急性期高敏感C反应蛋白对脑梗死预后的评估

目的探讨脑梗死急性期高敏感C反应蛋白（hs—CRP）对脑梗死远期预后的评估价值。方法选取首次急性脑梗死患者99例，在72h内检测血清hs—CRP，随访1年，将死亡及再发缺血性血管病变记录为终点事件。将所有患者分为CRP正常组（hs—CRP≤3mg／L）和CRP增高组（hs—CRP〉3mg／L），分别对两组患者进行生存分析比较。采用多变量Logistic回归分析hs—CRP增高、高血压、糖尿病、冠心病、高血脂、年龄、吸烟、饮酒等危险因素对终点事件的影响。结果hs—CRP〉3mg／L的患者较hs-CRP≤3mg／L的患者终点事件发生率显著增加（18．18％，5．45％；P=0．044；生存分析，log—rank检验）。多变量回归分析显示，hs—CRP增高（OR3．609；95％CI 0．869～14．992；P=0．047）和吸烟（OR4．094；95％CI1．092—15．340；P=0．037）与终点事件独立相关。结论脑梗死急性期hs—CRP增高可能是脑梗死发病1年内死亡和再发缺血性血管病变的独立危险因素。     

伴有颈动脉斑块的急性缺血性卒中患者急性期血清学相关指标水平的研究

目的探讨伴有颈动脉斑块的急性缺血性卒中患者三酰甘油(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、血尿酸(UA)、血同型半胱氨酸(Hcy)、IL-6及高敏C反应蛋白(hs-CRP)的水平的变化。方法选择201例伴有颈动脉斑块的急性缺血性卒中患者(脑卒中组),分为中青年组(年龄60岁) 100例和老年组(年龄≥60岁) 101例。同时选择100名健康体检者(对照组),分别检测其血脂、UA、Hcy、IL-6及hs-CRP水平,并对数据进行统计分析。结果急性缺血性卒中组TG、TC、HDL-C、LDL-C、UA、Hcy、IL-6、hs-CRP水平均明显高于对照组(均P 0. 05)。中青年组UA水平明显高于老年组(P 0. 05)。不稳定斑块患者IL-6、hs-CRP、UA均明显高于稳定斑块患者(均P 0. 05)。结论伴有颈动脉斑块的急性缺血性卒中患者血清学相关指标(UA、IL-6、hs-CRP)明显增高并可能与颈动脉斑块不稳定相关,高UA可能是青年脑卒中患者危险因素。     

血浆同型半胱氨酸水平与动脉粥样硬化性脑梗死的关系

目的探讨血浆同型半胱氨酸水平与动脉粥样硬化性脑梗死的关系,为动脉粥样硬化性脑梗死的预防提供指导依据。方法选择107例动脉粥样硬化性脑梗死患者为脑梗死组,同时选择同期本院健康体检者76例为对照组。所有研究对象均记录年龄、性别,吸烟、饮酒、高血压、糖尿病等既往史,测定血浆同型半胱氨酸(homocysteine,HCY)水平及空腹血糖(FBG)、甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C),应用彩色超声多普勒检查患者颈动脉内膜中层厚度(intimal-medial wall thickness,IMT)。根据颈动脉彩色超声多普勒检查结果将脑梗死组分为脑梗死伴颈动脉粥样硬化斑块组和脑梗死无斑块组,将对照组分为对照有颈动脉粥样硬化斑块组和对照无斑块组;脑梗死有斑块组和对照有斑块合并为斑块组,脑梗死无斑块组和对照无斑块组合并无斑块组。结果脑梗死组男性、高龄、吸烟、高血压患者较对照组增多,FBG、血浆TC、LDL-C、HCY水平均高于对照组,差异有统计学意义(P0.05)。多元Logistic回归分析显示吸烟、高血压、糖尿病、高血浆TC、LDL-C、HCY水平均是动脉粥样硬化性脑梗死的危险因素。Sperman秩相关显示HCY与吸烟、饮酒、高血压、糖尿病、TC、TG、LDL-C均无相关性。脑梗死组血浆HCY水平、IMT均高于对照组,斑块组血浆HCY、IMT水平均高于无斑块组,脑梗死有斑块组血浆HCY、IMT水平均高于脑梗死无斑块组,对照有斑块组血浆HCY、IMT水平均高于对照无斑块组,且差异均有统计学意义(P0.05);直线相关分析显示血浆HCY水平与IMT水平呈正相关(r=0.86,P0.05)。结论血浆HCY水平与脑梗死关系密切,高血浆HCY水平是动脉粥样硬化性脑梗死的独立危险因素,高血浆HCY水平主要通过加速动脉粥样硬化影响脑梗死的发病。     

