喹啉对癫(癎)大鼠海马神经元连接蛋白36表达的影响

目的:探讨喹啉对癫癎大鼠海马神经元连接蛋白36(Cx36)表达的影响.方法:64只SD大鼠随机分为正常对照组、癫癎模型组、地西洋治疗组和喹治疗组,每组16只大鼠.采用氯化锂-匹罗卡品诱导制作癫癎大鼠模型,地西泮治疗组子以1mg/kg地西泮治疗,喹啉治疗组予以60mg/kg喹啉治疗.术后分别采用Racine评分和脑电图检查判断癫癎发作情况.分别用免疫荧光染色法、Western blot法检测各组大鼠术后2h、4h时海马神经元Cx36的表达.结果:与正常对照组比较,癫癎模型组和地西泮治疗组大鼠术后2h、4h时海马神经元Cx36表达水平显著升高(均P<0.01).癫癎模型组和地西泮治疗组大鼠术后2h、4h时海马神经元Cx36表达水平比较差异无统计学意义.与癫癎模型组及地西泮治疗组比较,喹啉治疗组大鼠术后2h、4h时海马神经元Cx36表达水平显著降低(均P<0.01).结论:癫癎大鼠海马神经元Cx36表达水平升高,喹啉能抑制这一变化.     

癫持续状态的护理分析

2008-07—2012-07我院神经内科共收治癫持续状态患者50例,同时采用得当的护理措施效果良好。现报告如下。1临床资料选择我院神经内科2008-07—2012-07收治的癫持续状态患者50例为护理对象,年龄14～68岁,平均39.5岁;     

小儿癫持续状态126例病因分析

癫持续状态(SE)指的是一种惊厥持续30min以上,或连续多次发作,发作间期意识不恢复者〔1〕。SE是小儿神经内科的常见急症,如不及时控制,可造成不可逆的脑损害甚至死亡。为进一步对此病进行诊治,现将我院126例癫持续状态患儿的病因分析如下。1临床资料1.1一般资料本组资料来自2001-06～2005-12在我院门诊就诊及住院的126例患儿,男69例,女57例,年龄中位数为2岁(2个月～12岁)。均符合2001年5月ILAE(国际抗癫联盟)关于癫发作和对癫诊断的建议〔2〕。发作类型分为全面性SE和局灶性SE。既往有癫史46例,无癫史80例,发作后20min至…     

28例癫持续状态病人的护理体会

癫持续状态(Status epilepticus,SE)是神经科常见急危病之一,致残、致死率均较高,甚至一次发作就可造成不可逆性中枢神经系统和其他系统的损害[1],应及时进行抢救并加强护理。现将我科2001-2006年收治的28例SE病人护理体会介绍如下。1资料与方法1.1一般资料本组28例SE患者,男     

38例癫持续状态的病因分析

癫持续状态(SE)是神经内科急症之一,如不及时诊治病死率及致残率很高。为了进一步了解癫持续状态病因以准确地进行治疗,现将我院2004~2006年间收治的38例SE患者的病因分析如下。1资料与方法1.1一般资料本组男23例,女15例,年龄14~82岁,平均52岁。第一次SE 34例,2次以上出现S     

癫持续状态的急救与护理

癫持续状态是指癫发作持续时间长或反复发作、间歇较短的各种癫状态。临床上可引起意识、运动、行为和植物神经等不同障碍,若不及时控制,轻者造成大脑不可逆性损害,重者危及病人生命,故应作急症处理。本文收集了2004-01~2007-07住院的癫持续状态患者28例,由于抢救及时,护理得当均在较短时间内控制惊厥,意识恢复。现将抢救与体会总结如下。1临床资料本组28例,男18例,女10例。年龄8~63岁,平均25岁。大发作20例,小发作3例,局部发作5例。发作前有明显诱因22例,不明诱因6例。发作持续时间最长10h,最短2h,平均时间4h。28例癫持续状态发…     

