脑立体定向植入海马电极监测颞叶内侧癫痫的临床研究

目的 观察应用脑立体定向微创穿刺技术植入海马电极监测颞叶内侧癫痫的效果.方法 13例耐药性颞叶内侧癫痫患者,主要表现为复杂部分性癫痫发作及继发性全身强直阵挛性发作.根据临床症状、MRI等资料初步确定癫痫灶位于海马区域,在脑立体定向仪引导下于双侧海马植入8-触点深部电极,监测24 ～ 72 h,从而确认癫痫灶是否位于海马区域.结果 13例患者经过72 h监测,共监测到7例有29次临床发作,发作期脑电变化表现为在背景波形基础上出现阵发性高幅慢波或棘尖慢复合波,从某个电极点开始,迅速扩展到同侧其他电极点甚至对侧电极;头皮脑电在延迟1～2s后出现3～4 Hz的高幅δ节律.6例未监测到临床发作的患者,海马电极监测到发作性局灶性高幅慢波或尖慢综合波,而头皮电极未监测到明显异常.13例患者中6例接受选择性海马杏仁核切除或立体定向病灶损毁术,随访3～8个月,效果满意.结论 脑立体定向植入海马电极监测颞叶内侧癫痫是一种安全可靠的方法,可以判断癫痫病灶的起源,为外科进行选择性海马杏仁核切除提供有力依据,对于视频脑电图或其他手段难以记录到癫痫样波形或难以判断癫痫样放电起源的患者可进行脑立体定向深部电极脑电图监测.     

颞叶癫痫脑电图分析及病灶超微结构观察

目的 研究影像学检查无异常的颞叶癫痫患者,电生理异常与皮层棘波灶及海马超微病变的关系.方法 选择经CT或MRI检查未见异常的颞叶癫痫患者7例,术前做脑电图或24h视频脑电监测,术中在脑电监测下取颞叶大脑皮质棘波灶和海马组织,做电镜观察.结果 7例患者电生理检查均可见典型痫样放电.颞叶皮质痫灶和海马可见不同程度的神经元固缩,胶质细胞变性,胶质增生,突触数量及突触结构改变,血脑屏障破坏等改变.结论 影像学无异常的颞叶癫痫患者颞叶皮层痫灶和海马超微结构病理变化明显,特别是突触的变化,是导致癫痫患者脑电生理机能异常及癫痫反复自发性发作的形态学基础.     

颅内电极脑电图发作前期脑电活动特点在癫发作定位中的作用

目的分析颅内电极脑电图发作前期脑电活动特点,探讨其与不同发作起源部位及术后病理的关系,为癫定位诊断提供依据。方法回顾性分析19例症状性难治性癫病人的临床资料,根据颅内电极记录的发作起始部位不同,将病人分颞叶外癫(n=11)和颞叶癫(n=8)。分析两组发作前期脑电的放电类型以及病理结果。结果颞叶外癫病人发作前期脑电多表现为周期样节律性快活动,颞叶癫发作前期均表现为周期样多棘/棘-慢波放电。两组病人发作前期脑电活动的放电类型存在统计学差异(χ~2=40.358,P0.01)。术后病理结果显示局灶性脑皮质发育不良(focal cortical dysplasia,FCD)不同亚型之间的发作前期脑电活动存在统计学差异(χ~2=25.050,P0.01)。结论起源于颞叶外的癫,发作前期脑电活动多表现为周期样节律性快活动,病理分型以FCDⅡ型多见。而起源于颞叶的癫,发作前期则以周期样多棘/棘-慢波放电为主要放电表现,病理分型多见于FCDⅠ型。     

难治性颞叶内侧癫痫术前评估方法再评价

目的 通过难治性颢叶内侧癫痫术后随访1年以上,术后效果达到Engel's Ⅰ级(无发作)的患者,探讨各种术前评估方法确定癫痫灶的可靠程度.方法 65名术后随访超过1年,术后达到Engel's Ⅰ级疗效的难治性颞叶内侧癫痫患者,患者的发作症状学、神经影像和头皮脑电图进行回顾性分析.结果 所有患者的发作间期正电子发射断层扫描(PET)显示与手术侧一致的颞叶低代谢改变;41例患者发作前存在典型的颞叶内侧常见先兆,所有患者发作起始表现为意识障碍;28例患者有手术侧颞叶影像异常(图1),8例患者存在双侧颞叶异常,8例患者存在多脑叶影像异常,21例患者核磁共振检查未发现明显异常;20%患者发作间期偶有异常、80%患者存在多灶棘波、尖波、棘慢波;发作期脑电放电早期显示:20例患者无法确定起源侧别,45例患者可以确定侧别(手术侧),只有21例患者可以清楚的显示手术侧蝶骨电极起源.结论 患者的发作症状学分析和PET检查是难治性颞叶内侧癫痫术前评估中基本和重要的评估手段.     

