Abstract
Increasing evidence indicates that abnormal pain processing is present in the central nervous system of patients with Crohn’s disease (CD). The purposes of this study were to assess changes in gray matter (GM) volumes in CD patients in remission and to correlate structural changes in the brain with abdominal pain. We used a 3.0 T magnetic resonance scanner to examine the GM structures in 21 CD patients with abdominal pain, 26 CD patients without abdominal pain, and 30 healthy control subjects (HCs). Voxel-based morphometric analyses were used to assess the brain GM volumes. Patients with abdominal pain exhibited higher CD activity index and lower inflammatory bowel disease questionnaire scores than those of the patients without abdominal pain. Compare to HCs and to patients without abdominal pain, patients with abdominal pain exhibited lower GM volumes in the insula and anterior cingulate cortex (ACC); whereas compare to HCs and to patients with abdominal pain, the patients without abdominal pain exhibited higher GM volumes in the hippocampal and parahippocampal cortex. The GM volumes in the insula and ACC were significantly negatively correlated with daily pain scores. These results suggest that differences exist in the brain GM volume between CD patients in remission with and without abdominal pain. The negative correlation between the GM volumes in the insula and ACC and the presence and severity of abdominal pain in CD suggests these structures are closely related to visceral pain processing.
Highlights
Abdominal pain is an important clinical manifestation of Crohn’s disease (CD)
In our previous study [12], we found that, compare with healthy controls (HCs), patients with CD showed significant changes in gray matter (GM) volumes of multiple brain regions involved in pain, emotion, and homeostasis, and specific altered profiles of GM volume correlated with disease duration
We found the lowest GM volumes in the insula and anterior cingulate cortex (ACC) in remissive CD patients with abdominal pain
Summary
Abdominal pain is an important clinical manifestation of Crohn’s disease (CD). Such pain occurs in approximately 50% to 70% of patients during acute inflammation [1] and in a significant proportion of patients during clinical and/or endoscopic remission [2]. In our previous study [12], we found that, compare with healthy controls (HCs), patients with CD showed significant changes in GM volumes of multiple brain regions involved in pain, emotion, and homeostasis, and specific altered profiles of GM volume correlated with disease duration. These studies revealed changes in the GM structures in various brain regions, and pain has been associated with GM loss in numerous studies, the specific patterns of altered GM in patients with CD with or without abdominal pain have yet to be delineated
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