血小板-白细胞聚集体在进展性脑梗死中的作用

目的 探讨血小板-白细胞聚集体(platelet-leukocyte aggregation,PLA)在进展性脑梗死发病中的作用.方法 检测158例急性脑梗死患者血压、血糖、血脂、C反应蛋白(CRP)、纤维蛋白原、PLA,并分析进展性脑梗死发生的危险因素.结果 158例脑梗死中,37例发展为进展性脑梗死.进展性脑梗死组入院次日血小板-单核细胞聚集体( platelet-monocyte aggregations,PMA)高于无进展性脑梗死组(P＜0.05),而PLA、血小板-淋巴细胞聚集体(platelet-lymphocyte aggregations,PLyA)、血小板-中性粒细胞聚集体(platelet-neutrophilic aggregations,PNA)在两组间的比较无统计学意义(P＞0.05);PMA水平与血糖、血胆固醇、CRP、纤维蛋白原、收缩压呈正相关;收缩压(OR0.11,95％ CI 0.05 ～0.28,P=0.00)、PMA( OR 5.65,95％ CI 2.47 ～ 12.96,P=0.00)为进展性脑梗死发生的独立危险因素.结论 血小板-白细胞聚集体在进展性脑梗死的发病过程中发挥重要作用.     

参芎注射液对急性脑梗死患者血小板-白细胞聚集体的影响

目的 观察参芎注射液对急性脑梗死(ACI)患者血小板-白细胞聚集体(PLA)的影响.方法 将51例ACI患者随机分为阿司匹林组和阿司匹林+参芎注射液组,检测两组治疗前后PLA、血小板中性粒细胞聚集体(PNA)、血小板淋巴细胞聚集体(PLyA)和血小板单核细胞聚集体(PMA)的水平,以及血小板聚集率(PAR)、C反应蛋白(CRP)、血白细胞、血小板、血脂、血糖和纤维蛋白原(Fg)水平、美国国立卫生研究院卒中量表(NIHSS)评分的变化.结果 阿司匹林组:PLA、PNA、PLyA以及CRP均有下降趋势,但与治疗前比较差异无统计学意义,而PMA、PAR以及NIHSS评分较治疗前明显降低(均P<0.05).阿司匹林+参芎注射液组:PLA、PMA、PAR、CRP以及NIHSS评分较治疗前明显下降(均P<0.05),其中PMA和PAR下降较阿司匹林组更为明显(均P<0.05),而PNA、PLyA有下降趋势但与治疗前差异比较无统计学意义.两组治疗前后白细胞、血小板、血脂、血糖和Fg水平的差异均无统汁学意义.结论 参芎注射液具有协同抗血小板活化与聚集,抑制PLA,特别是PMA形成的作用,此外还具有一定的抗炎功效.     

急性脑梗死患者血小板-白细胞聚集体的动态变化及意义

目的探讨急性脑梗死患者血小板-白细胞聚集体(platelet-leukocyte aggregation,PLA)的动态变化及其临床意义。方法收集作者医院就诊的158例急性脑梗死患者以及30名健康体检者(对照组)为研究对象,根据瘫痪肢体肌力或神经功能评分量表(NIHSS)评分变化将脑梗死患者分为进展性脑梗死组和无进展脑梗死组,采用流式细胞技术检测健康对照组以及脑梗死患者不同时期的PLA水平。结果进展性脑梗死组血小板-单核细胞聚集体(platelet-monocyte aggregations,PMA)水平在进展期明显升高,而后逐渐下降(P<0.05),无进展脑梗死组PMA水平逐渐下降,差异有统计学意义(P<0.05);进展性和无进展脑梗死组PLA、血小板-淋巴细胞聚集体(platelet-lymphocyte aggregations,PLyA)、血小板-中性粒细胞聚集体(platelet-neutrophilic aggrega-tions,PNA)水平无明显动态变化(P>0.05);PMA水平与NIHSS评分呈正相关(r=0.12,P<0.05)。结论 PLA不仅在脑梗死的发病中发挥作用,而且可反映急性脑梗死患者病情的严重程度。     

