缺血性卒中合并脑白质病变的危险因素研究

目的 探讨缺血性卒中合并脑白质病变的患病情况及相关危险因素,通过对其干预以降低脑白质病变的发生率。方法 本研究连续入选2007年8月至2008年10月在北京天坛医院神经内科住院的缺血性卒中患者共483例,依据有无脑白质病变分成伴脑白质病变组和无白质病变两组,得出我院住院的缺血性卒中患者合并脑白质病变的患病率,以有无脑白质病变作为因变量,各种血管病危险因素作为自变量进行Logistic回归多因素分析。结果 我院住院的缺血性卒中患者脑白质病变的患病率为53.8%,随年龄增长发生率和病变严重程度增加（P均<0.01）。Logistic回归显示高龄［比值比（odds ratio,OR）=1.03,95%可信区间（confidence interval,CI）1.00～1.05,P<0.05］、高血压病（OR=1.77,95%CI 1.07～2.91,P<0.05）、卒中病史（OR=1.71,95%CI 1.02～2.88,P<0.05）、高血糖（OR=1.07,95%CI 1.00～1.15,P<0.05）和腔隙性脑梗死（OR=1.89,95%CI 1.17～3.06,P<0.05）是脑梗死患者合并脑白质病变的独立危险因素。结论 随年龄增长,脑白质病变的患病率和严重程度增加;高龄、高血压病、卒中病史、高血糖和腔隙性脑梗死是缺血性卒中患者合并脑白质病变的独立危险因素。     

缺血性卒中患者脑内微出血特点及危险因素的研究

目的 探讨脑内微出血在缺血性卒中患者中的发生率及在脑内各区域的分布情况,观察缺血性卒中亚型之间微出血发生率的差异,初步分析其相关因素及其与腔隙性脑梗死、脑白质病变等微小血管病变程度之间的关系。方法 连续入选261例心源性栓塞型、大动脉粥样硬化型及小动脉闭塞型3个亚型的缺血性卒中患者。记录患者一般临床资料及实验室检查结果,应用头颅磁共振梯度回波T2*加权成像（gradient-echoT2*-weighted,GRE-T2*）观察脑内微出血的数目及部位,同时观察腔隙性脑梗死数目和部位以及脑白质病变程度。结果 80例患者（30.70%）存在脑内微出血,数目为1～109个。微出血最常见于皮质-皮质下区（46.09%）,其次位于基底节区（27.80%）。各亚型中小动脉闭塞型患者脑内微出血的发生率最高（53.30%）。高血压、腔隙性脑梗死数目及脑白质改变程度为缺血性卒中患者脑内微出血发生的独立危险因素,比值比（odds ratio,OR）分别为4.364、1.190和1.310;脑内微出血的分级与腔隙性梗死分级（r =0.519,P <0.001）及白质改变程度（r =0.437,P <0.001）显著相关。结论 微出血在缺血性卒中患者特别是小动脉闭塞患者中发生率较高,微出血与腔隙性脑梗死数目及脑白质改变明显相关。     

糖尿病并发脑卒中的临床与相关因素探讨

目的　探讨糖尿病并发脑卒中的临床特点与相关因素 ,便于卒中防治。方法　住院糖尿病并发脑卒中患者 90例 ,均行颅脑CT检查 ,5例行MRI(1例行MRA)检查。并同时进行空腹血糖、血脂和血液流变学测定。结果　 90例根据影像学改变分为腔隙性脑梗死 5 0例 (其中多发性腔梗 36例 ,单发性腔梗 14例 ) ,脑梗死 2 5例 ,脑出血 8例 ,出血性脑梗死 3例 ,椎基底动脉供血不足 4例。病变部位 :基底节区 38例 ,侧脑室周围 2 0例。其余病例分布于额叶、小脑、脑干、丘脑等部位。脑梗死的平均空腹血糖值明显高于腔隙性脑梗死 (P <0 .0 1)。脑梗死的LDL c平均值也明显高于腔隙性脑梗死 (P <0 .0 1)。结论　糖尿病并发脑卒中以腔隙性脑梗死多见 (占 5 5 .6 % ) ,且病灶多发 ,分布广泛。病变好发部位以基底节区为主。高血糖及LDL c增高可能是糖尿病并发脑卒中的重要危险因素。     

