颞下锁孔入路的显微解剖与临床应用

目的进行颞下锁孔入路解剖学研究,探讨其临床应用价值.方法取甲醛固定的成人尸头标本15例(30侧),采用神经内镜辅助的显微外科技术进行颞下锁孔手术解剖学研究.并采用该入路手术切除8例颅内肿瘤.结果颞下锁孔入路可以充分暴露鞍上区、脚间窝、岩斜区及脑干腹外侧区的神经、血管结构;岩骨尖最大磨除面积为306mm2.肿瘤全切除7例(87.5%).结论经颞下锁孔入路能很好地处理鞍上、岩斜区、脚间窝以及脑干腹外侧区的病变.     

经眶上缘外侧锁孔入路鞍区内镜解剖及操作技术

目的探讨经眶上缘外侧锁孔入路鞍区的内镜解剖及操作技术。方法本组采用15具10％甲醛溶液固定的成人尸头和1例新鲜尸头,经眶上缘外侧锁孔入路应用内镜（0°镜、30°镜）对鞍区各间隙进行解剖观察并模拟手术操作。结果经眶上缘外侧锁孔入路开颅可达到经典翼点人路对骨窗的基本要求,通过使用内镜,可清晰的显露间隙Ⅰ、Ⅱ、Ⅲ、Ⅳ,尤其对重要穿通血管的显露更明确。结论经眶上缘外侧锁孔入路创伤小,暴露好;其中间隙Ⅰ、间隙Ⅲ是鞍区内镜探查最常使用且较为安全的间隙。     

翼点锁孔入路显微手术切除鞍区肿瘤

目的探讨翼点锁孔入路显微手术治疗鞍区及前颅底肿瘤的方法及效果。方法对19例鞍区及前颅底肿瘤采用翼点锁孔入路开颅显微手术切除。结果肿瘤全切除13例（68．4％）,次全切除4例（21．1％）,大部分切除2例（10．5％）。无手术死亡病例。术后随访2～18个月,失访2例,无肿瘤复发病例。结论翼点锁孔入路能够充分显露鞍区及前颅底,可达到传统翼点入路相似的手术效果,具有创伤小、脑组织暴露少、出血少、病人术后恢复快等优点。     

内镜辅助经单鼻孔-蝶窦入路切除垂体瘤的解剖及临床研究

目的 进行内镜辅助经单鼻孔-蝶窦入路切除垂体瘤的解剖研究，探讨其临床应用手术经验。方法 10例甲醛溶液固定的成人尸头模拟内镜辅助经单鼻孔-蝶窦手术入路，并进行显微解剖学观察；临床16例垂体瘤经该入路手术切除。结果 内镜辅助经单鼻孔-蝶窦入路对蝶窦、鞍区等结构显露良好，内镜可弥补显微镜的盲区。临床16例垂体瘤中，手术全切13例，近全切3例，效果满意，无相关严重并发症发生。结论 解剖及临床应用表明内镜辅助下行经单鼻孔-蝶窦入路具有对鞍区结构显露良好、肿瘤全切率高、手术创伤小、并发症少、病人术后恢复快等优点，是切除垂体瘤的理想术式。     

翼点锁孔入路神经内镜辅助下垂体腺瘤显微手术策略

目的 探讨翼点锁孔入路神经内镜辅助下垂体腺瘤显微手术策略.方法 选择翼点锁孔概念,利用神经内镜的辅助技术,对33例鞍区的垂体腺瘤患者先行单纯显微镜辅助下手术切除,然后再联合神经内镜切除肿瘤,比较两种方法的全切率.结果 33例患者中先用显微镜辅助下手术获得全切20例,次全切13例;13例次全切患者再联合神经内镜手术后获得全切8例,次全切5例.联合神经内镜手术获得全切的例数(28例)明显多于单纯显微镜手术(20例),差异有统计学意义(P<0.05).结论 利用翼点锁孔入路,神经内镜辅助下行垂体腺瘤显微手术能够克服手术中的死角.提高手术切除率,减少肿瘤残余,保护垂体柄,减少并发症,大大提高手术的效果.     

