经鼻-蝶窦入路的内镜鞍周解剖学研究

目的 通过经鼻蝶窦入路的内窥镜解剖学研究，为临床内镜经蝶手术提供形态学基础。方法 在10具已经动脉灌注染料的成人尸头上模拟扩大经鼻蝶窦手术入路，同时测量海绵窦内重要结构与鞍底的距离。结果 根据蝶窦后壁的骨性结构特征将蝶窦腔分为中间腔、旁中间腔及外侧腔5部分。扩大经蝶手术入路可清晰显示鞍底的骨膜、硬脑膜外层、海绵窦内侧壁，海绵窦内的颈内动脉及其分支血管、动眼神经、滑车神经、外展神经及眼神经等结构；打开堞骨平台可显示视神经、视交叉、垂体柄、鞍隔及视丘下部等解剖结构。结论 内窥镜扩大经鼻蝶手术入路可清晰显露蝶鞍周围的解剖结构，可适用于鞍旁、鞍上病变的手术治疗。     

蝶窦外侧壁和海绵窦内侧面观显微解剖研究

目的 为扩大经蝶手术和前方颅下手术提供蝶窦外侧壁和海绵窦内侧面观显微解剖参数。方法 对20具成人头颅标本，仿Janecka的标准面部移位入路切口(左侧)行两侧蝶窦外侧壁和海绵窦内侧面观显微解剖观察和测量。结果 蝶窦外侧壁的主要结构有视神经管隆起和颈内动脉隆起，而颈内动脉隆起缺失的出现率高达50％，此时，依照翼管-破裂孔-颈内动脉破裂孔段途径显露颈内动脉海绵窦段为一安全策略。内移颈内动脉海绵窦段，可以充分显露海绵窦外侧壁的颅神经。结论 掌握蝶窦外侧壁显微解剖和从内侧面显露、移动颈内动脉海绵窦段，有助于扩大经蝶手术和前方颅下手术对病变累及海绵窦的处理。     

内镜下经鼻-蝶窦入路蝶鞍周围解剖学研究

目的研究内镜下经鼻-蝶窦入路的解剖学,为临床内镜经蝶垂体病变手术提供形态学基础。方法选择10具经动脉灌注染料的成人尸体头部标本,男8具,女2具;模拟扩大经鼻-蝶窦手术入路,同时测量海绵窦内重要解剖结构与鞍底的距离。结果根据蝶窦后壁骨性结构特征将蝶窦腔分为中间腔、旁中间腔以及外侧腔等5个部分。扩大经鼻-蝶窦手术入路可清晰地显示鞍底的骨膜、硬脑膜外层、海绵窦内侧壁,海绵窦内的颈内动脉及其分支血管、动眼神经、滑车神经、外展神经及眼神经等重要解剖结构;打开蝶骨平台可显示视神经、视交叉、垂体柄、鞍膈及视丘下部等解剖结构。蝶鞍周围结构与鞍底中线的距离分别为视神经管隆起(5.72±1.56)mm,颈内动脉管隆起(5.42±1.38)mm,鞍膈(10.01±1.46)mm,视交叉(14.96±1.42)mm,海绵窦内颈内动脉(11.02±2.06)mm,海绵窦内动眼神经(13.75±1.79)mm,海绵窦内滑车神经(15.14±1.53)mm,海绵窦内外展神经(12.68±1.52)mm。结论内镜下扩大经鼻-蝶窦手术入路可清晰地显露蝶鞍周围的解剖结构,适用于鞍旁、鞍上病变的手术治疗。     

