视频脑电图和影像学检查对继发性癫痫患儿的诊断价值研究

目的:研究视频脑电图(V-EEG)和影像学检查对继发性癫痫患儿的诊断价值。方法:选取从2014年3月到2017年4月在我院接受诊治的癫痫患儿168例纳入本次研究。分别对所有患儿实施V-EEG和核磁共振成像(MRI)诊断,比较两种方式的诊断价值。结果:168例患儿中,V-EEG监测到154例有异常的脑电信号,其中120例有痫样放电,V-EEG显示痫样放电分布在左侧和右侧导联的比例较双侧导联明显更高(P0.05),MRI检测结果显示,140例患儿有颅内有关结构的病变亦或是发育异常,28例未发现异常。168例患儿中,发作类型为单纯部分型者72例,占比最高,为42.86%;主要病因中,颅内感染的发作类型以全身型为主,占11.31%。脑梗塞的发作类型以单纯部分型为主,占8.33%。颅内软化灶的发作类型以复杂部分型为主,占6.55%。颅内肿瘤的发作类型以单纯部分型为主,占6.55%。MRI定位主要在单侧,其中左侧占38.10%,右侧占29.76%;而经V-EEG监测显示异常放电154例,占91.67%,其中颅内感染和脑梗塞以及颅内肿瘤和颅内软化灶的阳性检出比例最高,分别为24.40%,13.10%,11.90%和10.71%。V-EEG诊断灵敏度和特异度均明显高于MRI(P0.05)。结论:V-EEG较MRI对继发性癫痫患儿的诊断价值更高,能够更加准确地提供诊断结果数据,值得在临床诊治过程中给予推广和应用。     

视频脑电图鉴别诊断癫痫患者睡眠障碍、认知障碍的临床价值研究

目的:探讨视频脑电图诊断癫痫患者睡眠障碍、认知障碍的临床价值。方法:选取2014年1月~2016年12月在我院神经内科进行诊治的癫痫患者236例作为癫痫组,另选取同期的健康患者家属或者其他健康体检者236例作为正常对照组,对两组进行视频脑电图联合睡眠参数分析;并对癫痫组视频脑电图联合认知参数进行分析。结果:癫痫组睡眠Ⅰ~Ⅱ期时间显著长于正常对照组且具有统计学差异(P=0.000),睡眠Ⅲ~Ⅳ期时间显著短于正常对照组且具有统计学差异(P=0.000),睡眠时相转换频率、觉醒指数均显著高于正常对照组且均具有统计学差异(P=0.000);清醒期、睡眠期不同痫样放电指数(IED)的WAIS-RC IQ和WMS-RC MQ均具有统计学差异(P0.05),10%IED≤50%者的WAIS-RC IQ和WMS-RC MQ均显著低于1%IED≤10%者且均具有统计学差异(P0.05),IED 10%可能是痫样放电影响患者认知功能的最低阈值。结论:视频脑电图在癫痫患者睡眠障碍、认知障碍识别中具有重要的临床价值。     

动态脑电图与常规脑电图应用于病毒性脑炎诊断的效果分析

目的:探讨动态脑电图与常规脑电图应用于病毒性脑炎的应用价值。方法:选取150例病毒性脑炎患者,随机分为两组,每组各75例,常规脑电图(REEG)组采用常规脑电图检查,动态脑电图(AEEG)组采用动态脑电图检查;观察并记录脑电图异常率,不同程度病情脑电图异常率的例数,评价动态脑电图与常规脑电图对病毒性脑炎的检测灵敏度和准确度。结果:AEEG组检出的脑电图异常率明显高于REEG组(P0.05)。不同程度病情脑电图检出的患者比例,两组相比,差异没有统计学意义(F=-0.085,P0.05)。REEG组中,轻度与中度病毒性脑炎检出率相比,差异没有统计学意义(P0.05),中度与重度病毒性脑炎检出率相比,差异没有统计学意义(P0.05),重度病毒性脑炎检出率明显高于轻度(P0.05)。AEEG组中,轻度与中度病毒性脑炎检出率相比,差异没有统计学意义(P0.05),重度病毒性脑炎检出率明显高于中度和轻度(P0.05),AEEG组重度病毒性脑炎检出率明显高于REEG组(P0.05)。结论:动态脑电图作为一种无创性检查,对于病毒性脑炎具有极好的检出率,灵敏度高,适用于病毒性脑膜炎的早期辅助诊断。     