眶上锁孔手术入路的解剖学研究及临床应用

目的研究眶上锁孔手术入路的显微解剖,并探讨该手术入路在治疗前循环动脉瘤及鞍区肿瘤中的临床应用。方法对10例成人尸头使用手术显微镜模拟经眉眶上锁孔手术入路,并应用此入路对我科76例患者(其中52例颅内前循环动脉瘤,24例鞍区肿瘤)进行了手术治疗。结果该手术入路可充分而清楚的显示鞍区及Willis环附近的解剖结构,52例动脉瘤全部手术夹闭成功,其中49例患者恢复良好,3例中残,无死亡。24例鞍区肿瘤,22例全切除,2例次全切除,未出现严重的并发症。结论该手术入路在临床上应用广泛,采用该入路治疗前循环动脉瘤及鞍区肿瘤安全、微创,值得临床推广应用。     

翼点锁孔入路鞍区神经内镜下解剖应用

目的 研究翼点锁孔入路鞍区各间隙的神经内镜解剖，为内镜辅助下该入路显微手术提供解剖学依据。方法15例尸头经翼点锁孔入路开颅后，神经内镜对鞍区五个间隙进行解剖结构观察。结果利用神经内镜可以更广泛清晰地显示鞍区不同间隙内的解剖结构，尤其是对细微结构如垂体上动脉及穿通动脉，利用成角内镜可“绕过”神经、血管观察其背后的结构。结论运用神经内镜可以消除翼点锁孔入路鞍区显微手术的显微外科解剖死角，减少术中脑组织及重要颅底血管、神经的牵拉，减少并发症的发生，从而提高鞍区手术的疗效。     

鞍结节脑膜瘤的影像学特征及翼点锁孔手术治疗

目的 探讨鞍结节脑膜瘤的影像学特点及翼点锁孔入路显微手术治疗的效果。方法 回顾性分析98例鞍结节脑膜瘤患者的临床资料,均采用翼点锁孔入路开颅显微手术切除肿瘤。结果 本组98例鞍结节脑膜瘤增强MRI呈显著均一强化,84例伴有脑膜尾征。本组肿瘤全切除80例,次全切除18例。本组无手术死亡病例。术后随访2月~10年,10例复发。结论 掌握鞍结节脑膜瘤的特征性影像学表现对于术前正确诊断具有重要价值。翼点锁孔入路显微手术治疗鞍结节脑膜瘤效果良好,具有创伤小、并发症少、病人术后恢复快等优点。     

翼点眶上小骨窗开颅显微手术切除大型鞍区肿瘤

目的 探讨应用翼点眶上小骨窗入路显微手术冶疗大型鞍区肿瘤的临床效果。方法 21例大型鞍区肿瘤均采用经翼点皮切口眶上小骨窗入路进行开颅手术。皮瓣按翼点入路切开，但仅采用经眶上小骨窗开颅，骨窗呈椭圆形，最大直径仅为3．5～4．0cm，前部尽量靠近颅前窝底，应用显微外科技术将鞍区肿瘤切除。结果 取得显微镜下全切除18例，次全切除3例，无1例手术死亡。仅有1例64岁老年病人术后并发高血压脑出血，于术后3个月死于8市部感染。其他多数病人术后仅出现较为短暂的多尿和低钠血症，经应用脑垂体后叶素和(或)长效尿崩停以及浓氯化钠溶液后效果良好，术后恢复良好。结论 采用经翼点皮切口眶上小骨窗入路显微外科技术切除鞍区大型肿瘤，均可做到显微镜下全切除或次全切除，且对脑组织损伤轻，肿瘤显露好，是较为理想的鞍区肿瘤手术入路。     

经蝶窦入路至鞍区及周围结构:显微解剖与内镜解剖的比较

目的比较经蝶入路至鞍区及周围结构的内镜手术与显微手术显露范围的差异。方法选10具汉族成人灌注尸头，采用经蝶入路，5具进行内镜解剖，5具进行显微解剖。结果采用经蝶入路，在蝶窦内内镜下可观察到更多的周围结构，利于确定鞍底、海绵窦与鞍结节位置。在显露硬膜下结构时，内镜下侧方可显露海绵窦外侧壁，前方可显露双侧嗅神经和直回。结论同显微经蝶手术相比，内镜经鼻蝶手术在蝶鞍周围区域的显露范围更宽广。     

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.     

Diagnostic Difficulties and Treatment Implications

Summary: Differentiation between types of epileptic seizures has been aided in recent years by the introduction of intensive neurodiagnostic techniques and the development of increasingly detailed classification systems. Paradoxically, these developments have not simplified the task of matching the appropriate antiepileptic drug to a particular seizure type. It is reasonable to assume that anticonvulsant drugs will have different effects on different types of seizures, but faulty, circular reasoning can enter the picture if one also assumes that responses of seizures to different drugs signify different seizure types. There are several examples of differential diagnoses that can fall prey to this problem, including the diagnosis between partial seizures with secondary generalization and generalized tonic-clonic seizures, and the diagnosis between complex partial seizures and absence seizures with automatisms, among others. Considerations of etiology in future classification systems can further complicate the problem: should one then choose an anticonvulsant drug on the basis of individual seizure type or on the basis of the type of epilepsy? Ramifications of this issue extend even to the drug approval process. Official sanction is not given for use of a drug for a seizure type not included in the original efficacy studies, even if later scientific evidence shows that seizure type to be related to a type that is included. New trials must be undertaken. These problems arise from how we choose to classify seizures.     

