脑梗死患者血清同型半胱氨酸与颅内外血管狭窄的相关性

目的探讨脑梗死患者血清同型半胱氨酸(Hcy)与颅内外血管狭窄的相关性。方法对行DSA检查的116例脑梗死患者进行分组,根据DSA所提示的颅内外血管狭窄的检查结果分为颅内外血管狭窄组(91例)、颅内外血管无狭窄组(25例);按狭窄部位又将狭窄组分为单纯颅内血管狭窄组(28例)、单纯颅外血管狭窄组(34例)及颅内外血管均有狭窄组(29例)。记录所有患者的常规危险因素,如年龄、性别、高血压、糖尿病、吸烟、饮酒及血生化指标如血清同型半胱氨酸(Hcy)、甘油三脂(TG)、胆固醇(CHO)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)等。结果(1)颅内外血管狭窄组血清Hcy升高的水平及比例明显大于对照组,分别为(17.6±10.1)mmol/L和(12.6±2.6)mmol/L,P=0.002;39.6%和16.0%,P=0.002。多元逐步Logistic回归分析发现,血清Hcy水平升高(OR=1.243,95%CI:1.047～1.476,P=0.013)、HDL降低(OR=0.089,95%CI:0.014～0.551,P=0.009)是颅内外血管狭窄的危险因素。(2)对于不同的狭窄亚组,血清Hcy升高的水平及比例在各组间无差异,分别为(18.1±10.9)mmol/L、(17.0±8.9)mmol/L、(17.7±10.7)mmol/L;比例分别为42.9%、38.2%、37.9%,P=0.11;多元逐步Logistic回归分析发现,血清Hcy升高是所有狭窄亚组的重要的危险因素(OR分别为1.367、1.232、3.846)。结论血清同型半胱氨酸水平升高是颅内外血管狭窄的危险因素。     

经颅多普勒监测蛛网膜下腔出血后脑血管痉挛的临床观察

目的总结应用经颅多普勒(TCD)监测蛛网膜下腔出血(SAH)后脑血管痉挛的临床价值。方法对2015-06—2016-05本院收治的78例SAH患者进行回顾性分析,均进行TCD监测,同时对患者进行数字减影血管造影(DSA)检查,观察各个时间段患者颅内血管血流速度变化,并以DSA检查结果作为标准判断TCD诊断颅内血管痉挛的价值。结果在7~10d时间段,患者的MCA、ACA、VA、BA血流速度达到峰值,后逐渐下降,颅内血管痉挛现象逐渐缓解;SAH患者MCA、ACA、VA、BA血流速度在7d、7~10d、10~14d三个时间段比较差异均具有统计学意义(P0.05);78例SAH患者,TCD诊断发生颅内血管痉挛59例,DSA诊断发生率颅内血管痉挛62例,TCD诊断SAH患者发生颅内血管痉挛的灵敏度为93.55%、特异度为93.75%、漏诊率为6.45%、误诊率为6.25%,TCD诊断颅内血管痉挛与DSA的一致性Kappa=0.816,P0.05。结论 TCD检查诊断SAH后出现颅内血管痉挛具有准确性高、无创等优点,值得临床推广应用。     