扩大经蝶入路显微镜与内镜的解剖学研究

研究背景目前普遍认为,传统经蝶入路对侵袭性垂体腺瘤的治疗效果较差,如何切除向蝶鞍外生长的肿瘤即成为神经外科的难题之一。本文通过研究扩大经蝶手术入路的解剖学特点,以为侵袭性垂体腺瘤的外科手术治疗提供理论依据。方法于成人尸头标本模拟内镜下扩大经蝶入路手术范围,并对相关解剖结构进行测量。结果 (1)蝶窦开口距鼻前棘52.62~63.16 mm,平均(59.68±4.28)mm;距后鼻孔上缘10.47~15.61 mm,平均(12.88±1.46)mm。(2)视神经和颈内动脉隆起率分别为11/20和17/20。(3)海绵窦内侧壁由一层硬脑膜组成,前、后、下海绵间窦和基底窦出现率分别为17/20、12/20、11/20和20/20。(4)双侧颈内动脉内缘在隐匿段间距为12.42~21.76 mm,平均(15.30±1.25)mm;在下水平段中点间距为10.42~18.43 mm,平均(14.03±1.19)mm;在前垂直段间距为16.75~24.88mm,平均(18.87±1.44)mm;在鞍结节内缘间距为9.97~16.18 mm,平均(12.73±0.94)mm。(5)颈内动脉海绵窦段与海绵窦内侧壁蝶鞍部之间有7侧直接接触(7/20);颈内动脉海绵窦段与海绵窦内侧壁蝶骨部之间均可见静脉丛伸入(20/20)。(6)共有9侧颈内动脉沿垂体下1/3走行(9/20)、7侧沿垂体下2/3走行(7/20)、3侧沿整个垂体走行(3/20)、1侧沿鞍底水平以下走行(1/20)。(7)有4侧(4/20)垂体出现侧突。结论扩大经蝶入路显露海绵窦内结构清晰,适用于处理由鞍内向海绵窦侵袭的垂体腺瘤。     

扩大经蝶手术入路相关的显微解剖学研究

目的详尽了解扩大经蝶入路到达颅底中央部手术相关显微外科解剖，为临床提供可靠的解剖学参数。方法15例颅骨干标本，进行骨性结构的观察和测量；15例尸头，显微镜下模拟手术入路，对涉及的结构进行显微解剖学观察、测量和拍照。结果扩大经蝶手术入路可以通过适当去除后组筛窦、鞍结节和蝶骨平台，显示额叶底部、视交叉前池、大脑前动脉A1和A2段、前交通动脉；通过切开海绵窦内侧壁可以显示颈内动脉海绵窦段及其分支；通过去除鞍背和蝶窦后壁，打开中上斜坡硬膜，可以显示桥脑、基底动脉及分支、小脑上动脉、大脑后动脉等结构。结论颅底中央部位置深在，组织关系复杂，血管神经丰富，毗邻结构重要。扩大经蝶入路可通过良好的视角显露鞍前、鞍旁及斜坡等颅底中央部的显微解剖结构。     

扩大经鼻蝶入路海绵窦的内镜解剖研究

目的通过对扩大经鼻蝶窦入路的内镜解剖学研究,为临床应用提供形态学基础.方法在10具动脉灌注染料的成人尸头上模拟扩大经鼻蝶窦手术入路,测量海绵窦内重要结构与鞍底的距离.结果扩大经鼻蝶手术入路可清晰显示鞍底的骨膜、硬脑膜外层、海绵窦内侧壁,及海绵窦内的颈内动脉及其分支血管、动眼神经、滑车神经、展神经及视神经等结构.结论内镜下行扩大经鼻蝶手术入路可清晰显露海绵窦及其内的解剖结构,适用于鞍内病变侵犯海绵窦的外科治疗.     

海绵窦内侧壁的显微解剖与扩大经蝶窦入路治疗侵袭海绵窦的垂体腺瘤（附103例分析）

目的研究海绵窦内侧壁结构的解剖特点，并探讨采用扩大经蝶窦入路治疗侵袭海绵窦垂体腺瘤的方法。方法在10具成人新鲜尸头上模拟扩大经蝶窦手术入路，观察海绵窦内侧壁结构的解剖特点。根据解剖学研究结果，指导临床采用扩大经蝶窦手术入路治疗侵袭海绵窦的垂体腺瘤103例。结果垂体侧方的海绵窦内侧壁薄弱，仅有一层疏松的纤维组织结构。颈内动脉是扩大经蝶窦入路海绵窦内所见的主要结构，可分为5段，有3个主要分支。颈内动脉海绵窦段主要的分支有脑膜垂体干、海绵窦下动脉和被囊动脉。向内侧走行的脑膜垂体干和被囊动脉是经蝶窦入路中较易损伤的血管。手术显微镜下全切除肿瘤62例（60．2％），次全切除38例（36．9％），大部切除3例（2．9％）；无手术死亡；手术并发症包括短暂性脑脊液鼻漏5例，暂时性脑神经功能损伤4例，垂体功能低下3例，颈内动脉损伤2例，永久性尿崩症1例。术后行放射治疗17例，γ刀治疗15例，药物治疗13例。随访3个月～8年，2例出现肿瘤复发而予以γ刀治疗。无再手术病例。结论扩大经蝶窦入路是切除侵袭海绵窦垂体腺瘤理想的入路；了解颈内动脉海绵窦段及其分支在解剖形态上的变化，对于减少术中出血，确保术中安全，具有重要意义。     

