血液透析相关性癫痫样发作临床研究

目的：探讨血液透析（血透）相关性癫痫样发作（HAS）的危险因素、临床特点以及防治措施。方法：回顾性分析总结1995年6月至2005年6月534例血透患者中15例有HAS病史的血透患者的临床资料。结果：HAS发病率为2．80％（15／534），发作类型为肌阵挛发作（9例，60．00％）、强直阵挛发作（3例，20．00％）、癫痫持续状态（2例，13．33％）、单纯部分发作（1例，6．67％）。危险因素贫血和促红细胞生成素（EPO）使用存在于14例患者中，其余的因素如高血压、电解质异常、药物使用存在率不高。地西泮治疗有效，复发率低。结论：贫血和EPO使用是HAS．发作的危险因素，肌阵挛发作是HAS的主要类型，地西泮治疗有效。     

青少年肌阵挛癫痫21例临床特点及脑电图分析

目的：总结青少年肌阵挛癫痫（JME）的临床及脑电图特点。方法：对21例JME患者的临床资料进行回顾性分析。结果：21例JME患者100%出现肌阵挛发作（MS）,81.0%（17/21）的患者有全面强直阵挛发作（GTCS）,28.6%（6/21）的患者有失神发作（AB）,EEG检查异常率为71.4%（15/21）,影像学均无异常。结论：JME是一种较常见的特发性全面性癫痫,详细询问病史结合规范的脑电图检查可提高检出率。     

妥泰单药治疗全身强直-阵挛发作34例临床研究

目的:研究妥泰单药治疗全身强直-阵挛发作癫痫的临床疗效和耐受性。方法:对34例全身强直-阵挛发作患者予以妥泰单药治疗24周,以治疗前3月的平均每月癫痫发作频率与单药治疗后9～24周平均每月癫痫发作频率进行比较,并观察脑电图的改变和药物耐受性。结果:单药治疗24周后有 20例(58.9％)癫痫发作频率较治疗前减少 75％以上,其中 9例(26.5％)现察期间停止发作,8例(23.5％)发作频率减少74～50％,总有效率为82.4％;治疗后脑电图有明显改善者占56.5％,与治疗前比较有显著性差异(P<0.001);无明显不良反应。结果:妥泰单药治疗全身强直-阵挛发作的总有效率与丙戊酸、苯妥英钠相近,治疗后脑电图有显著性改善,有良好耐受性。为全身强直-阵挛发作单药治疗的有效治疗药物之一。     

咪达唑仑持续静脉滴注治疗癫痫频繁发作65例疗效观察及护理

目的:总结咪达唑仑持续静脉滴注在治疗癫痫频繁发作中的疗效、不良反应及护理方法.方法:对65例癫痫频繁发作的患儿静脉应用咪达唑仑治疗,首先缓慢静脉推注1次(0.1～0.15 mg/kg),最大剂量＜3 mg,然后以1.0 μg/(kg·min)静脉维持,根据发作情况调整用药剂量,最大维持剂量为5.0 μg/(kg·min).惊厥控制24 h后逐渐减量直至停药.临床观察其疗效及不良反应.结果:24 h内控制发作42例(64.62%),减量前平均用药剂量为(1.75±0.38)μg/(kg·min);48 h内控制61例(93.85%),减量前平均用药剂量为(2.34±1.05)μg/(kg·min);72 h内控制61例(93.58%),减量前平均用药剂量为5.0 μg/(kg·min).用药期间不良反应:嗜睡58例(89.23%),共济失调18例(27.69%),呼吸道分泌物增多13例(20.00%),烦躁6例(9.23%),轻度血压下降37例(4.62%),1例在推注咪达唑仑过程中出现呼吸骤停.结论:咪达唑仑可快速、有效控制癫痫频繁发作,尤其是对全面性强直(或强直阵挛)发作疗效更为确切,在癫痫患儿的快速撤药或换药中可广泛应用.对不良反应的密切观察及临床精心护理也是治疗成功不可缺少的因素.     

