白醋并甲硝唑保留灌肠治疗肝性脑病的观察

目的探讨白醋并甲硝唑溶液保留灌肠治疗肝性脑病的效果。方法将78例肝性脑病患者随机分为观察组39例和对照组39例。2组均采用保肝、抗肝昏迷治疗；观察组在此基础上加用30％白醋100mL和0．2％甲硝唑注射液100mL保留灌肠，1次/d，第5天观察肝性肝性脑病的改善程度和清醒时间。结果观察组总有效率为84．62％，对照组61．54％；观察组平均清醒时间为（2．84±1．31）d，对照组为（3．76±1．45）d；2组比较差异有统计学意义。结论在常规保肝、抗昏迷治疗的基础上加用白醋并甲硝唑溶液灌肠治疗肝性脑病疗效较好。     

手术联合125I粒子植入治疗复发性脑胶质瘤

目的探讨手术联合125I粒子植入治疗复发性脑胶质瘤的临床效果。方法2007年2月至2009年12月收治49例复发脑胶质瘤患者,采用显微手术联合125I粒子植入治疗26例（观察组）,显微手术切除联合常规外放射治疗23例（对照组）,术后长期随访直至死亡,记录和分析两组患者的生存时间和并发症。结果全部病例随访22～158周,平均55．8周。观察组术后平均生存时间为（62．8±5．6）周,中位生存时间为55周;对照组平均生存时间为（46．9±4．8）周,中位生存时间为39周;两组生存期差异有统计学意义（P〈0．05）。观察组术后出现放射性脑病5例,癫痫7例;对照组术后出现放射性脑病6例,癫痫5例;两组并发症发生率分别为46．2％和47．8％,差异没有统计学意义（P〉0．05）。结论手术联合125I粒子植入治疗复发性脑胶质瘤疗效优于手术后补充外放射治疗,能安全有效地延长患者的生存时间。     

高压氧治疗一氧化碳中毒迟发性脑病疗效分析

目的观察高压氧(HBO)治疗一氧化碳中毒迟发性脑病(DEACMP)的临床疗效。方法将符合标准的一氧化碳中毒迟发性脑病患者70例随机分为对照组30例,采用常规综合治疗,治疗组40例,在常规治疗上加用高压氧治疗,治疗4个疗程评价疗效。结果对照组痊愈11例(36.67%),有效率为70.0%,治疗组痊愈29例(72.5%),有效率95.0%,治疗组有效率明显高于对照组(P<0.05),治愈时间较对照组缩短,差异有统计学意义(P<0.05)。结论高压氧可有效提高DEACMP的疗效,缩短病程。     

纳洛酮联合醒脑静治疗肝性脑病的疗效观察

目的：探讨纳洛酮联合醒脑静治疗肝性脑病的临床疗效。方法肝性脑病患者68例随机分为观察组与对照组各34例。2组均予以常规治疗，观察组加用纳洛酮、醒脑静治疗，对照组仅加用纳洛酮治疗，比较2组临床疗效。结果观察组总有效率91.18％，显著高于对照组的79.41％（P＜0.05）；治疗后观察组的血氨水平显著低于对照组，GCS评分显著高于对照组（P＜0.05）；观察组神志恢复时间较对照组显著缩短（P＜0.05）。结论纳洛酮联合醒脑静用于治疗肝性脑病能够显著改善患者的血氨水平以及肝功能，促进神志的恢复，疗效显著且不良反应少，值得推广应用。     

一氧化碳中毒迟发性脑病的病程及预后

目的 研究一氧化碳中毒迟发性脑病（DEACMP）的病程及预后。方法 对72例DEACMP患者的假愈期、临床表现、病程、预后及头部CT、MRI、脑电图（EEG）进行分析。结果 （1）本组病例中30d内病情开始好转者59.7%，31～60d病情开始好转者22.2%，〉60d病情开始好转者16.7%，总临床治愈率47.2%，有效率97.2%；（2）假愈期≤14d与≥15d的2组比较，前者病程显著长于后者，而后者的治愈率高于前者；（3）无明显假愈期患者病程长，预后差。结论 DEACMP的临床病程具有显著的自限性和可恢复性。     

