实验性大鼠血栓栓塞性脑梗死出血性转换的机制研究

目的研究大鼠血栓栓塞性脑梗死后并发出血性转换(hemorrhagic transformation,HT)的自然发生率、特点及溶栓治疗对其影响,探讨HT的可能机制.方法采用单一血栓大脑中动脉栓塞模型,通过伊文(氏)蓝、红四氮唑染色、病理观察以及动态MR扫描比较HT组和非HT组血-脑脊液屏障破坏范围、梗死体积、出血类型和部位以及栓塞后30、90 min开始溶栓对其影响.结果HT自然发生率为27.27%,30 min溶栓组为9.09%,有降低趋势.晚期溶栓不增加其发生率,但多发性血肿增多.HT组血-脑脊液屏障破坏范围、梗死体积[(207.33±15.42)和(178.00±54.91)mm3]均大于非HT组[(141.22±48.88)和(113.25±43.08)mm3,均P＜0.05].结论血栓栓塞性脑梗死HT发生率高,早期溶栓不增加其发生率,但溶栓治疗使多发性血肿的发生率增加.大面积梗死后血栓迁移、延迟再通与栓塞性脑梗死并发HT有关.     

急性缺血性脑卒中rt-PA静脉溶栓后出血性转化的特殊类型

目的溶栓后出血性转化(hemorrhagic transformation,HT)是重组组织型纤维蛋白溶酶原激活剂(rt-PA)治疗急性缺血性脑卒中的一个重要安全指标。HT有不同的亚型,而不同亚型的预后也不尽相同。我们对急性缺血性脑卒中患者rt-PA静脉溶栓后出现的特殊型HT进行分析。方法对发病3zh内的98例缺血性卒中患者用rt-PA(剂量0．6 mg/kg,最大剂量5 0 mg)进行静脉溶栓治疗,溶栓前后行头颅CT、MRI或数字减影血管造影(DSA)检查判断是否有HT,并判定这种HT与责任病灶的关系。结果溶栓后经CT或MRI检查发现4种特殊的远端HT类型,1例发生蛛网膜下腔出血(SAH),1例梗死部位的对侧出现明显占位效应的脑实质出血,1例出现梗死灶对侧的侧脑室出血,1例出现梗死部位对侧的腔隙性出血。这4例患者所引起的4类HT在临床上均为无症状,预后好。结论对急性缺血性脑卒中的溶栓治疗要坚持动态观和平衡观,对症状性出血性转化的诊断要慎重,充分考虑HT的分型和程度,从而正确判断HT对预后的影响。     

重组组织型纤溶酶原激活剂静脉溶栓治疗急性脑梗死疗效分析

目的探讨急性脑梗死患者使用rt-pA静脉溶栓的临床疗效和出血、死亡风险。方法回顾分析258例在4.5h内就诊的急性脑梗死患者,按是否静脉rt-pA溶栓分为静脉溶栓治疗组(简称溶栓组)和对照组。溶栓组196例患者按0.9mg·kg-1(最大量不超过90mg)静脉给予rt-PA,2组均给予脑梗死常规治疗。比较2组NIHSS评分、临床疗效、出血情况及死亡情况。结果溶栓组治疗后NIHSS评分和临床疗效均优于对照组,差异有统计学意义(P0.05),且2组颅内出血风险差异无统计学意义(P0.05)。溶栓组病死率较对照组低,差异有统计学意义(P0.05)。结论急性脑梗死患者4.5h内应用rt-PA静脉溶栓有显著临床疗效,并未增加颅内出血和死亡风险。     

早期静脉溶栓治疗急性轻型缺血性卒中的疗效观察

目的探讨早期静脉溶栓治疗急性轻型缺血性卒中的疗效及安全性。方法将70例首次急性轻型缺血性脑卒中患者随机分为溶栓组(35例)及未溶栓组(35例)。溶栓组于入院后给予重组组织型纤溶酶原激活剂(rt-PA)静脉溶栓治疗,未溶栓组给予阿司匹林(100 mg/d)口服。于出院时采用NIHSS评分评价患者神经功能缺损情况,治疗3个月后采用mRS评价患者预后。结果入院时溶栓组及未溶栓组患者一般临床资料差异无统计学意义(均P0.05)。与未溶栓组患者比较,溶栓组患者出院时NIHSS评分显著降低,预后良好的比率显著增高(P0.05~0.01)。两组患者均未发生症状性脑出血及死亡。结论静脉溶栓治疗可以显著改善轻型缺血性卒中患者的预后,并且不会增加其颅内出血的风险。     

