无症状脑梗死患者血清高敏C反应蛋白和肿瘤坏死因子-α水平的变化及其临床意义

目的：探讨无症状脑梗死（SCI）患者血清高敏C反应蛋白（hs-CRP）、肿瘤坏死因子-α（TNF-α）水平的变化及其在发病机制中的作用。方法：分别检测40例SCI、40例脑梗死（CI）患者、40例健康对照者血清hs-CRP和TNF-α含量。结果：SCI组和cI组hs—CRP含量分别为（8．86±0．96）和（16．32±1．88）mg／L，均显著高于对照组的（1．69±0．56）mg／L（P〈0．01），CI组hs—CRP含量亦显著高于SCI组（P〈0．05）；SCI组和CI组TNF-α含量分别为（1．92±0．73）和（2．56±0．91）ng／mL，显著高于对照组的（1．13±0．42）ng／mL（P〈0．01），CI组TNF-α含量亦显著高于SCI组（P〈0．05）。在SCI患者中，梗死灶数〉2个组（n=19）hs-CRP为（9．45±0．97）mg／L，显著高于梗死灶数≤2个组（n=17）的（7．21±0．75）mg／L（P〈0．01），两组TNF-α含量分别为（1．97±0．83）和（1．66±0．56）ng／mL，无显著差异。血压测定值越高，腔隙性梗死灶数量越多，未服降压药者梗死灶数量显著多于正规降压治疗者（P〈0．05）。结论：炎症过程参与了脑小血管病变；hs—CRP和TNF-α水平与脑缺血程度、神经功能缺损程度以及脑的小血管病变范围密切相关。高血压是腔隙性SCI最常见的病因，未降压治疗的重度高血压更易引起多发性腔隙性脑梗死。从预防再发的角度看，对SCI应尽早采取积极有效的治疗措施，高血压患者应尽早正规服用降压药。     

大动脉粥样硬化性脑梗死血清超敏C反应蛋白的临床意义

目的探讨大动脉粥样硬化不同机制所知脑梗死的血清超敏C反应蛋白（hs-CRP）的临床意义。方法采用中国缺血性卒中分型（CISS）分型方法,对临床诊断为大动脉粥样硬化型脑梗死根据发病机制分为4型,比较各组之间血清hs—CRP,并观察其余神经功能缺损程度以及不同机制类型梗死复发的关系。结果动脉一动脉栓塞型患者血清hs—CRP水平明显高于载体动脉阻塞穿支动脉型和混合型脑梗死组（P〈0．01）;低灌注／栓子清除障碍型患者血清hs—CRP水平明显高于载体动脉阻塞穿支动脉型（P=0．016）,其他各组间比较差异无统计学意义。动脉-动脉栓塞型患者中大于6mg／L的例数明显高于载体动脉阻塞穿支动脉型和混合型脑梗死组（P〈0．01）;低灌注／栓子清除障碍型患者中大于6mg／L的例数明显高于载体动脉阻塞穿支动脉型（P〈0．05）。中、重度神经功能缺损患者血清hs-CRP水平高于轻度神经功能缺损患者（P〈0．01）;重度神经功能缺损患者血清hs—CRP水平高于中度神经功能缺损患者（P〈0．01）。发病早期NIHSS与动脉一动脉栓塞型患者血清Hs．CRP水平升高成正相关（P=0．01）。动脉-动脉栓塞型和混合型卒中复发率明显高于载体动脉阻塞穿支动脉型（P=0．001,0．022）。结论血清hs—CRP可反映大动脉粥样硬化型脑梗死患者中斑块的稳定性,对早期诊断、病情判断以及复发风险有一定的预测价值。     

