Article
Blood spinal cord barrier disruption in patients with degenerative cervical myelopathy – potential to restore?
Störung der Blut-Rückenmark-Schranke bei Patienten mit degenerativer zervikaler Myelopathie – Potential zur Wiederherstellung?
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Authors
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Christian Blume
- Rheinisch-Westfälische Technische Hochschule Aachen, Neurochirurgie, Aachen, Deutschland
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Lars Ove Brandenburg
- Rheinisch-Westfälische Technische Hochschule Aachen, Institut für Anatomie und Zellbiologie, Aachen, Deutschland
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Verena Mainz
- Rheinisch-Westfälische Technische Hochschule Aachen, Klinik für Psychiatrie, Aachen, Deutschland
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Johannes Kalder
- Rheinisch-Westfälische Technische Hochschule Aachen, Institut für Anatomie und Zellbiologie, Aachen, Deutschland; Rheinisch-Westfälische Technische Hochschule Aachen, Klinik für Gefäßchirurgie, Aachen, Deutschland
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Marguerite Müller
- Rheinisch-Westfälische Technische Hochschule Aachen, Klinik für Neuroradiologie, Aachen, Deutschland
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Hans Rainer Clusmann
- Rheinisch-Westfälische Technische Hochschule Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
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Christian Andreas Mueller
- Rheinisch-Westfälische Technische Hochschule Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
| Published: | June 26, 2020 |
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Outline
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Objective: Blood spinal cord barrier (BSCB) disruption plays an elementary role in acute and neurodegenerative diseases of the spinal cord (SC). This study was set out to detect BSCB disruption in patients with degenerative cervical myelopathy (DCM) and possible recovery after surgical decompression of the cervical SC.
Methods: The study was prospectively enrolled with 58 DCM patients (25 female; 33 male; mean age 62.0 ± 12.0 years) of which 38 were included. As neurological healthy controls, 49 (17 female; 32 male; mean age 62.3 ± 14.4 years) patients with thoracic abdominal aortic aneurysm (TAAA) were recruited of which 38 were included. Preoperatively, CSF and blood serum samples were taken. All participants underwent neurological examination including mJOA and NDI. In eight DCM patients, samples could be collected three months postoperatively. To assess the status of the BSCB we used the Reiber diagnostic, measuring Albumin, IgG, IgA and IgM (all mg/dl). Quotients (CSF/serum) were calculated (n x 10-3) for all parameters (QIgG, QIgA, QIgM and QAlb ). The individual age-related reference range of QAlb for patients and controls were calculated: QAlb = (4 + age/15) × 10–3.
Results: Clinical status differed significantly between patients and controls (mJOA: DCM 10.4±3.2,TAAA17.4±1.2,p<.001; NDI: DCM 42.3±19.4, TAAA 4.6±7.7,p<.001). In the DCM group 32 patients showed a BSCB disruption. In the control group none of the patients had a BSCB disruption. QAlb as expression of BSCB impairment significantly differed between groups (QAlb: DCM: 12.6±8.2; TAAA: 5.1±1.8, p<.001). Intrathecal immunoglobulin concentrations significantly differed between groups (QIgGDCM5.8±3.9, TAAA 2.5±0.9, p<.001; QIgA DCM 3.4±2.4, TAAA 1.5±0.8, p<.001). Three months after decompressive surgery eight DCM patients agreed to be lumbar punctured again. Postoperatively, results reveal a reduction of QAlb in all patients (QAlb DCMpre 12.6±1.3, DCMpost 7.0±1.0, p<.001). In three patients BSCB disruption was completely restored.
Conclusion: DCM patients present with BSCB disruption. Higher concentrations of intrathecal immunoglobulin as an expression of pathological diffusion were detected. Postoperatively, BSCB seems to restore after decompressive surgery. These results indicate BSCB disruption to be a pathomechnism in DCM.
