Neurotransmitter alterations in the anterior cingulate cortex in Crohn's disease patients with abdominal pain: A preliminary MR spectroscopy study.
Neurotransmitter alterations in the anterior cingulate cortex in Crohn's disease patients with abdominal pain: A preliminary MR spectroscopy study.
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DOI：
10.1016/j.nicl.2018.09.008
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Xu M
中科院分区：
文献类型：
--
作者：
Lv K;Song W;Tang R;Pan Z;Zhang Y;Xu Y;Lv B;Fan Y;Xu M
已知克罗恩病（CD）在受影响的患者中引起腹痛以及中枢神经系统（CNS）的功能和结构改变。本研究旨在通过质子磁共振波谱（1H-MRS）技术检测伴有腹痛的CD患者双侧前扣带皮层（ACC）代谢物的变化，进一步探讨其神经机制。本研究招募了16名伴有腹痛的乳糜泻患者和13名无腹痛的乳糜泻患者，以及20名健康对照（hc）。临床评估包括0-10视觉模拟疼痛量表（VAS）、医院焦虑和抑郁量表（HADS）和克罗恩病活动指数（CDAI）。本研究选择双侧ACC作为感兴趣区域（ROI）。采用LCModel和Gannet定量分析双侧ACC代谢产物。统计学分析采用独立样本t检验和单因素方差分析（ANOVA）。采用Spearman相关分析来检验代谢物水平与临床评价之间的关系。结果显示，伴有腹痛的CD患者在双侧ACC中谷氨酸(Glu)/（肌酸 + 磷酸肌酸，总肌酸，tCr）水平明显高于无腹痛的CD患者（p = 0.003,0.009）。疼痛性CD组（Glutamate + Glutamine, Glx）/tCr水平高于非疼痛性CD组（p = 0.022）。此外，在疼痛CD组中，Glu/tCr和Glx/tCr水平与疼痛VAS评分有很强的相关性（ρ = 0.86,0.59,p < 0.05）。同时，伴有腹痛的CD患者γ-氨基丁酸+ (GABA+)/tCr水平显著低于hc （p = 0.002）。在一定程度上，CDAI与GABA+/tCr水平呈负相关（p = 0.088,ρ = −0.60）。乳糜泻伴腹痛患者疼痛加工的神经机制与神经化学代谢物密切相关。Glu和GABA的失衡可能在乳糜泻患者的腹痛过程中起关键作用。这种疼痛机制可能与脑肠轴上的肠道微生物群有关。首次对伴有腹痛的乳糜泻患者的脑代谢物进行了研究。采用1H-MRS在体内进行研究。伴有腹痛的ACC患者Glu和GABA水平发生改变。乳糜泻患者腹痛与疼痛加工中的神经递质有关。
Crohn's disease (CD) has been known to cause both abdominal pain alongside functional and structural alterations in the central nervous system (CNS) in affected patients. This study seeks to determine the alternations of metabolites in the bilateral anterior cingulate cortex (ACC) of CD patients with abdominal pain by using proton magnetic resonance spectroscopy (1H-MRS) to further explore the neural mechanism. Sixteen CD patients with abdominal pain and 13 CD patients without abdominal pain, were recruited alongside 20 healthy controls (HCs) for this study. Clinical evaluations, including the 0–10 Visual Analogue Scale (VAS) of pain, Hospital Anxiety and Depression Scale (HADS) and Crohn's Disease Activity Index (CDAI), were evaluated prior to MR scanning. This study selected the bilateral ACC as the region of interest (ROI). The metabolites of the bilateral ACC were quantitatively analyzed by LCModel and Gannet. A independent sample t-test and one-way analysis of variance (ANOVA) were performed for statistical analysis. Spearman correlation analyses were performed to examine the relationship between the metabolite levels and clinical evaluations. The results indicated that CD patients with abdominal pain exhibited significantly higher levels of Glutamate (Glu)/(creatine + phosphocreatine, total creatine, tCr) over CD patients without abdominal pain, and HCs (p = 0.003, 0.009, respectively) in the bilateral ACC. The level of (Glutamate + Glutamine, Glx)/tCr of pain CD group was higher than non-pain CD group (p = 0.022). Moreover, within the pain CD group, Glu/tCr and Glx/tCr levels correlated strongly with the VAS scores of pain (ρ = 0.86, 0.59 respectively, p < 0.05). Meanwhile, the results indicates that CD patients with abdominal pain have significantly lower levels of γ-aminobutyric acid plus (GABA+)/tCr (p = 0.002) than HCs. To some extent, CDAI demonstrated a trend of negative correlation with GABA+/tCr levels (p = 0.088, ρ = −0.60). The neural mechanism of CD patients with abdominal pain in pain processing is tightly associated with neurochemical metabolites. An imbalance in Glu and GABA may play a key role in abdominal pain processing for patients with CD. This mechanism of pain may associate with the intestinal microbiota on the brain-gut axis. The brain metabolite in CD patients with abdominal pain was firstly investigated. The study was conducted in vivo by using 1H-MRS. Glu and GABA levels altered in ACC of CD patients with abdominal pain. CD patients with abdominal pain in pain processing implicated neurotransmitters.
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作者：
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