依达拉奉联合降纤酶治疗脑梗死临床疗效观察

目的 观察依达拉奉联合降纤酶治疗急性脑梗死的临床效果及安全性.方法 90例急性脑梗死患者随机分为2组,分别采用降纤酶及依达拉奉联合降纤酶治疗,以疗程3d、7d、14d神经功能缺损程度评分观察疗效.结果 2组病人疗程3d、7d、14d神经功能缺损程度评分及疗效差异有统计学意义.结论 依达拉奉联合降纤酶治疗急性脑梗死安全有效.     

依达拉奉联合降纤酶治疗急性脑梗死疗效观察

目的观察依达拉奉联合降纤酶治疗急性脑梗死的疗效。方法将62例急性脑梗死患者随机分为联合治疗组30例和对照组32例。联合治疗组依达拉奉30 mg静滴,2次/d,降纤酶首日剂量10 U,第3、5天各5 U加入生理盐水250 mL中静滴,共用3次。对照组单用降纤酶,剂量及用法同依达拉奉联合降纤酶组。分别在2组治疗前和治疗后7、14、21 d对患者分别进行神经功能缺损程度评分(ESS)、Barthel指数评分及临床疗效评定。结果 2组治疗后7、14、21 d ESS评分、Barthel指数联合治疗组均优于对照组(P<0.05),21 d后治疗组显效率(60%)、有效率(97%)明显高于对照组的34%、75%(P<0.05)。结论依达拉奉联合降纤酶治疗急性脑梗死疗效显著。     

依达拉奉联合奥扎格雷钠治疗脑梗死临床研究

目的 观察依达拉奉联合奥扎格雷钠治疗脑梗死的疗效及安全性.方法 120例脑梗死患者随机分为2组,分别采用奥扎格雷钠及依达拉奉联合奥扎格雷钠治疗.以疗程14d神经功能缺损程度评分及2个月时日常生活能力指数评分(Barthel)为标准观察疗效.结果 治疗组显效率、总有效率、神经功能缺损程度评分和日常生活能力指数评分改变与对照组比较,差异均有统计学意义(均P<0.05),2组均无明显不良反应.结论 依达拉奉联合奥扎格雷钠治疗脑梗死安全有效,能显著改善患者的预后.     

尤瑞克林联合依达拉奉治疗急性后循环脑梗死疗效观察

目的观察尤瑞克林联合依达拉奉注射液治疗急性后循环脑梗死的疗效。方法将95例急性后循环脑梗死患者随机分为治疗组(尤瑞克林联合依达拉奉)45例和对照组(单用依达拉奉)40例,分别于入院时和治疗后14 d、28 d进行临床神经功能缺损程度(NIHSS)评分,治疗后90 d进行Barthel指数评分;分别在治疗前后测血液流变学并行经颅多普勒(TCD)检查。结果 2组治疗后14 d及28 d神经功能缺损评分均有明显改善,但治疗组与对照组的NIHSS、Barthel指数、血液流变学、TCD变化等比较差异均有统计学意义(P<0.05或P<0.01)。结论尤瑞克林联合依达拉奉可增加急性后循环脑梗死患者的脑血流,改善微循环,并有助于急性后循环脑梗死患者的神经功能恢复。     

依达拉奉注射液联合早期康复训练对急性脑梗死患者智力与记忆恢复的临床效果

目的：探讨依达拉奉注射液联合早期康复训练对急性脑梗死患者智力与记忆恢复的临床疗效。方法80例急性脑梗死患者随机分为治疗组和对照组。治疗组40例，采用依达拉奉注射液联合早期康复训练治疗；对照组予以丹参注射液治疗，不进行早期康复训练。2组均以14 d为一疗程，观察患者临床反应，并以评价患者神经功能缺损的CSS量表和评价日常生活能力的Barthel指数，分析2组临床效果。结果治疗14 d后，治疗组CSS量表评分和Barthel指数均优于对照组，差异有统计学意义（ P＜0.05）。结论依达拉奉注射液联合早期康复训练对急性脑梗死患者神经功能有极大的改善作用，有利于患者智力和记忆力恢复。     

