脑白质高信号与步态障碍的研究进展

脑白质高信号(WMH)是脑小血管病(CSVD)脑组织慢性低灌注的一个影像学表现,与新发小的皮质下梗死、腔隙性脑梗死、扩大的血管周围间隙、脑微出血和脑萎缩共同组成CSVD.目前国内大多聚焦于CSVD与认知及情感功能之间的研究,对CSVD所引起的步态障碍显得相对认识不足,而与WMH相关的步态障碍增加了CSVD患者的伤残率及病死率.本文就近年来国内外WMH与步态障碍之间的关联性、病理生理学机制、评价方法、干预措施等方面进行阐述,以期为将来临床诊断及其干预提供有益参考,从而提高老年人群的生活质量.     

脑小血管病的发病与诊治研究进展

随着经济快速发展人口老龄化加速,脑小血管病（CSVD）患者日益增多。CSVD是一种危害健康的常见慢性病,病因广泛,病机复杂,主要累及颅内小血管,可以引起一系列的临床症状、影像学改变,导致认知功能障碍和神经损伤,不仅降低了患者生活质量,还威胁到了患者生命健康,给老龄化社会带来严重危害。为了提高对CSVD的认识,本文主要对近年来CSVD病因、发病机制、临床表现、诊断及预防治疗方面进行综述,为临床医生及研究人员提供一些参考。     

脑小血管病与认知功能障碍

脑小血管病指脑小动脉及微动脉病变引起的脑缺血或出血性病变,它所导致的认知功能障碍是血管性认知功能障碍的重要亚型,临床表现包括腔隙综合征、认知功能障碍、步态障碍及情意障碍等.其影像学表现主要为腔隙性脑梗死、脑白质疏松、扩大的血管周围间隙及脑微出血等.     

维生素D水平与老年脑小血管病患者认知功能障碍的相关性研究

目的:分析老年脑小血管病（CSVD）患者的血清25-羟基维生素D［25（OH）D］水平与认知功能障碍之间的关系。方法:选择2019年12月至2020年12月于连云港市第二人民医院就诊的老年CSVD患者共97例,其中男56例、女41例,年龄65～85岁,依据蒙特利尔认知评估量表（MoCA）评分结果,分为CSVD认知正常组...     

盐酸多奈哌齐联合尼莫地平对脑小血管病性认知功能障碍患者MoCA评分的影响

脑小血管病(CSVD)是机体颅内微动脉、小动脉病变引起的颅内出血性损害或脑组织缺血,早期症状表现不明显,随着病情进展,患者认知功能损伤加重,患者表现为尿失禁、注意力不集中、认知障碍等,甚至诱发血管性痴呆等,若未及时有效治疗,可严重影响患者身体健康和生活质量,给家庭和社会带来压力[1, 2].尼莫地平是治疗CSVD的常见...     

维生素D水平与老年脑小血管病患者认知功能障碍的相关性研究

目的分析老年脑小血管病(CSVD)患者的血清25-羟基维生素D[25(OH)D]水平与认知功能障碍之间的关系。方法选择2019年12月至2020年12月于连云港市第二人民医院就诊的老年CSVD患者共97例, 其中男56例、女41例, 年龄65～85岁, 依据蒙特利尔认知评估量表(MoCA)评分结果, 分为CSVD认知正常组(50例)、CSVD认知障碍组(47例), 另选取同期健康老年人群作为对照组(30例), 收集3组受试者的临床资料和测定血清25(OH)D水平。计量资料组间比较采用单因素方差分析, 计数资料组间比较采用χ2检验, 多因素logistic回归分析分析CSVD患者出现认知功能障碍的危险因素, Pearson相关性分析分析认知障碍组MoCA评分与25(OH)D水平的关系。结果 CSVD认知正常组[(23.36±2.10)μg/L]、CSVD认知障碍组[(15.66±1.47)μg/L]25(OH)D水平较对照组[(34.03±2.17)μg/L]降低(F=13.764, P<0.05), 且CSVD认知障碍组的25(OH)D水平明显低于CSVD认知正常组水平(P<...     

脑小血管病性认知障碍血液学标志物的研究进展

如今,血管性认知障碍（vessel cognitive impairment,VCI）已成为痴呆的第2大病因,其中脑小血管病（cerebral small vessel disease,CSVD）被公认为VCI最常见的病因。临床实践中,脑小血管病认知功能障碍（CSVCI）的诊断主要通过神经量表评估、神经影像学等检查,并排除其他疾病导致认知功能障碍后得出诊断。近年来,因血液学标志物检测技术愈加成熟。众多学者认为,血液学标志物检测是一种简便、实用的检测手段,为CSVCI的临床诊断提供重要的参考价值,以此早期对CSVCI进行干预。本文主要对近10年CSVCI血液学标志物的研究进展作一综述。     

