显微外科手术治疗大型脑动静脉畸形

目的对显微外科手术治疗的13例大型脑动静脉畸形的手术治疗效果进行分析,探讨大型脑动静脉畸形的治疗策略和手术要点。方法共手术治疗13例大型动静脉畸形。外院曾行血肿外引流2例,血肿清除去骨瓣减压1例。全部位于功能区。Spetzler-Martin分级:Ⅳ级7例,Ⅴ级6例。4例行术前栓塞治疗。在我院均行动静脉畸形切除术。结果 6例无明显并发症。余7例主要并发症是偏盲、轻度失语、肌力下降及癫痫等,多数均逐渐恢复。10例动静脉畸形获全切,3例少量残留。残余动静脉畸形行伽玛刀治疗。结论动静脉畸形的最大危害是颅内出血,严重者可导致患者死亡。显微外科手术全切除是最有效的治疗方法。术前充分准备,采用正确的手术方法,术中术后控制血压,高级别大型动静脉畸形可以获得良好的治疗效果。     

大型脑动静脉畸形直接显微手术治疗的效果分析

目的通过总结大型脑动静脉畸形的显微手术经验,探讨脑动静脉畸形显微手术的效果以及正常灌注压突破对显微手术的影响。方法回顾性分析93例采用显微外科手术治疗的大型脑动静脉畸形病例,按照Spetzler—Martin分级,3级者37例,4级者35例,5级者21例。结果术后出现再出血及急性脑肿胀者3例（3．2％）,死亡2例。术后对91例患者进行随访,根据GOS分级,恢复良好82例（90．1％）,中残7例（7．7％）,重残2例（2．2％）。结论显微外科手术是治疗大型脑动静脉畸形的有效手段,术前精确的判断及术中精细的操作是手术成功的关键。正常灌注压突破对大型脑动静脉畸形直接显微手术无显著影响。     

CTA在非高血压自发性脑内血肿急诊手术中的指导作用

目的 探讨头颅多层螺旋CT血管造影(CT angiography,CTA)检查在非高血压自发性脑内血肿急诊显微外科手术治疗中的应用价值.方法 对27例需行急诊手术血肿清除的非高血压自发性脑内血肿患者,术前行头颅CTA检查,根据CTA检查结果做急诊开颅显微外科手术治疗,并对CTA在手术中的指导作用进行分析.结果 27例头颅CTA检查中,动脉瘤6例,动静脉畸形14例,烟雾病3例,无明显血管异常4例.术中探查发现动脉瘤6例,均予瘤颈夹闭;动静脉畸形14例,其中全切除12例,部分切除2例;烟雾病3例,均单纯血肿清除;海绵状血管瘤3例,均全切除;无明显原发病变1例,单纯血肿清除.术后均行头颅DSA检查,动静脉畸形残留2例,予伽玛刀治疗,烟雾病3例,无明显血管异常22例.格拉斯哥预后评分(GOS):Ⅰ级8例,Ⅱ级14例,Ⅲ～Ⅳ级5例.随访0.5-2年无再出血.结论 头颅CTA能简便、快速、无创地明确非高血压自发性脑内血肿患者中的动脉瘤、动静脉畸形、烟雾病等病因,提供直观的三维形态及解剖定位,有利于一期手术清除血肿及消除病因,降低手术风险,对非高血压性自发性脑内血肿的急诊显微外科手术治疗具有重要的指导作用.     

显微外科手术联合术前栓塞术治疗颅内动静脉畸形临床研究

目的评估显微外科手术联合术前栓塞术治疗颅内动静脉畸形的疗效。方法回顾性分析48例颅内AVM患者的临床资料,其中28例采用显微外科手术联合术前血管栓塞治疗(研究组),20例单纯采用手术治疗(对照组),比较2组手术疗效。结果研究组术中出血量、术后GOS评分、神经功能缺失情况与对照组相比均有显著性差异(P<0.05);Ⅲ～Ⅳ级颅内AVM研究组全切率89.3%,对照组为58.8%,2组比较有显著性差异(P<0.05);V级颅内AVM 2组全切率比较无明显差异(P>0.05)。结论显微外科手术联合术前栓塞术治疗颅内动静脉畸形疗效较好。     

