Abstract
Regional cortical thickness alterations have been reported in many chronic inflammatory and painful conditions, including inflammatory bowel diseases (IBD) and irritable bowel syndrome (IBS), even though the mechanisms underlying such neuroplastic changes remain poorly understood. In order to better understand the mechanisms contributing to grey matter changes, the current study sought to identify the differences in regional alterations in cortical thickness between healthy controls and two chronic visceral pain syndromes, with and without chronic gut inflammation. 41 healthy controls, 11 IBS subjects with diarrhea, and 16 subjects with ulcerative colitis (UC) underwent high-resolution T1-weighted magnetization-prepared rapid acquisition gradient echo scans. Structural image preprocessing and cortical thickness analysis within the region of interests were performed by using the Laboratory of Neuroimaging Pipeline. Group differences were determined using the general linear model and linear contrast analysis. The two disease groups differed significantly in several cortical regions. UC subjects showed greater cortical thickness in anterior cingulate cortical subregions, and in primary somatosensory cortex compared with both IBS and healthy subjects. Compared with healthy subjects, UC subjects showed lower cortical thickness in orbitofrontal cortex and in mid and posterior insula, while IBS subjects showed lower cortical thickness in the anterior insula. Large effects of correlations between symptom duration and thickness in the orbitofrontal cortex and postcentral gyrus were only observed in UC subjects. The findings suggest that the mechanisms underlying the observed gray matter changes in UC subjects represent a consequence of peripheral inflammation, while in IBS subjects central mechanisms may play a primary role.
Highlights
Inflammatory bowel diseases (IBD) such as ulcerative colitis (UC) are characterized by chronically recurring symptoms of abdominal pain associated with flares of mucosal inflammation
In irritable bowel syndrome (IBS), chronically recurring symptoms of abdominal pain and discomfort occur in the absence of mucosal inflammation or other identifiable nociceptive triggers, and symptom flares are often triggered by psychosocial stressors
Several pieces of evidence support the concept that IBD patients effectively engage endogenous pain inhibition systems [3], including greater engagement of a cortico limbic-pontine pain modulation network compared to IBS subjects [4]
Summary
Inflammatory bowel diseases (IBD) such as ulcerative colitis (UC) are characterized by chronically recurring symptoms of abdominal pain associated with flares of mucosal inflammation. Several pieces of evidence support the concept that IBD patients effectively engage endogenous pain inhibition systems [3], including greater engagement of a cortico limbic-pontine pain modulation network compared to IBS subjects [4] These differences in the engagement of endogenous pain modulation systems may explain the clinical observation that in uncomplicated UC, abdominal pain is not a prominent symptom even during flares. Several studies have applied multimodal brain imaging to investigate the presence of grey matter changes in patients with various chronic pain conditions without known nociceptive drive [5,6,7,8,9], with presumed nociceptive drive [10,11,12], and with known inflammatory drive [13,14,15,16,17,18]. The use of different analysis techniques by different groups, makes interpretive comparisons between studies and between different patient populations more difficult
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
