脊髓髓内肿瘤及显微外科治疗

目的 探讨脊髓髓内肿瘤的诊断和显微手术切除方法。方法 对16例脊髓髓内肿瘤手术患者进行回顾性研究。结果 肿瘤全切除10例,近全切除4例,大部切除2例,术后12例均有不同程度的改善和好转,1例肌力较术前减退,3例未见明显好转。随访3个月～4年,室管膜瘤复发1例,星形细胞瘤复发3例,其余未见复发。结论 脊髓髓内肿瘤应作显微手术切除,避免或减少脊髓损伤,尽量做到全切除,减少术后的复发。     

脊髓圆锥髓内肿瘤的诊断及显微手术治疗

目的探讨脊髓圆锥髓内肿瘤的诊断及显微手术技巧。方法回顾性分析9例显微手术切除的脊髓圆锥髓内肿瘤的临床资料。结果肿瘤全切2例,次全切5例,部分切除2例。术后随访648个月,症状明显改善8例,复发死亡1例,Mc Cormick分级：Ⅰ级6例,Ⅱ级2例。结论脊髓圆锥髓内肿瘤多为低级别胶质瘤或良性肿瘤。手术全切除较困难,但争取手术全切或次全切除可获得良好预后。     

显微手术治疗脊髓髓内肿瘤

目的探讨脊髓髓内肿瘤的显微手术治疗效果。方法回顾性分析经显微手术治疗的27例脊髓髓内肿瘤病人的临床资料。结果肿瘤全切除13例,次全切除10例,大部分切除4例。术后1月症状明显改善21例,稳定3例,加重3例。本组无死亡病例。术后随访6-24个月,复发2例;按McCormick脊髓功能状态分级：Ⅰ级17例,Ⅱ级6例,Ⅲ级3例,Ⅳ级1例。结论MRI是诊断脊髓髓内肿瘤的首选方法,显微手术切除脊髓髓内肿瘤是一种有效的手段。     

脊髓肿瘤的显微外科治疗

目的　探讨脊髓肿瘤的手术治疗效果。方法　回顾 3 8例脊髓肿瘤患者的诊断及显微手术切除方法。其中髓外 3 4例 ,髓内 4例。结果　肿瘤全切除 3 2例 (84 2 % ) ,次全切除 2例 ,大部分切除 4例 ,无手术死亡及严重致残 ,良性髓外及髓内肿瘤全切除后 ,多数患者脊髓功能在短期内即获改善 ,但是术前脊髓功能越差术后恢复越困难。结论　脊髓肿瘤应早期诊断并尽早手术治疗 ,术者娴熟的显微手术技巧可避免或减轻脊髓损伤。     

显微手术治疗脊髓髓内胶质瘤23例

目的:分析23例脊髓髓内胶质瘤显微手术治疗经验,评价其疗效和预后。方法:对9年来经显微手术治疗的23例脊髓髓内胶质瘤患者的肿瘤病理类型、肿瘤部位、临床症状、体征、辅助检查和临床疗效进行回顾性分析研究。结果:本组13例星形细胞瘤(56.5%)及10例室管膜瘤(43.5%),均于显微镜下肉眼全切除,全组无围手术期死亡。16例随访2个月至7.6年[平均(38±11)个月]。末次随访结束时(失访者按出院前的神经功能评定):肌力改善16例(69.6%)、不变2例(8.7%)、加重2例(8.7%)及死亡3例(13.0%)。随访中复发5例。结论:脊髓髓内胶质瘤宜早诊断并尽早接受手术治疗。显微神经外科技术可提高肿瘤全切,改善脊髓髓内胶质瘤的预后。星形细胞瘤应及时进行术后放疗和化疗。     

神经电生理监测下显微手术切除脊髓髓内肿瘤

目的 探讨在神经电生理监测下显微手术切除脊髓髓内肿瘤的效果。方法 回顾性分析2009年12月至2015年2月收治的102例髓内肿瘤患者临床资料。采用后正中入路手术切除肿瘤,所有手术均在神经电生理监测下进行。结果 肿瘤全切52例（50.98%）,大部分切除48例（47.06%）,部分切除2例（1.96%）。术后2周神经功能障碍改善16例（15.69%）,无变化20例（19.61%）,加重66例（64.7%）。98例随访3个月~2年,神经功能较术前改善94例（92.16%）,其中完全正常者67例（65.69%）;症状仍未恢复到术前4例（3.92%）,肿瘤复发4例（3.92%）。结论 采用显微手术切除髓内肿瘤是治疗该病的有效方法,术中神经电生理监测有助于手术的安全进行。     

