ABSTRACT
Avariety of brain regions identified as central pain-processing circuitry (‘‘central pain matrix’’), previously described in somatic pain studies (1,2) and well supported by neuroanatomical data (3) [in particular, the insula, the dorsal aspects of the anterior cingulate cortex (dACC), and the thalamus], have also been found to be activated consistently in response to visceral stimuli (4). However, other brain areas including somatosensory, limbic, paralimbic, and pontine regions have also been reported as activated by visceral stimulation though less consistently (4). Due to the lack of rigorous study designs able to isolate specific networks involved in various aspects of visceral stimulus processing [e.g., cognitive/affective influences on pain modulation, attention, anticipation, arousal, and autonomic responses to visceral stimuli (4)], functional brain imaging studies of functional disorders such as irritable bowel syndrome (IBS) to date have not clearly identified reproducible alterations in brain-gut interactions necessary to explain satisfactorily explain the phenomena of enhanced visceral perception, altered autonomic responses, or the frequently co-occurring nongastrointestinal symptoms such as fatigue, loss of energy, and other symptoms of physical discomfort. For example, it is not clear if the primary central abnormality in IBS is related to (i) enhanced selective attentional processes toward symptom-related cues (hypervigilance) and associated endogenous facilitation of visceral perception, (ii) a compromised endogenous pain inhibition system, or (iii) normal processing of pathological visceral input from the periphery.
