Using voxel-based morphometry (VBM), we studied cortical gray matter volume changes in patients with cervical spondylotic myelopathy (CSM) before and after cervical cord surgical decompression. We then discussed the structural damage mechanisms and the neural plasticity mechanisms involved in postsurgical CSM. Forty-five presurgical CSM patients, 41 of the same group followed-up 6 months after decompression surgery and 45 normal controls (NC) matched for age, sex and level of education underwent high-resolution 3-dimensional T1-weighted scans by 3.0 T MR. Then, VBM measurements were compared and cortical gray matter volume alterations were assessed among pre- or postsurgical CSM patients and NC, as well as correlations with clinical indexes by Pearson correlation. Compared with NC, presurgical CSM patients showed reduced gray matter volume in the left caudate nucleus and the right thalamus. After 6 months, postsurgical CSM patients had lower gray matter volume in the bilateral cerebellar posterior lobes but had higher gray matter volume in the brain-stem than did presurgical CSM patients. Postsurgical CSM patients had significantly lower gray matter volume in the left caudate nucleus but greater regional gray matter volume in the right inferior temporal gyrus, the right middle orbitofrontal cortex (OFC) and the bilateral lingual gyrus / precuneus /posterior cingulate cortex than did NC. Abnormal areas gray volume in presurgical CSM and postsurgical CSM patients showed no significant correlation with clinical data ( P > .05). Myelopathy in the cervical cord may cause chronic cerebral structural damage before and after the decompression stage, markedly in outlier brain regions involving motor execution/control, vision processing and the default mode network and in areas associated with brain compensatory plasticity to reverse downstream spinal cord compression and respond to spinal cord surgical decompression.

Objectives. To explore functional connectivity reorganization of the primary somatosensory cortex, the chronic microstructure damage of the cervical spinal cord, and their relationship in cervical spondylotic myelopathy (CSM) patients. Methods. Thirty-three patients with CSM and 23 healthy controls (HCs) were recruited for rs-fMRI and cervical spinal cord diffusion tensor imaging (DTI) scans. Six subregions (including leg, back, chest, hand, finger and face) of bilateral primary somatosensory cortex (S1) were selected for seed-based whole-brain functional connectivity (FC). Then, we calculated the apparent diffusion coefficient (ADC) and fractional anisotropy (FA) values of the cervical spinal cord. Correlation analysis was conducted between FC values of brain regions and DTI parameters of cervical spinal cord (ADC, FA), and their relationship with each other and clinical parameters. Results. Compared with the HC group, the CSM group showed decreased FC between areas of the left S1hand, the left S1leg, the right S1chest, and the right S1leg with brain regions. The mean FA values of the cervical spinal cord in CSM patients were positively correlated with JOA scores. Especially, the FApos values of bilateral posterior funiculus were positively correlated with JOA scores. The ADC and FA values of bilateral posterior funiculus in the cervical spinal cord were also positively correlated with the FC values. Conclusions. There was synchronization between chronic cervical spinal cord microstructural injury and cerebral cortex sensory function compensatory recombination. DTI parameters of the posterior cervical spinal cord could objectively reflect the degree of cerebral cortex sensory function impairment to a certain extent.