A clinical, haematological, and biochemical investigation of 62 epileptics is reported. Fifty-four of the patients were receiving anticonvulsant drugs and eight were untreated. None of the treated patients was anaemic, but 17 (38 per cent.) of 45 in whom the bone marrow was examined showed megaloblastic haemopoiesis. Treatment with folic acid in seven patients restored normoblastic haemopoiesis in all. Only seven of the 54 treated patients showed macrocytosis and only five showed hypersegmentation of the neutrophils in the peripheral blood. Serum folate concentrations were subnormal in 76 per cent. of the treated patients. With one exception, serum vitamin B12 concentrations were within the normal range, though significantly lower in the megaloblastic group than in the untreated patients. Only a small proportion of the treated patients excreted excess Figlu after a histidine load. Serum lactate dehydrogenase concentrations were normal in all patients. It was found that neither morphological changes in the peripheral blood nor biochemical investigations were reliable indications of megaloblastic haemopoiesis. All three major anticonvulsant drugs (phenobarbitone, phenytoin, and primidone) appear to be capable of causing folate deficiency. The possible mechanisms are discussed, and it is suggested that there may be a relationship between the anti-folate effect of the drugs and their therapeutic action. Attention is drawn to the possible consequences of prolonged drug-induced folate deficiency, which may be responsible for producing mental symptoms.