脑小血管病研究进展

<正>脑小血管病(cerebral small vessel disease,SVD)是在多种病因共同作用下引起颅内小血管病变,从而损伤脑深部灰质和脑白质,最终出现一系列病理学、神经影像学改变以及认知功能障碍的临床综合征[1]。颅内小血管主要包括脑小动脉、微动脉、毛细血管和小静脉,这些小血管对大脑最活跃的神经元代谢和脑网络复杂功能的维持必不可少[2]。小血管病变主要引起皮质下主要结构的病变,神经影像学可表现为深部脑梗     

脑小血管病及其病理改变

<正>脑动脉粥样硬化(atherosclerosis,AS)、脑小血管病(cerebral snmall-vessel disease,SVD)以及脑淀粉样血管病(cerebral amyloid angiopathy,CAA)是老年人脑中最常见的动脉血管异常性病变。影像学上脑白质的低信号、腔隙性脑梗死(1acunar in-farct,LI)和脑微出血(cerebral microbleed,CMB)改变,常提示存在SVD,是老年人常见的影像学改变。在病理学上,脑AS与SVD有相似的发病机制,如血浆蛋白从血管内渗出,吞噬脂质类的吞噬细胞在管壁聚集,血管纤维化等。此外,SVD由于损伤血管壁,而导致溢出的血浆蛋白进入脑室周围间     

阿尔茨海默病发病机制中的血管性病理因素

全球所有种族人群中脑血管性疾病是一种常见疾病，它是导致发病和死亡的一个主要原因，对老年人更是如此。脑血管的病理改变可以导致中风和痴呆。然而，它们大脑供血的主要血管和脑组织内血管的病理改变并不一样，一种病理改变是动脉粥样硬化，有的主要发生在颅外血管，如基底和颈内动脉，有的可能发生在血管末端引起广泛的脑供血不足导致脑缺氧，或在大脑前、中、后动脉导致局部缺血性改变，有时甚至引起明显的脑梗死。这种血管病变一方面可以导致急性脑死亡，另一方面也是更常见的是引起中风和瘫痪。然而，单次脑梗死发生或多次脑梗死发生导致痴呆并非罕见。血管性痴呆（vascular dementia），是一种单一因素类型痴呆，与它最相关的是“小血管病”，这种小血管病由于持续升高的血压引起小血管壁的增厚和管腔的狭窄（动脉硬化）导致脑内血管受损，并且引起脑缺血／缺氧。这种病变能影响多个脑皮质区，特别是脑白质，并且引起基底节多个微梗塞灶或微出血灶，多个脑组织丢失病灶积累增多，最后导致脑功能的丢失，即所描述的血管性痴呆。[第一段]     

脑小血管病引起的认知障碍磁共振波谱和弥散张量成像

脑小血管病(cerebral small vessel disease,SVD)的临床症状主要表现为认知障碍,病理学改变则表现为白质疏松和(或)腔隙性梗死.然而,目前尚不清楚SVD引起的认知障碍是否与白质损害程度相关.磁共振波谱分析能无创件榆测活体脑组织的代谢产物浓度,直接反映脑代谢;弥散张量成像是特异性观察脑白质的无创性新技术,通过平均弥散、各向异性等不同参数来定量评价脑白质的细微结构异常.磁共振波谱分析与弥散张量成像联合应用能更敏感地显示白质损害程度,为SVD引起的认知障碍提供研究工具.     

脑小血管病与抑郁

脑小血管病是导致老年人抑郁的主要原因之一,诊断主要依靠MRI,其影像学特征包括近期皮质下小梗死、假 定血管源性腔隙、假定血管源性脑白质高信号、血管周围间隙、脑微出血和脑萎缩。文章就近年来脑小血管病的不同 影像学特征与抑郁之间关系的进行综述,以期为临床早期发现高危人群的抑郁提供帮助。     

脑小血管病患者认知损害的机制和筛查

脑小血管病是指主要累及颅内小动脉和微动脉的一组疾病.脑小血管病在MRI上的主要特征性改变为弥漫性白质高信号、腔隙性梗死、微出血和血管周围间隙扩大,这些改变可能与认知损害存在相关性.目前,已有多种量表可用于脑小血管病所致认知损害的评价.     

