OBJECTIVE: We sought to identify central loci that activate in response to visceral stimuli (stool and pain). We had a particular interest in observing the anterior cingulate gyrus and frontal cortex in normals and in patients with intestinal disease, including inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). METHODS: Subjects underwent rectal balloon distention to a sensation of stool and to a sensation of pain while undergoing blood oxygenation level-dependent functional magnetic resonance imaging. Experiments were conducted in a Magnex 3.0-T whole body magnet with a Bruker Biospec console and a quadrature head coil. Four contiguous 5.0-mm oblique axial slices designed to optimize coverage of areas believed to be responsive to noxious stimulation were acquired. Activations were detected by using cross-correlation maps (p < 0.001) for individual subjects. The experimental groups were compared using both an analysis of variance and profile analysis. RESULTS: A significantly higher percentage of pixels activated in the anterior cingulate gyrus over both pain and stool conditions for the control group than for the IBS group and for the IBS group than for the IBD group (p < 0.035). Deactivation of left somatosensory cortex was greater for the IBS group than for the IBD group and greater for the IBD group than for the controls (p < 0.0065) in the boxcar condition. Frontal deactivation in controls compared with disease groups bordered on statistical significance. Profile analysis of the three groups across six regions of interest revealed that the control and IBD groups were distinguished by different profiles of response (p < 0.005). Nonparametric evaluation of the data suggests that, among the pixels in the anterior cingulate activating to pain, there are two patterns of response to pain-on/off and graded. This was true for both controls and disease groups. CONCLUSIONS: Normal controls and subjects with IBD and IBS share similar loci of activations to visceral sensations of stool and pain. Both activation and deactivation of particular regions of interest differentiate the three groups, as do profiles of patterned response across six of the regions of interest for the control and IBD groups.
OBJECTIVE: We sought to identify central loci that activate in response to visceral stimuli (stool and pain). We had a particular interest in observing the anterior cingulate gyrus and frontal cortex in normals and in patients with intestinal disease, including inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). METHODS: Subjects underwent rectal balloon distention to a sensation of stool and to a sensation of pain while undergoing blood oxygenation level-dependent functional magnetic resonance imaging. Experiments were conducted in a Magnex 3.0-T whole body magnet with a Bruker Biospec console and a quadrature head coil. Four contiguous 5.0-mm oblique axial slices designed to optimize coverage of areas believed to be responsive to noxious stimulation were acquired. Activations were detected by using cross-correlation maps (p < 0.001) for individual subjects. The experimental groups were compared using both an analysis of variance and profile analysis. RESULTS: A significantly higher percentage of pixels activated in the anterior cingulate gyrus over both pain and stool conditions for the control group than for the IBS group and for the IBS group than for the IBD group (p < 0.035). Deactivation of left somatosensory cortex was greater for the IBS group than for the IBD group and greater for the IBD group than for the controls (p < 0.0065) in the boxcar condition. Frontal deactivation in controls compared with disease groups bordered on statistical significance. Profile analysis of the three groups across six regions of interest revealed that the control and IBD groups were distinguished by different profiles of response (p < 0.005). Nonparametric evaluation of the data suggests that, among the pixels in the anterior cingulate activating to pain, there are two patterns of response to pain-on/off and graded. This was true for both controls and disease groups. CONCLUSIONS: Normal controls and subjects with IBD and IBS share similar loci of activations to visceral sensations of stool and pain. Both activation and deactivation of particular regions of interest differentiate the three groups, as do profiles of patterned response across six of the regions of interest for the control and IBD groups.
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