老年癫痫41例临床特点分析

目的研究老年癫痫的临床特点。方法回顾性分析大连医科大学附属第一医院癫痫门诊41例老年癫痫患者的临床资料。结果 41例患者70.7%为部分性发作,29.3%为全面性强直阵挛发作。病因分析：63.4%为脑血管病,9.8%为脑肿瘤,7.3%为代谢性疾病,14.6%病因不明。41例均为单药治疗,其中61.0%发作完全控制,有效率87.9%。结论老年癫痫多为继发性癫痫,病因明确,发作类型以部分性发作为主,抗癫痫药物单药治疗效果好。     

120例老年性癫痫的临床特点、治疗及预后

目的研究老年性癫痫的临床特点、治疗及预后。方法对120例老年性癫痫临床资料进行回顾性分析。结果老年性癫痫常见病因为脑血管疾病84例(70.0%),脑肿瘤19例(15.8%)、脑外伤和脑手术后癫痫12例(10.0%)、脑萎缩5例(4.2%)等。早发性与迟发性癫痫分别为42例和78例。发作类型大多数为局灶性发作76例(63.3%)或局灶性发作继发全身泛化44例(36.7%)。大多数患者对单一抗癫痫药反应良好。结论老年性癫痫常见原因为脑血管病、脑肿瘤、外伤和脑手术后;大多数发作为局灶性发作或局灶性发作继发全身泛化;对抗癫痫药反应良好。     

癫痫持续状态的临床研究

目的:探讨癫痫持续状态的病因、临床特点、诊断和治疗方法.方法:对51例癫痫持续状态患者的临床资料进行回顾性分析.结果:经积极治疗后48例患者得到有效控制,3例自动出院后死亡,病死率为5.9%.结论:脑血管病是癫痫持续状态最常见的病因,在有癞痫史的患者中停药或换药是最常见的诱因.尽早诊断,及时治疗可以提高抢救成功率.坚持服药,减少各种不良诱因是预防本病的关键.     

2013—2015年武汉大学人民医院神经内科抗癫痫药物的使用情况分析

目的 了解武汉大学人民医院抗癫痫药物的使用情况,为医护人员提供参考.方法 选取武汉大学人民医院2013年7月-2015年8月151份症状性癫痫病历进行回顾性分析,对患者的性别及年龄、病因、用药方案、抗癫痫药物的使用情况以及不良反应进行分类统计.结果 151例症状性癫痫患者中,男性多于女性;年龄多集中在51～64岁的患者;病因复杂,多集中在脑血管疾病、脑外伤、颅内感染3大原因;癫痫形式主要为全身性发作的强直阵挛性发作,抗癫痫治疗方案多采用单一用药的形式,而且丙戊酸钠和奥卡西平是临床上最常用的抗癫痫药物.结论 从药物流行病学角度考察了武汉大学人民医院神经内科抗癫痫药物的药物利用模式,对临床制定抗癫痫治疗方案具有积极的意义.     

神经外科病人预防癫痫发生的用药分析

目的 分析某医院收治的颅脑疾病病人预防癫痫发生的具体用药情况.方法 对某医院神经外科的出院病例进行回顾性调查,分析病人疾病种类、是否手术及具体手术类别,预防癫痫发作的药物使用情况.结果 所调查146例使用抗癫痫药物的病例中,以脑出血病人预防用抗癫痫药为多数;平均住院天数12.6 d;手术病例96例,平均手术时间是3.18 h;非手术病人50例.手术病人大多术后即刻或者术前1~3 d预防使用丙戊酸钠,住院期间预防用丙戊酸钠后无癫痫发作,术后无预防的癫痫发生率为6.8%.结论 该医院颅脑疾病病人预防癫痫发作以使用抗癫痫药丙戊酸钠为主,手术病人术后即刻或者术前预防用抗癫痫药术后癫痫的发生率明显降低.     

