Blood-brain barrier breakdown following traumatic brain injury: a possible role in posttraumatic epilepsy.
Blood-brain barrier breakdown following traumatic brain injury: a possible role in posttraumatic epilepsy.
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创伤性脑损伤后的血脑屏障分解：创伤后癫痫中可能作用。
DOI：
10.1155/2011/765923
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Shelef I
中科院分区：
文献类型：
--
作者：
Tomkins O;Feintuch A;Benifla M;Cohen A;Friedman A;Shelef I
最近的动物实验表明，血脑屏障(BBB)的开放在创伤后癫痫(PTE)的发病机制中起着关键作用。本研究旨在探讨轻度创伤性脑损伤(TBI)后癫痫患者血脑屏障紊乱的频率、程度和功能相关性。本研究共纳入37例颅脑损伤患者，其中19例为PTE。所有患者均接受脑电(EEG)记录和脑磁共振成像(BMRI)检查。使用新的定量技术评估BMRI对血脑屏障干扰的影响。使用标准化的低分辨率脑电磁断层扫描(SLORETA)定位皮质功能障碍。与对照组相比，脑外伤患者的脑电明显减慢，而PTE患者与非癫痫患者之间无明显差异。与非癫痫患者的25%相比，82.4%的PTE患者存在血脑屏障中断(P=.001)，甚至在创伤后数年仍可观察到。PTE患者伴有血脑屏障破坏的大脑皮质体积显著增大(P=.001)。在70%的患者中，慢波脑电活动定位于血脑屏障受损的同一区域，并与血脑屏障受损皮质的体积相关。最后，我们介绍了一位患有早期皮质功能障碍和血脑屏障衰竭的患者，两种病理的逐渐和平行的解决。我们的研究结果表明，轻度脑外伤后常可发现血脑屏障病变。PTE患者持续的血脑屏障破坏频率和程度增加。基于最近的动物研究和发现的血脑屏障受损区域和异常脑电活动之间的共存，我们认为血管病变在PTE的发病机制中发挥了作用。
Recent animal experiments indicate a critical role for opening of the blood-brain barrier (BBB) in the pathogenesis of post-traumatic epilepsy (PTE). This study aimed to investigate the frequency, extent, and functional correlates of BBB disruption in epileptic patients following mild traumatic brain injury (TBI). Thirty-seven TBI patients were included in this study, 19 of whom suffered from PTE. All underwent electroencephalographic (EEG) recordings and brain magnetic resonance imaging (bMRI). bMRIs were evaluated for BBB disruption using novel quantitative techniques. Cortical dysfunction was localized using standardized low-resolution brain electromagnetic tomography (sLORETA). TBI patients displayed significant EEG slowing compared to controls with no significant differences between PTE and nonepileptic patients. BBB disruption was found in 82.4% of PTE compared to 25% of non-epileptic patients (P = .001) and could be observed even years following the trauma. The volume of cerebral cortex with BBB disruption was significantly larger in PTE patients (P = .001). Slow wave EEG activity was localized to the same region of BBB disruption in 70% of patients and correlated to the volume of BBB disrupted cortex. We finally present a patient suffering from early cortical dysfunction and BBB breakdown with a gradual and parallel resolution of both pathologies. Our findings demonstrate that BBB pathology is frequently found following mild TBI. Lasting BBB breakdown is found with increased frequency and extent in PTE patients. Based on recent animal studies and the colocalization found between the region of disrupted BBB and abnormal EEG activity, we suggest a role for a vascular lesion in the pathogenesis of PTE.