42例缺血性卒中后癫痫发作危险因素探讨

目的：研究缺血性卒中患者继发早期癫痫发作和晚期癫痫发作的发病率、发作类型及缺血性卒中继发癫痫发作的临床危险因素。方法：分析山西省人民医院近3年来首发缺血性卒中的408例患者的年龄、性别、入院时意识、糖尿病、高血压、心源性疾病和卒中部位等的临床特征,随访6~12个月,其中缺血性卒中后继发癫痫发作患者42例,未继发癫痫发作患者366例。缺血性卒中后癫痫发作的患者依据癫痫发作的发生时间分为早期癫痫发作组（18例）和晚期癫痫发作组（24例）。分析缺血性卒中后早期癫痫发作和晚期癫痫发作的发病率、发作类型以及缺血性卒中后发生继发癫痫发作的临床危险因素。结果：缺血性卒中后癫痫发作的发病率为10.3%（42/408）,其中早期癫痫发作的发病率为4.4%（18/408）;晚期癫痫发作的发病率为5.9%（24/408）。早期癫痫发作的50.0%（9/18）为全面性强直-阵挛发作,晚期癫痫发作的58.3%（14/24）为单纯部分性发作。缺血性卒中后癫痫发作组与非癫痫发作组的临床特征经统计学比较,两组间心源性脑栓塞病例的发生率和累及皮质梗死的发生率比较差异有显著性（P〈0.05）。结论：缺血性卒中后早期癫痫发作以全面性发作为主,晚期癫痫发作以单纯部分性发作为主;心源性脑栓塞和累及皮质梗死是缺血性卒中后癫痫发生的危险因素。     

儿童脑损伤与创伤后癫痫

目的：研究住院康复的严重脑损伤儿童创伤后癫痫的发率、可能的危险因素及其发展。方法：回顾性分析７年所有入院儿童的病例资料和临床脑图记录，研究脑损伤后晚期癫痫儿童的情况。结果：１９９１年６月１日～１９９８年２月２８日共１０２例儿童受住院康复，随访时间为１８个月～８年，在脑损伤后８个月～５的时间里共９例患者出现创伤后癫痫，其中３例在损伤后第一曾有过强直－阵挛发作。其它的危险因素检测包括患者的年龄脑损伤原因、最初的Glasgow昏迷量表评分、神经图像的结果、气支持的时间。只有早期强直－阵挛发作（P＝０．００２…     

癫痫全身强直阵挛发作与自动症发作肌酶变化分析

目的:探讨全身强直阵挛发作与自动症发作时血清肌酶含量的变化。方法:癫痫患者86例,分成全身强直阵挛组64例和自动症发作组22例,同期门诊健康体检者28例为对照组;检测并比较癫痫发作后72 h内的血清肌酶浓度。结果:全身强直阵挛组及自动症发作组的乳酸脱氢酶(LDH)及肌酸磷酸激酶同工酶MB(CK-MB)高于对照组(P<0.05),全身强直阵挛组羟丁酸脱氢酶(HDBH)高于自动症发作组(P<0.05)。结论:全身强直阵挛发作与自动症发作时血清部分肌酶的含量存在变化。     

中年肌阵挛癫痫的预后及影响因素分析

目的探讨中年肌阵挛癫痫患者预后状况,并对其影响因素进行统计学分析。方法收治200例中年肌阵挛癫痫患者的资料,经治疗后200例中103例病情缓解,另97例病情未见好转,分别列入缓解组及未缓解组。应用统计学方法对所有研究对象的预后发作次数、患者文化程度、离院距离、肌阵挛癫痫发作类型、脑电图、头颅影像学检测结果及接受手术方式进行统计分析。结果肌阵挛癫痫发作次数5次以上、患者距离医院的距离在100km以上、头颅影像学检查结果阳性、手术方式等是中年肌阵挛癫痫患者预后的主要影响因素。结论中年肌阵挛癫痫患者的预后与多种因素有关,有针对性地对可能的危险因素进行预防,对于改善患者预后有很好的临床意义。     

干细胞移植中癫痫发作1例的护理

癫痫全面性强直（阵挛发作）是一组脑神经元异常放电所致的脑部疾病，它以全身抽搐和意识障碍为特征，先后经强直期、阵挛期、惊厥后期。自发作开始至意识恢复经过数分钟，醒后感觉头痛、疲乏，对抽搐过程无忆记。我们诊治1例脐血干细胞移植回输过程中的患在11h内有6次癫痫发作，现报告如下。     

全面强直阵挛癫痫静息态功能连接脑网络研究

目的 采用静息态功能MRI (fMRI)功能连接分析技术,观察全面强直阵挛癫痫患者发作间期静息态脑网络的改变,探讨强直阵挛癫痫的病理生理机制.方法 52例全面强直阵挛癫痫患者与57名止常志愿者(对照组)参与了,本研究.采集闭眼静息态fMRI数据.分别以双侧丘脑,双侧后扣带皮质为种子点,观察丘脑网络、默认网络(DMN)在患者中的功能改变.结果 组内单样本t检验结果提示,以双侧丘脑为种子点的功能连接模式主要分布于额顶叶,而以双侧后扣带皮质为种子点的功能连接模式主要表现为默认网络.进一步组间比较发现,患者的丘脑与双侧运动皮层及右侧岛叶的功能连接增强,而与DMN脑区及基底节的功能连接减弱;而DMN内部与后扣带皮质的功能连接在双侧颞极、内侧前额叶和缘上回的功能连接减弱,而与双侧角回、丘脑和左侧额上回的功能连接增强.结论 丘脑是强直阵挛癫痫网络的重要节点,它与运动皮层间增强的功能连接可能与癫痫发作时患者肌肉的强直阵挛有关.而默认网络内功能连接的异常可能与癫痫发作时的意识丧失有关.即使在发作间期,全面强直阵挛癫痫的脑功能也有着显著改变.     