52例癫持续状态的急救与护理

癫持续状态是指持续、频繁的癫发作。发作时间持续30h以上,或连续多次发作,发作间期意识不能恢复〔1〕。是一种神经内科常见急症。如不及时抢救,可短期内死亡。临床上在持续状态患者抢救过程中,快速控制发作,护理人员动态、综合地观察病情变化,有效预防并发症的发生,是抢救成功的关键。我科近4年间共收治癫持续状态患者52例。现将抢救过程中护理工作的一些体会报道如下。1资料与方法1.1一般资料52例患者,男33例,女19例,年龄6~70岁,平均20.3岁。发作类型:强直阵挛性发作32例,局部开始的强直阵挛发作10例,单纯部分发作4例。本组52例癫…     

AG490对氯化锂-匹罗卡品致癫大鼠星形胶质细胞活化及癫的影响

目的探讨匹罗卡品致癫大鼠海马肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)的表达、星形胶质细胞活化及JAK/STAT信号转导通路在颞叶癫发作中的作用。方法应用腹腔注射氯化锂-匹罗卡品(PILO)的方法建立颞叶癫模型,应用JAK/STAT信号转导通路特异性抑制剂AG490进行腹腔注射建立干预模型组;用Western blotting方法测定大鼠海马匀浆后TNF-α表达水平的变化,用免疫荧光观察AG-490阻滞JAK/STAT通路后对大鼠海马TNF-α表达水平与星形胶质细胞活化及癫发作的影响。结果 (1)PILO致癫模型组有80.00%(32/40)的大鼠达Racine分级Ⅳ级以上发作;10.00%(4/40)的雄性大鼠死亡;10.00%(4/40)的雄性大鼠未达Racine分级Ⅳ级发作,模型成功率为80.00%;1月后有自发发作者8只(25.00%8/32)。AG490干预组雄性大鼠Ⅳ级以上发作的发生率为75.00%(30/40);病死率为7.50%(3/40);17.50%(7/40)的雄性大鼠未达Ⅳ级发作,模型成功率为75%;1月后有自发发作者1只(3.3%1/30),AG490组Ⅳ级及以上发作及自发发作数与PILO致癫模型组比较,有显著性差异(P<0.05);(2)PILO致癫模型组TNF-α表达水平较对照组开始增高,AG490干预组TNF-α表达水平均较PILO致癫模型组明显降低(P<0.05);(3)PILO癫模型组可见阳性颗粒在星形胶质细胞内的空间分布,AG490腹腔注射建立干预后阳性颗粒的星形胶质细胞明显减少(P<0.05)。结论癫发作后TNF-α表达水平明显增高,提示星形胶质细胞增生。AG490可阻断JAK/STAT信号转导通路进而抑制星形胶质细胞活化,同时也可以影响癫大鼠的行为学变化,提示AG490对癫的发作可能有一定的抑制作用,其机制可能与其抑制星形胶质细胞增生有关。     

利多卡因泵入治疗难治性癫持续状态的疗效

癫持续状态(status epilepticus,SE)是临床急症,需要尽快终止,否者有致命危险。虽然常规抗癫药物治疗大部分癫发作都能被终止,但少数患者的癫发作仍不能终止或出现呼吸功能不全,需要其他治疗措施来迅速控制症状。利多卡因是一种作用于神经细胞的电压门控钠通道的局部麻醉药,广泛用于局麻、抗心律失常的治疗,自从1955     

癫持续状态相关原因分析及护理

癫持续状态或称癫状态,是指一次癫持续30min以上或持续多次发作,发作间歇意识或神志功能未恢复至正常水平。是神经科常见急症之一,致残率很高。任何类型癫均可出现颠持续状态,但通常是指全面强直—阵挛发作持续状态[1]。1资料与方法1.1一般资料2003-05~2006-05我们神经内     

