短暂性脑缺血发作及轻型卒中患者认知功能下降的随访研究

目的既往的研究对短暂性脑缺血发作(transient ischemic attack,TIA)及轻型卒中后的认知功能障碍的关注较少。我们将对此类患者发生认知功能障碍的危险因素进行探讨。方法我们筛选了2012年7月至12月期间,连续住院的TIA及轻型卒中患者。于发病后第3个月及第18个月各进行一次认知功能评估,截止至2014年3月31日。结果共209例TIA及轻型卒中患者入组。其中,共24例(11.5%)出现了认知功能显著下降。Logistic回归分析,结果显示:受教育年限(比数比OR=0.869,P=0.021),心房纤颤(OR=5.950,P=0.001)、多发性腔隙性脑梗死(OR=5.179,P=0.020)是TIA/轻型卒中患者中远期认知功能下降的独立危险因素。结论对于TIA/轻型卒中的患者有必要对其认知功能进行随访,对于有心房纤颤及颅内多发性腔隙性脑梗死的患者应关注其认知功能变化,加强随访,必要时尽早给予干预治疗措施,以减少其发生认知功能下降的风险。     

高龄与中低龄老年短暂性脑缺血发作/轻型卒中临床特点比较

目的对比高龄及中低龄老年短暂性脑缺血发作(TIA)/轻型卒中患者的临床特点及预后。方法收集2009年4月至2016年12月在江苏省人民医院老年神经科收治的老年TIA/轻型卒中患者232例,其中高龄(≥80岁以上)患者103例,中低龄老年(≥60岁且80岁)患者129例。比较高龄组和中低龄老年组以及预后良好组与预后不良组患者间临床特点差异,采用多因素Logistics回归分析影响高龄与中低龄老年TIA/轻型卒中患者预后的影响因素。结果与中低龄老年组相比,高龄组的卒中史、冠心病、房颤、痴呆、卒中后肺炎的比例以及预后不良的发生率明显较高(P0.05)。多因素分析显示,年龄≥80岁是TIA/轻型卒中预后不良的独立危险因素(OR=2.829,P=0.005)。NIHSS评分、卒中后肺炎、冠心病是高龄患者预后不良的独立危险因素(OR=1.607,P=0.007;OR=7.190,P=0.001;OR=3.153,P=0.026),NIHSS评分、卒中后肺炎、神经功能进展是中低龄老年患者预后不良的独立危险因素(OR=2.262,P=0.000;OR=4.341,P=0.023;OR=3.192,P=0.033)。结论高龄TIA/轻型卒中患者更易合并心脑血管基础病及痴呆,临床预后更差,有部分患者将面临致残的结局。     

腔隙性梗死患者轻度血管性认知损害危险因素分析

目的探讨腔隙性梗死后血管性认知损害的相关危险因素。方法共138例腔隙性梗死患者根据蒙特利尔认知评价量表分为认知功能正常55例、轻度认知功能障碍73例和重度认知功能障碍10例,采用单因素和多因素后退法Logistic回归分析筛查腔隙性梗死后血管性认知损害相关危险因素。结果关键部位梗死灶(OR=1.179,95%CI:0.870~2.472;P=0.012)和脑白质高信号3~4级(OR=2.005,95%CI:0.910~4.502;P=0.024)是腔隙性梗死患者出现血管性认知损害的独立危险因素。结论腔隙性梗死后血管性认知损害是多因素共同作用的结果,其中关键部位梗死灶和脑白质高信号3~4级是独立危险因素。     

缺血性卒中合并脑白质病变的危险因素研究

目的 探讨缺血性卒中合并脑白质病变的患病情况及相关危险因素,通过对其干预以降低脑白质病变的发生率。方法 本研究连续入选2007年8月至2008年10月在北京天坛医院神经内科住院的缺血性卒中患者共483例,依据有无脑白质病变分成伴脑白质病变组和无白质病变两组,得出我院住院的缺血性卒中患者合并脑白质病变的患病率,以有无脑白质病变作为因变量,各种血管病危险因素作为自变量进行Logistic回归多因素分析。结果 我院住院的缺血性卒中患者脑白质病变的患病率为53.8%,随年龄增长发生率和病变严重程度增加（P均<0.01）。Logistic回归显示高龄［比值比（odds ratio,OR）=1.03,95%可信区间（confidence interval,CI）1.00～1.05,P<0.05］、高血压病（OR=1.77,95%CI 1.07～2.91,P<0.05）、卒中病史（OR=1.71,95%CI 1.02～2.88,P<0.05）、高血糖（OR=1.07,95%CI 1.00～1.15,P<0.05）和腔隙性脑梗死（OR=1.89,95%CI 1.17～3.06,P<0.05）是脑梗死患者合并脑白质病变的独立危险因素。结论 随年龄增长,脑白质病变的患病率和严重程度增加;高龄、高血压病、卒中病史、高血糖和腔隙性脑梗死是缺血性卒中患者合并脑白质病变的独立危险因素。     