依达拉奉对急性脑梗死患者血清高敏感C反应蛋白及IL-8的影响

目的 通过观察依达拉奉对急性脑梗死患者血清高敏感C反应蛋白（highsensitive C-reactionprotein，hs—CRP），IL-8水平的影响及对神经功能的改善作用，探讨依达拉奉对急性脑梗死患者的疗效及其可能机制。方法选择60例急性脑梗死患者随机分为治疗组和对照组各30例，治疗组（30例）给予依达拉奉注射液30mg，2L4t／d。对照组给予丹参粉针400mg溶于生理盐250mL静滴，1次／d。连用15d。采用酶联免疫吸附实验检测治疗前、治疗后7d和15d的血清hs—CRP及IL-8水平变化，分别进行神经功能缺损程度评分。结果2组hs—CRP、IL-8水平在梗死后7d最高，随后逐渐降低。治疗组治疗前血清hs—CRP及IL-8水平和神经功能缺损总分与对照组比较，差异无统计学意义（P〉0．05）；治疗后7d及15d治疗组hs—CRP和IL-8水平及神经功能缺损总分均低于对照组（P〈0．01）。结论依达拉奉可降低患者血清hs—CRP水平和IL-8水平，减轻炎症反应，改善缺损的神经功能。通过降低血清hs—CRP和IL-8水平可能是其作用机制之一。     

急性脑梗死患者血清CRP、D-D水平变化的临床分析

目的分析急性脑梗死患者CRP、DD水平的变化与疾病诊断、治疗之间的关系及临床价值。方法测定82例急性脑梗死患者入院后第2、7、14、21天CRP、D-D的水平，并将其与我院体检中心82例健康患者的检查结果进行对比。结果观察组入院第2、7、14天CRP分别为（12．48±3．98）mg／L、（18．52±4．32）mg／L、（15．42士4．12）mg／L，对照组CRP为（3．15±0．96）mg／L，2组比较差异有统计学意义（P％0．05）。观察组轻、中、重度患者CRP分别为（9．89±0．98）mg／L、（20．41±1．62）mg／I．、（31．74±1．74）mg／I。，中、重度患者CRP均明显高于轻度患者（P〈O．05），重度患者CRP明显高于中度患者（P〈o．05）；观察组轻度、中度、重度患者D-D均明显高于对照组，各组间差异均有统计学意义（P＜0．05）。结论CRP、D-D水平的高低可以反映急性脑梗死患者炎症程摩及血栓情况，在疾病的诊断、治疗中一邑有转高的临床价值．     

急性脑梗死与超敏C反应蛋白的关系

目的探讨急性脑梗死患者血清超敏C-反应蛋白（hs—CRP）水平变化与脑梗死部位、严重程度及预后的关系。方法测定120例急性脑梗死患者和90名健康人血清hs—CRP的含量,按脑卒中患者临床神经功能缺损程度评分标准对患者进行评分,分组比较。结果脑梗死组血清CRP水平明显高于正常对照组（P〈0．01）。不同部位梗死患者血清hs—CRP水平比较没有差异。脑梗死轻、中、重型患者血清hs—CRP水平差异有统计学显著性（P〈0．05）。血清CRP水平越高的脑梗死患者病情越严重,临床预后差。结论血清hs—CRP水平增高与脑梗死的发生和严重程度有密切关系,而与病变部位无关。     

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.     

