Study Design: The e ect of epidural space perfusion with chilled saline solution (% 0.9 NaCl) on lipid peroxidation after experimental spinal cord injury in rats was evaluated. Objectives: The extent of lipid peroxidation is a useful parameter for evaluating the cellular disturbance caused by spinal cord trauma in experimental conditions. The protective e ects of hypothermia against neurological injury resulting from trauma or ischemia both in experimental and clinical situations have been demonstrated. Setting: Departments of Neurosurgery and Biochemistry, Cerrahpasa Medical School, Istanbul, Turkey. Methods: Twenty-®ve female Wistar Albino rats were used. There were ®ve rats in group I (sham-operated), seven rats in group II (trauma), and eight rats in group III (epidural cooling). The remaining ®ve rats were used for the pilot study to determine the spinal cord and body temperature. A clip compression method was used to produce acute spinal cord injury. In group III, 30 min after the trauma the injured spinal cord was cooled by perfusion of the epidural space with chilled saline solution (% 0.9 NaCl) with a¯ow rate of 5 ml/min for 30 min. At 2 h after trauma, all rats other than the ones used in the pilot study, were sacri®ced and the spinal cords were excised. The extent of lipid peroxidation in the spinal cord was assessed by measuring the tissue content of malonil dialdehyde (MDA). Results: The tissue MDA contents were 1.58 micromol MDA/gram wet weight (gww) in group 1 (sham-operated), 2.58 micromol MDA/gww in group 2 (trauma), and 1.77 micromol/ gww in group 3 (epidural cooling), the di erences being statistically signi®cant. Conclusion:The results indicated that epidural cooling of traumatized spinal cord is e ective in preventing secondary damage due to the peroxidation of lipid membranes.

Alterations in the composition of intervertebral disc extracellular matrix, mainly collagen and proteoglycans, may cause changes in mechanical properties of the disc, leading to dysfunction, nerve root compression, and herniation with severe clinical manifestations. Matrix metalloproteinases may be involved in degradation by hydrolysing extracellular matrix components. Inhibitors of matrix metalloproteinases, in contrast, function in the maintenance of degradation control. In this study, we investigated: (i) whether the level of matrix degradation correlated with the duration of the symptomatic disease, (ii) roles of matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of matrix metalloproteinases-2 (TIMP-2) in intervertebral disc degeneration. Nucleus pulposus of intervertebral discs were obtained from 22 patients and analysed for collagen and proteoglycan contents, and pro-MMP-2, TIMP-2 levels. Collagen content was determined as hydroxyproline and proteoglycan content was measured as glycosaminoglycans. The loss in matrix components did not correlate with the duration of the degenerative disc disease. Pro-MMP-2 levels were higher at early stages of the degenerative disc disease (r = -0.495, P < 0.05). TIMP-2 levels were similar in all samples. Pro-MMP-2 and TIMP-2 levels negatively correlated in herniated discs samples (r = -0.855, P < 0.01). Pro- MMP-2 levels negatively correlated with the collagen content in herniated disc material. Our findings may suggest a silent period of active disease prior to symptomatic outcome during which irreversible matrix loss occurs. Involvement of other proteolytic enzymes at different stages of the disease should also be investigated to help to control the degradation cascade at relatively early stages of disc degeneration before the clinical onset of disease.

A 63-year-old female presented with intracranial tuberculoma manifesting as severe headache.

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