Stroop color-naming task. Depressed (n = 58) and nondepressed control (n = 44) participants were required to name the color in which positive and negative adjectives, differing in the degree to which they described the person, were presented. These target adjectives were primed by emotional phrases that also varied according to degree of self-reference. Analyses indicated that depressed participants showed slower color-naming latencies for self-descriptive negative targets primed by self-descriptive negative phrases than for any other prime-target condition. No effect of prime-target relation was found for positive material with depressed participants, and nondepressed controls showed no effect of prime-target relation for material in either valence. These results support the hypothesis that negative information about the self is highly interconnected in the cognitive system of depressed patients.

Objective: While the efficacy ofcognitive-behaviour therapy (CBT)