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。     

缺血性卒中伴发癫(癎)的危险因素分析

目的 探讨缺血性卒中伴发癫(癎)的危险因素,以加强早期预防并改善预后.方法 根据斯堪地那维亚卒中评分(SSS)对101例发病<24 h的缺血性卒中伴发癫(癎)患者进行神经功能缺损程度评价,同时记录患者性别,年龄,既往史(高血压、冠心病、心房纤颤、2型糖尿病、高脂血症),电解质(血清钾、钠、氯),发病状态(安静、活动),缺血性卒中亚型(动脉粥样硬化性血栓性脑梗死、脑栓塞、腔隙性梗死),脑梗死后渗血,病灶部位(脑叶、基底节区),受累大脑半球侧别(左侧、右侧、双侧),脑萎缩及脑白质脱髓鞘病变等临床资料,分别进行单因素分析和多因素非条件Logistic回归分析.结果 单因素分析显示,与单纯缺血性卒中患者相比,缺血性卒中伴发癫(癎)者缺血性卒中亚型(脑栓塞)、脑梗死后渗血、病灶部位(脑叶,其中额叶所占比例达48.72%)、受累大脑半球侧别(右侧),以及神经功能缺损程度(SSS评分<30分)均存在明显差异(均P≤0.05);而性别、年龄、既往史、电解质指标、发病时状态、脑萎缩程度、脑白质脱髓鞘病变等因素,两组差异无统计学意义(均P>0.05).多因素非条件Logistic回归分析表明,脑栓塞(OR=0.152,95%CI:0.065～0.496;P=0.011)、脑梗死后渗血(OR=0.105,95%CI:0.020～0.549;P=0.008)、脑叶皮质受累(OR=0.099,95%CI:0.044～0.225;P=0.000)、SSS评分<30分(OR=0.145,95% CI:0.062～0.337;P=0.000)等因素为缺血性卒中伴发癫(癎)的主要危险因素,而右侧大脑半球受累(OR=0.638,95%CI:0.311～1.308;P=0.220)则不增加缺血性卒中伴发癫(癎)的风险.结论 具有脑栓塞、脑梗死后渗血、病灶位于脑叶(特别是额叶)、SSS评分<30分等因素的缺血性卒中患者易伴发癫(癎).     

脑小血管病患者认知状态与神经影像学特征的相关性分析

目的:本研究旨在探讨脑小血管病患者认知状态与皮质下腔隙性梗死部位及病灶数、白质病变和内侧颞叶萎缩之间的关系。方法:本研究纳入59例在上海交通大学医学院附属仁济医院神经内科脑血管病二级预防门诊登记的最近一次症状性缺血性卒中病史3个月的脑小血管病患者。根据详细的神经心理学评估结果,将59例患者分入无认知障碍组(24例)、轻度认知障碍组(22例)和血管性痴呆组(13例),采用头颅磁共振成像多重序列检查及斜冠状面重建,依据所得图像进行皮质下腔隙性梗死病灶计数、白质病变评分和内侧颞叶萎缩评分。结果:脑小血管病患者认知障碍的发生与皮质下腔隙性梗死病灶总数有关(P=0.004),其中皮质下白质部位腔隙性梗死病灶数在3组之间的差异有统计学意义(P=0.001);轻度认知障碍组和血管性痴呆组患者丘脑部位腔隙性梗死病灶数多于无认知障碍组的患者,但差异无统计学意义(P=0.058)。大部分的白质病变病灶位于额叶和顶枕叶,颞叶和基底节的白质病变较少。3组之间双侧额叶(P=0.033)和双侧基底节(P=0.009)的白质病变评分差异有统计学意义。59例患者中,43例完成磁共振成像斜冠状面重建。左右内侧颞叶萎缩一般呈同步发展;3组之间左或右内侧颞叶萎缩评分的差异均有统计学意义(P值均0.001)。在13例左内侧颞叶萎缩评分≥2分的患者中,11例为无认知障碍组和轻度认知障碍组患者;血管性痴呆组患者均有内侧颞叶萎缩,其中6例患者的左右侧平均内侧颞叶萎缩评分≥2分。多因素分析结果显示,皮质下白质腔隙性梗死病灶数[比值比:2.39(95%可信区间:1.19~5.80),P=0.005]和左内侧颞叶萎缩评分[比值比:10.21(95%可信区间:2.02~51.75),P=0.003]是脑小血管病认知功能的独立危险因素。结论:脑小血管病患者的认知损害程度与皮质下白质腔隙性梗死病灶数和左内侧颞叶萎缩评分相关。     

