Regional Neuroplastic Brain Changes in Patients with Chronic Inflammatory and Non-Inflammatory Visceral Pain

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.多项慢性炎症性疼痛性疾病中均已报道存在区域性皮层厚度改变，包括炎症性肠病（Inflammatory Bowel Disease, IBD）与肠易激综合征（Irritable Bowel Syndrome, IBS），但此类神经可塑性改变背后的具体机制仍未明确。为进一步阐明促成灰质改变的潜在机制，本研究旨在明确健康对照与两种伴或不伴慢性肠道炎症的慢性内脏痛综合征（chronic visceral pain syndromes）之间的区域性皮层厚度差异。本研究纳入41名健康对照者、11名腹泻型肠易激综合征（IBS）受试者及16名溃疡性结肠炎（Ulcerative Colitis, UC）受试者，所有受试者均接受了高分辨率T1加权磁化准备快速采集梯度回波扫描（high-resolution T1-weighted magnetization-prepared rapid acquisition gradient echo scans）。本研究采用神经影像实验室处理管线（Laboratory of Neuroimaging Pipeline）完成了结构影像预处理及感兴趣区（region of interests）内的皮层厚度分析。采用一般线性模型（general linear model）与线性对比分析（linear contrast analysis）检验组间差异。两种疾病组在多个皮层区域存在显著组间差异。与IBS受试者及健康对照者相比，溃疡性结肠炎受试者的前扣带皮层（anterior cingulate cortex）亚区及初级躯体感觉皮层（primary somatosensory cortex）的皮层厚度更高。与健康对照者相比，溃疡性结肠炎受试者的眶额皮层（orbitofrontal cortex）、岛叶（insula）中后段的皮层厚度更低；而肠易激综合征受试者的前岛叶皮层厚度更低。仅在溃疡性结肠炎受试者中观察到症状持续时间与眶额皮层、中央后回（postcentral gyrus）皮层厚度间存在强相关性。本研究结果提示，溃疡性结肠炎受试者所观察到的灰质改变机制为外周炎症（peripheral inflammation）介导的结果，而肠易激综合征受试者的灰质改变则可能主要由中枢机制（central mechanisms）主导。