Abstract
In the pathophysiology of lumbosacral radiculopathy, inflammation of the nerve root is of critical importance. Additionally, free radicals have been shown to be associated with some inflammatory process. This study was designed to investigate whether free radicals participate in the pathophysiology of nerve root involvement. We measured superoxide dismutase (SOD) activity in cerebrospinal fluid (CSF) of 31 patients with unilateral lumbosacral radiculopathy caused by a herniated disc using electron spin resonance (ESR) spectrometry. Then SOD activity was compared with the type of nerve root compression as seen on preoperative myelography. SOD activity in the normal control group was 7U/ml, while that in the hernia group remarkably decreased. The concentration gradient of SOD activity was different between central herniation and centrolateral herniation. Our findings indicate that free radicals are generated after nerve root compression. Under severe deficiency of SOD activity in CSF, serum SOD penetrates into CSF after further compression. In addition, SOD in CSF may play an important role in protecting against nerve root involvement.
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