The role of folate deficiency in the development of peripheral neuropathy caused by anticonvulsants.

To investigate the role of folate deficiency in neuropathy caused by anticonvulsants, electrophysiological studies of peripheral nerve function were carried out on 29 epileptic patients on long-term anticonvulsant therapy. All but three patients showed abnormalities in one or more electrophysiological measurements, the main abnormality being in amplitude of sensory nerve action potential--this was reduced or absent in 76% of patients. All patients had low concentrations of folate in serum and CSF, these being below the normal ranges in 19 patients. These 19 patients were treated with folate, either 5-formyltetrahydrofolate (10 patients) or folic acid (9 patients), over a period of one month. After therapy all patients had normal levels of folate in serum and CSF, slightly higher levels in CSF being obtained in those receiving 5-formyltetrahydrofolate. Folate therapy significantly reversed abnormalities in motor and sensory nerve distal latencies; the effect was greater with 5-formyltetrahydrofolate, apparently because this produced higher CSF folate concentrations than folic acid. We conclude that folate deficiency may be involved in the development of peripheral neuropathy due to anticonvulsants.