Brain Responses to Visceral and Somatic Stimuli in Patients With Irritable Bowel Syndrome With and Without Fibromyalgia

C.N.S. Center for Neurovisceral Sciences & Women's Health, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, USA.
The American Journal of Gastroenterology (Impact Factor: 10.76). 06/2003; 98(6):1354-61. DOI: 10.1111/j.1572-0241.2003.07478.x
Source: PubMed


Symptoms of irritable bowel syndrome (IBS) and fibromyalgia (FM) commonly coexist. We hypothesized that one of the mechanisms underlying this comorbidity is increased activation of brain regions concerned with the processing and modulation of visceral and somatic afferent information, in particular subregions of the anterior cingulate cortex (ACC).
Regional cerebral blood flow (rCBF) was assessed in age-matched female IBS (n = 10) and IBS + FM (n = 10) subjects using H(2)(15)O positron emission tomography during noxious visceral (rectal) and somatic pressure stimuli.
GI symptom severity was significantly higher in the IBS patients compared with the IBS + FM patients (p < 0.05). In addition, IBS + FM patients rated somatic pain as more intense than their abdominal pain (p < 0.05). Whereas the somatic stimulus was less unpleasant than the visceral stimulus for IBS patients without FM, the somatic and visceral stimuli were equally unpleasant in the IBS + FM group. Group differences in regional brain activation were entirely within the middle subregion of the ACC. There was a greater rCBF increase in response to noxious visceral stimuli in IBS patients and to somatic stimuli in IBS + FM patients.
Chronic stimulus-specific enhancement of ACC responses to sensory stimuli in both syndromes may be associated with cognitive enhancement of either visceral (IBS) or somatic (IBS + FM) sensory input and may play a key pathophysiologic role in these chronic pain syndromes.

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    • "In addition, the reporting of chronic pain may result from aberrant sensory processing within the CNS. Aberrant sensory processing is understood to be the underlying pain mechanism for those with FGID and fibromyalgia (Chang et al, 2003). It is also suggested that sympathetic overactivity contributes to central modulation, thus enhancing maladaptive behaviour "
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