Department of Molecular and Cellular Therapeutics, The Royal College of Surgeons in Ireland, Dublin 2, Ireland.
Epilepsy Res. 2012 Mar;99(1-2):156-66. doi: 10.1016/j.eplepsyres.2011.11.005. Epub 2011 Dec 23.
Applying a cross-sectional design, we set out to further characterize the significance of extrahippocampal brain atrophy in a large sample of 'sporadic' mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE+HS). By evaluating the influence of epilepsy chronicity on structural atrophy, this work represents an important step towards the characterization of MRI-based volumetric measurements as genetic endophenotypes for this condition.
Using an automated brain segmentation technique, MRI-based volume measurements of several brain regions were compared between 75 patients with 'sporadic' MTLE+HS and 50 healthy controls. Applying linear regression models, we examined the relationship between structural atrophy and important clinical features of MTLE+HS, including disease duration, lifetime number of partial and generalized seizures, and history of initial precipitating insults (IPIs).
Significant volume loss was detected in ipsilateral hippocampus, amygdala, thalamus, and cerebral white matter (WM). In addition, contralateral hippocampal and bilateral cerebellar grey matter (GM) volume loss was observed in left MTLE+HS patients. Hippocampal, amygdalar, and cerebral WM volume loss correlated with duration of epilepsy. This correlation was stronger in patients with prior IPIs history. Further, cerebral WM, cerebellar GM, and contralateral hippocampal volume loss correlated with lifetime number of generalized seizures.
Our findings confirm that multiple brain regions beyond the hippocampus are involved in the pathogenesis of MTLE+HS. IPIs are an important factor influencing the rate of regional atrophy but our results also support a role for processes related to epilepsy chronicity. The consequence of epilepsy chronicity on candidate brain regions has important implications on their application as genetic endophenotypes.
采用横断面设计,我们旨在通过评估癫痫慢性对结构萎缩的影响,在大量“散发性”海马硬化性内侧颞叶癫痫(MTLE+HS)患者中进一步确定海马外脑萎缩的意义。这项工作代表了朝着将基于 MRI 的容积测量作为该疾病的遗传内表型进行特征描述的重要一步。
使用自动脑分割技术,我们比较了 75 例“散发性”MTLE+HS 患者和 50 例健康对照者的几个脑区的 MRI 基于体积测量。通过线性回归模型,我们检查了结构萎缩与 MTLE+HS 的重要临床特征之间的关系,包括疾病持续时间、生活中部分和全身性癫痫发作次数以及初始诱发损伤(IPIs)的病史。
在同侧海马体、杏仁核、丘脑和大脑白质(WM)中发现明显的体积损失。此外,在左 MTLE+HS 患者中还观察到对侧海马体和双侧小脑灰质(GM)体积损失。海马体、杏仁核和大脑 WM 体积损失与癫痫持续时间相关。在有既往 IPIs 病史的患者中,这种相关性更强。此外,大脑 WM、小脑 GM 和对侧海马体体积损失与终生全身性癫痫发作次数相关。
我们的发现证实了除海马体外,多个脑区参与了 MTLE+HS 的发病机制。IPIs 是影响区域萎缩速度的重要因素,但我们的结果也支持与癫痫慢性相关的过程的作用。癫痫慢性对候选脑区的影响对它们作为遗传内表型的应用具有重要意义。