Inhibitor effect of dexketoprofen in rat model of pentylenetetrazol-induced seizures

Objectives: The relationship between epilepsy and inflammation is known, and it has been reported that there is an increase in cyclooxygenase (COX) levels in epilepsy. We aim to reveal the anticonvulsant effects of dexketoprofen in pentylenetetrazol (PTZ)-induced seizures in rats.

Materials and Methods: Forty-eight male Sprague-Dawley rats, 24 of them for EEG recording and 24 of them are for behavioral studies, were randomly divided in two groups: Group A for EEG recordings and Group B for behavioral assessment. A weight of 70 mg/kg PTZ was used for behavioral studies after dexketoprofen administration. Thirty-five milligrams per kilogram PTZ were used for EEG recording after dexketoprofen administration. The electrodes were implanted on dura over the left frontal cortex and the reference electrode was implanted over the cerebellum for EEG recording. The Racine convulsion scale (RCS), first myoclonic jerk (FMJ) onset time, and spike percentages were evaluated between the two groups.

Results: There was a significant (P< 0·05) difference between the RCS, FMJ onset time (P< 0·001), and spike percentage (P< 0·05) between the groups (Group 2 compared with Groups 3 and 4).

Conclusion: Dexketoprofen has an antiepileptic feature and this effect increases as the dosage increases, however it is currently unknown through which mechanism this drug shows its anticonvulsant effect. Dexketoprofen, in the group of NSAIDs, shows an anticonvulsant effect on PTZ-induced epilepsy model. This study suggests that dexketoprofen can preferably be used with NSAIDs for epileptic patients in clinical practice.     

手足口病伴神经系统症状85例分析

目的：探讨手足口病伴早期神经系统症状患者的临床特征及结局。方法对85例手足口病住院病例的临床表现、实验室检查、治疗转归及病原学等资料进行分析,其中热性惊厥（FC）62例,占72.94%,HFMD重症早期（易惊、肢体抖动、嗜睡）23例,占27.06%。结果（1）FC组主要表现为在发热第一天出现1-3次抽搐,持续1-10分钟不等,发作停止后神志恢复正常,无阳性病理神经征,部分有既往史和家族惊厥史;重症早期组主要表现为病后3-4天出现易惊、肢体抖动、嗜睡,于治疗后1-3天正常,无阳性病理神经征。（2）两组发热及皮疹持续时间的差异均无明显统计学意义,P均＞0.05。（3）多数患者存在血白细胞、C反应蛋白、糖升高及低钠血症,部分有心肌酶谱升高、心电图异常,以FC组为主。（4）病原检测：EV71-RNA（+）45例（52.94%）,CoxA 16-RNA（+）19例（22.35%）,肠道病毒通用核酸（+）12例（14.12%）,余9例（10.59%）检测均阴性,无交叉阳性结果。（5）平均住院5.86±1.89天,随访均未见后遗症。结论早期识别HFMD伴神经系统症状患者的病情及病因,有助于指导治疗及判断预后。     

Na+/Ca2+ Exchanger 3 is Downregulated in the Hippocampus and Cerebrocortex of Rats with Hyperthermia-induced Convulsion

Background:

Na⁺/Ca²⁺ exchanger (NCX) plays a crucial role in pentylenetetrazol-induced convulsion. However, it is unclear whether NCX is critically involved in hyperthermia-induced convulsion. In this study, we examined the potential changes in NCX3 in the hippocampus and cerebrocortex of rats with hyperthermia-induced convulsion.

Methods:

Twenty-one Sprague Dawley rats were randomly assigned to control group, convulsion-prone group and convulsion-resistant group (n = 7 in each group). Whole-cell patch-clamp method was used to record NCX currents. Both the Western blotting analysis and immunofluorescence labeling techniques were used to examine the expression of NCX3.

Results:

NCX currents were decreased in rats after febrile convulsion. Compared to the control group, NCX3 expression was decreased by about 40% and 50% in the hippocampus and cerebrocortex of convulsion-prone rats, respectively. Furthermore, the extent of reduction in NCX3 expression seemed to correlate with the number of seizures.

Conclusions:

There is a significant reduction in NCX3 expression in rats with febrile convulsions. Our findings also indicate a potential link between NCX3 expression, febrile convulsion in early childhood, and adult onset of epilepsy.     

东亚钳蝎提取物对癫痫小鼠大脑皮层NMDA受体和GABA_A受体的调节作用

目的研究BmKE对抗戊四氮致癫痫作用及其对致痫小鼠大脑皮层NMDAR和GABAAR的调节作用。方法观察戊四氮(PTZ)致癫痫模型小鼠,丙戊酸钠(VAP,阳性对照)治疗组和BmKE低(L)、中(M)、高(H)剂量治疗组小鼠癫痫发作的潜伏期,应用同位素3H分别标记MK-801和Muc imol,检测小鼠大脑皮层NMDAR和GABAAR的结合活性。结果BmKE(M)能显著延长PTZ致癫痫小鼠的发作潜伏期(P<0.05),BmKE(L)作用很小,BmKE(H)治疗组癫痫小鼠发作潜伏期的延长值比BmKE(M)治疗组低。PTZ显著升高致痫小鼠大脑皮层的NMDAR结合活性(P<0.05),BmKE(L)治疗组小鼠大脑皮层NMDAR结合活性降低,但是无显著性差异,BmKE(M)和BmKE(H)均极显著降低癫痫小鼠大脑皮层NMDAR结合活性(P<0.001)。BmKE(L)和BmKE(H)显著提高GABAAR结合活性(P<0.05),BmKE(M)极显著提高GABAAR结合活性(P<0.001)。结论适量的BmKE能够有效治疗戊四氮引起的癫痫,显著延长癫痫小鼠的发作潜伏期,BmKE抗癫痫的作用机理,可能与其抑制NMDAR结合活性,激活GABAAR的结合活性有关。     

