急性脑梗死患者脑血流中微栓子与颈动脉粥样硬化斑块的关系

目的 探讨急性脑梗死患者脑血流中微栓子与颈动脉粥样硬化斑块的关系.方法 67例急性脑梗死患者依据颈动脉超声检测分为颈动脉无斑块组(27例)和斑块组(40例),后者再分为不稳定斑块亚组(19例)和稳定斑块亚组(21例);对所有患者应用经颅多普勒仪进行脑血流中微栓子监测;比较各组间微栓子阳性率.结果 脑血流中微栓子阳性率颈动脉斑块组(30%)显著高于无斑块组(3.7%),不稳定斑块亚组(47%)显著高于稳定斑块亚组(14.3%)(均P<0.05).结论 颈动脉粥样硬化脑梗死患者脑血流中微栓子阳性率高;不稳定斑块更易脱落形成微栓子.     

急性脑梗死患者微栓子信号的影响因素及其与近期预后的关系研究

目的 探讨急性脑梗死患者微栓子信号的影响因素及其与近期预后的关系。方法 前瞻 性连续纳入2019 年1 月至2020 年1 月皖南医学院第二附属医院神经内科接诊的118 例急性脑梗死患者 作为研究对象,均经颅多普勒监测微栓子信号,根据微栓子信号是否阳性,分为阳性组和阴性组。采用单因 素和多因素Logistic回归分析微栓子信号的影响因素;随访6个月,观察脑梗死复发情况,通过Kaplan-Meier 生存曲线分析微栓子信号阳性与脑梗死复发的关系。结果 118例急性脑梗死患者中,36 例（30.51%）微 栓子信号阳性;阳性组有颈动脉斑块占比［69.44%（25/36）］、颈动脉重度狭窄率［55.56%（20/36）］、血小 板［（278.84±26.93）×109/L］、超敏C 反应蛋白水平［（13.87±3.58）mg/L］、美国国立卫生研究院卒中量 表（NIHSS）评分［（5.93±1.17）分］均明显高于阴性组,高密度脂蛋白胆固醇水平［（0.91±0.33）mmol/L］ 低于阴性组［分别为29.27%（24/82）、20.73%（17/82）、（215.48±16.53）×109/L、（9.87±2.07）mg/L、（4.88± 0.58）分、（1.23±0.65）mmol/L］,差异均有统计学意义（均P ＜ 0.05）。经多因素Logistic 回归分析,颈动 脉斑块（OR=7.425,95%CI：2.892～28.882）、重度狭窄（OR=2.692,95%CI：1.362～8.736）、高水平血小板 （OR=8.462,95%CI：1.425～16.465）均是微栓子信号阳性的独立危险因素（均P＜ 0.05）。 所有患者获得 随访,脑梗死复发15 例,其中阳性组脑梗死复发率为22.22%（8/36）,高于阴性组的8.54%（7/82）,差异有 统计学意义（χ2=4.223,P=0.040）;经Kaplan-Meier 生存曲线分析和Log-rank 检验,阳性组较阴性组患者 更易出现脑梗死复发（P＜ 0.05）。结论 急性脑梗死患者微栓子信号阳性与颈动脉斑块、重度狭窄和高 水平血小板有关,提示这部分患者近期预后更差,需要更加密切的随访,严格控制危险因素。     

急性脑梗死患者脑微栓子与颈动脉硬化的关系

目的 探讨急性脑梗死患者脑动脉系统微栓子(MES)与颈动脉硬化的关系.方法 收集急性脑梗死患者73例,进行脑动脉微栓子监测和颈动脉彩色多普勒超声检测,观察有脑动脉系统微栓子的病例数.结果 (1)41例有颈动脉斑块,32例无颈动脉斑块;(2)有颈动脉斑块者MES阳性率(46.34%)较无斑块者MES阳性率(21.88%)高(P<0.05);(3)颈动脉不稳定斑块MES阳性率(80%)较稳定性斑块MES阳性率(26.92%)高(P<0.01);(4)MES与颈动脉的狭窄程度、内膜增厚及斑块的个数无相关性.结论 颈动脉粥样硬化斑块的存在及不稳定性是导致脑动脉系统微栓子的重要因素之一,应高度重视,稳定颈动脉斑块是防治动脉至动脉栓塞的重要措施.     

