Abstract
EVIDENCE is accumulating to support the suggestion1 that folic acid (pteroyl glutamic acid) may play a role in epileptic phenomena. Grand mal epileptic patients undergoing anticonvulsant drug therapy are likely to develop megaloblastic anaemia as a result of disturbances in folic acid metabolism1, and it has been reported that correction of the folic acid deficiency by folate therapy results in an exacerbation of the frequency and intensity of epileptic episodes2,3. It is also known that folate and related pteridines possess convulsant properties in their own right when administered in high intravenous doses to rats, or given intracortically4.
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ROBERTS, P. Inhibition of high-affinity glial uptake of 14C-glutamate by folate. Nature 250, 429–430 (1974). https://doi.org/10.1038/250429a0
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DOI: https://doi.org/10.1038/250429a0
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