Prayson Richard A, Frater John L
Department of Anatomic Pathology, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
Ann Diagn Pathol. 2003 Jun;7(3):139-46. doi: 10.1016/s1092-9134(03)00010-8.
Cortical dysplasias or malformations due to abnormalities of cortical development are a well-recognized cause of intractable seizures. This study retrospectively examines the clinicopathologic features of 52 cases of extratemporal cortical dysplasia (from 135 total resections performed over a 16-year period). The study consists of 52 patients (27 males; 25 females) who underwent extratemporal resection for epilepsy at a mean age of 15.1 years (range, 3 months to 44.1 years). Seizure duration before surgery ranged from 7 to 372 months (mean duration, 129 months). Patterns of cortical dysplasia observed included diffuse architectural disorganization (n=48), neuronal cytomegaly (n=32), increased number of molecular layer neurons (n=32), balloon cells (n=19), gray matter heterotopia (n=3), neuronal glial clustering (n=3), and pial glial neuronal tissue (n=2). Five patients had coexistent nodular hamartomas. Coexistent tumors were present in five patients; including three dysembryoplastic neuroepithelial tumors, one ganglioglioma, and one low-grade fibrillary astrocytoma. Two patients had tuberous sclerosis. Follow-up was available in 50 patients (mean follow-up, 29 months). Thirty-eight patients (73%) had complete resolution or significant decrease in seizure frequency, 13 patients (25%) had increased seizures or no change in seizures, and one patient died in the postoperative period. In conclusion, (1). cortical dysplasia was identified in 38.5% of extratemporal resections for epilepsy; (2). the common cortical dysplasia patterns observed included diffuse cortical disorganization, neuronal cytomegaly, and increased molecular layer neurons; (3). 10% of extratemporal cortical dysplasia was associated with tumors; (4). improved seizure control was obtained in approximately three fourths of patients after resection; and (5). seizures associated with balloon cell dysplasia were less successfully managed with surgery.
由于皮质发育异常导致的皮质发育异常或畸形是难治性癫痫的一个公认病因。本研究回顾性分析了52例颞叶外皮质发育异常病例的临床病理特征(来自16年间进行的135例全切除术)。该研究包括52例患者(27例男性;25例女性),他们平均年龄为15.1岁(范围3个月至44.1岁)时接受了颞叶外癫痫切除术。术前癫痫发作持续时间为7至372个月(平均持续时间129个月)。观察到的皮质发育异常模式包括弥漫性结构紊乱(n = 48)、神经元巨细胞变(n = 32)、分子层神经元数量增加(n = 32)、气球样细胞(n = 19)、灰质异位(n = 3)、神经元胶质细胞聚集(n = 3)和软膜胶质神经元组织(n = 2)。5例患者并存结节性错构瘤。5例患者存在并存肿瘤;包括3例胚胎发育不良性神经上皮肿瘤、1例神经节胶质瘤和1例低级别纤维性星形细胞瘤。2例患者患有结节性硬化症。50例患者有随访资料(平均随访29个月)。38例患者(73%)癫痫发作完全缓解或发作频率显著降低,13例患者(25%)癫痫发作增加或无变化,1例患者在术后死亡。总之,(1). 在38.5%的颞叶外癫痫切除术中发现皮质发育异常;(2). 观察到的常见皮质发育异常模式包括弥漫性皮质紊乱、神经元巨细胞变和分子层神经元增加;(3). 10%的颞叶外皮质发育异常与肿瘤有关;(4). 大约四分之三的患者切除术后癫痫控制得到改善;(5). 与气球样细胞发育异常相关的癫痫手术治疗效果较差。