血清CysC、TGF-β1对老年腔隙性脑梗死患者早期神经功能恶化的预测价值

目的 探讨血清胱抑素C (CysC)、转化生长因子-β1 (TGF-β1)对老年腔隙性脑梗死(LI)患者早期神经功能恶化(END)的预测价值。方法 选取2020年1月至2021年12月琼海市人民医院神经内科收治的老年LI患者124例,采用多因素Logistic回归分析老年LI患者发生END的危险因素,分析血清CysC、TGF-β1对END的早期预测价值。结果 124例老年LI患者中发生END患者28例,发生率为22.58%。END组患者入院时NIHSS评分、病灶累及内囊后肢患者比例及血清CysC水平明显高于非END组,而END组患者血清TGF-β 1水平则低于非END组(P<0.05)。Logistic回归分析显示,NIHSS评分、病灶累及内囊后肢、血清CysC及TGF-β 1水平是LI患者发生END的危险因素(P<0.05)。CysC联合TGF-β 1检测对LI患者发生END预测的曲线下面积为0.867 (95%CI为0.791～0.943),灵敏度为85.7%,特异度为78.1%。结论 老年LI患者END发生率较高,可能与NIHSS评分高、病灶累及内囊后肢、血清CysC...     

脑梗死患者脑白质病变体积与血清同型半胱氨酸的相关性分析

目的分析脑梗死患者脑白质病变(WMLs)体积与血清同型半胱氨酸(Hcy)的相关性。方法选取我院收治的脑梗死患者80例,对80例患者的脑白质病变体积进行测量,并测定患者的Hcy水平,分析脑梗死患者脑白质病变体积与血清同型半胱氨酸水平的相关性。结果经多因素非条件Logistic回归分析显示,脑梗死患者的年龄、卒中史、腔隙梗死数目、颅内动脉狭窄及Hcy水平均是影响脑白质病变体积的独立危险因素(P0.05)。结论血清同型半胱氨酸水平与脑梗死患者脑白质病变体积有明显相关性,是决定患者脑白质病变体积的独立危险因素。     

脑白质疏松和陈旧性腔隙性脑梗死对首发缺血性卒中患者预后的影响

目的 探讨脑白质疏松和陈旧性腔隙性脑梗死对于首发缺血性卒中患者预后的影响。 方法 连续选取791例7 d以内首次发病的非心源性缺血性卒中患者。收集患者的人口学信息和脑血 管病的危险因素,评价患者的头颅磁共振成像包括脑白质疏松的严重程度、无症状性腔隙性脑梗死 的数量、缺血性卒中的病因分型以及急性梗死灶的分布特征,通过多因素Logistic回归分析脑白质疏 松和陈旧性腔隙性脑梗死与缺血性卒中患者预后相关的危险因素。 结果 分别有14例（1.8%）、38例（4.8%）患者在缺血性卒中发病1年内死亡、缺血性卒中或短暂性脑 缺血发作（transient ischemic attack,TIA）复发。多元Logistic回归发现：存在陈旧性腔隙性脑梗死、有 皮层新发脑梗死灶、入院后未给予抗血小板药物、出院时未服用他汀药物是缺血性卒中患者1年内 死亡的危险因素;而脑白质疏松对于缺血性卒中患者1年内的死亡无显著影响。冠状动脉粥样硬化性 心脏病、入院美国国立卫生研究院卒中量表（National Institute of Health stroke scale,NIHSS）评分<4 分、新发梗死灶的责任脑动脉闭塞或狭窄程度≥70%、出院时未给予抗血小板药物是缺血性卒中患 者1年内缺血性卒中或TIA复发的危险因素;而脑白质疏松和陈旧性腔隙性脑梗死对于缺血性卒中患 者1年内缺血性卒中或TIA的复发无显著影响。 结论 陈旧性腔隙性脑梗死是缺血性卒中患者1年内死亡的危险因素。而脑白质疏松和陈旧性腔隙 性脑梗死对于缺血性卒中患者1年内缺血性卒中或TIA的复发无显著影响。     