缺血性脑卒中患者颅内/外脑大动脉粥样硬化性狭窄的分布及其预测因素

目的探讨缺血性脑卒中患者脑动脉粥样硬化性狭窄的分布及其预测因素。方法对行数字减影血管造影(DSA)的连续的297例动脉粥样硬化性缺血性脑卒中患者进行分组,具有颅内/外大动脉狭窄(狭窄率＞50%)的241例患者作为狭窄组,未发现狭窄或轻度狭窄(≤50%)的56例患者作为小动脉闭塞对照组。按照狭窄部位又将狭窄组分3种模式:颅内与颅外狭窄并存(Ⅰ组,n=92)、单纯颅内动脉狭窄(Ⅱ组,n=102)及单纯颅外动脉狭窄组(Ⅲ组,n=47)。记录所有患者的常规危险因素如年龄、性别、高血压、糖尿病、长期吸烟、长期饮酒及血液学指标如血浆同型半胱氨酸(Hcy)、三酰甘油(TG)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)及纤维蛋白原(Fib)水平等。结果经多变量Logistic逐步回归分析,血浆Hcy水平升高〔OR为3．79,95% CI为(1．79,8．03)〕、长期吸烟〔OR为2．79,95% CI为(1．58,4．93)〕及高龄〔OR为1．34,95% CI为(1．13,1．59)〕是脑大动脉病变的独立预测因素;对于不同的狭窄分布,血浆Hcy水平升高(OR分别为Ⅰ组3．41,Ⅱ组4．49,Ⅲ组2．42)及长期吸烟(OR分别为Ⅰ组3．79,Ⅱ组4．40)几乎是所有狭窄模式的重要预测因子。其他危险因素中,高龄为Ⅰ组(OR为2．41)、Fib为Ⅰ组(OR为2．66)和Ⅲ组(OR为2．89)、TG升高(OR为1．77)为Ⅱ组的独立预测因子。结论颅内、外脑大动脉粥样硬化性病变的危险因子不同,可以部分解释中国患者颅内病变多于颅外病变的特点。高同型半胱氨酸血症及长期吸烟对颅内动脉病变的影响大于颅外,高纤维蛋白原血症为颅外动脉病变的特殊预测因子。     

伴有颅内动脉狭窄的缺血性脑卒中患者脑血管储备能力研究

目的 对伴有颅内动脉狭窄的缺血性脑卒中患者采用口服乙酰唑胺实验研究颅内大动脉血流储备能力.方法 对17例经磁共振血管显影(magnetic resonance angiography, MRA)/或经颅多谱勒超声(transcranial doppler ultrasonography, TCD)证实颅内动脉狭窄大于50%的缺血性脑卒中患者,按TOAST分型为动脉粥样硬化性脑梗死,通过TCD共测定187条颅内大血管血流速度,2 d后再口服乙酰唑胺2 g, 2 h后再行TCD检查,比较乙酰唑胺前后颅内大血管血流速度改变情况.结果 乙酰唑胺实验可使颅内血管血流速度明显增加.右颈内动脉(right internal carotid artery,RICA)、右大脑中动脉(right middle cerebral artery,RMCA)和右大脑后动脉(right posterior cerebral artery,RPCA)在乙酰唑胺后血流速度增加但无统计学差异(P值分别为0.086,0.258,0.084),而其他颅内血管在乙酰唑胺后血流速度显著增加(P值都小于0.05).非狭窄血管较狭窄血管乙酰唑胺后血流速度增加,但无统计学差异(P=0.08).中度狭窄血管与重度狭窄血管乙酰唑胺后血流速度改变无差异(P=0.65).结论 乙酰唑胺前后TCD可以准确测定颅内大动脉的血管血流储备能力,颅内狭窄血管较非狭窄血管血流储备能力有下降的趋势,而中度和重度狭窄血管血流储备能力无明显差异,但仍有待进一步的研究.     

散发性颅内破裂动脉瘤的流行病学研究

目的探讨散发性颅内破裂动脉瘤的流行病学特点。方法应用病例对照研究,对100例散发性颅内破裂动脉瘤病人及116例非颅内动脉瘤病人进行流行病学调查,采用卡方检验及多元Logistic多因素回归分析对各相关危险因素进行统计学分析。结果单因素分析结果表明:63%的散发性颅内破裂动脉瘤病人在40～59岁之间;颅内动脉瘤组与非颅内动脉瘤组在性别(P=0.036,OR=1.794)、吸烟(P=0.005,OR=2.327)、血压(P=0.005,OR=2.161)和空腹血糖(P<0.001,OR=4.114)等方面的差异具有统计学意义。以年龄、性别、吸烟、饮酒、冠心病史、血压和空腹血糖等因素为自变量,Logistic多因素回归加权分析表明:性别(P<0.001,OR=9.435)、吸烟(P<0.001,OR=0.098)、高血压(P=0.016,OR=2.195)和空腹血糖(P<0.001,OR=4.019)仍与颅内动脉瘤的发生明显相关。结论散发性颅内破裂动脉瘤好发于40～59岁之间;女性、吸烟、高血压及空腹血糖增高是颅内动脉瘤的危险因素。     

