进展性脑梗死患者血浆溶血磷脂酸和酸性磷脂水平的变化及其意义

目的 探讨进展性脑梗死(PCI)患者血浆溶血磷脂酸(LPA)和酸性磷脂(AP)水平的变化及其意义.方法 93例急性脑梗死(ACI)患者,根据发病后48 h内病情变化分为PCI组(35例)和非PCI(NPCI)组(58例).检测两组发病后6 h、24 h、3 d、7 d、14 d、21 d血浆LPA和AP的水平,并与正常对照组(50人)比较.结果 与正常对照组比较,PCI组与NPCI组患者发病6 h～14 d时血浆LPA、AP水平均明显增高(均P<0.01);与NPCI组比较,PCI组患者发病6 h～14 d时血浆LPA、AP水平均明显增高(均P<0.01).结论 ACI患者血浆LPA和AP水平均增高,其中PCI患者血浆LPA、AP水平较NPCI患者更高.血浆LPA、AP水平可提示ACI患者病情进展趋势.     

人血浆脂蛋白相关磷脂酶A2与缺血性脑血管病的关系

目的探讨Lp-PLA2与缺血性脑血管病的关系,为预测缺血性脑血管病的发生提供准确简便快捷的方法。方法选择缺血性脑血管病患者98例为病例组和30例健康者为对照组,病例组包括短暂性脑缺血发作组21例,无症状脑梗死组31例,症状性脑梗死组46例。病例组与对照组均采用双抗体酶联免疫吸附测定法(ELISA)检测血浆Lp-PLA2水平,同时检测血浆CHOL、TG、LDL-C、HDL-C水平。结果①病例组患者血浆Lp-PLA2水平明显高于对照组(P<0.01);②有症状脑梗死组患者血浆LP-PLA2水平高于短暂脑缺血发作组和无症状脑梗死组(P<0.01),三组比较差异有统计学意义;③无症状脑梗死组患者血浆Lp-PLA2水平高于短暂性脑缺血发作组(P<0.01)。结论 Lp-PLA2可能与缺血性脑血管病的严重程度有关,Lp-PLA2可以作为预测缺血性脑血管病风险的一个生物学标志物。     

血浆同型半胱氨酸水平对急性脑梗死预后的影响及干预治疗的作用

目的探讨血浆同型半胱氨酸(Hcy)水平对急性脑梗死(ACI)预后的影响及干预治疗的作用。方法采用荧光法检测152例ACI患者发病<24h(治疗前)、1个月和6个月时血浆Hcy水平。按发病<24h时血浆Hcy水平将患者分为正常Hcy组、高Hcy组,后者又分为干预治疗组[给予叶酸5mg/d、维生素(Vit)B620mg/d、VitB120.5mg/d,连续6个月]和常规治疗对照组(常规治疗组)。在发病后各时点对3组患者进行美国国立卫生研究院卒中量表(NIHSS)和Barthel指数(BI)评分。结果治疗6个月时,干预治疗组血浆Hcy水平比治疗前以及常规治疗组明显降低(均P<0.01);正常Hcy组和干预治疗组NIHSS评分明显低于、BI评分明显高于常规治疗组(均P<0.05)。结论血浆Hcy水平增高的ACI患者预后较差,对高Hcy血症干预治疗可以改善ACI的预后。     

急性脑梗死患者血浆谷胱甘肽过氧化酶浓度的改变及其与GPx-3启动子基因多态性的关系

目的探讨急性脑梗死(ACI)患者血浆谷胱甘肽过氧化酶(GPx)浓度的改变及其与GPx-3启动子基因多态性的关系。方法检测94例ACI患者和80例正常对照者血浆GPx浓度。在ACI患者发病第1d进行神经功能缺损程度评分(NDS)。采用聚合酶链反应-连接酶检测方法(PCR-LDR)检测ACI患者GPx-3启动子基因多态性。结果ACI组发病第1d血浆GPx浓度明显低于正常对照组(P<0.01),发病第14d时血浆GPx浓度与正常对照组比较,差异无统计学意义(P>0.05)。有GPx-3启动子基因多态性的ACI患者,血浆GPx浓度和NDS明显低于无GPx-3启动子基因多态性的患者(P<0.05～0.01)。结论ACI患者血浆GPx浓度明显降低,有GPx-3基因多态性的患者血浆GPx浓度下降更明显,神经功能缺损程度更重。     

