Artikel
Degenerative cervical myelopathy – Chronic trauma leads to alterations of endogenic inflammatory and angiogenetic mediator concentrations in CSF
Degenerative zervikale Myelopathie – Chronisch traumatische Schädigungen des Rückenmarks führen zu Veränderungen endogener inflammatorischer und angiogenetischer Mediator – Konzentrationen im Liquor
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Autoren
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Christian Blume
- RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
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Hans Clusmann
- RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
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Lars Ove Brandenburg
- RWTH Aachen Uniklinikum, Institut für Anatomie und Zellbiologie, Aachen, Deutschland
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Matthias Florian Geiger
- RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
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Marguerite Müller
- RWTH Aachen, Klinik für Neuroradiologie, Aachen, Deutschland
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Christian Andreas Mueller
- RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
| Veröffentlicht: | 8. Mai 2019 |
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Gliederung
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Objective: Endogenous immune mediated reactions of inflammation and angiogenesis are components of the secondary injury of the spinal cord in patients with degenerative cervical myelopathy. Aim of this study is to detect and identify the alteration of certain mediators in the cerebrospinal fluid (CSF) in patients with chronic spinal cord injury (SCI) compared control group.
Methods: Patients with DCM (n=28; 14 female; mean age 62.3±10.8) and indication for surgery were included. CSF samples were taken preoperatively. A control group of patients (n=38; 13 female; mean age 65.0±15.0), with abdominal aortic aneurysm (AAA), requiring surgery was established. Patients of this group received a CSF drainage for intrathecal pressure monitoring, samples were taken preoperatively. The neurological status of patients and controls was evaluated prior surgery including NDI and mJOA. Controls with any neurological deficit or history of neurological diseases were excluded. Samples were examined via ELISA tests. Protein-concentrations of inflammatory and angiogenic factors were measured in CSF pg/ml: Angiopoietin-2, VEGF-A and C (Vascular Endothelial Growth Factor), RANTES (Regulated And Normal T cell Expressed and Secreted), Interleukin (IL) 1 beta and IL 8.
Results: Patients and controls did not differ in terms of age and gender distribution. The groups clearly distinguished in their neurological status (mJOA: DCM 10.8±3.3, AAA 17.3±1.2, p<0.001; NDI: DCM 45±19.7, AAA 5.3±8.6, p<0.001). Statistically significant differences in concentrations of mediators between the groups were detected: Angiopoetin 2 (DCM 271.4±90.6, AAA 476.6±230.6, p<0.001), IL 8 (DCM 60.2±70.2, AAA 250.5±638.9, p=0.011) RANTES (DCM 3.1±9.9, AAA 2.6±3.1, p=0.039). Subgroup analysis of patients with mild and moderate (n=15) clinical myelopathy versus patients with severe (n=10) neurological status, measured by mJOA score, showed significant differences in concentrations of Angiopoetin 2 (mild and moderate: 230.0±76.9, severe 319.9±86.1, p=0.016). The duration of symptoms in patients with DCM on the other hand had no influence on mediator concentrations in CSF.
Conclusion: Proangiogenetic mechanisms (Angiopoetin 2 and IL-8) were significantly reduced in patients with DCM. Comparable with known angiogenetic reactions in SCI, however these immune mediated reactions seem to be suppressed over a longer period of time in chronic SCI. Furthermore Angiopoetin 2 alterations are associated with the clinical severity of DCM.
