Blockade of sodium channels by phenytoin protects ultrastructure and attenuates lipid peroxidation in experimental spinal cord injury.

Spinal cord injury (SCI) involves a series of pathological events. Abnormal sodium influx has been implicated as one of the key events in the pathophysiology of the SCI. Pharmacological blockade of sodium channels can reduce secondary injury and increase recovery from trauma. The aim of the present study was to show the neuroprotective effect of phenytoin, a sodium channel blocker, after experimental SCI. Control and laminectomy-only groups were not injured. 50 g-cm weight drop injury was produced in the trauma group. In the treatment groups, methylprednisolone (30 mg/kg) and phenytoin (1 mg/kg, 10 mg/kg, or 30 mg/kg) were given intraperitoneally immediately after injury. Malondialdehyde (MDA) levels in the spinal cord samples were examined for lipid peroxidation. Spinal cord ultrastructure was evaluated and grading system was used for quantitative evaluation. Trauma increased tissue MDA levels. Treatment with methylprednisolone and phenytoin decreased MDA levels compared to trauma in all doses. Significant ultrastructural neuroprotection was observed with 30 mg/kg of phenytoin treatment according to general neural score. This ultrastructural neuroprotection of phenytoin was not different from methylprednisolone. Phenytoin appears to protect spinal cord against injury by decreasing lipid peroxidation and lessening neuronal damage associated with SCI in rats.