Tang's comparisons between kainic acid-induced seizures, hypoxia, hypoglycemia and hemorrhage suggest that the kainic acid-induced changes utilize the same pathological pathways as the other three conditions (95) . Indeed there are clear interrelations between all such conditions with prolonged seizures resulting in metabolic acidosis and an environment of relative hypoxia and hypoglycemia, and prolonged and severe hypoglycemia resulting in seizures in the generalized tonic-clonic form. The eventual histopathological outcome from these events culminates in varying degrees of neuronal loss, gliosis and even necrosis. If this is the case, it is difficult to proclaim that the genetic expression changes are actually specific to the process of epileptogenesis. Another study reported in abstract form (21) and cited in Lukasiuk et al's review revealed distinct differences in gene expression between the kainic acid and pilocarpine models of epileptogenesis, despite being studied in as exacting an environment of the same laboratory.