GSH & Epilepsy & Seizures

Superoxide dismutase and glutathione peroxidase function in progressive myoclonus epilepsies
Ben-Menachem E, Kyllerman M, and others. [Epilepsy Res 2000 Jun;40(1):33-9.] "Progressive myoclonic epilepsies (EPM) are difficult to treat and refractory to most antiepileptic drugs. Besides epilepsy, EPMs also involve continuous neurological deterioration. Oxidative stress is thought to be an important factor in this process. We therefore analyzed a series of antioxidant enzymes in the blood of patients and compared with healthy age matched controls. In addition patients were given high doses of N-acetylcysteine (NAC), a glutathione percursor to determine if symptoms of EPM would improve. Five patients, four with EPM 1 (Unverricht-Lundborg disease) and one patient with EPM2 (Lafora body disease) were treated with 6 g/day of NAC. NAC improved markedly and stabilized the neurological symptoms in patients with EPM 1 but had a doubtful effect in the patient with EPM 2."

Glutathione peroxidase deficiency and childhood seizures
Beutler E, Curnutte JT, Forman L. [Lancet 1991 Sep 14;338(8768):700 - Comment on: Lancet. 1991 Jun 15;337(8755):1443-4.]
4 children with intractable seizures, repeated infections, and intolerance to anticonvulsants had evidence of glutathione peroxidase deficiency. 2 had low intracellular enzyme activity but normal blood selenium and high plasma glutathione peroxidase concentrations. The other 2 had low intracellular glutathione peroxidase activity with low circulating glutathione peroxidase and selenium concentrations. The clinical state of the children improved after discontinuation of anticonvulsant medication and selenium substitution.

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