Objective To study the relationships between cognitive impairment in patients with lacunar infarcts and quantitative CT measures and to determine the independent correlative factors of cognitive impairment.Methods Neu...Objective To study the relationships between cognitive impairment in patients with lacunar infarcts and quantitative CT measures and to determine the independent correlative factors of cognitive impairment.Methods Neuropsychological examination was conducted for 128 patients with acute lacunar infarct.Number,location,and volume of infarcts,cerebral atrophy index and severity of white matter lesions(WMLs) were measured and recorded.Results The number of lacunar infarcts in cognitive impairment (CI) group was significantly larger than that in cognitive normal(CN) group.Mean width of sulcus and sylvian fissure,index of frontal horn and ventricular-brain ratio(VBR) were significantly different in both groups.There were more patients with 3 grades or 4 grades WMLs in CI group(62%) than those in CN group(22%).The total volume of lacunar infarcts showed no statistically significant difference.Logistic regression analysis indicated that the number of lacunar infarcts in frontal subcortex and thalamus,the volume of infarcts in anterior periventricular white matter,width of cerebral sulcus and sylvian fissure were correlated with cognitive impairment respectively.Additionally,age and education were correlative factors of cognitive impairment in patients with lacunar infarct.Conclusion Correlative factors of cognitive impairment in patients with lacunar infarct are not merely one feature,but a combination of infarct features(number,location,and volume),cortical atrophy and host factors(age and education).展开更多
Hypertension is a primary risk factor for the progression of cognitive impairment caused by cerebral small vessel disease,the most common cerebrovascular disease.Howeve r,the causal relationship between hypertension a...Hypertension is a primary risk factor for the progression of cognitive impairment caused by cerebral small vessel disease,the most common cerebrovascular disease.Howeve r,the causal relationship between hypertension and cerebral small vessel disease remains unclear.Hypertension has substantial negative impacts on brain health and is recognized as a risk factor for cerebrovascular disease.Chronic hypertension and lifestyle factors are associated with risks for stro ke and dementia,and cerebral small vessel disease can cause dementia and stroke.Hypertension is the main driver of cerebral small vessel disease,which changes the structure and function of cerebral vessels via various mechanisms and leads to lacunar infarction,leukoaraiosis,white matter lesions,and intracerebral hemorrhage,ultimately res ulting in cognitive decline and demonstrating that the brain is the to rget organ of hypertension.This review updates our understanding of the pathogenesis of hypertensioninduced cerebral small vessel disease and the res ulting changes in brain structure and function and declines in cognitive ability.We also discuss drugs to treat cerebral small vessel disease and cognitive impairment.展开更多
