Patterns of cortical thickness alterations in degenerative cervical myelopathy: associations with dexterity and gait dysfunctions.

Degenerative cervical myelopathy (DCM) can lead to significant brain structural reorganization. The association between the cortical changes and specific motor symptoms in DCM has yet to be fully elucidated. We investigated the associations between cortical thickness changes with neurological symptoms, such as dexterity and gait abnormalities, in patients with DCM in a case-control study. A 3 Tesla MRI scanner was used to acquire high-resolution T1-weighted structural scans from 30 right-handed patients with DCM and 22 age-matched healthy controls. Pronounced cortical thinning was observed in DCM patients relative to healthy controls, particularly in the bilateral precentral and prefrontal gyri, left pars triangularis, left postcentral gyrus, right transverse temporal and visual cortices (P ≤ 0.04). Notably, cortical thickness in these regions showed strong correlations with objective motor deficits (P < 0.0001). Specifically, the prefrontal cortex, premotor area and supplementary motor area exhibited significant thickness reductions correlating with diminished dexterity (R² = 0.33, P < 0.0007; R² = 0.34, P = 0.005, respectively). Similarly, declines in gait function were associated with reduced cortical thickness in the visual motor and frontal eye field cortices (R² = 0.39, P = 0.029, R² = 0.33, P = 0.04, respectively). Interestingly, only the contralateral precuneus thickness was associated with the overall modified Japanese Orthopaedic Association (mJOA) scores (R² = 0.29, P = 0.003). However, the upper extremity subscore of mJOA indicated an association with the visual cortex and the anterior prefrontal (R² = 0.48, P = 0.002, R² = 0.33, P = 0.0034, respectively). In conclusion, our findings reveal patterns of cortical changes correlating with motor deficits, highlighting the significance of combining objective clinical and brain imaging assessments for understanding motor network dysfunction in DCM.