托吡酯、卡马西平与丙戊酸钠治疗脑炎继发癫痫的效果观察

目的分析托吡酯、卡马西平与丙戊酸钠治疗脑炎继发癫痫效果。方法选取我院在2014年2月至2016年2月期间收治的150例脑炎继发癫痫患者为本次研究对象,并根据用药的不同分成3组,托吡酯组、卡马西平组以及丙戊酸钠组,每组患者各50例。托吡酯组给予托吡酯药物的口服治疗、卡马西平组给予卡马西平药物的口服治疗、丙戊酸钠组给予丙戊酸钠药物的口服治疗。分析三组患者的治疗效果以及不良反应发生情况,并进行对比。结果托吡酯组的有效率为82%;卡马西平组有效率为78%;戊酸钠组有效率为80%,三组患者的总有效率差异不显著,无统计学意义(P>0.05);托吡酯组、卡马西平组以及丙戊酸钠组患者的不良反应发生率分别为6.0%、20%、12%,卡马西平组不良反应发生率明显高于丙戊酸钠组和托吡酯组,丙戊酸钠组患者的不良反应发生率明显高于托吡酯组,三组差异对比有统计学意义(P<0.05)。结论对于脑炎继发癫痫患者的治疗而言,采用托吡酯、卡马西平以及丙戊酸钠均可达到理想的临床疗效,但卡马西平药物以及丙戊酸钠药物的不良反应发生率较高,托吡酯药物药物不良反应发生率较低,可以有效提升患者的安全性,应用价值较高。     

伴中央-颞区棘波儿童良性癫痫患者首次治疗分别使用丙戊酸钠、卡马西平、托吡酯的疗效比较

目的：比较丙戊酸钠、卡马西平、托吡酯作为伴中央-颞区棘波儿童良性癫痫（benign epilepsy with centro-temporal spikes,BECT）患儿首次治疗用药的疗效。方法：回顾性选取2019年2月—2022年2月本院收治的BECT患儿100例,依据用药方法不同分为丙戊酸钠组（40例）、卡马西平组（30例）、托吡酯组（30例）。比较各组临床疗效、认知功能、生活质量、首药治疗失败时间、药物不良反应事件发生情况、家长满意度。结果：三组总有效率、操作智商、语言智商、总智商评分、生活质量评分、家长满意度比较,差异无统计学意义（P>0.05）;卡马西平组首药治疗失败时间晚于丙戊酸钠组、托吡酯组（P<0.05）,且丙戊酸钠组患儿的首药治疗失败时间晚于托吡酯组（P<0.05）;丙戊酸钠组、卡马西平组药物不良反应事件发生率低于托吡酯组（P<0.05）,但丙戊酸钠组、卡马西平组药物不良反应事件发生率比较,差异无统计学意义（P>0.05）。结论：卡马西平、丙戊酸钠、托吡酯治疗BECT的疗效相当,均能够提升患者认知功能、生活质量、家长满意度,但与托吡酯相...     

卡马西平、托吡酯与丙戊酸钠缓释片对脑炎继发癫痫的疗效及不良反应观察

目的探究卡马西平、托吡酯以及丙戊酸钠缓释片对脑炎继发癫痫的治疗效果,并进行安全评价。方法脑炎继发性癫痫患者120例,分为三组,分别口服卡马西平、托吡酯以及丙戊酸钠缓释片进行治疗,以治疗效果和不良反应率作为评价指标,并进行统计学分析。结果托吡酯组的总有效率最高,卡马西平组最低,但三组差异无统计学意义（P〉0.05）;而托吡酯组的不良反应发生率最低,仅为10.0%,与其他两组相比,差异具有统计学意义（P〈0.05）。结论卡马西平、托吡酯以及丙戊酸钠缓释片对脑炎继发性癫痫的治疗效果旗鼓相当,但是托吡酯在临床应用中的不良反应率较低,因此托吡酯更加适用于癫痫的临床上治疗。     