短暂性症状伴梗死的相关危险因素分析及再发缺血性脑卒中的风险预测

目的探讨短暂性症状伴梗死(transient symptoms with infarction,TSI)患者的相关危险因素及进展为缺血脑卒中的风险。方法 145例短暂性脑缺血发作患者在发病24h内行头颅磁共振及DWI检查,根据DWI检查结果分为短暂性脑缺血发作(transient ischemic attack,TIA)组和TSI组,比较2组患者的一般临床资料情况。发病7d后分别对2组患者进行随访,比较脑梗死复发的发生率。结果与TIA组相比,TSI组C反应蛋白、有TIA和卒中史、中性粒细胞数/淋巴细胞数比值(NLR)、高同型半胱氨酸血症、低密度脂蛋白(LDL-C)、ABCD2评分、运动障碍、发作次数3次的比例显著升高,差异有统计学意义(P0.05)。Logistic回归分析显示,既往有TIA和卒中史(OR=2.485,95%CI 1.433～4.302)、高同型半胱氨酸血症(OR=1.803,95%CI 1.171～2.775)、NLR升高(OR=3.134,95%CI 1.734～5.654)、症状发作次数3次(OR=2.669,95%CI 1.287～5.606)及运动障碍(OR=2.055,95%CI 1.204～3.493)均与TSI患者的发生呈正相关。TSI组患者7d后随访再发TIA及脑梗死的风险显著高于TIA组。结论既往有TIA和卒中史、NLR升高、高同型半胱氨酸血症、发作次数3次及运动障碍是TSI的独立危险因素,对其危险因素进行早期干预,可减少TSI的发病率及卒中复发的风险。     

腔隙性脑梗死合并脑微出血临床及影像学特征研究

目的探讨腔隙性脑梗死患者合并脑微出血(cerebral microbleeds,CMBs)的临床及其影像学特征。方法采用前瞻性研究方法,连续收集2013年8月~2015年9月在本院神经内科住院的腔隙性脑梗死患者120例,根据有无CMBs将患者分为有CMBs组(39例)和无CMBs组(81例),比较2组间基本临床资料、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CMBs发生的独立危险因素。结果 120例腔隙性脑梗死患者中合并CMBs39例(32.5%),其中2组年龄(t=6.373,P0.001)、高血压病(χ~2=5.385,P=0.02)、高尿酸(χ~2=4.474,P=0.04)、腔隙性脑梗死数目(t=8.773,P0.001)以及脑白质疏松程度评分(t=7.964,P0.001)比较差异具有统计学意义。Logistic回归分析显示,年龄、高血压病、腔隙性脑梗死数目以及脑白质疏松程度评分是腔隙性脑梗死患者发生CMBs的独立危险因素。结论腔隙性脑梗死患者CMBs发生与年龄、高血压病、腔隙性脑梗死数目以及脑白质疏松程度有关。     

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。     

Homocysteine, silent brain infarcts, and white matter lesions: The Rotterdam Scan Study

Silent brain infarcts and white matter lesions are frequently seen on magnetic resonance imaging in healthy elderly people and both are associated with an increased risk of stroke and dementia. Plasma total homocysteine may be a potentially modifiable risk factor for stroke and dementia. We examined whether elevated total homocysteine levels are associated with silent brain infarcts and white matter lesions. The Rotterdam Scan Study is a population-based study of 1,077 people aged 60 to 90 years who had cerebral magnetic resonance imaging. The cross-sectional relation of total homocysteine with silent infarcts and white matter lesions was analyzed with adjustment for cardiovascular risk factors. The mean plasma total homocysteine level was 11.5 micromol/l (standard deviation 4.1). The risk of silent brain infarcts increased with increasing total homocysteine levels (odds ratio 1.24/standard deviation increase, 95% confidence interval 1.06-1.45). The severity of periventricular white matter lesions and extent of subcortical white matter lesions were also significantly associated with total homocysteine levels, even after excluding those with silent brain infarcts. The overall risk of having either a silent brain infarct or severe white matter lesions was strongly associated with total homocysteine levels (odds ratio 1.35/standard deviation increase, 95% confidence interval 1.16-1.58). We concluded that total homocysteine levels are associated with silent brain infarcts and white matter lesions independent of each other and of other cardiovascular risk factors.     

