Park Jun T, Chugani Harry T
Division of Pediatric Epilepsy, Department of Pediatrics, Rainbow Babies & Children's Hospital, Case Western University School of Medicine, Cleveland, Ohio.
Division of Pediatric Neurology, Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan, Division of Pediatric Neurology, Nemours DuPont Hospital for Children, Wilmington, Delaware, Department of Neurology and Pediatrics, Thomas Jefferson University School of Medicine, Philadelphia, Pennsylvania, USA.
Epileptic Disord. 2017 Mar 1;19(1):24-34. doi: 10.1684/epd.2017.0900.
To recognize epileptic spasms (ES) as a seizure type after traumatic brain injury (TBI), accidental or non-accidental, in infants and children. In the process, we aim to gain some insight into the mechanisms of epileptogenesis in ES. A retrospective electronic chart review was performed at the Children's Hospital of Michigan from 2002 to 2012. Electronic charts of 321 patients were reviewed for evidence of post-traumatic epilepsy. Various clinical variables were collected including age at TBI, mechanism of trauma, severity of brain injury, electroencephalography/neuroimaging data, and seizure semiology. Six (12.8%) of the 47 patients diagnosed with post-traumatic epilepsy (PTE) had ES. Epileptic spasms occurred between two months to two years after TBI. All patients with ES had multiple irritative zones, manifesting as multifocal epileptiform discharges, unilateral or bilateral. Cognitive delay and epileptic encephalopathy were seen in all six patients, five of whom were free of spasms after treatment with vigabatrin or adrenocorticotropic hormone. The risk of PTE is 47/321(14.6%) and the specific risk of ES after TBI is 6/321 (1.8%). The risk of ES appears to be high if the age at which severe TBI occurred was during infancy. Non-accidental head trauma is a risk factor of epileptic spasms. While posttraumatic epilepsy (not ES) may start 10 years after the head injury, ES starts within two years, according to our small cohort. The pathophysiology of ES is unknown, however, our data support a combination of previously proposed models in which the primary dysfunction is a focal or diffuse cortical abnormality, coupled with its abnormal interaction with the subcortical structures and brainstem at a critical maturation stage.
认识到癫痫性痉挛（ES）是婴幼儿创伤性脑损伤（TBI）后，无论是意外还是非意外损伤后的一种发作类型。在此过程中，我们旨在深入了解ES癫痫发生的机制。2002年至2012年在密歇根儿童医院进行了一项回顾性电子病历审查。对321例患者的电子病历进行审查，以寻找创伤后癫痫的证据。收集了各种临床变量，包括TBI时的年龄、创伤机制、脑损伤严重程度、脑电图/神经影像学数据以及发作症状学。47例诊断为创伤后癫痫（PTE）的患者中有6例（12.8%）发生了ES。癫痫性痉挛发生在TBI后2个月至2年之间。所有ES患者均有多个激惹区，表现为多灶性癫痫样放电，单侧或双侧。所有6例患者均有认知延迟和癫痫性脑病，其中5例在使用vigabatrin或促肾上腺皮质激素治疗后痉挛消失。PTE的风险为47/321（14.6%），TBI后ES的特定风险为6/321（1.8%）。如果严重TBI发生在婴儿期，ES的风险似乎较高。非意外性头部外伤是癫痫性痉挛的一个危险因素。根据我们的小样本队列，虽然创伤后癫痫（而非ES）可能在头部受伤10年后开始，但ES在两年内开始。ES的病理生理学尚不清楚，但我们的数据支持先前提出的模型组合，其中主要功能障碍是局灶性或弥漫性皮质异常，再加上在关键成熟阶段与皮质下结构和脑干的异常相互作用。
