型半胱氨酸的代谢与缺血性卒中的相互关系

高同型半胱氨酸血症被认为是卒中的独立危险因素。本文以同型半胱氨酸代谢途径为背
景,以同型半胱氨酸及相关血脂致动脉粥样硬化为基础,阐述同型半胱氨酸与缺血性卒中的关系。其
中,同型半胱氨酸水平与卒中的严重程度成正比,维生素降低同型半胱氨酸对卒中预后的影响各研
究结果不一。高同型半胱氨酸血症与各型缺血性卒中的关系研究结果仍存在争议。     

非痴呆性血管性认知障碍的研究进展

血管性认知障碍（vascular cognitive impairment,VCI）是由脑血管病危险因素（如高血压、 糖尿病、高脂血症和高同型半胱氨酸血症等）、显性脑血管病（出血性及缺血性卒中）及非显性脑血 管病（脑白质疏松和慢性脑缺血等）引起的一组从轻度认知功能损害到痴呆的临床综合征。非痴呆 性血管性认知障碍（vascular cognitive impairment-no dementia,VCIND）是VCI的早期阶段,其中约一半 患者会在5年内进展为痴呆。血管性痴呆（vascular dementia,VD）在治疗上尚未发现行之有效的方法, 但又是唯一可以预防的痴呆。发现VCIND危险因素并进行早期干预,对于寻求延缓痴呆进展的二级 预防策略至关重要。现从VCIND的概念、流行病学、诊断标准及影响因素等方面进行综述,以期能够 早期识别相关危险因素,防治VCI。     

急性缺血性卒中1年血管源性死亡危险因素分析

目的 分析急性缺血性卒中患者随访1年血管源性死亡的相关影响因素，为早期评估高危急性缺血
性卒中患者、积极控制危险因素、降低死亡率提供临床依据。
方法 回顾性纳入2014年1月-2018年9月于河北省任丘康济新图医院神经内科住院的急性缺血性
卒中患者，收集患者临床基线资料及实验室检查结果。采用多因素Cox回归分析方法分析急性缺血性
卒中患者1年内血管源性死亡的危险因素。
结果 研究共纳入符合入排标准的急性缺血性卒中患者3 6 61例，随访1年内死亡患者16 0
例（4.4%），其中血管源性死亡136例（3.7%），其中包括缺血性血管性死亡3.1%（114例），出血
性血管性死亡0.1%（4例），心源性血管性死亡0.2%（8例），其他血管性死亡0.3%（10例），非血
管源性死亡0.7%（24例）。非血管源性死亡患者作为删失数据，最终共纳入急性缺血性卒中患者
3637例。多因素Cox回归分析显示年龄＞60岁（OR 1.084，95%CI 1.062～1.105，P＜0.001）、颈动脉
狭窄（OR 1.835，95%CI 1.288～2.614，P =0.001）、入院时NIHSS评分（OR 1.200，95%CI 1.164～1.237，
P ＜0.001）、脂蛋白a（OR 1.001，95%C I 1.000～1.001，P ＜0.001）、白细胞计数（OR 1.093，
95%CI 1.031～1.159，P =0.003）、纤维蛋白原水平（OR 1.092，95%CI 1.025～1.164，P =0.006）、血肌
酐（OR 1.004，95%CI 1.001～1.007，P =0.009）是血管源性死亡的独立危险因素。HDL-C（OR 0.378，
95%CI 0.208～0.686，P =0.001）是血管源性死亡的保护因素。
结论 急性缺血性卒中1年内血管源性死亡的危险因素为高龄、颈动脉狭窄、入院时NIHSS评分、脂
蛋白a水平、白细胞计数、纤维蛋白原及血肌酐水平。高密度脂蛋白为其保护因素。     

血管性认知障碍的早期预警因子

血管性认知障碍是指脑血管病及其危险因素引起的从轻度认知损害到痴呆的一类综合征。目前的研究认为,包括腔隙性脑梗死(LI)、白质高信号(WMH)、脑微出血(CMBs)、扩大的血管周围间隙(EPVS)等在内的脑小血管病(CSVD)、脑组织N-乙酰天门冬氨酸(NAA)/肌酸(Cr)比值降低、全脑血流灌注减少、动脉粥样硬化和动脉僵硬化、颈动脉狭窄、颅内动脉搏动指数增高、颅内血管对高/低碳酸血症的反应性降低、自发性微栓子、血清高血同型半胱氨酸,以及低TT3、脑脊液高α1-抗胰凝乳蛋白酶、YKL-40和NF-L等分子标志物均可作为血管性认知障碍的早期预警因子。磁共振和超声技术的应用为这些早期预警因子的检出提供了有力帮助。     

