Volume of White Matter Hyperintensities,and Cerebral Micro-Bleeds

PurposeIn the past years the significance of white matter hyperintensities (WMH) has gained raising attention because it is considered a marker of severity of different pathologies. Another condition that in the last years has been assessed in the neuroradiology field is cerebral microbleeds (CMB). The purpose of this work was to evaluate the association between the volume of WMH and the presence and characteristics of CMB.Material and methodsSixty-five consecutive (males 45; median age 70) subjects were retrospectively analyzed with a 1.5 Tesla scanner. WMH volume was quantified with a semi-automated procedure considering the FLAIR MR sequences whereas the CMB were studied with the SWI technique and CMBs were classified as absent (grade 1), mild (grade 2; total number of CMBs: 1–2), moderate (grade 3; total number of CMBs: 3–10), and severe (grade 4; total number of CMBs: >10). Moreover, overall number of CMBs and the maximum diameter were registered.ResultsPrevalence of CMBs was 30.76% whereas WMH 81.5%. Mann–Whitney test showed a statistically significant difference in WMH volume between subjects with and without CMBs (p < 0.001). Pearson analysis showed significant correlation between CMB grade, number and maximum diameter and WMH. The better ROC area under the curve (Az) was obtained by the hemisphere volume with a 0.828 (95% CI from 0.752 to 0,888; SD = 0.0427; p value = 0.001). The only parameters that showed a statistically significant association in the logistic regression analysis were Hemisphere volume of WMH (p = 0.001) and Cholesterol LDL (p = 0.0292).ConclusionIn conclusion, the results of this study suggest the presence of a significant correlation between CMBs and volume of WMH. No differences were found between the different vascular territories.     

脑大动脉病变与脑白质高信号的相关性研究进展

脑大、小血管共同构成了脑的血管树,它们在结构和功能上有一定的相关性。近年来,脑 大血管病变与脑小血管病之间相关关系的研究逐渐受到重视。大动脉粥样硬化、动脉延长扩张及管 壁僵硬度增大从不同侧面反映了大血管病变的特点,脑白质高信号是脑小血管病重要的影像学表现。 本文对动脉粥样硬化、动脉延长扩张及僵硬度增大与脑白质高信号之间的相关性进行综述,以探讨 脑大血管病变与脑小血管病的关系。     

脑小血管病脑白质损伤动物模型

脑小血管病是导致认知功能减退、步态情感障碍和痴呆的重要脑血管疾病,脑白质弥漫 性损伤是该病的重要影像学特征。结合国内外近年来相关研究内容,本文对不同的脑小血管病白质 损伤动物模型制作进行了系统性回顾,包括单一型动物模型如双侧颈总动脉狭窄模型、脑淀粉样血 管病模型、Notch3 转基因小鼠模型、自发性高血压大鼠模型、易卒中型肾血管性高血压大鼠模型,以 及由两个或两个以上单一型动物模型组合而成的复合型动物模型等。     

脑小血管病变和抑郁的关系

脑小血管病变是指一组累及脑部小动脉、细动脉和静脉以及毛细血管病变的总称,影像学特点主要包括脑白质病变、腔隙性脑梗死和微出血。脑小血管病变与抑郁的发病及预后相关,其主要的作用机制为小血管病变破坏了皮质-纹状体-苍白球-丘脑皮质环路。本文针对脑小血管病变与抑郁的关系这一热点问题,分别从脑白质病变、腔隙性脑梗死及微出血与抑郁的关系方面对其进行阐述。     

