Progression from frontal-parietal to mesial-temporal epilepsy after fluid percussion injury in the rat
Progression from frontal-parietal to mesial-temporal epilepsy after fluid percussion injury in the rat
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DOI：
10.1093/brain/awh337
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发表时间：
2005-01-01
期刊：
影响因子：
14.5
通讯作者：
Miller, JW
中科院分区：
文献类型：
--
作者：
D'Ambrosio, R;Fender, JS;Miller, JW
我们最近描述了大鼠创伤后癫痫（PTE）的体内模型，其中在单次流体冲击损伤（FPI）发作后出现慢性自发性复发性癫痫发作。在受伤后的前 2 个月内研究的 PTE 是局灶性的，癫痫发作主要源自受伤部位或周围的额顶叶新皮质。然而，也观察到源自不同且不明确的病灶的罕见双侧癫痫发作。为了阐明创伤后癫痫发生机制和双侧癫痫发作的发生，我们对大鼠进行了长达 7 个月的损伤研究。体内配对硬膜外和深度电极记录表明，前海马体演变成癫痫病灶，引发双侧癫痫发作。受伤后两周后，额顶叶癫痫发作率随时间保持恒定，而海马癫痫发作率随时间大幅增加，表明不同的机制介导新皮质和海马创伤后癫痫发生。由于这些病灶的时间演变不同，癫痫综合征的特点是受伤后早期以额叶-顶叶癫痫发作为主，但在稍后的时间点以颞叶癫痫发作为主。病理分析表明，进行性海马和颞叶皮层病理学与双侧癫痫发作频率和持续时间的增加相平行。这些结果表明，FPI 诱导的额顶叶癫痫 (FPE) 进展为具有双重病理学的内侧颞叶癫痫 (MTLE)。这些观察结果确立了 FPI 诱导的 PTE 与人类 PTE 之间的许多相似之处，并进一步验证其作为临床相关的 PTE 模型。
We recently described an in vivo model of post-traumatic epilepsy (PTE) in the rat where chronic spontaneous recurrent seizures appear following a single episode of fluid percussion injury (FPI). PTE, studied during the first 2 months post-injury, was focal and seizures originated predominantly from the frontal-parietal neocortex at or around the injury site. However, rarer bilateral seizures originating from a different and undefined focus were also observed. To shed light on the Posttraumatic Epileptogenic mechanisms and on the generation of bilateral seizures, we studied rats up to 7 months post-injury. In vivo paired epidural and depth-electrode recordings indicated that the anterior hippocampus evolves into an epileptic focus which initiates bilateral seizures. The rate of frontal-parietal seizures remained constant over time after 2 weeks post-injury, while the rate of hippocampal seizures greatly increased over time, suggesting that different mechanisms mediate neocortical and hippocampal post-traumatic epileptogenesis. Because of different temporal evolution of these foci, the epileptic syndrome was characterized by predominant frontal-parietal seizures early after injury, but by predominant mesio-temporal seizures at later time points. Pathological analysis demonstrated progressive hippocampal and temporal cortex pathology that paralleled the increase in frequency and duration of bilateral seizures. These results demonstrate that FPI-induced frontal-parietal epilepsy (FPE) progresses to mesial-temporal lobe epilepsy (MTLE) with dual pathology. These observations establish numerous similarities between FPI-induced and human PTE and further validate it as a clinically relevant model of PTE.