PO10-TU-71 Does disc herniation incite noncompressive inflammatory myelopathy?

Abstract

Purpose: Demyelination of cervical spinal cord is usually attributed to neuroinflammation. However, focal demyelination of cervical spinal cord may also follow physical trauma. We report here our experience of focal cervical cord demyelination due to cervical spondylosis and cervical hyperextension-flexion injury. Method: Six patients (M=5, F = 1) between the age group of 21–45 years presented with features of cervical myelopathy. In 4 of these cases (M=3, F = 1), there was an extensive area of focal demyelination in the cervical spinal cord extending from a single or two-level cord compression by spondylotic bar. Despite adequate surgical decompression, there was persistent spinal cord demyelination in the post-operative MRI and these patients had chronic myelopathic signs with little or no improvement following surgery. In 2 other cases (M=2), focal demyelination was associated with previous history of cervical cord hyperextension-flexion injury. None of these patients had any disseminated demyelination elsewhere in the central nervous system and had normal MRI of brain and visual evoked potentials. Conclusion: We propose that focal demyelination of cervical spinal cord can occur after physical trauma, and hyperintense MRI signal within the spinal cord of patients with spondylotic myelopathy is likely to represent focal demyelination rather than myelomalacia. Our clinical experience is consistent with the pathology of demyelination in spondylotic cervical myelopathy which was first reported by Brain and Wilkinson. It is possible that in at-risk patients, post-traumatic cervical cord demyelination is the initial clinical syndrome with the potential of disseminated demyelination over time and space. Symptoms of multiple sclerosis may also be precipitated or exacerbated by cervical cord trauma.