脑动脉微栓子与颈动脉硬化的关系

目的探讨急性脑梗死患者脑动脉系统微栓子（MES）与颈动脉硬化的关系。方法收集急性脑梗死患者146例,进行脑动脉和颈动脉彩色多普勒超声检测,对有脑动系统微栓子的病例进行监测。结果（1）82例有颈动脉斑声,64例无颈动脉斑块;（2）有颈动脉斑块者MES阳性率（46．34）较无斑块者MEs阳性率（21．88）高（P〈0．05）;（3）颈动脉不稳定斑块MES阳性率（80％）较稳定性斑块MES阳性率（26．92％）高（P〈0．01）;（4）MES与颈动脉的狭窄程度、内膜增厚及斑块的个数无相关性。结论颈动脉粥样硬化斑块的存在及不稳定性是导致脑动脉系统微栓子的重要因素之一,应高度重视,稳定颈动脉斑块是防治动脉栓塞的重要措施。     

微栓子信号的发生率及其临床意义

目的探讨常规接受微栓子监测检查患者的微栓子信号发生率以及其相关临床特征。方法连续纳入自2016年7月至2018年12月接受常规30 min微栓子监测以及常规TCD检查中探及到微栓子信号的患者,收集基线信息。结果共5 886例患者进行了30 min微栓子监测检查,其中50例存在微栓子信号,阳性率0.85%。大脑中动脉微栓子信号的出现率最高,达84%。46%(23/50)微栓子来源于动脉,包括8例动脉粥样硬化性脑动脉或颈动脉狭窄、10例颅内动脉、4例烟雾病和1例ANCA相关性动脉炎; 30%(15/50)提示心脏来源的微栓子,包括1例心房颤动、4例人造瓣膜和10例卵圆孔未闭;其他原因微栓子来源占24%(12/50),包括8例从右到左分流和4例未知来源。微栓子阳性的患者脑白质病变及认知障碍发生率高,分别为72%及68%。结论微栓子信号较罕见,不同的疾病微栓子信号的临床意义及机制可能不一样。     

无症状性颈动脉粥样硬化狭窄的微栓子监测及干预治疗

目的探讨对无症状性颈动脉粥样硬化狭窄患者进行微栓子监测及干预治疗在缺血性卒中、短暂性脑缺血发作(TIA)预防中的应用价值。方法选择我院经超声诊断为无症状性颈动脉粥样硬化狭窄50%以上的患者84例,随机分为研究组和对照组各42例,对照组仅给予危险因素干预治疗,研究组在危险因素干预治疗基础上予阿托伐他汀钙片20mg,1次/d+阿司匹林肠溶片100mg或氯吡格雷片75mg,1次/d。分别于治疗前、治疗后6个月、1a进行微栓子监测,随访期1a。观察2组随访时微栓子阳性率及1a内累计微栓子阳性率和脑缺血事件的发生率。结果(1)治疗前研究组13例(30.95%)、对照组17例(40.48%)监测到微栓子信号,差异无统计学意义(P0.05);随访6个月时研究组7例(16.67%)、对照组18例(42.86%)监测到微栓子信号,1a时研究组4例(9.52%)、对照组13例(30.92%)监测到微栓子信号,差异有统计学意义(P0.05);1a内研究组累计13例(30.95%)、对照组累计24例(57.14%)监测到微栓子信号,差异有统计学意义(P0.05)。(2)随访期内,2组共发生同侧脑缺血事件10例,其中研究组3例(TIA 1例,脑梗死2例),对照组7例(TIA 3例,脑梗死4例),差异无统计学意义(P0.05)。结论无症状性颈动脉狭窄患者存在斑块脱落的危险,微栓子信号的出现提示脑缺血事件的风险增高,积极干预治疗可以降低其微栓子信号的发生率,并有降低1a内脑缺血事件的趋势。     

