Related Experiment Videos
Neurotransmitter alterations in the anterior cingulate cortex in Crohn's disease patients with abdominal pain: A
Kun Lv1, Wenwen Song2, Rui Tang1
1The First Clinical Medical College of Zhejiang Chinese Medical University, Hangzhou, China; Department of Radiology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
Purpose:
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.
Methods:
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.
Results:
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).
Conclusion:
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.