Article
Degenerative cervical myelopathy – Accumulation of proinflammatory eotaxin-1 in postoperative CSF samples compared to preoperative and healthy controls. Advice for extended inflammation and neurotoxicity?
Degenerativer zervikaler Myelopathie: Akkumulation von proinflammatorischem Eotaxin-1 im postoperativen Liquorproben im Vergleich zu preoperativen und gesunden Kontrollen. Hinweise für eine verlängerte Inflammation und Neurotoxizität?
Search Medline for
Authors
-
Andreas Müller
- Universitätsklinikum RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
-
Verena Mainz
- Universitätsklinikum RWTH Aachen, Institute of Anatomy and Cell Biology, Aachen, Deutschland
-
Ulf Bertram
- Universitätsklinikum RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
-
Tobias Schmidt
- Universitätsklinikum RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
-
Thomas Pufe
- Universitätsklinikum RWTH Aachen, Institute of Anatomy and Cell Biology, Aachen, Deutschland
-
Hans Clusmann
- Universitätsklinikum RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
-
Christian Blume
- Universitätsklinikum RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
| Published: | May 25, 2022 |
|---|
Outline
Text
Objective: Endogenous immune mediated reactions of inflammation are a component of the secondary injury of the spinal cord in patients with degenerative cervical myelopathy (DCM). Eotaxin-1 (CCL11), which is a chemokine and eosinophil chemoattractant, is elevated in the cerebro-spinal fluid (CSF) of patients with neuroinflammatory disorders. The study aim is to identify the eotaxin-1 alterations in CSF of patients with DCM before and after surgery and to compare those to a control group.
Methods: Patients with DCM (n=50; 21 female; mean age 62.9±11.1SD) were included. CSF samples were taken pre- and postoperatively. A control group of patients (n=51; 17 female; mean age 61.1±16.6), with abdominal aortic aneurysm (AAA), requiring surgery was established. The neurological status of participants was evaluated prior surgery including NDI and mJOA. Samples were examined via ELISA tests. Protein-concentrations of CCL11 were measured in CSF pg/ml.
Results: Groups did not differ in terms of age and gender distribution. Groups differed regarding their neurological status (mJOA: DCM 10.98±3.0, AAA 17.27±1.2, p<0.001; NDI: DCM 40±20.7, AAA 6±8.3, p<0.001), and in CCL11 concentrations: DCM 2,96±0.52, AAA 1.76±1.03, p<0.001). A significant increase of CCL11 was observed three month after surgery (5.71±2.75). These values were significantly increased both in comparison to the controls and to the preoperative values (p<0.001). Subgroup analysis of clinical data via correlations showed no significant differences in concentrations of CCL11.
Conclusion: Microglia express the CCL11 receptor and CCL11 promote microglial migration, and increase microglial expression of reactive oxygen species, which reinforce neurotoxicity. A definitive answer to the question of whether inflammation and neurotoxicity have a significant influence on the maintenance of DCM even after surgery cannot yet be given in the absence of a correlation with clinical outcome data. Larger case numbers are necessary to answer this question with certainty.