内囊后肢梗死的临床特征及危险因素

目的探讨内囊后肢梗死患者的临床特征及危险因素。方法选择局限于内囊后肢的梗死患者94例,以同期年龄相近、性别相同94例未分类脑梗死患者为对照,比较两组危险因素分布的差异。并进一步对内囊后肢梗死患者亚组的危险因素进行比较,即进展性运动障碍组与非进展性组以及白质疏松与无白质疏松组、有多发腔隙性脑梗死(LI)组与无多发LI组的危险因素分布。结果内囊后肢梗死组患者的高血压患病率、吸烟率、高同型半胱氨酸血症(Hhcy)率较未分类脑梗死组高(P0.05)。进展性运动障碍组与非进展组的危险因素比较,无显著差异(P0.05)。结论内囊后肢梗死大多数为穿支动脉病变所致,高血压、吸烟、Hhcy是内囊后肢梗死的主要危险因素。内囊后肢梗死容易发生进展性运动功能障碍及预警综合征,其病理机制与内囊后肢固有的穿支动脉病变以及运动纤维分布特征有关。     

无症状性脑梗死的危险因素和影像学特征

目的　探讨神经内科非脑卒中老年住院患者中无症状性脑梗死 (SBI)的发生率、危险因素、影像学特征及其临床意义。方法　神经内科非脑卒中老年住院患者 2 6 0例均行CT或MRI检查 ,从年龄、影像学特征 (病灶大小 ,部位、类型等 )、危险因素等方面进行统计学分析。结果　在神经内科非脑卒中老年住院患者中 ,SBI发生率为 31 15 % ,有随年龄增长而上升的趋势 ;男性多于女性 (1 79∶1) ;CT/MRI显示病灶直径多在0 3cm～ 1 5cm之间 ,95 %为腔隙性脑梗死 ,71 6 %分布于基底节区、内囊等 ;SBI患者伴发高血压病、糖尿病、缺血性心脏病、高脂血症、吸烟、动脉硬化等明显高于非SBI者 (P <0 0 1)。结论　高龄、高血压病、糖尿病、缺血性心脏病、高脂血症、吸烟、动脉硬化均为SBI危险因素。影像学所见多为基底节区、内囊腔隙性梗死。     

卒中及短暂性脑缺血发作患者不同部位脑萎缩的危险因素

目的脑萎缩是卒中后痴呆的重要危险因素,探索卒中及短暂性脑缺血发作患者不同部位脑萎缩的危险因素,为降低卒中后痴呆发的发生提供潜在干预靶点。方法纳入连续住院的卒中及短暂性脑缺血发作(transient ischemic attack,TIA)患者,采集患者一般危险因素及血管性危险因素,完成头颅MRI和/或头颅CT扫描及半定量测定,包括陈旧性腔隙性脑梗死数量、额叶萎缩、顶叶萎缩、颞中叶萎缩及广泛脑萎缩的程度。结果共519例卒中及TIA患者完成4种脑萎缩的测量。Logistic回归分析结果显示:除年龄外,女性(比数比OR=2.447,P=0.007)、腔隙性脑梗塞病灶数(OR=1.414,P=0.027)是额叶萎缩的独立危险因素;缺血性卒中病史(OR=2.224,P=0.024)是顶叶萎缩的独立危险因素;颅内/外大血管狭窄(OR=2.584,P=0.015)、脑白质变性评分(OR=1.112,P=0.007)及腔隙性脑梗塞病灶数(OR=1.158,P=0.042)是颞中叶萎缩的独立危险因素;而糖尿病(OR=2.109,P=0.001)、心房纤颤(OR=1.934,P=0.015)、脑白质变性评分(OR=1.098,P=0.002)是广泛脑萎缩的独立危险因素。结论糖尿病、心房纤颤、腔隙性脑梗塞数及脑白质变性是卒中及TIA患者脑萎缩的危险因素,可对对上述高危人群尽早干预,减小此类患者发生痴呆的可能。     

