丙戊酸钠脑病1例报告

现报告丙戊酸钠脑病1例如下.1病例男,45岁.因"发作性四肢抽搐40年,加重2d"于2010年6月10日入院.患者5岁始出现发作性四肢抽搐伴意识丧失、尿便失禁,每次发作持续约1 ～3 min,诊断为原发性癫(癎),予口服苯妥英钠治疗;后因控制欠佳逐步调整为苯妥英钠、苯巴比妥及氯硝西泮联合治疗.入院前1个月患者不规则服药,入院前2d患者抽搐伴意识丧失再发,持续30 min未缓解,拟"癫(癎)持续状态"入急诊室治疗,予地西泮、甘露醇等治疗后症状缓解.但此后2d内患者四肢抽搐反复发作而入院.查体:神志清晰,认知功能正常,查体无异常体征.血常规、肝肾功能、血糖、电解质及苯妥英钠与苯巴比妥血药浓度均正常.入院后再次出现抽搐伴意识丧失发作持续15 min未缓解,故予丙戊酸钠400 mg静注,继以1 mg/(kg·h)静滴维持;抽搐控制,意识恢复.次日将丙戊酸钠改为1 g/d口服,此后1周无癫(癎)发作.入院第9d患者出现嗜睡及阵发性右上肢抽动,第10 d表现为昏睡,肢体抽动较前频繁;第11d昏迷并反复出现抽搐.肝功能、肾功能、电解质及血糖均正常,血丙戊酸钠浓度为65.34 mg/L(50～100 mg/L),血氨263μmol/L(18～72 μmol/L).EEG示弥漫性高波幅慢波及中等波幅尖波.头颅MRI示两侧额叶、颞叶、岛叶及基底节区片状T2WI高信号、弥散加权成像(DWI)为高信号病灶,T1WI增强后扫描无强化.     

托吡酯导致高氨血症1例报告

<正>1临床资料患者,男,65岁,因3 h前四肢抽搐1次于2014年9月22日入院。患者3 h前突发四肢抽搐,意识丧失,头眼右偏,持续约2 min后抽搐自行缓解。既往高血压史8 y;2型糖尿病史4 y;脑梗死史4 y,遗留左肢麻木;癫痫史2 y,服用拉莫三嗪100 mg/次,2次/d,因发作未完全控制于5 m前加用托吡酯50 mg/次,2次/d,加用托吡酯后出现反应迟钝。入院查体:BP:120/80 mmH g(1 mmH g=0.133 kP a),神清,精神萎     

遗传性血浆蛋白C缺陷症致大脑静脉窦血栓形成一例

临床资料 患者,女性,30岁,因"突发左侧肢体无力伴四肢抽搐1d余"于2011年8月收住我科.患者入院前1d在工作时突发左侧肢体乏力,伴有头痛.数分钟后出现双上肢屈曲,双下肢伸直,继而四肢抽搐,意识不清,症状持续2 min后缓解;发病1h后至外院摄头颅CT示右侧额顶叶出血,诊治(具体不详)过程中再发上述发作1次.发病4h后收住我院治疗.入院时体检:体温37℃,脉搏70次/min,呼吸20次/min,血压:125/75 mm Hg(1 mm Hg =0.133 kPa);意识模糊,双侧瞳孔对称等大,对光反射灵敏,肌力、痛觉检查欠配合.腱反射双侧对称(++),双侧病理征阴性.既往体健,发病前半个月曾有间断服用避孕药物去氧孕烯炔雌醇片.入院诊断考虑:(1)脑出血,右侧顶叶;(2)症状性痫性发作.入院后查头颅MRI及磁共振静脉造影示两额顶叶多发脑肿胀及出血,上矢状窦血栓形成(图1).予低分子质量肝素抗凝等治疗后复查磁共振静脉成像示上矢状窦前部显示良好.     