CTA在脑动静脉畸形出血急诊显微外科手术治疗中的指导意义

目的 探讨多层螺旋CT血管造影(CTA)存脑动静脉畸形(AVM)出血急诊显微外科手术治疗中的指导意义. 方法 同顾性分析四川省人民医院神经外科自2004年8月至2007年10月应用CTA指导急诊显微外科手术治疗脑AVM出血的21例患者的临床资料. 结果 本组21例脑AVM患者均行血肿清除及脑AVM的显微外科手术治疗,畸形血管伞切15例.部分切除5例,1例延髓血管畸形未能切除.痊愈6例(皮层下非功能区血肿5例,小脑血管畸形1例),好转14例(皮层下功能区血肿7例,小脑血肿4例,基底节区血管畸形3例),死亡1例(延髓血管畸形).结论 CTA可完成脑AVM的诊断,指导脑AVM出血的急诊显微外科手术治疗.     

复杂脑动静脉畸形的显微外科手术治疗效果分析

目的 探讨显微外科手术治疗复杂脑动静脉畸形的诊治要点。方法 回顾性分析苏州大学附属第一医院神经外科2011年1月—2021年1月通过单纯显微手术切除及复合手术治疗的38例复杂脑动静脉畸形患者的临床资料,根据Spetzler-Martin分级,Ⅲ级24例,Ⅳ级9例,Ⅴ级5例。畸形血管团平均大小为5.9 cm(3.5～12.3 cm),位于功能区27例,非功能区11例,术前行CTA、DSA及MRI检查,术后行CT、CTA或DSA检查,定期随访,格拉斯哥预后评分(GOS)评价神经功能障碍。结果 所有患者中,28例接受介入加手术综合治疗,10例接受单纯显微手术切除。术后影像学示,35例(92.1%)全切,3例(7.9%)较术前明显缩小。术后随访6～79个月,其中恢复良好34例(GOS=4～5分),中度残障2例(GOS=3分),重度残障1例(GOS=2分),死亡1例(GOS=1分)。结论 显微外科手术切除是治疗复杂脑动静脉畸形的有效方法之一,通过和血管内介入栓塞紧密结合,加之术前精准影像学评估,术中导航、荧光血流监测技术的应用及术中科学的显微操作,均是手术成功的关键。     

脑动静脉畸形显微手术治疗23例分析

目的 探讨显微手术治疗脑动静脉畸形（AVM）的效果。方法 对23例脑动静脉畸形惠者根据临床表现、头颅CT或MRI及脑血管造影实施显微手术切除，先行阻断供血动脉，再阻断引流静脉，从而全切畸形团。结果 23例患者除3例术后复查脑血管造影部分残留外，均获全切。结论 显微手术治疗脑动静脉畸形可使手术更加安全，是行之有效的治疗方法。     

显微手术治疗脑动静脉畸形35例

目的 探讨显微手术治疗脑动静脉畸形的疗效及其手术适应症，进而提高手术疗效。方法 对我院近8年来显微手术治疗脑动静脉畸形35例进行回顾性总结。结果 全切27例，次全切3例，部分切除 夹闭主要供血动脉1例，夹闭主要供血动脉2例，活检2例，恢复良好31例，病残2例，死亡2例。结论 显微手术治疗脑动静脉畸形疗效良好，合理选择手术适应症、手术方式及应用显微神经外科技术是取得良好疗效的重要因素。     

脑外型海绵状血管瘤的诊断与显微外科治疗

目的 探讨脑外型海绵状血管瘤的术前诊断及显微外科治疗的效果.方法 通过对18例脑外海绵状血管瘤诊治过程的回顾性分析,包括术前诊断、临床表现、神经影像学特征及显微外科治疗方法.结果 全切除10例,部分切除8例.17例术后症状均改善,全切10例无复发.结论 显微外科手术切除病灶是目前治疗本病最可靠的方法,能否全切与术前评估、术者经验及显微操作技术等有关;放射治疗有效.     

脑动静脉畸形的显微外科手术治疗

脑动静脉畸形的显微外科手术治疗蒋太鹏，朱贤立，付友增，陈耕野，林宁我们于１９８９年１１月至１９９４年１１月共收治脑动静脉畸形２７例，均在显微操作下行全切和部分切除，现报告如下：临床资料１．一般资料：２７例ＡＶＭ患者中，男性１４例，女性１３例。年龄９～...     

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.     

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.     

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.     

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.