老年人癫痫发作的临床分析

目的 探讨老年人癫痫发作的临床特点，以期为临床诊治提供帮助。方法 回顾分析因癫痫发作而住院的187例中33例首发年龄在60岁以上的老年病人。结果 60岁以上首次癫痫发作的33例占同期癫痫发作而住院的187例的17．65％，男性多于女性，脑血管病为主要原因，脑血管病2周内继发癫痫发作13例，发作次数1－3次，仅4例需用抗癫痫药，2周后继发癫痫发作15例，发作较频，全部需服抗癫痫药。发作形式以部分性发作为主（57．58％），头颅CT或MRI检查发现病灶在皮层的发生率最高（54．55％）。结论 老年癫痫发作有其自身特点。     

236例症状性癫痫病因分析

目的探讨症状性癫痫的病因及不同年龄段病因构成特点。方法对236例症状性癫痫患者的病因特点进行回顾分析。结果 20岁以下及60岁以上症状性癫痫患者起病者各110例。最多见的病因为脑血管病(19.9%),其次为脑外伤(14.4%),药物、毒物及代谢紊乱(12.7%),中枢神经系统感染(12.3%)。20岁以下的患者以颅内感染、皮质发育障碍为多见,2~39岁年龄段则以颅内感染为首位,其次脑血管病(主要为脑缺血和脑血管瘤)、脑肿瘤等;40岁以上的患者以脑血管病为第一位病因,其次是脑外伤、神经系统变性疾病等占多数。结论症状性癫痫常见的病因依次是脑血管病,脑外伤,药物、毒物及代谢紊乱,中枢神经系统感染,且不同年龄段病因的构成明显不同。     

丙戊酸钠致高氨血症脑病和癫痫加重1例

1例78岁男性患者,诊断为脑卒中后癫痫.2020年7月19日给予丙戊酸钠缓释片(0.5 g,bid)抗癫痫治疗.8月20日因抽搐再次发作,自行调整丙戊酸钠用量为2 g,bid,2 d后出现抽搐频繁发作及乳酸、血氨升高.入院后考虑丙戊酸钠过量致高氨血症脑病可能性大,立即停用丙戊酸钠,同时给予降血氨对症治疗,调整抗癫痫药物...     

老年性癫痫患者的临床特征和脑电图分析

目的分析和总结老年性癫痫患者临床特征,脑电图特点及临床意义。方法对60例60岁后发病的老年性癫痫患者的临床特征,脑电图及神经影像学资料等进行分析。结果 60例患者中,复杂部分性发作是最常见的发作类型。48例为症状性癫痫,12例为隐源性癫痫。脑血管病,脑肿瘤,代谢中毒性疾病,颅内感染,脑外伤等是最常见病因。脑电图异常以局灶性慢波最为常见。50例随防患者中,40例控制良好。结论老年人群是癫痫的高发人群。正确认识临床特征和脑电图特点是诊断治疗的关键。     

颅脑手术后抗癫痫药物预防癫痫疗效分析

目的：分析抗癫痫药物在脑外科治疗中的使用情况,探讨抗癫痫药物在颅脑手术后癫痫的预防作用以及各种药物作用的强弱。方法：查阅2001～2007年医院神经外科住院患者的病例资料,利用spss软件分析术后使用抗癫痫药是否对术后癫痫的发生率产生影响,并比较4种常用抗癫痫药对术后癫痫的预防作用。结果：非癫痫患者有预防性用药的93例,术后无发作的89例,发作4例;未使用抗癫痫药物的38例,术后无发作的36例,发作2例。有预防性用药与无预防性用药的术后癫痫发生率分别为4．30％和5．26％（P〉0．05）,两组无统计学差异。苯妥英钠、苯巴比妥钠、丙戊酸钠、卡马西平4种抗癫痫药对非癫痫患者术后癫痫的预防作用无统计学差异。结论：对于非癫痫手术的患者,预防性使用抗癫痫药效果并不理想。外科中常用的四种抗癫痫药物在预防作用方面比较并无统计学差异。     

