眉间锁孔入路手术的显微解剖学研究

目的 观察眉问锁孔入路手术的显露范围并测量相关解剖学参数,以为临床应用提供依据.方法 应用眉间锁孔入路模拟手术并结合局部解剖对12具(24侧)成年国人尸头标本进行研究.形成约3.00 cm×2.50 cm大小骨窗,于手术显微镜下观察显露范围,并测量相关解剖学参数.选择1例典型鞍区脑膜瘤患者,施行眉间锁孔入路手术,观察手术疗效及预后.结果 手术显微镜下观察骨窗显露范围.可见额极、额底、筛板、鸡冠、嗅沟、嗅柬、蝶骨平台、鞍结节、前床突、后床突、小脑幕、视交叉、视神经、颈内动脉、大脑前动脉、大脑中动脉、大脑镰、上矢状窦、胼胝体、前连合和终板等组织结构;打开终板,可见第三脑室.测量双侧眶上孔(眶上切迹)之间距离为(45.92±5.86)mm;双侧滑车上切迹之间距离为(33.14±4.23)mm;鼻额缝至双侧内眦连线距离(16.25±1.52)mm;骨窗中心点至视交叉前缘中心点距离(64.30±3.20)mm,至鞍结节中心点距离(57.38±2.72)mm,至鞍膈中心点距离(67.04±2.89)mm,至终板中心点距离(66.18±3.79)mm,至前交通动脉距离(60.64±4.61)mm.1例患者施行眉间锁孔入路肿瘤切除术,疗效满意.结论 眉间锁孔入路手术可较好地显露前颅底及鞍区中线附近的解剖结构,推荐用于前颅底和鞍区中线附近病变的手术以及前交通动脉动脉瘤的夹闭,具有切口小、骨窗小、刨伤小、额叶损伤少、嗅觉易保留等优点,但也存在并发感染、脑脊液漏的风险,且不适用于脑肿胀患者.     

经眶上锁孔入路切除鞍区颅咽管瘤

目的探讨经眶上锁孔入路切除鞍区颅咽管瘤的应用价值。方法对7例位于鞍上,肿瘤上下径为3．5～6cm的颅咽管瘤患者(部分囊性变者4例,完全实性者3例),作眉弓内弧形小切口,在眶上铣开一直径为2．5cm的半圆形小骨瓣,术中根据肿瘤位置,从视交叉前间隙,视神经外侧间隙和颈内动脉外侧间隙切除肿瘤。术中除注意保护视神经、垂体柄、下丘脑之外,还应防止损伤颈内动脉、后交通动脉、脉络膜前动脉和大脑后动脉发出的到下丘脑和前穿质部位穿通动脉的损伤。结果术中6例病人肿瘤全切除,1例病人次全切除,术后5例病人出现不同程度的尿崩症及电解质紊乱,经药物治疗后好转,6例病人视力改善。结论眶上锁孔入路切口小,但能提供鞍上区足够的手术空间,足以显露鞍区病变及其邻近结构,且减少了脑牵拉和手术创伤,有利于颅咽管瘤的全切除,是一种安全有效的处理鞍区病灶手术入路途径。     

内镜辅助眶上锁孔入路治疗垂体瘤的临床解剖学研究

目的探讨内镜辅助眶上锁孔入路治疗垂体瘤的可行性。方法21例福尔马林固定尸体头部标本用于鞍区各解剖结构,特别是垂体柄、视神经、视交叉及其供血动脉特点的观察,总结手术可利用的间隙、应保护的结构;在9例新鲜尸头上模拟进行内镜辅助眶上锁孔入路手术,进一步验证其可行性及优势。结果颈内动脉床突上段长度14.5±1.3mm(8.1～18.5mm),发向垂体柄、视神经或视交叉的穿支动脉的支数分别为:大脑前或前交通动脉3.0支(2～6支),颈内动脉2.1支(1～5支),后交通动脉3.2支(3～6支),基底动脉1.4支(1～3支)。视神经颅内段长度为11.4±2.7mm(6.1～17.6mm),第1间隙面积为44.8±3.4mm2(7.0～100.8mm2),手术可通过第1间隙或(和)第2间隙进行。结论通过眶上锁孔入路治疗向鞍上发展的垂体瘤有充足的操作空间,具有视神经、视交叉减压充分,利于保护其供血动脉的优点。     

眶上锁孔入路的临床应用

目的探讨眶上锁孔入路的临床合理应用。方法选择2000年6月-2004年6月鞍区病变患36例，其中垂体肿瘤30例，鞍区脑膜瘤3例，颅咽管瘤2例，后交通动脉瘤1例；采用眶上锁孔入路，沿眉弓做切口，切口长度约5cm，骨窗范围长约3．5cm，宽2．5cm，弧形切开硬脑膜，在显微镜和神经内镜的辅助下完成手术。结果36例中30例垂体肿瘤手术全切除率为80．00％(24／30)，次全切除率13．33％(4／30)；脑膜瘤3例均达到辛普森Ⅱ级切除；颅咽管瘤2例，1例全切除，1例次全切除；夹闭后交通动脉瘤1例。16例垂体肿瘤患于手术后出现一过性尿崩症，2例伤口发生脑脊液漏，1例手术后额叶内小血肿，1例手术后视力较术前减退，1例伤口感染。手术中嗅神经保留完好，无一例死亡。结论眶上锁孔入路可增加手术的安全性，减少创伤，对于部分颅前窝及鞍区病变，眶上锁孔入路完全可以替代传统的经额手术入路。     