急性脑梗死静脉溶栓后症状性脑出血的危险因素研究进展

<正>静脉溶栓是唯一被证实治疗急性脑梗死的有效方法,且对于适用溶栓的患者静脉注射重组组织纤溶酶原激活物(rt-PA)是最佳选择,但其增加了症状性脑出血(symptomatic intracerebral hemorrhage,SICH)的风险。据统计急性脑梗死患者应用rt-PA溶栓后出现SICH约占6%。最近一项随机对照试验研究显示,急性脑梗死患者应用rt-PA溶栓后     

前-后循环急性脑梗死静脉溶栓疗效比较及安全评价

目的探讨前-后循环急性脑梗死静脉溶栓疗效差异及安全性评价。方法对前-后循环急性脑梗死120例,其中前循环64例及后循环56例急性脑梗死进行rt-PA静脉溶栓治疗,比较两组间神经功能恢复情况;并通过Logistic回归分析影响急性脑梗死rt-PA静脉溶栓后出血风险的独立危险因素。结果两组患者经溶栓治疗后24h、2w神经功能较溶栓治疗前均有明显恢复(P<0.01),两组之间溶栓治疗后24h神经功能恢复差异无统计学意义,但两组之间溶栓治疗后2w神经功能恢复差异有统计学意义(P<0.05);Logistic回归分析表明高血压病、心房纤颤、糖尿病及吸烟增加rt-PA静脉溶栓出血风险。结论在急性脑梗死的rt-PA静脉溶栓治疗中,前循环疗效优于后循环,且高血压病、心房纤颤、糖尿病及吸烟影响rt-PA静脉溶栓疗效,有增加出血风险可能,从而影响患者日后生活质量。     

血压对急性脑梗死静脉溶栓患者脑血流及预后的影响

目的探讨降血压对急性脑梗死静脉溶栓患者脑血流及短期预后的影响。方法选取我科收治合并高血压的急性脑梗死(ACI)患者86例为研究对象,入院后行阿替普酶静脉溶栓治疗,随机分为观察组及对照组,观察组入院后继续应用降压药物,维持血压120～140/80～90mmHg(1mmHg=0.133kPa),对照组血压低于180/100mmHg时不降压,1周后启动降压治疗。观察2组患者静脉溶栓后梗死侧脑血流、梗死体积变化,NIHSS评分变化,出血并发症、90d良好预后(mRS≤2)。结果观察组脑血流较对照组降低,但差异无统计学意义;梗死体积、NIHSS评分变化、出血并发症及90d良好预后的患者和对照组比较,差异无统计学意义(P0.05)。结论急性脑梗死患者静脉溶栓后及时降压治疗,没有明显降低梗死侧脑血流,没有扩大脑梗死体积,对患者的短期预后无明显影响,但控制血压可能降低溶栓后出血转化。     

肝素预防急性脑梗死尿激酶溶栓后再瘫痪的临床观察

目的 探讨急性脑梗死瘫痪患者尿激酶溶栓后肝素持续静脉注射预防再瘫痪的疗效及安全性.方法 将36例溶栓成功患者按随机数字表法分成两组,治疗组18例溶栓后即用肝素1000 U/h持续静脉注射,监测部分凝血酶原时间(aPTT),调节肝索用量.保持aPTT在正常值1.5～2.0倍之间,连用5 d.对照组18例溶栓后24 h 口服阿司匹林0.1 g,1次/d.对两组7 d内发生再瘫痪及脑出血的例数,第14天神经功能缺损程度评分(NIHSS)进行统计学比较.结果 治疗组再瘫痪0例.无症状脑出血5例;对照组再瘫痪5例,无症状腩出血2例;两组再瘫痪发生率差异有统计学意义,脑出血发生率差异无统计学意义.第14天两组神经功能缺损程度评分差异有统计学意义.结论 急性脑梗死肢体瘫痪患者在尿激酶溶栓成功后应用肝素抗凝,维持aPTT在正常值的1.5～2.0倍,对于预防再瘫痪是有效和安全的.     

rt-PA静脉溶栓治疗急性脑梗死的疗效分析

目的研究发病4.5h内的急性脑梗死患者使用rt-PA静脉溶栓的疗效。方法 2015-06—2016-12收治的发病4.5h内急性脑梗死患者125例,分为溶栓组65例和对照组60例。溶栓组给予rt-PA静脉溶栓及脑梗死常规治疗,对照组给予阿司匹林及其他常规治疗。2组分别在治疗前和治疗后24h和7d进行NIHSS评分。结果治疗前后溶栓组的NIHSS评分改善明显,与对照组比较,差异有统计学意义(P0.05)。结论急性脑梗死患者发病在4.5h内应用rt-PA静脉溶栓有显著临床疗效。     

