额叶癫(痫)与颞叶癫(痫)的临床与电生理对比分析

目的:对比分析额叶癫(痫)、颞叶癫(痫)发作期临床及脑电图表现.方法:统计2011～2012年视频脑电图(V-EEG)监测中发作的额叶癫(痫)和颞叶癫(痫)各30例,进行病因、影像学以及发作间期、发作期脑电图(EEG)和临床表现对比分析.结果:额叶癫(痫)、颞叶癫(痫)在发作间期、发作期的EEG及临床表现均有各自典型特征,如额叶癫(痫)各年龄段均有发作,颞叶癫(痫)主要集中于成人,额叶癫(痫)发作间期EEG诊断意义不大,额叶癫(痫)发作间期EEG具有一定病灶提示价值,发作期颞叶癫(痫)有先兆者居多且多数为口及消化系统自动症,而额叶癫(痫)多为过度动作,动作夸张且易出现姿势性扭转强直等.结论:V-EEG监测对于具有发作期的额叶癫(痫)、颞叶癫(痫)的诊断具有重要价值.     

发作间期的高频振荡定位药物难治性癫(痫)致(痫)灶(附1例报告并文献复习)

目的:报道对1例药物难治性癫电患者应用深部电极脑电图(EEG)长程监测发现的发作间期高频振荡分布及与其它辅助检查、临床症状的一致性,结合手术后疗效,分析高频振荡对药物难治性癫(痫)的定位价值.方法:记录患者自然安静睡眠高频振荡脑电活动5 min,对比围发作期症状、影像学资料、常规神经电生理资料,分析深部电极记录的高频振荡与其它资料的一致性,根据高频振荡进行手术后的临床效果评价,并结合文献资料进行分析.结果:29岁男性患者临床发作表现提示可能为右额病灶,PET-CT示右额中回低代谢,MRI表现为双海马萎缩,头皮EEG显示右额尖慢波,颅内电极高频振荡位于双颞叶内侧和右额,自然睡眠期左侧颞叶内侧最频发且波幅高(自动检测),深部电极EEG提示右额为起源灶(术后8h内癫(痫)持续状态,与惯常发作有异),主要参考发作间期高频振荡分布,进行立体定向射频热凝毁损左侧颞叶内侧后,患者术后4个月仅留先兆,不影响正常工作生活.结论:在患者安静睡眠期记录颅内电极发作间期高频振荡5 min,可以显示患者的潜在致(痫)灶,帮助临床定位.     

癫(痫)患者脑磁共振表现与脑电图异常的相关性

目的:探讨癫(痫)患者脑电图(EEG)异常部位与脑磁共振(MRI)异常部位的相关性.方法:收集2015年1月～2016年8月在南京脑科医院住院的290例癫(痫)患者的EEG及MRI结果进行回顾性分析.结果:EEG癫(痫)波检出率在MRI异常组为98.5％,显著高于MRI正常组(79.5％)(P＜0.05).耐药性癫(痫)的发生率在MRI异常组(26.1％)显著高于MRI正常组(10.3％)(P＜0.05).MRI异常部位与EEG异常部位的重合率在海马硬化组(95％)和脑发育不良组(84.6％)显著高于其它各组.耐药性癫(痫)的发生率在脑发育不良组(50％)及海马硬化组(30％)高于其他各组.结论:癫(痫)患者在MRI上显示海马硬化及脑发育不良时,其作为癫(痫)病灶存在的可能性极大,且耐药性癫(痫)的发生率高.     

以心功能障碍为初始唯一症状的颞叶内侧癫(痫)1例报告

癫(痫)先兆或发作时有自主神经症状或以自主神经症状为主的发作文献中早有记载,如1889年Jackson S等报告颞叶内侧癫(痫)发作有心率变化[1].少数病人心功能障碍为源于海马或岛叶的癫(痫)发作时的唯一症状[2].本文报告1例以心悸为主要症状的源于颞叶内侧的癫(痫)发作病例. 1病例报告 患者李某某,男性,54岁.2001年,患者开始出现突发性心悸的症状.2007年开农用车时心悸发作不慎翻车落入沟里受伤,送医后进行颅内穿刺抽液.     

热凝毁损杏仁核对痫性放电的抑制作用

目的探讨热凝毁损杏仁核对头皮痫性放电的抑制作用。方法对本院2005年1月~2006年5月收治的58例癫痫患者常规进行24小时视频脑电监测、偶极子分析,对有痫性放电的患者机器人辅助立体定向引导深部电极植入杏仁核,记录其电活动,其后热凝毁损杏仁核,复查深部电极和头皮脑电。结果58例癫痫患者全部记录到头皮棘尖波,56例(96.55%)存在杏仁核痫性放电。热凝毁损杏仁核后,其痫性放电消失42例,明显减少14例,无无效者,复查头皮脑电棘尖波消失20例,明显减少32例,无明显差别者6例。结论热凝毁损杏仁核可明显抑制包括颞叶内侧放电的半球痫性放电。     

