Evaluating the Role of Perilesional Tissue in Pathobiology of Epileptogenesis of Vascular Malformations of the Central Nervous System.

R T Rajeswarie, H R Aravinda, A Arivazhagan, N Nandeesh Bevinahalli, Malla Bhaskara Rao, Anita Mahadevan
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Abstract

Background and purpose: Seizures are common presentation of cerebral vascular malformation (CVM). Topography and haemodynamic alterations are proposed as mechanisms for epileptogenesis, but the role of glial/neuronal alterations in perilesional tissue has not received much attention. Identification of the exact pathophysiologic basis could have therapeutic implications. To evaluate whether angioarchitectural factors of CVM or alterations in neuroglial/stroma of the adjacent cortex contribute to seizures.

Method: The clinical, imaging and histological characteristics of arteriovenous malformation (AVM) and cerebral cavernous malformation (CCM) with and without seizures was evaluated using neuroimaging imaging and digital subtraction angiography parameters and histopathology by morphology and immunohistochemistry.

Results: Fifty-six cases of CVM were diagnosed over a 2-year study period. Of these, 32 had adequate perilesional tissue for evaluation (AVM, 24; CCM, 8). Seizures at presentation was seen in 12/24 (50%) of AVM and 5/8 (62.5%) CCM. In AVM, hemosiderin deposition and gliosis in parenchyma (p=0.01) had significant association with seizure. Siderotic vessels in the adjacent cortex was exclusively seen only in CCM with seizures (p=0.018). Angioarchitectural features of CVM on imaging and neuronal alterations in adjacent cortex on histology failed to show any statistically significant difference between the two groups (p>0.05).

Conclusions: We propose that changes in adjacent cortex appear to be epileptogenic rather than the malformation per se. Reactive gliosis and hemosiderin deposits in perilesional tissue in AVM and siderotic vessels in CCM were associated with seizure. This explains the better outcomes following extended lesionectomy that includes epileptogenic perilesional tissues.

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评估病灶周围组织在中枢神经系统血管畸形癫痫发生病理生物学中的作用。
背景与目的:癫痫发作是脑血管畸形(CVM)的常见表现。地形和血流动力学改变被认为是癫痫发生的机制,但神经胶质/神经元改变在病变周围组织中的作用尚未得到太多关注。确定确切的病理生理基础可能具有治疗意义。评估CVM的血管构建因素或相邻皮质神经胶质/基质的改变是否与癫痫发作有关。方法:应用神经影像学和数字减影血管造影参数,结合形态学和免疫组织化学方法对伴有和不伴有癫痫发作的动静脉畸形(AVM)和脑海绵状血管瘤(CCM)的临床、影像学和组织学特征进行评价。结果:在2年的研究期间,诊断出56例CVM。其中32例有足够的病变周围组织进行评估(AVM, 24例;12/24(50%)的AVM和5/8(62.5%)的CCM在发病时出现癫痫发作。在AVM中,含铁血黄素沉积和实质胶质瘤与癫痫发作有显著相关性(p=0.01)。相邻皮质侧缩血管仅在癫痫发作的CCM中可见(p=0.018)。两组CVM影像学血管建筑学特征及相邻皮层组织学上神经元改变差异无统计学意义(p>0.05)。结论:我们认为邻近皮质的改变似乎是癫痫性的,而不是畸形本身。AVM的反应性胶质瘤和含铁血黄素沉积在病灶周围组织和CCM的含铁血黄素血管与癫痫发作有关。这解释了包括致痫性病变周围组织在内的扩展病变切除术的更好结果。
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