高原地区急性脑梗死患者静脉溶栓后出血转化的因素分析及列线图预测模型构建

目的 通过分析高原地区急性脑梗死(ACI)患者静脉溶栓后出血转化(HT)发生的影响因素,建立并评估个体化预测高原地区ACI患者静脉溶栓后HT发生风险的列线图模型。方法 选取2018年5月至2020年3月该院收治的ACI并进行重组组织型纤溶酶原激活剂(rt-PA)静脉溶栓治疗的患者162例为研究对象,并根据静脉溶栓治疗后是否发生HT将其分为HT组（34例）和非HT组（128例）。采用Logistic回归模型,分析ACI患者静脉溶栓后HT发生的影响因素。应用R语言(R 3.6.3)中的rms程序包绘制预测ACI患者静脉溶栓后HT发生风险的列线图模型。采用研究对象工作特征曲线(ROC)、校准曲线及Hosmer-Lemeshow拟合优度检验评估列线图模型进行验证。结果 Logistic回归模型显示,ACI患者静脉溶栓后HT的发生与糖尿病、脑梗死面积、发病至溶栓时间、NIHSS评分、血小板及D-二聚体密切相关(P<0.05)。ROC结果显示,预测ACI患者静脉溶栓后HT发生风险的AUC(95%CI)为0.831(0.727~0.935)。校准曲线为斜率接近为1的直线,Hosmer-Lemeshow拟合优度检验χ²=9.761,P=0.282。结论 该研究基于糖尿病、脑梗死面积、发病至溶栓时间、NIHSS评分、血小板、D-二聚体这6项影响因素构建的预测高原地区ACI患者静脉溶栓后HT发生风险的列线图模型,具有良好的区分度与准确度。     

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.     

Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity

Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.     

Pediatric Epilepsy Surgery

Summary: The use of implantable arrays of epidural electrodes has made it possible to carry out extraoperative electrocorticography (ECoG) and functional localization in the awake child. This has permitted cortical excisions that are determined by criteria similar to those obtained during surgical procedures performed under local anesthesia in adults. In addition, the method also permits simultaneous ECoG and video monitoring during the child's symptomatic seizures, providing additional important localizing information that is impractical to obtain in operations under local anesthesia. We report our experience with 75 children, ages 5 months to 15 years, whom we have managed with epidural electrode arrays. The method of extraoperative ECoG is described and illustrative cases are presented to demonstrate its feasibility and utility in children. In addition, we call attention to gliomas as a common cause of chronic focal seizures in children. Of 49 children undergoing resection and followed for from 1 to 14 years (mean of 5.8 years), 32 (65%) are either seizure free or have had a significant reduction in seizure frequency that has unambiguously improved their quality of life. The results are analyzed further by relating the surgical outcome to each of the pathologic entities that caused the seizures. This analysis reveals the variety of neurological conditions that commonly cause intractable focal seizure disorder in children and distinguishes those pathologic entities in which the seizure disorder is apt to respond to surgical intervention from those that will not.     

Un nouveau cadre conceptuel de travail pour une psychiatrie revisitée ? Introduction à deux articles de E. Kandel

In two articles which appeared in the American Journal of Psychiatry and that were subsequently translated for Évolution Psychiatrique, E. Kandel examines the bases for a reinterpreted psychiatry that is prepared to confront the major challenge of the 3rd millenium: that of insight into the mind and brain. This requires a major reorganization of the discipline, which involves a reinvestment of the scientific approach and a critical  assessment of the data provided by psychoanalytical psychiatry and cognitive neurosciences. Seven concepts have therefore been proposed for interactive re-examination: consciousness, the unconscious, memory, emotion, development, desire, impulse. The dynamic relations existing between genetics and the environment allow one to see how evolutions are possible from actions at different levels, both psychotherapeutic and pharmacological. Imaging and other techniques provide additional objective information to the process of human interaction which remains the basis of psychiatry. A common framework for psychiatry and the neurosciences, a reconsideration and renewal of the psychoanalytical approach are both possible and necessary.     

