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Alternative Medicine Review, March, 2007 by Alan R. Gaby
Forty-three teenagers and adults with uncontrolled epilepsy were randomly assigned to receive, in double-blind fashion, 600 IU/day vitamin E or placebo for three months. After a one-week washout period, each patient received the alternate treatment for an additional three months. Anticonvulsant medications were continued as previously. The mean seizure frequency decreased by 25.7 percent during the placebo period and by 13.8 percent during the vitamin E period compared with baseline. (89)
Although the research on efficacy is conflicting, vitamin E is relatively safe and may be considered for adjunctive treatment in epileptic patients, particularly children.
Manganese
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In rats, manganese deficiency increased susceptibility to electroshock-induced convulsions. In addition, hydralazine-induced seizures in rats were prevented by prior administration of manganese. (90)
In humans with epilepsy, whole-blood manganese levels were significantly lower by 20-41 percent than in controls. (91-96) Manganese concentrations in epileptic patients did not correlate with seizure frequency or the type, dose, or plasma levels of anticonvulsant medication. Concentrations of other minerals, such as zinc and copper, were generally normal, suggesting that the association between manganese deficiency and epilepsy was not due to general malnutrition. Patients whose epilepsy was a result of trauma had significantly higher blood manganese concentrations than patients with no history of trauma, (92) which suggests that manganese deficiency is a primary contributing factor, rather than a consequence, of epilepsy or its treatment.
One group of practitioners stated that unspecified doses of manganese were helpful in controlling epileptic seizures. (97) In a case report, a 12-year-old boy with poorly controlled epilepsy and a low blood manganese level experienced fewer seizures after treatment with 20 mg manganese daily. A dose of 10 mg/day was tried initially for three weeks, but was not effective. (91)
Taurine
Taurine acts as a modulator of membrane excitability in the central nervous system by inhibiting the release of other neurotransmitters and decreasing mitochondrial release of calcium. (98) Taurine concentrations have been found to be elevated in serum, but decreased in the brain, of some patients with epilepsy. In contrast, serum concentrations of most other amino acids were lower in patients with epilepsy than in healthy controls. Taurine administration partially corrected these low serum amino acid concentrations. (99-102)
Taurine has been administered orally or intravenously at a wide range of doses (200 mg/day to 21 g/ day) for varying periods of time to patients with severe, intractable epilepsy. In some studies, a significant reduction in seizure frequency was observed, (103-107) whereas no benefit was seen in others. (108) According to one report, taurine was effective against partial epilepsy but had little effect on generalized epilepsy. The beneficial effects of taurine frequently diminished or disappeared after a few weeks of treatment. One possible explanation for the loss of efficacy is that high-dose taurine caused amino acid imbalances, as suggested by the appearance of generalized aminoaciduria in a patient during treatment daily with 2.0-2.5 g taurine. It has been suggested that the optimal dose of taurine to treat epilepsy might be in the range of 100-500 mg/day, and in one report a loss of antiseizure activity was seen in some patients when the dose was increased above 1.5 g/day. While additional studies are needed to determine taurine's optimal dosage range, no specific dosage regimen has been shown to produce long-lasting improvement of epilepsy.
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