依达拉奉治疗急性脑梗死疗效观察

目的观察依达拉奉治疗急性脑梗死疗效。方法对比分析2组患者治疗前及治疗后7d、14d神经功能缺失评分及疗程满2周后神经功能恢复总有效率。结果治疗组在神经功能恢复及总有效率方面明显优于对照组。结论依达拉奉治疗急性脑梗死疗效确切,有利于急性脑梗死患者神经功能缺损的康复。     

依达拉奉联合氯吡格雷治疗急性脑梗死疗效分析

目的评价依达拉奉注射液联合氯吡格雷治疗急性脑梗死(acute cerebral infarction,ACI)的临床疗效。方法选择发病72 h内的急性脑梗死患者70例,随机分为依达拉奉加氯吡格雷组35例(治疗组)及常规治疗组35例(对照组),进行神经功能缺损评分和日常生活能力(ADL)评分,神经功能缺损评分采用美国国立卫生院卒中量表(NI HSS),ADL评分采用Barthel指数。结果治疗组与对照组NI HSS,ADL评分在治疗后7 d、14 d、21 d均有统计学差异(P0.05)。结论依达拉奉和氯吡格雷联合治疗能有效改善急性脑梗死患者神经功能缺损和日常生活能力,能显著改善预后。     

依达拉奉治疗急性脑梗死76例临床分析

目的 观察依达拉奉治疗急性脑梗死的临床疗效.方法 选择76例急性脑梗死患者,随机分为治疗组42例,对照组34例,2组均给予缺血性脑血管病常规治疗,治疗组同时给予依达拉奉30mg静滴,2次/d,14d为一个疗程.治疗前,治疗后7d、14d、21d分别进行一次神经功能缺损评分、欧洲卒中量表评分、Barthel生活质量评分,观察治疗效果.结果 治疗21d后治疗组总有效率95.24%,对照组总有效率79.41%,2组之间疗效有显著差异(P<0.05).结论 依达拉奉治疗急性脑梗死安全有效,值得临床应用.     

尤瑞克林联合依达拉奉治疗急性大面积脑梗死临床研究

目的探讨尤瑞克林联合依达拉奉治疗急性大面积脑梗死的临床疗效及安全性。方法 180例急性大面积脑梗死患者随机分为对照组、治疗A组、治疗B组,每组各60例,3组均给予抗血小板聚集,脱水降颅内压、他汀、神经营养剂,根据病情调整血压、血糖、防治并发症等常规治疗,治疗A组在常规对照组基础上加用依达拉奉,治疗B组在治疗A组基础上联合尤瑞克林,3组疗程14d。于治疗前和治疗后14d监测3组C反应蛋白(CRP)的变化,治疗前和治疗后14、90d对3组患者进行神经功能缺损(NIHSS)评分、日常生活能力(Barthel指数评分)评定,并评估90d的临床疗效,记录不良反应。结果治疗14d后治疗B组CRP降低较治疗A组及对照组明显(P0.05),治疗B组14d、90d神经功能缺损程度、90d日常生活能力及临床疗效均优于治疗A组及对照组(P0.05),不良反应未明显增加。结论尤瑞克林联合依达拉奉治疗急性大面积脑梗死安全、有效。     

丁苯酞联合依达拉奉治疗急性脑梗死60例疗效观察

目的观察丁苯酞联合依达拉奉治疗急性脑梗死的临床疗效。方法将我院2007-10～2010-10收治的120例急性脑梗死患者随机分为治疗组60例和对照组60例,2组均给予常规治疗,治疗组在此基础上联合应用丁苯酞和依达拉奉,对照组则单独使用依达拉奉,疗程14 d,一个疗程后评价疗效。结果治疗组总有效率93.3%,对照组为68.3%,2组比较差异有统计学意义(P<0.05);治疗14 d后患者神经功能缺损评分比较,治疗组明显优于对照组(P<0.05),且2组均无明显不良反应。结论丁苯酞联合依达拉奉治疗急性脑梗死疗效显著,可快速改善神经功能,且无明显不良反应,值得临床上推广。     

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.