Demyelination in degenerative cervical myelopathy: a systematic review and meta-analysis of autopsy and imaging studies.

BACKGROUND

Degenerative cervical myelopathy (DCM) is the leading cause of spinal cord dysfunction in adults, marked by progressive neurological deficits in spinal compression. The pathophysiology is driven by chronic spinal cord injury, yet the role of demyelination is not well defined. This systematic review and meta-analysis assesses the prevalence of demyelination in DCM and its relation to clinical measures.

METHODS

A literature search was conducted across MEDLINE, EMBASE, Scopus, Web of Science, and the Cochrane Library, following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Studies reporting demyelination in DCM through autopsy, histopathology, or spinal cord imaging were included. Data were extracted and analyzed using random-effects meta-analysis.

RESULTS

Twenty-seven studies (364 DCM patients) were included. The GLMM random-effects model across 16 autopsy studies (n = 85) yielded an exploratory pooled proportion of 75.2% (95% CI: 16.8-97.6). In DCM patients, magnetization transfer ratio (MTR) was significantly reduced in the ventral column, the dorsal column, and the whole cord. The reduction was greatest in the ventral column (pooled MD = - 5.88, 95% CI: -9.00 to - 2.77, p = 0.0002).Meta-analysis of five independent studies demonstrated a significant positive correlation between MTR and baseline neurological function (pooled r = 0.38, 95% CI: 0.14-0.57).

CONCLUSION

Demyelination is a prominent histopathological feature of DCM. Comparison of autopsy and imaging studies generates a conceptual hypothesis of ventral-to-dorsolateral spatiotemporal disease progression that has not been directly demonstrated and requires prospective longitudinal validation. MTR is significantly and positively associated with baseline clinical severity, supporting its potential role as a myelin-sensitive biomarker in DCM. Additional research is warranted to define the progression of demyelination in DCM and guide the development of targeted therapeutic interventions.