Article
Blood-spinal cord barrier disruption in patients with degenerative cervical myelopathy
Blut-Myelon Schrankenstörung bei Patienten mit degenerativer zervikaler Myelopathie
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Authors
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Christian Blume
- RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
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Matthias Florian Geiger
- 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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Marguerite Müller
- RWTH Aachen, Klinik für Neuroradiologie, Aachen, Deutschland
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Verena Mainz
- RWTH Aachen Uniklinikum, Klinik für Psychiatrie, Aachen, Deutschland
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Hans Clusmann
- RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
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Christian Andreas Mueller
- RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
| Published: | May 8, 2019 |
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Outline
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Objective: Disruption of the blood-spinal cord barrier (BSCB) is associated with several acute and neurodegenerative diseases causing secondary injuries to the spinal cord. Aim of this study is to prove the presence of BSCB disruption in patients with degenerative cervical myelopathy (DCM) and give a possible explanation for the onset of secondary injuries.
Methods: Twenty-one patients (12 female; 9 male; mean age 63.3±11.6 years) with DCM were prospectively included. All patients had an indication for neurosurgical decompression. As controls 33 patients (12 female; 21 male; mean age 62.3±15.2 years) with abdominal aortic aneurysm (AAA) and indication for surgery were included. These Patients (AAA) routinely received CSF drainage prior surgery for intraoperative intrathecal pressure monitoring. Samples of CSF and blood serum were taken simultaneously from each participant. All participants underwent neurological examination including mJOA and NDI. Regarding BSCB disruption and intrathecal immunoglobulin (Ig) concentrations the samples were examined for Albumin, IgG, IgA and IgM (all mg/dl). Quotients (CSF/serum) were standardized calculated according to the Reiber diagnostic: QIgG (n x 10-3), QIgA (n x 10-3), QIgM (n x 10-3) and QAlb (n x 10-3) 21. The individual age related references ranges of QAlb for patients and controls were calculated: QAlb=(4 + age/15) × 10–3.
Results: Patients and controls differed significantly in their clinical status (mJOA: DCM 10,1±3,1, AAA 17,6±1,2, p<.001; NDI: DCM 46,3±20,9, AAA 6,0±8,9, p<.001). There were no statistical differences concerning gender and age. The CSF/Serum quotient of Albumin (QAlb (n x 10-3)), as an expression of BSCB disruption, was significantly increased in the DCM patients compared to the controls (DCM: 10,0±3,4; AAA: 4,7±1,9, p<.001). Intrathecal Immunoglobulin concentrations of IgG (QIgG: DCM 4,6±1,6; AAA 2,4±0,8; p<.001) and IgA (QIgA: DCM 2,6±1,1; AAA 1,4±0,7; p<.001) differed significantly between the groups. The Reiber diagnostic showed no intrathecal synthesis of Ig. Thus, higher concentrations of Ig were caused increased BSCB permeability and diffusion.
Conclusion: Patients with DCM seem to have an increased permeability and disruption of the BSCB. A possible explanation for the initiation of secondary structural damage via immune mediated inflammatory response and further deterioration of the course of this disease.
