Neuroendocrine, Cognitive and Structural Imaging Characteristics of Women on Longterm Sickleave with Job Stress–Induced Depression

A recent increase in long-term sick leave (LTSL) in Sweden affects mostly women in the public sector. Depression-related diagnoses account for most of the increase, and work-related stress has been implicated. We examined dexamethasone/corticotropin-releasing hormone (dex/CRH) test responses, magnet...

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Veröffentlicht in:Biological psychiatry (1969) 2006-10, Vol.60 (8), p.867-873
Hauptverfasser: Rydmark, Ingrid, Wahlberg, Kristina, Ghatan, Per Hamid, Modell, Sieglinde, Nygren, Åke, Ingvar, Martin, Åsberg, Marie, Heilig, Markus
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Sprache:eng
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Zusammenfassung:A recent increase in long-term sick leave (LTSL) in Sweden affects mostly women in the public sector. Depression-related diagnoses account for most of the increase, and work-related stress has been implicated. We examined dexamethasone/corticotropin-releasing hormone (dex/CRH) test responses, magnetic resonance imaging measures of prefrontocortical and hippocampal volumes, and cognitive performance in 29 female subjects fulfilling three core criteria: 1) LTSL>90 days; 2) unipolar depression or maladaptive stress reaction with depressed mood; 3) job-related stress given as a reason for disability. This group was compared with 28 healthy matched controls. The cortisol response to CRH differed markedly between the two groups ( p = .002), with a dampened response in patients. This difference remained after removing subjects on antidepressant drugs ( p = .006) or smokers ( p = .003). Neither hippocampal nor prefrontocortical volumes differed. Performance on hippocampus-dependent declarative memory tests did not differ between groups, but the LTSL group had impaired working memory. Our most salient finding is an attenuated dex-CRH response in patients on LTSL due to job-stress related depression. This is opposite to what has been described in major depression. It remains to be established whether this impairment is the end result of prolonged stress exposure, or a pre-existing susceptibility factor.
ISSN:0006-3223
1873-2402
DOI:10.1016/j.biopsych.2006.04.029