小儿热性惊厥研究

热性惊厥是小儿时期因体温升高诱发的一种特殊的癫痫综合征。研究发现其与遗传有关,有较明确的基因位点。机体细胞及体液免疫紊乱成为易复发的原因之一。在血生化方面,血清铁、钙的含量降低也是重要的易感因素。由于其对智能发育影响尚不确定,故预防性抗惊厥治疗尚需进一步探讨。     

Secondary generalization of hippocampal kindled seizures in rats: examining the role of the piriform cortex

A primary feature of epilepsy is the potential for focal seizures to recruit distant structures and generalize into convulsions. Key to understanding generalization is to identify critical structures facilitating the transition from focal to generalized seizures. In kindling, development of a primary site leads progressively to secondarily generalized convulsions. In addition, subsequent kindling of a secondary site results in rapid kindling from that site, presumably because of its facilitated access to the primary kindled network. Here, we investigated the role of the piriform cortex in convulsive generalization from a secondary site kindled in the hippocampus after primary site amygdala kindling. In a necessarily complicated design, rats initially experienced forebrain commissurotomy to lateralize the experiment to one hemisphere. Then the amygdala was kindled and, 3 weeks later, it was electrically-triggered into status epilepticus, which destroyed the ipsilateral piriform cortex. This experience occurred several days before secondary site kindling of the dorsal hippocampus. In rats with complete piriform cortex loss, there was no disruption in kindling or convulsive seizure expression from the hippocampus. However, when damage also involved parts of the perirhinal, insular and entorhinal cortices, convulsive expression was blocked. Although other evidence suggests that piriform lesions affect generalization of primary site kindling, the present study shows that they do not alter secondary site kindling in the dorsal hippocampus. The additional involvement of parahippocampal cortical areas in convulsive expression suggests an important functional association between these cortical regions and the hippocampus in seizure propagation and clinical expression.     

良性家族性婴儿惊厥疾病基因与染色体8q24的连锁分析

目的 :对 5例中国良性家族性婴儿惊厥 ( BFIC)家系进行基因定位研究。方法 :选择 D8S50 2 、D8S537等 STR作为 DNA标记 ,应用聚合酶链反应 ( PCR) ,变性聚丙烯酰胺凝胶电泳 ( PAGE)和银染技术 ,采用 LINKAGE软件包中的 MLINK程序进行连锁分析。结果 :在常染色体显性 ( AD)模式下 ,在标记位点 D8S50 2 处 ,5个家系在重组率为 0 .0 5 0 ,外显率为 70 %时 ,获得两点对数优势计分 ( LOD)值总和为 0 .337;在标记位点 D8S537处 ,5个家系在外显率为 70 % ,重组率从 0 .0 0 0到 0 .40 0之间 ,获得两点 L OD值总和均为负值。结论 :不能认为位点D8S50 2 和 D8S537与 BFIC疾病基因存在连锁关系     

Effects of MK-801, dantrolene, and FK506 on convulsive seizures and brain nitric oxide production in seizure-susceptible EL mice

To clarify the role of nitric oxide (NO) in the pathogenesis of seizures in susceptible EL mice, we investigated effects of three drugs potentially related to NO production, MK-801, dantrolene, and FK506, on convulsive seizures and brain NO metabolites (NOx). MK-801 or dantrolene, but not FK506, suppressed convulsive seizures in EL mice; only MK-801 reduced NOx in the brain. Our results suggested involvement of the N-methyl-D-aspartate receptor-channel complex and intracellular calcium mobilization, but not calcineurin, in the convulsions of EL mice.     

病毒性肠炎伴良性婴幼儿惊厥12例临床分析

目的分析病毒性肠炎伴良性婴幼儿惊厥的临床特点。方法对2005年1月～2006年12月我院儿科住院诊断为病毒性肠炎伴良性婴幼儿惊厥患儿进行临床观察和出院后12个月以上的随访。结果12例发病年龄6～30个月，秋冬季发病10例，均为全身性发作，一次病程中平均发作1．6次，发作期间脑电图（EEG）背景正常，血生化、脑影像学正常，惊厥停止后未行抗癫治疗，无一例复发，全部病例无癫痫和热性惊厥家族史，精神运动发育正常。结论本组患儿具有以下特点：①6个月-2岁高发，秋冬季多发，无家族史；②无热惊厥于病程的1-3d发生，全身性发作，无脱水及酸中毒，无血电解质紊乱；③脑影像学正常，EEG正常；④全部病例无复发，预后好。     

首剂联合应用安定和苯巴比妥治疗新生儿惊厥的临床观察

目的 探讨安定联合苯巴比妥治疗新生儿缺氧缺血性脑病发生惊厥的疗效.方法 将156例病例随机分为两组,再给予常规首剂苯巴比妥止惊基础上,治疗组加用安定,分别观察治疗1、5、15 min止惊效果.结果 治疗组与对照组迅速有效率和总有效率进行比较,结果显示治疗组的迅速有效率和总有效率明显高于对照组,差异具有显著性(P<0.05).结论 首剂联合应用安定和苯巴比妥治疗新生儿缺氧缺血性脑病发生惊厥疗效显著,值得临床推广.