This study semi-quantitatively analyzed the effects of leukoaraiosis.Patients with moderate or severe lacunar infarction were found to exhibit low scores on the Montreal Cognitive Assessment Scale （F=12.02,P=0.000）,...This study semi-quantitatively analyzed the effects of leukoaraiosis.Patients with moderate or severe lacunar infarction were found to exhibit low scores on the Montreal Cognitive Assessment Scale （F=12.02,P=0.000）,and prolonged P300 Cz2.0 latency （F=16.04,P=0.000）.Correlation analysis revealed that the occurrence of leukoaraiosis was negatively correlated with Montreal Cognitive Assessment scores （r=-0.416,P=0.000）,and positively correlated with P300 Cz2.0 latency （r=0.538,P=0.000）.These findings indicate that leukoaraiosis aggravates cognitive impairment in patients with lacunar infarction,such that more severe leukoaraiosis is associated with more severe cognitive decline.展开更多
Cerebral small vessel disease（CSVD） is a common etiology of vascular cognitive impairment with no dementia（V-CIND）. Studies have revealed that cerebral microbleeds（CMBs）, a feature of CSVD, contribute to cogniti...Cerebral small vessel disease（CSVD） is a common etiology of vascular cognitive impairment with no dementia（V-CIND）. Studies have revealed that cerebral microbleeds（CMBs）, a feature of CSVD, contribute to cognitive impairment. However, the association between CMBs and dementia conversion in individuals with V-CIND is still unclear. Here, we analyzed the predictive role of CMBs in the conversion from V-CIND to dementia in CSVD patients. We recruited and prospectively assessed 85 patients with CSVD and V-CIND. V-CIND was evaluated using a series of comprehensive neuropsychological scales, including the Chinese version of the Montreal Cognitive Assessment and the Clinical Dementia Rating. MRI assessments were used to quantify lacunar infarcts, white matter hyperintensities, CMBs, and medial temporal lobe atrophy. Eighty-two of the 85 patients completed the assessment for dementia conversion at a 1-year follow-up assessment. Multivariate logistic regression analyses were conducted to examine independent clinical and MRI variables associated with dementia conversion. Twenty-four patients（29.3%） had converted to dementia at the 1-year follow-up, and these individuals had significantly more CMBs in the fronto-subcortical circuits. Multivariate logistic regression analyses revealed that the patients with CMBs in the fronto-subcortical circuits（odds ratio = 4.4; 95% confidence interval： 1.602-12.081, P = 0.004） and 5 or more CMBs overall（odds ratio = 17.6, 95% confidence interval： 3.23-95.84, P = 0.001） had a significantly increased risk of dementia at the 1-year follow-up. These findings indicate that CMBs in the fronto-subcortical circuits may be predictive of dementia conversion in CSVD patients with V-CIND, and thus extend the clinical significance of CMBs.展开更多