同型半胱氨酸与缺血性卒中

同型半胱氨酸(Hcy)即2-氨酸-4-巯基丁酸,又名高半胱氨酸,是蛋氨酸(Met)代谢的重要中间产物。1964年,Gibson等率先报告高同型半胱氨酸血症与血管性疾病和血栓形成有关。自1969年McCully提出高同型半胱氨酸血症是导致动脉粥样硬化的主要因素以来,已有大量研究证实高同型半胱氨酸血症是缺血性卒中的独立危险因子,但近年又有临床试验得出不同结论。笔者拟就同型半胱氨酸与缺血性卒中之间的关系作如下综述。一、同型半胱氨酸代谢特点     

高同型半胱氨酸血症与糖尿病合并血管性痴呆的相关性分析

目的探讨高同型半胱氨酸血症与糖尿病合并血管性痴呆的相关性。方法选取糖尿病合并血管性痴呆患者、非痴呆性血管性认知功能障碍患者、单纯糖尿病患者各60例,分别设为痴呆组、认知障碍组、对照组,采用简易精神状态量表与蒙特利尔认知评估量表进行评估,比较其认知功能评分。采血测定血浆同型半胱氨酸水平,比较3组同型半胱氨酸水平、高同型半胱氨酸血症发生率。根据高同型半胱氨酸血症发生情况将每组分为A组(高同型半胱氨酸血症)、B组(非高同型半胱氨酸血症),比较其认知功能评分。结果 3组MMSE评分、MoCA评分比较差异均有统计学意义(P0.05)。3组同型半胱氨酸水平、高同型半胱氨酸血症发生率比较差异均有统计学意义(P0.05)。痴呆组、认知障碍组、对照组中,A组MMSE评分、MoCA评分均低于B组(P0.05)。高同型半胱氨酸血症与糖尿病合并血管性痴呆呈正相关(r=0.809,P0.05)。结论高同型半胱氨酸血症与糖尿病合并血管性痴呆密切相关,同型半胱氨酸水平越高,认知功能损害越严重。     

同型半胱氨酸与缺血性卒中

同型半胱氨酸（Hcv）即2-氨酸-4-巯基丁酸，又名高半胱氨酸，是蛋氨酸（Met）代谢的重要中间产物。1964年，Gibson等率先报告高同型半胱氨酸血症与血管性疾病和血栓形成有关。自1969年Mccully提出高同型半胱氨酸血症是导致动脉粥样硬化的主要因素以来，已有大量研究证实高同型半胱氨酸血症是缺血性卒中的独立危险因子，但近年又有临床试验得出不同结论。笔者拟就同型半胱氨酸与缺血性卒中之间的关系作如下综述。     

进展性缺血性卒中相关危险因素临床分析

目的探讨进展性缺血性卒中的临床相关因素。方法分析我院神经内科322例急性脑梗死患者临床资料,将其分为进展性卒中组及非进展性卒中组,对两组患者的高血压病史,糖尿病史,空腹及三餐后2h血糖、入院时收缩压、舒张压、高脂血症、高同型半胱氨酸血症及颅内血管狭窄情况进行比较。结果进展组患者中有高血压、糖尿病史及高脂血症、高同型半胱氨酸血症者较非进展组多见(P<0.05),进展组患者空腹及餐后2h血糖水平较非进展组高(P<0.05),进展组与非进展组患者入院时收缩压及舒张压水平未见显著差异(P>0.05),进展组患者颅内主要供血动脉狭窄较非进展组多见(P<0.05)。结论高血压、糖尿病史、血糖水平、高脂血症、高同型半胱氨酸血症及颅内血管狭窄与进展性卒中的发生相关。     

非痴呆性血管性认知障碍的影响因素研究

目的探讨非痴呆性血管性认知障碍的影响因素。方法选取唐山市工人医院2014年1月-2016年1月非痴呆性血管性认知障碍(vascular cognitive impairment no dementia,VCIND)患者为研究对象,同期认知功能正常者为对照组。对比VCIND组和对照组的血管病危险因素、生化指标、甲状腺激素水平的差异,采用Logistic回归分析VCIND的独立危险因素。结果研究共纳入VCIND组115例,对照组147例。VCIND组患者高血压(73.9%vs 53.1%,P=0.001)及既往卒中史(60.9%vs 34.7%,P0.001)比例显著高于对照组。VCIND组空腹血糖(P0.001)、同型半胱氨酸(P0.001)、甘油三酯水平显著高于对照组(P=0.022)。VCIND组游离三碘甲状腺原氨酸(free triiodothyronine,FT3)水平显著低于对照组[(2.80±0.39)pg/ml vs(2.90±0.27)pg/ml,P=0.043]。多因素分析显示,卒中病史[比值比(odds ratio,OR)6.461,95%可信区间(confidence interval,CI)2.835~14.725,P0.001]、同型半胱氨酸(OR 15.726,95%CI 7.198~34.358,P0.001)、血糖水平(OR 1.864,95%CI 1.367~2.541,P0.001)是VCIND的独立危险因素,而FT3(OR 0.351,95%CI0.192~0.647,P0.001)是VCIND的保护性因素。结论卒中病史、高血糖水平、高同型半胱氨酸血症是VCIND的独立危险因素,而FT3是VCIND的保护性因素。     