伴有颈动脉斑块的急性前循环脑梗死患者的微栓子研究

目的 探讨颈动脉斑块、微栓子和急性前循环脑梗死的关系。方法 选择住院的急性前循环脑梗死患者65例,经颈动脉超声检查分为伴有颈动脉斑块组45例和不伴有颈动脉斑块组20例,2组均行微栓子监测。结果 伴有颈动脉斑块组与不伴有颈动脉斑块组吸烟、高血压病、糖尿病、高脂血症相比无明显差异(P>0.05); 伴有颈动脉斑块患者的微栓子阳性率为38%,不伴有颈动脉斑块患者为13%,2组相比有明显差异(P<0.05); 软斑组微栓子阳性率为45%,硬斑组微栓子阳性率为18%,2组相比有明显差异(P<0.05)。结论 急性前循环脑梗死患者多有颈动脉斑块,软斑块是微栓子的主要来源,微栓子是急性脑梗死发病的重要危险因素,对二者早期干预是防治脑卒中的重要措施之一。     

100例微栓子阳性脑梗死患者的多因素分析

目的探讨微栓子(microembolus,MES)阳性与缺血性脑卒中高危因素的关系及其临床意义。方法根据经颅多普勒监测100例MES阳性的缺血性脑卒中患者和74例MES阴性的缺血性脑卒中患者临床资料,分析各卒中高危因素与MES的关系。结果MES阳性与年龄、性别、超重、吸烟、酗酒、高血压、高尿酸血症、卒中家族史无关;与高血脂、糖尿病、高纤维蛋白原血症、高红细胞压积、高同型半胱胺酸血症、颈动脉不稳定斑块显著相关(P<0.05)。结论病变的颈动脉、异常的血流及血液成分是颅内微栓子主要促成因素,其阳性说明患者有活动性栓子,易发生或易再发缺血性卒中。     

112例脑动脉系统微栓子监测的临床研究

目的　研究脑动脉系统微栓子 (MES)的产生机制及其相关因素。方法　将 112例 MES监测的临床资料进行总结分析。结果　本组微栓子检出率为 33.93% ,且全部见于有明显脑卒中症状者 ;脑梗死 MES检出率为35 .87%且以原发性大面积梗死为主 ;MES阳性与病程有明显相关 ,病程 <72 h易检出微栓子 ,阳性率为 4 7.72 % ;颅内血管狭窄是微栓子产生的主要原因 ;颈动脉异常与正常组微栓子出现率无明显差异 ,但发现本组病例中微栓子出现以左侧为主 ,与颈动脉病变部位一致率为 5 5 .5 5 % ;确定微栓子来源于有病变的颅外颈动脉 2例 ,来源于有病变的颅内颈动脉系 5例 ,来源于同时伴有颅内外血管病变 12例 ,表明颅内外动脉同时伴有病变时微栓子检出率增高 ;MES的阳性率与血液成分无相关性 ,但在血液成分异常组中血粘度增高以及血小板聚集降低 MES阳性率明显增高。结论　脑动脉系统中监测到微栓子说明患者有活动的栓子来源 ,易发生或复发脑梗死 ,TCD能正确的监测、判断脑循环中微栓子 ,确定其发生率、性质、来源以及与疾病的联系     

