难治性枕叶癫痫的术前定位与手术治疗

目的探讨难治性枕叶癫痫的术前定位与手术方法。方法对经手术治疗且随访时间6个月以上的9例枕叶癫痫患者的临床资料进行回顾性分析。采用发作症状评估、影像学检查、长程视频头皮脑电图监测、颅内电极脑电图记录等方法综合术前定位。根据术前定位确定的致痫灶部位与范围采用不同的手术方法。7例病人采用颅内电极置入术来精确定位。局部枕叶皮层切除2例,枕叶大部或全部切除4例,全枕叶或后头部脑叶离断3例;同期经枕入路切除或离断颞叶内结结构3例。结果术后随访6个月至2年,术后癫痫无发作6例,发作1次1例,发作减少90%以上2例。结论难治性枕叶癫痫经手术治疗可以取得较好的疗效,颅内电极脑电图记录有助于致痫灶准确定位,并指导术中切除部位与功能保护。     

MRI和CT阴性表现的脑致痫灶定位研究

目的回顾性分析难治性癫痫手术治疗的临床资料,探讨MRI和CT阴性表现病例的致痫灶定位方法.方法经MRI和CT检查呈阴性表现的癫痫患者42例,应用发作症状评估、长程头皮和颅内电极视频脑电图（video-EEG）监测等方法综合定位致痫灶.结果36例（85.7%）患者可以明确定位致痫灶,其中位于颞叶19例,额叶12例,额叶＋颞叶3例,顶枕叶2例;多灶性起源或定位不明确者6例,2例放弃手术.40例脑致痫灶组织均有不同程度的病理改变.结论一些局灶性皮质发育不良、微发育不良等细微脑组织改变通过现有的MRI和CT影像学检查尚难以发现,而它们常常是导致癫痫发作的病理基础.综合分析患者的临床发作特点,特别是长程EEG监测资料,可为大部分的此类病例明确定位脑致痫灶.     

难治性癫痫致痫灶的术前常用评估方法及有效性分析

目的分析难治性癫痫致痫灶的术前常用评估方法的定位价值,为术前评估方法的合理选择提供依据。方法回顾性分析2011年9月至2013年10月手术治疗的76例难治性癫痫的临床资料,分别评估症状学、头皮及颅内脑电图、影像学检查在术前致痫灶定位中的有效性。结果分别有88.1%、44.7%、82.9%的病人通过临床症状学、头颅MRI、头皮脑电图监测可获得一定价值的定侧或定位信息;在难治性颞叶内侧癫痫中,手术侧海马头M:RS NAA/(Cr+Cho)比值较对侧明显降低(P0.05),当双侧海马头NAA/(Cr+Cho)比值的不对称指数%0.08时,判断NAA/(Cr+Cho)比值较小一侧为致痫灶所在侧别的准确率更高。19例头颅MRI阴性并接受PET-CT检查的病人中,68.4%可获得一定价值的定侧或定位信息;仍有68.4%的病例需要通过颅内脑电图监测来进一步明确致痫灶的部位及范围。结论临床症状学分析及头皮脑电图监测对颅内电极的植入及致痫灶切除术有着重要的参考价值;MRI及MRS检查在难治性颞叶内侧癫痫的术前评估中存在一定的参考价值;PET-CT对于头颅MRI检查阴性的病例在癫痫手术中仍有着一定的参考价值;颅内脑电图监测对于致痫灶的判断及癫痫手术切除范围的限定仍有着决定性的意义。     

颅内电极脑电监测定位致痫灶

目的 探讨颅内埋置电极脑电图(iEEG)监测定位致痫灶的意义及其安全性。方法 对38例经无创方法难以定位的难治性癫痫病人，采用颅骨钻孔或骨瓣开颅方法埋置硬膜下和(或)深部电极，行长程视频脑电监测定位致痫灶。根据术中致痫灶定位、术后病理、术后疗效和EEG复查结果分析iEEG监测定位致痫灶的准确性。结果8例埋置深部电极，13例埋置硬膜下电极，17例联合应用硬膜下电极和深部电极。颅内电极埋置4～22d，平均9d；脑电监测8～226h，平均128h．根据癫痫发作初始期iEEG，32例(84．2％)病人准确定位了致痫灶，无颅内出血和感染等严重并发症发生。结论选择性应用硬膜下和深部电极长程视频脑电监测是一种安全、有效的检查方法；癫痫发作初始期异常放电的节律和范围是可靠的致痫灶定位指标．     

