血浆PTX3对动脉瘤性蛛网膜下腔出血后脑血管痉挛的预测价值

目的 分析血浆正五聚蛋白3(Pentraxin 3,PTX3)对动脉瘤性蛛网膜下腔出血后脑血管痉挛的预测价值。方法 收集本院2016年2月-2019年2月186例动脉瘤性蛛网膜下腔出血患者作为研究对象,经颅多普勒检测仪检测大脑中动脉(Middle cerebral artery,MCA)流速,MCA平均流速(Mean velocity of MCA,MCA Vm)>120 cm/s,且同侧Lindegaard≥3为血管痉挛组(92例),其余为无血管痉挛组(94例); 收集2组一般资料; 酶联免疫吸附(Enzyme linked immunosorbent assay,ELISA)法检测血浆中PTX3水平; 绘制受试者工作特性曲线(Receiver operator characteristic curve,ROC)分析血浆中PTX3对动脉瘤性蛛网膜者发生脑血管痉挛的诊断价值; 以血浆PTX3水平<4.73 ng/mL和≥4.73 ng/mL分为PTX3低表达组和PTX3高表达组,分析血浆PTX3水平与一般资料的关系; Logistic分析影响动脉瘤性蛛网膜下腔出血患者发生脑血管痉挛的因素。结果 无血管痉挛组与血管痉挛组年龄、治疗方法、高血压病史、Fisher分级、Hunt-Hess分级存在明显差异(P<0.05); 与无血管痉挛组比较,血管痉挛组血浆PTX3水平升高(P<0.05); ROC曲线显示,血浆PTX3水平预测动脉瘤性蛛网膜下腔出血患者发生脑血管痉挛的ROC曲线下面积为0.777,截断值为4.73 ng/mL,其敏感性为68.50%、特异性为74.50%; 血浆PTX3水平与年龄、治疗方法、Fisher分级、Hunt-Hess分级关系密切(P<0.05); Logistic分析显示,PTX3、年龄、Fisher分级、Hunt-Hess分级是影响动脉瘤性蛛网膜下腔出血患者发生脑血管痉挛的独立危险因素。结论 动脉瘤性蛛网膜下腔出血脑血管痉挛患者血浆PTX3水平升高,PTX3对动脉瘤性蛛网膜下腔出血患者发生脑血管痉挛具有一定诊断价值。     

Rho激酶抑制剂对动脉瘤性蛛网膜下腔出血后迟发性脑血管痉挛的疗效研究

目的 探讨Rho 激酶抑制剂对动脉瘤性蛛网膜下腔出血(aSAH)后迟发性脑血管痉挛(DCVS)的治疗效果.方法 按照是否应用Rho 激酶抑制剂对35 例自发性性蛛网膜下腔出血后发生迟发性脑血管痉挛的患者资料和治疗效果进行回顾性分析.结果 Rho 激酶抑制剂对迟发性脑血管痉挛临床症状改善率81.25%,与常规治疗组47.37%相比,具有统计学差异(P＜0.05);治疗后,Rho 激酶抑制组脑血流速度低于对照组(P＜0.05).结论 Rho 激酶抑制剂能明显缓解aSAH 后迟发性脑血管痉挛的临床症状,为神经外科防治迟发性脑血管痉挛提供了临床依据.     

法舒地尔联用尼莫地平预防动脉瘤性蛛网膜下腔出血后迟发性脑血管痉挛的疗效观察

目的探讨法舒地尔联用尼莫地平对预防动脉瘤性蛛网膜下腔出血后脑血管痉挛的疗效及不良反应。方法在入院后即常规给予尼莫地平静脉持续泵入的同时,将50例动脉瘤性蛛网膜下腔出血患者在作动脉瘤栓塞治疗后,均给予腰大池引流及"3H"疗法,并随机分成2组,治疗组加用盐酸法舒地尔30mg静滴,3次/d,连用14d,观察2组血管痉挛的发生情况及不良反应。结果治疗组症状性脑血管痉挛1例,无症状性脑血管痉挛3例,对照组症状性脑血管痉挛3例,无症状性脑血管痉挛10例,2组间差异有统计学意义(P<0.05)。不良反应方面2组比较差异无统计学意义。结论法舒地尔联用尼莫地平在预防动脉瘤性蛛网膜下腔出血所致血管痉挛的疗效优于单用尼莫地平,安全性亦较高。     