神经内镜下经鼻扩大入路至中颅底的解剖学研究

目的明确神经内镜下经鼻扩大入路至中颅底的各种重要解剖标志,探讨该入路临床应用的影响因素和手术特点。方法分别运用直径4 mm,长度18 cm的0°、30°和45°硬质内镜(Karl Storz),在动脉灌注后的成人尸头上模拟手术过程,神经导航的引导下经双侧鼻腔扩大入路对中颅底进行内镜解剖。测量各个解剖标志之间的距离。结果蝶窦后壁可分为鞍区、鞍上区、海绵窦区和斜坡区。在蝶窦后壁可见鞍底、后组筛房、蝶骨平台、鞍结节、斜坡、斜坡隐窝、海绵窦、颈内动脉隆起、视神经管隆起、颈内动脉-视神经隐窝。在蝶窦腔的外侧壁可见眶尖隆起、上颌神经隆起、下颌神经隆起和翼管神经,并分别形成视神经颈内动脉和动眼神经三角、V_1~V_2三角、V_2~V_3三角。两侧颈内动脉-视神经隐窝内侧距离为(11.3±1.2)mm,两侧垂体前部距离为(12.2±2.1)mm,两侧垂体中部距离为(21.5±2.5)mm,两侧垂体后部距离为(17.6±3.4)mm,垂体前后径为(9.1±2.9)mm。硬膜内的鞍上区又可分为视交叉上部、视交叉下部、鞍背后部和脑室部。在剪开海绵窦和垂体之间的硬膜后,海绵窦段的颈内动脉可分为三叉神经段、后曲段、下水平段、前曲段和上水平段。结论神经内镜经鼻扩大入路至中颅底可清晰显示鞍区、鞍上区和海绵窦区的解剖结构,为该区域的病变提供一条有价值微侵袭的手术方法。颈内动脉-视神经隐窝是该区域手术的关键性标志。     

扩大经蝶窦入路颈内动脉海绵窦段显微镜、内镜下的解剖学研究

目的研究扩大经蝶窦入路颈内动脉海绵窦段的显微镜及内镜下的解剖特点。方法在10具动静脉灌注染料的成人新鲜尸头上模拟扩大经蝶窦手术入路，在显微镜及内镜下观察颈内动脉海绵窦段的走行特点，及颈内动脉海绵窦段与垂体的关系，测量双侧颈内动脉海绵窦段在不同水平的距离。结果颈内动脉海绵窦段分为5段，有3个动脉分支，其在蝶窦外侧壁上形成颈内动脉隆突，与视神经隆突形成视神经-颈动脉凹陷，是内镜手术中确定中线的标志。颈内动脉前曲段的内侧缘距垂体中线的距离为（11．94±1．90）mm（9．02～14．86mm），后曲段的内侧缘距垂体中线的平均距离为（7．96±2．07）mm（5．64～11．58mm）。结论颈内动脉海绵窦段是扩大经蝶窦手术入路中最重要的解剖结构。内镜下扩大经蝶窦手术可清晰显示海绵窦内的颈内动脉及其分支血管和神经等重要的组织结构，是处理由鞍内侵犯海绵窦内侧壁病变的良好手术方式。     

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.     

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.     

Treatment Considerations in Anticonvulsant Monotherapy

Summary: The long-standing practice of polypharmacy in treating epilepsy is giving way to use of monotherapy. Monotherapy can improve seizure control as well as reduce the risk of serious idiosyncratic reactions, dose-related side effects, and complex drug interactions. Monotherapy also offers improved compliance and cost-effectiveness. The basis of monotherapy is accurate diagnosis and assessment of the patient's seizure type(s), followed by selection of a single appropriate anticonvulsant drug. Many patients currently treated with multiple anticonvulsants can be successfully converted to monotherapy with a carefully monitored program in which troublesome and redundant drugs are gradually withdrawn from the therapeutic regimen.