急性脑梗塞与脑出血相关因素的对比研究

目的:探讨不同危险因素在脑卒中发生的情况及不同危险因素在脑梗死与脑出血间的差异。方法:将收治的卒中患者共408例,其中脑梗死281例,脑出血127例,均预先对各项资料进行编码,输入计算机数据库。所有患者均进行系统的临床和辅助检查,生化指标为集体测定,脑卒中诊断经过MRI或CT确诊。结果:1、高血压、吸烟是脑卒中最重要的危险因素。2、脑出血患者首诊舒张压(P=0．014)、缓解期舒张压(P=0．006)、HDL(P=0．034)、较脑梗塞患者高,其差别有统计学意义;其TC(P=0．047)、吸烟(P=0．007)、心脏病病史(P=0．020)、糖尿病病史(0．000)、卒中家族史(P=0．033)、心脏病家族史(P=0．040)较脑梗塞患者低或少,其差别有统计学差异。3、与脑梗塞相比,吸烟(OR=0. 226,95％CI=0．107—1．623)、糖尿病病史(OR=0．094,95％CI=0．023—2．401)、心脏病病史(OR=0．046,95％CI=0．236-0．905)对脑出血危险较小;高血压病史(OR=1．096,95％CI=0．542-0.895)是脑出血唯一危险因素。结论:高血压、吸烟是脑卒中最重要的危险因素;脑梗塞与脑出血的危险因素并不完全一致。     

颅内动脉中重度狭窄的危险因素研究

目的 探讨颅内动脉狭窄的危险因素。方法 2006年4月～12月连续收集急性缺血性卒中患者136例，所有病例均行脑血管数字减影血管造影（DSA）或经颅多普勒超声（TCD）联合磁共振血管成像（MRA）确定是否存在颅内血管狭窄。63例（46.3%）颅内动脉存在中度以上狭窄患者作为病例组，73例（53.7%）无明显颅内动脉狭窄患者作为对照组，对两组患者的危险因素进行统计学分析。研究变量包括人口学因素、既往病史及个人史。结果 单变量分析发现两组患者间高血压、脂代谢紊乱、缺血性心脏病、吸烟史水平间差别有显著性意义（P <0.05）；多元logistic回归分析发现，高血压病（OR =2.631，95%CI 1.124～6.160，P =0.026）、脂代谢紊乱（OR =2.255，95%CI 1.060～4.797，P =0.035）是颅内动脉狭窄的独立危险因素。结论 高血压、脂代谢紊乱可能是导致颅内动脉狭窄形成的独立危险因素，应进行大样本的队列研究加以证实。     

经颅多普勒超声椎动脉血流速度减低的病理机制与鉴别诊断

目的 探讨缺血性卒中患者椎动脉血流速度减低的病理机制及超声鉴别诊断.方法 纳入经颅多普勒超声(transcranial Doppler ultrasound,TCD)显示椎动脉血流速度减低的缺血性脑卒中患者168例,以数字血管减影(digital subtraction angiography,DSA)为"金标准"进行分组,比较各组椎动脉峰值流速(systolic velocity,Vs)及血管搏动指数(pulsatility index,PI)的差异.结果 椎动脉正常组41 例(24.4%);椎动脉发育不良/变异组55例(32.7%);椎动脉狭窄组72例(42.8%).正常组双侧椎动脉Vs及PI无统计学差异(P＞0.05);狭窄组患侧椎动脉Vs 低于健侧(P=0.000),PI 双侧对比无统计学差异(P＞0.05);发育变异组患侧椎动脉Vs 低于健侧(P=0.001),PI则高于健侧(P=0.004).不同病变类型血流动力学的比较显示,椎动脉起始段≥70%狭窄者、椎动脉变异者及颅内段闭塞者Vs均低于正常椎动脉(均P＜0.05),椎动脉起始段轻-中度狭窄者Vs与正常椎动脉无统计学差异(P=0.195);正常椎动脉PI与上述各组比较均有统计学差异(P＜0.05),椎动脉起始段≥70%狭窄者PI最低(0.77±0.37),低于正常椎动脉、椎动脉变异、椎动脉起始段轻-中度狭窄及颅内段闭塞者(均P＜0.05);而颅内段闭塞者PI则明显高于上述各组(1.47±0.13,P=0.000).结论 TCD椎动脉血流速度减低可见于椎动脉正常、发育不良/变异、起始段重度狭窄/闭塞以及颅内段闭塞,双侧椎动脉血流速度和PI对称性的比较对于鉴别诊断具有重要意义.     

