RECENT studies have established a relationship between vitamin B6 metabolism and convulsive disorders of the nervous system. Pyridoxine deficiency in young animals and human infants and the administration of pyridoxine antagonists in animals have been observed to cause convulsive activity which is rapidly alleviated by administration of pyridoxine1,2. Several instances have been reported of children with abnormally high vitamin B6 requirements1,3. On ordinary dietary vitamin B6 intake, they appear, at least as regards their nervous system, to be suffering from a relative vitamin B6 deficiency and are subject to convulsions which are rapidly terminated by pyridoxine administration, or entirely prevented by pyridoxine supplementation of the diet. In order to investigate further the nature of the cerebral metabolic disturbances occurring in vivo in vitamin B6 deficiency, measurements of cerebral blood flow, oxygen consumption, and respiratory quotient were made in one of these pyridoxine-dependent children during a period of seizure activity induced by withdrawal of pyridoxine from the diet and immediately after its alleviation by parenteral administration of pyridoxine.