Opioids and the developing organism: A comprehensive bibliography, 1984–1988

A comprehensive bibliography of the literature concerned with opioids and the developing organism for 1984-1988 is presented. Utilized with companion papers (Neurosci. Biobehav. Rev. 6:439-479; 1982; 8:387-403; 1984), these articles cover the clinical and laboratory references beginning in 1875. For the years 1984, 1985, 1986, 1987, and 1988, a total of 877 citations were recorded. A series of indexes accompanies the citations in order to make the literature more accessible. These indexes are divided into clinical and laboratory topics, and subdivided into such topics as the type of opioid explored and the general area of biological interest (e.g., physiology).     

La biologie et le futur de la psychanalyse : un nouveau cadre conceptuel de travail pour une psychiatrie revisitée

The American Journal of Psychiatry has received a number of letters in response to my earlier “Framework” article (1). Some of these are reprinted elsewhere in this issue, and I have answered them briefly there. However, one issue raised by some letters deserves a more detailed answer, and that relates to whether biology is at all relevant to psychoanalysis. To my mind, this issue is so central to the future of psychoanalysis that it cannot be addressed with a brief comment. I therefore have written this article in an attempt to outline the importance of biology for the future of psychoanalysis.     

Facteurs de risque environnementaux à la schizophrénie

Schizophrenia is currently a major concern, its prevalence being estimated at around 1% and its social consequences being severe. The elucidation of the pathophysiology of the disease is difficult due to the great variability of clinical expressions, the instability of the clinical symptoms during the evolution and the absence of reliable biological markers. The existence of a familial aggregation in schizophrenia is well known, the risk of presenting the disease for first-degree relatives of patients being 5 to 10 times higher than the risk observed in the general population. The genetic component was further confirmed by twin and adoption studies. Although the concordance for the disease is higher (40 to 70%) among monozygotic twins as compared with dizygotic twins (15%) it does not reach 100%, which implies that environmental factors modulate the effects of the genotype. However, the role of these factors and especially their interaction with genetic factors remain unclear but the implications of some specific environmental factors are well documented by recent research data. The current literature on sex differences in schizophrenia is consistent. Several studies have suggested that male and female patients may differ in age at the onset and expression of clinical symptoms. Complications during pregnancy or birth-giving may increase the risk of developing schizophrenia later in life. The major complications are oxygen deprivation during pregnancy, bleeding, maternal malnutrition or infection (exposure to influenza, for example). A low birth weight is associated with an increased risk of schizophrenia. Psychoses are more common among people living in an urban environment and among those born during winter months. Schizophrenia is probably more prevalent in people who are living promiscuously, are subject to toxic abuse, poor nutrition and stress but here more precise data are needed. Moreover, immigrants have a higher risk of developing psychotic disorders. In addition, head traumas are associated with an increased risk of schizophrenia. Though they are contentious, some studies suggest that substance abuse (cannabis use in European countries) is related to the development of schizophrenia, especially in people with genetic vulnerability. Moreover, substance misuse may worsen the symptoms. If the environment is sufficiently stressful, people with a high genetic vulnerability will develop some degree of mental illness, including schizophrenia. Conversely, a less stressful or a protective environment may decrease the risk of its onset in persons with a predisposition to schizophrenia.     

Introduction: Goals

Summary: Epilepsy is characterized by recurrent seizures. Many epilepsies with focal seizures as well as convulsive generalized seizures respond satisfactorily to antiepileptic drugs (AEDs) that reduce repetitive firing (e.g., phenytoin, carbamazepine, and valproate) or that augment GABA_A-mediated inhibition (e.g., phenobarbital and benzodiazepines). A number of drugs presently under development, such as NMDA receptor antagonists, loreclezole, losigamone, meth-ysticine, and dextromethorphan, are promising in acute animal models of otherwise drug-resistant convulsant activity. As a result of recent studies in both experimental models and surgically resected human epileptic brain, the prospects for development of AEDs have significantly improved. Several new AEDs recently have reached the commercial market or are in experimental or clinical trials. A comparative presentation of the standing of the new AEDs with respect to their efficacy and side effects is necessary, but still very difficult. Because initial experience with new AEDs is restricted to populations with severe drug-resistant epilepsy, the crucial question whether potential new AEDs can alter prognosis is not yet definitively answered. There is a clear need to compare the effects of standard AEDs and new AEDs in naive patients and over longer follow-up periods. Moreover, because of the strong desire to develop antiepileptic therapy that directly treats the primary etiology of a given epileptic syndrome , or modifies the neurobiological processes that cause recurrent seizures, better experimental epilepsy models for chronic epilepsy and further clinical studies are necessary to increase the knowledge on the pathophysiology of distinct epileptic syndromes. In this respect, studies on the differences between responders and nonresponders to a given AED treatment are extremely valuable.