各类型脑卒中患者的踝肱指数研究

目的 通过测量各种类型脑卒中患者的踝肱指数(ankle-brachial index ABI),定量评估各类型脑卒中与颅内动脉粥样硬化程度的相关性,探讨ABI是否可作为评估颅内动脉硬化狭窄的指标之一.方法 选取各类型脑卒中住院患者共227例,正常对照组88例.使用博士血管多谱勒超声测量仪,测量所有病例组与对照组的ABI,比较两组受试者的ABI.并分析ABI与脑卒中的相关性.结果 227例脑卒中患者中,动脉血栓形成性脑梗死119例,其ABI为(0.905±0.133);腔隙性梗死42例,其ABI为(0.908±0.160);分别与对照组ABI(0.980±0.108)比较,有统计学差异(P＜0.05).心源性脑栓塞组、蛛网膜下腔出血组、脑出血组的ABI值分别与对照组比较,无统计学差异(P＞0.05).相关分析显示高血压(OR=3.963)和ABI(OR=2.225)与脑卒中明显相关(P＜0.05).结论 ABI可反映动脉血栓形成性脑梗死和腔隙性梗死均与脑动脉硬化明显相关,可作为颅内动脉粥样硬化狭窄的初步筛查手段.     

实验性高血压所致的基底动脉结构改变及血管紧张素转换酶抑制剂的影响

探讨高血压大鼠基底动脉结构的变化及血管紧张素转换酶抑制剂对其的影响。选用易卒中型肾血管性高血压大鼠模型 ,分为高血压组、卡托普利治疗组、假手术正常血压对照组。分别于肾动脉狭窄术后 4、8、12周处死动物 ,取基底动脉 ,制片后分别用光镜和透射电镜观察 ,并进行体视学定量分析。术后 4周时高血压组基底动脉光镜下无明显形态学变化 ,8周和 12周时中膜厚度、壁腔比值均比同时期正常血压对照组增加 ,有显著性差异 (P <0 .0 5 ) ;卡托普利治疗后中膜厚度、壁腔比值均小于高血压组 ,差异有显著性 (P <0 .0 5 )。术后 4周高血压组基底动脉平滑肌细胞间隙略增宽 ;术后 8周细胞器肿胀 ,部分溶解 ,间质轻度水肿 ;12周时平滑肌细胞肌丝变性、断裂、溶解 ,内质网扩张 ,线粒体部分空泡变性 ,细胞坏死。卡托普利组各时期超微结构改变不明显。表明高血压可致基底动脉肥厚和超微结构破坏 ,而卡托普利可以预防高血压所致的基底动脉结构破坏。     

Mixed Stroke

Purpose To summarize the chnical, autoptic and animal experimental dala of stroke, propose the concept of mixed stroke (MS) and demonstrate the enoiogy, pathogenesis, clinical mainfestations, prophylaxis and treatment of MS Background At present. stroke still is classified in the national and international academic fields as two main groups: hemorrhage and ischema In fact, thc cerebral vascular disease with hemorrhage forus and ischema focus at the same time is not rare moreover, this type of stroke has special etiology, pathogenesis and clinical manifestations. But it is always made a main dagnosis and neglected the other nature of coexistent focus on either clinical or pathological diagnosis according to traditional classification of stroke Data sources and methods Mort of pablished originsl articles about MS in our department and laboralory wcre reviewed. Resulta The clinical autoptic and animal experimental dats all prcved that hemorrhage and infarction could occur in the course of a stroke simultaneously or in suecession during a short time, which demonstrated the existence of MS It was found clinically that MS patients all had the hustory of hypcrtension and in the autoptic data the MS patients dying of stroke all had typical hypertensive changes in the heart and kidney. and had hypertensive arteriosclerosis in the cerebral arteriole and small artery. MS was cas lily thdueed in stroke-prone renovascular hypertensivc rats This kind of rats are free from genetic deficiency and arc not affected by senile factor, so their cerebral vascular foci are mainly induced by the single factor -hypertension. TThese indicate definitely that hypertensive cerebral vascular lesion is the basis inducing MS. The main lesions of hypertensive cerebral arteriole and small artery were hyalinosis and fibrinoid of the walls, and the formation of microaneurysms or hyperplasla of iniernal and external layers The math lcsions of hypertensive cerebral capillaries were increasing vascular permeability. mural damage. edema of brain tissuc surroumding the vessel. stenotie lumen and leakage of bloed cells These lcsions in varying degrees were observed at different part of thc same brain or at different length of the same vessel at the same time, on the basis of which both hemocrhagic stroke and ischemic stroke could occurr These indicate the brain of the same patient with hypertension has pathomocpliological base of hemorrhagic strokc and ischemic stroke at the same time After after acute cerebral vascular disease occurring, it can be complicated by the other opposite nature of focus during a short time owing to oppression. draw. vascular spasm, metabolic disotder. sharp fluctuation of systemic blood pressure and other factors. The MS patients often had alterations of consciousness and the sign5 of meningeal irritation. were easlily complicated by multiple system organ failure Few cascs had distinct mulufocal cerebral lesions climcally. but after a careful cxamination of the nervous system. bilateral pathologic reflexes were often found. CT or MRI is an important means to diagnose Mis and should be used in 1 -Sd after the onset The measures of treatment for MS should be more vigorous and reliable The factors aggravating pathological lesion should be paid special attention to prevent When MS suspected of occurring clinically, rational neutral measures of treatment are advisable With MS definitely diagnosed the doctors should treat the main foous positively. keep homeostasis, prevent the disorder of hypothafamic function. select proper drugs and treat mfection positively Preventing multiple system organ failure is a key to decrease the mortality of MS. Having spent many years exploring, we establish the anunal model of coexistent infarction and hemorrhage on the basis of stroke-prone renovascular hypertensive rats The incidence of MS up to 95% was found in the group. which were given an inIection of fiblinogen and resperpine. As this model can stimulate the clinical evolution of stroke very well and has very high incidence. it Is a good animal model of MS. conclusions It is essential to list MS as a type of stroke singly. Valuing and studying MS are im ponant for the whole fieid studying pathogenesis. prophylaxis and treatment of stoke.     