卡马西平与丙戊酸钠对儿童癫痫部分性发作脑电图的临床对照研究

目的:探究卡马西平与丙戊酸钠对儿童癫痫部分发作患儿发作脑电图影响,并实施组间对照研究。方法:选择2017年1月至2020年1月于我院接受治疗的81例癫痫部分性发作患儿为研究对象,按照其接受治疗的差异将其分为卡马西平组(40例)和丙戊酸钠组(41例),对比两组患儿接受药物治疗后脑电图以及脑电地形图变化情况。结果:(1)卡马西平组患儿接受治疗后脑电图检测显示间歇期痫样活动减少≥50%者占比高达67.50%(27/40),而丙戊酸钠组占比仅为43.90%(18/41),两组比较差异明显(P<0.05);(2)脑电背景活动变化比较显示,治疗后卡马西平组患儿α波无影响者占比65.00%,明显高于丙戊酸钠组36.59%,同时丙戊酸钠组患儿δ波数(20 s内)药物治疗后变化较卡马西平组更为明显;(3)脑电功率比较显示,卡马西平组患儿治疗后仅θ频段相对功率出现明显变化(P<0.05),但丙戊酸钠组患儿α频段相对功率、θ频段相对功率和θ频段绝对功率均出现明显变化(P<0.05)。结论:丙戊酸钠应用于儿童癫痫部分性发作时患儿脑电背景活动会明显变慢,甚至有出现间歇期痫样放电的风险,而卡马西平相对更为稳定,对患儿脑电图的影响更小,安全性更高。     

CO中毒继发癫痫的脑电图和经颅多普勒改变的关系研究

目的:探讨一氧化碳(Carbon monoxide,CO)中毒继发癫痫的经颅多普勒(Transcranial Doppler,TCD)和脑电图(Electroencephalogram,EEG)特征的关系。方法:对我院自2011年6月至2015年5月收治的145例CO中毒患者的临床资料和EEG、TCD特征进行检查,并分析其与继发癫痫的相关性。结果:145例CO中毒患者中,EEG结果显示正常患者93例(64.13%);异常患者52例(35.86%)。TCD正常患者90例(62.07%),异常55例(37.93%)。主要表现为颈内动脉系统血流动力学的改变,大脑前动脉流速与病情严重程度成正相关,TCD血流速度增加或减慢不对称,脑血流速度升高比率显著高于脑血流速度减低比率。无论在睡眠期还是清醒期EEG异常患者全导阵发性3.0~4.0Hz的棘慢波均存在放电。患者出现EEG、TCD异常与年龄、癫痫家族史、发热温度、持续时间、继发癫痫类型以及24h内发作次数有关。继发癫痫39例,占EEG异常患儿的75.00%,占TCD异常患儿的72.73%。继发癫痫患者中,15例额区放电日后发生发生癫痫14例(93.33%),19例枕区放电16例(84.21%)发生癫痫,13例Rolandic区放电8例(61.54%)发生癫痫,5例广泛性棘慢波者继发癫痫的有1例(20%)。结论:EEG、TCD检查异常的CO中毒患者中具有较高的继发癫痫的发病率,中枕区和额区阵发性异常放电者更容易继发癫痫。     

益生菌联合常规药物对难治性癫痫患儿的疗效及对脑电图的影响CSCD

目的 探讨益生菌联合常规药物对难治性癫痫患儿的治疗效果及对患儿脑电图的影响,为该类患儿的治疗提供参考。方法 选取2020年1月至2022年5月我院收治的104例难治性癫痫患儿作为研究对象,按照随机数表法分为对照组和联合组。对照组患儿采用常规药物治疗,联合组在对照组的基础上联用益生菌治疗。对比两组患儿治疗前后癫痫发作频率、脑电图情况、炎症因子[白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)]、神经递质[γ-氨基丁酸(GABA)、5-羟色胺(5-HT)]水平及治疗后的临床疗效和用药安全性。结果 治疗前两组患儿癫痫发作频率、脑电图各频段相对功率以及IL-6、TNF-α、GABA和5-HT水平差异均无统计学意义(均P>0.05)。治疗后两组患儿癫痫发作频率、脑电图θ频段相对功率及IL-6、TNF-α水平均降低,且联合组患儿以上指标水平均低于对照组(均P<0.05)。治疗后两组患儿GABA和5-HT水平均升高,且联合组的GABA和5-HT水平高于对照组(均P<0.05)。两组患儿临床疗效分布差异有统计学意义,联合组总有效率高于对照组(94.23%vs 80.77%,P<0.05)。治疗期间两组患儿的不良反应发生率对比差异无统计学意义(P>0.05)。结论 对难治性癫痫患儿采用益生菌联合常规药物治疗能有效降低其癫痫发作频率,改善脑电图相应频段的相对功率,减轻炎症反应,抑制异常兴奋,且疗效显著,安全性高。     

