高热惊厥214例临床分析

本文分析了214例高热惊厥,结果为:检出率4.35％;男女之比为1.61:1;好发年龄为6个月～6岁(93.5％);首发年龄为6个月～4岁(89.9％);惊厥发作时体温多在39℃以上(74.6％);惊厥发作多在发热后12h内(72.4％);每次热病中惊厥发作1～3次(99.5％);惊厥持续时间多在15min内(91.0％);致惊厥发作的热性疾病以上呼吸道感染为最多;214例中63例复发,其中2例转癫痫,61例尚未发现智力低下或其他异常。从2例转癫痫的临床及脑电图看,提示惊厥发作愈重,持续时间愈长,转癫痫的可能性愈大。     

儿童热性惊厥复发危险因素分析

目的:研究热性惊厥患儿的复发危险因素。方法:结合36例热性惊厥患儿的临床及脑电图资料,研究其复发因素情况。结果:复发共19例(53.0%),复发危险因素与惊厥家族史、初次发作体温<38.5℃、初次发作年龄<1岁及复杂型热性惊厥有关(P<0.01)。结论:对有复发危险因素儿童应密切随访,一旦发热,及早采取适当的干预措施。     

硫喷妥钠治疗小儿难治性惊厥持续状态疗效观察

目的 探讨对小儿难治性惊厥持续状态的有效治疗方法。方法 对14例小儿难治性惊厥持续状态采用硫喷妥钠治疗并观察疗效。结果 硫喷妥钠治疗有效率为100％，1例出现呼吸抑制，3例于停药后复发。结论 硫喷妥钠对小儿难治性惊厥持续状态有明显疗效，但易发生呼吸抑制。惊止后应维持一段时间，以免复发。     

Prevention of arginine-vasopressin-induced motor disturbances by a potent vasopressor antagonist

The antivasopressor analog d(CH2)5Tyr(Me) arginine-vasopressin completely blocked the convulsive-like behavior and other severe motor disturbances which are normally observed following a second central arginine-vasopressin injection. This vasopressor antagonist appears to be selective for arginine-vasopressin-induced motor disturbances, in that the convulsive and motor effects of pentylenetetrazol and somatostatin were not altered significantly by pretreatment with the central antagonist. Results suggest that arginine-vasopressin-induced motor disturbances are mediated via central receptors. The classic antidiuretic (V2) type of arginine-vasopressin receptor does not appear to be involved, since the agonist 1-desamino-8-D-arginine-vasopressin did not elicit convulsive-like behavior or other severe motor disturbances 2 days following a first ('priming') injection of arginine-vasopressin.     

Lignocaine–induced convulsion does not induce c–fos protein (c–Fos) in rat hippocampus

Recent studies have shown that proto–oncogene c–fos mRNA is induced in the central nervous system by a variety of stimuli including generalised convulsions. In this study, the expression of c–fos protein (c–Fos) following lignocaine–induced convulsions was examined and compared with that following convulsions induced by non–anesthetic convulsants, such as pentylenetetrazol, kainic acid and electroconvulsive shocks, in rat brain.
Administration of 120 mg kg^-1 lignocaine by the intraperitoneal route induced generalised convulsions in all rats examined within 10 min. C–Fos was markedly induced in the piriform cortex and amygdala, and slightly induced in the neocortex and thalamus, while no c–Fos expression was observed in the hippocampus. In contrast, c–Fos expression following generalised convulsions induced by non–anaesthetic convulsants was very marked in the hippocampal region, piriform cortex and amygdala, and extended to the thalamus and neocortex.
These results contradict those of previously reported local cerebral metabolic studies using 2–deoxyglucose as a metabolic marker, and suggest that lignocaine–induced convulsions, unlike those induced by non–anaesthetic convulsants, may not cause severe sequelae (plastic changes) in the hippocampus.     

一氧化氮及一氧化氮合酶在遗传性癫痫易感大鼠惊厥发作中的作用

目的：探讨一氧化氮、一氧化氮合酶在遗传癫痫易感大鼠惊厥发作中的变化及作用。方法：选择惊厥评分在30－40的P77PMC大鼠35只，均分A－G7组，A组为对照组、G组预先30min腹腔注射一氧化氮合酶抑制剂L－NAME，分别于铃声刺激致惊后0．5、1、2、4,12h断头处死，取出脑组织分离双侧大脑皮层、海马等组织匀浆，测定一氧化氮及一氧化氮合酶，分别统计并进行t检验。结果：惊厥后0．5－1h皮层、海马一氧化氮、一氧化氮合酶逐渐升高，2h达峰值，4－12h恢复正常，应用L－NAME后，一氧化氮、一氧化氮合酶升高被抑制，但大鼠惊厥评分增高并致1例惊厥后死亡和明显延长惊厥持续时间。结论：惊厥后大鼠体内一氧化氮、一氧化氮合酶合成增加，给予合成酶抑制后能明显下降，但能加重惊厥程度和延长持续时间，提示一氧化氮于惊厥后升高，可能作为内源性抑制性性质，在惊厥发作自行终止机制中具有重要作用。     

梭曼中毒动物中枢神经系统病变与惊厥的关系

用神经组织学方法观察了兔、猫、狗、猴梭曼中毒急救治疗后CNS的病理变化.结果表明,CNS病变程度随着惊厥持续时间的延长而加重,抗惊剂可以保护CNS免受损伤.不同种动物梭曼引起的CNS病变基本相似,均为神经细胞的缺血性改变.主要病变包括大脑皮质、丘脑、海马、小脑和脊髓的神经细胞尼氏体溶解、核浓缩和细胞表面结痂.由于CNS病变与惊厥有密切关系,因此梭曼中毒后必须应用抗惊剂.     

膀胱冲洗液适宜温度的临床探讨

目的 :确定最适温度的膀胱冲洗液 ,最大限度的减少膀胱痉挛的次数和强度 ,减少出血 ,提高病人生活质量。方法 :采用六组不同温度冲洗液对术后病人行持续膀胱冲洗 ,记录膀胱痉挛次数 ,膀胱出血程度及体温变化的情况。结果 :随着冲洗液温度升高 ,膀胱痉挛平均次数减少 ,冲洗前后患者体温差逐渐变小 ,2 0℃～ 3 0℃温度组术后冲洗液红细胞计数平均数明显低于其它温度组。结论 :2 0℃～ 3 0℃是持续膀胱冲洗的最适温度     

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。     

良性家族性新生儿惊厥 KCNQ2 基因新突变

目的 对一个中国良性家族性新生儿惊厥(benign familial neonatal convulsions，BFNC)家系进行基因诊断，并探讨其分子发病机理。方法 对该家系进行详细的临床检查及疾病基因的连锁分析。应用聚合酶链反应(polymerase chain reaction，PCR)-DNA直接测序，并用PCR-单链构象多态(single strand conformation polymorphism，SSCP)对先证者、家系内16人及家系外72名无血缘关系的正常入进行KCNQ2基因突变分析。结果 连锁分析提示该家系与KCNQ2基因连锁，并排除与KCNQ3基因连锁。PCR—DNA直接测序在先证者发现．KCNQ2基因突变193ldelG，PCR—SSCP发现家系内其他患者均出现与先证者相同的异常SSCP条带，而72名正常人未出现此异常条带。结论 KCNQ2基因突变是中国人BFNC的发病原因之一，193ldelG是国内外未曾报道过的新突变，连锁分析结合基因突变分析可对BFNC患者进行基因诊断。