Treatment of Status Epilepticus in Adults: Guidelines of the Italian League Against Epilepsy

Summary:  Status epilepticus (SE) is a medical emergency which can lead to significant morbidity and mortality and requires prompt diagnosis and treatment. SE is differentiated into generalized or partial SE on the basis of its electro-clinical manifestations. The guidelines for the management of SE produced by the Italian League against Epilepsy also distinguish three different stages of SE (initial, established and refractory), based on time elapsed since the onset of the condition and responsiveness to previously administered drugs. Treatment should be started as soon as possible, particularly in generalized convulsive SE, and should include general support measures, drugs to suppress epileptic activity and, whenever possible, treatments aimed at relieving the underlying (causative) condition. Benzodiazepines are the first line antiepileptic agents, and i.v. lorazepam is generally preferred because it is associated with a lower risk of early relapses. If benzodiazepines fail to control seizures, i.v. phenytoin is usually indicated, though i.v. phenobarbital or i.v. valproate may also be considered. Refractory SE requires admission to an intensive care unit (ICU) to allow adequate monitoring and support of respiratory, metabolic and hemodynamic functions and cerebral electrical activity. In refractory SE, general anesthesia may be required. Propofol and thiopental represent first line agents in this setting, after careful assessment of potential risks and benefits.     

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。     

成人顽固性癫痫持续状态的临床分析

目的 探讨成人顽固性癫痫持续状态（RSE）的危险因素、临床特点、治疗及预后。方法 54例癫痫持续状态（SE）．58次发作事件，分为RSE组和非顽固性癫痫持续状态（NRSE）组．对病因、诱因、临床表现、辅助检查、预后等进行对比分析。结果 RSE占SE的43．1％，病毒性脑炎是RSE最主要的病因（P=0．001），相反，既往癫痫发作在NRSE中更常见（P=0．000），相应地药物治疗的改变引起的SE多为NRSE（P=-0．003）；RSE组GCS评分及预后较NRSE组均差（均P=0．000）。结论 SE经一、二线抗癫痫药治疗后仍有很大一部分难以控制，病毒性脑炎是导致RSE的一个重要病因，其预后较差．目前对RSE的治疗还缺乏十分合理的方案。     

Changes in microtubule-associated protein-2 (MAP2) expression during development and after status epilepticus in the immature rat hippocampus

In this study, we analyzed the spatiotemporal expression patterns of the high-molecular weight (MAP2a and b) and low-molecular weight (MAP2c and d) cytoskeletal microtubule-associated protein-2 (MAP2) isoforms with Western blotting, and the cellular localization of the high-molecular weight MAP2 isoforms with immunocytochemistry in the hippocampi of 1- to 21-day-old rats. Moreover, the temporal profile (from 30 min to 1 week) of MAP2 isoform reactivity to kainic acid-induced status epilepticus was studied in P9 rats. During development, the expression of the high-molecular weight MAP2 isoforms significantly increased, while the low-molecular weight isoforms decreased, the most prominent changes occurring during the second postnatal week. This developmental increase in the high-molecular weight MAP2 expression was also confirmed with immunocytochemistry, which showed increased immunoreactivity, particularly in the molecular layers of the dentate gyrus, and in CA1 and CA3 stratum radiatum. In 9-day-old rats, status epilepticus resulted in a rapid transient increase (about 210%) in the high-molecular weight MAP2 expression, without any effect on the low-molecular weight MAP2. Moreover, disturbed dendritic structure in the CA1 and CA3 stratum radiatum was manifested as formation of varicosities 3h after the kainic acid treatment. The strictly developmentally regulated MAP2 isoform expression suggests different functional roles for these proteins during the postnatal development in the rat hippocampus. Moreover, high-molecular weight MAP2s may play a role in nerve cell survival during cell stress.     

Treatment of Status Epilepticus

Summary: Status epilepticus, particularly the convulsive form, is a medical emergency, warranting prompt and aggressive treatment. To do this, one must have a thorough understanding of the pharmacology of the anticonvulsant agents. Therapy should be directed toward rapid termination of the status epilepticus, prevention of seizure recurrence, and treatment of any underlying cause. Most importantly, one should establish and adhere to a standard treatment protocol for best results.     