脑梗死患者的亚临床炎症及胰岛素抵抗

目的观察脑梗死患者的亚临床炎症及胰岛素抵抗(IR)情况。方法检测114例脑梗死患者(脑梗死组)血清C-反应蛋白(CRP)、白介素-6(IL-6)及空腹胰岛素(Fins)、空腹血糖(FPG)、血脂、血压水平,分析胰岛素敏感指数(ISI)与炎症指标的关系,并与70例非脑梗死患者(对照组)进行比较。结果⑴脑梗死组血清CRP水平[(2.73±0.87)mg/L]、IL-6水平[(0.14±0.03)ng/ml]明显高于对照组[(1.63±0.93)mg/L、(0.12±0.03)ng/ml](均P<0.01),ISI(-4.31±0.53)明显低于对照组(-3.92±0.43)(P<0.01);⑵脑梗死组中,CRP>8.2mg/L患者的ISI(-4.63±0.71)明显低于CRP≤8.2mg/L患者的ISI(-4.18±0.54)(P<0.05)。结论脑梗死患者存在血清炎症的证据及IR;并且IR和亚临床炎症反应水平相一致。     

超早期去骨瓣减压术对大面积脑梗死老年患者神经功能及血小板活化能力水平的影响

目的探讨超早期去骨瓣减压术对大面积脑梗死老年患者神经功能及血小板活化能力水平的影响。方法将郑州中康医院2018年6月至2019年6月收治的123例大面积脑梗死老年患者按照手术时间分组,对照组61例发病24~48 h内行去骨瓣减压术,观察组62例超早期(发病24 h内)行去骨瓣减压术。观察两组患者的疗效、神经功能、血小板活化能力水平及手术并发症。结果观察组疗效优于对照组(P<0.05);观察组术后1个月、6个月末用美国国立卫生研究院卒中量表(NIHSS)评分较对照组低(P<0.05);观察组术后1周末血小板淋巴细胞聚集体(PlyA)、血小板-单核细胞聚集体(PMA)、血小板-白细胞聚集体(PLA)及血小板中性粒细胞聚集体(PNA)的百分比水平较对照组低(P<0.05);观察组手术并发症发生率(6%)较对照组(20%)低(P<0.05)。结论超早期去骨瓣减压术可降低大面积脑梗死老年患者血小板活化水平,改善神经功能,提高治疗效果并减少手术并发症。     

急性腔隙性脑梗死患者血清C反应蛋白和白介素-8水平的变化及临床意义

目的 探讨急性腔隙性脑梗死患者血清高敏C反应蛋白(hs-CRP)、白介素-8水平(IL-8) 的变化及其在发病机制中的作用.方法 分别检测36例腔隙性脑梗死和36例脑梗死患者及36例健康对照者血清hs-CRP和IL-8含量.结果 腔梗组和脑梗组hs-CRP含量分别为(10.42±0.68)mg/L和(18.45±1.28)mg/L,均显著高于对照组的(1.28±0.47)mg/L(P<0.01),CI组hs-CRP含量亦显著高于健康对照组(P<0.01);腔梗组和脑梗组IL-8含量分别为(29.65±18.24)ng/ml和(36.57±19.01)ng/ml,显著高于对照组的(25.98±16.87)ng/ml(P<0.01).在脑梗患死者中,大面积脑梗死组(≥9ml,n=16)hs-CRP为(21.36±1.48)mg/L,显著高于小面积脑梗死组(<9ml,n=20)的(15.30±0.97)mg/l(P<0.01),2组IL-8含量分别为(38.1±19.87)ng/ml和(33.45±18.67)ng/mL,差异亦有统计学意义(P<0.01).结论 炎症过程参与了脑小血管病变;hs-CRP和IL-8水平与脑缺血程度以及脑的小血管病变范围密切相关.hs-CRP 及IL-8是预测脑梗死患者病情严重程度的重要生化指标.     