后循环梗死的危险因素分析

目的 探讨后循环梗死的主要危险因素.方法 回顾性分析216例急性后循环梗死患者的临床资料.根据头颅MRI的表现,将患者分为近段组、中段组、远端组、混合组以及单灶组、多灶组、单侧病灶组、双侧病灶组、腔隙性梗死(腔梗)组与非腔梗组;分析各组的危险因素.同时与同期住院的前循环梗死患者的危险因素进行对比.结果 216例后循环梗死患者中,有高血压为76.9%、糖尿病为36.6%、高脂血症为30.1%、既往有卒中史为26%、心脏疾病为22.2%;近段病变为6%,中段病变为24.5%,远段病变最高为49%;近端组的平均年龄[(57.92±12.81)岁]显著低于其他组(P<0.01),高脂血症发生率(61.5%)显著高于其他组(P<0.01);既往卒中史在多病灶组、双侧病灶组及腔梗组中明显高于单病灶、单侧病灶及非腔梗组(均P<0.01),而高脂血症在单病灶组中高于多病灶组,单侧病灶组高于双侧病灶组(均P<0.05).后循环梗死组平均年龄[(69.42±11.25)岁]大于前循环梗死组[(65.93±11.22)岁](P<0.01);高脂血症、糖尿病、既往卒中史发生率高于前循环梗死组(分别为20.7%、16.9%、14.6%)(P<0.05～0.01),而吸烟率(18.5%)低于前循环梗死组(38.5%)(P<0.01).结论 后循环梗死常见的危险因素是高血压、糖尿病、高脂血症与既往卒中史.与前循环梗死组相比,后循环梗死组年龄较大、血管危险因素患病率高.     

Virchow-Robin spaces relate to cerebral small vessel disease severity

BACKGROUND AND PURPOSE: Virchow-Robin spaces (VRs) are perivascular spaces surrounding the deep perforating brain arteries. VRs dilatation is pathologic, and it could be a manifestation of cerebral small vessel disease. In the present study we assessed the relation between VRs and silent ischemic lesions in a cohort of patients with cerebral small vessel disease. METHODS: We divided dilated VRs on MRI (1.5 Tesla) into three semi-quantitative categories in 165 first ever lacunar stroke patients. We counted asymptomatic lacunar infarcts and graded white matter lesions, and compared the prevalence of vascular risk factors in different categories of VRs. We also determined independent predictors of silent ischemic lesions. RESULTS: VRs at basal ganglia level related to age, hypertension, asymptomatic lacunar infarcts, and white matter lesions. VRs at basal ganglia level predicted silent ischemic lesions (odds ratio 10.58 per higher VRs category; 95 %- confidence interval 3.40 - 32.92). CONCLUSION: Dilated VRs in the basal ganglia relate to the severity of cerebral small vessel disease and might be a manifestation of the same small vessel abnormality that causes silent ischemic lesions. This adds a role for VRs as a potential marker for small vessel disease.     

Silent intracerebral lesions identified on magnetic resonance imaging in patients presenting with initial stroke--comparative studies of the affected hemisphere and the contralateral one]

Among patients who had undergone MRI examinations with a clinical suspicion of stroke, we selected 82 patients with initial cerebral infarction being located only in a unilateral cerebral hemisphere. Seventeen (21%) subjects had wedge-shaped lesions including cerebral cortex (the cortical type), 65 (79%) had them predominantly in white matter and/or territory of the deep perforators (the subcortical type). Fifty nine cases out of total 82 (72%:9 in the cortical type, 50 in the subcortical type) had the silent cerebral infarction in the contralateral hemisphere to the affected side found on the 1.5 tesla superconductive system T2 weighted magnetic resonance imaging. Among them, 57 had the contralateral small cortical and/or subcortical (white matter) infarction, the other 2 cases had the contralateral lacunar infarction in the basal ganglia-internal capsule area as the silent lesion. The incidence of the cortical type was high in cases without the silent cerebral infarction in the contralateral hemisphere. It might be suspected that the cortical type had tendency to present clinical symptoms caused by initial stroke without prior silent cerebral infarction. The author proposed that the cerebral embolism might play an important role in showing the sudden onset clinical symptoms of the cortical type. And the author also proposed that there might be a difference in the development of clinical symptoms between the silent cerebral infarction located in the basal ganglia-internal capsule area and the cortical-subcortical (white matter) area.     

