急性脑梗死患者脑微出血的相关危险因素分析

目的 探讨急性脑梗死（ACI）患者脑微出血（CMB）的相关危险因素,为CMB的预防提供参考.方法 取本院自2011年以来入院的ACI患者84例,均进行MRI磁敏感加权成像（SWI）检查,根据患者有无CMB分为CMB组52例和无CMB组32例.分析2组患者的一般资料及相关临床指标,得出ACI合并CMB的危险因素.结果 CMB组患者年龄显著大于无CMB组,CMB组患者有高血压史、脑卒中史和吸烟史比例显著高于无CMB组;CMB组血HDL水平显著高于无CMB组,血LDL水平显著低于无CMB组,差异均具有统计学意义（P＜0.05）.结论 在ACI患者中,CMB的发生与否与患者年龄、高血压史、脑卒中史和吸烟史以及血HDL、LDL水平直接关联,这对往后临床预测ACI患者发生CMB具有一定的借鉴意义.     

脑淀粉样变血管病在癫痫中的研究进展

脑淀粉样血管病（Cerebral amyloid angiopathy,CAA）是年龄依赖性疾病,主要影响老年患者,其特征为脑叶出血、脑微出血、非创伤性蛛网膜下腔出血和皮质表面铁沉着症,是一组异质性较高的疾病,老年人自发性颅内出血的主要原因,如患者出现痴呆、精神症状、反复或多发性脑叶出血应考虑CAA的可能性。癫痫可能是这种疾病的后遗症之一,文献研究发现CAA患者的癫痫发作可能与CAA一种独特的亚型即CAA相关性炎症（CAA-related inflammation,CAA-ri）有关,这是一种炎症形式,是散发性CAA少见的临床表现。CAA-ri是中枢神经系统血管炎的一种特殊类型,CAA患者有时候出现一些不典型的临床表现,即其临床表现无特异性,比如头痛、癫痫、行为改变、局灶性神经体征、意识受损合并不对称T2加权磁共振成像高信号病变等,临床医生就得考虑是CAA-ri。虽然CAA-ri较为少见,但是及时诊断很重要,因为一旦出现癫痫发作,表面CAA患者的炎症可能已经到了一个很严重的地步,因此及时识别和加以处理尤为重要,文献表明,大多对免疫抑制剂反应良好。由于其少见性,目前对CAA中癫痫发生的研...     

脑淀粉样血管病研究现状

<正>脑淀粉样血管病(cerebral amyloid angiopathy,CAA)是由淀粉样蛋白沉积在脑皮质、皮质下及软脑膜动脉的一种常见于老年人的脑小血管病,主要累及中小动脉,很少累及静脉,临床上以反复性多发性脑叶出血、认知功能减退等为主要表现~([1])。β淀粉样蛋白(Aβ)在脑血管壁上过量沉积是其主要发病机制。CAA已成为老年人自发性脑出血的常见病因之一,CAA相关性脑出血至少约占自发性脑出血的20%~([2])。     

血浆同型半胱氨酸与不同类型脑小血管病相关性分析

目的：分析血同型半胱氨酸（Hcy）与不同类型脑小血管病的相关性。方法纳入脑小血管病患者123例（病例组）,其中单纯脑白质疏松症（LA）39例,腔隙性梗死（LI）35例,脑微出血（CMB）16例,脑白质疏松并腔隙性梗死和（或）脑微出血33例,40例健康者为对照组。对2组患者均进行Hcy检测。结果LA、LI、CMB及脑白质疏松并腔隙性梗死和（或）脑微出血组血浆同型半胱氨酸均高于对照组（P＜0.05）,脑白质疏松并腔隙性梗死和（或）脑微出血组血浆同型半胱氨酸明显高于其他3组脑小血管病组（P＜0.05）,LA、LI及CMB血浆同型半胱氨酸无明显差异。结论Hcy与脑小血管病（SVB）的病情严重程度具有密切关系。     