综合降低血氨浓度治疗乙肝肝硬化引起的肝性脑病

目的通过综合降低血氨浓度，观察治疗乙肝肝硬化引起的肝性脑病的临床疗效。方法将56例乙肝肝硬化出现肝性脑病患者随机分为综合降低血氨治疗组（包括口服乳果糖、醋酸灌肠、乙酰谷酰胺静脉注射，n=30）和乙酰谷酰胺治疗组（n=28），1周治疗后观察临床疗效。结果综合治疗组显效21例（70．0％），有效9例（30．0％），无效0例，无死亡，总有效率100％；而乙酰谷酰胺治疗组显效8例（28．6％），有效8例（28．6％），无效7例（25．0％），死亡5例（17．8％），总有效率为57．1％，2组总有效率比较差异有统计学意义（P〈0．001）。综合治疗组死亡率和血氨浓度也显著降低（P〈0．05）。结论综合降低血氨浓度是控制乙肝肝硬化患者肝性脑病的有效方法，可显著降低肝性脑病的发生，降低患者死亡。     

门冬氨酸和鸟氨酸联合治疗肝性脑病的疗效观察

目的观察联合使用门冬氨酸和鸟氨酸治疗各种肝硬化引起肝性脑病患者的临床疗效，探讨其对生化指标的影响。方法收集2004-08-2007-08乙肝、丙肝和酒精性肝硬化住院患者84例，住院期间均出现不同程度的肝性脑病，分为门冬氨酸和鸟氨酸治疗组与乙酰谷酰胺治疗组（各42例），治疗5～7d观察2组患者的临床表现，记录临床症状、体征的变化．检测治疗前后患者血氨和肝功能，判断临床疗效变化。结果2组患者均经过5～7d治疗后，门冬氨酸和鸟氨酸治疗组患者显效22例（52．4％）．有效16例（38．1％），无效4例（9．5％），无死亡病例，总有效率为90．5％；乙酰谷酰胺治疗组患者显效16例（38．1％），有效14例（33．3％），无效8例（19．1％），死亡4例（9．5％），总有效率为71．4％。2组总有效率比较，差异有统计学意义（P〈0．05）。另外，发现门冬氨酸和鸟氨酸治疗组患者的血氨水平比乙酰谷酰胺治疗组显著下降（P〈0．05），而2组之间的血清谷丙转氨酶、谷草转氨酶、碱性磷酸酶、谷氨酰转肽酶、胆红素和凝血酶原时间均无明显变化（P〉0．05）。结论降低血氨是治疗肝性脑病的重要步骤，门冬氨酸联合鸟氨酸是控制肝性脑病发生的有效药物。     

依达拉奉联合地塞米松治疗急性一氧化碳中毒后迟发性脑病疗效观察

目的 观察依达拉奉联合地塞米松对急性一氧化碳中毒后迟发性脑病( DEACMP) 的治疗作用.方法 将80 例有昏迷史的DEACMP患者分为治疗组(40例)和对照组(40例).对照组予高压氧、脑细胞活化剂、烟酸治疗.治疗组在对照组治疗的基础上加用依达拉奉30mg+生理盐水100ml静滴,2次/d,连续治疗7～14d;地塞米松10mg静滴,1次/d,连续5d.观察并比较2组治疗效果.结果 治疗组有效率(92.5%)明显高于对照组(70.0%),2组之间差异有统计学意义(χ2=6.65,P<0.01).结论 应用依达拉奉、地塞米松、高压氧等综合治疗DEACMP,多数患者可以获得满意的疗效.     

急性一氧化碳中毒后迟发性脑病患者血清白介素水平的变化及其临床意义

目的 探讨急性一氧化碳（CO）中毒后迟发性脑病（DEACMP）患者血清白介素（IL）水平变化及其临床意义。方法 采用酶联免疫吸附法检测34例DEACMP患者治疗前、后血中IL-2、4、6的水平，并与30名健康人和30例急性CO中毒（ACMP）患者进行比较。结果 （1）DEACMP组治疗后血中IL-2、4、6的含量显著高于治疗前（均P〈0．01），但仍显著低于ACMP组和健康对照组（均P〈0．01）；（2）ACMP组血IL-2、4、6的含量明显高于健康对照组（均P〈0．01）。结论 DEACMP的发生与神经免疫病理损伤有关，血中IL-2、4、6的水平可以反映DEACMP患者机体的免疫状态。     

依达拉奉联合高压氧治疗一氧化碳中毒迟发性脑病的疗效

目的观察依达拉奉联合高压氧治疗一氧化碳中毒迟发性脑病(DEACMP)的疗效。方法将50例DEACMP患者随机分为观察组和对照组各25例。在常规治疗基础上,观察组给予依达拉奉联合高压氧治疗,对照组仅给予高压氧治疗,治疗30d后评定疗效。结果治疗组总有效率90%,对照组总有效率70%,2组疗效比较差异有统计学意义(P0.05)。结论依达拉奉联合高压氧治疗DEACMP疗效确切。     

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.