脑梗死急性期血浆纤维蛋白原水平与预后的随诊观察

目的了解脑梗死急性期血浆纤维蛋白原水平(fibrinogen,FIB)的影响因素,评价急性期FIB水平与脑梗死预后的相关性。方法选取自2000年1月～2002年5月在北京协和医院神经科住院治疗的116例脑梗死患者,应用凝血酶法(Clauss法)定量测定起病10d内血浆FIB水平,并对患者进行随访分析。通过线形回归分析评价急性期血浆FIB水平的影响因素。应用Kaplan—Meier法计算累积生存概率,分析急性期血浆FIB水平与脑梗死患者复发和死亡事件的相关性。结果临床分型为腔隙性脑梗死的患者血浆FIB(2．78±0．76g／L)浓度显著低于其他类型脑梗死患者(3．30±1．05g／L),且这一差异不受性别、糖尿病、高血压、吸烟、饮酒、病灶大小、感染等因素影响 (t=4．030,P<0．005)。病灶小于2cm的脑梗死中,大、小血管病变患者的血浆FIB浓度无显著差别(2．78±0．72g／ L比2．95±0．77g／L,P=0．478)。急性期FIB浓度高的患者(FIB浓度为前25百分位)病后1年时的预后较FIB低者(FIB浓度在后75百分位)差,前者复发和死亡事件概率(19．2％)高于后者(6．3％),P=0．047。远期的预后情况在两组间无明显差异(23．1％比14．3％,P=0．19)。结论脑梗死急性期FIB水平在不同类型脑梗死间存在差异, 且与1年内脑梗死复发或死亡事件相关。     

脑血栓形成复发的危险因素研究

目的：探讨脑血栓形成复发的危险因素。方法：收集首发441例脑血栓形成患者的临床资料,采用前瞻性队列研究,随访1年,记录终点事件。结果：脑血栓形成1年复发率为t3．8％;年龄（P=0．002,OR=1．044,95％CI=1．015～1．073）、高血压病史（P=0．040,OR=I．944,95％CI=1．032～3．663）、纤维蛋白原（P=0．000,OR=I．932,95％CI=1．386～2．666）为影响脑血栓形成复发的因素。结论：高龄、高血压病史及纤维蛋白原升高是脑血栓形成复发的重要危险因素。     

重度颈动脉狭窄患者介入或药物治疗效果的长期随访

目的研究重度颈动脉狭窄患者的预后及其影响因素，前瞻性评价介入治疗或药物治疗的效果。方法103例脑卒中或TIA合并重度颈动脉狭窄患者意向性分组，分为介入组与药物治疗组。前者40例择期给予脑血管内支架置入术，后者63例给予抗血小板药物治疗。随访主要终点为发病2年时功能预后（mRS评定）；次要终点为血管事件（发病1、2年或2年以上）的发生率。结果两组的基线资料（性别、年龄、病史、收缩压、血脂、NIHSS、mRS）差异无统计学意义。在随访2年时，Logistic回归表明选择介入治疗是功能预后不良（mRS 3-6分）的独立保护性因素（RR=0．13，P=0．001，95％CI 0．036-0．460）。在发病1年和2年时血管事件发生率差异有统计学意义，介入组的血管事件发生率低于药物组（1年时，介入组：药物治疗组=12．5％：42．9％，OR 0．19，95％CI 0．07-0．55，P=0．001；2年时，介入组：药物治疗组=17．5％：47．6％，OR 0．23，95％CI 0．09-0．60，P=0．002）。进一步随访（随访时间2年以上）发现，两组血管事件发生的中位数时间分别为55个月和54个月，Kaplan-Meier分析结果提示差异无统计学意义。Cox回归提示选择介入治疗或药物治疗不是血管事件发生的独立影响因素（RR=1．063，95％CI 0．40～2．83，P=0．900）。结论对于重度颈动脉狭窄患者，介入治疗较单纯药物治疗能获得较好的功能预后；介入治疗能减少脑卒中或TIA发病后1年或2年时血管事件的发生；但是随访2年以上时，介入治疗未能减少血管事件发生。     