不同年龄脑梗死患者TOAST分型与血脂和纤维蛋白原的相关分析

目的：对不同年龄脑梗死患者TOAST分型与血脂和纤维蛋白原（Fg）进行相关分析。方法：回顾性分析427例45-89岁脑梗死患者的临床资料,并按不同年龄段分成3组。结合TOAST分型对3组患者的三酰甘油（TG）、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL—C）、高密度脂蛋白胆固醇（HDL—C）、Fg予以分析。结果：①TG、TC、LDL—C水平随着年龄增高而降低CP〈0．05）;HDL—C、Fg水平随年龄增长而增高（P〈0．05）;②随着年龄增长,心源性脑检塞型脑梗死和女性患者的发生比例明显增高（P〈0．05）。结论：对75岁以上的脑梗死患者应重视联合降纤治疗;心源性脑栓塞的发生率随年龄增长增高。需重视对合并有导致雌激素水平低下因素的高龄女性的脑梗死预防。     

TIA患者颈动脉内中膜厚度与血清指标水平的关系及对脑梗死的预测价值

目的 探讨短暂性脑缺血发作(TIA)患者颈动脉内中膜厚度(IMT)与血清指标水平的关系及对脑梗死的预测价值。方法 选择2016年3月-2018年3月在本院首次诊断为TIA的54例患者作为TIA组,同期体检的健康志愿者作为对照组,检测颈动脉IMT及血清超敏C反应蛋白(hs-CRP)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、总胆固醇(TC)、甘油三酯(TG)、同型半胱氨酸(Hcy)的水平,随访TIA患者1年内的脑梗死发生率。结果 与对照组比较,TIA组的IMT及血清hs-CRP、LDL-C、TC、Hcy水平明显增高(P<0.05),且IMT与血清hs-CRP、LDL-C、TC、Hcy水平呈正相关,血清HDL-C、TG水平无明显差异(P>0.05); TIA组中1年内发生脑梗死患者的IMT及血清hs-CRP、LDL-C、Hcy水平明显高于未发生脑梗死患者(P<0.05),且IMT增厚及hs-CRP、LDL-C、Hcy水平增高是TIA组患者1年内发生脑梗死的危险因素(P<0.05); IMT预测TIA患者1年内发生脑梗死的最佳截点为1.090,敏感性为78.57%、特异性为58.33%。结论 TIA患者颈动脉IMT增厚与血清炎症、脂代谢、Hcy指标水平相关,且对1年内脑梗死的发生具有预测价值     

中青年人脑梗死同型半胱氨酸及血脂水平与颈动脉粥样硬化的关系

目的探讨中青年脑梗死患者血清同型半胱氨酸（HCY）及血脂水平与颈动脉斑块性质之间的关系。方法中青年脑梗死患者86例为测试组,中青年体检健康者78例作为对照组,两组均通过生化分析仪及相关试剂检测血清中HCY、总胆固醇（TCHO）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-c）、脂蛋白a（LPa）水平,同时根据颈动脉超声检查测量两组颈动脉内中膜厚度（IMT）、有无斑块及斑块性质组成百分比。结果测试组血清HCY、qCHO、LDL-C、TG水平、IMT厚度明显增高,两组比较差异明显（P〈0．05）;两组斑块构成类型分布差异明显（P〈0．05）。结论中青年脑梗死HCY水平、血脂水平可能与颈动脉斑块不稳定性的发生有相关。     

绝经期女性脑梗死患者雌激素水平与血脂关系研究

目的 研究绝经期女性脑梗死患者血清中雌二醇(E2)、血脂含量变化,探讨雌激素对缺血性脑血管疾病的关系。方法 取78名绝经期女性脑梗死患者和62名对照组患者空腹静脉血,测定血清E2、甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋门胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白-AI(Apo-AI)及载脂蛋白B100(Apo-B100)。结果脑梗死组E2水平(12.86pg/ml)低于对照组(25.59pg/ml),有显著差异(P<0.01)。脑梗死组TG、TC、LDL-C、Apo-B100显著高于对照组(P分别<0.01、0.01、0.01、0.05),脑梗死组HDL-C显著低于对照组(P<0.01),脑梗死组ApoA-I与对照组相比无显著性差异(P>0.05)。雌激素水平与TG、TC、LDL-C、Apo-B100呈显著负相关(r分别为-0.63、-0.44、-0.57、-0.30,P<0.01),与HDL-C呈显著正相关(r=0.53,P<0.01)。结论 雌激素水平降低可导致血脂谱异常改变,从而促进动脉粥样硬化,低雌激素水平可能是缺血性脑血管病发生的危险因素之一。     