单纯性糖耐量受损对脑梗死患者病情严重程度及预后的影响

目的 探讨单纯性糖耐量受损对脑梗死患者病情严重程度及预后的影响.方法 随机选择脑梗死后正常血糖患者32例、单纯性糖耐量受损患者43例和糖尿病患者34例,发病1、4周均用美国国立卫生院卒中评分(National Institutes of Health Stroke Scale,NIHSS)评定患者的病情严重程度,用Barthel生活指数(Barthel index,BI)评定患者的日常生活能力,用改良的Rankin量表(modified Rankin Scale,mRS)评定患者的病残程度,并于12、24周时再次进行BI及mRS.结果 单纯性糖耐量受损组及糖尿病组发病1周时的NIHSS分别为6(0～23)和5.5(0～22),与正常血糖组3(0～16)相比,差异有统计学意义(P均<0.05);而糖尿病组、单纯性糖耐量受损组发病1周时的NIHSS评分之间的差异无统计学意义(P>0.05).单纯性糖耐量受损组发病4周、12周及24周时的预后不良率分别为61.4%、46.5%及32.6%,糖尿病组分别为55.9%、47.1%及50.0%,与正常血糖组的28.1%、18.8%及9.4%相比,差异均有统计学意义(P均<0.05);而单纯性糖耐量受损组与糖尿病组两组之间的差异均无统计学意义.结论 伴发单纯性糖耐量受损的脑梗死患者病情较重,预后不良;积极监测和治疗单纯性糖耐量受损可能成为改善脑梗死患者预后的有效措施之一.     

经颅多普勒超声检测脑血流自动调节下限的初步应用

目的研究经颅多普勒（TCD）在脑血流自动调节下限检测中的应用,拓宽TCD的应用范围。方法利用TCD检测SD大鼠大脑中动脉（MCA）的血流速度,同步记录有创血压,按照临界关闭压（CCP）的理论测定脑血流自动调节下限,与常用的缓慢放血降低血压,绘制脑血流自动调节曲线法测定的自动调节下限进行比较。结果缓慢放血降低血压过程中,MCA的血流速度和颈总动脉的血流量下降趋势完全一致(r=0.95116±0.05736,P<0.001),可以用MCA的血流速度代替血流量计算CCP。CCP法检测到的脑血流自动调节下限为（70.88±24.05）mmHg（1mmHg=0.133kPa）,与放血降低血压利用血流速度和血流量变化测定的结果［分别为（72.88±26.26）mmHg和（75.63±22.22）mmHg］高度相关（r分别为0.79455和0.73846,P均<0.001）,数值相近,来源于同一群体（P分别为0.96758和0.81768）,前者可以代替后两者。结论TCD检测MCA的血流速度,同步记录动脉血压,按照CCP理论测定脑血流自动调节下限,切实可行,结果可靠,可以准确、快捷地反映脑血流动力学变化。     