Seizures in alcohol-dependent patients: epidemiology, pathophysiology and management

The relationship between alcohol and seizures is complex and multifaceted. The prevalence of epilepsy in alcohol-dependent patients of western industrialised countries may be at least triple that in the general population, whereas the prevalence of alcoholism is only slightly higher in patients with epilepsy than in the general population. The seizure threshold is raised by alcohol drinking and declines on cessation of drinking. As a result, during withdrawal from alcohol, usually 6-48 hours after the cessation of drinking, seizures may occur. Alcohol acts on the brain through several mechanisms that influence seizure threshold. These include effects on calcium and chloride flux through the ion-gated glutamate NMDA and GABA receptors. During prolonged intoxication, the CNS adapts to the effects of alcohol, resulting in tolerance; however, these adaptive effects seem to be transient, disappearing after alcohol intake is stopped. Although the relationship of seizures to alcohol use is likely to be dose dependent and causal, the available clinical data do not suggest that alcohol use results in seizure genesis. However, a genetic predisposition to alcohol withdrawal seizures is possible. Other seizures in alcohol-dependent individuals may be due to concurrent metabolic, toxic, infectious, traumatic, neoplastic and cerebrovascular diseases and are frequently partial-onset seizures. Alcohol abuse is a major precipitant of status epilepticus (9-25% of cases), which may even be the first-ever seizure type. Prompt treatment of alcohol withdrawal seizures is recommended to prevent status epilepticus. During the detoxification process, primary and secondary preventative measures can be taken. A meta-analysis of controlled trials for the primary prevention of alcohol withdrawal seizures demonstrated a highly significant risk reduction for seizures with benzodiazepines and antiepileptic drugs and an increased risk with antipsychotics. A meta-analysis of randomised, placebo-controlled trials for the secondary prevention of seizures after alcohol withdrawal showed lorazepam to be effective, whereas phenytoin was ineffective. Because withdrawal seizures do not recur if the patient remains abstinent, long-term administration of antiepileptic drugs is unnecessary in abstinent patients. The first seizure not related to alcohol withdrawal should not result in permanent drug treatment in an alcohol-dependent patient, because of poor compliance and the high likelihood of remission. The treatment of alcohol dependence is more important and should be prioritised before the prevention of further seizures.     

Refractory generalised convulsive status epilepticus : a guide to treatment

The patient with status epilepticus has continuous or rapidly repeating seizures. Generalised convulsive status epilepticus (GCSE) is the most common form of the disorder and is a life-threatening condition that requires prompt medical management. Status epilepticus that does not respond to first-line benzodiazepines (lorazepam or diazepam) or to second-line antiepileptic drugs (phenytoin/fosphenytoin, phenobarbital or valproate) is usually considered refractory and requires more aggressive treatment.The optimal treatment of refractory GCSE has not been defined, but patients should be treated in an intensive care unit, as artificial ventilation and haemodynamic support are required. Invasive haemodynamic monitoring is often necessary and EEG monitoring is essential.The drug treatment of refractory GCSE involves general anaesthesia with continuous intravenous anaesthetics given in doses that abolish all clinical and electrographic epileptic activity, often requiring sedation to the point of burst suppression on the EEG. Barbiturate anaesthetics, pentobarbital in the US and thiopental sodium in Europe and Australia, are the most frequently used agents and are highly effective for refractory GCSE both in children and adults. Indeed, they remain the only way to stop seizure activity with certainty in severely refractory cases. Other options are midazolam for adults and children and propofol for adults only.Regardless of the drug selected, intravenous fluids and vasopressors are usually required to treat hypotension. Once seizures have been controlled for 12-24 hours, continuous intravenous therapy should be gradually tapered off if the drug being administered is midazolam or propofol. Gradual tapering is probably not necessary with pentobarbital or thiopental sodium. Continuous EEG monitoring is required during high-dose treatment and while therapy is gradually withdrawn. During withdrawal of anaesthetic therapy, intravenous phenytoin/fosphenytoin or valproate should be continued (these agents having been administered during earlier phases of GCSE) to ensure an adequate baseline of antiepileptic medication so as to prevent the recurrence of status epilepticus. If additional medication is needed, the most appropriate antiepileptic drugs are gabapentin for focal seizures and levetiracetam and topiramate for all seizure types, as these drugs can be started at high doses with a low risk of idiosyncratic reactions.Even with current best practice, mortality in patients who experience refractory GCSE is about 50% and only the minority return to their premorbid functional baseline. Therefore, new treatment options are urgently needed. The ideal new drug for refractory GCSE would be one that has the ability to stop seizures more effectively and safely than current drugs, and that has neuroprotective properties to prevent the brain damage and neurological morbidity caused by GCSE.     

