Description

The role of specific brain regions in the pathophysiology of clinical depression is poorly understood. However, one brain area, the prefrontal cortex, is emerging as likely being directly involved in clinical depression. The authors review accepted clinical diagnostic criteria for depression and show how these relate to the behavioral changes seen after prefrontal cortex damage in man and other animals. Information from structural (MRI, CT) and functional imaging (SPECT, PET) is then examined for direct evidence of prefrontal cortex abnormalities in clinically depressed subjects.

Functional imaging studies, with few exceptions, demonstrate prefrontal lobe hypo metabolism in primary and secondary depression, with severity of depression often correlating with the degree of frontal inactivity. These studies imply that dysfunction of the prefrontal cortex, particularly with respect to its role in modulating limbic activity, could conceivably produce many of the symptoms seen in clinical depression. Viewing clinical depression as a disease involving dysfunction of the prefrontal cortex and connected brain regions may prove helpful in both the clinical management of depression and in clarifying future avenues for research. Depression 2:59–72 (1994). © 1994 Wiley-Liss, Inc.Belief in a concerned God has been shown to be associated with lower depression through the mediation of hopelessness. This study hypothesized that this relationship would also be true longitudinally. Shortly after admission to treatment and 8 weeks later, 136 adults with clinical depression completed the Beck Depression Inventory, the Beck Hopelessness Scale, and the Religious Well-Being Scale (RWB). Logistic regression models supported an association of baseline RWB, but not baseline hopelessness, with a 50% reduction in symptoms after 8 weeks. Persons in the upper third of RWB at admission were 75% more likely to have a response to treatment than persons in the lower
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Journal of Annals of Behavioural Science