卡马西平中毒致癫癎持续状态一例报告

临床资料:患者女性,34岁,以意识不清3h ,伴肢体抽搐1h于2 0 0 3年9月14日入院。患者于入院前3h ,因与家人争吵后服用卡马西平(CBZ)约10 0片后出现意识不清,于入院前1h突发肢体抽搐,发作时眼球上吊、角弓反张、牙关紧闭、颜面青紫,约10min自行缓解,仍意识不清,反复发作4次,小便失禁。既往癫病史10余年,间断服用卡马西平,已基本控制发作。查体:血压130 / 80mmHg(1mmHg =0 133kPa) ,意识不清,双瞳孔散大,直径5 5mm ,光反应迟钝,口唇青紫,牙关紧闭,双肺呼吸音清晰,心律齐,心率10 6次/min ,未闻及杂音。双侧Babinski征( )。实验室检查:血…     

睑阵挛伴失神癫癇发作1例报告

睑阵挛伴有或不伴有失神癫发作 ,在 2 0 0 1年国际癫发作分类中单独列为泛化性癫发作的一种类型。我院电视录像脑电图 (videoEEG)监测诊断 1例睑阵挛伴失神癫发作 ,现报告如下。1　资料1 1　临床资料 :患者男性 ,13岁。因“反复发作性眨眼、复视 3年 ,伴发作意识丧失、四肢抽搐”于 1999年 1月 13日入院。患者1996年始有反复眼睑快速跳动 ,伴复视发作 ,每日发作数次至数十次 ,持续数秒至十余秒 ,神志清楚。期间伴有意识丧失 ,四肢抽搐发作 ,1～ 2次 /月 ,抽搐发作有时发生于反复眨眼持续长时间后出现 ,曾使用卡马西平和苯巴比妥治…     

基底动脉支架内急性闭塞静脉加动脉介入溶栓抢救成功一例

患者男性,64岁,因"言语不利、左侧肢体活动不利20 d"于2006年7月21日入院.既往有高血压病史2年.入院查体:血压160/100 mm Hg(1 mm Hg=0.133 kPa),意识清楚,言语尚可,脑神经检查未见明显异常,颈软无抵抗.四肢肌力、肌张力正常,双下肢病理征可疑阳性.化验示血常规正常.人院后行全脑血管造影示基底动脉近心端狭窄95%,遂行球囊扩张及支架植入术,术后造影见基底动脉近心端狭窄消失,远端血流恢复正常.术后口服氯吡格雷75 mg/d、阿司匹林100 mg,每日3次,低分子肝素钙0.4 ml皮下注射1次/12 h(共2 d).     

癫持续状态继发垂体前叶功能减退一例

临床资料患者女性,36岁,因“发作性抽搐10年余,再发伴呼之不应6h”于2003年4月25日就诊于四川大学华西医院。10余年前,患者因发作性四肢抽搐伴意识丧失在当地医院诊断为癫强直阵挛发作,予抗癫药物(具体不详)治疗后控制良好,4年前自行停药。1个月前,患者无明确诱因再次出现强直阵挛发作,当地医院给予丙戊酸钠0.2g,每日2次口服,入院前3d,患者连续值夜班并漏服药物2次,于入院前6h出现呼之不应、双目上视、牙关紧闭、口吐白沫、口唇发绀,伴有四肢抽搐及小便失禁,持续约2min,每间隔20min左右重复发作,发作间期仍呼之不应,持续约6h,直至就诊于…     

肌阵挛发作 癫 共济失调

<正>病历摘要患者男性,16岁。发作性意识丧失伴肢体抽搐4年、双上肢抖动2年、加重2个月,于2013年9月4日入院。患者于4年前玩游戏时出现双眼反复眨眼,随即意识丧失、呼之不应,伴四肢抽搐、双眼上翻、面部发紫,无大小便失禁和舌咬伤,每次发作持续约2 min后自行缓解。当地医院诊断为"癫",予左乙拉西坦(开浦兰)500 mg(2次/d)口服后仍间     

DSA示穿支动脉发育不良的内囊预警综合征1例报告

<正>1临床资料患者,男,44岁。因发作性右侧肢体活动不灵1 y加重1d于2015年9月5日入院,近1 y反复出现右侧肢体活动不灵,约7~8次,每次发作约持续数小时,最长时间约10 h后完全缓解;既往史:发现高血压病4 y,最高血压150/100 mmHg,平时服用"施慧达",血压维持约120~130/90 mm Hg;入院时神经科查体未见明显异常。入院美国国立卫生研究院     

