DWI对MCA狭窄患者卒中亚型的诊断

目的:评价弥散加权MRI(Diffusion-weighted imaging,DWl)对MCA狭窄患者急性梗死的诊断价值。方法:经TCD／MRA诊断的症状性大脑中动脉粥样硬化性狭窄(以下简称MCA闭塞性病变:middle cerebral artery occlesive disease MCAOD)患者,分别于病后1周内行头颅水抑制MRI成像(Fluid-attenuated inversion recovery,FLAIR)及DWI检查,比较FLAIR、DWI所示梗死灶的类型和数量。结果:238例症状性MCAOD患者的FLAIR结果表明,单发腑梗死137例(57.6％),多发性脑梗死101例(42.4％)。其中皮层区域内梗死82例(34.5％),深部小梗死120例(50.4％),变界区梗死143例(60.1％)。而内交界区梗死、半卵园中心梗死以及伴随的皮层小梗死的发生率分别为52.9％、22.7％、13.0％,84例MCAOD患者的DWl结果表明,73.8％患者呈多发性脑梗死表现,皮层区域内梗死、交界区梗死、深部小梗死的发生率分别为46.4％、56％和44.0％,而皮层播散性小梗死(22.6％)、半卵园中心梗死(29.1％)的诊断率高于FLAIR结果。结论:DWI对于微小梗死以及多发梗死的诊断明显优于FIAIR成像,尤其对于皮层播散性小梗死灶以及半卵园中心梗死的诊断更敏感,利于卒中亚型的诊断及卒中机制的判断。     

动脉硬化性大脑中动脉狭窄或闭塞所致脑梗死类型

目的探讨动脉硬化性大脑中动脉狭窄或闭塞性疾病(MCAOD)所致脑梗死的类型。方法对50例经颅脑MRA或DSA确诊的症状性MCAOD患者进行研究,依据其头部弥散加权成像(DWI)和T2W的改变对脑梗死分型。结果50例患者共发现57条动脉硬化性大脑中动脉狭窄或闭塞,未发现病灶的有6(占12．0%)个大脑半球,多发性脑梗死和单发脑梗死分别见于13(占22．8%)个和38(占66．7%)个大脑半球。脑分水岭梗死、流域性脑梗死、半卵圆区脑梗死、多发性散在点状脑梗死(MSSI)、腔隙性脑梗死分别见于18(占31．6%)个、12(占21．1%)个、6(占10．5%)个、2(占3．5%)个和1(占1．8%)个大脑半球。结论MCAOD可引起各种类型的脑梗死,脑分水岭梗死约占1/3,动脉粥样硬化性血栓形成约占1/5,纹状体内囊梗死约占1/5,主要发病机制与动脉-动脉栓塞和低灌注有关。     