立体定向颅内脑电图在难治性癫痫治疗中的价值(附30例临床分析)

目的探讨立体定向颅内脑电图技术(SEEG)在难治性癫痫术前评估及癫痫灶定位中的作用与价值。方法回顾性分析中国医科大学航空总医院癫痫中心对于头皮脑电、电子计算机断层扫描(computed tomography, CT)、头颅磁共振(MRI)难以定位的药物难治性癫痫患者30例,根据其临床和术前影像学检查结果,设计SEEG方案并进行电极置入,长程记录发作3次以上并给予电刺激,结合发作间期及发作期深部脑电图确定致痫灶,手术切除后随访患者发作改善情况。结果 15例患者监测到局灶性发作,13例监测到区域性发作,2例患者监测到频繁全面性发作,30例患者均无电极植入后并发症,其中28例参照颅内脑电图结果行外科手术治疗,术后随访6～18个月,癫痫发作消失18例,5例缓解90%,5例缓解50%以上,无手术并发症。结论立体定向颅内脑电图在头皮脑电及磁共振难以明确致痫灶的难治性癫痫治疗中有重要的地位,为癫痫外科提供定位诊断价值,提高手术效果,减少手术并发症。     

颅内电极监测对顽固性颞叶癫痫致痫灶的定位价值

目的:探讨发作期及发作间期颅内电极监测对癫痫灶的定位作用。方法:20例难治性颞叶癫痫,经临床、影像学及头皮脑电图不能确定致痫灶部位,应用立体定向技术,在患者双侧颞叶植入硬膜下条状电极,进行长时间视频脑电图监测,记录发作期和发作间期的脑电图变化,并与头皮脑电图、MRI进行比较,分析癫痫灶部位,进行手术治疗,术后跟踪随访,评估致痫灶定位的准确性。结果:20例癫痫病人颅内电极埋藏时间1～5天,每个患者至少监测到2次临床发作,每一病例均记录发作间期和发作期的异常放电活动。15例发作间期与发作期定侧一致,2例发作间期为双侧棘波病灶,3例发作间期定位与发作期不一致。按Engel术后效果分级:手术效果满意(癫痫发作消失)13例(65%),显著改善3例(15%),良好3例(15%),无效1例(5%)。所有病例均未出现因颅内电极埋藏而致的并发症。结论:对于致痫灶不能定位的难治性癫痫,应用颅内电极记录方法,尤其是发作期起始时脑电图变化,可以确定致痫灶位置,为癫痫手术治疗提供可靠的依据。     

额叶癫癎发作的癫癎灶定位

目的 通过分析40例额叶癫痫发作患者术前定位的临床资料，探讨额叶癫痫发作的癫痫灶综合定位方法。方法 应用临床发作症状评估、MRI／CT扫描、单光子发射计算机体层摄影术(SPECT)检查、长程视频脑电图监测以及颅内电极记录等方法综合定位额叶癫痫患者的癫痫灶。结果 应用非侵袭性检查可以为45．0％的患者进行额叶癫痫灶定位；结合颅内脑电图长程记录，癫痫灶定位率可达90．0％；当影像学检查阴性时，78．9％的患者可以定位癫痫灶。结论 应用临床发作症状学评估、影像学检查、长程视频脑电图监测以及颅内脑电图长程记录相结合的综合定位方法，可以显著提高额叶癫痫发作的癫痫灶定位效果。     

枕叶癫痫的术前定位

目的:通过回顾分析9例枕叶癫痫患者的临床资料,讨论枕叶癫痫的临床特征和致痫灶的术前定位。方法:应用临床发作症状评估、CT/MRI扫描、SPECT/PET检查、长程视频脑电图监测、颅内电极记录以及皮层脑电监测等方法综合定位枕叶癫痫患者的致痫灶。结果:视觉先兆及头或眼向一侧偏转是最常见的发作早期改变;发作形式以复杂部分性发作为主,也可以继发全面性发作。致痫灶位于枕叶内侧面2例,背外侧面7例,其中致痫灶位于枕叶与顶叶的临界区1例,枕叶与颞叶的临界区或累及颞叶后部4例。术后随访1年以上,按照Engel's术后效果分级:Ⅰ级5例,Ⅱ级2例,Ⅲ级1例,Ⅳ级1例。结论:视觉先兆的出现常常提示致痫灶位于枕叶,MRI检查以及发作初始期头和眼向一侧偏转等症状学特点均有较高的定侧定位价值。当其他方法定位致痫灶较困难时,应用颅内电极记录有助于定位。     