缺血性血管性认知障碍与血浆生化预测指标的探讨

目的探讨血浆生化指标与血管认知障碍的相关性及预测指标。方法蚌埠市第一人民医院选取2013-12—2016-12 490例缺血卒中患者,3个月无复发,随诊3a,观测血浆生化指标与血管性认知障碍的相关性,患者使用《精神障碍诊断与统计手册IV》(DSMIV)标准,132例诊断为血管认知障碍(vascular cognitive impairment,VCI),采用简易精神状态量表(MMSE)对认知障碍程度进行评估,358例为非血管认知障碍患者,所有患者应用美国国立卫生院神经功能缺损评分(National Institute of Health Stroke Scale,NIHSS)对神经功能进行临床评估,日常生活活动能力量表(ADL)对日常生活能力进行评估,所有患者入院后行血浆生化指标检测、血常规、凝血6项、头CT、MRI影像检查。结果在人口特征因素分析中,在缺血性卒中患者血管认知障碍与认知正常组之间,年龄、吸烟、饮酒、高血压差异有统计学意义,在血浆生化指标分析中,高同型半胱氨酸、低密度脂蛋白在血管认知障碍与认知正常组之间差异有统计学意义;有意义指标用Logistic二分类回归分析血浆生化指标对血管认知障碍影响分析,年龄(OR0.43,95%CI为0.25~0.726)、吸烟(OR0.63,95%CI为0.14~0.289)、饮酒(OR5.567,95%CI为1.128~25.43)、高血压(SBP≥160 mmHg)(OR12.17,95%CI为3.33~44.36)、同型半胱氨酸(OR1.025,95%CI为0.99~1.052),低密度脂蛋白(OR0.873,95%CI为0.6~1.271),余指标差异无统计学意义。结论高同型半胱氨酸血症和高密度脂蛋白血症对血管认知障碍有显著影响,可以作为独立危险因素,二者联合可以作为血管认知障碍的早期预测指标。     

Vascular aspects of cognitive impairment and dementia

Hypertension and stroke are highly prevalent risk factors for cognitive impairment and dementia. Alzheimer''s disease (AD) and vascular dementia (VaD) are the most common forms of dementia, and both conditions are preceded by a stage of cognitive impairment. Stroke is a major risk factor for the development of vascular cognitive impairment (VCI) and VaD; however, stroke may also predispose to AD. Hypertension is a major risk factor for stroke, thus linking hypertension to VCI and VaD, but hypertension is also an important risk factor for AD. Reducing these two major, but modifiable, risk factors—hypertension and stroke—could be a successful strategy for reducing the public health burden of cognitive impairment and dementia. Intake of long-chain omega-3 polyunsaturated fatty acids (LC-n3-FA) and the manipulation of factors involved in the renin–angiotensin system (e.g. angiotensin II or angiotensin-converting enzyme) have been shown to reduce the risk of developing hypertension and stroke, thereby reducing dementia risk. This paper will review the research conducted on the relationship between hypertension, stroke, and dementia and also on the impact of LC-n3-FA or antihypertensive treatments on risk factors for VCI, VaD, and AD.     

Dementia, stroke, and vascular risk factors; a review

Interest in dementia has increased over the past few decades. Stroke is an important cause of cognitive problems. The term vascular cognitive impairment is now used to describe dementia attributed to stroke or deep white matter lesions detected on imaging. Although vascular cognitive impairment is increasingly diagnosed, Alzheimer's disease remains the most common dementia worldwide. The relationship between Alzheimer's disease and vascular cognitive impairment is unclear, although there exists significant overlap, which prompts physicians to consider them opposite ends of a disease spectrum, rather than separate entities. There is also substantial evidence that stroke risk factors such as hypertension, diabetes; lipid disorders, etc. are independently associated with an increased risk of Alzheimer's disease and vascular cognitive impairment. Evidence suggests that these risk factors have a cumulative effect on Alzheimer's disease development but not on vascular cognitive impairment. This is more marked in Alzheimer's disease patients in the presence of the ε4 allelic variant of apolipoprotein E. How these risk factors increase the risk of dementia is largely unknown. Physicians must be aware that stroke causes dementia; that vascular risk factors appear to be independent risk factors in developing dementia, and that poststroke care must include cognitive assessment.     