脂蛋白相关磷脂酶A2水平、微栓子信号与大动脉粥样硬化型急性脑梗死患者短期预后的关系

目的研究大动脉粥样硬化型急性脑梗死患者住院时的脂蛋白相关磷脂酶A2水平、微栓子信号对其短期预后的影响。方法募集起病72 h内的大动脉粥样硬化型急性脑梗死患者238例,收集其入院时的临床资料及实验室资料等。根据改良Rankin量表评分将患者分为预后良好组(0~2分)和预后不良组(2分)。将研究对象分为4组:脂蛋白相关磷脂酶A2正常、微栓子信号阴性组(NL/NM);脂蛋白相关磷脂酶A2正常、微栓子信号阳性组(NL/IM);脂蛋白相关磷脂酶A2升高、微栓子信号阴性组(IL/NM);脂蛋白相关磷脂酶A2升高、微栓子信号阳性组(IL/IM)。采用非条件Logistic回归分析脂蛋白相关磷脂酶A2水平、微栓子信号与急性脑梗死短期预后的关系。结果急性脑梗死患者预后不良组入院时的脂蛋白相关磷脂酶A2水平、微栓子信号阳性率均高于预后良好组(均P0.05)。经多因素调整后,与NL/NM相比,NL/IM、IL/NM和IL/IM组发生预后不良的OR值(95%CI)分别为0.719(0.112~4.627)、4.687(1.506~14.588)和14.868(3.373~65.538)。结论急性脑梗死患者入院时脂蛋白相关磷脂酶A2水平是其短期预后不良的独立危险因素,微栓子信号阳性显著放大了高水平脂蛋白相关磷脂酶A2对发生短期预后不良的作用,脂蛋白相关磷脂酶A2/微栓子信号是大动脉粥样硬化型急性脑梗死短期预后不良的预测指标。     

Behavioral dopamine signals

Lesioning and psychopharmacological studies suggest a wide range of behavioral functions for ascending midbrain dopaminergic systems. However, electrophysiological and neurochemical studies during specific behavioral tasks demonstrate a more restricted spectrum of dopamine-mediated changes. Substantial increases in dopamine-mediated activity, as measured by electrophysiology or voltammetry, are related to rewards and reward-predicting stimuli. A somewhat slower, distinct electrophysiological response encodes the uncertainty associated with rewards. Aversive events produce different, mostly slower, electrophysiological dopamine responses that consist predominantly of depressions. Additionally, more modest dopamine concentration fluctuations, related to punishment and movement, are seen at 200-18,000 times longer time courses using voltammetry and microdialysis in vivo. Using these responses, dopamine neurotransmission provides differential and heterogeneous information to subcortical and cortical brain structures about essential outcome components for approach behavior, learning and economic decision-making.     

Safety signals and agoraphobia

The safety-signal analysis of agoraphobia is critically examined. This examination suggests that safety signals developed from an aversive context have limited potential as therapeutic variables. A safety-signal formulation of agoraphobia is presented within a stimulus control framework that emphasizes a competition between positive and aversive reinforcement contingencies.     

Pancreatic glucagon signals postprandial satiety

The hypothesis that prandial increases in circulating pancreatic glucagon initiates an important peripheral satiety signal is reviewed. Glucagon administration at the beginning of meals reduces the size of test meals in animals and humans and reduces the size of spontaneous meals in rats. Exogenous glucagon may also interact synergistically with cholecystokinin to inhibit feeding. These appear to be satiety effects because they are behaviorally specific in rats and subjectively specific in humans. Glucagon's pharmacological satiety effect is complemented by compelling evidence for a necessary contribution of endogenous glucagon to the control of meal size: administration of glucagon antibodies increases both test and spontaneous meal size in rats. Under many, but not all, conditions exogenous glucagon's satiety effect appears to originate in the liver and to be relayed to the brain via hepatic vagal afferents. Analysis of the central processing of this signal, however, has barely begun. How glucagon changes are transduced into neural afferent signals also remains an open question. The only hypothesis that has been extensively tested is that stimulation of hepatic glucose production initiates the satiety signal, but this is neither convincingly supported nor clearly rejected by currently available data. It is also not yet clear whether glucagon contributes to some forms of obesity or has potential use as a therapeutic tool in the control of eating disorders. Of the several proposed controls of hunger and satiety, glucagon appears to be one of the most likely to be physiologically relevant. This encourages further analysis of its behavioral characteristics, its neural mechanisms, and its clinical potential.     

Feeding signals and brain circuitry

Food intake is a major physiological function in animals and must be entrained to the circadian oscillations in food availability. In the last two decades a growing number of reports have shed light on the hormonal, cellular and molecular mechanisms involved in the regulation of food intake. Brain areas located in the hypothalamus have been shown to play a pivotal role in the regulation of energy metabolism, controlling energy balance. In these areas, neuronal plasticity has been reported that is dependent upon key hormones, such as leptin and ghrelin, that are produced by peripheral organs. This review will provide an overview of recent discoveries relevant to understanding these issues.     