大鼠蛛网膜下隙出血脑血管痉挛模型的建立

目的 采用两种注血方法建立大鼠蛛网膜下隙出血早期脑血管痉挛模型,比较两种制备方法对脑血管痉挛程度的影响.方法 分别采用枕大池一次注血和二次注血法制备蛛网膜下隙出血早期基底动脉痉挛动物模型,HE染色观察基底动脉形态变化,计算基底动脉血管横截面积;透射电子显微镜观察基底动脉超微结构变化.结果 光学显微镜观察,枕大池一次注血组和二次注血组大鼠颅底有凝血块沉积;一次注血组大鼠基底动脉血管横截面积略有缩小[(2.68±0.48)×10-2mm2],但与假手术组比较差异无统计学意义(q=2.630,P=0.070),二次注血组大鼠基底动脉血管横截面积[(2.41±0.24)×10-2mm2]显著小于假手术组(q=4.660,P=0.003),但与一次注血组之间差异无统计学意义(q=2.031,P=0.166).电子显微镜观察,一次注血组大鼠基底动脉内弹力层局部变薄,内皮细胞胞质少量空泡形成,胞膜损伤崩解,中膜平滑肌细胞空泡样变性;二次注血组大鼠中膜平滑肌细胞和内皮细胞胞质空泡样变性,内皮细胞胞膜受损.结论 经枕大池注血法可复制蛛网膜下隙出血早期脑血管痉挛动物模型,以二次注血法所复制的脑血管痉挛模型更为稳定.     

颅内动脉瘤性蛛网膜下隙出血并发Takotsubo心肌病

目的探讨颅内动脉瘤性蛛网膜下隙出血并发Takotsubo心肌病临床特点。方法回顾分析14例颅内动脉瘤性蛛网膜下隙出血并发Takotsubo心肌病患者的临床资料、血清心肌酶谱[包括肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、氨基末端B型利尿钠肽前体(NT-pro BNP)]水平、心电图和超声心动图表现。结果 14例患者入院时(初次检查)血清心肌酶谱[CK(591.93±248.78)IU/L、CK-MB(27.07±7.66)IU/L、NT-pro BNP(8685.36±3963.44)IU/L]水平即升高,2周复查时下降[CK(137.79±29.93)IU/L、CK-MB(14.36±5.58)IU/L、NT-pro BNP(577.14±203.37)IU/L],治疗前后差异具有统计学意义(t=7.090,P=0.000;t=4.897,P=0.000;t=7.778,P=0.000)。入院时心电图表现为ST段抬高或压低、T波倒置、QT间期延长,超声心动图呈节段性左室壁运动异常,左心室射血分数(36.07±6.15)%,2周复查时升至(56.43±3.18)%(t=13.381,P=0.000),1个月后恢复正常。结论颅内动脉瘤性蛛网膜下隙出血可诱发Takotsubo心肌病,患病率约4.58%,患者预后良好。超声心动图对早期筛查至关重要,急性期可通过冠状动脉造影术明确诊断。     