How to evaluate the patient after a first seizure

The primary care physician who is approached by a patient or the parents of a patient who has had a first seizure must determine that a seizure has indeed occurred and then ascertain the type of seizure before any treatment is prescribed. While there is a variable recurrence risk after generalized tonic-clonic and partial seizures, certain types, such as absence seizures, have a high recurrence risk. Studies disagree on whether all patients with a first seizure require treatment, especially considering the side effects that can accompany anticonvulsant drugs. If the diagnosis is uncertain, waiting for a second seizure before starting treatment is usually a good idea. Electroencephalography should be done and, depending on results, followed by electrocardiography, a fasting glucose test, and/or computed tomography. If the diagnosis is certain, computed tomography or magnetic resonance imaging is useful in ruling out structural lesions as the cause of the seizure. The dosage of an anticonvulsant drug that is appropriate for the patient can then be determined by slowly increasing the dosage of one drug at a time until the patient becomes seizure-free without clinical toxicity.     

Bilateral pneumothoraces and pneumomediastinum complicating a generalized tonic-clonic seizure

Patients often present to the emergency department following a generalized tonic-clonic seizure, particularly of new onset. Complications associated with seizures usually arise from injuries sustained from loss of consciousness or during convulsive activity. This report describes a patient with an idiopathic seizure who developed postictal alveolar edema and delayed bilateral pneumothoraces and pneumomediastinum. A literature search revealed only 1 other case of this potentially life-threatening pulmonary complication from seizures.     

Selective frontal,parietal, and temporal networks in generalized seizures

Are "generalized" seizures truly generalized? Generalized tonic-clonic seizures are classified as either secondarily generalized with local onset or primarily generalized, without known focal onset. In both types of generalized seizures widespread regions of the nervous system engage in abnormally synchronous and high-frequency neuronal firing. However, emerging evidence suggests that all neurons are not homogeneously involved; specific nodes within the network may be crucial for the propagation and behavioral manifestations of generalized tonic-clonic seizures. Study of human tonic-clonic seizures has been limited by problems with patient movement and variable seizure types. To circumvent these problems, we imaged generalized tonic-clonic seizures during electroconvulsive therapy, in which seizure type and timing are well controlled. (99m)Tc-hexamethylpropylene amine oxime injections during seizures provide a "snapshot" of cerebral blood flow that can be imaged by single photon emission computed tomography (SPECT) after seizure termination. Here we show that focal regions of frontal and parietal association cortex show the greatest relative signal increases. Involvement of the higher-order association cortex may explain the profound impairment of consciousness seen in generalized seizures. In addition, focal involvement of the dominant temporal lobe was associated with impaired retrograde verbal memory. Similar focal increases were also seen in imaging of spontaneous secondarily generalized tonic-clonic seizures. Relative sparing of many brain regions during both spontaneous and induced seizures suggests that specific networks may be more important than others in so-called generalized seizures.     

Glass ingestion from fracture of a laryngoscope bulb.

A 22-month-old child had a generalized tonic-clonic seizure during attempted orotracheal intubation and broke the laryngoscope bulb with his teeth. The glass was swallowed but passed uneventfully through the gastrointestinal tract. The possibility of this unusual complication should be considered when patients at risk for seizures are intubated by the orotracheal route.     

Sudden unexpected death in a mouse model of Dravet syndrome

Sudden unexpected death in epilepsy (SUDEP) is the most common cause of death in intractable epilepsies, but physiological mechanisms that lead to SUDEP are unknown. Dravet syndrome (DS) is an infantile-onset intractable epilepsy caused by heterozygous loss-of-function mutations in the SCN1A gene, which encodes brain type-I voltage-gated sodium channel Na_V1.1. We studied the mechanism of premature death in Scn1a heterozygous KO mice and conditional brain- and cardiac-specific KOs. Video monitoring demonstrated that SUDEP occurred immediately following generalized tonic-clonic seizures. A history of multiple seizures was a strong risk factor for SUDEP. Combined video-electroencephalography-electrocardiography revealed suppressed interictal resting heart-rate variability and episodes of ictal bradycardia associated with the tonic phases of generalized tonic-clonic seizures. Prolonged atropine-sensitive ictal bradycardia preceded SUDEP. Similar studies in conditional KO mice demonstrated that brain, but not cardiac, KO of Scn1a produced cardiac and SUDEP phenotypes similar to those found in DS mice. Atropine or N-methyl scopolamine treatment reduced the incidence of ictal bradycardia and SUDEP in DS mice. These findings suggest that SUDEP is caused by apparent parasympathetic hyperactivity immediately following tonic-clonic seizures in DS mice, which leads to lethal bradycardia and electrical dysfunction of the ventricle. These results have important implications for prevention of SUDEP in DS patients.     