大脑中动脉狭窄与其深穿支供血区单发脑梗死的关系

目的 分析大脑中动脉(MCA)深穿支供血区单发脑梗死的形态学表现,进一步探讨其与MCA狭窄的关系.方法 连续入选2005年1月至2006年12月于北京协和医院神经科住院治疗急性脑梗死,并经头颅DWI检查明确急性梗死灶为单发,且位于MCA深穿支供血区域的55例患者;所有患者均行TCD和MRA检查,颅外颈内动脉狭窄>50%以及有可疑心源性栓子来源的患者从研究中排除.根据是否存在病灶同侧MCA狭窄将入选患者分为两组:MCA狭窄组(14例)与MCA正常组(41例).测量DWI上急性梗死灶的直径、面积和体积,并将直径≤2 cm归为经典腔隙性梗死,直径>2 cm归为纹状体内囊梗死.DWI上的梗死灶区分为基底节区、侧脑室体旁和同时累及上述2个部位,并判断MRI T2>像上皮质下多发陈旧性小梗死灶或白质疏松是否存在.结果 55例患者中,病灶侧MCA狭窄患者14例(25.5%),MCA正常患者41例(74.5%).MCA狭窄组中经典腔隙性梗死占71.4%,MCA正常组中经典腔隙性梗死占67.3%,差异无统计学意义(χ2=0.147,P=0.701).MCA狭窄组与正常组患者MCA深穿支梗死病灶的大小(包括直径、面积及体积)差异均无统计学意义.MCA正常组和MCA狭窄组病灶在基底节区、侧脑室体旁及基底节区+侧脑室体旁分布的比例依次为:正常组31.7%、17.1%和51.2%;狭窄组35.7%、28.6%和35.7%,两组间差异无统计学意义(χ2=1.272,P=0.529).同时存在皮质下多发陈旧性小梗死灶或白质疏松的患者在MCA正常组有23例(56.1%),在MCA狭窄组有3例(21.4%),二者差异有统计学意义(χ2=5.033,P=0.025).结论 MCA深穿支供血区梗死具有不同的发病机制,MCA狭窄和穿支动脉本身病变均可造成深穿支供血区单发脑梗死.梗死灶的大小、体积及梗死发生的部位与是否存在同侧大脑中动脉狭窄无明显相关性,而同时存在皮质下多发陈旧性小梗死灶或白质疏松对穿支动脉病变有提示作用.     

大脑中动脉重度狭窄或闭塞患者脑梗死病灶类型与CT灌注成像分析

目的比较大脑中动脉(MCA)重度狭窄或闭塞患者不同脑梗死病灶类型的灌注状态。方法对89例MCA严重狭窄或闭塞患者进行头颅320排CTA+CT灌注成像检查,比较不同梗死病灶类型患者MCA闭塞率、侧支循环程度、MCA供血区灌注情况。结果 89例患者中,穿支动脉梗死(PAI)8例(9.0%)、皮质分支动脉梗死(PI)7例(7.9%)、大面积梗死(LTI)7例(7.9%)、分水岭梗死(BZI)43例(48.3%)、多发性脑梗死(MI)13例(14.6%)、无梗死灶11例(12.4%);不同类型梗死灶间MCA M1段病变、血管闭塞及不良侧支循环比率差异无统计学意义(均P0.05)。不同类型梗死灶局部脑血流量(rCBF)患健比、达峰时间(TTP)患健比差异有统计学意义(均P0.05)。BZI组rCBF患健比显著高于LTI组与无梗死灶组(均P0.05);LTI组及BZI组TTP患健比显著高于无梗死灶组及PAI组(均P0.05),MI组TTP患健比较无梗死灶组升高(P0.05)。LTI组MCA供血区低灌注发生率显著高于无梗死灶组(P0.05)。不同亚型BZI组间低灌注异常及不良侧支循环率差异有统计学意义(均P0.05),各灌注参数、MCA M1段病变及闭塞比率差异无统计学意义(均P0.05)。结论 LTI为失代偿期表现,低灌注发生率最高,其余类型为代偿期表现。皮质下型分水岭梗死较其他亚型侧支循环差,低灌注发生率更高,与血流动力学受损为主要病因的观点相符。MCA重度狭窄或闭塞患者脑梗死病灶类型以BZI为主。     

116例大脑中动脉病变患者脑梗死类型分布和脑灌注异常分析

目的 应用神经影像检查,分析大脑中动脉闭塞性疾病(MCAOD)患者梗死类型分布和脑灌注异常. 方法 对经CT血管造影(CTA)证实的116例MCAOD患者的CT平扫、CT灌注成像(CTP)和CTA的影像资料进行回顾性分析,确定其脑梗死类型分布和脑灌注改变. 结果 116例患者中,CTA共检出133条大脑中动脉(MCA)狭窄或闭塞,其中单侧者99例,双侧者17例.其中MCA闭塞25条,重度狭窄39条,中、轻度狭窄69条.CT或MRI显示腔隙性脑梗死(LIS)45例,各型分水岭脑梗死(CWSI)38例,流域性脑梗死26例,纹状体内囊梗死(SCI)10例,未检出梗死病灶14例.CTP显示MCA供血区内脑血流灌注异常96例,其中58例有MCA供血区的大范围血流灌注减低.未检出血流灌注异常者37例. 结论 由于MCA狭窄的部位、程度和发病机制的不同以及侧支循环的建立,MCAOD可造成不同类型的脑梗死和血流灌注异常.     