皮质发育不良癫(痫)发作间期脑电图在术前评估的定位价值

目的:探讨头皮脑电图(EEG)在局灶性皮质发育不良(focal cortical dysplasia,FCD)癫(痫)病人发作间期的特点及定位致(痫)区的意义.方法:选择自2010年5月～2013年5月我中心收治的50例行颅内电极埋置术,并经病理证实为FCD的患者为研究对象.将颅内电极脑电图(intracranial e-lectrodes EEG,IEEG)发作间期放电(interictal discharge,IID)与头皮脑电图(EEG) IID分为四种类型:A型独立棘波;B型重复棘慢波;C型多棘波;D型阵发性快活动.IEEG发作期放电(ictal discharg,ID)分为3型:Ⅰ型阵发性快活动;Ⅱ型棘波节律;Ⅲ型小于8 Hz的节律性电活动.将50例患者头皮EEG-IID与IEEG-ID分析比较.结果:50例头皮EEG-IID的A、B、C、D各型的波形、部位与IEEG-ID相比,其间均有显著性差异.6例头皮EEG-IID在D型中,5例IEEG-ID为Ⅰ型,术后随访预后均为EngleⅠ级;10例头皮EEG-ID在C型中,7例IEEG-ID为Ⅰ型,术后随访为Engle Ⅰ级的6例;C、D型Engle Ⅰ级1 2例.而头皮EEG-IID中A型16例,术后随访EngleⅠ级的4例,定位意义明显弱于其它类型.结论:50例中头皮EEG-IID以棘波、尖波波形较为多见,且范围较IEEG-IID广泛.经过由皮层到头皮的传导,不论是IID还是ID,异常放电形式均有可能发生改变.头皮EEG的C、D型IID较为局限,定位可靠性较高.     

颅内电极皮层电刺激皮层后放电的抑制规律研究

目的:通过对后放电(AD)进行脉冲刺激抑制的研究,为皮层电刺激(ECS)治疗癫(痫)摸索合理的刺激参数.方法:回顾性研究2011～2012年行癫(痫)颅内电极埋置术并接受ECS病人的脑电图(EEG)资料共10例,如患者反复出现AD,即在相同位置给予相同参数的短暂脉冲刺激(BPS),有时可终止AD,对皮层AD的抑制规律进行分析.结果:对64个点重复刺激后可重复出现AD触点45个(70％),对这45个AD点给予BPS,其中13个(29％)在刺激后2s内AD终止,对比不同的AD波形、频率、部位、时相、累及范围、是否远隔、刺激潜伏期与BPS干预效果相关.结论:当在AD波形的负相峰及下降期,AD波形表现为棘慢波及节律性波,BPS潜伏期越短时,BPS干预AD更加有效.     

颞叶内侧型癫痫海马杏仁复合体发作间期的痫性放电特征与范围

目的探索颞叶内侧型癫痫海马杏仁复合体区发作间期痫性放电的特征与范围,为立体定向射频毁损提供可靠依据。方法 235例经多导长程视频脑电加偶极子定位检查提示为颞叶内侧型癫痫患者,经机器人辅助定位在海马杏仁复合体区植入深部电极,监测并分析其放电特征与范围,根据监测结果实施射频毁损术。结果 235例患者均检测到发作间期的痫性放电,共6种形式;痫性放电中心部位波动于靶点下20 mm至靶点上10mm。平均位于靶下6.3507±5.0325 mm。放电范围在垂直于颞叶长轴方向为5~35 mm,平均14.2639±5.1011mm。颅底与放电中心的距离波动于2~25 mm,平均为9.0097±2.9232 mm。结论颞叶内侧型癫痫的痫性放电部位与传统定位的靶点有一定差异,且放电范围各不相同,应以深部电极监测结果实施毁损。     

多项睡眠图联合长程视频脑电图监测癫(痫)患者夜间睡眠呼吸事件82例报告

目的:探讨癫(痫)患者睡眠中(痫)性放电对睡眠呼吸事件的影响.方法:对临床确诊的82例成人癫(痫)患者进行多项睡眠图(PSG)和长程视频脑电图(V-EEG)监测,分析其夜间睡眠中发作性事件情况,并探讨(痫)性放电及抗癫(痫)药的影响.结果:癫(痫)组入睡潜伏期、快速眼动(REM)睡眠潜伏期增加,浅睡期所占比例增多,深睡期所占比例减少,睡眠效率降低,夜间觉醒次数增多,睡眠呼吸暂停指数增高,与对照组比较差异均有显著意义(P＜0.01).周期性腿动事件与对照组比较无明显差异.(痫)性放电和抗癫(痫)药对睡眠呼吸暂停指数和周期性腿动指数未见明确影响.结论:癫(痫)患者存在睡眠结构紊乱和睡眠呼吸障碍,觉醒事件、呼吸事件、腿动事件三者之间相互影响,采用PSG联合V-EEG同步监测有利于全面分析睡眠结构与癫(痫)呼吸事件之间的关系.     

同步EEG-功能性MRI对颞叶癫痫致痫灶的定位作用

目的 探讨同步EEG-功能性MRI(fMRI)对颞叶癫痫致痫灶的定位作用.方法 对17例症状性颞叶癫痫患者进行同步EEG-fMRI检查.对EEG出现痫样放电时的fMRI数据进行分析,将痫样放电导致的脑组织血氧水平依赖信号改变区域叠加在MRI图像上,确定癫痫灶的位置;并与手术中脑皮质电极和深部电极EEG确定的致痫灶位置进行比较.结果 10例患者同步EEG-fMRI与皮质电极和深部电极EEG确定的致痫灶的位置和范围完全相同;另外7例患者同步EEG-fMRI确定的致痫灶中心位置与皮质电极和深部电极EEG相同,但范围比后者显示的扩大.癫痫灶切除术后14例发作控制,3例发作频率明显降低.结论 同步EEG-fMRI对颞叶癫痫致痫灶的定位准确,无创伤性;对手术定位具有可靠的指导作用.     

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.     

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.     

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.     

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.     

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.