Effects of Propofol on Epileptiform Activity and Hippocampal Morphology in Febrile Convulsions and Pilocarpine Induced SeizuresAylin Bican1*, Ibrahim Bora1, Ilker M Kafa2 and Mustafa A Kurt2
- *Corresponding Author:
- Aylin Bican
Department of Neurology
Uludag University, Faculty of Medicine
Gorukle Bursa, Turkey
E-mail: [email protected]
Received Date: June 05, 2012; Accepted Date: August 21, 2012; Published Date: August 23, 2012
Citation: Bican A, Bora I, Kafa IM, Kurt MA (2012) Effects of Propofol on Epileptiform Activity and Hippocampal Morphology in Febrile Convulsions and Pilocarpine Induced Seizures. J Clin Exp Pathol 2:123. doi: 10.4172/2161-0681.1000123
Copyright: © 2012 Bican A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.