颈内和大脑中动脉狭窄与闭塞的梗死类型及卒中机制的研究

目的 研究单侧动脉粥样硬化性MCA/ICA狭窄与闭塞的急性缺血性脑卒中患者在DWI上的梗死类型及发病机制.方法 起病48h内DWI诊断的急性脑梗死伴有动脉粥样硬化性MCA/ICA狭窄与闭塞的131例患者,有潜在心源性栓子患者除外.急性期DWI上梗死病灶分为：（1）单发病灶（小的穿动脉梗死灶;大的穿动脉梗死灶,皮层支梗死,大面积梗死,分水岭梗死）;（2）多发梗死病灶.结果 131例患者,ICA51例,MCA80例.ICA出现最多的梗死类型：穿支动脉伴分水岭梗死,但与MCA比较,皮层支伴分水岭梗死具有统计学意义（8/51,P=0.001）.MCA以穿支动脉伴皮层支梗死最多,且与ICA比较,具有统计学意义（12/80,P=0.003）.MCA中任何皮层支梗死与狭窄程度无关,ICA中任何分水岭梗死与狭窄程度相关.结论 颈内和大脑中动脉狭窄与闭塞在DWI上的梗死类型有明显的不同,提示有着不同的卒中发病机制.     

大脑中动脉区梗死的DWI特点及与其供血动脉狭窄的关系

目的 探讨大脑中动脉(MCA)区脑梗死磁共振扩散加权成像(DWI)成像病灶分布特点及与其供血动脉狭窄程度的关系.方法 回顾性的分析经颅脑磁共振成像(MRI)的DWI序列诊断的急性脑梗死,选择病灶位于MCA分布区,且完善其供血动脉检查,包括头颈部CTA,或颅脑MRA加颈部血管超声的患者108例,排除心源性栓塞、特殊血管病变导致的脑梗死.将梗死按照部位分为腔隙型梗死(SSSI)、皮层下梗死(SI)和混合型梗死(MI),供血动脉分为正常、轻度(50％)、重度(50％)和闭塞.比较不同类型梗死组的供血动脉狭窄的发生率.结果 各种梗死类型的发生率之间差异无统计学意义(x2=1.08,P＞0.05).单纯MCA病变者53例(53/108,49.1％),单纯ICA病变者28例(28/108,25.9％),单纯MCA病变高于单纯ICA病变(x2=12.35,P＜0.01).同侧血管正常者以LI类型的梗死多见,而单纯ICA病变者以MI类型的梗死多见(x2=10.22;10.54,P＜0.01);三种梗死类型在单纯MCA病变患者中差异无统计学意义(x2=0.25,P＞0.05);在单纯MCA病变者中,SI梗死类型多见于MCA闭塞患者(x2=7.45,P＜0.05).LI梗死类型多见于MCA轻度或重度狭窄患者(x2=6.39,P＜0.05).结论 结合DWI和相应血管检查对于明确MCA区动脉粥样硬化性脑梗死的病因和机制有一定帮助.基底节区的腔隙梗死,相应血管检查正常提示小血管病的可能大;MCA存在一定狭窄则可能是穿支受累造成;ICA病变多累及皮层,包括皮层型分水岭区梗死;而不同程度的MCA病变其梗死形态没有本质区别,皮层下梗死更多见MCA闭塞患者.     