以癔症样发作为表现的苯妥英钠中毒1例

正1病例患者,男性,75岁。因"发作性四肢抽搐、神智不清55年,下肢不能行走、情绪不稳2个月"入院。患者55年前出现发作性四肢抽搐,伴意识不清、口唇咬破、小便失禁,诊断为癫痫,多年来一直服苯妥英钠片0. 1g,3次/d、鲁米那钠片30 mg,2次/d治疗,症状控制平稳。近10年来患者反复出现头晕、恶心于当地医院神经内科门诊就诊,并于2008年4月、2010年8月、2010年10月、2011年8月多次因发作性眩     

Epilepsy and anomalies of neuronal migration: MRI and clinical aspects

Neuronal migration disorders are the result of disturbed brain development. In such disorders, neurons are abnormally located. In diagnosing these conditions, magnetic resonance imaging is superior to any other imaging technique. This enables us to improve our knowledge of the clinical correlates of neuronal migration. With reference to migrational disorder, a retrospective study of all 303 patients with epileptic seizures referred for magnetic resonance imaging during a 3-year period was performed, 13 patients (aged 12-41, mean age 27) were identified. They represent 4.3% of the entire study group. Of the patients with known epilepsy, 6.7% and of the mentally retarded, 13.7% had migrational disorders. Four patients had schizencephaly as the dominant finding, one was classified as hemimegalencephaly, 2 had isolated heterotopias, and 6 had localized pachy- and/or poly-microgyria. The clinical pictures are complex. Ectopias of grey matter are recognised foci of epilepsy, but from an epileptological and a clinical viewpoint little attention has been given to these disorders. The present study shows that malmigration is not rare in epilepsy patients, especially not in the mentally retarded.     

Hepatic Considerations in the Use of Antiepileptic Drugs

Summary: Virtually all of the major antiepileptic drugs (AEDs) can cause hepatotoxicity, although fatal hepatic reactions are rare. The mechanisms, incidences, and risk profiles for such reactions differ from drug to drug. With carbamazepine and phenytoin, hepatotoxicity may be due to drug hypersensitivity. Although the profiles of patients at risk have not been well-defined for these two antiepileptic drugs, it would appear from reports in the literature that older adolescents and adults are at higher risk than children of developing serious or fatal hepatotoxicity. Once hepatotoxicity develops, mortality rates are 10–38% with phenytoin and 25% for carbamazepine. The risk profile for valproate fatal hepatotoxicity has been more clearly defined. Those at primary risk of fatal hepatic dysfunction are children under the age of 2 years who are receiving multiple anticonvulsants and also have significant medical problems in addition to severe epilepsy. The risk is considerably lower for patients over the age of 2 years on valproate monotherapy. In contrast to the risk profile with other AEDs, adults receiving valproate as monotherapy have the lowest risk of hepatotoxicity. Fatal hepatic dysfunction coincident with valproate may be the result of aberrant drug metabolism. Concomitant use of AEDs that induce microsomal P450 enzymes (e.g., phenytoin and phenobarbital) may enhance the production of a toxic metabolite, and hence the greater risk of hepatotoxicity with polypharmacy.     

Vascular Malformations and Epilepsy: Clinical Considerations and Basic Mechanisms

Summary: Vascular malformations (VMs) are associated with epilepsy. The natural history of the various VMs, clinical presentation, and tendency to provoke epilepsy determine treatment strategies. Investigations have probed the mechanisms of epileptogenesis associated with these lesions. Electrophysiologic changes are associated with epileptogenic cortex adjacent to VMs. Putative pathophysiologic mechanisms of epileptogenesis include neuronal cell loss, glial proliferation and abnormal glial physiology, altered neurotransmitter levels, free radical formation, and aberrant second messenger physiology.     

Classification of methods in transcranial Electrical Stimulation (tES) and evolving strategy from historical approaches to contemporary innovations

