Abstract
Purpose: We aimed to find out the distributed functional connectome of white matter in patients with functional dyspepsia (FD).Methods: 20 patients with FD and 24 age- and gender-matched healthy controls were included into the study. The functional connectome of white matter and graph theory were used to these participants. Two-sample t-test was used for the detection the abnormal graph properties in FD. Pearson correlation was used for the relationship between properties and the clinical and neuropshychological information.Results: Patients with FD and healthy controls showed small-world properties in functional connectome of white matter. Compared with healthy controls, the FD group showed decreased global properties (Cp, S, Eglobal, and Elocal). Four pairs of fiber bundles that are connected to the frontal lobe, insula, and thalamus were affected in the FD group. Duration and Pittsburgh Sleep Quality Index positively correlated with the betweenness centrality of white matter regions of interest.Conclusion: FD patients turned to a non-optimized functional organization of WM brain network. Frontal lobe, insula, and thalamus were key regions in brain information exchange of FD. It provided some novel imaging evidences for the mechanism of FD.
Highlights
Functional dyspepsia (FD) is one of the most prevalent functional gastrointestinal disorders, with high prevalence (5–11% of the population) (Ford et al, 2015)
We aimed to reveal the functional connectome of white matter (WM) in FD patients
There was no significant difference in age and sex between the FD patients and healthy controls (Table 1)
Summary
Functional dyspepsia (FD) is one of the most prevalent functional gastrointestinal disorders, with high prevalence (5–11% of the population) (Ford et al, 2015). FD is characterized by four main symptoms: bothersome postprandial fullness, early satiety, epigastric burning, and epigastralgia (Enck et al, 2017). FD negatively affects the quality of life in patients and is a healthcare burden for society for its recurrent nature of the symptoms (El-Serag and Talley, 2003; Lacy et al, 2011). In the absence of detectable organic causes, FD was referred to be a functional disorder, which was thought to result from the dysregulation in brain–gut interaction (Koloski et al, 2012). The neural basis of FD remains poorly understood.
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