MedWire News: Patients with functional dyspepsia display abnormal brain activity that fluctuates in line with their symptoms, an international research team has shown.
Writing in Gastroenterology, they suggest that the areas of the brain displaying abnormal activation may be involved in determining the severity of dyspepsia symptoms.
Functional dyspepsia is thought to result from abnormal processing of visceral sensation at the level of the central nervous system; previous research has identified stimulation-related changes in brain activity but few studies have focused on resting brain activity.
To address this shortfall, Fanrong Liang (Chengdu University of Traditional Chinese Medicine, Sichuan, China) and team mapped changes in resting brain glycometabolism in 40 patients with functional dyspepsia and 20 healthy controls.
Analysis of positron emission tomography-computed tomography images revealed a number of differences between patients and controls.
Specifically, compared with healthy subjects, patients with functional dyspepsia had significantly higher levels of glycometabolism in the bilateral insula, anterior cingulate cortex (ACC), middle cingulate cortex (MCC), cerebellum, thalamus, prefrontal cortex, precentral gyrus, postcentral gyrus, middle temporal gyrus, superior temporal gyrus, putamen, right parahippocampal gyrus, claustrum, and left precuneus.
Furthermore, the increased activity in the ACC, insula, thalamus, MCC, and cerebellum observed in the dyspepsia patients was significantly correlated with the severity of their symptoms, as assessed by both symptom index of dyspepsia scores and Nepean dyspepsia index scores.
Accordingly, glycometabolism in the ACC, insula, thalamus, MCC, and cerebellum of patients with more severe functional dyspepsia was significantly higher than that of patients with less severe functional dyspepsia.
Liang and co-authors say that their study reveals an increase in resting cerebral brain glycometabolism in patients with functional dyspepsia, as well as showing a correlation between this abnormal brain activity and symptom severity.
"The glycometabolism increase in these regions might relate to the abnormal homeostatic regulation of functional dyspepsia patients," they suggest.
"We hypothesize that the hyperactivity of ACC, MCC, thalamus, insula, and cerebellum are involved in the pathologic mechanism of functional dyspepsia, and that ACC, MCC, thalamus, insula, and cerebellum are the key regions associated with the severity of functional dyspepsia."
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