血浆脂蛋白相关磷脂酶A2检测对颈动脉斑块稳定性的预测价值

目的检测动脉粥样硬化脑梗死(ACI)患者及健康体检者血浆脂蛋白相关磷脂酶A2(Lp-PLA2)水平,探讨颈动脉斑块稳定性与血浆Lp-PLA2水平相关性。方法采用双抗体夹心酶联免疫吸附法(ELISA)检测血浆Lp-PLA2水平,同时检测血脂、纤维蛋白原等生化指标;行颈动脉彩色多普勒超声检查,评估颈动脉斑块稳定性。结果不稳定斑块组血浆Lp-PLA2水平明显高于稳定斑块组(P<0.01)。结论血浆Lp-PLA2水平可作为颈动脉斑块稳定性的预测指标。     

急性脑梗死患者血浆神经肽Y与血清一氧化氮合酶水平的变化及其临床意义

目的探讨急性脑梗死(ACI)患者血浆神经肽Y(NPY)、血清一氧化氮合酶(NOS)水平的变化及其临床意义。方法分别用放射免疫法、化学比色法、酶法检测30例ACI患者(ACI组)(发病<48 h和第12 d)及27名正常对照者(NC组)血浆NPY、血清结构型NOS(cNOS)、诱导型NOS(iNOS)及三酰甘油(TG)水平,头颅MRI检查测量脑梗死灶体积,应用美国国立卫生研究院卒中量表(NIHSS)评定神经功能缺损程度。结果与NC组比较,ACI组NPY水平差异无统计学意义;血清cNOS水平发病<48 h显著降低(P<0.01),并与梗死体积、同期NIHSS评分呈负相关(r=-0.368、-0.457,均P<0.05),与NIHSS评分差值呈正相关(r=0.466,P<0.05);血清iNOS水平发病<48 h显著升高(P<0.01),与梗死体积、同期NIHSS评分及两次检测的血TG水平呈正相关(r=0.390、0.362、0.411、0.395,均P<0.05),与NIHSS评分差值呈负相关(r=-0.461,P<0.05)。NPY差值与cNOS差值呈负相关(r=-0.369,P<0.05)。结论 ACI患者发...     

血浆Lp-PLA2水平与动脉粥样硬化脑梗死患者危险因素的相关性

目的探讨血浆Lp-PLA2水平与动脉粥样硬化脑梗死患者危险因素的相关性,以期为诊断和治疗动脉硬化脑梗死提供理论依据。方法 2014-01—2015-01就诊我院的急性动脉粥样硬化性脑梗死(ACI)患者62例为观察对象,同期选取健康者62例作对照,对2组一般资料、生化指标及血浆Lp-PLA2水平等进行分析,血浆Lp-PLA2和ACI患者常见危险因素的相关性。结果观察组中高血压史和糖尿病史明显多于对照组,差异有统计学意义(P0.05);观察组HDL-C水平低于对照组,血浆Lp-PLA2水平明显高于对照组,差异均有统计学意义(P0.05);血浆Lp-PLA2水平与性别呈正相关,而与吸烟、饮酒史呈负相关(P0.05);而与年龄、高血压史、糖尿病史及生化指标无相关性(P0.05)。结论血浆Lp-PLA2水平与ACI患者常见部分危险因素有相关性,可能是ACI重要的危险因素。     