脑小血管病

目的探讨伴皮质下梗死和白质脑病的常染色体显性遗传性脑动脉病(cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy,CADASIL)患者脑微出血(cerebral microbleeds,CMBs)的分布特征及临床意义。方法回顾性纳入2017年6月-2019年12月北京协和医院基因确诊的连续CADASIL患者21例(CADASIL组),以及性别匹配的高血压动脉硬化性脑小血管病患者21例(高血压脑小血管病组)。所有患者均行头MRI检查(含T2^*/SWI序列),盲法读片并记录CMBs的数量和部位,分析两组CMBs分布的差异。结果CADASIL组年龄和常见血管病危险因素比例均低于高血压脑小血管病组。CADASIL组47.6%患者检出CMBs(共计115个),而高血压脑小血管病组高达95.2%(共计218个)。CADASIL组CMBs分布以丘脑最常受累(45.2%),其次是脑叶(皮层/皮层下,35.7%)、基底节(11.3%)。高血压脑小血管病组则以丘脑以外的基底节CMBs最多见(35.3%),其次是脑叶(26.6%)、丘脑(19.2%)、脑干(16.1%)。CADASIL患者丘脑CMBs/总CMBs比例、丘脑CMBs/(基底节CMBs+脑干CMBs)比例均高于高血压脑小血管病组(均P<0.001)。结论CADASIL患者CMBs分布以丘脑最常见,其次是皮层/皮层下区域,而高血压脑小血管病患者则以丘脑以外的基底节、脑干更常见。     

脑小血管病的新进展

脑小血管病（small vessel disease，SVD）越来越受到广大神经科学研究者的重视，在今年的国际卒中会议和欧洲卒中会议上都提出了“小血管病引起大问题”的论点。SVD的影像学表现包括腔隙性梗死、脑白质疏松和微出血。Hachinski教授指出，痴呆足疾病分子生物学的一种终末状态，是经过20年的分子生物学改变，从轻度认知障碍到严重认知障碍，     

脑小血管病与颅内大动脉病变关系的研究进展

脑大、小血管在结构和功能上密切相关。越来越多的证据表明脑小血管病常与颅内大动 脉病变共存,严重程度具有一定相关性。颅内大动脉粥样硬化、颅内动脉延长扩张和颅内动脉僵硬 度增加分别反映了颅内大血管的结构和功能改变。本文就脑小血管病与不同颅内大动脉病理变化之 间共存及互相影响的研究现状进行综述,以探讨脑大、小血管病的关系。     

血脑屏障与脑小血管病

脑小血管病是指主要累及直径400μm以下的脑微小动脉血管病,临床表现为无症状性脑梗死,各种腔隙综合征和血管性认知功能障碍,影像学表现为腔隙性脑梗死灶,脑白质缺血性损害,微出血及血管间隙扩大的多种病因性疾病。血脑屏障渗透性的改变与脑小血管病之间有着重要的关系,即血管内皮及相关结构功能障碍导致血脑屏障渗透性增加,造成血液成分漏出到血管周围组织和脑实质内,继发相应的病理生理改变,导致脑小血管病相关的影像学和病理变化。     

血尿酸与脑小血管病患者血管性轻度认知障碍的相关性研究

目的 探讨血尿酸（uric acid,UA）与脑小血管病（cerebral small vessel disease,CSVD）患者血管性轻度 认知障碍（vascular mild cognitive impairment,VaMCI）的相关性。 方法 选择2015年10月-2017年6月于潍坊医学院附属医院就诊的87例CSVD患者和44例体检者,根据 蒙特利尔评估表（montreal cognitive assessment,MoCA）将CSVD患者分为VaMCI组47例和认知正常组40 例,用Logistic回归分析及Pearson相关分析来分析尿酸与脑小血管病患者轻度认知障碍的相关性。 结果 CSVD认知正常组及轻度认知障碍组血UA水平（[ 315.15±56.76）μmol/L,（363.32±42.58） μmol/L]高于对照组（[ 269.66±40.21）μmol/L]（均P<0.001）,且CSVD轻度认知障碍组血尿酸水平 高于认知正常组（P <0.001）。轻度认知损害组UA水平与其MoCA总分、视空间与执行能力、记忆、语 言呈负相关（r =-0.351,P =0.015;r =-0.456,P =0.001;r =-0.408,P =0.004;r =-0.329,P =0.024）。 Logistic回归分析结果显示,血UA水平[比值比（odds ratio,OR）1.020,95%可信区间（confidence interval, CI）1.009～1.032,P =0.01]是CSVD患者轻度认知障碍的独立危险因素。 结论 CSVD血管性轻度认知障碍患者血UA升高,且血UA是CSVD患者轻度认知障碍的危险因素。UA 水平与CSVD血管性轻度认知障碍患者蒙特利尔评估总分、视空间与执行能力、记忆、语言呈负相关。     