大脑中动脉狭窄程度与不同急性脑梗死模式的相关性研究

目的探讨大脑中动脉(MCA)狭窄程度与不同急性脑梗死病变模式的关系。方法回顾性分析324例急性脑梗死患者,根据头颅磁共振弥散加权成像(DWI)和磁共振血管成像(MRA),MCA狭窄程度分为轻、中、重度,患者梗死模式分为:单发性梗死(包括小的穿支动脉供血区梗死、大的穿支动脉供血区梗死、皮质分支动脉供血区梗死和大面积梗死)、分水岭梗死(CWI)和多发性梗死。比较不同模式的急性脑梗死患者的MCA病变情况。结果 324例急性脑梗死患者中,MCA狭窄致穿支动脉(PAI)梗死最为多见,占137例(42.28%);PAI患者MCA重度狭窄率与其他单发性梗死、多发性梗死和内分水岭梗死(IWI)患者相比较,差异具有统计学意义(P0.01)。内分水岭梗死、多发性梗死和大面积梗死的MCA重度狭窄率高于小穿支动脉梗死、大穿支动脉梗死、皮质穿支动脉梗死和外分水岭梗死(P0.05),而内分水岭梗死、多发性梗死和大面积梗死之间的MCA重度狭窄率相比差异无统计学意义(P0.05)。结论 MCA狭窄致PAI最为多见,但是MCA重度狭窄并非是PAI的重要原因;MCA重度狭窄易导致CWI(尤其是IWI)和多发性梗死;MCA重度狭窄也是导致LTI重要原因之一。     

大脑中动脉严重狭窄或闭塞卒中类型分析

目的探讨大脑中动脉严重狭窄或闭塞患者卒中类型特点及其发病机制。方法经TCD确诊的大脑中动脉狭窄或闭塞患者,依据头部CT和(或)MRI所示梗死灶进行卒中分型。结果169例大脑中动脉严重狭窄或闭塞患者,卒中类型各亚型以腔隙性脑梗死(LI)最为常见,占38.46%,其次为分水岭梗死(WI)占19.23%。流域性脑梗死、弥散性多发点状脑梗死、半卵园中心梗死与MCA严重狭窄或闭塞程度有关。结论大脑中动脉严重狭窄或闭塞患者卒中类型以腔隙型脑梗死、分水岭梗死为主。卒中类型多种多样,血管检查应该作为缺血性脑血管病的常规检查。     

大脑中动脉狭窄患者急性脑梗死发病机制:一项弥散加权磁共振和微栓子监测研究

目的我们前瞻性研究了30例经颅多谱勒超声(TCD)和核磁血管成像(MRA)检查证实大脑中动脉(MCA)狭窄,并在该供血区域出现急性缺血性卒中患者,以探讨MCA狭窄的可能机制。方法全部病人均进行微栓子监测以及弥散加权磁共振(DWI)检查。急性梗死分成单发和多发梗死,梗死部位分成皮层梗死(CI)、交界区梗死(BI)和深穿支动脉梗死(PAI)。微栓子信号(MES)和DWI梗死病灶分别由两位不同的医生在不知道对方资料的情况下确认。结果DWI结果发现急性多发脑梗死和单发梗死各15例(50%)。多发梗死病人中,成链状排列的BI最常见(11例,占73%)。单发梗死中只有PAI是最常见的类型(10例,占67%)。10例(33%)病人检测到MES,每30min内MES的中位数为15(3-102)个。MES在多发梗死中的发生频率(9/15,60.0%)明显高于单发梗死(1/15,6.7%)(P=0.002)。MES的数目能预测DWI上脑梗死的数目(线性回归,调整后R2=0.475,P<0.01)。结论MCA狭窄梗死最常见的原因有两个:①穿支动脉闭塞引起的皮层下小的腔隙性梗死;②由动脉-动脉的栓子不能被清除而造成的多发小梗死,尤其是在交界区更明显。     

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.     

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.     

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.     

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.     

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.     

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.