脑小血管病的研究进展

正脑小血管病(cerebral small vessel disease,CSVD)是一类多种病因导致脑小动脉、小静脉及毛细血管受累的病理过程,所造成的脑实质损害主要位于皮质下结构,包括腔隙性脑梗死(lacunar infarctions,LI)、脑白质损害、脑微出血(cerebral microbleeds,CMB)等。CSVD与脑卒中、痴呆、老年关系密切,其重要性不亚于动脉粥样硬化性血栓形成。因此,     

血管性认知功能损害研究值得重视的问题

血管性认知功能损害(VCI)是指由血管因素导致或与之伴随的认知功能损害,除卒中外,血管性脑的损害及高血压、糖尿病、冠心病等血管性危险因素也是重要原因。VCI是异质性的临床状态,涵盖了从轻微认知损害到血管性痴呆的各种表现,皮质下缺血性小血管病是其中最常见的类型,以执行功能受损和伴发淡漠、抑郁障碍为特征。对VCI的诊断主要依据临床表现并参考各自不同的表现类型。应按照临床证据和指南要求规范进行治疗干预。     

脑小血管病与血管性认知损害:关注神经影像学

脑小血管病(cerebral small vessel disease,CSVD)是老年人群功能丧失、残疾和认知损害的重要原因,皮质下CSVD可导致腔隙性梗死和进展性脑白质损害.CSVD性认知功能障碍是血管性认知损害(vascular cognitive impairment,VCI)的重要亚型,其所致的痴呆约占血管性痴呆的36%~67%.随着技术的发展,神经影像学及其相关标志物已成为诊断CSVD及认知损害的有力手段,在脑认知学相关领域内也可探寻到CSVD发病机制的线索.神经影像学血管性改变报道标准(STandards for ReportIng Vascular changes on nEuroimaging,STRIVE)确立了代表CSVD的6种关键性损伤的神经影像学标志物,包括近期皮质下小梗死、假定血管源性的腔隙灶、假定血管源性的白质高信号、血管周围间隙、脑微出血和脑萎缩.文章对CSVD所致VCI与影像学特征的相关性进行综述.     

脑小血管病与脑血流储备

脑小血管病是指脑内小血管病变及其导致的脑组织改变.脑血流储备功能发生的血管和脑小血管病的病变血管处于相同节段,因此可利用脑血流储备检测评价脑小血管病的血管病变.     

脑小血管疾病动物模型

脑小血管疾病是直径30～300 μm的大脑皮质/穿髓小动脉的病变,可导致血管性痴呆进而影响患者的生活质量.目前的热点集中在探讨其发病机制方面.文章对脑小血管疾病目前的常用动物模型进行了综述,旨在为其基础研究提供参考.     

Hypersignaux de la substance blanche chez la personne âgée : physiopathologie,troubles cognitifs associés et pistes de prévention

White matter hyperintensities (WMH), also known as leukoaraïosis are very common neuroradiological manifestations in the elderly. The main risk factors for WMH are age and high blood pressure. The vascular origin of these lesions is classically accepted and WMH are considered as one feature of the small vessel disease. WMH may be associated with clinical symptoms, depending notably on their importance according to age. They are associated with increased mortality, strokes and changes in cognition with a higher risk of dementia (vascular dementia or Alzheimer's disease). Modification of vascular risk factors could have a beneficial effect, but few evidences from controlled trials are available.     

