Abstract

Abstract
Epidemiological and recent prospective analyses of long Febrile Seizures (FS) support the idea that such seizures
can provoke Temporal Lobe Epilepsy (TLE) in some children. Because of the high prevalence of these seizures, if
epilepsy was to arise as their direct consequence, this would constitute a significant clinical problem. Animal studies
have revealed that exposure of hippocampal neurons to FS early in life, particularly prolonged or frequently repetitive
FS, or together with brain malformation, may lead to sustained dysfunction of these cells including long-term memory
impairment or epileptogenesis, in spite of the absence of neuronal damage. We established a hyperthermia model
of febrile convulsions in young adult rats, and studied the effects of propofol treatment general anesthetic acting via
GABA-A receptor on epileptiform activity and the morphological features of medial temporal lobe.
We found statistically significant neuronal losses in the CA1, CA3 and dentate gyrus regions of hyperthermiaapplied
rats as compared to the control rats. We also observed that propofol administration suppressed epileptic
discharges in EEG and prevented clinical seizures behaviors. It took a median of 11 (range, 6-40) minutes for propofol
to stop seizures. We conclude that prevention of epilepsy-related damage can be achieved via epileptogenesis-based
clinical approaches, and that propofol is an effective agent in the hyperthermia-induced status epilepticus model.

Keywords: Epileptogenesis; Febrile convulsions; Pilocarpine; Hippocampus; Propofol