​Stress is often a powerful pain killer. Stress activates several brain-orchestrated pain inhibitory actions, including the activation of the hypothalamus-pituitary-adrenal axis (HPA-axis) resulting in the release of cortisol. The latter is often regarded as the major stress hormone in the human body, and besides its powerful anti-inflammatory action it also exerts endogenous analgesia. However, severe and chronic stress often leads to a maladaptive response inside the central nervous system. Especially when the person’s brain decides that the stress level is too high or too much (to cope with), the brain switches to a status that in the end will be maladaptive. This implies several brain mechanisms, including the decreased availability of two major inhibitory neurotransmitters in the central nervous system: serotonin and GABA (gamma-aminobutyric acid) - two major neurotransmitters responsible for enabling brain-orchestrated endogenous analgesia. Most clinicians nowadays are aware of the possibility that pain can be either nociceptive or neuropathic in nature. 

In response to severe and chronic stress, the brain’s capacity to produce serotonin and GABA reduces, resulting in decreased capacity to inhibit pain. This on its own opens to paths to, or accelerates the hyperexcitability of the central nervous system …. Also the HPA-axis becomes exhausted, resulting in less production of the ‘body’s natural stress coping drug’ cortisol, again diminishing the body’s capacity to inhibit pain. 

References & further reading:
http://www.ncbi.nlm.nih.gov/pubmed/24316519
http://www.ncbi.nlm.nih.gov/pubmed/21636214
http://www.ncbi.nlm.nih.gov/pubmed/18255166
Related Pain in Motion-post:
http://www.paininmotion.be/EN/news-stress-adaptation.html

Jo Nijs