Vascular dementia: Different forms of vessel disorders contribute to the development of dementia in the elderly brain

The diagnosis of vascular dementia (VaD) describes a group of various vessel disorders with different types of vascular lesions that finally contribute to the development of dementia. Most common forms of VaD in the elderly brain are subcortical vascular encephalopathy, strategic infarct dementia, and the multi infarct encephalopathy. Hereditary forms of VaD are rare. Most common is the cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Sporadic forms of VaD are caused by degenerative vessel disorders such as atherosclerosis, small vessel disease (SVD) including small vessel arteriosclerosis, arteriolosclerosis, and lipohyalinosis, and cerebral amyloid angiopathy (CAA). Less frequently inflammatory vessel disorders and tumor-associated vessel lesions (e.g. angiocentric T-cell or angiotropic large cell lymphoma) can cause symptoms of dementia. Here, we review and discuss the impact of vessel disorders to distinct vascular brain tissue lesions and to the development of dementia in elderly individuals. The impact of coexisting neurodegenerative pathology in the elderly brain to VaD as well as the correlation between SVD and CAA expansion in the brain parenchyma with that of Alzheimer's disease (AD)-related pathology is highlighted. We conclude that “pure” VaD is rare and most frequently caused by infarctions. However, there is a significant contribution of vascular lesions and vessel pathology to the development of dementia that may go beyond tissue damage due to vascular lesions. Insufficient blood blow and alterations of the perivascular drainage mechanisms of the brain may also lead to a reduced protein clearance from extracellular space and subsequent increase of proteins in the brain parenchyma, such as the amyloid β-protein, and foster, thereby, the development of AD-related neurodegeneration. As such, it seems to be important for clinical practice to consider treatment of potentially coexisting AD pathology in cognitively impaired patients with vascular lesions.     

From hemobiology to vascular disease: A review of the potential of gliclazide to influence the pathogenesis of diabetic vascular disease

Patients with type II diabetes commonly die from thrombotic vascular disease. Large vessel occlusion due to thrombosis or atherosclerotic stenosis is a process accelerated by diabetes and results in premature death. Diabetic small vessel disease, with its unique microangiopathic process, underlies many of the large vessel changes as well as causing retinopathy and nephropathy. The microangiopathic changes produce a prothrombotic tendency that has been widely reported in type II diabetes. There is reduced endothelial cell production of prostacyclin and the activators of fibrinolysis, together with increased platelet reactivity. In addition, there is increased lipid peroxidation and oxidative stress due to excess free-radical activity and impaired antioxidant defenses particularly in the presence of microvascular disease. The development of many of these abnormalities is associated with poor long-term glycemic control. However, the changes are also seen in atherosclerosis in nondiabetic patients where the progression of the disease can be modified by antiplatelet agents and antioxidants. The process of vascular damage is accelerated by diabetes, often due to co-existing disease and aging, although it is now clear that improvement in long-term glycemic control by lowering blood glucose levels to near to the nondiabetic state reduces the development of small and large vessel disease. Although the biochemical mechanism underlying this observation remains uncertain, protein glycosylation and increased platelet reactivity are implicated and interrelated. Increased oxidative stress due to excess free-radical activity may be central to diabetic vascular disease as endothelial cell damage, lipoprotein oxidation, modification of both platelet reactivity and arachidonic acid cascade are all properties of free radicals and their reaction products lipid peroxides. All sulfonylureas are excellent hypoglycemic agents and improve long-term prognosis, but gliclazide has additional effects in modulating the prothrombotic tendency of diabetes as it has powerful free-radical scavenging properties. This unique effect associated with improvements in platelet reactivity and fibrinolysis is independent of glycemic control and may prevent vascular disease or slow its progression.     

