大型听神经瘤显微手术治疗策略(附26例分析)

目的探讨大型听神经瘤的显微手术治疗策略。方法回顾性分析26例大型听神经瘤采用枕下乙状窦后入路显微外科手术切除的经验。结果肿瘤全切除21例（80.8％），次全切除5例（19．2％）。肉眼下面神经解剖保留20例（76．9％），术后House—Brackman面神经功能分级Ⅰ～Ⅱ级10例（38．5％），Ⅲ～Ⅵ级16例（61．5％）。结论采用枕下乙状窦后入路显微外科手术切除大型听神经瘤，面神经可获得解剖和功能的保护，并发症与病死率低，临床疗效良好。     

大型听神经瘤的显微外科手术切除

目的 总结64例大型听神经瘤显微外科手术的体会,探讨面、听神经功能保留的可能性和可行性。方法 59例采用单侧枕下入路,5例巨大型累及岩尖斜坡采用经岩入路,所有病例均采用显微外科技术行肿瘤切除术。结果 肿瘤全切除56例（88％）,次全切除7例,大部切除1例。面神经解剖保留57例（89％）,功能保留43例（67％）。术前尚有听力22例,术后听力保存6例（27％）手术,死亡1例（1．5％）。结论 大部分大型听神经瘤采用显微外科技术可行Ⅰ期全切除和面神经的保留,强调保护桥脑腹外侧静脉丛和小脑前下动脉的重要性。对大型听神经瘤亦应争取面神经和听力的保留。     

听神经瘤手术治疗的临床体会

目的 总结104例听神经瘤手术切除的体会，以提高此类手术的治疗效果。方法 经CT或MRI扫描检查确诊，应用显微外科技术，经枕下-乙状窦后入路行肿瘤切除术。结果 肿瘤全切89例（85．58％），次全切和大部切除15例（14．42％）；术后死亡2例（1．92％）。术中面神经解剖保留89例（85．58％），听神经解剖保留25例（24．04％），术后7例（6．73％）听力保存或有所改善。结论 肿瘤大小与肿瘤全切率及面、听神经保留率密切相关。合适的体位，正确的切除方法及较强的功能保护观念，是提高听神经瘤手术疗效的关键。     

听神经瘤的显微外科治疗和面神经功能保护的探讨

目的 探讨听神经瘤的显微外科手术技巧及保留面神经的技术。 方法 福建医科大学附属第一医院神经外科自2002年8月至2010年12月经枕下乙状窦后（骨瓣成型、锁孔）入路显微手术治疗听神经瘤患者168例,术中在面肌肌电图监测下采取囊内切除与囊壁切除交替进行、双向会合、锐性分离面神经等技术切除肿瘤,并回顾性分析显微手术的技巧和疗效。 结果 肿瘤全切149例(88.69％),部分切除19例(11.31％);面神经解剖学保留146例(86.9％);死亡2例(1.19％)。术后6个月按House Blackmann标准评估面神经功能：Ⅰ、Ⅱ级91例(54.16％),Ⅲ、Ⅳ级52例(30.95％),Ⅴ、Ⅵ级25例(14.89％)。 结论 经枕下乙状窦后（骨瓣成型、锁孔）入路显微手术治疗听神经瘤安全有效;利用术中面肌肌电图监测可以提高面神经解剖保留率;熟练掌握显微手术技巧是全切肿瘤、解剖保留面神经的关键。     

显微外科手术治疗巨大听神经鞘瘤（附32例报告）

目的探讨巨大听神经鞘瘤显微外科手术的方法、疗效及并发症的预防。方法回顾性分析32例巨大听神经鞘瘤的显微外科手术情况。结果所有病例均通过枕下乙状窦后入路显微外科手术切除。肿瘤全切除(SimpsonⅠ~Ⅱ级)30例(93.8%),次全切除(SimpsonⅢ级)2例。面神经解剖保留19例(59.4%),按House-Brackmann标准,面神经功能Ⅰ级9例(28.1%),Ⅱ~Ⅲ级13例(40.6%),Ⅳ级以上8例(25.0%);死亡1例。结论熟练的显微外科手术技术能使巨大听神经鞘瘤获得良好的全切除率,巨大听神经鞘瘤的面神经解剖及功能保留尚有难度,需进一步改善提高。     

