纳洛酮治疗急性脑梗死48例临床分析

目的 观察急性脑梗死患者血浆β－内啡肽变化和纳洛酮的治疗效果。方法 将我院1999年6月－2000年12月住院的98例急性脑梗死患者分成两组，治疗前后分别采取空腹静脉血2ml，用放免法检测β－EP的含量，同时对患者的神经系统功能缺失进行评分，评价临床疗效。结果 （1）治疗组总有效率89．58％，对照组总有效率58％，治疗组的疗效明显高于对照组（P＜0．01）。（2）急性期2组患者血浆β-内啡肽均升高，随着临床症状的好转，β－EP含量均有明显下降，治疗组下降更为明显（P＜0．01）。结论 纳洛酮应早期应用，其作用迅速、疗效好，价格低廉，且无不良反应。     

纳洛酮对早产儿血浆β-内啡呔的影响

目的探讨早产儿疾病中血浆β-EP(β-内啡肽)的变化及纳洛酮对其影响.方法将我院NICU住院的早产儿49例,从两方面进行比较(1)无合并症的早产儿与正常足月儿比较.(2)患病早产儿应用纳洛酮治疗与不用纳洛酮治疗,监测其血浆β-EP水平.结果正常早产儿血浆β-EP比正常足月儿高(P＜0.05);患病早产儿经纳洛酮治疗组血浆β-EP明显下降(P＜0.01).结论早产儿β-EP血浆水平比足月儿高,纳洛酮能有效降低早产儿血浆β-EP水平,从而拮抗β-EP对呼吸、循环的抑制作用,提高治愈率.     

纳洛酮联合门冬氨酸鸟氨酸对肝性脑病血清β-内啡肽血氨水平的影响

目的探讨纳洛酮联合门冬氨酸鸟氨酸对肝性脑病血清β-内啡肽、血氨水平的影响。方法选取肝性脑病患者76例,随机分为对照组38例,给予常规治疗方案;研究组38例,在常规治疗基础上给予纳洛酮与门冬氨酸鸟氨酸治疗。观察2组临床疗效及治疗前后的肝功能指标(ALT、AST、总胆红素)、血氨浓度以及β-内啡肽变化。结果研究组总有效率81.58%,对照组为65.79%,2组比较差异有统计学意义(χ2=5.05,P0.001);与治疗前相比,2组治疗后β-内啡肽、血氨水平及肝功能指标均明显下降,差异均有统计学意义(P0.05),治疗后研究组β-内啡肽、血氨水平均低于对照组,差异有统计学意义(P0.05)。结论纳洛酮联合门冬氨酸鸟氨酸治疗肝性脑病疗效显著。     

金尔伦(盐酸纳洛酮)治疗急性重型脑外伤的临床研究

目的：探讨金尔伦（盐酸纳洛酮）在急性重颅脑外伤中的运用效果及其机制,方法:146列急性重型颅脑损伤病人随机分成金洋伦治疗组（n=75)和对照组（n=71),观察治疗早期病人生命体征,颅内压,头颅CT变化和远期疗效,以及治疗前后血,脑脊液中β－内肽变化情况,结果,金尔伦治疗组早期病人呼吸循环较快恢复稳定,呼吸异异常（29．3％）,心律异常（30．7％）,及伤后1周颅内压显著升高（20％）和重度脑水肿者（20％）均较对照组明显减少（P＜0．01）,金尔伦组1周后意识;转清醒率（54．7％）及伤后3个月恢复良好率（42．7％）,显著高于对照组（P＜0．05）,重残及死亡率（37．3％）明显减少（P＜0．05）,金尔伦组病人β－内啡肽下降程度及速度较对照组显著加快（P＜0．01）,结论：金尔伦可以降低急性重型颅脑外伤病人颅内压的升高幅度,缩短昏迷时间,降低伤残率,促进病人神经功能恢复,改善预后,其机制可能是拮工抑制伤后β－内啡肽的释放。     

亚低温联合纳洛酮治疗脑出血的临床对比研究

目的 观察亚低温联合纳洛酮治疗脑出血的临床疗效及对血浆神经肽Y(NPY)、β-内啡肽(β-EP)的影响。方法 将我院1999年6月～2003年4月住院的98例急性脑出血病人随机分成两组,两组综合治疗相同,治疗组加用亚低温联合纳洛酮治疗:治疗前后分别采取空腹静脉血2 ml,用放免法检测NPY、β-EP的含量,同时对病人的神经功能缺损进行评分,评价临床疗效。结果 (1)治疗组总有效率91.7％,对照组总有效率64％,治疗组的有效率明显高于对照组(P<0.01);(2)急性期两组病人血浆NPY、β-内啡肽均升高,治疗后NPY、β-EP含量均下降,治疗组下降更为明显(P<0.01)。结论 亚低温联合纳洛酮治疗可以明显改善脑出血病人神经功能及预后,早期应用效果好。     

中风患者急性脑水肿血浆β-内啡肽和强啡肽的变化及纳洛酮对其影响的研究

目的:探讨两种内阿片肽与卒中后脑水肿的关系及纳洛酮对阿片肽、脑水肿的作用。方法:脑出血和脑梗塞随机分成治疗组(纳洛酮)和对照组,治疗前后抽血检测血浆β-内啡肽和强啡肽值,CT测定脑水肿CT值。结果:纳洛酮治疗后内阿片肽值下降,脑水肿减轻,治疗效果优于对照组,脑梗塞更加明显。结论:脑卒中病情轻重与内阿片肽值,脑水肿密切相关,阿片受体拮抗剂可减轻脑水肿,促进神经机能恢复。     