Drug therapy reviews: drug therapy of status epilepticus.

Drug treatment of status epilepticus is reviewed. Tonic-clonic, focal motor, complex partial and absence status epilepticus are discussed. In managing tonic-clonic status epilepticus one should: (1) maintain vital functions at all times, (2) identify and treat precipitating factors and (3) administer an intravenous loading dose of phenytoin sodium or phenobarbital sodium. Careful use of i.v. diazepam sometimes helps to achieve these objectives. Intravenous phenytoin sodium and phenobarbital sodium provide definitive, long-term control of tonic-clonic seizures but must be administered slowly and require time to reach peak brain concentrations. Intravenous diazepam appears to enter and exit from the brain rapidly and may control seizures while therapeutic brain concentrations of long-acting drugs are being achieved. Phenytoin, phenobarbital and diazepam should not be administered intramuscularly in treating status epilepticus. Treatment of focal motor and complex partial status epilepticus is similar to that of tonic-clonic status epilepticus, but i.v. diazepam is required less frequently and loading doses of phenytoin and phenobarbital sometimes can be given more slowly. Status epilepticus of the absence type is managed with i.v. acetazolamide sodium or diazepam. Paraldehyde, muscle relaxants, general anesthesia and lidocaine may be tried when conventional therapies fail.     

Prevention or modification of epileptogenesis after brain insults: experimental approaches and translational research

Diverse brain insults, including traumatic brain injury, stroke, infections, tumors, neurodegenerative diseases, and prolonged acute symptomatic seizures, such as complex febrile seizures or status epilepticus (SE), can induce "epileptogenesis," a process by which normal brain tissue is transformed into tissue capable of generating spontaneous recurrent seizures. Furthermore, epileptogenesis operates in cryptogenic causes of epilepsy. In view of the accumulating information about cellular and molecular mechanisms of epileptogenesis, it should be possible to intervene in this process before the onset of seizures and thereby either prevent the development of epilepsy in patients at risk or increase the potential for better long-term outcome, which constitutes a major clinical need. For identifying pharmacological interventions that prevent, interrupt or reverse the epileptogenic process in people at risk, two groups of animal models, kindling and SE-induced recurrent seizures, have been recommended as potentially useful tools. Furthermore, genetic rodent models of epileptogenesis are increasingly used in assessing antiepileptogenic treatments. Two approaches have been used in these different model categories: screening of clinically established antiepileptic drugs (AEDs) for antiepileptogenic or disease-modifying potential, and targeting the key causal mechanisms that underlie epileptogenesis. The first approach indicated that among various AEDs, topiramate, levetiracetam, carisbamate, and valproate may be the most promising. On the basis of these experimental findings, two ongoing clinical trials will address the antiepileptogenic potential of topiramate and levetiracetam in patients with traumatic brain injury, hopefully translating laboratory discoveries into successful therapies. The second approach has highlighted neurodegeneration, inflammation and up-regulation of immune responses, and neuronal hyperexcitability as potential targets for antiepileptogenesis or disease modification. This article reviews these areas of progress and discusses the challenges associated with discovery of antiepileptogenic therapies.     

