Natural approaches to epilepsy

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

Dimethylglycine

Dimethylglycine, a metabolite of betaine, demonstrated anticonvulsant activity in mice in one study, (109) but not in another. (110)

In a case report, a 22-year-old mentally handicapped man with mixed complex, partial, and grand mal seizures had been having 16-18 generalized seizures per week, despite therapeutic levels of phenobarbital and carbamazepine. His mother began giving him 90 mg dimethylglycine twice daily because of a suggestion it might improve his stamina. Within one week his seizure frequency dropped to three per week. Two attempts to withdraw dimethylglycine resulted in a dramatic increase in seizures. (111)

In follow-up studies, administration of dimethylglycine to 24 epileptic patients in doses of 300-810 mg/day for up to 30 days did not produce any improvement. (112,113) It was suggested that the one patient who benefited from dimethylglycine may have had an isolated metabolic defect that was overcome by treatment with this compound.

Thiamine

Severe thiamine deficiency can cause seizures in both alcoholic and non-alcoholic patients; these seizures are reversible with thiamine supplementation. Low thiamine status was found in 25 percent of 620 epileptic patients attending an outpatient clinic in one study, and in 31 percent of 72 patients in another study. (114,115) In a placebo-controlled trial, supplementation of epileptic patients with 50 mg thiamine daily for six months was associated with significant improvements in tests of both verbal and non-verbal IQ. (113) Thus, suboptimal thiamine status may be a factor in the impaired cognitive function seen in some patients with epilepsy.

Folic Acid

Seizures occur in some infants with cerebral folate deficiency, a syndrome that also includes slow head growth, psychomotor retardation, cerebellar ataxia, and other neurological abnormalities. This syndrome is caused by impaired transport of folate across the blood-brain barrier into the central nervous system. The transport defect can be overcome by administration of folinic acid (an active form of folic acid), which bypasses the blocked folate transport mechanism. There are several case reports in which administration of folinic acid (2.5-20 mg twice daily in one study, 0.5-1.0 mg/kg body weight per day in another) resulted in improvement or complete control of seizures in infants. (116,117)

In patients with seizures not due to cerebral folate deficiency, folic acid supplementation is of little or no benefit with respect to seizure control, and may even exacerbate seizures in some instances (see below). However, folate deficiency is common in patients with epilepsy and may have negative effects on other aspects of health. Subnormal serum or erythrocyte folate concentrations have been observed in 19-88 percent of patients with epilepsy in different studies. (49,50,118-122) Low folate levels were found more frequently among inpatients than outpatients, and in those with coexisting psychiatric illness than those without psychiatric illness. Folate deficiency is due primarily to the use of anticonvulsant medications (e.g., phenytoin, valproate, carbamazepine, phenobarbital, and primidone), which interfere with folic acid absorption. (123-125)