The finding of low pyridoxine levels among children assessed, in the population of Kitgum District as well as in the children assessed in Western Equatoria in South Sudan is notable, in the light of a condition known as pyridoxine-dependent seizures (PDS) and pyridoxine-responsive seizures. Hunt et al, (1954) first described pyridoxine dependent seizures (PDS) (23) with an autosomal recessive inheritance. PDS is due to defective binding of pyridoxine to its apoenzyme, glutamate decarboxylase, which catalyzes the conversion of glutamic acid, a critical nutrient, into gamma-aminobutyric acid (GABA), an inhibitory central nervous system neurotransmitter. The resultant reduced levels of GABA lower the seizure threshold, leading to intractable seizures (24, 25,26, 27, appendix Z).