尿激酶超早期静脉溶栓治疗急性脑梗死20例疗效观察

目的 观察应用尿激酶超早期静脉溶栓治疗急性脑梗死的有效性和安全性.方法 治疗组20例,尿激酶100万～150万 U溶于生理盐水100 mL中静滴,30 min内滴完;对照组20例给予常规治疗,分别在溶栓前、溶栓后1 d、7 d和14 d通过神经功能缺损评分评价疗效.结果 2组治疗后1 d、7 d和14 d的神经功能缺损评分比较差异有统计学意义(P＜0.05);治疗组总有效率为90%,对照组总有效率为75%,2组比较差异有统计学意义(P＜0.05);2组均无致死性出血和药物过敏反应.结论 应用尿激酶超早期静脉溶栓治疗急性脑梗死安全、有效.     

尿激酶静脉溶栓治疗急性脑梗死34例临床疗效分析

目的 评价应用尿激酶静脉溶栓治疗急性脑梗死的有效性和安全性.方法 治疗组34例静脉滴注尿激酶100万U(体质量≤50公斤)或150万U(体质量＞50公斤)溶于生理盐水100ml或150ml中,半小时内滴完;对照组30例按常规治疗,并分别在溶栓前、溶栓后24h、1周、3周时间点,采用脑卒中患者神经功能缺损评分表进行评价.结果 治疗组总有效率为91.17%,对照组总有效率为66.66%,2组比较差异有非常显著性(P＜0.01);不同剂量尿激酶治疗前、治疗后24h、1周及3周神经功能缺损评分比较差异无显著性(P＞0.05).结论 尿激酶静脉溶栓治疗急性脑梗死剂量为100万U(体质量≤50公斤)或150万U(体质量＞50公斤)较符合治疗剂量个体化原则,且安全、有效.     

颈动脉注射小剂量尿激酶治疗急性脑梗死疗效观察

目的观察颈内动脉注射尿激酶溶栓治疗急性脑梗死的疗效及安全性。方法对60例急性脑梗死患者随机分为2组,对照组给予常规治疗,治疗组在对照组治疗基础上应用30万U尿激酶溶入20ml生理盐水中,进行患侧颈动脉推注溶栓治疗。分别对治疗前后患者神经功能缺损程度进行评定,观察治疗前后2组总有效率、显效率。结果2组比较,神经功能缺损评分有显著性差异。治疗组总有效率、显效率明显优于对照组,差异均有统计学意义(P<0.01)。结论颈动脉小剂量尿激酶溶栓治疗急性脑梗死安全、有效。     

动脉溶栓治疗急性脑梗死临床观察

目的探讨尿激酶动脉溶栓治疗急性脑梗死的临床疗效。方法将2010-03-2011-03我院诊治的60例急性脑梗死患者随机分为对照组（常规对症治疗）和观察组（对症治疗基础上,给予尿激酶进行动脉内溶栓治疗）,对2组患者的神经功能缺损评分（NDS）、临床疗效进行比较。结果观察组患者与治疗前相比,治疗后2h和2周的NDS明显降低,差异有统计学意义（P〈0.05）;在治疗24h和2周后,与对照组相比,观察组NDS明显降低,差异有统计学意义（P〈0.05）。与对照组的总有效率（76.7%）相比,观察组的总有效率明显增高（96.7%）,差异有统计学意义（P〈0.05）。结论对于急性脑梗死患者,动脉溶栓治疗具有较好的临床疗效,值得临床推广。     

超早期尿激酶静脉溶栓治疗急性脑栓塞64例疗效分析

目的观察超早期尿激酶静脉溶栓治疗急性脑栓塞的临床效果。方法选择我院收治的64例急性脑栓塞患者为研究对象,随机分为对照组和观察组。对照组采用常规治疗,观察组采用超早期尿激酶静脉溶栓治疗,比较2组治疗效果、治疗前后神经功能缺损改善情况。结果观察组总有效率达100%,显著高于对照组的62.5%。观察组治疗后24h、2周神经功能缺损评分显著优于对照组。2组不良反应发生率差异无统计学意义(P0.05)。结论超早期尿激酶静脉溶栓治疗急性脑栓塞疗效确切,安全可靠,值得临床推广应用。     