How complex interactions of ischemic brain infarcts, white matter lesions, and atrophy relate to poststroke dementia

BACKGROUND: Cerebrovascular disease is a major factor related to cognitive impairment. However, behavioral correlates of ischemic brain lesions are insufficiently characterized. OBJECTIVE: To examine magnetic resonance imaging correlates of dementia in a large, well-defined series of patients with ischemic stroke. METHODS: Detailed medical, neurological, and neuropsychological examinations were conducted 3 months after ischemic stroke for 337 of 486 consecutive patients aged 55 to 85 years. Infarcts (type, site, side, number, and volume), extent of white matter lesions (WMLs), and degree of atrophy were categorized according to magnetic resonance images of the head. The definition for dementia of the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III) was used. RESULTS: Dementia was diagnosed in 107 (31.8%) of the patients and stroke-related dementia in 87 (25.8%). Volumes, numbers, distinct sites of infarcts, extent of WMLs, and degree of atrophy were different for the demented and nondemented subjects. Particularly, volumes of infarcts in any (right- or left-sided) superior middle cerebral artery territory (27.3 vs 13.7 cm(3), P =. 002) and left thalamocortical connection (14.8 vs 4.0 cm(3), P =. 002) differentiated the 2 groups. Logistic regression analysis showed that the correlates of any dementia included the combination of infarct features (volume of infarcts in any superior middle cerebral artery: odds ratio [OR], 1.11; frequency of left-sided infarcts: OR, 1.21), extent of WMLs (OR, 1.3), medial temporal lobe atrophy (OR, 2.1), and host factors (education; OR, 0.91). In the patients with stroke-related dementia, the main correlate was volume of infarcts in the left anterior corona radiata (OR, 1.68). CONCLUSION: Correlates of poststroke dementia do not include merely 1 feature but a combination of infarct features, extent of WMLs, medial temporal lobe atrophy, and host features.     

皮质下缺血性脑血管病MRI与血管性痴呆的相关性研究

目的:探索皮质下缺血性脑血管病MRI表现与血管性痴呆之间的关系。方法:对比分析了皮质下多发梗死28例痴呆患者和33例非痴呆患者的MRI表现,采用Logistic回归分析皮质下缺血性血管性痴呆的影像学相关高危因素。结果:痴呆组中顶叶皮质下、内囊膝部和丘脑的梗死发生率,顶叶皮质下、侧脑室体旁前部、内囊膝部和丘脑平均梗死数目,4级LA的出现率以及所有脑萎缩指标均明显大于对照组(P<0.05)。但Logistic回归后,只有平均脑沟宽度、侧脑室指数和丘脑梗死的数目进入了方程。结论:皮质下缺血性血管性痴呆可能与脑萎缩的程度和丘脑梗死的数目密切相关。     

MRI pontine hyperintensity after supratentorial ischemic stroke relates to poor clinical outcome

BACKGROUND AND PURPOSE: MRI studies in patients with atherosclerosis often reveal ill-defined hyperintensity in the pons on T2-weighted images. This pontine hyperintensity (PHI) does not fulfill the criteria of a brain infarct, and its clinical relevance is not established. We examined the frequency, as well as the radiological and clinical correlates, of PHI in poststroke patients. METHODS: Three hundred nineteen patients were studied 3 months after supratentorial ischemic stroke with the use of 1.0-T MRI. Brain infarcts, atrophy, white matter hyperintensities, and PHI were registered. The clinical outcome was assessed 3 and 15 months after the stroke. RESULTS: Of the patients, 152 (47.6%) had PHI. The risk factors for stroke did not differ in patients without or with PHI. PHI was related to a higher frequency (P=0.002) and larger volume (P<0.001) of supratentorial brain infarcts, to parietal (P=0.020) and temporal (P=0.002) atrophy, to central atrophy (P< or =0.040), and to white matter hyperintensity grade (P<0.001). Brain infarcts that affected the corpus striatum (putamen, caudate, and pallidum) (P< or =0. 011) or pyramidal tract (P<0.001) were more frequent in patients with PHI. The 3- and 15-month outcomes were worse in patients with PHI (P< or =0.004). The total volume of brain infarcts (OR 1.22), mean atrophy (OR 3.59), and PHI (OR 3.76) were independent correlates of a poor 15-month outcome. CONCLUSIONS: PHI after supratentorial ischemic stroke deserves attention because it relates to poor clinical outcome.     