Transcranial Electrical Stimulation (tES) encompasses all methods of non-invasive current application to the brain used in research and clinical practice. We present the first comprehensive and technical review, explaining the evolution of tES in both terminology and dosage over the past 100 years of research to present day. Current transcranial Pulsed Current Stimulation (tPCS) approaches such as Cranial Electrotherapy Stimulation (CES) descended from Electrosleep (ES) through Cranial Electro-stimulation Therapy (CET), Transcerebral Electrotherapy (TCET), and NeuroElectric Therapy (NET) while others like Transcutaneous Cranial Electrical Stimulation (TCES) descended from Electroanesthesia (EA) through Limoge, and Interferential Stimulation. Prior to a contemporary resurgence in interest, variations of transcranial Direct Current Stimulation were explored intermittently, including Polarizing current, Galvanic Vestibular Stimulation (GVS), and Transcranial Micropolarization. The development of these approaches alongside Electroconvulsive Therapy (ECT) and pharmacological developments are considered. Both the roots and unique features of contemporary approaches such as transcranial Alternating Current Stimulation (tACS) and transcranial Random Noise Stimulation (tRNS) are discussed. Trends and incremental developments in electrode montage and waveform spanning decades are presented leading to the present day. Commercial devices, seminal conferences, and regulatory decisions are noted. We conclude with six rules on how increasing medical and technological sophistication may now be leveraged for broader success and adoption of tES.     

Carbamazepine Efficacy and Utilization in Children

Summary: Carbamazepine is effective for preventing partial and generalized tonic-clonic seizures in children. Although absence epilepsies are more common in children than adults, an estimated 80% of children with epilepsy have seizure types or epilepsies that are potentially responsive to carbamazepine. The differential diagnosis of ictal staring is an especially important issue in children because absence and atypical absence seizures are more prevalent in children than adults. Age-related pharmacokinetic differences and drug interactions are major considerations in children. On average, children have higher clearance rates of carbamazepine, shorter half-lives, and higher ratios of carbamazepine-10, 11-epoxide to carbamazepine than adults. In addition, children with severe epilepsy are more likely to require multiple-drug therapy, which can lead to complex drug interactions. When carbamazepine is administered along with valproate, drug protein binding interactions can cause intermittent side effects.     

Neonatal Seizures: Problems in Diagnosis and Classification

Summary: The clinical identification of neonatal seizures is critical for the recognition of brain dysfunction; however, diagnosis is often difficult because of the poorly organized and varied nature of these behaviors. Current classification systems are limited in their ability to communicate motor, autonomic, and electroencephalo-graphic features of seizures precisely and to provide a basis for uniform effective diagnosis, therapy, and determination of prognosis. Recent investigations of neonates, utilizing bedside electroencephalographic/polygraphic/ video monitoring techniques, have provided the basis for improved diagnosis and classification of seizures in the newborn. These studies have demonstrated that not all clinical phenomena currently considered to be seizures require electrocortical epileptiform activity for their initiation or elaboration. In addition, the specific clinical character of the phenomena considered to be seizures, the clinical state of the infant, and the character of the EEG indicate the probable pathophysiological mechanisms involved and suggest probable etiologies, prognosis, and therapy. Similarities between animal models that demonstrate reflex physiology and neonates with motor automatisms and tonic posturing suggest that these clinical behaviors may not be epileptic in origin but, rather, primitive movements of progression and posture mediated by brainstem mechanisms. Although not all clinical behaviors currently considered to be neonatal seizures may have similar pathophysiological mechanisms, they are clinically significant because they all indicate brain dysfunction.     

Valproate Monotherapy in the Management of Generalized and Partial Seizures

Summary: For decades, therapeutic tradition has promoted the concept of polypharmacy in the management of epilepsy. In recent years, however, studies have shown that, for most patients, monotherapy can provide comparable or better seizure control than administration of multiple anticonvulsants, while diminishing the potential for adverse reactions, drug interactions, and poor compliance. Valproate is an important monotherapeutic agent that is highly effective in the control of idiopathic primary and secondarily generalized epilepsies, and partial seizures that do not generalize. Comparative studies have found that valproate is at least as effective as phenytoin and carbamazepine in the treatment of generalized and partial seizures. Given the similar efficacy, other factors such as pharmacokinetics and side effects may therefore determine anticonvulsant selection for monotherapy.     

Un nouveau cadre conceptuel de travail pour la psychiatrie

In an attempt to place psychiatric thinking and the training of future psychiatrists more centrally into the context of modern biology, the author outlines the beginnings of a new intellectual framework for psychiatry that derives from current biological thinking about the relationship of mind to brain. The purpose of this framework is twofold. First, it is designed to emphasize that the professional requirements for future psychiatrists will demand a greater knowledge of the structure and functioning of the brain than is currently available in most training programs. Second, it is designed to illustrate that the unique domain which psychiatry occupies within academic medicine, the analysis of the interaction between social and biological determinants of behavior, can best be studied by also having a full understanding of the biological components of behavior.