The processing of proprioceptive signals

Simple and two-choice reaction times were investigated in two experiments using proprioceptive stimuli. The form of the stimulus was the release of the passively supported forearm. The responses were to halt the falling arm and to activate a microswitch held in the hand. Latencies were also determined from the EMG activity. The findings indicated that the latency of two-choice situations were not significantly different from the simple situation, and that compatible responses were significantly faster than incompatible responses.     

Microembolic signals in subarachnoid hemorrhage

Microembolic signals (MES) detected by transcranial Doppler (TCD) have been reported in subarachnoid hemorrhage (SAH), although their origin and contribution to brain ischemia remain uncertain. We conducted a prospective study to evaluate the frequency of MES among patients with SAH and to determine their origin. Twenty-seven patients with SAH, comprising 15 aneurysmal and 12 non-aneurysmal patients, participated in the study. TCD evaluation was performed using a 2 MHz probe. Patients were studied three times per week during their in-patient stay to detect vasospasm, and then each middle cerebral artery (MCA) was monitored for 30 min using the Monolateral Multigate mode to detect MES. Using this method, MES were detected in 7 out of 15 patients (47%) with aneurysmal SAH and were not seen in non-aneurysmal patients (p = 0.007). Vasospasm occurred in 52% (14/27) of cases. However, clinical signs and symptoms of vasospasm were identified in only 18.5% (5/27). There was no significant relationship between MES and vasospasm (p = 0.224). Also, no relationship was found between MES and the location of the aneurysm (p = 0.685). Thus, in this study MES were only detected in aneurysmal SAH. However, we did not find a relationship between the location of the aneurysm and MES, or the presence of vasospasm and MES. Therefore, MES in patients with SAH may also originate from vascular pathology other than the aneurysm sac or vascular spasm.     

Functional source separation from magnetoencephalographic signals

We propose a novel cerebral source extraction method (functional source separation, FSS) starting from extra-cephalic magnetoencephalographic (MEG) signals in humans. It is obtained by adding a functional constraint to the cost function of a basic independent component analysis (ICA) model, defined according to the specific experiment under study, and removing the orthogonality constraint, (i.e., in a single-unit approach, skipping decorrelation of each new component from the subspace generated by the components already found). Source activity was obtained all along processing of a simple separate sensory stimulation of thumb, little finger, and median nerve. Being the sources obtained one by one in each stage applying different criteria, the a posteriori "interesting sources selection" step is avoided. The obtained solutions were in agreement with the homuncular organization in all subjects, neurophysiologically reacting properly and with negligible residual activity. On this basis, the separated sources were interpreted as satisfactorily describing highly superimposed and interconnected neural networks devoted to cortical finger representation. The proposed procedure significantly improves the quality of the extraction with respect to a standard BSS algorithm. Moreover, it is very flexible in including different functional constraints, providing a promising tool to identify neuronal networks in very general cerebral processing.     

基于脑电信号的身份识别方法*☆

基于脑电信号的身份识别是通过采集试验者的脑部信号来进行身份认证。对于同一个外部刺激或者主体在思考同一个事件的时候,不同人的大脑所产生的认知脑电信号不同。选取与运动意识想象有关的电极后,分析不同个体在特定状况下脑电的个体差异,采用以回归系数、能量谱密度、相同步、线性复杂度多种信号处理结合方法对运动想象脑电信号进行处理来进行特征提取。组合多元特征向量并运用多层BP神经网络对不同个体的脑电信号进行分类,并在不同的意识想象及不同数据长度、不同的波段对试验者进行识别率验证分析。结果表明,不同运动想象的平均识别率均在80%以上,其中以想象舌头运动的识别率较高,达到90.6%,不同波段的识别率也表明意识想象的模式及相应波段对身份认别有较大的影响。