脑小血管病步态障碍的影像特征与危险因素研究

目的 探讨与脑小血管病（cerebral small vessel disease,CSVD）步态障碍相关的影像特征。 方法 连续收集2018年7-9月在青岛西海岸新区人民医院神经内科住院的CSVD患者,记录入组 患者的性别、年龄、吸烟史、控制不良的高血压、高脂血症、HbA1c、无症状性梗死、室周白质高信 号（periventricular white matter hyperintensities,PWMHs）评分、深部白质高信号（deep white matter hyperintensities,DWMHs）评分、皮质萎缩（外侧裂比值）、皮质下萎缩（尾状核指数）及颞叶海马萎缩 （海马沟回比）等资料。按照Holden步行功能分级（functional ambulation classification,FAC）≤3,分为跌 倒低风险组（low risk of falling,LRF）和高风险组（high risk of falling,HRF）,采用多因素Logistic回 归分析CSVD患者步态障碍的独立危险因素。 结果 研究共纳入102例CSVD患者,其中HRF组59例（57.8%）。单因素分析提示HRF组与LRF组的年龄 （P＜0.001）、HbA1c（P =0.007）、PWMHs（P =0.002）、DWMHs（P＜0.001）、外侧裂比值（P＜0.001）、尾 状核指数（P =0.003）及海马沟回比（P＜0.001）差异有统计学意义,多因素Logistic回归分析显示年龄 （OR 1.173,95%CI 1.053～1.306,P =0.004）、DWMHs（OR 8.883,95%CI 2.674～29.512,P＜0.001）及外 侧裂比值（OR 1.433,95%CI 1.028～1.999,P =0.034）是CSVD步态障碍的独立危险因素。 结论 CSVD患者步态障碍的独立危险因素包括年龄、皮层萎缩及DWMHs评分。     

MRI correlates of dementia after first clinical ischemic stroke

BACKGROUND AND PURPOSE: Dementia after first clinical stroke frequently has been found, but the clinical and radiological correlates have not been fully detailed. We examined magnetic resonance imaging (MRI) correlates of dementia in a large well-defined series of patients with first clinical ischemic stroke. METHODS: Detailed medical, neurological and neuropsychological examination was conducted 3 months after ischemic stroke for 273 patients with first clinical stroke from a consecutive series of 486 patients aged 55-85 years. MRI of the head categorised infarcts (type, site, side, number, volume), extent of white matter lesions (WMLs) and degree of atrophy. The DSM-III definition for dementia was used. RESULTS: Dementia was diagnosed in 79 (28.9%) of the patients with first clinical stroke. Volumes, numbers, distinct sites of infarcts, extent of WMLs and degree of atrophy were different for the demented and nondemented subjects. Logistic regression analysis showed that the correlates of dementia included the combination of infarct features (volume of infarcts in left-sided anterior corona radiata; OR 1.86), extent of WMLs (OR 1. 37), medial temporal lobe atrophy (OR 3.4) and host factors (low education; OR 1.11). The additive effect of having more than one correlate was detected (OR 2.53). CONCLUSIONS: Dementia occurring after first clinical stroke is frequent and not solely due to a single stroke, but contain a combination of infarcts features, extent of WMLs, medial temporal lobe atrophy and host factors reflecting more than one underlying pathology.     

Frequency of white matter lesions and silent lacunar infarcts

White matter lesions and silent lacunar infarcts are related to and may result from cerebral small vessel disease. Reported frequencies of these lesions vary largely among studies. Differences in imaging techniques, rating scales, cut-off points in lesion severity grading and study populations contribute to the variation, in addition to differences in risk factor profiles across studies. In this paper, we will firstly discuss general methodological issues that may influence reported frequencies of white matter lesions and silent lacunar infarctions, and then review published data. We will focus on the results from population-based studies and only briefly comment on patient series of stroke and dementia.     

Blood pressure, white matter lesions and medial temporal lobe atrophy: closing the gap between vascular pathology and Alzheimer's disease?

