Sendrowski K, Sobaniec W, Sobaniec-Lotowska M E, Artemowicz B
Department of Pediatric Neurology and Rehabilitation, Medical University of Białystok, Poland.
Adv Med Sci. 2007;52 Suppl 1:161-5.
The aim of the study wad to estimate a potentially neuroprotective effect of topiramate (TPM) in the experimental model of FS.
24 young male rats divided in 4 groups were involved in the study. Febrile seizures were induced by placing the animals in 45 degrees C warm water bath for four consecutive days. TPM at the dose 80 mg/kg b.m. was administered: before the FS and immediately after the FS. FS group and control rats received only normal saline. Thereafter hippocampal slices were prepared to performing histological and morphometric examination.
Morphometric investigations revealed that FS caused death of 60% of the neurons in sector CA1 and a half of them in sector CA3. Histological examinations of hippocampal slices showed that TPM at a dose of 80 mg/kg b.m., administered before the seizures, considerably improved CA1 and CA3 pyramidal cell survival. Similar neuroprotective effect, but in a markedly lesser degree was observed when TPM was administrated after the FS.
Our findings seem to confirm that FS exert a strong destructive effect on the sensitive hippocampal neurons and on the neuroprotective properties of TPM in this process, which may have practical implications. It can be assumed that in children with recurrent and prolonged FS, prophylactic drug administration could prevent hippocampal sclerosis and development of symptomatic epilepsy.
本研究旨在评估托吡酯（TPM）在热性惊厥（FS）实验模型中的潜在神经保护作用。
24只雄性幼鼠被分为4组参与研究。通过将动物连续4天置于45摄氏度的温水浴中诱导热性惊厥。以80mg/kg体重的剂量给予TPM：在热性惊厥发作前及发作后立即给药。FS组和对照组大鼠仅接受生理盐水。此后制备海马切片以进行组织学和形态学检查。
形态学研究显示，热性惊厥导致CA1区60%的神经元死亡，CA3区有一半的神经元死亡。海马切片的组织学检查表明，在惊厥发作前给予80mg/kg体重剂量的TPM，可显著提高CA1和CA3锥体细胞的存活率。当在热性惊厥发作后给予TPM时，观察到类似的神经保护作用，但程度明显较小。
我们的研究结果似乎证实，热性惊厥对敏感的海马神经元具有强烈的破坏作用，并且在此过程中TPM具有神经保护特性，这可能具有实际意义。可以推测，对于复发性和持续性热性惊厥的儿童，预防性给药可以预防海马硬化和症状性癫痫的发生。
