Cortical volume reductions as a sign of secondary cerebral and cerebellar impairment in patients with degenerative cervical myelopathy

• Published in: NeuroImage clinical Vol. 30; p. 102624
• Main Authors: Jütten, Kerstin, Mainz, Verena, Schubert, Gerrit Alexander, Fabian Gohmann, Robin, Schmidt, Tobias, Ridwan, Hani, Clusmann, Hans, Mueller, Christian Andreas, Blume, Christian
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 01-01-2021; Elsevier
• Subjects: Degenerative cervical myelopathy; Gray matter volume alterations; Regular; Voxel-based morphometry; Degenerative cervical myelopathy; Voxel-based morphometry; Gray matter volume alterations
• ISSN: 2213-1582; 2213-1582
• DOI: 10.1016/j.nicl.2021.102624

•Degenerative cervical myelopathy is the most common cause of chronic impairment of the spinal cord.•MRI-based anatomical assessment of cerebral and cerebellar areas revealed significant tissue volume reduction in DCM patients compared to healthy controls.•Disease severity correlated with cerebral and cerebellar atrophy in the primary motor cortex, primary somatosensory cortex and cerebellar areas.•Chronic injury to the spinal cord seems to have impact on remote anatomical structures in the brain.
This study investigated supra- and infratentorial structural gray and white matter (GM, WM) alterations in patients with degenerative cervical myelopathy (DCM) as an indicator of secondary harm due to chronic cervical cord compression and micro trauma. With MRI-based anatomical assessment and subsequent voxel-based morphometry analyses, pre- and postoperative volume alterations in the primary motor cortex (MI), the primary somatosensory cortex (SI), the supplementary motor area (SMA), and the cerebellum were analyzed in 43 DCM patients and 20 controls. We assessed disease-related symptom severity by the modified Japanese Orthopaedic Association scale (mJOA). The study also explored symptom severity-based brain volume alterations as well as their association with clinical status. Patients had lower mJOA scores (p = .000) and lower GM volume than controls in SI (p = .016) and cerebellar regions (p = .001). Symptom severity-based subgroup analyses revealed volume reductions in almost all investigated GM ROIs (MI: p = .001; CB: p = .040; SMA: p = .007) in patients with severe clinical symptoms as well as atrophy already present in patients with moderate symptom severity. Clinical symptoms in DCM were associated with cortical and cerebellar volume reduction. GM volume alterations may serve as an indicator of both disease severity and ongoing disease progression in DCM, and should be considered in further patient care and treatment monitoring.