Abstract

Endogenous immune mediated reactions of inflammation and angiogenesis are components of the spinal cord injury in patients with degenerative cervical myelopathy (DCM). The aim of this study was to identify alteration of certain mediators participating in angiogenetic and inflammatory reactions in patients with DCM. A consecutive series of 42 patients with DCM and indication for surgical decompression were enrolled for the study. 28 DCM patients were included, as CSF samples were taken preoperatively. We enrolled 42 patients requiring surgery for a thoracic abdominal aortic aneurysm (TAAA) as neurologically healthy controls. In 38 TAAA patients, CSF samples were taken prior to surgery and thus included. We evaluated the neurological status of patients and controls prior to surgery including NDI and mJOA. Protein-concentrations of factors with a crucial role in inflammation and angiogenesis were measured in CSF via ELISA testing (pg/ml): Angiopoietin 2, VEGF-A and C, RANTES, IL 1 beta and IL 8. Additionally, evaluated the status of the blood-spinal cord barrier (BSCB) by Reibers´diagnostic in all participants. Groups evidently differed in their neurological status (mJOA: DCM 10.1 ± 3.3, TAAA 17.3 ± 1.2, p < .001; NDI: DCM 47.4 ± 19.7, TAAA 5.3 ± 8.6, p < .001). There were no particular differences in age and gender distribution. However, we detected statistically significant differences in concentrations of mediators between the groups: Angiopoietin 2 (DCM 267.1.4 ± 81.9, TAAA 408.6 ± 177.1, p < .001) and VEGF C (DCM 152.2 ± 96.1, TAAA 222.4 ± 140.3, p = .04). DCM patients presented a mild to moderate BSCB disruption, controls had no signs of impairment. In patients with DCM, we measured decreased concentrations of angiogenic mediators. These results correspond to findings of immune mediated secondary harm in acute spinal cord injury. Reduced angiogenic activity could be a relevant part of the pathogenesis of DCM and secondary harm to the spinal cord.

Highlights

  • Endogenous immune mediated reactions of inflammation and angiogenesis are components of the spinal cord injury in patients with degenerative cervical myelopathy (DCM)

  • We evaluated the neurological status of patients and controls prior to surgery including Neck Disability Index (NDI) and mJOA

  • Evaluated the status of the blood-spinal cord barrier (BSCB) by Reibersdiagnostic in all participants. Groups differed in their neurological status

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Summary

Introduction

Endogenous immune mediated reactions of inflammation and angiogenesis are components of the spinal cord injury in patients with degenerative cervical myelopathy (DCM). In patients with DCM, we measured decreased concentrations of angiogenic mediators These results correspond to findings of immune mediated secondary harm in acute spinal cord injury. Migration of these cells and activation of inflammatory reactions in the central nervous system (CNS) is mediated by fractalkine (CX3CL1)[9] Regarding these pathomechanisms, inflammatory immune mediated reactions seem to be an important part of the pathophysiology of DCM. Other pathophysiological factors of DCM include disturbed intracellular energy metabolism and mediated cell i­njury[22]. In this context, Vascular Endothelial Growth Factor (VEGF) is a well-known factor of vascular angiogenesis, homeostasis and ­pathology[23]. VEGF C–deficient animal models detected defects of lymphatic v­ essels[40]

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