糖调节受损与颅内外动脉闭塞性病变的相关性

目的观察非糖尿病缺血性卒中患者糖调节受损（IGR）的发病率，并研究IGR与颅内外动脉粥样硬化性狭窄或闭塞（简称颅内外动脉闭塞性病变）的相关性。方法以非糖尿病且空腹血糖水平（FPG）〈7．0mmol／L的缺血性卒中患者为研究对象（病程3周至半年）。依据经颅多普勒超声和头颅磁共振血管成像结果，将被研究者分为狭窄组（大血管病变组）与非狭窄组（小血管病变组）；依据口服葡萄糖耐量试验（OGTT），5．6mmol／L≤FPG〈7．0mmol／L和（或）7．8mmol／L≤OGTT2h血糖〈11．1mmol／L者诊断为IGR，OGTT2h血糖≥11．1mmol／L者诊断为糖尿病。结果（1）160例缺血性卒中患者中IGR及糖尿病的患病率分别为35．6％（57／160）和21．8％（35／160）；其中狭窄组为40．9％（45／110）和26．3％（29／110），非狭窄组为24．0％（12／50）和12．0％（6／50），两组比较前者明显高于后者（P=0．038，0．042）；（2）Logistic回归分析显示OGTT2h血糖、低高密度脂蛋白胆固醇及缺血性卒中家族史为颅内外动脉闭塞性病变的独立危险因素（OR=1．362、0．149、7．518，P=0．019、0．003、0．002）。结论经OGTT发现，IGR在缺血性卒中患者中普遍存在，尤其伴有颅内外动脉闭塞性病变者更为常见。而OGTT2h血糖是IGR患者导致颅内外动脉闭塞性病变的独立危险因素。     

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.     

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.     

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.     

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.     

The influence of comorbid depression on seizure severity

PURPOSE: To determine the relation between depressive symptoms and seizure severity among people with epilepsy. METHODS: A postal questionnaire was used to survey a nationwide community sample about seizures and depression. The Seizure Severity Questionnaire (SSQ) assessed the severity and bothersomeness of seizure components. The Centers for Epidemiological Studies-Depression scale categorized levels of depression. RESULTS: Respondents categorized as having current severe (SEV, n = 166), mild-moderate (MOD, n = 74), or no depression (NO, n = 443) differed significantly in SSQ scores (all p < 0.0001). People with SEV or MOD reported significantly worse problems than did those with NO depression for overall seizure recovery (mean, 5.3, 4.9, 4.5, respectively); overall severity (5.0, 4.5, 4.2); and overall seizure bother (5.3, 4.8, 4.4) (all p < 0.005). Cognitive, emotional, and physical aspects of seizure recovery also were rated worse among people with SEV than with NO depression (all p < 0.05). Symptoms of depression were significantly correlated with higher levels of all components of generalized tonic-clonic seizure severity (r = 0.33-0.48; all p < 0.0001), and partial seizures (r = 0.31-0.38; all p < 0.01). CONCLUSIONS: Clinically depressed people with epilepsy reported higher levels of perceived severity and bother from seizures, as well as greater problems with overall seizure recovery than did nondepressed people experiencing similar types of seizures. The pervasive influence of depressive symptoms on reports of seizure activity suggests that people with epilepsy should be screened for depression. These data highlight the importance of detecting and treating depression among people with epilepsy.     

Une phénoménologie de la dépendance à l'alcool. Une expérience primordiale de la « nostrité »

The phenomenological approach to alcoholism interestingly focuses on specific dynamics of interpersonal relationships displaying the founding of the Self from a primary “us” and its original basis in the human feast. Priorities for treatment intervention recommend to involve social setting and relationships of the patients, reaching their active participation to a motivational and long term group treatment, underlying the specific therapeutic effect of world exchanges. Biopsychosocial determination of alcoholism could be primarily based on components of interpersonal relationships. Regarding social background, drinking is one of the most famous supports for the achievement of the feast, a founding marker of present time. Taking an existential point of view, the feast appears as the heart of mankind because it presents a primary “us”, a plural state which indicates the beginning and founding of the Self from the others. During the feast, we regularly have to reach our Self from the “us” while avoiding two main dangers, drunkenness, an increase in the dizziness of upright verticality, and addiction, an opposite vertical surrender to alcohol and falling into in the alcoholic relapse, both situations imply a spatial domination and the disappearance of others. Treatment programs of alcohol addicts need to integrate the necessity of reaching the existential basic trust from the support of a group to the appropriation of the community which can be defined as an original “usness”.