急性脑梗死超早期尿激酶静脉溶栓治疗体会

目的观察中等剂量尿激酶在急性脑梗死超早期静脉溶栓治疗的有效性和安全性。方法选择发病在6h内的急性脑梗死患者47例,随机分为治疗组23例,对照组24例,治疗组一次性应用尿激酶75万～100万U静脉溶栓治疗。观察溶栓后1d、7d、14d2组神经功能缺损评分（NIHSS）变化。以溶栓后出血转化、24h内再梗死及死亡等作为安全指标。结果 2组治疗前后NIHSS评分比较差异有统计学意义（P〈0.01）,治疗组24h内出血转化1例,对照组再梗死1例,死亡1例。结论中等剂量尿激酶静脉溶栓治疗超早期急性期脑梗死临床疗效显著、安全。     

尿激酶溶栓联合脑保护剂治疗急性脑梗死的疗效观察

目的评价尿激酶联合脑保护剂对急性脑梗死(6～12h)静脉溶栓的疗效及安全性。方法 凡符合入组标准的患者接受尿激酶75万~125万U溶于生理盐水100~200ml内,20min内滴完,随后静滴25％硫酸镁极化液、低分子右旋糖酐、丹参、20％甘露醇、胞二磷胆碱、七叶皂甙及尼莫通或口服尼莫地平等脑细胞保护剂,治疗前及治疗后2h、24h、7d、14d进行神经功能缺损评分及疗效评价。结果 起病6～12h的急性脑梗死尿激酶溶栓后不同时间神经功能缺损评分及有效率和总有效率与对照组比较有显著性差异(P<0.01),虽6h内溶栓组比6～12h溶栓组疗效好,24h溶栓组后神经功能缺损评分均高于6～12h溶栓组(P<0.05),但2周后疗效评价二组间却无显著性差异(P>0.05)。结论起病6~12h的急性脑梗死并非溶栓治疗的绝对禁区,只要合理选择病例,及早联合使用脑保护剂,同样能获得理想的疗效。     

重组人组织型纤溶酶原激酶衍生物治疗急性脑梗死的疗效观察

目的：探讨重组人组织型纤溶酶原激酶衍生物（rPA ）治疗急性脑梗死的疗效与安全性。方法根据治疗方案将155例急性脑梗死患者分为观察组（84例）与对照组（71例）,观察组在常规治疗基础上给予rPA治疗,对照组在常规治疗基础上给予尿激酶治疗。结果（1）治疗前,2组美国国立卫生院神经功能缺损量表（NHISS）评分、Barthel 指数（BI）相比差异无统计学意义（P＞0.05）。治疗后,观察组 NHISS评分显著低于对照组,BI显著高于对照组,差异有统计学意义（P＜0.05）。（2）观察组治疗效果显著优于对照组,差异有统计学意义（P＜0.05）。（3）观察组不良反应发生率显著低于对照组,差异有统计学意义（P＜0.05）。结论 rPA治疗急性脑梗死的疗效确切、安全性高,是治疗急性脑梗死的理想药物之一。     

小剂量尿激酶溶栓治疗急性脑梗死临床观察

目的 观察尿激酶静脉溶栓治疗急性脑梗死的临床有效性及安全性.方法 应用小剂量尿激酶超早期(发病6 h内)静脉溶栓治疗急性脑梗死19例,于溶栓前及溶栓后24 h、10 d进行神经功能缺损及日常生活指数量表评分,同时观察脑内及其他系统有无出血并发症.结果 溶栓后24 h神经功能缺损及日常生活指数评分与溶栓前相比均有改善,P...     

磁共振血管成像-弥散成像不匹配在尿激酶静脉溶栓治疗急性脑梗死中的应用

目的 研究磁共振血管成像-弥散成像(MRA-DWI)不匹配在尿激酶静脉溶栓治疗急性脑梗死中的临床应用价值.方法 符合溶栓标准且溶栓前行1.5 T超导磁共振(MRI)检查的36例急性脑梗死病人,根据MRI检查结果分为MRA-DWI不匹配组及MRA-DWI匹配组,给予尿激酶静脉溶栓治疗,比较2组间治疗前后神经功能缺损评分变化及不良反应的发生率.结果 溶栓治疗后第1天及第14天2组神经功能缺损评分比较差异有统计学意义(P＜0.01),溶栓治疗后第14天MRA-DWI不匹配组基本治愈率50.00%,总有效率94.44%, MRA-DWI匹配组基本治愈率5.55%,总有效率66.66%,2组比较差异有统计学意义(P＜0.05);2组溶栓后48h内不良反应的发生率(11.11%、55.56%)比较差异有统计学意义(P＜0.05). 结论磁共振血管成像-弥散成像不匹配能准确预测缺血半暗带,指导尿激酶静脉溶栓治疗急性脑梗死.     

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.     

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.     

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.     

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.