血清缺血修饰蛋白、钙调蛋白表达水平与脑小血管病患者神经功能受损的相关性分析

目的研究血清缺血修饰蛋白(ischemia modified albumin, IMA)、钙调蛋白(CaM)表达水平与脑小血管病(cerebral small vessel disease, CSVD)患者神经功能受损的相关性。方法回顾性分析2020年4月至2021年12月在聊城市第三人民医院住院治疗的CSVD患者的140例临床资料, 在患者入院时, 采用酶联免疫吸附法测定患者血清中CaM水平, 采用白蛋白-钴结合实验测定患者血清中IMA水平, 采用美国国立卫生院卒中量表(NIHSS)量表对患者的神经功能进行评价, 参照国立神经病学与中风研究所(NINDS)评价患者短暂性脑缺血情况, 评价患者尿失禁情况、步态障碍情况, 采用蒙特利尔认知评估(MoCA)量表对患者的认知功能进行评价。分析CSVD患者血清IMA和CaM表达水平的影响因素, 分析CSVD患者神经功能受损程度的影响因素及其与患者血清IMA和CaM表达水平的相关性。结果患者的性别、年龄、有无步态障碍、有无尿失禁等与患者血清IMA、CaM表达水平均无相关性(均P > 0.05);认知功能障碍患者、头晕和眩晕患者、短暂性脑缺血...     

老年痴呆症与脑出血90d病死率有关

目的探讨老年痴呆症或认知功能障碍与ICH后病死率之间的关联。方法根据影像学表现将脑出血患者分为脑叶出血组和非脑叶出血组,记录患者一般情况和影像学信息,老年痴呆症和认知功能障碍史。评估脑出血患者7 d和90 d死亡风险。结果共143例进入本研究,平均年龄。脑叶出血57例,非脑叶出血86例。ICH患者发病早期病死率较低,但90 d病死率达49.7%,伴老年痴呆症或认知功能障碍患者的病死率则上升至81.8%。在脑叶出血组患者发病初期(7 d)病死率增加与低GCS有关,90 d后病死率增加与痴呆或认知功能障碍史、年龄、抗血小板药物史关;而非脑叶出血组发病7 d病死率增加与低和出血量有关,90d后病死率增加与年龄、抗凝血剂史、舒张压、出血量和低GCS有关。结论老年痴呆症或认知功能障碍史较常见于脑出血,且为脑叶出血病死率的预测因素。     

脑小血管病与认知功能障碍研究进展

脑小血管病是引起世界上高达1/5中风患者,老年人认知功能下降的一个重要因素。近年来有关脑SVD的微循环障碍、病理生理发病机制及其继发的认知功能障碍,越来越受到人们的关注。MRI在研究脑小血管病相关认知功能障碍发挥重要作用。本文对脑小血管病及其与认知功能损害机制研究综述如下。     

脑小血管病认知障碍的药物治疗研究进展

脑小血管病（CSVD）是导致血管性认知障碍的主要原因,老年人群发病率高。目前针对CSVD认知障碍的药物治疗尚无明确的标准和特定的药物。本文围绕CSVD认知障碍的降压治疗、抗血小板治疗、溶栓治疗、他汀治疗以及尚处于临床研究阶段的治疗药物和相关临床前研究药物进行了综述。     

阿托伐他汀联合胞磷胆碱对脑小血管病合并轻度认知功能障碍患者血脂水平的影响

目的探讨阿托伐他汀联合胞磷胆碱对脑小血管病(CSVD)合并轻度认知功能障碍(MCI)患者低密度脂蛋白胆固醇(LDL-C)水平的影响。方法选取医院2016年5月至2018年5月收治的CSVD合并MCI患者142例,按随机数字表法分为对照组和观察组,各71例。两组患者均给予胞磷胆碱钠胶囊,观察组患者加用阿托伐他汀钙片。两组均连续治疗6个月。结果观察组患者临床总有效率为91.55%,明显高于对照组的70.42%(P <0.05);治疗后,两组患者蒙特利尔评估量表(MoCA)各维度评分和总分、生活质量量表(SF-36)各领域评分均明显升高(P <0.05);观察组治疗后三酰甘油(TG)、总胆固醇(TC)、LDL-C均明显下降,高密度脂蛋白胆固醇(HDL-C)水平明显升高(P <0.05),且观察组上述指标改善均明显优于对照组(P <0.05);对照组与观察组不良反应发生率相当(5.63%比2.82%,P> 0.05)。结论阿托伐他汀联合胞磷胆碱治疗CSVD合并MCI疗效确切,可改善患者的血脂水平和认知功能,显著提高生活质量,且安全性较高。     

TGF-β信号转导通路与遗传性脑小血管病

转化生长因子-β（transforming growth factor β,TGF-β）是一类具有生物活性的调节因子,广泛表达于内皮细胞、神经细胞、成纤维细胞、上皮细胞等。TGF-β可通过介导Smad依赖通路和非Smad依赖通路参与多种遗传性脑小血管病（cerebral small vessel disease,CSVD）,如CADASIL、CARASIL、HTRA1基因突变相关CSVD（症状携带者）、Fabry病等的发生发展。TGF-β信号通路可能通过影响内皮细胞功能、血管壁结构改变、血脑屏障通透性增加等导致CSVD。但此通路的调节异常不能作为一元论来解释CSVD的发生。本文将对TGF-β蛋白家族及其受体,TGF-β信号转导通路及其转导机制,TGF-β信号通路与遗传性CSVD等方面进行综述。     