Vascular cognitive deterioration and stroke

Vascular cognitive impairment, the recent modification of the terminology related to vascular burden of the brain, reflects the all-encompassing effects of vascular disease or lesions on cognition. It incorporates the complex interactions between vascular aetiologies, risk factors and cellular changes within the brain and cognition. The concept covers the frequent poststroke cognitive impairment and dementia, as well as cerebrovascular disease (CVD) as the second most common factor related to dementia. CVD as well as vascular risk factors including arterial hypertension, history of high cholesterol, diabetes or forms of heart disease are independently associated with an increased risk of cognitive impairment and dementia. Traditional vascular risk factors and stroke are also independent factors for the clinical presentation of Alzheimer's disease (AD). In addition to these vascular factors, CVD/strokes, infarcts and white-matter lesions may trigger and modify the progression of AD as the most common cause of neurodegenerative dementia. The main subtypes of previously defined vascular dementia (VaD) include the cortical VaD or multi-infarct dementia also referred as poststroke VaD, subcortical ischaemic vascular disease and dementia or small-vessel dementia and strategic-infarct dementia. Whilst CVD is preventable and treatable, it is clearly a major factor in the prevalence of cognitive impairment in the elderly worldwide.     

Prevention of vascular dementia

Stroke is an important public health problem worldwide. Those at high risk of stroke may be at high risk of cognitive impairment and dementia after stroke. Modifiable cardiovascular risk factors in midlife including hypertension, alcohol use, cigarette smoking, and certain dietary factors may be important targets for prevention of vascular causes of cognitive impairment. These same types of factors may also be associated with Alzheimer disease. Better control of cardiovascular disease risk factors might lead to delay or prevention of vascular dementia and Alzheimer disease.     

Homocysteine in neuropsychiatric disorders of the elderly

OBJECTIVE: There is increasing interest in homocysteine as a risk factor for neuropsychiatric disorders such as stroke, dementia, depression and Parkinson's disease. This article reviews the current literature on the relationship between homocysteine and these disorders to ascertain if any clinical recommendations can be made. METHOD: A MEDLINE and EMBASE search was made for English language publications between 1966 and 2002 using the search terms 'Homocysteine' and 'Stroke', 'Dementia', 'Vascular Dementia', 'Alzheimer's dementia', 'Cognition disorders or cognitive decline or memory disorders', 'Depression or depressive disorders' or 'Parkinson's disease'. In addition, individual articles were hand searched for relevant references. RESULTS: Cross-sectional studies consistently suggest that elevated homocysteine increases the risk of stroke, and may also increase the risk of leukoariosis, vascular dementia (VaD), cognitive impairment and Alzheimer's disease (AD). Longitudinal studies of homocysteine as a risk factor are few and inconsistently supportive of these associations. No intervention trials to determine the effect of lowering homocysteine levels have yet been published. The pathological mechanisms for homocysteine-mediated disease await complete elucidation. Mild hyperhomocysteinemia is common in the elderly population, and folate supplementation can decrease homocysteine levels. CONCLUSION: The epidemiological evidence for homocysteine as a risk factor for neuropsychiatric disease is an emerging area of great interest. Screening the population for hyperhomocysteinemia cannot be recommended at this stage, but individuals at increased risk of cerebrovascular disease or cognitive impairment should be investigated and treated for elevated homocysteine levels.     

老年缺血性脑卒中后轻度血管性认知障碍的影响因素

目的分析老年缺血性脑卒中后轻度血管性认知障碍(VCI)的影响因素。方法对患者一般资料、体格检查、认知评估及影像学资料进行收集与调查,并行单因素分析与Logistic回归分析。结果老年缺血性卒中后轻度VCI的发生与患者年龄、文化程度、冠心病、糖尿病、高血压、卒中次数、发病部位及卒中面积有关;与性别、BMI、吸烟、饮酒等无明显相关。Logistic回归分析显示,文化程度为老年缺血性脑卒中后轻度VCI发生的保护因素,而年龄、冠心病、糖尿病、高血压、卒中次数、发病部位及卒中面积是危险因素。结论老年缺血性脑卒中后轻度VCI发生的危险因素众多,临床上可进行针对性的早期干预。     