102例大型听神经瘤的手术治疗

目的：总结102例大型听神经瘤手术切除的体会，以提高此类肿瘤的手术治疗效果。方法：采用一侧枕下乙状窦后入路切除肿瘤，其中64例采用超声吸引和显微手术治疗。结果：94例（92．2％）肿瘤获全切除。面神经解剖保留87例（85．3％），根据House-Brackmann面神经功能分级标准，I－Ⅱ级47例（54．1％），Ⅲ-Ⅳ级35例（40．2％），Ⅴ-Ⅵ级5例（5．7％）。结论：采用显微手术技术，绝大多数听神经瘤均可在保留面神经解剖完整的前提下获得手术全切除。     

听神经瘤显微手术与面神经保护

目的探讨大中型听神经瘤的显微手术治疗及面神经保护技巧。方法自2007年9月至2011年9月在面神经电生理监测下采用枕下乙状窦后入路显微手术切除大中型听神经瘤142例。结果肿瘤全切除136例（95．7％）,次全切除6例（4．3％）。术中面神经解剖保留132例（93．0％）,面神经与肿瘤粘连紧密无法保留10例（7．0％）。本组无长期昏迷及死亡病例。术后出现颅内感染3例、后组颅神经受损7例、眼睑闭合不能90例,无脑脊液漏病例。所有病人术后均随访3个月到2年,无术后复发病例;按House—Braekmann分级评估面神经功能,Ⅰ～Ⅱ级78例（54．9％）,Ⅲ～Ⅳ级53例（37．3％）,Ⅴ～Ⅵ级11例（7．8％）。结论充分了解桥脑小脑角区显微解剖知识,特别是了解听神经瘤与面神经的解剖关系,有助于提高手术效果。娴熟的操作技巧是手术成功的关键,术中监测及面神经的保留有助于面神经功能的保护。     

大中型听神经瘤的显微手术治疗及面神经的保护

目的 探讨显微手术治疗大中型听神经瘤的疗效及保护面神经的方法。方法 23例大中型听神经瘤（直径>2 cm）患者均在电生理监测下采用枕下乙状窦后入路显微手术切除,术后对其面神经功能进行随防。结果 肿瘤全切除15例,近全切除8例;面神经保留22例,保留率为95.7%;术后面神经功能House-Brackmann分级:1级3例,2级10例,3级6例,4级2例,5级1例,6级1例。术后所有病人随访3~24月,发生脑脊液漏者1例,长期昏迷1例,无死亡病例。结论 显微手术与面神经的电生理监测为全切除大中型听神经瘤并保留面神经提供了保障。     

大型、巨大型听神经瘤的显微手术治疗

目的 探讨显微神经外科技术在大型听神经瘤切除术中的应用。方法 通过对285例大型、巨大型听神经瘤显微外科手术治疗的病例进行统计分析。结果 应用显微外科技术将肿瘤全切除262例,次全切除23例。面神经保留率达69.5％,听神经保留率32％。结论 对大型、巨型的听神经瘤选择不同的手术入路,应用显微外科技术,可提高肿瘤全切除率,有效地保护颅神经的功能。     

大型听神经瘤显微手术治疗的临床体会

目的总结25例听神经瘤手术切除的体会,探讨如何全切肿瘤并避免对周围重要结构的损害。方法对经显微手术治疗的25例大型听神经瘤的临床资料进行回顾性分析。结果本组大型听神经瘤25例,全切除22例,次全切除3例;面神经保留20例;依据House—Brackmann大型听神经瘤评定法评定面神经术后功能,其中Ⅰ级3例,Ⅱ级5例,Ⅲ级4例,Ⅳ级8例,Ⅴ～Ⅵ级5例。本组无1例死亡。结论根据术前和术中的策略,选择好手术人路和运用好显微外科技术可以提高大型听神经瘤的切除率、面神经功能保护率及减少手术并发症。     

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.     

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.     

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.     

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.     

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.     

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.