老年人慢性肾功能不全与脑小血管病变

目的 探讨老年人慢性肾功能不全(CKD)与脑小血管病变(SVD)的关系.方法 老年CKD组152例和老年对照受试者158例,均为男性,记录人口学资料和血管危险因素,根据头颅MRI结果 半定量评估脑白质病变(WML)和计算腔隙性梗死数(LI). 结果 (1)与对照组比较,老年CKD组高血压(30.9%对19.0%)、糖尿病(23.7%对14.6%)患病率明显升高(X2值分别为5.91和4.19,P<0.05);(2)与对照组比较,老年CKD组WML2级(34.9%对24.1%)和3级(25.7%对16.5%)比率明显升高(X2=4.37和3.96,P<0.05);LI患病率明显升高,为45.4%对25.3%(X2=13.70,P<0.05);除外高血压和糖尿病对照组仍得到类似的结果 ;(3)多元Logistic回归分析显示,年龄、高血压和肾小球滤过率(GFR)与老年CKD患者SVD的发生密切关联(OR值分别为3.47、3.63和1.91). 结论 高血压和糖尿病町能是老年CKD的危险因素;老年CKD与脑SVD密切关联;年龄、高血压和GFR降低可能是老年CKD患者脑SVD的独立危险因素.     

ADMA/DDAH系统与脑白质疏松症的关系

脑白质疏松症(LA)是深部脑小血管病变(SVD)引起的弥漫性脑缺血,可导致脑白质区神经传导纤维脱髓鞘疾病,是脑损害的一个早期标志。一氧化氮(NO)是血管内皮舒张因子,由体内的一氧化氮合酶(NOS)催化产生。非对称性二甲基精氨酸(ADMA)是NOS的内源性竞争抑制物。ADMA增加使NO生成减少,导致血管内皮功能障碍。二甲基精氨酸二甲胺水解酶(DDAH)是内源性ADMA的主要代谢酶,是决定血浆ADMA浓度的关键因素。ADMA/DDAH通路可能通过血管内皮损伤机制影响LA。     

Vasculopathy and vasculitis in systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune connective tissue disease, where vascular lesions are one of the typical symptoms. The pathological process often involves skin vessels, renal glomeruli, the cardiovascular system, brain, lung alveoli, and gastrointestinal tract vessels. This review presents possible adverse mechanisms underlying the cause and effect relationship of various factors causing vascular lesions in SLE patients. The generally accepted hypothesis links vascular damage in SLE with the deposition of immune complexes in the vascular endothelium. The anti-endothelial cell antibodies (AECA), antiphospholipid antibodies and anti-double stranded DNA antibodies present in SLE, that directly or indirectly affect endothelial cells, causing inflammatory damage to the vessel wall, and their role, have been discussed. It has been stressed that although the suggested role of AECA in vasculitis pathogenesis has not been fully established, evidence, however, has demonstrated that AECA is a factor causing endothelial damage in SLE patients. On the other hand, issues concerning cellular adhesion molecules which enable leukocyte adhesion and rolling along the endothelial cell surface, and their extravascular migration, focus on the role they may be playing in SLE patients with vasculitis. A potential role of soluble forms of adhesion molecules, pentraxin 3, medications, infections in the pathogenesis of this disease has also been shown. Special attention has been given to the role of type 3 hepatitis virus in vascular damage in SLE.     

脑小血管病与认知功能障碍

脑小血管病是指颅内小动脉和做动脉病变引起脑的缺血或出血损害,是血管性认知功能障碍的重要亚型。其主要的影像学表现为腔隙性脑梗死、脑白质疏松和脑做出血。脑小血管病的临床分类主要包括腔隙综合征、Binswanger脑病、脑淀粉样血管病、伴有皮质下腑梗死和白质肭痫的常染色体显性遗传性脑动脉病、伴有皮质下脑梗死和白质脑病的常染色体隐性遗传性脑动脉病及其它较少见的小血管病。其临床表现则丰要为静灶腑血管病（静灶腔隙性脑梗化、脑微出血和部分白质疏松）、各类腔隙综合征和血管性认知功能障碍。     

小动脉硬化性脑小血管病与睡眠障碍

研究显示,脑小血管病可通过脑组织损害影响神经回路、局部脑血流量改变及神经内分泌改变等机制造成睡眠障碍,且脑小血管病所致的卒中后抑郁和脑萎缩均可能与睡眠障碍有关.反过来,睡眠障碍可损害血脑屏障和脑血管自动调节功能,增高脑小血管病的发病风险.两者相互联系,互为因果,共同影响患者预后和生存质量.