Central processing of noxious stimuli in patients with irritable bowel syndrome compared to healthy controls.

摘要

Irritable Bowel Syndrome (IBS) is a complex disorder of unknown etiology. Research into the pathophysiology of IBS suggests the involvement of psychological, hormonal, immunological, genetic, cardiovascular, and autonomic nervous system factors, as well as peripheral and central sensitization of pain signals in the etiology and/or maintenance of IBS. Visceral hyperalgesia is consistently observed in IBS patients. However, recent investigations have found evidence of somatic hyperalgesia, not seen in earlier studies, suggesting the possibility of a dysfunction in central pain regulatory mechanisms.; Evidence suggests a role for central sensitization in IBS pain. Psychophysical investigations into dysregulation of the endogenous pain regulatory mechanisms of temporal summation and diffuse noxious inhibitory controls (DNIC) have been consistently demonstrated in other chronic pain conditions such as Fibromyalgia and Temporomandibular Disorder, which show high comorbidity with IBS.; The primary objective of this investigation was to explore the role of central sensitization in IBS pain by assessing both efferent (DNIC) and afferent (temporal summation) central modulation of nociception in IBS patients. Group differences in psychological, autonomic nervous system, and general pain measures were also assessed.; Forty eight pre-menopausal females (27 with IBS) participated in this investigation. No group differences were seen in temporal summation or the DNIC effect on temporal summation. Similarly, no group differences were seen in any general pain measures or in sympathetic tone. IBS subjects reported significantly greater stress than Controls on measures of; state anxiety, depression, catastrophizing, and anger-out expression. IBS subjects also demonstrated significantly lower levels of DNIC than Controls during noxious tonic conditioning stimuli. However, non-noxious conditioning stimuli also produced an apparent DNIC effect in a counterbalanced design. After controlling for non-specific effects occurring in the non-painful conditioning protocol (distraction, and psychological measures associated with DNIC), IBS subjects continue to show deficient DNIC (p 0.01).; This is the second investigation that has attempted to account for non-specific effects in the investigation of DNIC. Only by controlling for non-specific effects, can evidence of deficient DNIC can be attributed to dysregulation in endogenous analgesic mechanisms. Further studies are needed to elucidate whether deficient DNIC is a cause or consequence of IBS pain.