In a child, a convulsive seizure in association with fever may mean 1 of 6 things. 1. The fever may be a consequence of a spontaneous seizure, the results of an excess of muscular energy and heat. 2. The seizure may be the result of excess hydration or of antibiotics given to combat an infection. 3. The fever may be a seizure phenomenon, the result of a paroxysmal seizure discharge in the region of the hypothalamus. 4. The seizure may be due not to the fever but to bacterial toxins. 5. It may be the secondary result of cerebral pathology induced by an invasion of the brain by the infectious organisms. 6. The seizure may be due to no one of these, but be the direct response of the young child's organism to high fever in association with some infection. In addition, the seizure may not be the consequence of fever, but both fever and seizure a consequence of toxic action on brain cells. Curious features as yet not satisfactorily explained are. 1. Fever-induced seizures belong predominantly to the very young. 2. Almost invariably the febrile seizure, if there is such, is the child's initial seizure. 3. Response to fever is almost invariably a convulsion rather than some other manifestations of epilepsy. A study was made of 1,136 persons whose first convulsive seizure occurred in the first decade of life, 298 having had fever-induced seizures (usually with subsequent non-febrile), 838 having had none. The two groups were compared with respect to age at the first seizure, the presence of antecedent brain pathology, the sex of patients and whether seen in clinic or office. Extreme youth and absence of pathology were most often associated with febrile seizures. Among a total of 407 fever-activated cases, 76.9% subsequently experienced nonfebrile seizures. In 22% an interval of five years or longer separated the last febrile seizure from the first nonfebrile one. With respect to the type of subsequent seizures, an undue proportion of patients had only psychomotor seizures, suggesting that febrile seizures may sometimes be attended by temporal lobe lesions. Febrile seizures are usually innocuous, but if prolonged, focal or attended by much cyanosis or protracted coma, they may cause brain damage. Of 392 patients who sustained brain injury in the first 10 years of life, febrile seizures were blamed for the injury and the continuing epilepsy in 5.4%. Most notable of these findings, however, is the confirmation of what others have reported, that the genetic influence in children having fever-induced seizures is unduly high. In the author's group, this influence, as measured by the incidence of epilepsy among near relatives, is approximately double the genetic influence in young children having only nonfebrile seizures. If we accept the view that evidence of hereditary transmission is the hall-mark of essential epilepsy, then a febrile seizure is epilepsy; but more than that, it is an unusually pure culture of epilepsy. This conclusion has a corollary. Fever-activated epilepsy is short lived. The majority of children with a history of fever-induced seizures have had only one or two. Therefore, the more pure or essential the epilepsy, the better the outlook for spontaneous recovery. Seizures uncomplicated by some acquired pathology of the brain tend to be short lived, perhaps even self-limited—limited by the stabilizing influence of age.