Benign juvenile myoclonic epilepsy

Two patients with long-standing, poorly controlled seizures presented to a university hospital emergency department. Both patients had myoclonic jerks on waking and evidence of absence seizures as well as generalized tonic-clonic seizures. A diagnosis of benign juvenile myoclonic epilepsy was made, and the seizures were controlled with valproic acid.     

Severe attacks of familial hemiplegic migraine, childhood epilepsy and ATP1A2 mutation

We studied four members of a family suffering from typical attacks of familial hemiplegic migraine (FHM) caused by a new mutation, R548C, of ATP1A2 gene in exon 12. One individual had also childhood absence epilepsy and generalized tonic-clonic seizures (GTCS). GTCS were followed by a severe attack of hemiplegic migraine at four times. Sodium valproate enabled control of both the epileptic seizures and the most severe FHM attacks. This association of FHM and epileptic seizures and their control with the same treatment suggest similar pathophysiological mechanisms.     

癫(癎)患者抑郁障碍发生率及相关因素调查

目的：探讨癫痫患者抑郁发生率和相关危险因素。方法：运用自制问卷对患者的个人及家庭一般情况进行调查记录，采用Zung抑郁自评量表对104例癫痫患者进行筛选、抑郁评定，并对不同因素对癫痫患者抑郁发病率的影响进行比较。结果：104例癫痫患者中有55例52．9％合并有抑郁症状，其中37例（35．6%）有严重抑郁，8例（17．3％）为中、轻度抑郁。复杂性部分发作患者抑郁的患病率为73．5％，明显高于强制-阵挛发作的42．8％，两者差别有统计学意义（P〈O．01）。结论：癫痫患者的抑郁是严重的医疗和社会问题其发生与癫痫发作的类型，频率病程和社会家庭的支持有关。     

Juvenile myoclonic epilepsy presenting as a new daily persistent-like headache

New daily persistent headache (NDPH) is a recognized subtype of chronic daily headache with a unique presentation of a daily headache from onset typically in individuals with minimal or no prior headache history. Various secondary mimics of NDPH have now been documented but at present there has been no association made between primary epilepsy syndromes and new daily persistent-like headaches. A case patient is presented who developed a daily continuous headache from onset who 3 months after headache initiation had her first generalized tonic-clonic seizure. Further investigation into her history and her specific EEG pattern suggested a diagnosis of juvenile myoclonic epilepsy (JME). Her NDPH and seizures ceased with epilepsy treatment. Clinically relevant was that the headache was the primary persistent clinical symptom of her JME before the onset of generalized tonic-clonic seizures. The current case report adds another possible secondary cause of new daily persistent-like headaches to the medical literature and suggests another association between primary epilepsy syndromes and distinct headache syndromes.     

Ertapenem-associated seizures in a peritoneal dialysis patient

OBJECTIVE: To report a case of a patient undergoing peritoneal dialysis who developed refractory seizures after 2 doses of ertapenem. CASE SUMMARY: A 56-year-old white man with end-stage renal disease requiring continuous ambulatory peritoneal dialysis experienced 5 seizures following 2 doses of ertapenem 500 mg given intravenously. The first generalized tonic-clonic seizure occurred 16 hours after the second ertapenem dose and lasted 3 minutes. Three hours after his first seizure, the patient experienced 2 more seizures 15 minutes apart, lasting 3 minutes each. After suffering a fifth seizure, the patient became apneic and pulseless and was not resuscitated, as he had previously requested a "do not resuscitate" status. DISCUSSION: Carbapenem treatment has been associated with simple partial, complex partial, and generalized tonic-clonic seizures, with generalized seizures representing the most frequently occurring type. Safety data from 7 published clinical trials of ertapenem revealed a seizure incidence of 0.18%. To our knowledge, there are no previously published reports of ertapenem neurotoxicity in patients undergoing peritoneal dialysis. Moreover, little information is available regarding the pharmacokinetics of carbapenems in end-stage renal disease. Ertapenem pharmacokinetics were not tested in any patients receiving peritoneal dialysis during published clinical trials. CONCLUSIONS: Our patient experienced 5 seizures, possibly induced by ertapenem, as validated by the Naranjo probability scale. Clinicians administering ertapenem to patients undergoing peritoneal dialysis should use caution, as clinical experience with the agent is limited and pharmacokinetic data are lacking.