Clinical lacunar syndromes as predictors of lacunar infarcts. A comparison of acute clinical lacunar syndromes and findings on diffusion-weighted MRI

OBJECTIVES: To evaluate if patients with acute lacunar syndromes have acute lacunar infarcts or other types of cerebral lesions on diffusion-weighted MRI. METHODS: Patients with acute lacunar syndromes underwent echo-planar diffusion MRI of the brain within 3 days after stroke onset. Localization and size of lesions with hyperintense signal were determined, compared with clinical characteristics and with findings on follow-up T2-weighted MRI. RESULTS: Twenty-three patients participated in the study. Thirteen patients had pure motor stroke, 1 pure sensory stroke, 8 sensorimotor stroke, and 1 ataxic hemiparesis. Twenty-two patients had at least one lesion with increased signal on diffusion-weighted MR images. These acute lesions were in the internal capsule/ basal ganglia/thalamus in 13 patients, subcortical white matter in 5 patients, brainstem in 2 patients, cortex (multiple small lesions) in 1 patient, and cortex + basal ganglia in 1 patient. The median volume of the lesions was 0.6 ml on the initial examination and on follow-up, of 17 patients after 1 to 5 months, 0.5 ml. CONCLUSIONS: Almost all patients with acute ischemic lacunar syndromes have acute lesions on echo-planar diffusion-weighted MRI within 3 days after stroke onset. These lesions are mostly small and subcortical, compatible with lacunar infarcts caused by single penetrating artery occlusion, but in a minor proportion of patients (2 of 23 in our study) a cortical involvement is found.     

初发腔隙性梗死病人与代谢综合征关系的研究

目的 探讨腔隙性梗死病人代谢综合征的患病率及与各亚型之间的关系.方法 选择138例初发腔隙性梗死患者及年龄、性别相匹配的138例初发动脉硬化性皮层梗死患者,根据有无白质损害,观察腔隙性梗死患者代谢综合征的患病率及与腔隙性梗死亚型的关系.结果 皮层梗死组代谢综合征的患病率（45.7%）高于腔隙性梗死组（35.9%）（P〈0.01）.无白质损害的腔隙性梗死患者代谢综合征的患病率高于有白质损害者,皮层梗死组代谢综合征患病率高于有白质损害的腔隙性梗死组.结论 代谢综合征的患病率与不伴白质损害的腔隙性梗死明显相关,皮层梗死的患病率高于有白质损害的腔隙性梗死,与各型梗死之间的发病机制不同有关.     

Correlation study between small vessel disease and early neurological deterioration in patients with mild/moderate acute ischemic stroke

Aims: Cerebral small vessel disease (SVD) refers to a group of pathological processes that affect small arteries, arterioles, venules, and capillaries of the brain. We hypothesized that imaging markers of SVD could be associated with neurological deterioration during acute phase of mild/moderate ischemic stroke. Methods: We performed a prospective cohort with 687 consecutive patients with acute ischemic stroke and also with admission NIHSS score below 12 points. Imaging markers of SVD include silent lacunar infarction, deep cerebral microbleeds (CMBs), brain atrophy, periventricular and semiovale white matter hyperintensities, basal ganglia and semiovale enlarged perivascular spaces as well as SVD burden rating scale, which were evaluated and calculated, respectively. Early neurology deterioration (END) was defined as an increment of NIHSS score ≥2 points in the first 72 h after admission. Results: None of these imaging markers and rating scale of SVD significantly correlated with END after adjusted for major confounders. Post hoc analysis indicated similar negative results in different age, TOAST classification and infarction location subgroups. Only silent infarction (OR 2.42, 95%CI 1.33–5.10) and deep CMBs (OR 2.10, 95%CI 1.08–3.72) seemed to be predictors for END in female patients. However, due to the increased type I error in multiple comparisons, these relationships should not be regarded as statistically significant. Conclusion: In patients with mild/moderate acute ischemic stroke, imaging markers of SVD did not correlate with END.     