Poststroke epilepsy: epidemiology, pathophysiology and management

Seizures and status epilepticus can be a presenting feature of acute stroke. They may occur in its early (<7 days) clinical course or be a remote (>7 days) complication. Most seizures are single, either partial or generalised. Early and remote seizures seem to have different predictors and pathogenesis. Seizures are more frequent in severe and disabling strokes, haemorrhagic strokes and those with cortical involvement. The risk of epilepsy is higher for patients with early seizures, cortical infarctions and lobar haemorrhages and in dependent patients. Early or remote seizures do not have a significant influence on dependency or mortality, although seizures and status epilepticus can be a direct cause of death.Treatment can be started after a first or a recurrent seizure. Treatment options include phenytoin, carbamazepine, valproic acid (valproate sodium) and the new antiepileptic drugs (AEDs). New AEDs can be used to decrease the likelihood of drug interactions and adverse effects in patients who do not tolerate the classic AEDs and in treatment failures with classic AEDs. Large observational studies to define prognostic factors for poststroke seizures in specific stroke subtypes are needed. Randomised controlled trials of AED prophylaxis for acute and remote seizures are essential to improve the evidence level of current guidelines and recommendations.     

Lacosamide for epileptic seizures in patients with co-morbidities and unusual presentations of epilepsy

Numerous patients who are prescribed antiepileptic drugs (AEDs) for epileptic seizures are already receiving other agents for the treatment of co-morbid conditions, which frequently occur alongside epilepsy. This raises additional clinical considerations and makes the use of AEDs with good safety profiles and fewer drug-drug interactions attractive. Second and third-generation anticonvulsant drugs are associated with fewer pharmacological interactions and improved tolerability compared with first-generation drugs. Furthermore, second and third-generation anticonvulsant drugs are associated with linear pharmacokinetic profiles and differing mechanisms of action, making them ideal for pluripathological and polymedicated patients. In this report, we highlight the efficacy of one such agent, lacosamide, in five patients with co-morbidities and unusual presentations of epilepsy, including a patient with paraneoplastic encephalitis caused by microcytic lung carcinoma, one with a brain tumour and one with Alzheimer's disease, as well as a case of catamenial epilepsy and one of refractory convulsive status epilepticus. In all patients, lacosamide was associated with a substantial reduction in seizure frequency and effective control of seizure episodes. Treatment was generally well tolerated in all patients, indicating that lacosamide is an effective treatment option for a variety of patients with epileptic seizures.     

New pharmacotherapy for epilepsy

In the majority of cases, epilepsy develops in three phases: (i) initial brain damaging insult (eg, head trauma, stroke, status epilepticus), resulting in (ii) epileptogenesis, which in turn leads to (iii) recurrent seizures (epilepsy). The current treatment of epilepsy, however, focuses exclusively on the prevention or suppression of seizures, ie, the end result of the disease process. Recent findings regarding the sequence of neurobiological changes leading to epilepsy and its molecular basis have raised the question of whether the disease process of epileptogenesis can be prevented, or at least modified in such a way that the epilepsy that develops is milder, easier to treat, non-progressive and without cognitive decline and drug-resistance. Furthermore, if epilepsy has already emerged, can the harmful effects of seizures on the brain be alleviated? Experimental data indicate that attenuation of the severity of the initial insults associated with seizure activity by anti-epileptic drugs improves the outcome by reducing epileptogenesis, resulting in a milder disease. Although there are no true anti-epileptogenic compounds that interfere with the molecular cascades underlying epileptogenesis, there are several new concepts that offer new targets for the treatment of epileptogenesis and disease modification, including neurotrophins, neuropeptides, caspase inhibitors and anti-inflammatory agents.     