Prospects for prevention and treatment of vascular cognitive impairment

With the aging population and rising prevalence of vascular disease in developed and developing countries, increasing numbers of individuals are at risk of cognitive impairment. Despite the potential of the therapeutics that are currently under investigation, none have yet fulfilled their promise for the prevention and treatment of dementia. The term vascular cognitive impairment (VCI) describes individuals with significant cognitive impairment arising from vascular disease. Risk factors predisposing to stroke correlate with brain changes, cognitive loss and Alzheimer's disease pathology. The volume of the infarcts and white matter changes, silent lacunar infarcts, and global and regional brain atrophy may be imaged non-invasively, targeted as surrogates of the dementia processes and considered parameters to be targeted for interventional strategies. As the greatest chance to prevent cognitive impairment and its progression is by intervening in the early stages or prior to any change, the development of preventative therapeutics is an important strategy. Non-invasive magnetic resonance imaging techniques may help to identify a subgroup of patients in whom infarct prevention, via risk factor control, may be of paramount importance. As the pathophysiology of dementia becomes more fully understood by coupling neuropsychological with neuroimaging, genetic and pathological features, there is the potential for the establishment of diagnostic criteria of the early phase of VCI and the testing of novel interventional strategies.     

White matter and cognitive function in schizophrenia

Abnormalities of cerebral white matter, oligodendrocytes, and myelin have been observed in schizophrenia with in-vivo imaging and post-mortem biochemistry. White-matter abnormalities are also frequently associated with cognitive impairment in both healthy and diseased individuals, and cognitive dysfunction is an important component of schizophrenia. While many studies have documented these associations, only a handful have examined the role of white matter in cognitive function in schizophrenia. In this paper, we explore what is known about white-matter deficits in relation to schizophrenia, cognitive deficits, or both together, in order to generate a theoretical model for the role that compromise of white matter might play in producing cognitive impairment in schizophrenia.     

Enhancement of oligodendrocyte autophagy alleviates white matter injury and cognitive impairment induced by chronic cerebral hypoperfusion in rats

Cognitive impairment caused by chronic cerebral hypoperfusion(CCH) is associated with white matter injury(WMI), possibly through the alteration of autophagy. Here, the autophagy—lysosomal pathway(ALP) dysfunction in white matter(WM) and its relationship with cognitive impairment were investigated in rats subjected to two vessel occlusion(2VO). The results showed that cognitive impairment occurred by the 28th day after 2VO. Injury and autophagy activation of mature oligodendrocytes and neuronal a...     

Vascular cognitive impairment and Alzheimer’s disease: role of cerebral hypoperfusion and oxidative stress

Cerebrovascular disease may lead to a wide range of cognitive changes, referred to collectively as vascular cognitive impairment. Stroke increases the risk of cognitive impairment and dementia, and may contribute to the progression of Alzheimer's disease (AD). Apart from clinical stroke itself, vascular risk factors are associated with the development of cognitive impairment and dementia. Animal models involving a temporary or permanent interruption of blood flow in the common carotid arteries develop nonprogressive cognitive impairment. Oxidative stress during cerebral hypoperfusion in animal models plays a key role in neuronal death and may thus contribute to the development of cognitive impairment in cerebrovascular disease. Genetic and pharmacological interventions to inhibit the major source of reactive oxygen species, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, are neuroprotective in experimental cerebral ischemia. Recent studies have demonstrated that inhibition of NADPH oxidase activity can mitigate cognitive impairment in rodent models of cerebral hypoperfusion. In this article, we review the evidence linking cognitive impairment and/or AD with NADPH oxidase-dependent oxidative stress, including the renin-angiotensin system.     

高压氧辅助治疗对急性脑梗死伴认知功能障碍患者认知功能及神经功能恢复情况的影响分析

目的探讨对急性脑梗死伴认知功能障碍患者采用高压氧辅助治疗对认知功能及神经功能恢复情况的影响。方法42例急性脑梗死伴认知功能障碍患者,根据治疗方法不同分为实验组及对照组,每组21例。对照组仅给予常规急性脑梗死药物治疗,实验组在常规急性脑梗死药物治疗基础上给予高压氧治疗。比较两组患者入院当天、治疗第30天简易精神状态检查量表(MMSE)评分及入院当天、治疗第3天、第30天美国国立卫生研究院卒中量表(NIHSS)评分。结果入院当天,两组患者MMSE评分比较差异无统计学意义(P>0.05);治疗第30天,实验组患者MMSE评分为(24.2±3.5)分,高于对照组的(21.3±2.6)分,差异具有统计学意义(P<0.05)。入院当天、治疗第3天,两组患者NIHSS评分比较差异无统计学意义(P>0.05);治疗第30天,实验组患者NIHSS评分为(12.2±1.7)分,明显低于对照组的(14.3±2.4)分,差异具有统计学意义(P<0.05)。结论高压氧辅助治疗对急性脑梗死患者认知功能及神经功能的恢复可能有促进作用。