人工全髋表面置换技术的历史与现状

作为全髋置换术(THR)的一种替代技术,全髋表面置换术(THSR)通过保留股骨头、颈骨块而恢复髋关节正常的生物力学特性及关节的稳定性,并由于未破坏股骨髓腔结构而具有易翻修的潜力。在其发展长达半个多世纪的三个技术时期中,通过不断积累经验,使得假体系统在材料、设计及固定方法等技术参数方面获得长足改进。但仍存在尚待解决的问题。新一代金-金全髋表面假体系统的问世是髋关节置换术的一个重要历程碑,在不到10年的临床随访中其早期疗效非常满意,但中、长期疗效尚不确定,需待与其它方法作进一步长期的、随机化对照性研究。     

The nature and timing of excitotoxic neuronal necrosis in the cerebral cortex,hippocampus and thalamus due to flurothyl-induced status epilepticus

Summary Flurothyl-induced status epilepticus was studied by light and electron microscopy (LM, EM) to determine the time course and structural features of neuronal necrosis in the vulnerable brain regions in epilepsy. The cerebral cortex, hippocampus and thalamus were examined after closely spaced recovery periods of up to 1 week. The results showed that acidophilic neurons appeared simultaneously in neurons of the neocortex, hippocampus and thalamus, and that this occurred within 1 h following the end of the epilepsy. The corresponding features of acidophilic neurons by EM were mitochondrial flocculent densities and large discontinuities in cell and nuclear membranes. Dark neurons were ubiquitous during the epilepsy, but recovered almost universally. A few dark neuronal forms persisted and underwent cytorrhexis after 12-h recovery or longer. Axon-sparing dendritic lesions characteristic of excitotoxic neuronal death were found in the neuropil of the neocortex, and in both vulnerable CA1 and resistant CA3 neurons of the hippocampus. Other than acute edema, glial changes were absent. The findings support an excitotoxic mechanism in epilepsy-induced selective neuronal necrosis also in brain regions outside the hippocampus, and contrast with previous reports in ischemia and hypoglycemia in that neuronal necrosis occurs virtually immediately after an epileptic insult. No maturation of cell damage, as described in ischemia, was seen. Furthermore, even exceedingly dark neuronal forms and massive dendritic swelling must be considered sub-lethal or prelethal cellular changes. Lethal cellular changes include acidophilia by LM, cell membrane breaks, and mitochondrial flocculent densities by EM.Supported by the Alberta Hertage Foundation for Medical Research, the Swedish Society of Medicine, the Swedish Medical Research Council, the Magnus Bergvall Foundation, and the Research Funds of the Karolinska Institute.     

低收入大学生一般自我效能感、主观幸福感研究

近年来 ,低收入大学生作为高校中的一个特殊群体逐渐受到研究者和教育者的关注。目前对低收入大学生的一般自我效能感 (generalself -efficacy)和主观幸福感的研究还不多见。一般自我效能感是指个体对各种挑战或新情境的应对能力的总体信心[1] 。一般自我效能感描述的是个体有效地应对各种紧张情境的广义而稳定的个人能力感 ,它与身心健康存在一定的关系[1- 2 ] 。主观幸福感 (subjectivewell-being)是指人们对于自己是否幸福的主观感受 ,是反应心理健康水平的重要指标之一。研究低收入大学生的一般自我效能感和幸福感的特点及其关系对于揭…     

A computer program for calculating the acid-base parameters in samples of blood using a mini-computer

Summary A computer program is presented and evaluated, which calculates all acid-base parameters from data provided by either the indirect Astrup method or the direct method using empirical formulae derived from the Siggaard-Andersen curve nomogram. The program is implemented on a PDP 8 in a multi-user FOCAL environment and can be adapted to other electronic calculators.     

Short term status epilepticus in rats causes specific behavioral impairments related to substantia nigra necrosis

Summary Status epilepticus (SE) was induced for 40 min by flurothyl in well oxygenated rats. This insult resulted in selective destruction of up to 65% of the substantia nigra pars reticulata. We investigated the short and long term behavioral effects of this damage. No deficits were observed in sensorimotor reactivity, locomotor coordination, spontaneous or apomorphine-stimulated locomotor activity in the rats with induced epilepsy. However, these rats exhibited a long-lasting enhancement of amphetamine-stimulated locomotor activity. We propose that this selective impairment is caused by the necrosis of the pars reticulata. This damage might lead to deficient regulation either of mesostriatal dopamine neurons innervating nc. accumbens, or of neurons in the mesencephalic reticular formation mediating the locomotor response initiated in the nc. accumbens.