| Summary: | Rationale/statement of the problem : Despite numerous studies on the influence of psychosocial stress on hypothalamic-pituitary-adrenal axis (HPA) system responsivity, heterogeneous results have been found with regard to depression in remission. In addition, knowledge concerning cognitive functioning in the remitted state is also narrow showing thus far inconsistent results. The present study investigated the effect of psychosocial stress on the cortisol response and cognitive performance in patients recovered from depression in comparison to healthy controls. Methods : Eighty patients who have recovered from depression for at least 6 months (average: 31 months) and 80 healthy matched controls were investigated on the effects of psychosocial stress (TSST) on the performance in an affective go/nogo task. Cortisol responses, behavioral inhibition, reaction time performance and emotional-cognitive functioning were analyzed. We hypothesized that stress vulnerability of cognitive performance is positively correlated to HPA system responsiveness (measured by salivary cortisol) in both healthy subjects and remitted patients but larger in remitted patients compared to healthy controls. Results : Thus far, preliminary analyses reveal no abnormal stress-associated HPA system response in patients recovered from depression in comparison to healthy controls. However, remitted patients showed impaired attentional set shifting in the go/nogo task. This impairment was positively correlated with the duration of illness. Conclusion : Our study is the first to investigate affective go/nogo task performance and effects of a stress challenge test in patients recovered from depression. Our data demonstrate that attentional set shifting deficits are not only present during acute episodes but also in remission. These deficits seem to be correlated with the duration of illness. Nonetheless, restored stress-associated HPA system function suggests recovery of the HPA system reactivity to psychosocial stress in patients remitted from depression. This in turn suggests that the observed cognitive impairment is not mediated by abnormal HPA responses.Cognitive impairment in the area of executive functioning may be considered a specific trait marker that persists after clinical and neuroendocrinological remission.
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