血浆脂蛋白磷脂酶A2与脑梗死严重程度及预后的相关性研究

目的 探讨血浆脂蛋白磷脂酶A2(lipoprotein-associated phospholipase A2,Lp-PLA2)水平与急性脑梗死(acute cerebral infarction,ACI)患者病情严重程度及预后的相关性。方法 选取2017—2019年江苏大学附属昆山医院神经内科住院的207例急性脑梗死患者,检测Lp-PLA2及高密度脂蛋白(HDL)、低密度脂蛋白(LDL)、脂蛋白a[LP(a)]、同型半胱氨酸水平(Hcy),详细记录患者有无高血压史、糖尿病史、吸烟、饮酒史。采用美国国立卫生研究所卒中量表评分(NIHSS)评估脑梗死严重程度,通过患者3个月的改良Rankin量表(mRS)评分评估其短期预后,分析LP-PLA2水平与脑梗死严重程度与预后的相关性。结果 Lp-PLA2(OR=1.016,95%CI:1.011～1.021,P0.01)、LDL(OR=1.574,95%CI:1.137～2.178,P=0.006)、Hcy(OR=1.044,95%CI:1.008～1.082,P=0.017)、年龄(OR=1.071,95%CI:1.041～1.101,P0.01)、吸烟(OR=0.256,95%CI:0.139～0.471,P0.01)为脑梗死患者病情严重程度的独立危险因素,性别、饮酒、高血压史、糖尿病史、HDL、LP(a)则差异无统计学意义(P0.05)。Lp-PLA2(OR=1.03,95%CI:0.986～1.067,P0.01)、吸烟(OR=0.397,95%CI:0.16～0.984,P=0.046)、脑梗死病情的严重程度(OR=0.04,95%CI:0.009～0.167,P0.01)是影响脑梗死预后的独立危险因素。结论 除传统的吸烟、LDL、Hcy、年龄危险因素外,Lp-PLA2亦是影响脑梗死患者病情严重程度的独立危险因素,且影响脑梗死患者的预后。Lp-PLA2或可作为标志物用于预测脑梗死病情严重程度及预后。     

缺血性脑卒中患者血清尿酸水平与颅内动脉狭窄的关系

目的 研究缺血性脑卒中患者血清尿酸水平与颅内动脉狭窄的关系.方法 对60例缺血性脑卒中患者进行数字减影血管造影检查,根据其颅内动脉狭窄程度分为狭窄组与无狭窄组.检测其血清尿酸、血脂及同型半胱氨酸(Hcy)水平,并进行比较.结果 根据DSA检查结果,将患者分为狭窄组(45例)和无狭窄组(15例).狭窄组男性、高血压、糖尿病、吸烟史、饮酒史、高血脂的比率及血尿酸水平显著高于无狭窄组(P ＜0.05～0.01).Logistic回归分析显示,高血压是颅内动脉狭窄的独立危险因素(OR=55.730,95％CI:1.100 ～2823.152;P ＜0.05).结论 高尿酸与颅内动脉狭窄有关,但不是其独立危险因素.     

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.     

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.     

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.     

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.     

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.     

Pediatric Epilepsy Surgery

Summary: The use of implantable arrays of epidural electrodes has made it possible to carry out extraoperative electrocorticography (ECoG) and functional localization in the awake child. This has permitted cortical excisions that are determined by criteria similar to those obtained during surgical procedures performed under local anesthesia in adults. In addition, the method also permits simultaneous ECoG and video monitoring during the child's symptomatic seizures, providing additional important localizing information that is impractical to obtain in operations under local anesthesia. We report our experience with 75 children, ages 5 months to 15 years, whom we have managed with epidural electrode arrays. The method of extraoperative ECoG is described and illustrative cases are presented to demonstrate its feasibility and utility in children. In addition, we call attention to gliomas as a common cause of chronic focal seizures in children. Of 49 children undergoing resection and followed for from 1 to 14 years (mean of 5.8 years), 32 (65%) are either seizure free or have had a significant reduction in seizure frequency that has unambiguously improved their quality of life. The results are analyzed further by relating the surgical outcome to each of the pathologic entities that caused the seizures. This analysis reveals the variety of neurological conditions that commonly cause intractable focal seizure disorder in children and distinguishes those pathologic entities in which the seizure disorder is apt to respond to surgical intervention from those that will not.