目的探讨原发性高血压并腔隙性脑梗死(lacunar infarction,LI)患者认知功能障碍的相关危险因素。方法选择2016年10月-2017年6月在新疆医科大学第一附属医院高血压科住院的原发性高血压患者292例,根据是否合并腔隙性脑梗死分为2组,高血压...目的探讨原发性高血压并腔隙性脑梗死(lacunar infarction,LI)患者认知功能障碍的相关危险因素。方法选择2016年10月-2017年6月在新疆医科大学第一附属医院高血压科住院的原发性高血压患者292例,根据是否合并腔隙性脑梗死分为2组,高血压并LI患者186例(高血压并LI组),高血压非LI组(高血压组)106例。检测所有受试者的血脂、同型半胱氨酸,行颈部血管B超、头颅多普勒、头颅CT或MRI、动态血压检查,同时采集病史,采用简易精神评估量表(mini-mental state examination,MMSE)进行认知功能测定,依据MMSE评分及相关评估结果分为认知正常患者及认知障碍患者,对认知功能障碍组行单因素差异性分析(P<0.05),对相关危险因素进行二元Logistic回归分析。结果认知正常患者174例,认知障碍患者118例,高血压并LI组MMSE评分[(25.55±3.86)分]低于高血压组[(27.28±2.66)分](P<0.01);高血压并LI组认知功能障碍的比例(47.31%)高于高血压组(28.30%)(P<0.05);二元Logistic回归分析显示:年龄、受教育年限、合并冠心病、颈部血管斑块阳性、夜间收缩压为原发性高血压合并LI患者发生认知功能障碍的独立危险因素。颈部血管斑块阳性的原发性高血压合并LI患者发生认知功能障碍的风险为斑块阴性患者的2.59倍。患有冠心病的原发性高血压合并LI患者发生认知功能障碍的风险为无冠心病患者的2.87倍。结论年龄、受教育年限、夜间收缩压、合并冠心病、颈部血管斑块阳性是原发性高血压并LI患者发生认知功能障碍的重要危险因素。展开更多
目的研究初次发病的腔隙性脑梗死(lacunar infarction,LI)患者认知功能障碍的发病率及相关危险因素。方法前瞻性选取首次发病、病程<2周的LI患者,发病72h内应用简易智力状态检查量表(mini-mental state examination,MMSE)对LI患者进...目的研究初次发病的腔隙性脑梗死(lacunar infarction,LI)患者认知功能障碍的发病率及相关危险因素。方法前瞻性选取首次发病、病程<2周的LI患者,发病72h内应用简易智力状态检查量表(mini-mental state examination,MMSE)对LI患者进行认知功能评定。结果60例患者中21例(35%)出现了不同程度的认知功能障碍。Logistic回归分析显示LI患者认知功能障碍的出现与高血压、糖尿病、高脂血症及高同型半胱氨酸(HHcy)有关(P<0.05)。结论首次发病的LI常可出现认知功能障碍,高血压、糖尿病、高脂血症及HHcy与认知功能障碍的关系密切。展开更多
目的探讨老年腔隙性脑梗死部位与认知功能障碍的关系及随时间发展的趋势。方法选择98例老年腔隙性脑梗死患者，另选同期健康体检的老年人60例为对照组。分别对患者急性期（脑梗死发生3～4周）、12个月、24个月以及对照组采用中文版蒙特...目的探讨老年腔隙性脑梗死部位与认知功能障碍的关系及随时间发展的趋势。方法选择98例老年腔隙性脑梗死患者，另选同期健康体检的老年人60例为对照组。分别对患者急性期（脑梗死发生3～4周）、12个月、24个月以及对照组采用中文版蒙特利尔认知评估量表（MoCA）进行认知功能评估，观察腔隙性脑梗死部位与认知功能障碍的关系及随时间发展的趋势。结果各部位腔隙性脑梗死患者注意力集中、执行功能得分均显著低于对照组，病变部位在小脑区的患者记忆得分显著低于其他各组，病变部位在大脑皮层的患者命名得分显著低于其他各组，病变部位在小脑区和脑干区的患者定向力得分显著低于其他各组。病变部位在内囊及基底节区、脑干区、大脑皮层区与小脑区的患者抽象思维和语言得分显著低于病变部位在丘脑区的患者和对照组。随访结果发现，各病变部位的患者在24个月随访的 MoCA 得分总分均显著低于急性期的得分。差异均有统计学意义（ P ﹤0.05）。结论老年腔隙性脑梗死患者存在认知功能障碍，其认知功能障碍与梗死的部位相关，且随着病变进展出现缓慢恶化的趋势。展开更多
目的探讨非高密度脂蛋白(non-HDL-C)与腔隙性脑梗死(LI)认知障碍的关系。方法回顾性分析2017年1月~2018年11月就诊于我院神经内科符合LI诊断标准的患者171例,参照MoCA量表进行评分,分为认知障碍组和非认知障碍组,测量总胆固醇及高密度...目的探讨非高密度脂蛋白(non-HDL-C)与腔隙性脑梗死(LI)认知障碍的关系。方法回顾性分析2017年1月~2018年11月就诊于我院神经内科符合LI诊断标准的患者171例,参照MoCA量表进行评分,分为认知障碍组和非认知障碍组,测量总胆固醇及高密度脂蛋白,并计算non-HDL-C水平。对non-HDL-C与LI认知障碍之间的关系进行Logistic多因素回归分析。结果调整潜在混杂因素后,与non-HDL-C最低四分位组相比,non-HDL-C最高四分位组患者认知障碍患病率较高[OR=3.806(95%CI):1.475~9.822,P=0.006]。随着non-HDL-C的增高,患者认知障碍可能进一步增加(P for trend=0.004)。结论Non-HDL-C与认知障碍呈现正相关,且随着non-HDL-C水平增高,认知障碍可能会出现增加的趋势。展开更多
基金This study was supported by Shaanxi Science Technology Study Development Plan Item(No.2006K13-G7-6)Xi'an Science Technology Study Development Plan Item(No.GG05140).