脑淀粉样血管病的影像学标志物及临床相关性研究进展

脑淀粉样血管病（cerebral amyloid angiopathy,CAA）是一种多见于老年人群中的脑小血管病, 不同于高血压导致的脑小血管病易累及脑深部区域,CAA多累及皮层及软脑膜小血管。多发脑叶微出 血是CAA患者常见的影像学表现,研究认为其与症状性脑叶出血及进行性认知功能下降相关。随着 近年来对脑小血管病影像学表现的深入研究,发现皮层蛛网膜下腔出血与皮层表面含铁血黄素沉 积是CAA相对特异的影像学表现,并且与短暂性局灶性神经系统症状发作相关。此外,脑白质高信号、 小梗死灶等脑小血管病影像学标志均在CAA患者中出现,提示除外临床较关注的出血性改变,CAA患 者的缺血性损伤也是导致临床症状的重要因素。     

中老年高血压患者血压昼夜节律波动类型对脑微出血的影响

目的 探讨中老年高血压患者血压昼夜节律波动类型与脑微出血(CMB)的关系.方法 选取有高血压病的中老年患者,通过24 h动态血压仪监测血压及颅脑磁敏感加权成像(SWI)序列检测脑微出血,对年龄分组后,比较脑微出血患者的危险因素,并通过Logistic回归分析不同血压昼夜节律波动类型和CMB、CMB发生位置的关系.结果 ...     

脑微出血与脑卒中相关性的临床研究

目的通过核磁共振T2*加权梯度回波成像(MRI GRE-T2*WI)筛查脑微出血(CMB),探讨CMB与卒中发生、发展之间的关系,及其与卒中危险因素之间的联系。方法纳入脑血管病患者140例,其中腔隙性脑梗死组58例、脑梗死组42例,脑出血组40例;另收集同期30例住院或门诊非血管病患者作为对照组。登记所有患者血压、血脂、血糖、既往史等基线资料,行MRI GRE-T2*WI扫描,记录各组脑微出血发生例数、部位、数目,进行统计分析。结果所有170例患者中,CMB患者的血压、血脂、血糖等较无CMB患者高,症状明显,对比明确(P均<0.05);各脑卒中组的CMB发生率均明显高于对照组(P均<0.05);各脑卒中组CMB分级构成不同(P<0.05),脑出血组CMB重度发生率明显高于其它各组;有CMB的各脑卒中组CMB总体均数比较,自发性脑出血组>腔隙性脑梗死组>脑梗死组。结论高血压病、糖尿病、高脂血症是影响CMB发生的显著因素;CMB作为微出血病变,在预测脑出血病变方面具有一定意义,可通过对CMB的诊断了解脑部出血的部位等基本信息,为以后的治疗带来方便;MRI GRE-T2*WI扫描的诊断方法为脑出血病变的常规诊断方法,此种方法在诊断脑出血病变准确度高,优势明显,因此,对于临床的诊断治疗具有显著的价值,可推广。     

增龄相关性脑小血管病谱系的病理基础及其影像学特点

增龄相关性脑小血管病谱系（spectrum o f a ge-related cerebral small vessel diseases， ArCSVDS）是指随着年龄的增长，脑小动脉、微动脉、毛细血管、微静脉、小静脉出现老化的一组脑 小血管病（cerebral small vessel disease，CSVD），包括深穿支动脉病（deep perforating arteriopathy，DPA） 和β淀粉样蛋白（β-amyloid，Aβ）有关的脑淀粉样血管病（cerebral amyloid angiopathy，CAA）。以往的 研究往往将这两种疾病视为独立的实体，然而最近的研究发现，无论从年龄、高血压等相似的脑血 管病危险因素，还是从潜在的相互作用角度出发，DPA与CAA是一组ArCSVDS疾病，血脑屏障（blood brain barrier，BBB）破坏、内皮细胞损伤、血管周围Aβ是连接DPA与CAA的共同发病机制，而且有 30%～68%的患者两者可以重叠发病。     

增龄相关性脑小血管病治疗新进展

随着全球预期寿命的延长,增龄相关性脑小血管病（cerebral small vessel disease,CSVD）患 病率不断增加。最近研究显示,深穿支动脉病（deep perforating arteriopathy,DPA）和脑淀粉样血管病 （cerebral amyloid angiopathy,CAA）均属于增龄相关性脑小血管病谱系（spectrum of age-related cerebral small vessel diseases）疾病,两者存在重叠性,且相互作用。增龄相关性CSVD治疗包括特异性及非特 异性治疗。非特异性治疗包括控制血管危险因素、抗血小板治疗及静脉溶栓等。特异性治疗方面,最 近研究提示抗炎治疗对增龄相关性CSVD或许有效;而针对CAA相关性炎症,已显示其对类固醇和（或） 环磷酰胺有良好的反应。随着对增龄相关性CSVD发病机制的进一步了解,未来可能会出现更多特异 性的治疗方法。     

