癫痫之前的神经损害影响远期结局

圣迭戈——伦敦北部癫痫持续状态儿童监督研究的Richard Chin博士在美国癫痫学会年会上报告，既往神经损害是儿童惊厥性癫痫持续状态后发生长期癫痫以及严重认知和运动障碍的唯一独立预测因子。

Richard Chin博士

研究者对126例中位年龄为3.6岁的儿童在惊厥性癫痫持续状态(CSE)后中位随访8.5年。结果显示，在之前有神经损害的患儿中，随访中发生活动性癫痫的比值比为7.195%置信区间(CI)为1.8~27.7，认知功能障碍的比值比为16.3(95%CI，4.3~61.1)，运动功能障碍的比值比为9.8(95%CI，3.0~31.2)。最初发作的持续时间以及是否为局灶性、全身、连续性或间断发作对预后均无预测作用。总体而言，“如果在发作前拥有良好的神经发育，则预后将会非常好，”

最多见的是小儿高热惊厥病例，这是最常见的儿科CSE病因。关于这一点，研究显示，在高热惊厥后进入研究的30例患儿中，无1例在随访期间发生活动性癫痫或严重运动功能障碍；1例之后诊断为自闭症的患者发生严重认知功能障碍。其中28例患儿的MRI正常，1例患儿有神经纤维瘤病证据，另1例患者有单侧海马体积缩小，不伴有信号改变。尽管一直认为持续高热惊厥是之后发生颞叶内侧硬化（MTS）的一个重要危险因素，但“未能找到支持这一观点的证据。无一持续高热惊厥患儿发生MTS。高热惊厥与之后发生颞叶内侧硬化之间的关系并非我们一度认为的那么强”。

51例有远处症状的CSE的患儿既往曾被诊断为大脑性麻痹、缺氧性脑损伤和其他问题；在随访期间，48例(94%)发生活动性癫痫，32例(63%)有严重运动功能受损，37例(73%)发生严重认知功能障碍。17例患儿发生急性症状性CSE发作；仅1例在随访期间发生活动性癫痫和严重认知功能障碍。1例由肺炎球菌性脑膜炎引起发作的患儿的MRI显示遗留MTS。研究中多数其他患儿被归类为特发性或隐源性CSE发作——多数在随访期间发生活动性癫痫和严重运动或认知功能障碍。

Chin博士披露无相关利益冲突。

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By: M. ALEXANDER OTTO, Clinical Neurology News Digital Network

SAN DIEGO – Prior neural impairment is the only independent predictor of long-term epilepsy and major cognitive and motor impairments following convulsive status epilepticus in children, researchers reported at the annual meeting of the American Epilepsy Society.

Investigators with the North London Status Epilepticus in Childhood Surveillance Study assessed 126 children a median of 8.5 years following convulsive status epilepticus (CSE) at a median age of 3.6 years.

Among children with prior neurologic impairment, the odds ratio for active epilepsy at follow-up was 7.1 (95% confidence interval, 1.8-27.7), for cognitive impairment, 16.3 (95% CI, 4.3-61.1), and for motor impairment, 9.8 (95% CI, 3.0-31.2).
 
Outcomes were not predicted by the duration of the original attack or by whether it was focal or generalized or continuous or intermittent.

Overall, "if you have good neurologic development before status, your outcome is going to be very good," said senior investigator Dr. Richard Chin, director of the epilepsy center at the University of Edinburgh.

That’s often the case with pediatric febrile seizures, the most common cause of pediatric CSE. True to the point, none of the 30 children who entered the study following febrile seizures had active epilepsy or major motor impairments at follow-up; one child with a subsequent autism diagnosis had major cognitive impairment. MRIs were normal in 28 of the children; one child had evidence of neurofibromatosis and another had a unilateral hippocampal volume reduction without signal change.

Although prolonged febrile seizures have long been thought to be a significant risk factor for subsequent mesial temporal sclerosis (MTS), "we didn’t find evidence of that. None of our children with prolonged febrile seizures developed MTS. The relationship between febrile seizures and subsequent mesial temporal sclerosis is not as strong as once believed," Dr. Chin said.

The 51 children who entered the study with remote symptomatic CSE had previous diagnoses of cerebral palsy, hypoxic brain injury, and other problems; 48 (94%) had active epilepsy, 32 (63%) had major motor deficits, and 37 (73%) had major cognitive impairments at follow-up.

Seventeen children had suffered acute symptomatic CSE attacks; only one had active epilepsy and major cognitive impairment at follow-up. MRIs in a child whose attack was brought on by pneumococcal meningitis suggested left MTS.

Most of the rest of the children in the study were classified as having had an idiopathic or cryptogenic CSE attack – the majority had active epilepsy at follow-up and major motor or cognitive impairments.

Dr. Chin said that he had no disclosures.