动脉瘤性蛛网膜下腔出血后脑血管痉挛危险因素的分析

目的 探讨动脉瘤性蛛网膜下腔出血后脑血管痉挛的危险因素.方法 回顾性分析93例动脉瘤性蛛网膜下腔出血患者的临床资料,研究脑血管痉挛的危险因素.结果 93例动脉瘤性蛛网膜下腔出血患者中共有28例患者(30.1％)发生脑血管痉挛.Hunt-Hess分级≥Ⅲ级血管痉挛发生率明显高于Hunt-Hess分级Ⅰ-Ⅱ级,差异有统计学意义(P＜0.01);Fisher分级≥Ⅲ级血管痉挛发生率明显高于Fisher分级Ⅰ-Ⅱ级,差异有统计学意义(P＜0.01);白细胞计数＞ 15×109的患者脑血管痉挛发生率(41.9％,18/43)明显升高(P＜0.05).结论 Hunt-Hess分级≥Ⅲ级、Fisher分级≥Ⅲ级、白细胞计数增高是蛛网膜下腔出血后脑血管痉挛的危险因素.     

动脉瘤性蛛网膜下腔出血患者脑脊液中一氧化氮浓度的动态变化

目的探讨蛛网膜下腔出血后脑脊液中一氧化氮浓度的动态变化及其与脑血管痉挛的关系。方法采集57例动脉瘤性蛛网膜下腔出血(aSAH)患者脑脊液标本(采集时间为入院后即刻,出血后第3、5、7、10、14天),采用镉粒还原法检测脑脊液中NO浓度。结果出血后第3天脑脊液中NO浓度即有明显降低(P<0.05),在出血后第7～10天达到最低(P<0.01),而后逐渐升高。症状性脑血管痉挛患者NO浓度明显低于未痉挛者及无症状的脑血管痉挛患者。结论症状性脑血管痉挛的发生与脑脊液中NO浓度降低有一定相关性。     

Copeptin在动脉瘤性蛛网膜下腔出血患者血浆中的水平测定

目的对Copeptin在蛛网膜下腔出血患者血液中的浓度进行检测,探讨其与蛛网膜下腔出血的严重性的关系。方法收集37例动脉瘤性SAH患者的血液标本作为实验组,20例体检健康作为对照组者,所有标本均采用夹心ELSISA的方法对Copeptin进行检测,研究其在不同Fisher分级、脑内血肿、Hunt-Hess分级、脑血管痉挛、脑梗死、GOS评分之间的差异。结果实验组copeptin平均值明显高于对照组[(16.28±3.65)pmol/L vs(4.03±1.12)pmol/L)],Hunt-Hess分级Ⅲ~Ⅴ级、Fisher分级3级、合并ICH、GOS分级Ⅰ~Ⅲ级患者的Copeptin平均水平明显增高,血管痉挛、脑梗死、动脉瘤的位置、性别对Copeptin的浓度无明显影响。结论 Copeptin发病早期血液浓度和蛛网膜下腔出血的严重性有关。     

尼莫地平防治蛛网膜下腔出血后脑血管痉挛疗效观察

目的 探讨尼莫地平防治蛛网膜下隙出血后脑血管痉挛的疗效.方法 将70例蛛网膜下腔出血后脑血管痉挛的患者随机分为尼莫地平组(观察组)和对照组,对照组用脱水、止血等常规疗法,观察组在常规疗法基础上加用尼莫地平.结果 尼莫地平组防治蛛网膜下腔出血后脑血管痉挛疗效优于对照组,2组疗效比较差异有统计学意义(P＜0.01) .结论 尼莫地平防治蛛网膜下隙出血后脑血管痉挛安全有效.     

脑血管痉挛活体动物模型的研究进展

蛛网膜下腔出血引起的脑血管痉挛是导致蛛网膜下腔出血患者不良预后的主要原因之一,其发生机制至今尚未完全明了。因此,寻找一种理想的蛛网膜下腔出血后脑血管痉挛动物模型将对脑血管痉挛发生机制及临床防治的研究起到巨大的推动作用,但目前尚无一种用于研究蛛网膜下腔出血后症状性脑血管痉挛的理想模型。本文就应用各种动物制作脑血管痉挛模型的研究进展进行综述。     

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.     

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.     

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.