轻度胃肠炎伴良性婴幼儿惊厥临床分析和远期随访研究

目的：研究轻度胃肠炎伴良性婴幼儿惊厥（BICE）的临床特点以指导临床治疗。方法：对2009年1月至2010年6月乌鲁木齐市儿童医院神经内科病房收治的21例BICE患儿的临床资料和出院后24～42月的随访结果进行回顾性分析。结果：21例BICE患儿男女比例为1：0．62;年龄8～26个月,其中12～24个月16例（76．2％）。发病季节9—11月份高发。惊厥发生时间无热惊厥后24h内出现急性胃肠炎（BE）者3例,在急性胃肠炎后第1～5天出现惊厥18例,以3d内最多（76．1％）。13例（61．9％）出现2次以上惊厥,平均发作次数为2．1次,9次惊厥因疼痛哭闹所诱发（20．5％）,惊厥持续时间40S～3min,无惊厥持续状态,发作形式为全面强直一阵挛发作。4例有热性惊厥家族史。发作间期监测V—EEG,3例睡眠期见两枕部、中央区低-中波幅不典型尖慢波散发,5例见睡眠纺锤波及慢波改变,3例头颅CT示外部性脑积水,其余未见异常。13例（61．9％）大便轮状病毒抗原阳性,8例阴性。出院后18例进行24～42个月随访,无1例复发,精神运动发育正常。结论：BICE1～2岁发病率高,以秋冬季多见。轮状病毒为主要病因,部分患儿有热性惊厥家族史。惊厥多发生在急性胃肠炎病程1～3d,早期频繁发作,但无惊厥持续状态,发作形式为全身强直一阵挛发作,发作间期EEG及头颅影像学正常。预后良好。     

Anticonvulsant therapy for status epilepticus

AIMS: To determine whether a particular anticonvulsant is more effective or safer than another or placebo in patients with status epilepticus, and to summarize the available evidence from randomized controlled trials, and to highlight areas for future research in status epilepticus. METHODS: Randomized controlled trials of participants with premonitory, early, established or refractory status epilepticus using a truly random or quasi-random allocation of treatments were included. RESULTS: Eleven studies with 2017 participants met the inclusion criteria. Lorazepam was better than diazepam for reducing risk of seizure continuation [relative risk (RR) 0.64, 95% confidence interval (CI) 0.45, 0.90] and of requirement of a different drug or general anaesthesia (RR 0.63, 95% CI 0.45, 0.88) with no statistically significant difference in the risk of adverse effects. Lorazepam was better than phenytoin for risk of seizure continuation (RR 0.62, 95% CI 0.45, 0.86). Diazepam 30 mg intrarectal gel was better than 20 mg in premonitory status epilepticus for the risk of seizure continuation (RR 0.39, 95% CI 0.18, 0.86). CONCLUSIONS: Lorazepam is better than diazepam or phenytoin alone for cessation of seizures and carries a lower risk of continuation of status epilepticus requiring a different drug or general anaesthesia. Both lorazepam and diazepam are better than placebo for the same outcomes. In the treatment of premonitory seizures, diazepam 30 mg intrarectal gel is better than 20 mg for cessation of seizures without a statistically significant increase in adverse effects. Universally accepted definitions of premonitory, early, established and refractory status epilepticus are required.     

儿童睡眠癫痫电持续状态的临床与脑电图变化

目的探讨儿童睡眠癫痫电持续状态(ESES)临床和脑电图变化。方法收集2009年6月至2011年8月本院诊断ESES的患儿31例,分析其临床资料。结果 21例患儿单药控制临床发作疗效欠佳,丙戊酸钠联合用药治疗反应良好,首发年龄越小,则发作和EEG异常的持续时间越长。药物及激素治疗效果越差。13例(42%)予甲泼龙冲击治疗,9例(69%)在甲泼尼龙冲击疗程结束后癫痫发作控制,或发作减少50%以上,3例(23%)发作无改善。5例(38%)神经心理损伤及运动倒退情况明显好转,2例(15%)好转半年后再次出现神经心理倒退,6例(46%)较治疗前无变化。结论甲泼尼龙对ESES临床治疗疗效不一。对于消除中央区-颞区电持续续状态效果明显,但对特发性枕区癫痫伴ESES现象及年龄<2岁癫痫患儿疗效欠佳。