脊髓髓内肿瘤的显微外科治疗

目的 总结脊髓髓内肿瘤的治疗经验.方法 回顾性分析36例经显微手术治疗的脊髓髓内肿瘤病人的临床资料,术中超声辅助定位5例.结果 室管膜瘤17例,低级别星形细胞瘤(WHO I ～II级)8例,高级别星形细胞瘤(WHO Ⅲ～Ⅳ级)3例,血管母细胞瘤3例,海绵状血管瘤2例,脂肪瘤、转移瘤、畸胎瘤各1例.室管膜瘤全切率82.4%,低级别星形细胞瘤为50.0%,高级别星形细胞瘤为33.3%,血管母细胞瘤、海绵状血管瘤和转移瘤均全切,脂肪瘤和畸胎瘤次全切.术后随访3个月,根据McCormick脊髓功能状态分级:I级23例,II级7例,Ⅲ级3例,Ⅳ级3例.结论 显微手术切除脊髓髓内肿瘤是目前最有效的治疗措施.术中超声有助于术中肿瘤定位,减少手术创伤.     

脊髓髓内肿瘤的显微手术治疗

目的研究脊髓髓内肿瘤的显微手术技巧。方法回顾分析了25例采用显微手术切除的脊髓髓内肿瘤病例。结果全切除18例,次全切除4例,部分切除3例。术后随访3～78个月,19例结果良好,6例结果差(3例死亡)。结论显微手术治疗脊髓髓内肿瘤大多数结果良好。不同类型的肿瘤采用不同的手术方法,熟练的显微技术和对脊髓保护的意识是手术成功的关键。     

脊髓髓内肿瘤的诊断及显微手术治疗

目的总结分析脊髓髓内肿瘤的诊断及显微手术治疗经验。方法回顾分析2000年1月至2005年5月收治的43例脊髓髓内肿瘤的临床特征、影像学表现、诊断及显微手术治疗效果;随访1～4年,并采用McCormick评分标准评价患者术前、术后的脊髓功能。结果肿瘤全切28例,次全切7例,部分切除8例。术后患者症状好转31例,无变化6例,加重6例,无手术死亡。结论①显微手术治疗脊髓髓内肿瘤效果良好,尤其对室管膜瘤、海绵状血管瘤等可做到全切而不产生明显的后遗症。②脂肪瘤因全切困难,且术后多数症状加重,要严格掌握手术时机及适应证。③对其它类型的髓内肿瘤,有症状者应积极早期手术治疗。     

脊髓髓内胶质瘤的显微神经外科手术处理

目的总结脊髓髓内胶质瘤显微神经外科手术治疗的经验。方法1999年至2005年共手术治疗脊髓髓内胶质瘤71例,男39例,女32例,年龄4~68岁(平均38.1岁),病程2个月~9年;肿瘤直径占脊髓横断面的60%~90%,长度跨越4~11个椎体;临床表现按McCormick神经功能分级:Ⅰ级11例,Ⅱ级49例,Ⅲ级8例,Ⅳ级3例。早期42例采用传统椎板切除术,后期29例采用整块切除棘突及椎板后再回植重建的方法进入椎管,在显微镜下沿脊髓后正中裂切开脊髓显露肿瘤并分块切除。结果手术全切肿瘤59例(83%),大部分切除12例(17%)。术后病理诊断:室管膜瘤51例(72%),星形细胞瘤19例(27%),恶性小圆细胞瘤1例(1%)。术后近期症状较术前加重或出现新的神经损害症状者40例(56%),症状改善或无变化者31例(44%)。随访6个月~6年,52例(73.2%)恢复正常工作或学习,13例(18.3%)可自理生活,6例(8.5%)不能自理生活;肿瘤复发2例。患者功能预后与术前神经功能分级密切相关,术前神经损害症状越轻,术后恢复越好。结论显微神经外科手术切除脊髓髓内胶质瘤是目前最有效的治疗措施,最佳手术时机是在患者尚未发生严重神经损害症状之前。     

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.     

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.     

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.