Natural approaches to epilepsy

Alternative Medicine Review, March, 2007 by Alan R. Gaby

While correction of folate deficiency is desirable, administration of large doses of folic acid can decrease blood levels of phenytoin, phenobarbital, and carbamazepine, (126-129) potentially interfering with seizure control. An increase in seizure frequency has been seen in some, (130) but not all, (131-133) studies in which high-dose folic acid (5 mg three times per day) was given to drug-treated epileptic patients. In addition to interfering with anticonvulsant medication, high-dose folic acid itself may be epileptogenic. Intravenous administration of 14.4 mg folic acid induced a tonic-clonic seizure in one epileptic patient, although other patients experienced no adverse effects from 75 mg folic acid given intravenously. (134) One woman with epilepsy had an increase in seizure frequency and severity after receiving 0.8 mg folic acid per day, which was prescribed because she was planning to become pregnant. (135) A cause-effect relationship in this case is uncertain.

Based on these observations, modest doses of folic acid should be used to treat folate deficiency in epileptic patients. A study of pregnant epileptic women taking anticonvulsant drugs found that a folic acid dose of 100-1,000 mcg/day was sufficient to prevent folate deficiency and did not impair seizure control. (136)

Folic acid has also been used to treat phenytoin--induced gingival hyperplasia. In a small double-blind study, use of a 0.1-percent folic acid mouth rinse for six months significantly reduced the severity of this condition, whereas a placebo was ineffective. Patients used 5 mL of the mouth rinse twice daily, spitting it out after rinsing for two minutes (this solution should not be swallowed, as doing so would provide 10 mg/day of folic acid). Oral, rather than topical, administration of folic acid (3-4 mg/day) produced little or no improvement in phenytoin-induced gingival hyperplasia. (137,138)

Biotin

Serum biotin levels were below normal in 74 percent of 264 epileptic patients on long-term anticonvulsant therapy. (139) Low biotin levels appear to result from an acceleration of biotin catabolism by phenytoin, carbamazepine, and phenobarbital. (140,141) In addition, carbamazepine and primidone may inhibit intestinal absorption of biotin. (142) Interestingly, dermatitis and ataxia, side effects of many anticonvulsants, are also observed in patients with an inborn error of biotin-dependent enzymes.

There is no evidence that biotin supplementation interferes with the effect of anticonvulsants. To the contrary, correction of biotin deficiency might reduce seizure frequency, as suggested by the fact that biotin-responsive seizures have occurred in some patients with inborn errors of biotin metabolism. (143)

Vitamin D

Patients taking anticonvulsants are at increased risk of developing vitamin D deficiency, apparently because these drugs induce liver enzymes that inactivate vitamin D. (144,145) Rickets, (146) osteomalacia, (147) and low bone mineral contentx48 have been reported in drug-treated epileptic patients. The frequency with which these disorders occurred has varied widely in different studies, in part because of differences in sun exposure.