Cerebral Small Vessel Diseases and Sleep Related Strokes

Background and Purpose: Sleep related Stroke (SRS) is common and has been associated with cerebral small vessel diseases (SVD) in ischemic strokes (ISs). We tested the hypothesis that SRS is associated with SVD in both ischemic and hemorrhagic stroke. Methods: Prospectively collected data from patients consecutively enrolled after intracerebral hemorrhage (ICH) related to SVD or after IS were analyzed. Symptom onset was recorded as SRS versus awake. Each ICH was grouped according to lobar and deep locations. The IS cohort was etiologically characterized based on the Causative Classification of Stroke system. Frequencies of SRS within and between ICH and IS cohorts as well as its associations (etiology, risk factors) were analyzed. Results: We analyzed 1812 IS (mean age 67.9 years ± 15.9 years, 46.4% female) and 1038 ICH patients (mean age 72.5 years ± 13.0 years, 45.4% female). SRS was significantly more common among SVD-related ICH patients (n = 276, 26.6%) when compared to all IS (n = 363, 20.0%, P < .001) and in both, small artery occlusion (SAO) related IS and lobar ICH within the respective IS and ICH cohorts (16.3% SRS versus 9.1% awake for SAO within all IS, P < .001; and 57.1% SRS versus 47.7% awake for lobar bleeds within all ICH, P = .008). These associations remained significant after controlling for age, sex and risk factors. Conclusions: SRS was associated with SVD. The SAO etiology and cerebral amyloid angiopathy related lobar ICH suggest that the presence of SVD can interact with sleep or arousal related hemodynamic changes to cause ischemic and hemorrhagic stroke.     

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。     

Prestroke Statins,Progression of White Matter Hyperintensities,and Cognitive Decline in Stroke Patients with Confluent White Matter Hyperintensities

Cerebral white matter hyperintensities (WMH) are a consequence of cerebral small vessel disease. Statins have been shown to reduce recurrent stroke among patients with various stroke subtypes, including lacunar stroke, which also arises from small vessel disease. In this study, we investigated the hypothesis that prestroke statin use would reduce the progression of WMH and/or cognitive decline among stroke patients with confluent WMH. Patients (n = 100) were participants of the VITAmins To Prevent Stroke magnetic resonance imaging substudy. All patients had confluent WMH on magnetic resonance imaging at baseline. Eighty-one patients completed the 2-year follow-up. We assessed general cognition and executive function using the mini-mental state examination and Mattis dementia rating scale–initiation/perseveration subscale, respectively. We compared the change in volume of WMH and cognition between prestroke statin use and prestroke nonstatin use groups. We also evaluated the effects of prestroke statin use on incident lacunes and microbleeds. The prestroke statin use group (n = 51) had less WMH volume progression (1.54 ± 4.52 cm³vs 5.01 ± 6.00 cm³, p = 0.02) compared with the prestroke nonstatin use group (n = 30). Multivariate linear regression modeling identified prestroke statin use as an independent predictor of WMH progression (β = –0.31, p = 0.008). Prestroke statin use was also associated with less decline (Mattis dementia rating scale–initiation/perseveration subscale; β = 0.47, p = 0.001). No association was observed with changes in mini-mental state examination scores. There were no between group differences on incident lacunes or incident microbleeds. Prestroke statin use may reduce WMH progression and decline in executive function in stroke patients with confluent WMH.

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