Sensorimotor Network Alterations and Compensation in Cervical Spondylotic Myelopathy: A 7 T Task-Based and Resting-State Functional MRI Study

BACKGROUND AND OBJECTIVES: Cervical spondylotic myelopathy (CSM) is a leading cause of spinal cord dysfunction, yet the central neural mechanisms underlying motor impairment and recovery remain unclear. METHODS: This study used the first 7 T functional MRI (fMRI) study in patients with CSM to investigate sensorimotor network alterations. Sixteen patients with CSM and age-matched healthy controls underwent task-based fMRI during hand grasping and resting-state fMRI. Ten patients completed 3-month postoperative follow-up imaging. Clinical severity was assessed using Japanese Orthopaedic Association (JOA) scores. RESULTS: Task-based fMRI during hand movements revealed compensatory bilateral recruitment in patients with CSM compared with controls, with significantly increased activation in the ipsilateral primary motor cortex (M1; peak: 45, -21, 56; T = 7.93, P < .001) and contralateral cerebellum (peak: -21, -52, -28; T = 7.23, P < .001). Cerebellar hyperactivation correlated negatively with JOA total scores (peak: -26, -56, -24; T = 10.74, P < .001) and dexterity subscales (T = 9.05, P < .001), indicating severity-dependent compensation. Resting-state analysis revealed widespread increases in sensorimotor network connectivity. The strongest alterations were observed in bilateral M1 connectivity (T = 14.65, P < .001), bilateral primary sensory cortex connectivity (T = 14.53, P < .001), and M1-supplementary motor area (SMA) connections (right M1 to left SMA: T = 13.21, P < .001; bilateral SMA: T = 13.89, P < .001). Intracerebellar networks showed marked hyperconnectivity (bilateral cerebellar lobule VI: T = 15.35, P < .001; bilateral cerebellar lobule IV-V: T = 14.25, P < .001). Resting-state connectivity strength was negatively correlated with both JOA total scores and dexterity subscales. CONCLUSION: This 7T fMRI study reveals that CSM induces compensatory reorganization involving the contralateral cerebellum and ipsilateral motor cortex, with severity-dependent hyperconnectivity. These findings clarify mechanisms of motor compensation and suggest cerebellar-focused rehabilitation as a potential therapeutic strategy.