观察卡马西平和托吡酯与丙戊酸钠治疗脑炎继发癫痫的临床效果

目的 观察卡马西平、托吡酯、丙戊酸钠治疗脑炎继发癫痫的临床效果.方法 选取2010年1月-2012年1月灌云县人民医院接受治疗的108例脑炎继发癫痫患者作为研究对象,将其随机分为卡马西平组、托吡酯组和丙戊酸钠组,各36例.观察3组患者的临床疗效.结果 治疗后卡马西平组、丙戊酸钠组和托吡酯组总有效率分别为75.63%（25/36）、77.78%（28/36）和79.63%（29/36）,3组间比较差异无统计学意义（P＞0.05）.结论 卡马西平、托吡酯、丙戊酸钠治疗脑炎继发癫痫的疗效相当;对脑炎继发癫痫患者采取单药治疗时,卡马西平对部分性发作有较好疗效,托吡酯与丙戊酸钠适宜治疗各种类型脑炎继发癫痫患者,同时托吡酯具有较少不良反应.     

卡马西平、托吡酯与丙戊酸钠治疗脑炎继发癫痫的临床疗效分析

目的分析卡马西平、托吡酯与丙戊酸钠治疗脑炎继发癫痫的临床疗效。方法从本院2016年1月至2017年11月接受的脑炎继发癫痫患者中抽取69例,按照药物不同将其分为A、B、C组,均23例。A组采用卡马西平、B组采用托吡酯、C组采用丙戊酸钠进行治疗,观察三组患者临床疗效和不良反应发生情况。结果 A、B、C三组患者临床疗效差异无统计学意义(P>0.05);但B组托吡酯治疗后不良反应发生率显著低于A组和C组,组间比较结果 P<0.05。结论在脑炎继发癫痫治疗中,采用卡马西平、托吡酯与丙戊酸钠治疗均有显著疗效,三种药物治疗效果差异不大,但应用托吡酯治疗后,患者不良反应发生率较低,安全性更高。     

托吡酯、丙戊酸钠、卡马西平治疗脑炎后癫痫的有效性分析

目的探讨托吡酯、丙戊酸钠、卡马西平治疗脑炎后癫痫的有效性。方法根据随机数字表法进行2016年2月至2018年2月135例脑炎后癫痫压患者分成不同组。甲组给予卡马西平治疗,乙组采用丙戊酸钠进行治疗,丙组用托吡酯治疗。比较三组脑炎后癫痫压治疗效果;症状改善时间;治疗不良反应率。结果三组脑炎后癫痫压治疗效果无显著差异,P> 0.05;三组症状改善时间无显著差异,P> 0.05;三组的治疗不良反应率依次是丙组低于乙组,乙组低于甲组,且组间均差异显著,P <0.05。结论托吡酯、丙戊酸钠、卡马西平治疗脑炎后癫痫的有效性相当,但其中托吡酯不良反应最少,丙戊酸钠次之,而卡马西平不良反应最多。     

托吡酯卡马西平与丙戊酸钠治疗脑炎继发癫痫的效果观察

目的对托吡酯、卡马西平及丙戊酸钠治疗脑炎继发癫痫的效果进行观察。方法采纳2017年1月至2019年1月在我院进行治疗的脑炎继发癫痫患者180例,并根据患者入院治疗时间分为A组、B组、C组各60例,分别给予托吡酯、卡马西平、丙戊酸钠治疗,将三组患者的治疗效果进行对比。结果 A组患者给予托吡酯治疗后,治疗效果明显高于B组、C组患者(P <0.05),B组、C组患者的治疗效果无明显差异(P> 0.05)。结论上述三种药物均可对脑炎继发癫痫患者起到较好的治疗效果,但托吡酯治疗效果更佳,临床可将托吡酯作为治疗脑炎继发癫痫患者的首选药物。     