癫痫持续状态大鼠内质网应激预适应对海马神经元保护作用的实验研究

目的 探讨2-脱氧葡萄糖诱导内质网应激预适应对癫痫持续状态大鼠海马神经元的保护作用及其可能机制。方法 采用2-脱氧葡萄糖连续腹腔注射诱导内质网应激,并在此基础上制备氯化锂-匹罗卡品癫痫持续状态大鼠模型。Nissl染色观察癫痫持续状态后海马神经元损伤情况、计数海马CA1和CA3区存活神经元数目;免疫组织化学检测海马CA3区内质网应激标志物葡萄糖调节蛋白78（GRP78）和X盒结合蛋白1（XBP-1）表达变化。结果 与癫痫持续状态组相比,癫痫持续状态后第7天时内质网应激预适应组大鼠海马存活神经元数目增加,以CA1区显著（t=5.353,P=0.000）。癫痫持续状态组大鼠发作后6 h,海马CA3区GRP78和XBP-1表达水平升高且高于对照组（均P=0.000）,于发作第2天达峰值水平（均P=0.000）;内质网应激预适应组大鼠发作前海马CA3区GRP78和XBP-1表达即高于对照组（均P=0.000）,GRP78在发作后24 h和2 d时维持在峰值水平（均P=0.000）,XBP-1在发作后24 h达峰值水平（P=0.000）;内质网应激预适应组大鼠海马CA3区GRP78和XBP-1表达在癫痫持续状态前,以及癫痫持续状态后6、12、24 h均高于癫痫持续状态组（均P=0.000）,至第2和7天时与癫痫持续状态组之间差异无统计学意义（P〉0.05）。结论 经2-脱氧葡萄糖诱导的内质网应激预适应对癫痫持续状态大鼠海马神经元具有保护作用,而XBP-1-GRP78信号转导通路的活化可能是其机制之一。     

大鼠癫痫持续状态后水通道蛋白-4的表达

目的 探讨癫痫持续状态（SE）后大鼠水通道蛋白-4（AQP4）的表达变化与脑水肿形成之间的关系。方法 54只SD大鼠随机分为对照组（n=6），SE后6h，12h，24h，48h，72h，96h，120h，168h组（n=6）。腹腔注射锂-匹罗卡品建立大鼠SE模型，免疫组织化学染色和逆转录PCR方法检测AQP4蛋白和基因在SE形成后的表达。结果 SE后AQV4蛋白和mRNA24h表达水平明显增加，48h达到高峰，持续72h后下降，168h时仍有表达。SE后AQP4表达变化和脑水肿形成过程在时间上呈明显的正相关（r=0．73，氏0．05）。结论 SE后AOP4表达明显增强，在时间上与脑水肿形成呈正相关，提示AQP4在SE后脑水肿形成过程中起着重要作用。     

In vitro status epilepticus causes sustained elevation of intracellular calcium levels in hippocampal neurons

Calcium ions and calcium-dependent systems have been implicated in the pathophysiology of status epilepticus (SE). However, the dynamics of intracellular calcium ([Ca2+]i) levels during SE has not yet been studied. We have employed the hippocampal neuronal culture (HNC) model of in vitro SE that produces continuous epileptiform discharges to study spatial and dynamic changes in [Ca2+]i levels utilizing confocal laser scanning microscopy and the calcium binding dye, indo-1. During SE, the average [Ca2+]i levels increased from control levels of 150-200 nM to levels of 450-600 nM. This increased [Ca2+]i was maintained for the duration of SE. Following SE, [Ca2+]i levels gradually returned to basal values. The duration of SE was shown to affect the ability of the neuron to restore resting [Ca2+]i levels. Both N-methyl-D-aspartate (NMDA) receptor-gated and voltage-gated Ca2+ channels (VGCCs) contributed to the increased calcium entry during SE. Moreover, this elevation in [Ca2+]i occurred in both the nucleus and cytosol. These results provide the first dynamic measurement of [Ca2+]i during prolonged electrographic seizure discharges in an in vitro SE model and suggest that prolonged epileptiform discharges give rise to abnormal sustained increases in [Ca2+]i levels that may play a role in the neuronal cell damage and long-term plasticity changes associated with SE.     

