BackgroundLittle is known about the changes of brain structural and functional connectivity networks underlying the pathophysiology in migraine. We aimed to investigate how the cortical network reorganization is altered by frequent cortical overstimulation associated with migraine.Methodology/Principal FindingsGray matter volumes and resting-state functional magnetic resonance imaging signal correlations were employed to construct structural and functional networks between brain regions in 43 female patients with migraine (PM) and 43 gender-matched healthy controls (HC) by using graph theory-based approaches. Compared with the HC group, the patients showed abnormal global topology in both structural and functional networks, characterized by higher mean clustering coefficients without significant change in the shortest absolute path length, which indicated that the PM lost optimal topological organization in their cortical networks. Brain hubs related to pain-processing revealed abnormal nodal centrality in both structural and functional networks, including the precentral gyrus, orbital part of the inferior frontal gyrus, parahippocampal gyrus, anterior cingulate gyrus, thalamus, temporal pole of the middle temporal gyrus and the inferior parietal gyrus. Negative correlations were found between migraine duration and regions with abnormal centrality. Furthermore, the dysfunctional connections in patients' cortical networks formed into a connected component and three dysregulated modules were identified involving pain-related information processing and motion-processing visual networks.ConclusionsOur results may reflect brain alteration dynamics resulting from migraine and suggest that long-term and high-frequency headache attacks may cause both structural and functional connectivity network reorganization. The disrupted information exchange between brain areas in migraine may be reshaped into a hierarchical modular structure progressively.

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Objective To investigate the dynamics underlying the sustained effect of acupuncture as a possible explanation of earlier findings that acupuncture stimulation at the vision-related acupuncture point, GB37, cannot specifically change the functional MRI (fMRI) signals of the visual cortex compared with stimulation at an adjacent non-meridian point. Methods The 'on-off' experimental design was separated into four series conditions: 1 min of baseline scanning at the beginning, then two stimulation epochs separated by a 50 s 'rest' period, and then a 1 min 'rest' epoch. The standard General Linear Model (GLM) approach and multi-conditions analysis were used. Results Results from the multi-conditions analysis were different from those from the standard GLM analysis. We found that the neural signal of the limbic-paralimbic-neocortical system after acupuncture stimulus lasted longer than the putative period. Furthermore, the fMRI signal changes in the occipital cortex showed different temporal patterns between GB37 and the non-meridian point. Conclusions Owing to the sustained effect of acupuncture, standard GLM analysis may be unsuitable for 'on-off' design acupuncture studies and lead to uncertain and contradictory results. The findings from this study suggest that acupuncture at GB37 can induce complex brain activity in the vision cortex. The state-related neural signal may reflect one of the significant characteristics underlying acupuncture.

Recent neuroimaging studies have shown local brain aberrations in functional dyspepsia (FD) patients, yet little attention has been paid to the whole-brain resting-state functional network abnormalities. The purpose of this study was to investigate whether FD disrupts the patterns of whole-brain networks and the abnormal functional connectivity could reflect the severity of the disease. The dysfunctional interactions between brain regions at rest were investigated in FD patients as compared with 40 age- and gender- matched healthy controls. Multivariate pattern analysis was used to evaluate the discriminative power of our results for classifying patients from controls. In our findings, the abnormal brain functional connections were mainly situated within or across the limbic/paralimbic system, the prefrontal cortex, the tempo-parietal areas and the visual cortex. About 96% of the subjects among the original dataset were correctly classified by a leave one-out cross-validation approach, and 88% accuracy was also validated in a replication dataset. The classification features were significantly associated with the patients’ dyspepsia symptoms, the self-rating depression scale and self-rating anxiety scale, but it was not correlated with duration of FD patients (p>0.05). Our results may indicate the effectiveness of the altered brain functional connections reflecting the disease pathophysiology underling FD. These dysfunctional connections may be the epiphenomena or causative agents of FD, which may be affected by clinical severity and its related emotional dimension of the disease rather than the clinical course.