经前纵裂大脑镰入路锁孔手术治疗鞍结节脑膜瘤

目的 探讨经前纵裂大脑镰入路锁孔手术治疗压迫视神经并累及视神经管的鞍结节脑膜瘤的疗效。方法 回顾性分析2017年5月~2021年5月经前纵裂大脑镰入路锁孔手术治疗的9例鞍结节脑膜瘤的临床资料。9例肿瘤压迫视神经并累及视神经管。结果 9例肿瘤均全切除,术后随访6个月~2年,无复发。术前15侧（83.33%）眼睛存在视力受损,术后均改善。术后出现假性脑膜膨出1例,无尿崩症。结论 对于压迫视神经并累及视神经管的鞍结节脑膜瘤,经前纵裂大脑镰入路锁孔手术提供了一种经颅入路替代方法,可以很好地暴露血管和视神经管,获得良好的手术效果。     

锁孔入路开颅手术(附106例报告)

目的：评价用锁孔入路开颅术显微切除垂体腺瘤、颅咽管瘤、鞍结节脑膜瘤、脑胶质瘤、听神经瘤及直视下夹闭后交通动脉瘤、前交通动脉瘤的效果及安全性。方法：对垂体腺瘤、颅咽管瘤、脑膜瘤、后交通动脉瘤及前交通动脉瘤于眶上外侧，右颞叶胶质瘤于右颞，听神经瘤于耳后，分别作一直径2．5cm骨瓣，显微镜下切除肿瘤或直视下夹闭动脉瘤。结果：垂体腺瘤77例中65例达到全切除，12例为次全切除；颅咽管瘤11例、鞍结节脑膜瘤6例、胶质瘤1例及听神经瘤7例，均予全切；4例颅内动脉瘤均夹闭成功。 所有患恢复良好，未发生与手术入路有关的并发症。结论：采用锁孔入路，能够安全切除直径在55mm 以下的大型、巨大型垂体腺瘤，以及30－70mm的颅咽管瘤、鞍结节脑膜瘤、听神经瘤，并可直视下夹闭前、后交通动脉瘤。     

眶上锁孔入路治疗基底动脉上段动脉瘤的解剖学研究及初步临床应用

目的探讨眶上锁孔入路治疗基底动脉上段动脉瘤的可行性和适应证,并报告其初步临床应用经验。方法 8具福尔马林固定的尸头标本,完成眶上锁孔入路开颅后,通过视神经颈内动脉三角(即第二间隙),观察基底动脉上段的显露,并在神经导航系统辅助下完成解剖数据测量。在临床应用中,经眶上锁孔入路夹闭基底动脉上段动脉瘤9例。结果眶上锁孔入路通过第二间隙可显露基底动脉上1/3段,双侧小脑上动脉和大脑后动脉(P1段和部分P2段)。可观察到的基底动脉最低点与后床突水平间的直线距离为(5.0±1.2)mm,磨除后床突,距离可显著增加(3.4±1.0)mm(P0.05)。可观察到的基底动脉延长线最远点到颅前窝的垂直距离为(12.4±2.3)mm,去除眉弓及部分眶顶,距离可显著增加(3.3±1.2)mm(P0.05)。9例基底动脉上段动脉瘤通过眶上锁孔入路成功夹闭,术后随访6～12个月,病人恢复好。结论眶上锁孔入路可显露不高于颅前窝水平10mm,不低于后床突水平5mm的基底动脉。磨除后床突和切除眉弓及部分眶顶可分别增加基底动脉近端、远端的显露。眶上锁孔入路中,经第二间隙夹闭基底动脉上段动脉瘤是手术最佳路径。     

神经内镜下经鼻蝶入路鞍上区域手术的应用解剖

目的探讨经鼻蝶入路和翼点入路对鞍上区暴露的差异,为内镜下经鼻蝶入路进入鞍上区的手术方法建立解剖学基础。方法在12例成人尸颅标本上,分别模拟经鼻蝶入路和翼点入路,暴露鞍上区,观察视神经、视交叉、垂体柄、颈内动脉及其分支。比较两个入路对于鞍上区重要结构的显露。结果翼点入路下,鞍结节后缘至视交叉前缘距离为5.35±1.38mm,两侧视神经内缘间距10.58±1.46mm,小脑幕游离缘长度6.73±0.84mm,后交通动脉长度16.52±2.98mm,前交通动脉长度2.11±0.35mm。神经内镜下经鼻蝶入路可以暴露视神经、视交叉、垂体柄、颈内动脉、大脑前动脉、大脑中动脉、前交通动脉、后交通动脉等结构,对于颈内动脉分叉以上结构暴露欠佳。结论经鼻蝶入路可以完全暴露第Ⅰ、Ⅱ间隙内的神经血管结构,对于第Ⅲ、Ⅳ间隙内结构显露较差,可以在微侵袭条件下部分代替翼点入路。     

