Does chronic occupational stress cause brain damage?
Cerebral Cortex

Cerebral Cortex publishes papers on the development, organization, plasticity, and function of the cerebral cortex, including the hippocampus. Studies with clear relevance to the cerebral cortex, such as the thalamocortical relationship or cortico-subcortical interactions, are also included.

During the last decade, Western societies have been facing increasing reports about a new work-related phenomenon. It affects healthy, productive, and highly functional individuals typically working long hours for many years without a normal weekend recovery. These persons complain of stereotyped symptoms, including memory and concentration problems, sleeplessness, profound fatigue, and a feeling of being emotionally drained, which they attribute to occupational stress. This condition is frequently misinterpreted as depression because of partially shared symptoms. However, it is seldom helped by anti-depressant medications and seems to represent a separate construct. The underlying mechanisms are unknown, and there is an ongoing discussion whether the described disabilities are caused by stress, if they could be associated with cerebral changes, or if we are confronted with a new medical condition.

Psychosocial stress, initially defined by Lazarus and Folkman (1987), is thought to result from an ?imbalance between demands and resources.? An adequate coping with stress stimuli involves specific networks in the brain, which encompass the structures processing emotion (primarily the amygdala), and parts of the frontal lobe that are involved in cognitive modulation of emotion (the anterior cingulate cortex (ACC) and the medial prefrontal cortex (mPFC).


We hypothesized that repeated, chronic stress could lead to damage of the brain areas which modulate stress perception, leading to a vicious cycle with impaired ability to cope with stress and a further facilitation of stress perception. To measure whether such damage could exist, we used measurements of the cortical thickness and of the volumes of specific brain structures known to be involved with the processing of psychosocial stress stimuli, including the amygdala. These measures were carried out using brain MRIs compared between 40 subjects reporting symptoms of chronic occupational stress (on average 38 years old) and 40 matched controls. We found that in stressed subjects, there was a significant thinning of the mesial prefrontal cortex (see below). Furthermore, in the frontal cortex, which is essential for our cognitive functions, the normal thinning effect of age was more pronounced than in the controls. In addition, the amygdala volumes were increased in subjects with occupational stress and the increase was positively correlated with the degree of perceived stress.

Together, these data suggest that chronic occupational stress may indeed be associated with specific changes in brain regions involved with the processing and modulation of stress stimuli.

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