Cognitive Dysfunction Associated with Antiepileptic Drug Therapy

Summary: Epilepsy is frequently associated with cognitive dysfunction. However, the reasons for this correlation are unclear. Possible influential factors include patient age; duration, frequency, etiology, and type of seizures; hereditary factors; psychosocial issues; and antiepileptic drug (AED) therapy. Whereas many of these factors are beyond the physician's control, AED therapy is one element that can be addressed in treatment decisions by recognizing the potential cognitive effects of particular AEDs. For example, phenobarbital impairs memory and concentration; phenytoin affects attention, problem solving ability, and performance of visuomotor tasks. In contrast, carbamazepine may affect concentration, while valproate would appear to have minimal effects on cognition. Moreover, cognitive effects of AEDs are amplified with coadministration of multiple anticonvulsants (polytherapy). A review of studies on the cognitive effects of monotherapy with AEDs, as opposed to those of polytherapy, provides evidence that drug-related cognitive dysfunction can be reversed if patients are switched to a simpler therapeutic regimen. Future research should be directed toward developing reliable measures for assessing and monitoring cognition, and understanding the particular cognitive side effects of each AED. Physicians also need to revise their opinions about which side effects are "tolerable" for epileptic patients.     

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.     

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.     

Carbamazepine Efficacy in Adults With Partial and Generalized Tonic-Clonic Seizures

Summary: Carbamazepine and phenytoin are drugs of choice in initial monotherapy for adult partial and secondarily generalized tonic-clonic seizures. These designations reflect the results of the Veterans Administration Epilepsy Cooperative Study Group of 1985. An earlier comparative study of carbamazepine and phenytoin by Ramsay and associates found both drugs equally effective in controlling new-onset seizures. Among the advantages of carbamazepine is that it causes relatively few cognitive and dysmorphic side effects. Its disadvantages are its unavailability in parenteral formulation and its metabolic autoinduction. The latter must be compensated for by planned dosage increases to maintain therapeutic plasma steady-state levels during the first 2 or 3 months of treatment. Carbamazepine is judged a drug of choice in the treatment of these secondarily generalized tonic-clonic seizures, and the drug of choice in children, adolescents, and women susceptible to the dysmorphic side effects associated with other anticonvulsant agents.     

Etiologic and Preventive Aspects of Epilepsy in the Child–Bridging the Gap Between Laboratory and Clinic

Summary: Four broad categories of basic phenomena are pertinent to developing ways to prevent epilepsy. These include mechanisms of epileptogenesis, ictal initiation and temporary entrainment by the seizure discharge of normally functioning brain, seizure propagation, and control mechanisms that function both to restrain the cascade of epileptic events culminating in a seizure and to arrest the epileptic event and restore the interictal state. In newborns and children, hypoxia-ischemia is a major factor leading to epileptogenesis, and several schemes are proposed to classify, quantify, and prevent hypoxic-ischemic encephalopathy. Control mechanisms must be better understood in order to develop prophylactic recommendations for epilepsy, and an experimental model of "kindling antagonism" may increase our understanding of these. Programs of prevention of seizures in children will evolve only if basic researchers and clinicians work productively together to develop an adequate understanding of factors important in epileptogenesis and antiepileptogenic control mechanisms.     

Predisposing and Causative Factors in Childhood Epilepsy

Summary: We review information from large studies of defined populations, examining the role of known factors and especially of prenatal and perinatal factors in contributing to nonfebrile seizure disorders of early childhood. We depend especially, but not exclusively, on the recently completed analyses from the Collaborative Perinatal Project of the National Institute of Neurological and Communicative Disorders and Stroke, the NCPP. About 4% of children in the NCPP who had at least one non-febrile nonsymptomatic seizure by the age of 7 years had a previous seizure during acute neurologic illness, such as meningitis or during the acute illness after trauma. Many such seizures should potentially be preventable. Of children with seizures, 10% had had a neonatal seizure and 13% had had a febrile seizure. Among the hundreds of prenatal and perinatal factors explored as predictors of childhood seizure disorders, the principal predictors identified were congenital malformations of the fetus, cerebral and noncerebral; family history of certain neurologic disorders; and neonatal seizures. In agreement with the British National Child Development Study, labor and delivery factors in the NCPP appeared to contribute very little to childhood seizure disorders. Maldevelopment, rather than damage at birth to an initially intact nervous system, appeared to be the more common mechanism. Most seizure disorders of early childhood remained unexplained by the large set of prenatal and perinatal characteristics examined.     

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.