Characterizing immune involvement in degenerative cervical myelopathy: a systematic review.

OBJECTIVE: Degenerative cervical myelopathy (DCM) is the most common cause of cervical spinal cord impairment in adults. It is described as progressive, age-related spinal cord compression due to degenerative changes in the spinal column. While the mechanical pathology of DCM is well characterized, the immune system's role in the disease's neurological progression and potential as a therapeutic target remains unclear. The authors aimed to comprehensively review the available literature on immunological involvement in DCM pathogenesis. Understanding the interactions between inflammation, apoptosis, and neurodegeneration in DCM may provide insights into novel treatment strategies. METHODS: A systematic literature review was conducted in the PubMed database through August 1, 2024, following PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. Papers met inclusion criteria for the review if they reported on molecular, histological, CSF, or peripheral markers of immune involvement or the immune response, causation, or relation to DCM. Systematic reviews, case reports, or animal studies were excluded. Studies were screened by two blinded authors based on relevance and synthesized to assess the immune environment in DCM. RESULTS: A total of 113 studies were identified, with 10 meeting the inclusion criteria. Findings revealed elevated proinflammatory cytokines in the CSF of DCM patients, including interleukin-8 and tumor necrosis factor-α, as well as increased oligoclonal IgG bands and blood-spinal cord barrier disruption. Histological analysis demonstrated apoptosis via Fas-mediated pathways, impaired autophagy, and increased staining for activated myeloid cells in DCM tissue compared to controls. Peripheral immune profiling indicated increased M2 macrophages and activated CD4 T cells in DCM patients. Furthermore, serum S100b postoperative values and perioperative CSF levels of neurofilament light chain and glial fibrillary acidic protein correlated significantly with clinical improvement and favorable outcomes following treatment. This review is limited by the number of eligible studies, causal interpretation and temporal bias, and lack of standardized interstudy biomarker analysis. These findings identify an immune component of DCM neurodegeneration that may influence disease severity and treatment response. CONCLUSIONS: There is a significant interplay between immune responses and DCM disease progression, revealing how inflammatory mechanisms can influence clinical outcomes and treatment efficacy. Further studies are warranted to understand the immune component of DCM and pave the way for targeted immunotherapies alongside surgical decompression.