儿童抗癫痫药物治疗药物监测

抗癫痫药物（AEDs）是治疗癫痫的主要药物,现有27种抗癫痫药物,这使得治疗药物监测（TDM）的应用越来越广泛,同时,抗癫痫药物也是进行TDM最常见的药物。第一代抗癫痫药物卡马西平、苯巴比妥、苯妥英钠、乙琥胺、扑米酮、丙戊酸在TDM方面积累了很多经验,现在TDM将更多地应用于新的抗癫痫药物如醋酸艾司利卡西平、非氨酯、加巴喷丁、拉科酰胺、拉莫三嗪、左乙拉西坦、奥卡西平、吡仑帕奈、哌拉西坦、普瑞巴林、瑞替加滨、卢非酰胺、司替戊醇、噻加宾、托吡酯、氨己烯酸和唑尼沙胺。本文通过对样本类型、样本的采集和处理、参考范围的概念进行综述,旨在为儿童抗癫痫用药的药物监测提供依据。     

基于马尔可夫模型比较丙戊酸钠、托吡酯和苯妥英钠治疗癫痫的经济性

目的:比较丙戊酸钠、托吡酯和苯妥英钠治疗癫痫的经济性。方法:计算机检索Pro Quest、Pub Med、Springer、中国期刊全文数据库、中文科技期刊全文数据库、万方数字化期刊全文数据库,收集关于丙戊酸钠、托吡酯和苯妥英钠治疗癫痫的经济性研究,运用Tree Age Pro 2011.1.0.12.1软件构建马尔可夫(Markov)模型,通过计算成本-效果比(CER)对3种药物的经济性作出评价。结果:共纳入6项研究。苯妥英钠的CER值为29.99,丙戊酸钠的CER值为2 664.52,托吡酯的CER值为6 657.25,即苯妥英钠<丙戊酸钠<托吡酯。结论:单从经济学方面考虑,苯妥英钠是治疗癫痫最经济、有效的药物。由于纳入研究数量偏少,该结论有待大样本、高质量的研究进一步验证。     

卡马西平、苯妥英钠、丙戊酸钠治疗成人强直—阵挛性发作260例疗效观察

本文对260例强直—阵挛性发作的患者分别采用卡马西平、苯妥英钠、丙戊酸钠治疗。结果三组的显效率分别为43.2%、20.9%、18.6%。总有效率分别为90.1%、83.7%、68%。卡马西平组与苯妥英钠组和丙戊酸钠组比较有统计学意义。另外,苯妥英钠的毒副反应大于卡马西平和丙戊酸钠。     

Topiramate potentiates the antiseizure activity of some anticonvulsants in DBA/2 mice

Topiramate (1-50 mg/kg, intraperitoneally (i.p.)) was able to antagonize audiogenic seizures in DBA/2 mice in a dose-dependent manner. Topiramate at dose of 2.5 mg/kg i.p., which per se did not significantly affect the occurrence of audiogenic seizures in DBA/2 mice, potentiated the anticonvulsant activity of carbamazepine, diazepam, felbamate, lamotrigine, phenytoin, phenobarbital and valproate against sound-induced seizures in DBA/2 mice. The degree of potentiation induced by topiramate was greatest for diazepam, phenobarbital and valproate, less for lamotrigine and phenytoin and not significant for carbamazepine and felbamate. The increase in anticonvulsant activity was associated with a comparable increase in motor impairment. However, the therapeutic index of the combination of all drugs+topiramate was more favourable than that of antiepileptics+ saline, with the exception of carbamazepine or felbamate+topiramate. Since topiramate did not significantly influence the total and free plasma levels of the anticonvulsant drugs studied, we suggest that pharmacokinetic interactions, in terms of total or free plasma levels, are not probable. However, the possibility that topiramate can modify the clearance from the brain of the anticonvulsant drugs studied cannot be excluded. In addition, topiramate did not significantly affect the hypothermic effects of the anticonvulsants tested. In conclusion, topiramate showed an additive effect when administered in combination with some classical anticonvulsants, most notably diazepam, phenobarbital, lamotrigine, phenytoin and valproate.     