伴智能障碍的脑白质疏松症患者相关危险因素分析

目的分析伴智能障碍的脑白质疏松症(LA)患者的相关危险因素。方法 207例LA患者分为伴有智能障碍组和无智能障碍组,对患者的性别、年龄、高血压病史、糖尿病史、冠心病史及既往脑梗死病史等进行相关因素分析和Logistic回归分析。结果两组年龄、高血压病史、糖尿病史、既往脑梗死病史和LA的严重程度均有显著差异。多因素回归分析最终入选模型的变量是年龄、高血压病史、既往脑梗死病史和重度LA。结论高龄、高血压病史、既往脑梗死病史和重度LA,对LA是否伴智能障碍有独立的提示作用。     

Clinical determinants of dementia and mild cognitive impairment following ischaemic stroke: the Sydney Stroke Study

BACKGROUND: Dementia following stroke is common but its determinants are still incompletely understood. METHODS: In the Sydney Stroke Study, we performed detailed neuropsychological and medical-psychiatric assessments on 169 patients aged 50-85 years, 3-6 months after a stroke, and 103 controls with a majority of both groups undergoing MRI brain scans. Stroke subjects were diagnosed as having vascular mild cognitive impairment (VaMCI) or vascular dementia (VaD) or no cognitive impairment by consensus. Demographic, functional, cerebrovascular risk factors and neuroimaging parameters were examined as determinants of dementia using planned logistic regression. RESULTS: 21.3% of subjects were diagnosed with VaD, with one case in those aged 50-59 years, 24% in those aged 60-69 years and 23% in those 70-79 years. There was no difference by sex. The prevalence of VaMCI was 36.7%. VaD subjects had lower premorbid intellectual functioning and had 0.9 years less education than controls. The VaD and VaMCI groups did not differ from the no cognitive impairment group on any specific cerebrovascular risk factor, however overall those with impairment had a greater number of risk factors. They did not differ consistently on depression severity, homocysteine levels and neuroimaging parameters (atrophy, infarct volume and number of infarcts) except for an excess of white matter lesions on MRI and greater number of infarcts in the VaD and VaMCI groups. On a series of logistic regression analyses, stroke volume and premorbid function were significant determinants of cognitive impairment in stroke patients. CONCLUSION: Post-stroke dementia and MCI are common, especially in older individuals. Cerebrovascular risk factors are not independent risk factors for VaD, but stroke volume is a significant determinant of dementia. Premorbid functioning is a determinant of post- stroke impairment.     

Vascular cognitive impairment,a cardiovascular complication

Over the past two decades, the term vascular cognitive impairment (VCI) has been used to refer to a spectrum of cognitive decline characterized by executive dysfunction, associated with vascular pathology. With 30% of stroke survivors showing cognitive impairments, it is regarded as the most common cause of cognitive impairment. This is a narrative review of available literature citing sources from PubMed, MEDLINE and Google Scholar. VCI has a high prevalence both before and after a stroke and is associated with great economic and caregiver burden. Despite this, there is no standardized diagnostic criteria for VCI. Hypertension has been identified as a risk factor for VCI and causes changes in cerebral vessel structure and function predisposing to lacuna infarcts and small vessel haemorrhages in the frontostriatal loop leading to executive dysfunction and other cognitive impairments. Current trials have shown promising results in the use of antihypertensive medications in the management of VCI and prevention of disease progression to vascular dementia. Prevention of VCI is necessary in light of the looming dementia pandemic. All patients with cardiovascular risk factors would therefore benefit from cognitive screening with screening instruments sensitive to executive dysfunction as well as prompt and adequate control of hypertension.     

Vascular dementia prevention: a risk factor analysis

Brain injury from ischemic or hemorrhagic cerebrovascular disease (CVD) produces decline in cognitive functions and vascular dementia (VaD). Likewise, CVD may cause VaD from hypoperfusion of susceptible brain areas. CVD may also worsen degenerative dementias such as Alzheimer's disease. Significant advances have been made in the identification and control of risk factors for stroke and cardiovascular disease. The main risk factors for VaD include age, hypertension and absence of antihypertensive medication, diabetes, cigarette smoking, history of cardiovascular disease (coronary heart disease, congestive heart failure, peripheral vascular disease), atrial fibrillation, left ventricular hypertrophy, hyperhomocysteinemia, orthostatic hypotension, cardiac arrhythmias, hyperfibrinogenemia, and sleep apnea. Recently identified risk factors include chronic infection and elevation of C-reactive protein, particularly in patients with diabetes. Evidence from controlled clinical trials strongly suggests that control of vascular risk factors, in particular hypertension, could prevent the development of dementia.