BACKGROUND: Vascular factors are recognized as important risk factors for Alzheimer's disease, although it is unknown whether these factors directly lead to the typical degenerative pathology such as medial temporal lobe atrophy. We set out to investigate the relation between blood pressure and medial temporal lobe atrophy in patients with senile and presenile Alzheimer's disease with or without white matter lesions. METHODS: We determined the relation between blood pressure and pulse pressure and medial temporal lobe atrophy on MRI in 159 patients with Alzheimer's disease, stratified on white matter lesions and age at onset of dementia. RESULTS: There was a linear relation between systolic blood pressure and pulse pressure (both in tertiles) and the severity of medial temporal lobe atrophy (p(trend) = 0.05 and p(trend) 0.03, respectively). A significant relation was found between pulse pressure [beta = 0.08 (95% CI: 0.00-0.15; p = 0.05) per 10 mm Hg] and (borderline significant) systolic blood pressure [beta = 0.05 (95% CI: -0.01 to 0.11; p = 0.1) per 10 mm Hg] and medial temporal lobe atrophy. White matter lesions and age-stratified analysis revealed a significant association between systolic blood pressure and pulse pressure and medial temporal lobe atrophy, only in the subsample with white matter lesions and in the subsample with a senile onset of dementia. The relations were independent of severity of dementia and diabetes mellitus. CONCLUSIONS: Systolic blood pressure and pulse pressure are associated with medial temporal lobe atrophy in Alzheimer's disease, especially in the presence of white matter lesions and in patients with a late onset of dementia. Our finding may be another step in providing a rationale on how vascular factors could ultimately result in Alzheimer's disease.     

Focal Atrophy and Cerebrovascular Disease Increase Dementia Risk among Cognitively Normal Older Adults

BACKGROUND AND PURPOSE: This study investigated the association of medial temporal lobe (MTL) atrophy and cerebrovascular disease (white matter hyperintensities [WMH], subclinical infarcts) with the risk of developing Alzheimer's disease (AD) among cognitively normal older adults. METHODS: Risk of developing AD was examined for 155 cognitively normal older adults (77.4 years, 60% women, 81% white). The MTL volumes and the presence of WMH and of subclinical infarcts were determined from brain magnetic resonance imaging (MRI) at the beginning of the study. Follow-up cognitive evaluations (average 4.3 years) identified those who developed AD. RESULTS: The presence of either MTL atrophy or subclinical infarcts was independently and significantly associated with a greater risk to develop AD (OR [95% CI]: 4.4 [1.5, 12.3] and 2.7 [1.0, 7.1], respectively). In addition, those participants with both MTL atrophy and at least one brain infarct had a 7-fold increase in the risk of developing AD (OR [95% CI]: 7.0 [1.5, 33.1]), compared to those who had neither of these conditions. CONCLUSIONS: In cognitively normal older adults, markers of neurodegeneration (as reflected by MTL atrophy) and of cerebrovascular disease (as reflected by infarcts on MRI) independently contribute to the risk to develop AD.     

Magnetic resonance imaging white matter hyperintensities and mechanism of ischemic stroke.

BACKGROUND AND PURPOSE: We sought to determine the relations between infarct subtype and white matter hyperintensities (WMHIs) on MRI. MATERIALS AND METHODS: We studied 395 ischemic stroke patients with 1. 0-T MRI. The number of lacunar, border-zone, and cortical infarcts was registered. WMHIs were analyzed in 6 areas. Univariate and multivariate statistical analyses were used to find the risk factors for different infarct subtypes and to study the connections between WMHIs and brain infarcts. RESULTS: Lacunar infarcts were associated with hypertension (odds ratio [OR], 1.79; 95% CI, 1.17 to 2.73), alcohol consumption (OR, 1.96; 95% CI, 1.17 to 3.28), and age (OR, 1. 03; 95% CI, 1.00 to 1.06). Border-zone infarcts were associated with carotid atherosclerosis (OR, 2.20; 95% CI, 1.15 to 4.19). Atrial fibrillation (OR, 3.02; 95% CI, 1.66 to 5.50) and carotid atherosclerosis (OR, 1.94; 95% CI, 1.12 to 3.36) were independent positive predictors, and history of hyperlipidemia (OR, 0.44; 95% CI, 0.26 to 0.75) and migraine (OR, 0.48; 95% CI, 0.25 to 0.93) were negative predictors for cortical infarcts. Patients with lacunar infarcts had more severe WMHIs than patients with nonlacunar infarcts in all WM areas (P相似文献