Anticonvulsants in the treatment of bipolar mania

A series of antiepileptic drugs have been investigated in terms of their ability to treat mania (with later applications for the treatment of bipolar depression and prevention of relapses). These include divalproex, carbamazepine, oxcarbazepine, gabapentin, lamotrigine, levetiracetam, tiagabine, topiramate and zonisamide. Although these drugs are all antiepileptic in action, they bring about these effects by different mechanisms; in particular, their impact on GABA differs significantly. Perhaps for this reason, their impact on mania varies greatly, with double-blind significant results evident only for valproate, carbamazepine and oxcarbazepine. Only valproate and carbamazepine are approved by the US FDA for use in mania; oxcarbazepine has never been found significantly effective in large-scale studies. Of the other options, both gabapentin and topiramate failed in large-scale investigations; tiagabine failed in small sample reports. Although lamotrigine has been successful in the prevention of depression relapse in bipolar disorder, it has not been effective in treating mania. Finally, there are no findings of large scale double-blind studies on the use of levetiracetam and zonisamide. A review of the kinetics, side effects and complications of the antiepileptic drugs indicates that carbamazepine is useful, and has adverse event benefit over all other options. The potential of zonisamide awaits further testing.     

Testing of prototype antiepileptics in hippocampal slices

Summary The effects of six prototype anticonvulsant drugs, phenytoin, carbamazepine, midazolam, phenobarbital, ethosuximide and sodium valproate, were evaluated in two different experimental models of epileptiform activity using the in vitro slice preparation from the rat hippocampus. The relative potencies of the agents were determined: a) in the complete absence of synaptic transmission by recording spontaneous burst firing from the CA 1 pyramidal cell layer in a low calcium high magnesium solution and b) during blocked synaptic inhibition by observing the activity of each drug upon orthodromically evoked population spikes in penicillin containing medium. The rank order of potencies was a) in low Ca²⁺: carbamazepine, phenytoin, midazolam, phenobarbital, valproate, ethosuximide; b) in penicillin containing medium: midazolam, phenobarbital, carbamazepine, phenytoin, valproate, ethosuximide. These observations illustrate that the use of multiple paradigms is warranted when examining the mechanisms of action of new anticonvulsants.     

Effects of anti-epileptic drugs on glutamine synthetase activity in mouse brain.

1. Glutamine synthetase (GS) is a key enzyme in the regulation of glutamate neurotransmission in the central nervous system. It is responsible for the conversion of glutamate to glutamine, and for the detoxification of ammonia. 2. We have investigated the effects of single and repeated intraperitoneal administration of a range of established and new anti-epileptic drugs on GS activity in mouse brain. 3. Four hours after the final dose, animals were sacrificed and the brains removed for analysis of GS activity. 4. Both single and repeated doses of phenytoin and carbamazepine were found to reduce enzyme activity (P<0.05). 5. Single doses of phenobarbitone, felbamate and topiramate were without effect, however repeated administration of these drugs dose-dependently reduced GS activity (P<0.05). 6. Single and repeated doses of sodium valproate, vigabatrin, lamotrigine, gabapentin, tiagabine, levetiracetam and desglycinyl-remacemide were found to have no effect on GS activity. 7. The reduction in enzyme activity demonstrated is unlikely to be related to the anti-epileptic actions of these drugs, but may contribute to their toxicity.     

Imperatorin enhances the protective activity of conventional antiepileptic drugs against maximal electroshock-induced seizures in mice