三种抗癫痫药对癫痫患者脑电图的背景影响比较研究

目的:研究对比三种抗癫痫药(苯妥因钠、丙戊酸钠、卡马西平)对癫痫患者脑电图的背景影响。方法:选取我院于2009年3月至2011年2月收治的60例癫痫患者,随机分为苯妥因钠(PHT)、卡马西平(CBZ)和丙戊酸钠(SVP)组各20例,动态观察各组患者于治疗期间痫样波放电的频度和EEG背景的变化。结果:EEG痫样波放电的抑制率以SVP最为明显,而CBZ在EEG背景活动影响方面均比其他两组显著。结论:三种药物对癫痫波放电的抑制顺序是SVP>PHT>CBZ,SVP组明显优于其他两组。     

术中皮质脑电图监测癫痫病灶切除13例分析

目的:探讨继发性癫痫术中运用皮质脑电图监测切除癫痫病灶的疗效。方法:对13例继发性癫痫患者术前经多次常规脑电图、24h动态脑电图检查定位并联合CT、MRI等检查结果,确定癫痫病灶的准确位置。在皮质脑电图精确定位监测下手术切除致痫灶。结果:13例癫痫患者均通过皮质脑电图监测,准确定位,切除致痫灶,切除病灶后的棘波、尖波,棘、尖慢复合波减少或完全消失。结论:利用皮质脑电图监测手术切除痫灶是治疗继发性癫痫最有效的方法之一。     

复杂性热性惊厥脑电图特征与癫痫发生的相关性

目的：探讨复杂性热性惊厥脑电图特征与癫痫发生的相关性。方法：2012年3 月到2014 年5 月选择在我院诊治为复杂性热 性惊厥的呼吸道感染患儿86 例作为观察组,同期选择在我院诊治的非热性惊厥的呼吸道感染患儿86 例作为对照组,两组都进 行脑电图监测与认知功能判定,对癫痫发生情况进行判定与分析。结果：观察组的言语智商、行为智商与总智商评分都明显低于 对照组(P<0.05)。观察组的癫痫发生率为9.3 %,脑电图异常率为8.1 %;而对照组的癫痫发生率为1.2 %,脑电图异常率为2.3 %, 对比差异都有统计学意义(P<0.05)。在观察组患儿中,Spearman 相关性分析显示脑电图异常与癫痫发生存在明显正向相关性(r=0. 349,P<0.05)。结论：复杂性热性惊厥伴随有脑电图异常,与癫痫发生存在明显正向相关性,损害患儿的认知功能。     

柴胡对癫痫模型电活动的调制

目的 :研究柴胡对癫痫发作的影响。方法 :以家兔和大鼠为实验对象 ,用毛果芸香碱致痫 ,采用脑电图和细胞外玻璃微电极记录技术 ,观察柴胡对癫痫模型大脑皮层放电及海马脑片场电位的影响。结果 :腹腔注射柴胡后可使癫痫发作次数及发作持续时间显著减少 ,发作间隔时间显著延长 ,(P <0 .0 5 ) ,脑片旁滴注柴胡后使致痫大鼠海马脑片诱发场电位幅度平均降低 2 0 .4 1% ,恢复时间平均为 6 .86min ,(P <0 .0 1)。结论 :柴胡注射液能明显抑制癫痫模型电活动 ,提示柴胡具有抗痫作用     

注射用丹参多酚酸盐联合丙戊酸钠治疗脑卒中后癫痫患者的疗效分析

目的:研究注射用丹参多酚酸盐联合丙戊酸钠对脑卒中后癫痫的临床疗效和安全性。方法:选择2016年1月～2019年4月东南大学附属中大医院江北院区神经内科住院的80例脑卒中后癫痫患者,将其随机分为两组。对照组的40例患者仅给予丙戊酸钠治疗,观察组的40例患者给予丹参多酚酸盐联合丙戊酸钠治疗。比较两组治疗后的脑电图检查结果、癫痫症状控制情况。结果:治疗后,观察组总有效率为明显高于对照组(97.50%vs. 80%,P0.05);两组的累及导联数、痫样放电、发作持续时间、发作次数较治疗前以及血清神经元特异性烯醇化酶(Neuron specific enolase,NSE)水平均较治疗前明显降低(P0.05),且观察组以上指标均明显低于对照组(P0.05)。两组的嗜睡、皮疹、头痛、感觉异常、恶心呕吐的发生率比较差异无明显统计学意义(P0.05)。结论:注射用丹参多酚酸盐联合丙戊酸钠治疗脑卒中后癫痫的疗效明显优于单用丙戊酸钠治疗,其可更有效控制癫痫症状,且安全性较高。     