Nonconvulsive status epilepticus

Nonconvulsive status epilepticus (NCSE) is a heterogeneous disorder with multiple subtypes. Although attempts have been made to define and classify this disorder, there is yet no universally accepted definition or classification that encompasses all subtypes or electroclinical scenarios. Developing such a classification scheme is becoming increasingly important, because NCSE is more common than previously thought, with a bimodal peak, in children and the elderly. Recent studies have also shown a high incidence of NCSE in the critically ill. Although strong epidemiological data are lacking, NCSE constitutes about 25-50% of all cases of status epilepticus. For the purposes of this review, we propose an etiological classification for NCSE including NCSE in metabolic disorders, NCSE in coma, NCSE in acute cerebral lesions, and NCSE in those with preexisting epilepsy with or without epileptic encephalopathy. NCSE is still underrecognized, yet potentially fatal if untreated. Diagnosis can be established using an electroencephalogram (EEG) in most cases, sometimes requiring continuous monitoring. However, in comatose patients, diagnosis can be difficult, and the EEG can show a variety of rhythmic or periodic patterns, some of which are of unclear significance. Although some subtypes of NCSE are easily treatable, such as absence status epilepticus, others do not respond well to treatment, and debate exists over how aggressively clinicians should treat NCSE. In particular, the appropriate treatment of NCSE in patients who are critically ill and/or comatose is not well established, and large-scale trials are needed. Overall, further work is needed to better define NCSE, to determine which EEG patterns represent NCSE, and to establish treatment paradigms for different subtypes of NCSE.     

锂-匹鲁卡品诱导癫痫持续状态大鼠海马神经元线粒体及细胞核的变化

BACKGROUND： Mitochondrial damage plays a key role in neuronal damage. OBJECTIVE： To observe ultrastructural damage to mitochondria and nuclei, as well as caspase-3 expression, in hippocampal CA3 neurons of lithium-pilocarpine-induced status epilepticus rats. DESIGN, TIME AND SETTING： The neuropathological, randomized, controlled study was performed at the Animal Experimental Center, Shandong University, China in May 2008. MATERIALS： A total of 75 healthy, adult, male, Wistar rats were randomly assigned into model （n = 45） and control （n = 30） groups. Lithium-pilocarpine （Sigma, USA） was used in this study. METHODS： Rats in the model group were intraperitoneally injected with lithium chloride （3 mEq/kg）, and 24 hours later with pilocarpine （45 mg/kg）, to induce seizures for 2 hours. Rats in the control group were intraperitoneally infused with the same volume of saline. Rat hippocampal CA3 tissue was obtained at 3, 12, and 24 hours following status epilepticus. MAIN OUTCOME MEASURES： Neuronal changes were observed under an optical microscope. Ultrastructural changes in mitochondria and nuclei were observed using an electron microscope. caspase-3 mRNA levels were quantified by semiquantitative RT-PCR. RESULTS： After 3 hours of status epilepticus, mitochondria with swollen cristae and ruptured membranes were observed by electron microscopy. Nuclei with marginated chromatin were observed after 24 hours status epilepticus. RT-PCR results demonstrated increased caspase-3 expression at 12 hours, and significantly increased expression at 24 hours following termination of status epilepticus. This was in accordance with acidophilia occurrence, as indicated by hematoxylin-eosin staining, and time of ultrastructural damage to nuclei. CONCLUSION： In lithium-pilocarpine-induced status epilepticus rat models, ultrastructural damage to mitochondria in hippocampal neurons occurred during early stages, followed by increased caspase-3 expression and nuclear changes. These results suggested that mitochondrial damage plays a key role in neuronal damage following status epilepticus.     

妥泰对海人酸致癎大鼠海马神经元线粒体损伤的保护作用

目的观察海人酸（KA）诱导的癫痫持续状态（SE）、大鼠海马CA3区神经元线粒体超微结构的损伤及妥泰（TPM）的保护作用。方法用TPM干预。用KA诱导大鼠SE2h,并于癫痫终止后3h制作脑切片,用光镜观察神经元的大体损伤,并用电镜进一步观察线粒体的超微结构。结果KA组和TPM组大鼠均出现了线粒体超微结构的损伤,TPM组大鼠的损伤明显减轻。结论KA诱导的SE可导致海马神经元线粒体损伤,妥泰对此具有保护作用。     

妥泰对海人酸致大鼠海马神经元线粒体损伤的保护作用

目的观察海人酸(KA)诱导的癫持续状态(SE)、大鼠海马CA3区神经元线粒体超微结构的损伤及妥泰(TPM)的保护作用。方法用TPM干预。用KA诱导大鼠SE 2h,并于癫终止后3h制作脑切片,用光镜观察神经元的大体损伤,并用电镜进一步观察线粒体的超微结构。结果KA组和TPM组大鼠均出现了线粒体超微结构的损伤,TPM组大鼠的损伤明显减轻。结论KA诱导的SE可导致海马神经元线粒体损伤,妥泰对此具有保护作用。