神经内镜下经筛蝶入路视神经管减压术相关解剖及影像学研究

目的提高神经内镜下经筛蝶入路行视神经管减压术的安全性与准确性。方法选用6例(12侧)成人头颅干性标本,行眼眶三维CT扫描并重建,在CT图片上测量并利用公式计算相关参数;分别沿水平面和矢状面切开头颅标本,测量相关解剖学参数。对比CT影像与实体解剖两种方法所测得的相关数据。选用6例(12侧)灌注头颅湿性标本,模拟神经内镜下经筛蝶入路视神经管减压术,内镜下进行观察和测量。结果视神经管颅口、眶口、管中段处的周长分别为(16.42±1.56)mm、(17.32±1.60)mm和(13.58±1.42)mm。内镜下视神经管颅口、眶口及管中段可磨除内壁的最大有效宽度分别为(7.82±2.63)mm、(8.05±2.77)mm和(6.92±2.01)mm。鞍结节隐窝中心点和视神经管颅口内侧壁中点连线与横坐标之间的角度为(17.23±1.34)°。在视神经管眶口处,眼动脉位于视神经正下方2侧(16.7%)和外下方10侧(83.3%)。结论神经内镜下经筛蝶入路视神经管减压术是一种入路直接、减压充分的微创手术。术前仔细阅读CT影像资料并作相关测量,结合多种定位方法能提高手术准确性。     

内镜经眶上锁孔入路视神经管减压的解剖学研究

目的在尸头标本上,探讨经眶上锁孔硬膜外入路行神经内镜下视神经管减压术的可行性。方法以直径4 mm的0°和30°硬质神经内镜对10例(共20侧)成人尸头标本,行眶上锁孔硬膜外视神经管减压术,记录入路相关解剖结构并测量相关数据。结果通过眶上锁孔硬膜外入路,神经内镜可清晰显露蝶骨嵴、前床突、视神经管内口与镰状韧带,并完成对视神经管外壁及上壁的磨除减压。经测量,额骨颧突至视神经管内口距离为(59.32±2.27)mm,视神经管内口上壁中点至颈内动脉距离为(3.80±0.93)mm。结论神经内镜经眶上锁孔硬膜外入路可对视神经管上壁与外侧壁进行充分减压,具有安全、微创与有效的特点。     

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 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.     

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.     

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.     

Anticonvulsant Drugs and Cognitive Function: A Review of the Literature

Summary: Alterations of cognitive function are separate from disturbances of behavior seen in association with epilepsy. The nature of the cognitive disability may to a certain extent depend on the seizure type. Partial seizures, mainly derived from a temporal lobe focus, impair memory tasks, while generalized seizures seem to have more effect on attentional abilities. A number of studies, reviewed in this paper, suggest that anticonvulsant drugs further impair cognitive function. Maximal impairments are seen in patients receiving polytherapy: rationalization of polytherapy improves cognitive abilities. Studies in children and adults have allowed differentiation of the effects of various commonly used antiepileptic agents. Maximal cognitive deficits are seen with. phenytoin, while phenobarbital and sodium valproate induce moderate disturbances, and carbamazepine seems relatively free from such toxicity. Further research is needed on the interrelationship between types of seizure disorders, types of anticonvulsant medications, and cognitive function.     

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.     

Effects of NMD A- and AMPA-Receptor Antagonists on Different Forms of Epileptiform Activity in Rat Temporal Cortex Slices

Summary: Lowering extracellular magnesium induces different patterns of epileptiform activity in rat hippocampus and entorhinal cortex. Short recurrent epileptiform discharges in the hippocampus are stable over time, whereas seizurelike events (SLEs) in the entorhinal cortex, the subiculum, and the neighboring neocortex develop into late recurrent discharges which are not blocked by clinically employed antiepileptic drugs. We tested the sensitivity of the different epileptiform discharge patterns to. /V-methyl-D-aspartate (NMDA)- and non-NMDA-receptor antagonists. As NMDA-receptor antagonist we used dextrorphan, ket-amine, and 2-aminophosphonovalerate (2APV); as α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA)-receptor antagonist we employed the quinoxaline derivative glutamate 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The findings show that the different patterns of epileptiform activity, including the late recurrent discharges, are sensitive to all NMDA-receptor antagonists. However, when dextrorphan was employed to suppress seizure-like events, later recurrent discharges did not develop during the remaining time course of the experiment. CNQX reversibly suppressed recurrent discharges in the hippocampus and SLEs in the entorhinal cortex. However, late recurrent discharges become insensitive to CNQX, even at a high concentration of 60 μM m. This finding suggests a prominent role for NMDA receptors in the generation of late recurrent discharges.