Somatic Manifestations of Posttraumatic Stress

Syndromes characterized by somatic and/or visceral pain and discomfort are commonly observed in individuals with a history of traumatic stress. For example, irritable bowel syndrome and fibromyalgia are more common in patients with a history of abuse, and similar symptoms have been reported by soldiers following most wars (post Gulf War Syndrome). Aversive early life events increase the vulnerability of individuals to develop viscerosomatic pain syndromes during stressful situations in adult life, presumably by permanently increasing stress responsiveness. While acute stress induced inhibition of somatic pain perception has been well characterized in rodents, the mechanisms underlying stress- induced enhancement of visceral and somatic pain perception are not known. However, a series of observations in patients with IBS and FM support a role for altered responsiveness of central stress systems in the development of stress-induced hyperalgesia: they include preattentive hyperresponsiveness to auditory stimuli, increased activation of attentional mechanisms, including the anterior cingulate cortex, increased emotional responses to stressors, increase central levels of stress mediators such as corticotropin releasing factor (CRF) and substance P (SP), and altered activity of the hypothalamic pituitary adrenal (HPA) axis. Several of these findings seen in human patients, can also be demonstrated in animal models of enhanced stress responsiveness. Aversive early life events in terms of postnatal maternal stressors permanently alter the expression of central stress mediators, endogenous pain modulation systems, central opioid mechanisms, HPA axis responsiveness and produce anxiety like behaviors in the adult animal. Pharmacologic inhibition of central stress mediators such as CRF and SP can reverse some of these abnormalities. A better understanding of the role of genetic factors as well as early life aversive experiences as vulnerability factors for the development of viscerosomatic pain syndromes will help to develop preventive interventions in susceptible individuals.

Supported by NIH grants DK 48351 (EAM), AR 46122 (LC), NR 04881 (BN) and P50 DK64539 (EAM)