新生儿窒息时β-EP的变化及纳洛酮对其影响

目的　探讨新生儿窒息时血浆 β -EP( β -内啡肽 )的变化及纳洛酮对其影响。 方法　将符合诊断的 3 6例足月新生儿分组讨论 ,并进行统计学分析。结果　 ( 1)血浆 β -EP水平 :重度窒息组高于轻度窒息组 (P <0 0 5 ) ,轻度窒息组高于非窒息组 (P >0 0 5 )。 ( 2 )纳洛酮治疗后 1h后 β -EP浓度开始下降 (P <0 0 5 ) ,3d后继续下降 ,与用药前比较 (P <0 0 1)有显著性意义。 结论　窒息程度越重 ,血浆 β -EP水平越高。纳洛酮能明显降低血浆 β -EP水平 ,提高治愈率 ,降低病死率。     

奥卡西平对癫痫患者Hcy CRP及认知功能的影响

目的探讨奥卡西平对癫痫患者同型半胱氨酸(Hcy)、C反应蛋白(CRP)及认知功能影响。方法选取巩义市人民医院2015-01-2017-12收治的癫痫患者100例,按照随机数字表法分为观察组50例与对照组50例。对照组给予苯妥英钠治疗,观察组给予奥卡西平治疗,2组疗程均为12周。比较2组疗效,治疗前后血浆Hcy和CRP水平、MoCA评分和P300电位潜伏期时长变化及不良反应发生情况。结果观察组总有效率(92.00%)高于对照组(72.00%)(P0.05)。2组治疗后血浆Hcy和CRP水平降低(观察组:t=11.905、29.791,对照组:t=6.627、12.243,P0.05);观察组治疗后血浆Hcy和CRP水平低于对照组(t=8.562、26.363,P0.05)。2组治疗后MoCA评分增加(观察组:t=16.664,对照组:t=10.845,P0.05);观察组治疗后MoCA评分高于对照组(t=5.386,P0.05)。2组治疗后P300电位潜伏期时长降低(观察组:t=17.946,对照组:t=6.835,P0.05);观察组治疗后P300电位潜伏期时长低于对照组(t=9.969,P0.05)。观察组不良反应发生率(14.00%)低于对照组(36.00%)(P0.05)。结论奥卡西平治疗癫痫的疗效显著,且可降低患者Hcy和CRP水平,改善患者认知功能。     

大剂量盐酸纳洛酮治疗脑梗死疗效分析

目的观察大剂量盐酸纳洛酮对24h内发病未经溶栓脑梗死患者的治疗效果。方法在24h内发病失去溶栓机会和(或)溶栓禁忌的脑梗死患者采用盐酸纳洛酮针3.2mg/次,连用72h,观察治疗前后血中β-内啡肽变化以及脑梗死症状的缓解及预后情况。结果总有效率达91.7%,明显高于对照组(69.5%),(χ2=4.34,P<0.05)。结论早期大剂量盐酸纳洛酮治疗脑梗死疗效确切;早期合理使用盐酸纳洛酮(内源性吗啡样物质拮抗剂)可减轻、阻止甚至逆转由β-内啡肽所造成的局部脑缺血、水肿、梗死性病理过程,防止神经缺血性损害扩展。     

纳洛酮对急性重症非心源性脑梗死患者血浆BNP水平的影响

目的观察纳洛酮对急性重症非心源性脑梗死患者血浆BNP的影响,探讨其脑保护作用机制。方法将116例重症非心源性脑梗死患者(NIHSS≥8,GCS≤8分)随机分为治疗组(n=58)和对照组(n=58),对照组入院后给予常规治疗,治疗组在常规治疗的基础上给予盐酸纳洛酮静脉注射,分别于入院1、3、7d检测血浆BNP水平,同时进行NIHSS、GCS评分,根据脑水肿CT值判断脑水肿程度。结果 2组3d、7d时血浆BNP水平均明显增高,脑水肿较重,神经功能缺损严重,与对照组相比,治疗组血浆BNP水平下降,脑水肿、神经功能缺损程度均减轻(P0.05)。结论纳洛酮可显著改善急性重症非心源性脑梗死神经功能缺损程度,减轻脑水肿,其神经保护作用可能与下调血浆BNP水平有关。     

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.     

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.     

Epilepsy and anomalies of neuronal migration: MRI and clinical aspects

Neuronal migration disorders are the result of disturbed brain development. In such disorders, neurons are abnormally located. In diagnosing these conditions, magnetic resonance imaging is superior to any other imaging technique. This enables us to improve our knowledge of the clinical correlates of neuronal migration. With reference to migrational disorder, a retrospective study of all 303 patients with epileptic seizures referred for magnetic resonance imaging during a 3-year period was performed, 13 patients (aged 12-41, mean age 27) were identified. They represent 4.3% of the entire study group. Of the patients with known epilepsy, 6.7% and of the mentally retarded, 13.7% had migrational disorders. Four patients had schizencephaly as the dominant finding, one was classified as hemimegalencephaly, 2 had isolated heterotopias, and 6 had localized pachy- and/or poly-microgyria. The clinical pictures are complex. Ectopias of grey matter are recognised foci of epilepsy, but from an epileptological and a clinical viewpoint little attention has been given to these disorders. The present study shows that malmigration is not rare in epilepsy patients, especially not in the mentally retarded.     

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.     

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.     

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.