颅内电极监测技术在癫痫手术中的应用

目的探讨颅内电极监测技术在难治性癫痫外科治疗中的应用价值。方法对头皮脑电图及影像学等非侵袭性检查难以确定致痫灶或致痫灶与重要功能区关系密切的51例难治性癫痫患者,行颅内电极埋置术,长程视频脑电图监测确定致痫灶,并行脑皮层电刺激功能区测定,再次手术切除致痫灶。结果术后致痫灶切除效果按Engel分级：I级32例,Ⅱ级13例,Ⅲ级5例,Ⅳ级1例。术后发生头皮愈合不良3例,延长住院时间后治愈。无脑脊液漏及永久性神经功能缺失发生。结论颅内电极监测可以精确定位致痫灶,皮层电刺激术对脑功能区定位可靠、方便,故对于采用非侵袭性检查不能明确致痫灶或致痫灶与重要功能区关系密切的难治性癫痫患者,颅内电极监测结合皮层电刺激术可以提高其治愈率,并有效降低并发症发生率。     

颅内电极脑电图监测对癫痫致痫灶的定位作用

目的探讨颅内电极脑电图（EEG）监测对癫痫致痫灶的定位作用。方法对经临床、影像学和常规EEG检查不能确定致痫灶部位的20例难治性颞叶癫痫患者，应用立体定向技术，经双侧颞叶植入硬膜下条状电极进行长时间EEG监测，观察发作期及发作间期EEG变化，结合常规EEG、MRI检查结果对癫痫灶进行综合定位；术后随访，评估致痫灶定位的准确性。结果20例患者颅内电极埋藏时间为1—5d，每例监测到／〉2次临床发作并记录发作间期和发作期的异常放电活动。20例患者发作期颅内电极EEG均能准确定位，15例致痫灶发作间期与发作期一致，2例发作间期为双侧棘波，3例发作间期定位与发作期不一致。术后按Engel疗效分级：发作消失13例（65％），显著改善3例（15％），良好3例（15％），无效1例（5％）。未出现因颅内电极安置所致的并发症。结论颅内电极EEG监测可为癫痫手术治疗提供可靠的病灶定位依据。     

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.     

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.     

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.     

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.     

The influence of comorbid depression on seizure severity

PURPOSE: To determine the relation between depressive symptoms and seizure severity among people with epilepsy. METHODS: A postal questionnaire was used to survey a nationwide community sample about seizures and depression. The Seizure Severity Questionnaire (SSQ) assessed the severity and bothersomeness of seizure components. The Centers for Epidemiological Studies-Depression scale categorized levels of depression. RESULTS: Respondents categorized as having current severe (SEV, n = 166), mild-moderate (MOD, n = 74), or no depression (NO, n = 443) differed significantly in SSQ scores (all p < 0.0001). People with SEV or MOD reported significantly worse problems than did those with NO depression for overall seizure recovery (mean, 5.3, 4.9, 4.5, respectively); overall severity (5.0, 4.5, 4.2); and overall seizure bother (5.3, 4.8, 4.4) (all p < 0.005). Cognitive, emotional, and physical aspects of seizure recovery also were rated worse among people with SEV than with NO depression (all p < 0.05). Symptoms of depression were significantly correlated with higher levels of all components of generalized tonic-clonic seizure severity (r = 0.33-0.48; all p < 0.0001), and partial seizures (r = 0.31-0.38; all p < 0.01). CONCLUSIONS: Clinically depressed people with epilepsy reported higher levels of perceived severity and bother from seizures, as well as greater problems with overall seizure recovery than did nondepressed people experiencing similar types of seizures. The pervasive influence of depressive symptoms on reports of seizure activity suggests that people with epilepsy should be screened for depression. These data highlight the importance of detecting and treating depression among people with epilepsy.     

Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity

Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.