Lipid Peroxidation and Antioxidants in Childhood Epilepsy

Summary

Evidence linking vitamin E deficiency with neurological abnormalities indicates that vitamin E may have an important central nervous system role relating to membrane stability and function. In an experimental model, vitamin E (α-tocopheryl acetate) reduced seizure activity. Vitamin E inhibits the effects of oxidation in brain tissues (antioxidant) and is a free radical scavenger. Free radical scavengers have been implicated in the epileptic brain injury caused by prolonged seizures due to hyperoxia. Vitamin E is a membrane stabilizer protecting membranes from peroxidation damage. Clinical studies in children have shown reduced plasma levels of vitamin E in seizure patients receiving antiepileptic drugs (AEDs). An uncontrolled, non-blind clinical trial suggested that add-on vitamin E improved seizure control in some patients. Since vitamin E deficiency hypothetically exacerbates epileptic seizures in patients receiving AEDs, treatment of the vitamin E deficiency should improve seizure control and/or neurological function. A prospective, modified crossover, randomized, double-blind, placebo-controlled clinical trial of add-on vitamn E therapy (400 IU/day) was then carried out in 24 epileptic patients who were refractory to AEDs. There was a significant reduction of seizures in 10 of 12 patients. This result was significantly different from that with controls given placebo (0 of 12, p < 0.05).This result did not appear to be due to the effects of change in the plasma levels of the co-medication. There were no adverse side effects. This therapeutic observation accords with previous reports and some experimental studies. This finding may be very important to the 10 %–20 % of the epileptic population whose seizures are inadequately controlled with the best anticonvulsant drugs presently available.