急性缺血性卒中患者脑微出血相关因素分析

【摘要】
目的 探讨急性缺血性卒中患者合并脑微出血（cerebral microbleeds,CMB）的情况及其相关因素。
方法 本研究采用单中心、前瞻性研究方法,连续收集2011年1月～2012年6月于北京市第六医院神经内科住院的急性缺血性卒中患者302例,根据有无CMB将患者分为有CMB组（83例）和无CMB组（219例）,比较两组间一般临床资料、生化指标及影像学特点是否存在差异,并采用多因素逐步Logistic回归模型分析CMB发生的独立危险因素。
结果 302例患者中,合并有CMB者83例（27.5%）,其中年龄（t=3.67,P<0.001）、高血压（χ2=4.76,P=0.03）、卒中史（χ2=5.46,P=0.02）、纤维蛋白原（t=2.33,P=0.02）、腔隙性脑梗死数目（Z=-5.04,P<0.001）以及脑白质疏松程度评分（Z=-7.88,P<0.001）两组间比较差异具有显著性。Logistic回归分析显示,纤维蛋白原［比值比（odds ratio,OR）1.469,95%可信区间（confidence interval,CI）1.366～1.602;P=0.037］、腔隙性脑梗死数目（OR 1.636,95%CI 1.200～2.231;P=0.002）以及脑白质疏松程度评分（OR 1.700,95%CI 1.502～1.980;P<0.001）是急性缺血性卒中患者CMB发生的独立危险因素。
结论 CMB的发生与纤维蛋白原含量、腔隙性脑梗死数目以及脑白质疏松程度相关。     

Microbleeds in hereditary cerebral hemorrhage with amyloidosis-Dutch type

In a hereditary variant of cerebral amyloid angiopathy (CAA), cerebral hemorrhage with amyloidosis-Dutch type, supratentorial microbleeds were found to occur independently of the presence of hypertension, whereas hypertension probably contributed to the development of cerebellar microbleeds. This predictable hereditary variant of CAA may be a useful model to study microbleeds in relation to CAA.     

Cerebral amyloid angiopathy in the elderly

Cerebral amyloid angiopathy (CAA) results from deposition of β‐amyloid in the media and adventitia of small arteries and capillaries of the leptomeninges and cerebral cortex and is a major cause of lobar intracerebral hemorrhage and cognitive impairment in the elderly. CAA is associated with a high prevalence of magnetic resonance imaging markers of small vessel disease, including cerebral microbleeds and white matter hyperintensities. Although advanced CAA is present in approximately ¼ of brains with Alzheimer disease (AD), fewer than half of CAA cases meet pathologic criteria for AD. This review will discuss the pathophysiology of CAA and focus on new imaging modalities and laboratory biomarkers that may aid in the clinical diagnosis of individuals with the disease. Ann Neurol 2011;70:871–880     

Clinical and radiological differences between patients with probable cerebral amyloid angiopathy and mixed cerebral microbleeds

Journal of Neurology - The key imaging features of cerebral amyloid angiopathy (CAA) are lobar, cortical, or cortico-subcortical microbleeds, macrohaemorrhages and cortical superficial siderosis...     

Spatial relation between microbleeds and amyloid deposits in amyloid angiopathy

Advanced cerebrovascular β‐amyloid deposition (cerebral amyloid angiopathy, CAA) is associated with cerebral microbleeds, but the precise relationship between CAA burden and microbleeds is undefined. We used T2*‐weighted magnetic resonance imaging (MRI) and noninvasive amyloid imaging with Pittsburgh Compound B (PiB) to analyze the spatial relationship between CAA and microbleeds. On coregistered positron emission tomography (PET) and MRI images, PiB retention was increased at microbleed sites compared to simulated control lesions (p = 0.002) and declined with increasing distance from the microbleed (p < 0.0001). These findings indicate that microbleeds occur preferentially in local regions of concentrated amyloid and support therapeutic strategies aimed at reducing vascular amyloid deposition. Ann Neurol 2010     

