Abstract

Tuina, a method of traditional Chinese manual manipulation, is an effective alternative therapy for neuropathic pain (NP), but its analgesic mechanism remains unclear. In this study, we used resting-state functional magnetic resonance imaging (R-fMRI) to explore the analgesic mechanism of Tuina in an NP rat model. After undergoing surgery to induce chronic compression of the dorsal root ganglion (CCD), one group of rats underwent Tuina at the ipsilateral BL40 acupoint once a day for 10 min during the 25 days following surgery while another group did not. Behavioral tests were performed at baseline, on the third day following surgery, and once a week for the next 4 weeks. R-fMRI was performed at baseline and 7 days and 28 days following surgery. Behavioral testing revealed that the Tuina group presented a significant response improvement to mechanical and thermal nociception stimuli compared to the untreated group 2 weeks following CCD surgery. Interestingly, rats submitted to Tuina presented higher measures of spontaneous neuronal activity in basal forebrain region, primary somatosensory cortex barrel field, dentate gyrus, secondary somatosensory cortex, striatum, descending corticofugal pathways, and globus pallidum of the left hemisphere 4 weeks after the CCD surgery compared to rats having undergone CCD only. In addition, on the 28th day, the ALFF signals of the left dentate gyrus, left secondary somatosensory cortex, left striatum, and bilateral primary cingulate cortex were significantly increased while those in the right dentate gyrus and bilateral periaqueductal gray were significantly decreased compared to those on the 7th day. Correlation analysis showed that the ALFF values of the left descending corticofugal pathways and globus pallidum had a positive correlation with mechanical withdrawal threshold and paw withdrawal thermal latency tests. Altogether, these results indicate that NPP induced by CCD surgery affects the plasticity of the cerebral cortex, and that Tuina alleviate pain behavior by promoting cortical remodeling.

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