Dubé Céline, Richichi Cristina, Bender Roland A, Chung Grace, Litt Brian, Baram Tallie Z
Department of Anatomy/Neurobiology, University of California, Irvine, CA 92697-4475, USA.
Brain. 2006 Apr;129(Pt 4):911-22. doi: 10.1093/brain/awl018. Epub 2006 Jan 30.
Experimental prolonged febrile seizures (FS) lead to structural and molecular changes that promote hippocampal hyperexcitability and reduce seizure threshold to further convulsants. However, whether these seizures provoke later-onset epilepsy, as has been suspected in humans, has remained unclear. Previously, intermittent EEGs with behavioural observations for motor seizures failed to demonstrate spontaneous seizures in adult rats subjected to experimental prolonged FS during infancy. Because limbic seizures may be behaviourally subtle, here we determined the presence of spontaneous limbic seizures using chronic video monitoring with concurrent hippocampal and cortical EEGs, in adult rats (starting around 3 months of age) that had sustained experimental FS on postnatal day 10. These subjects were compared with groups that had undergone hyperthermia but in whom seizures had been prevented (hyperthermic controls), as well as with normothermic controls. Only events that fulfilled both EEG and behavioural criteria, i.e. electro-clinical events, were considered spontaneous seizures. EEGs (over 400 recorded hours) were normal in all normothermic and hyperthermic control rats, and none of these animals developed spontaneous seizures. In contrast, prolonged early-life FS evoked spontaneous electro-clinical seizures in 6 out of 17 experimental rats (35.2%). These seizures consisted of sudden freezing (altered consciousness) and typical limbic automatisms that were coupled with polyspike/sharp-wave trains with increasing amplitude and slowing frequency on EEG. In addition, interictal epileptiform discharges were recorded in 15 (88.2%) of the experimental FS group and in none of the controls. The large majority of hippocampally-recorded seizures were heralded by diminished amplitude of cortical EEG, that commenced half a minute prior to the hippocampal ictus and persisted after seizure termination. This suggests a substantial perturbation of normal cortical neuronal activity by these limbic spontaneous seizures. In summary, prolonged experimental FS lead to later-onset limbic (temporal lobe) epilepsy in a significant proportion of rats, and to interictal epileptifom EEG abnormalities in most others, and thus represent a model that may be useful to study the relationship between FS and human temporal lobe epilepsy.
实验性长时间发热性惊厥(FS)会导致结构和分子变化,从而促进海马体兴奋性过高,并降低对进一步惊厥剂的惊厥阈值。然而,这些惊厥是否会引发迟发性癫痫,正如人们在人类身上所怀疑的那样,仍不清楚。此前,对运动性惊厥进行行为观察的间歇性脑电图未能在婴儿期经历实验性长时间FS的成年大鼠中证明自发性惊厥。由于边缘性惊厥在行为上可能很微妙,因此我们在此使用慢性视频监测并同时记录海马体和皮质脑电图,来确定成年大鼠(约3月龄开始)在出生后第10天经历持续性实验性FS后是否存在自发性边缘性惊厥。将这些实验对象与经历过热但惊厥得到预防的组(热对照)以及正常体温对照组进行比较。只有同时满足脑电图和行为标准的事件,即电临床事件,才被视为自发性惊厥。所有正常体温和热对照大鼠的脑电图(记录时长超过400小时)均正常,且这些动物均未发生自发性惊厥。相比之下,17只实验大鼠中有6只(35.2%)在早期经历长时间FS后出现了自发性电临床惊厥。这些惊厥表现为突然僵住(意识改变)和典型的边缘性自动症,同时脑电图上出现波幅增加、频率减慢的多棘波/尖波串。此外,实验性FS组中有15只(88.2%)记录到发作间期癫痫样放电,而对照组均未记录到。大多数在海马体记录到的惊厥之前,皮质脑电图波幅会降低,这种情况在海马体发作前半分钟开始,并在惊厥终止后持续存在。这表明这些边缘性自发性惊厥对正常皮质神经元活动有重大干扰。总之,长时间实验性FS会导致相当比例的大鼠出现迟发性边缘性(颞叶)癫痫,并且大多数其他大鼠会出现发作间期癫痫样脑电图异常,因此这是一个可能有助于研究FS与人类颞叶癫痫之间关系的模型。