Abstracts

Increased T2 signal intensity in the hippocampus is occasionally seen following status eplepticus. In animal models and in human pathological specimens, seizure induced hippocampal injury and mesial temporal sclerosis is most marked in area CA1, or the Sommer sector, of the hippocampus. We have measured the relative distribution of T2 signal hyperintensity in the fields of the hippocampal body in MRIs done shortly after febrile status epilepticus (SE) in order to determine the distribution of signal intensity in the acute phase of hippocampal injury following febrile status eplepticus. As part of a prospective study, children presenting to the hospital with febrile SE were imaged within 72 hours following the episode of febrile SE. Febrile SE was defined as 30 minutes of continuous seizure activity or intermittent seizure activity without recovery inbetween in a child with a febrile seizure. MRIs were visually inspected for increased T2 signal. In those with eidence of increased T2 signal, the mid section of the body of each affected hippocampus was divided into 8 radial sectors for determination of the circumferential distribution of T2 signal intensity. This T2 intensity map was then compared to the location of hippocampal subdivisions. To date we have examined the acute MRIs of 38 children from a pilot study and 70 children from the current FEBSTAT prospective study. Of these, seven subjects had markedly increased hippocampal T2 signal on fast spin echo oblique coronal series. Visual inspection of these hippocampi suggested that the maximal increased T2 signal was located in the lateral and inferior portions of the hippocampal body, approximately the region of CA1. Circumferential measurement of T2 signal confirmed the impression of visual analysis that the highest signal was located in the CA1 area and to a lesser degree in CA4. The subiculum had lower T2 signal intensity than all the regions of the hippocampus examined. Hippocampal T2 signal intensity is abnormally increased in a some children following febrile status epilepticus. The distribution of this increased signal in the regions of the hippocampal body appears to approximate the distribution of the most profound cell loss in mesial temporal sclerosis with area CA1 being most affected. This distribution is compatible with the hypothesis that the status induced injury may be the precursor of mesial temporal sclerosis. (Supported by NINDS - R01 NS43209 Consequences of Prolonged Febrile Seizures in Childhood.)