急性脑卒中与便秘57例分析

目的 探讨急性脑卒中与便秘的关系。方法 57例脑卒中患者分成动脉粥样硬化血栓性脑梗死（ATI）组23例；腔隙性梗死（LI）组23例；脑出血（ICH）组11例，观察各组便秘发生率并进行比较。结果 脑卒中者第1周便秘发生率50.88％，显著高于正常老年人对照组（P〈0．05）。基底节区脑卒中者便秘发生率57．1％，明显高于非基底节卒中者（P〈0.05）。结论 脑卒中患者急性期常发生便秘，基底节区脑卒中者便秘发生率较非基底节区脑卒中者高。     

MRI findings of small subcortical “lacunar-like” infarction resulting from large vessel disease

Small subcortical infarctions resulting from large-vessel disease are often observed. It is important to distinguish these from pure lacunar infarction resulting from small-vessel disease because the investigations and examinations differ. We investigated the differences on brain magnetic resonance imaging (MRI) between small subcortical "lacunar-like" infarcts resulting from large-vessel disease and pure lacunar infarcts. Thirteen subjects with small lacunar-like infarcts (size < 2 cm), resulting from large-vessel disease, and 30 subjects with lacunar infarcts (< 2 cm), without large-vessel disease were studied. We measured infarction size using a 1.5-T MRI device and evaluated silent subcortical hyperintensity lesions using the modified Scheltens' score. Large-vessel lesion was confirmed by conventional angiography, duplex carotid scan, and magnetic resonance angiography. There was no difference in the mean age of the two groups. Cerebrovascular risk factors and atherosclerotic complications were also comparable for the two groups. Progressive stroke was more common in the lacunar-like infarction group than in the lacunar infarction group (P = 0.004). Scores for periventricular hyperintensity, white matter hyperintensity, basal ganglia hyperintensity, and total subcortical hyperintensity scores were significantly higher in the lacunar infarction group than in the lacunar-like infarction group. The difference in basal ganglia hyperintensity scores was remarkable (P = 0.001). The enlargement of the perivascular space was also significantly greater in the lacunar infarction group than in the lacunar-like infarction group. These findings seem to reflect differences in the pathogenesis of infarction between the two groups. Silent subcortical hyperintensity lesions and enlargement of perivascular space are useful for between distinguishing small lacunar-like infarct resulting from large-vessel disease and pure lacunar infarction. This may have significant implications for the management of patients with lacunar-sized infarctions. It suggests that the pathogenesis of lacunar-sized infarction is variable.     

急性脑梗死患者脑白质病变因素风险评估

目的探讨脑白质病变对急性脑梗死患者预后的影响。方法选择驻马店市中心医院收治的282例急性脑梗死患者,根据MRI检查结果分为脑白质病变组(115例)和无脑白质病变组(167例),对2组临床资料(性别、年龄、糖尿病、高血压、房颤、高血脂)情况进行统计,同时对全部患者随访90d,评价患者的预后情况。结果脑白质病变组和无脑白质病变组男女比例及平均年龄差异无统计学意义(P0.05)。而脑白质病变组糖尿病、高血压、房颤、高血脂的发生率及预后不良率、病死率显著高于无脑白质病变组(P0.01)。结论急性脑梗死患者若在影像学检查中发现脑白质病变,需对相关危险因素进行积极干预,可有效改善预后,降低病死率。     

缺血性脑卒中患者脑微出血与脑白质病变的相关性研究

目的 探讨缺血性脑卒中患者脑微出血与脑白质病变的相关性。方法 选取2018年1月-2019年12月本院收治的缺血性脑卒中患者; 通过核磁共振成像扫描患者头部观察各脑区脑微出血、脑白质病变情况,并对脑微出血情况进行分级,对脑白质病情情况进行评分; 采用Logstic回归分析法分析各危险因素与脑微出血、脑白质病变的关系; 通过spearman相关分析法分析脑微出血分级与脑白质病变评分的相关性。结果 有脑微出血患者中皮质及皮质下出现脑微出血占比61.46%明显高于基底及丘脑23.96%及幕下区41.10%(P<0.05); 有脑白质病变患者中额区脑白质病变占比69.44%明显高于颞区14.81%、顶枕区6.48%、基底节3.70%(P<0.05); Logstic回归分析显示年龄>60岁、有高半胱氨酸血症及合并心房颤动是发生脑微出血的独立危险因素(P<0.05),年龄>60岁是发生脑白质病变的独立危险因素(P<0.05); 脑微出血各级与脑白质病变各评分均呈正相关(r=0.327,0.311,0.401,0.362,P<0.05)。结论 年龄>60岁是缺血性脑卒中患者发生脑微出血及脑白质病变的危险因素; 在缺血性脑卒中患者中脑微出血与脑白质病变呈正相关