Treatment and prevention of primary intracerebral hemorrhage

Intracerebral hemorrhage (ICH), which constitutes 10 to 15% of all strokes and affects approximately 65,000 people each year in the United States, has the highest mortality rate of all stroke subtypes. Hypertension, cerebral amyloid angiopathy, and anticoagulation underlie the majority of cases of ICH. Warfarin not only increases the risk but also increases the severity of ICH by causing hematoma expansion. With the advent of gradient-echo magnetic resonance imaging, patients with underlying cerebral amyloid angiopathy or hypertensive vasculopathy can be identified, and measures can be taken to prevent ICH. Initiating an antihypertensive regimen in a patient with nonlobar microbleeds suggestive of hypertensive vasculopathy, and withholding warfarin in patients with lobar microbleeds suggestive of cerebral amyloid angiopathy, are emerging prevention strategies. Although a treatment for cerebral amyloid angiopathy does not exist, agents targeting beta-amyloid metabolism and bioactivity are promising candidates. Strategies for preventing warfarin-associated hemorrhage include strict monitoring of anticoagulation levels and using agents such as direct thrombin inhibitors. The future of ICH management lies in therapies targeted at the pathophysiological steps in ICH. Potential treatments include glutamate receptor antagonists for preventing glutamate excitotoxicity, matrix metalloproteinase and thrombin inhibitors for preventing perihematomal edema, and recombinant activated factor VII for preventing hematomal expansion.     

Small Cortical Infarcts Transformed to Lobar Cerebral Microbleeds: A Case Series

Cerebral microbleeds (MBs) have been often observed due to the development of imaging devices, and are classified to deep and lobar MBs. Lobar MBs are strongly associated with cerebral amyloid angiopathy. Here, we report 3 cases of lobar MBs that developed after small cortical ischemic stroke. One case underwent carotid artery stenting for severe carotid stenosis, one was diagnosed with artery-to-artery embolism, and the other was embolic stroke of undetermined source. New small cortical infarctions were detected with diffusion-weighted magnetic resonance imaging (MRI). Initial MRI revealed no hemorrhage around the ischemic lesion on T2*-weighted gradient-recalled echo or susceptibility-weighted imaging (SWI) at the onset of stroke. Follow-up SWI after 12-20 months revealed lobar MBs in the previously detected ischemic lesions, and high-intensity lesions remained around the MBs on fluid-attenuated inversion recovery imaging. These cases revealed that cerebral MBs developed through the transformation of small cortical infarctions. All cases showed lobar MBs, and these MBs existed in the previously detected ischemic lesions at a chronic stage. Lobar MBs present around ischemic lesions may predict embolic infarcts.     

Cerebral amyloid angiopathy: An overview

Cerebral amyloid angiopathy (CAA) is characterized by amyloid deposition in cortical and leptomeningeal vessels. Several cerebrovascular amyloid proteins (amyloid β‐protein (Aβ), cystatin C (ACys), prion protein (AScr), transthyretin (ATTR), gelsolin (AGel), and ABri (or A‐WD)) have been identified, leading to the classification of several types of CAA. Sporadic CAA of Aβ type is commonly found in elderly individuals and patients with Alzheimer’s disease. Cerebral amyloid angiopathy is an important cause of cerebrovascular disorders including lobar cerebral hemorrhage, leukoencephalopathy, and small cortical hemorrhage and infarction. We review the clinicopathological and molecular aspects of CAA and discuss the pathogenesis of CAA with future perspectives.     

磁共振指导下脑微出血的精准诊疗

脑微出血（cerebral microbleeds,CMBs）作为脑小血管病的一种,与各种血管危险因素密切 相关,其中脑叶CMBs还与淀粉样脑血管病相关。CMBs不仅提高了复发症状性脑出血的风险,还可能引 起认知障碍甚至痴呆。本文主要就CMBs在磁共振磁敏感序列的影像特点和诊断标准等方面进行综 述,通过神经影像学检查方法提高CMBs诊断的准确率,为CMBs的精准诊断和治疗提供重要依据。     

Cerebral amyloid angiopathy presenting as a mass lesion

A rare clinical presentation of cerebral amyloid angiopathy is reported. Our patient presented with the clinical and radiological signs of a right frontal mass lesion suggesting a brain tumor, and a biopsy provided the diagnosis of cerebral amyloid angiopathy. A brief review of the pathology and clinical features of cerebral amyloid angiopathy is presented.