gms | German Medical Science

Objective: The aim of this prospective study was to evaluate the different alterations of inflammatory angiogenic mediators in cerebrospinal fluid (CSF) and blood serum (BS) in patients with cervical spondylotic myelopathy (CSM).

Methods: In patients with CSM who underwent lumbar myelography CSF and BS were sampled. Patients were monitored for neurological symptoms including NDI and mJOA. Clinical follow up with examination, BS sampling for protein concentrations, and questionnaires were performed preoperatively (preop) and 5 days, 6 weeks, 3, 6, 9, 12 and 18 months postoperatively (postop). A control group with preop CSF and BS samples was formed from patients with abdominal aortic aneurysm surgery (AAA-group), who had a lumbar drain for intradural pressure monitoring. The control group was monitored to exclude neurological signs of CSM (mJOA). The samples were evaluated with ELISA. Following angiogenic protein-concentrations were measured in CSF and BS in pg/ml: PDGF-BB (Platelet-derived growth factor), RANTES (regulated on activation, normal T cell expressed and secreted), Endoglin, Angiopoietin-2, Endothelin-1, VEGF-A, C, D (Vascular Endothelial Growth Factor), FGF-1 and 2 (Fibroblast Growth Factor), EGF (Epidermal Growth Factor and Interleukins (IL-1, 6, 8, 10, 17)

Results: Overall 26 patients were included. CSM-group 14 patients (mean age 64 years), AAA-group 12 patients (mean age 58 years (p=0.178)). Mean preop scores: mJOA CSM-group 9.2, AAA-group 17.0 (p=<0,001); NDI CSM-group 49.7, AAA-group 1.2 (p=<0.001). We identified significant differences in the CSF preop: Angiopoietin-2 CSM-group 243.6 vs AAA-group 388.2 (p=0.022); VEGF-A CSM-group 12.3 vs AAA-group 5.0 (p=0.019); IL-1alpha CSM-group 100.3±86.5 vs AAA-group 38.3±52.1 (p=0.047); IL-1beta CSM-group 20.9±25.9 vs AAA-group 0.9±0.6 (p=0.031). In BS, only Endoglin was different in CSM-group 1526.9 vs AAA-group 975.4 (p=0.024). In the clinical follow up examinations of the CSM-group mJOA and NDI showed significant improvement from the third month postop.

Conclusion: The groups are clearly distinguished regarding the clinical signs of myelopathy. Higher concentrations of some angiogenic factors in the CSF are associated with the diagnosis of CSM. Thus, they could contribute to an increased induction of angiogenesis (VEGF-A, Endoglin) and a dysregulation of microvascular permeability (Angiopoietin-2) in patients with CSM. These factors may serve as tools for further research on prognosis and pathophysiology. A limitation is the non-availability of postoperative CSF, in general.