P-选择素基因S290N和P-选择素糖蛋白配体-1基因M62I多态性与缺血性脑梗死血小板白细胞聚集体的相关性探讨

目的探讨血小板白细胞聚集体在缺血性脑梗死中的变化以及与P-选择素基因S290N和P-选择素糖蛋白配体-1基因M62I多态性的关系。方法选取58例缺血性脑梗死患者作为病例组,20例正常人群作为对照组。病例组分为大动脉粥样硬化性脑梗死(LAA)19例,小动脉闭塞性脑梗死(SAO)39例。运用流式细胞技术检测所有受试者的血小板白细胞聚集体(PLA)、血小板单核细胞聚集体(PMA)、血小板淋巴细胞聚集体(PLy A)和血小板中性粒细胞聚集体(PNA)水平。并运用基因测序方法检测P-选择素基因S290N和P-选择素糖蛋白配体-1基因M62I多态性。结果 PMA%在病例组与对照组、LAA与对照组、SAO与对照组间差异有统计学意义(P=0.000,P=0.018,P=0.000)。PNA%在病例组与对照组、LAA与对照组间差异有统计学意义(P=0.045,P=0.002)。PNA%在LAA组SELP基因S290N位点SS和SN基因型间差异有统计学意义(P=0.008)。PLA%在LAA组PSGL-1基因M62I位点MM、MI和Ⅱ基因型间差异有统计学意义(P=0.046)。结论 PMA和PNA与缺血性脑梗死发病有关,SELP基因S290N位点SN基因型以及PSGL-1基因M62I位点MM基因型会增加LAA发生风险。     

急性腔隙性脑梗死患者血清C-反应蛋白和白介素-8水平的变化及临床意义

目的 探讨急性腔隙性脑梗死患者血清高敏C-反应蛋白(hs-CRP)、白介素-8水平(IL-8) 的变化及在发病机制中的作用.方法 分别检测36例腔隙性脑梗死、36例脑梗死和36例健康对照者血清hs-CRP和IL-8含量.结果 腔梗组和脑梗组hs-CRP含量分别为(10.42±0.68)、(18.45±1.28)mg/L,均显著高于对照组的(1.28±0.47)mg/L(P＜0.01),CI组hs-CRP含量亦显著高于健康对照组(P＜0.01);腔梗组和脑梗组IL-8含量分别为(29.65±18.24)、(36.57±19.01)ng/ml,显著高于对照组的(25.98±16.87)ng/ml(P＜0.01),在脑梗患者中,大面积脑梗死(≥9ml)hs-CRP为(21.36±1.48)mg/L,显著高于小面积脑梗死组(<9ml)的(15.30±0.97)mg/L(P＜0.01),2组IL-8含量分别为(38.1±19.87)、(33.45±18.67)ng/ml,差异亦有统计学意义(P＜0.01).结论 炎症过程参与了脑小血管病变;hs-CRP和IL-8水平与脑缺血程度以及脑的小血管病变范围密切相关.hs-CRP 及IL-8是预测脑梗死患者病情严重程度的重要生化指标.     

急性脑梗死患者血小板参数的临床观察

目的 探讨周围血中血小板计数(PLT)、平均血小板体积(MPV)和血小板体积分布宽度(PDW)在急性脑梗死中的变化及临床意义.方法 我们对2006-07～2008-05的104例急性脑梗死患者与80例正常健康人采取血液标本,测定PLT、MPV、PDW进行对比做相关性分析.结果 急性脑梗死组MPV、PDW较正常对照组明显增大,有显著差异(P<0.01).急性脑梗死组PLT较正常对照组明显减少,有显著差异(P<0.01).结论 血小板功能异常是脑梗死的一个独立危险因素,血小板参数的检测可间接反映血小板的功能,对脑梗死的预防研究有一定的意义.     

C-反应蛋白和皮质醇预测恶性脑梗死的价值

目的研究联合检测血清C-反应蛋白(CRP)和皮质醇预测恶性脑梗死(MCI)的临床价值。方法检测73例大脑中动脉供血区大面积脑梗死患者血清CRP和皮质醇水平,依据临床症状和脑CT检查将患者分为MCI组和非MCI组,应用受试者工作特征曲线(ROC)进行评价。结果MCI组患者血清CRP和皮质醇分别为(17.90±4.30)mg/L和(1059.95±226.67)nmol/L,非MCI组患者血清CRP和皮质醇分别为(12.87±4.31)mg/L和(858.48±300.55)nmol/L,MCI组患者血清CRP和皮质醇高于非MCI组,差异有显著性(P0.01)。CRP诊断MCI的灵敏度和特异度分别为87.1%和85.7%。皮质醇诊断的灵敏度和特异度分别为71.0%和64.3%。平行诊断试验:灵敏度为96.26%,特异度为55.11%。系列诊断试验:灵敏度为61.845,特异度为94.895。结论脑梗死患者血清CRP和皮质醇为预测MCI的敏感指标;联合检测血清CRP和皮质醇有助于提高诊断的敏感性(平行诊断试验)和特异性(系列诊断试验)。     

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.     

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.     

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.     

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.     

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.     

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.