27例学龄前难治性颞叶癫痫患儿临床报道

目的探讨学龄前难治性颞叶癫痫患儿影像学、电生理特点及手术方法和疗效。方法回顾性分析解放军联勤保障部队第九八八医院神经外科中心自2014年6月至2019年1月行手术治疗的27例学龄前难治性颞叶癫痫患儿资料,术前评估结合临床发作表现,MRI、磁共振波谱分析(MRS)、正电子发射断层扫描(PET-CT)等影像资料,以及发作间期和发作期视频脑电图(VEEG)资料;术中应用皮层脑电图(ECoG)与深部电极监测定位异常放电区域,指导手术切除致痫灶范围。术后采用Engel分级评估疗效。结果27例患儿均有典型颞叶癫痫临床表现,MRI发现一侧颞叶及海马异常信号影,发作间期及发作期VEEG提示异常放电起始于一侧额颞部。术中ECoG及深部电极监测均发现颞叶明显持续或阵发性尖波、棘波、棘慢复合波等癫痫样放电。27例患儿均采用标准前颞叶+病灶切除+周边异常放电颞叶皮质扩大切除术,其中2例患儿切除部分岛叶长回及额盖皮质热灼处理。随访6个月,EngelⅠ级患儿22例,EngelⅡ级患儿3例,EngelⅢ级患儿2例。结论早期手术、术中ECoG与深部电极联合监测下适度扩大切除范围是改善学龄前难治性颞叶癫痫患儿手术疗效的关键因素。     

立体定向杏仁核海马毁损治疗颞叶癫痫

目的探讨立体定向杏仁核海马毁损治疗颞叶癫痫的原理、方法和疗效。方法患者头部安装MD～2000立体定向框架。使其平行于颞角长轴。针对12例颞叶顽固性癫痫患者,应用头部MRI扫描定位,局麻下深部电极行杏仁核及海马脑电监测和射频毁损术。结果射频毁损前12例患者深部电极均记录到杏仁核和海马区棘波、尖波或多棘波,术后显示痴样放电消失。术后随访9～18个月．癫痫发作完全控制者58．3％（7／12）,显著改善33．3％（4／12）。结论立体定向杏仁核海马毁损术治疗颞叶顽固性癫痫是一种安全有效的微创治疗方法,值得临床推广。     

青霉素致大鼠急性癫痫模型全身性放电起源的实验研究

目的 探讨青霉素致大鼠急性癫痫模型全身性放电起源的定位特征.方法 给10只SD大鼠各铺设皮层、海马和杏仁核电极共7对,用青霉素300万U·kg-1腹腔注射建立急性全身性癫痫模型,同时脑电记录,观察全身性癫痫样放电起始阶段的脑电特征.结果 脑电显示全身性癫痫样放电起始阶段杏仁核最早出现连续性棘波.结论 青霉素诱导的急性全身性癫痫大鼠模型癫痫样放电并非完全同步化,杏仁核为癫痫易感区,可能参与放电起源.     

间断性海马电刺激治疗顽固性颞叶癫痫的研究

目的 探讨间断性电刺激海马结构治疗顽固性颞叶癫痫.方法 对10例颞叶内侧型癫痫的患者行立体定向经枕入路钻孔,沿海马长轴置入脑深部普通4导电极;视频脑电监测并定侧定位致痫灶(海马);选择刺激区域,给予高频低电流间断电刺激,每天分别选取同一时间段刺激2次,间隔6h,连续刺激2～3d.在刺激区域记录脑电活动,并分析和统计刺激前、后的棘波数量变化.结果 在电刺激期间,6例刺激前、后比较棘波数减少＞50％,3例减少＞30％,1例效果不明显,棘波数减少＜10％.10例经急性电刺激前、后棘波数比较,影像未显示海马硬化的病例较有海马硬化的病例棘波数减少幅度大.结论 通过统计电刺激前后脑电图中棘波数量的变化,呈现出棘波数明显减少,证实了间断电刺激海马治疗颞叶内侧型癫痫的有效性和可行性.     

颞叶癫痫海马萎缩与头皮脑电发作时放电相互矛盾的手术策略(附5例临床分析)

目的本文报告了一侧海马硬化对侧颞叶头皮脑电放电的临床特点、手术策略及预后。方法本组回顾了5例MRI提示海马萎缩,头皮EEG表现为发作放电在海马萎缩对侧。采用深部电极检查并与头皮EEG和MRI检查结果进行了比较,手术方法为前颞叶切除加海马-杏仁和切除术。结果5例病人均有发作先兆表现;发作放电时头皮EEG表现出的痫样放电波在海马萎缩对侧5例,发作放电间期的头皮EEG表现出的痫样放电波与海马萎缩同侧者3例,1例在海马萎缩对侧,1例为双颞叶弥漫性放电;深部电极检查与MRI结果一致;术后随访2~4年,Ⅰ级4例,Ⅱ级1例。结论颞叶癫痫发作间期痫样放电比发作期痫样放电定位更为准确;MRI与头皮EEG检查结果不一致时,深部电极检查有助于术前定位。     

额叶癫痫的特点及手术治疗

目的 :分析额叶癫痫的临床特征、发作期及发作间期脑电图特点 ,探讨额叶癫痫手术治疗。方法 :应用视频脑电图对 9例额叶癫痫患者进行长程监测 ,并对其中 6例记录颅内脑电图。分析癫痫发作的临床表现及脑电图特点 ,定位致痫灶 ,行手术切除。结果 :额叶癫痫的发作特点为 :发作频繁而短暂 ,以睡眠期发作为主 ,常见过度运动 ,姿势性强直 ,发声等发作症状。发作期可见棘波节律 ,广泛低幅快活动 ,节律性慢波等特征性脑电活动。颅内电极记录可清晰显示异常脑电活动的发作起源及扩散情况 ,有助于定位致痫灶。手术切除病灶及致痫灶 ,效果满意。结论 :额叶癫痫是一组具有特征性的癫痫综合征 ,颅内电极记录有助于揭示其脑电活动变化。对于难治疗性额叶癫痫 ,准确定位致痫灶是手术成功的关键。     

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.