The effects of imperatorin (8-isopentenyloxypsoralen; 9-(3-methylbut-2-enyloxy)-7H-furo[3,2-g]chromen-7-one) on the anticonvulsant activity of four conventional antiepileptic drugs (carbamazepine, phenobarbital, phenytoin and valproate) were studied in the mouse maximal electroshock seizure model. Results indicate that imperatorin (30 and 40 mg/kg, i.p.) significantly potentiated the anticonvulsant activity of carbamazepine against maximal electroshock-induced seizures by reducing its median effective dose (ED(50)) from 10.3 to 6.8 (by 34%; P<0.05) and 6.0 mg/kg (by 42%; P<0.01), respectively. Similarly, imperatorin (40 mg/kg, i.p.) markedly enhanced the antielectroshock action of phenobarbital and phenytoin, by lowering their ED(50) values from 19.6 to 12.2 mg/kg (by 38%; P<0.05-phenobarbital) and from 12.8 to 8.5 mg/kg (by 34%; P<0.05-phenytoin) in the maximal electroshock seizure test. In contrast, imperatorin (40 mg/kg, i.p.) did not affect the protective action of valproate against maximal electroshock-induced seizures in mice. Imperatorin at lower doses of 20 and 30 mg/kg had no significant effect on the anticonvulsant activities of conventional antiepileptic drugs in the mouse maximal electroshock seizure model. Pharmacokinetic evaluation of interaction between imperatorin (30 mg/kg, i.p.) and carbamazepine (6.8 mg/kg, i.p.) revealed a significant increase in total brain carbamazepine concentration after imperatorin administration, indicating a pharmacokinetic nature of interaction between these drugs. In cases of phenobarbital and phenytoin, imperatorin (40 mg/kg, i.p.) did not alter significantly total brain concentrations of phenytoin and phenobarbital in mice, and thus, the observed interactions in the maximal electroshock seizure test between imperatorin and phenobarbital or phenytoin were pharmacodynamic in nature. The present study demonstrates that imperatorin enhanced the antiseizure effects of carbamazepine, phenobarbital and phenytoin in the mouse maximal electroshock seizure model. However, the combination of imperatorin with carbamazepine, despite its beneficial effects in terms of seizure suppression in mice, was complicated by a pharmacokinetic increase in total brain carbamazepine concentration in experimental animals. In contrast, the combinations of imperatorin with phenytoin and phenobarbital, due to their beneficial antiseizure effects and no pharmacokinetic interactions between drugs in the brain compartment of experimental animals, deserve more attention and are of pivotal importance for epileptic patients as advantageous combinations from a clinical viewpoint.     

New anti-epileptic drugs for the 21st century

Prior to 1993, there were only six major drugs available in the US for the treatment of patients with epilepsy. These included phenobarbital (PB), phenytoin (PHT), carbamazepine (CBZ), primidone (PRIM), valproic acid/sodium valproate (VPA) and ethosuximide (ESX). Of these drugs, VPA has the broadest spectrum of activity and ESX the most limited. Despite these six agents, as well as several secondary drugs, it is estimated that over 30% of patients have inadequate seizure control, while others, whose disease is adequately controlled, suffer from bothersome adverse events (AEs). Since 1993, ten new drugs have entered the worldwide market (not all in the US). Those released include felbamate (FBM), gabapentin (GBP), lamotrigine (LTG), topiramate (TPM), tiagabine (TGB), oxcarbazepine (OXC), levetiracetam (LVT), zonisamide (ZNS), clobazam (CLB) and vigabatrin (VGB). The purpose of this article is to review each of the above drugs, looking at efficacy, safety, tolerability and where they may play a role in the current treatment of epilepsy.     

New anti-epileptic drugs for the 21st century

Prior to 1993, there were only six major drugs available in the US for the treatment of patients with epilepsy. These included phenobarbital (PB), phenytoin (PHT), carbamazepine (CBZ), primidone (PRIM), valproic acid/sodium valproate (VPA) and ethosuximide (ESX). Of these drugs, VPA has the broadest spectrum of activity and ESX the most limited. Despite these six agents, as well as several secondary drugs, it is estimated that over 30% of patients have inadequate seizure control, while others, whose disease is adequately controlled, suffer from bothersome adverse events (AEs). Since 1993, ten new drugs have entered the worldwide market (not all in the US). Those released include felbamate (FBM), gabapentin (GBP), lamotrigine (LTG), topiramate (TPM), tiagabine (TGB), oxcarbazepine (OXC), levetiracetam (LVT), zonisamide (ZNS), clobazam (CLB) and vigabatrin (VGB). The purpose of this article is to review each of the above drugs, looking at efficacy, safety, tolerability and where they may play a role in the current treatment of epilepsy.     

