小儿非癫痫性发作临床分析

目的　对小儿时期的各种非癫痫性发作进行分析。方法　对 3 2例疑似非癫痫性发作的患儿进行临床分析 ,同时进行录像脑电图或 2 4h动态脑电图监测。结果　 3 2例患儿发作期及发作间期脑电图均无异常放电 ,证实为非癫痫性发作 ,以生理性发作最多 (16例 ,占 5 0 % ) ,其平均年龄最小 (3 .5岁 )。结论　儿童时期存在多种形式的非癫痫性发作 ,以生理性发作最多 ,且非癫痫性发作易被误诊为癫痫及其他疾病 ,采用动态脑电图监测对诊断及鉴别诊断均有指导意义     

Influence of aminophylline and strychnine on the protective activity of excitatory amino acid antagonists against maximal electroshock-induced convulsions in mice

Summary Aminophylline reversed the protective action of both, D-3-(2-carboxypiperazine-4-yl)-1-propenyl-1-phosphonic acid (D-CPP-ene — a competitive NMDA antagonist) and valproate (used as a conventional antiepileptic drug for comparative purposes) against maximal electroshock-induced seizures. The respective ED₅₀ values of aminophylline were 55.7 and 98.4mg/kg i.p. However, aminophylline (up to 100mg/kg i.p.) did not influence the protective efficacy of 1-(4-aminophenyl)-4-methyl-7,8-methyl-enedioxy-5H-2, 3-benzodiazepine (GYKI 52466 — a non-NMDA antagonist). Strychnine affected the protection provided by D-CPP-ene, GYKI 52466, and valproate against maximal electroshock — the ED₅₀ values of strychnine for the reversal of the anticonvulsive effects of D-CPP-ene, GYKI 52466 or valproate were 0.082, 0.35 and 0.28mg/kg s.c., respectively.An involvement of strychnine sensitive glycinergic receptor-mediated events in the mechanism of the anticonvulsive activity of excitatory amino acid antagonists and valproate may be postulated. The ineffectiveness of aminophylline to reduce the anticonvulsive effects of GYKI 52466 may distinguish a new class of antiepileptic drugs offering an advantage over conventional antiepileptics in patients with epilepsy, requiring aminophylline for pulmonary reasons.     

Cerebrospinal fluid purine metabolites after complex febrile convulsions

Adenosine monophosphate, inosine monophosphate, inosine, adenosine, guanosine, adenine, guanine, hypoxanthine, xanthine and uric acid were determined in cerebrospinal fluid (CSF) of 15 children after complex febrile seizures (CFS) and in 27 after simple febrile seizures (SFS), and compared with those in a control group of 63 children. There was no statistically significant difference between the groups for any of these metabolites, suggesting that CFS and SFS neither significantly disturb the metabolism of nucleotides, nucleosides or bases nor significantly deplete neuron adenosine triphosphate levels.     

Frontal versus transcorneal stimulation to induce maximal electroshock seizures or kindling in mice and rats

Frontal stimulation, i.e. electrical stimulation where electrodes are pressed on the skin of the intact frontal skull of mice or rats, may represent a more humane alternative to the widely used transcorneal stimulation to induce electroshock seizures. The aim of this work was to directly compare transcorneal and frontal stimulation in eliciting maximal electroshock-induced seizures (MES) in mice and the anticonvulsant effect of carbamazepine (CBZ) and phenytoin (PHT) on thus produced seizures. In addition, we stimulated mice and rats repeatedly via transcorneal and frontal electrodes to see whether kindling is produced by this procedure. Two electroshock tests were used in mice, i.e. maximal electroshock seizure threshold (MEST) test and MES generated by supramaximal stimulation (50 mA). Frontal stimulation resulted in lower convulsive threshold than in the case of corneal stimulation. Both CBZ and PHT produced dose-dependent increases in seizure threshold for both sites of stimulation, i.e. transcorneal and frontal. As regards type of electrodes, higher doses of PHT were required to increase seizure threshold in the case of frontal than transcorneal stimulation. Supramaximal stimulation (50 mA) yielded comparable ED₅₀ values regardless of the site of stimulation. Furthermore, once-daily stimulation of mice, regardless of the placement of electrodes, did not induce any changes in convulsive threshold. We also attempted to kindle mice and rats via corneal and frontal electrodes by repetitive electrical stimulation using currents which initially did not produce generalized clonic seizures. Mice were stimulated once daily for 2 s with 3 mA (corneal electrodes) or 2 mA (frontal electrodes) and rats were stimulated twice daily for 4 s at 8 mA (corneal electrodes) or 5 mA (frontal electrodes). With corneal stimulation in rats there was a clear progression of kindling development which was not the same in nature when compared with corneally-stimulated mice. Frontal stimulation did not produce kindling. Moreover, corneal stimulation was better tolerated by rats, while in mice high mortality was seen after either method of current delivery. Our data indicate that frontal electrodes can be used as an alternative to transcorneal stimulation to produce MES by supramaximal or threshold current intensities as screening procedures in antiepileptic drug (AED) development. Nevertheless, this type of stimulation cannot be used to produce minimal electroshock seizures and seems not to be useful to produce kindling in rats and mice.     

Temporal Lobe Epileptogenesis and Epilepsy in the Developing Brain: Bridging the Gap Between the Laboratory and the Clinic. Progression, But in What Direction?