高频电刺激对大鼠海马脑片癫痫样放电特性影响的研究

本文采用电极阵列检测技术,在大鼠海马脑切片上诱导出稳定的癫痫样放电,分析、研究130 Hz的高频电刺激(high-frequency stimulation,HFS) CA3区时,海马切片在癫痫发作间期放电(inter-ictal discharges,IID)和发作期放电(ictal discharges,ID)的各项参数、癫痫样放电地起始位点、传播方向和传输速率以及各频段的功率谱密度.结果显示:高频电刺激可以有效地降低癫痫发作期的幅值、减少持续时间、增长潜伏时间、抑制癫痫样放电由IID向ID的转变等.提示高频电刺激抑制癫痫的作用机制是通过促进神经元之间的抑制性传输系统,并且抑制海马神经元之间的兴奋性连接,从而达到抑制效果.     

De Novo Loss-of-Function Mutations in CHD2 Cause a Fever-Sensitive Myoclonic Epileptic Encephalopathy Sharing Features with Dravet Syndrome

Dravet syndrome is a severe epilepsy syndrome characterized by infantile onset of therapy-resistant, fever-sensitive seizures followed by cognitive decline. Mutations in SCN1A explain about 75% of cases with Dravet syndrome; 90% of these mutations arise de novo. We studied a cohort of nine Dravet-syndrome-affected individuals without an SCN1A mutation (these included some atypical cases with onset at up to 2 years of age) by using whole-exome sequencing in proband-parent trios. In two individuals, we identified a de novo loss-of-function mutation in CHD2 (encoding chromodomain helicase DNA binding protein 2). A third CHD2 mutation was identified in an epileptic proband of a second (stage 2) cohort. All three individuals with a CHD2 mutation had intellectual disability and fever-sensitive generalized seizures, as well as prominent myoclonic seizures starting in the second year of life or later. To explore the functional relevance of CHD2 haploinsufficiency in an in vivo model system, we knocked down chd2 in zebrafish by using targeted morpholino antisense oligomers. chd2-knockdown larvae exhibited altered locomotor activity, and the epileptic nature of this seizure-like behavior was confirmed by field-potential recordings that revealed epileptiform discharges similar to seizures in affected persons. Both altered locomotor activity and epileptiform discharges were absent in appropriate control larvae. Our study provides evidence that de novo loss-of-function mutations in CHD2 are a cause of epileptic encephalopathy with generalized seizures.     

Complicated relationship between autism with regression and epilepsy

We retrospectively evaluated a set of 205 children with autism and compared it to the partial sub-set of 71 (34.6%) children with a history of regression. From 71 children with regression, signs of epileptic processes were present in 43 (60.6%), 28 (65.12%) suffered clinical epileptic seizures, and 15 (34.9%) just had an epileptiform abnormality on the EEG. In our analysis, autistic regression is substantially more associated with epileptic process symptoms than in children with autism and no history of regression. More than 90% of children with a history of regression also show IQ < 70 and reduced functionality. Functionality and IQ further worsens with the occurrence of epileptic seizures (98% of children with regression and epilepsy have IQ < 70). We proved that low IQ and reduced functionality significantly correlate rather with epileptic seizures than just sub-clinical epileptiform abnormality on EEG. Clinical epileptic seizures associated with regression significantly influence the age of regression and its clinical type. The age of regression is higher compared to children with regression without epileptic seizures (in median: 35 months of age in patients with seizures while only 24 months in other patients). Patients with seizures revealed regression after 24th months of age in 68% of cases, while patients without seizures only in 27%. However, coincidence with epilepsy also increased the occurrence of regression before the 18th month of age (23% of patients), while only 4% of patients without epilepsy revealed regression before the 18th month. Epileptic seizures are significantly associated especially with behaviour regression rather than speech regression or regression in both behaviour and speech. Also epileptic seizures diagnosed before correct diagnosis of autism were significantly associated with delayed regression (both behavioural and speech regression).     