阻塞性睡眠呼吸暂停综合征患者血浆脂蛋白相关磷脂酶A_2含量的变化

目的观察阻塞性睡眠呼吸暂停综合征(OSAS)患者血浆脂蛋白相关磷脂酶A2(Lp-PLA2)水平的变化特点,探索OSAS相关性脑卒中的病理生理学机制,为临床抗栓治疗提供依据。方法经临床和辅助检查确诊的OSAS患者40例(OSAS组)、伴OSAS的急性脑梗死患者36例(OSAS伴脑梗死组)以及不伴OSAS的急性脑梗死患者38例(脑梗死组)纳入本研究,另选取年龄、性别匹配的36名健康者作为对照组。采用ELISA法检测各组血浆Lp-PLA2水平。结果发病24h时,OSAS组、OSAS伴脑梗死组以及脑梗死组患者血浆LpPLA2水平均显著高于对照组(均P0.01),且OSAS伴脑梗死组血浆Lp-PLA2水平高于OSAS组和脑梗死组(均P0.01)。至发病后21d,OSAS伴脑梗死组患者血浆Lp-PLA2含量仍高于脑梗死组和对照组(P0.01),而脑梗死组和对照组血浆Lp-PLA2水平比较差异无统计学意义(P0.05)。结论 OSAS患者血浆LpPLA2水平升高,提示其体内存在Lp-PLA2相关性炎性反应,LP-PLA2可作为一种理想的分子标记物用于判断OSAS患者体内炎性反应状态;OSAS伴脑梗死患者炎性反应明显且持续时间较长,可能为早期强化抗炎治疗提供理论依据。     

急性脑梗死患者血清脂蛋白相关磷脂酶A2水平的改变及其与病情的关系

目的 研究急性脑梗死(ACI)患者血清脂蛋白相关磷脂酶A2(LP-PLA2)水平的改变及其与病情的关系.方法 91例ACI患者按照美国国立卫生研究院卒中量表(NIHSS)评分分为轻型ACI组(NIHSS评分＜4分)、中型ACI组(4～15分)、重型ACI组(＞15分).应用酶联免疫吸附法测定ACI患者及31名正常对照者的血清LP-PLA2水平.ACI患者NIHSS评分与血清LP-PLA2水平的关系用Spearman相关分析.结果 ACI组的血清LP-PLA2水平显著高于正常对照组(P＜0.01);重型ACI亚组血清LP-PLA2水平又显著高于中型ACI亚组和轻型ACI亚组(均P＜0.01).经Spearman相关分析,ACI患者的NIHSS评分与血清LP-PLA2水平呈正相关(r=0.485,P＜0.001).结论 ACI患者的血清LP-PLA2水平显著升高,病情越重者升高越明显.     

动脉粥样硬化性脑梗死患者血浆脂蛋白相关磷脂酶A2水平及相关性研究

目的分析血浆脂蛋白相关磷脂酶A2(Lp-PLA2)水平与动脉粥样硬化脑梗死(ACI)患者常见危险因素的相关性。方法采用双抗体夹心酶联免疫吸附法(ELISA)检测血浆Lp-PLA2水平,同时检测血脂、纤维蛋白原等生化指标;行头颅核磁共振检查计算脑梗死面积大小;使用美国国立卫生研究院卒中量表(NIHSS)进行神经功能缺损程度评估。结果 ACI组血浆Lp-PLA2水平明显高于对照组(P<0.01);血浆Lp-PLA2水平随脑梗死面积增加而呈递增趋势(P>0.05);神经功能缺损程度越重,血浆Lp-PLA2水平越高(P<0.05);血浆Lp-PLA2水平与性别、CRP呈正相关,与吸烟、饮酒呈负相关,与年龄、高血压病、糖尿病、TC、TG、HDLC、LDLC、Fib、Lp(a)均无关。结论血浆Lp-PLA2升高可能是ACI重要危险因素。     

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.     

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.     

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.     

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.     

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.     

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.