Direct comparison of the genomic responses of brain in response to ischemic stroke, intracerebral hemorrhage, kainic acid induced seizures, hypoglycemia and hypoxia was made by Tang et al in 2002. Significantly, marked overlap of regulated genes was found throughout all disease states. In particular, all genes induced by kainic acid were also induced by ischaemia, hemorrhage or hypoglycemia. This suggests a multifactorial mechanism of injury for kainic acid induced seizures that mimics or utilizes the same pathways as those associated with ischaemia, hypoglycemia or hemorrhage (95) . Whether seizures themselves primarily induce these genomic changes or secondarily act through periods of ischemic or hypoglycemic during seizure episodes remain unclear. What is clear, however, is the similarities in histological changes seen in these conditions with marked neuronal loss, fibrillary gliosis with vacuolation and enlarged reactive astrocytes variously reported following severe hypoglycemia and ischemia, with or without associated status epilepticus (1, 13, 51, 52) .