Epileptic activity during early postnatal life in the AY-9944 model of atypical absence epilepsy

Atypical absence epilepsy (AAE) is an intractable disorder characterized by slow spike-and-wave discharges in electroencephalograms (EEGs) and accompanied by severe cognitive dysfunction and neurodevelopmental or neurological deficits in humans. Administration of the cholesterol biosynthesis inhibitor AY-9944 (AY) during the postnatal developmental period induces AAE in animals; however, the neural mechanism of seizure development remains largely unknown. In this study, we characterized the cellular manifestations of AY-induced AAE in the mouse. Treatment of brain slices with AY increased membrane excitability of hippocampal CA1 neurons. AY treatment also increased input resistance of CA1 neurons during early postnatal days (PND) 5–10. However, these effects were not observed during late PND (14–21) or in adulthood (7–10 weeks). Notably, AY treatment elicited paroxysmal depolarizing shift (PDS)-like epileptiform discharges during the early postnatal period, but not during late PND or in adults. The PDS-like events were not compromised by application of glutamate or GABA receptor antagonists. However, the PDS-like events were abolished by blockage of voltage-gated Na⁺ channels. Hippocampal neurons isolated from an in vivo AY model of AAE showed similar PDS-like epileptiform discharges. Further, AY-treated neurons from T-type Ca²⁺ channel α1G knockout (Ca_v3.1^−/−) mice, which do not exhibit typical absence seizures, showed similar PDS-like epileptiform discharges. These results demonstrate that PDS-like epileptiform discharges during the early postnatal period are dependent upon Na⁺ channels and are involved in the generation of AY-induced AAE, which is distinct from typical absence epilepsy. Our findings may aid our understanding of the pathophysiological mechanisms of clinical AAE in individuals, such as those with Lennox–Gastaut syndrome.     

Localizational concepts in epilepsy: past, present and future

The clinical seizure pattern, particularly the initial phenomena, plus the EEG, when satisfactory recording of the seizure onset can be achieved, determine the primary localization of epileptic phenomena. The EEG has also demonstrated, by the presence of interictal epileptiform spike discharges, the presence of a second-order localization of epileptic phenomena, namely, the location and extent of cortex adjacent to the site of origin of the neuronal seizure discharge that is recruited into action in a clinical epileptic seizure. Experience with cortical resection in the treatment of focal epilepsy has demonstrated the importance of a third-order localization of epileptic phenomena, namely, how much of the potentially epileptogenic cortex must be excised in order to produce a satisfactory reduction of the seizure tendency.     

Rosiglitazone Suppresses In Vitro Seizures in Hippocampal Slice by Inhibiting Presynaptic Glutamate Release in a Model of Temporal Lobe Epilepsy

Peroxisomal proliferator-activated receptor gamma (PPARγ) is a nuclear hormone receptor whose agonist, rosiglitazone has a neuroprotective effect to hippocampal neurons in pilocarpine-induced seizures. Hippocampal slice preparations treated in Mg²⁺ free medium can induce ictal and interictal-like epileptiform discharges, which is regarded as an in vitro model of N-methyl-D-aspartate (NMDA) receptor-mediated temporal lobe epilepsy (TLE). We applied rosiglitazone in hippocampal slices treated in Mg²⁺ free medium. The effects of rosiglitazone on hippocampal CA1-Schaffer collateral synaptic transmission were tested. We also examined the neuroprotective effect of rosiglitazone toward NMDA excitotoxicity on cultured hippocampal slices. Application of 10μM rosiglitazone significantly suppressed amplitude and frequency of epileptiform discharges in CA1 neurons. Pretreatment with the PPARγ antagonist GW9662 did not block the effect of rosiglitazone on suppressing discharge frequency, but reverse the effect on suppressing discharge amplitude. Application of rosiglitazone suppressed synaptic transmission in the CA1-Schaffer collateral pathway. By miniature excitatory-potential synaptic current (mEPSC) analysis, rosiglitazone significantly suppressed presynaptic neurotransmitter release. This phenomenon can be reversed by pretreating PPARγ antagonist GW9662. Also, rosiglitazone protected cultured hippocampal slices from NMDA-induced excitotoxicity. The protective effect of 10μM rosiglitazone was partially antagonized by concomitant high dose GW9662 treatment, indicating that this effect is partially mediated by PPARγ receptors. In conclusion, rosiglitazone suppressed NMDA receptor-mediated epileptiform discharges by inhibition of presynaptic neurotransmitter release. Rosiglitazone protected hippocampal slice from NMDA excitotoxicity partially by PPARγ activation. We suggest that rosiglitazone could be a potential agent to treat patients with TLE.