Summary:  The origins of human mesial temporal lobe epilepsy and hippocampal sclerosis are still not well understood. Hippocampal sclerosis and temporal lobe epileptogenesis involve a series of pathologies including hippocampal neuronal loss and gliosis, axonal reorganization, and maybe hippocampal neoneurogenesis. However, the causality of these events is unclear as well as their relation to the factors that may precipitate epileptogenesis. Significant differences between temporal lobe epileptogenesis in the adult and immature brain may require differential approaches. Hereditary factors also may participate in some cases of hippocampal sclerosis. The key point is to identify the significance of these age-dependent changes and to design preventive treatments. Novel strategies for the prevention and treatment of mesial temporal lobe epilepsy and hippocampal sclerosis may include rational use of neuroprotective agents, hormonotherapy, immunizations, and immunotherapy.     

高热惊厥脑干听觉诱发电位的分析

本文报道了30例高热惊厥患儿的脑干听觉诱发电位检测结果。结果提示,高热惊厥患儿脑干听觉诱发电位异常率较高,以Ⅰ—Ⅴ波峰间期延长为主,同时Ⅰ、Ⅲ、Ⅴ波耳间差值增大。文中讨论了这一结果与高热惊厥发病年龄特征的关系。     

Nonepileptic Posttraumatic Seizures

Summary: Purpose: Epileptic posttraumatic seizures (PTSs) are a well-recognized consequence of head injury (HI), but HI and nonepileptic seizures (NESs) have not been related. We describe a significant subset of patients with NESs who had their seizures attributed to HI.
Methods: We reviewed the records of all patients diagnosed with NES at the University of Maryland Medical Center over a 6-year period (1989–1995) and selected patients with seizures attributed to a head injury occurring ≥3 years before the onset of their seizures.
Results: Of 157 patients with video-EEG confirmed NES, 37 (24%) had the onset of their seizures attributed to an HI. Their average age was 34 years (range, 15–56 years); 68% were women. Nonepileptic PTS usually developed within the first year after HI (89%). Convulsive symptoms were present in 54%. Whereas epileptic PTSs characteristically follow severe HI, the majority (78%) of our patients with nonepileptic PTSs sustained only mild HI. Before their HI, 76% of our patients were employed, working in the home, or students, but only 11% could continue those activities after developing nonepileptic PTSs.
Conclusions: Nonepileptic PTSs are frequently mistaken for epileptic PTSs and result in serious disability. The misdiagnosis of nonepileptic PTSs leads to ineffective and inappropriate treatment. Patients with intractable seizures after HIS, articularly mild HIS, should be carefully evaluated for NESs.     

儿童失神癫(癎)脑电图的多尺度特征

目的:研究儿童失神癫癎脑电图的多尺度定量特征。方法:对15例失神癫癎患儿10次临床发作和20次亚临床癎样放电的脑电图进行子波分析,提取失神癫癎发作过程中脑电信号的多尺度定量典型特征,与发作前10 s及发作后10 s的脑电信号进行比较,并与12例正常同龄儿童脑电图进行比较。结果:研究显示儿童失神癫癎发作过程中脑电信号的多尺度典型特征主要表现为12尺度(对应频率3 Hz)的节律性活动显著增强,发作时20尺度(低频大尺度,对应频率0．12 Hz)结构与频率3 Hz的结构具有非正常的跳跃式尺度关系,3 Hz节律性棘慢复合波与大尺度(频率1 Hz以下)背景低频放电结构共同存在。发作过程中分尺度功率主要集中在20尺度和12尺度,其演变规律为20尺度能量逐渐减低,12尺度能量逐渐增加。10次临床发作的脑电信号均显示上述特征。发作前10 s和后10 s的脑电多尺度信号中仍然存在隐性的3 Hz棘慢复合波成分,与一般认为3 Hz棘慢复合波突起突止不同．而从传统的脑电图上无法分辨出发作前后的这些多尺度细节的定量特征。亚临床癎样放电的多尺度特征与发作期无明显差别,但持续时间短。结论:子波分析作为一种新的信号分析方法,适合于脑电信号的分析,可以获得比传统视觉脑电图更多的定量信息。通过对失神癫癎患儿的脑电信号进行子波分析,得到其发作过程中典型的多尺度定量特征,有助于失神癫癎发作的临床辅助诊断、预后评价以及神经电生理机理的基础研究。     

小儿热性惊厥的脑电图

本文对296例小儿热性惊厥脑电图进行分析。结果:小儿热性惊厥脑电图(EEG)异常率48.65％,主要以阵性高幅慢波为主(77.78％)。小儿癫痫脑电图异常率(89.61％)。主要以阵发性棘慢波和局灶性改变为主(62.78％)。二周后EEG复查热性惊厥EEG大部分恢复正常(83.35％)。而小儿癫痫EEG未有恢复正常的。热性惊厥发作次数愈多,发作持续时间愈长EEG改变愈明显,二周后脑电图恢复正常的愈少。这对小儿热性惊厥的诊断和预后判定有重要价值。     

听源性惊厥易感大鼠室旁核神经元c—fos表达的研究

目的为下丘脑室旁核参与惊厥应答提供形态学资料。方法：以听源性忭厥易大鼠为动物模型，用免疫组织化学ＡＢＣ法显示下丘脑室旁核神经元即早基因ｃ－ｆｏｓ的表达。