纹状体梗死患者黑质弥散变化的弥散张量研究

目的 观察纹状体梗死后黑质的弥散变化,探讨纹状体梗死后黑质的继发性损害及其意义.方法 收集首次发病、单侧纹状体梗死、非纹状体梗死、病程在3个月以上的患者各20例分别作试验组和临床对照组,募集健康志愿者20名作对照研究.研究对象均进行1次弥散张量成像(DTI),试验组与临床对照组进行改良Rankin量表(mRS)、Barthol指数(BI)的评分,评估患者脑梗死的预后以及日常生活能力,同时对部分有类似帕金森病症状的患者采用统一帕金森病综合评分量表(Unified Parkinson's Disease Rating Scale,UPDRS)的第Ⅲ分量表评价其严重程度.结果 DTI的参数分析显示:分别与临床对照及健康对照比较,试验组梗死灶同侧黑质的平均弥散量(mean diffusion,MD)值分别升高30.86%(t=40.07,P=0.000)及31.42%(t=42.64,P=0.000),临床对照组梗死灶同侧黑质的MD值与健康对照组比较差异无统计学意义.与没有帕金森病样症状的患者比较,试验组患者中4例出现帕金森病样症状患者梗死灶同侧黑质的MD值升高22%(t=18.03,P=0.01),同时患侧黑质的MD值的上升与其帕金森病样症状的严重程度呈正相关(r=0.97,P=0.03).结论 纹状体梗死可以导致同侧黑质的继发性损害,而且这种继发性损害可能是部分帕金森综合征的发病原因.     

卒中后神经可塑性的研究进展

卒中后神经功能缺损的自行改善与残存脑组织的可塑性有关。神经递质、神经特异性蛋白、神经营养因子、神经抑制因子和神经干细胞等因素在此过程中起着重要作用。研究神经可塑性发生机制和影响因素 ,有助于指导卒中后的康复治疗。     

卒中后神经可塑性的研究进展

卒中后神经功能缺损的自行改善与残存脑组织的可塑性有关。神经递质、神经特异性蛋白、神经营养因子、神经抑制因子和神经干细胞等因素在此过程中起着重要作用。研究神经可塑性发生机制和影响因素,有助于指导卒中后的康复治疗。     

脑梗死急性期血清MMP-9的动态变化及其与脑梗死分型关系的研究

目的　探讨微循环分子标志物的改变与脑梗死临床分型和病情的关系 ,以指导临床的诊治。方法　收集急性脑梗死病人 4 7例 ,分别测定 4 8小时内、第 3天和第 5天的血清MMP 9含量 ,然后分析它与病情轻重、临床分型及预后的关系。结果　脑梗死后MMP 9的含量升高 ,升高幅度和变化规律在OCSP各亚型不同 ;MMP 9在大梗死组的含量显著高于其它组 ;MMP 9与NIHSS呈正相关 ,r=0 4 87;Logistic回归显示 4 8小时内的血清MMP 9含量是预后的独立预测因素。结论　脑梗死后血清MMP 9水平升高 ,并与病灶大小成正比 ,但与病变部位关系不大 ;此外 ,MMP 9可能对病情的严重程度和预后有预示作用。     

局灶性脑梗死继发逆行性神经纤维变性及其临床意义

目的应用磁共振弥散张量成像(diffusion tensorimaging,DTI)技术前瞻性动态观察皮质下或脑干局灶性脑梗死后,病灶上方继发的神经纤维逆行性变性的过程,探讨其对神经功能恢复的影响。方法选择具有单侧内囊区或脑干的独立病灶的脑梗死患者16例,选择年龄及性别相匹配的健康志愿者16名作为对照组。患者分别在发病的第1周(W1)、第4周(W4)、第12周(W12)进行DTI检测和美国国立卫生研究院卒中评分(national institutes of health stroke scale,NIHSS)、简式Fugl-Meyer运动功能评分法(FM)和Barthel生活指数(Barthel Index,BI)评分。计算半卵园中心的DTI参数和各临床评分在观察期内变化的百分数绝对值,分析两者之间的相关关系。结果与对照组比较,病灶上方半卵园中心的部分弥散各向异性(fractional anisotropy,FA)值在各个时间点均明显减少(患者组W1:(0.43±0.02),W4:(0.39±0.01),W12:(0.33±0.02),分别与对照组比较:(0.46±0.01),P<0.01),而平均弥散量(mean diffusivity,MD)无统计学差异(P>0.05)。患者从W1至W12,半卵园中心FA值减少的百分数的绝对值与NIHSS评分减少百分数的绝对值之间(r=-0.49,P<0.05)及与FM增加百分数的绝对值之间(r=-0.56,P<0.05)呈负相关,与BI变化的百分数的绝对值之间无明显相关(P>0.05)。结论局灶性皮质下脑梗死可引起神经纤维逆行性的继发性变性,而且这种逆行性的神经纤维继发性变性会持续存在并可能阻碍患者神经功能的恢复。