Effect of antiepileptic drugs on cognitive function in individuals with epilepsy: a comparative review of newer versus older agents

Several 'new' antiepileptic drugs (AEDs), i.e. oxcarbazepine, vigabatrin, lamotrigine, zonisamide, gabapentin, tiagabine, topiramate and levetiracetam have been introduced into clinical practice within the last decade. Most of these new drugs are at least as effective as the 'old' AEDs [phenytoin, phenobarbital (phenobarbitone), valproic acid (sodium valproate) and carbamazepine] and, in general, they seem to be better tolerated than the old drugs. The new AEDs might have less influence on cognitive functions but the aspect has not been systematically studied. Neuropsychological testing has been the major method of objectively examining cognitive function related to the use of AEDs but a number of methodological problems blur the results. Alteration of cognition might reflect a chronic adverse effect of AEDs but the negative effects of the drugs are only one of several factors that may influence cognition. In addition, subjective complaints about cognitive deficits (e.g. memory problems or attention) may also reflect other aspects of adverse effects than those concerning specific cognitive functions (e.g. mood and anxiety). This review focuses on studies of the cognitive effects of the new AEDs, and in particular on studies that compare cognitive effects of the old and new drugs. In general, the new AEDs seem to display no or minor negative cognitive effects. In studies in which new AEDs have been compared with old AEDs, there was a tendency in favour of the new AEDs in some of the studies.     

Influence of retigabine on the anticonvulsant activity of some antiepileptic drugs against audiogenic seizures in DBA/2 mice

Retigabine (D-2319, 0.5-20 mg/kg i.p.) antagonised dose dependently audiogenic seizures in DBA/2 mice. Retigabine at 0.5 mg/kg i.p., a dose that per se did not affect the occurrence of audiogenic seizures significantly, potentiated the anticonvulsant activity of carbamazepine, diazepam, felbamate, lamotrigine, phenytoin, phenobarbital and valproate against sound-induced seizures in DBA/2 mice. The degree of additivity for the effect induced by retigabine was greatest for diazepam, phenobarbital, phenytoin and valproate, less for carbamazepine and lamotrigine and least for felbamate. The increase in anticonvulsant activity was usually associated with a comparable increase in motor impairment. However, the therapeutic index of combined treatment (drugs plus retigabine), was more favourable than the same drug plus vehicle. Since retigabine had no significant influence on the total and free plasma levels of the anticonvulsant drugs, pharmacokinetic interactions, in terms of total or free plasma levels, are not probable. However, the possibility that retigabine modifies the clearance of the anticonvulsant drugs from the brain cannot be excluded. Retigabine had no significant effect on the hypothermic effects of the anticonvulsants tested. In conclusion, retigabine showed an additive effect when administered in combination with classical anticonvulsants, most notably diazepam, phenobarbital, phenytoin and valproate.     

Synthetic cannabinoid WIN 55,212-2 mesylate enhances the protective action of four classical antiepileptic drugs against maximal electroshock-induced seizures in mice

The aim of this study was to determine the effect of WIN 55,212-2 mesylate (WIN — a non-selective cannabinoid CB1 and CB2 receptor agonist) on the protective action of four classical antiepileptic drugs (carbamazepine, phenytoin, phenobarbital, and valproate) in the mouse maximal electroshock seizure (MES) model. The results indicate that WIN (10 mg/kg, i.p.) significantly enhanced the anticonvulsant action of carbamazepine, phenytoin, phenobarbital and valproate in the MES test in mice. WIN (5 mg/kg) potentiated the anticonvulsant action of carbamazepine and valproate, but not that of phenytoin or phenobarbital in the MES test in mice. However, WIN administered alone and in combination with carbamazepine, phenytoin, phenobarbital and valproate significantly reduced muscular strength in mice in the grip-strength test. In the passive avoidance task, WIN in combination with phenobarbital, phenytoin and valproate significantly impaired long-term memory in mice. In the chimney test, only the combinations of WIN with phenobarbital and valproate significantly impaired motor coordination in mice. In conclusion, WIN enhanced the anticonvulsant action of carbamazepine, phenytoin, phenobarbital and valproate in the MES test. However, the utmost caution is advised when combining WIN with classical antiepileptic drugs due to impairment of motor coordination and long-term memory and/or reduction of skeletal muscular strength that might appear during combined treatment.