血清超敏C反应蛋白对脑梗死预后的评价

目的 调查超敏C反应蛋白(HS-CRP)对脑梗死预后的预测价值.方法 选择67例脑梗死患者,分为HS-CRP增高组(16例)和HS-CRP正常组(51例),检测其脑梗死后HS-CRP的水平,随访1年,比较两组终点事件的发生率.使用多因素逻辑回归分析对各个危险因素与终点事件的相关性进行统计分析.结果 67例脑梗死患者在随访1年期间,共20例(29.9％)患者发生了终点事件,其中包括:缺血性脑血管病13例(19.4％)、冠心病5例(7.5％)和死亡2例(3.0％).HS-CRP增高组终点事件的发生率较正常组显著增加(50％vs 23.5％,P＜0.05).通过多因素逻辑回归分析,HS-CRP＞5 mg/1是终点事件发生的独立危险因素(OR:2.911；95％ CI:1.385 to 15.605；P＜0.05).结论 HSCRP增高与脑梗死患者的不良预后相关,脑梗死后常规检测HS-CRP具有重要的现实意义.     

急性脑梗死患者血清抵抗素水平及相关性研究

目的 探讨脑梗死患者血清抵抗素水平变化及其与糖代谢、脂质代谢、超敏C反应蛋白(hs-CRP)等的相关性.方法 采用酶联免疫吸附法测定82例脑梗死患者血清抵抗素水平,同时检测血清瘦素、胰岛素、空腹血糖(FBG)、三酰甘油(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)及hs-CRP水平,计算定量胰岛素敏感性检测指数(QUICKI).另收集健康体检者50名为对照组.对所有受试者进行身高、体质量、腰围、臀围、收缩压(SBP)、舒张压(DBP)测量,并计算体质量指数(BMI)及腰臀比(WHR).结果(1)两组间性别比、年龄和BMI差异无统计学意义(P＞0.05),脑梗死组WHR、SBP和DBP均明显高于对照组(P＜0.01).(2)脑梗死组血清抵抗素、瘦素、胰岛素、FBG、LDL-C及hs-CRP均明显高于对照组(P＜0.05),而血清HDL-C和QUICKI均低于对照组(P＜0.05),两组间TC和TG比较差异无统计学意义(P＞0.05).(3)单因素直线相关分析结果显示,抵抗素与BMI、SBP、DBP、胰岛素、FBG、LDL-C和hs-CRP呈正相关(P＜0.05),与QUICKI和HDL-C呈负相关(P＜0.05),与WHR、瘦素、TC和TG无相关性(P＞0.05).(4)多元逐步回归分析结果显示,抵抗素与BMI、SBP、LDL-C和hs-CRP呈正相关(P＜0.05),而与HDL-C和QUICKI呈负相关(P＜0.05).结论 急性脑梗死患者血浆抵抗素水平明显升高,提示抵抗素在动脉粥样硬化性脑梗死的发生过程中具重要调控作用.抵抗素不但参与糖代谢紊乱和脂质代谢紊乱的发生,而且与高血压、肥胖以及动脉粥样硬化炎性反应等有关.     

老年腔隙性脑梗死患者血清胆红素和血脂水平的相关性研究

目的研究老年腔隙性脑梗死患者血清胆红素和血脂水平,探讨它们在老年腔隙性脑梗死发病机制中的作用。方法78例老年腔隙性脑梗死患者（腔梗组）,与72例无腔隙性脑梗死患者（对照组）,抽空腹静脉血,测定血清总胆红素（TBIL）、直接胆红素（DBIL）、间接胆红素（IBIL）、甘油三酯（TG）,总胆固醇（TC）,低密度脂蛋白胆固醇（LDL-C）,高密度脂蛋白胆固醇（HDL-C）水平及TC／HDL-C比值,两组进行比较。结果在老年人腔隙性脑梗死患者中TG、TC、LDL—C、TC／HDL—C水平明显高于对照组（P〈0．05）,而TBIL、DBIL、IBIL、HDL-C水平明显低于健康对照组（P〈0．05）。结论TG、TC、LDL-C水平,TC／HDL—C比值升高,TBIL、DBIL、IBIL、HDL-C水平降低与老年人腔隙性脑梗死发病密切相关。老年腔隙性脑梗死患者存在胆红素和脂质代谢紊乱,胆红素和脂质代谢紊乱参与了老年腔隙性脑梗死事件的发生。     

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.