文摘Objective To study the relationships between cognitive impairment in patients with lacunar infarcts and quantitative CT measures and to determine the independent correlative factors of cognitive impairment.Methods Neuropsychological examination was conducted for 128 patients with acute lacunar infarct.Number,location,and volume of infarcts,cerebral atrophy index and severity of white matter lesions(WMLs) were measured and recorded.Results The number of lacunar infarcts in cognitive impairment (CI) group was significantly larger than that in cognitive normal(CN) group.Mean width of sulcus and sylvian fissure,index of frontal horn and ventricular-brain ratio(VBR) were significantly different in both groups.There were more patients with 3 grades or 4 grades WMLs in CI group(62%) than those in CN group(22%).The total volume of lacunar infarcts showed no statistically significant difference.Logistic regression analysis indicated that the number of lacunar infarcts in frontal subcortex and thalamus,the volume of infarcts in anterior periventricular white matter,width of cerebral sulcus and sylvian fissure were correlated with cognitive impairment respectively.Additionally,age and education were correlative factors of cognitive impairment in patients with lacunar infarct.Conclusion Correlative factors of cognitive impairment in patients with lacunar infarct are not merely one feature,but a combination of infarct features(number,location,and volume),cortical atrophy and host factors(age and education).
基金supported by the National Natural Science Foundation of China,Nos.82274611 (to LZ),82104419 (to DM)Capital Science and Technology Leading Talent Training Project,No.Z1 91100006119017 (to LZ)+3 种基金Beijing Hospitals Authority Ascent Plan,No.DFL20190803 (to LZ)Cultivation Fund of Hospital Management Center in Beijing,No.PZ2022006 (to DM)R&D Program of Beijing Municipal Education Commission,No.KM202210025017 (to DM)Beijing Gold-Bridge Project,No.ZZ20145 (to DM)。
文摘Hypertension is a primary risk factor for the progression of cognitive impairment caused by cerebral small vessel disease,the most common cerebrovascular disease.Howeve r,the causal relationship between hypertension and cerebral small vessel disease remains unclear.Hypertension has substantial negative impacts on brain health and is recognized as a risk factor for cerebrovascular disease.Chronic hypertension and lifestyle factors are associated with risks for stro ke and dementia,and cerebral small vessel disease can cause dementia and stroke.Hypertension is the main driver of cerebral small vessel disease,which changes the structure and function of cerebral vessels via various mechanisms and leads to lacunar infarction,leukoaraiosis,white matter lesions,and intracerebral hemorrhage,ultimately res ulting in cognitive decline and demonstrating that the brain is the to rget organ of hypertension.This review updates our understanding of the pathogenesis of hypertensioninduced cerebral small vessel disease and the res ulting changes in brain structure and function and declines in cognitive ability.We also discuss drugs to treat cerebral small vessel disease and cognitive impairment.
文摘This study semi-quantitatively analyzed the effects of leukoaraiosis.Patients with moderate or severe lacunar infarction were found to exhibit low scores on the Montreal Cognitive Assessment Scale （F=12.02,P=0.000）,and prolonged P300 Cz2.0 latency （F=16.04,P=0.000）.Correlation analysis revealed that the occurrence of leukoaraiosis was negatively correlated with Montreal Cognitive Assessment scores （r=-0.416,P=0.000）,and positively correlated with P300 Cz2.0 latency （r=0.538,P=0.000）.These findings indicate that leukoaraiosis aggravates cognitive impairment in patients with lacunar infarction,such that more severe leukoaraiosis is associated with more severe cognitive decline.
基金supported by the Medical Scientific Research Foundation of Guangdong Province,China(No.A2015160)
文摘Cerebral small vessel disease（CSVD） is a common etiology of vascular cognitive impairment with no dementia（V-CIND）. Studies have revealed that cerebral microbleeds（CMBs）, a feature of CSVD, contribute to cognitive impairment. However, the association between CMBs and dementia conversion in individuals with V-CIND is still unclear. Here, we analyzed the predictive role of CMBs in the conversion from V-CIND to dementia in CSVD patients. We recruited and prospectively assessed 85 patients with CSVD and V-CIND. V-CIND was evaluated using a series of comprehensive neuropsychological scales, including the Chinese version of the Montreal Cognitive Assessment and the Clinical Dementia Rating. MRI assessments were used to quantify lacunar infarcts, white matter hyperintensities, CMBs, and medial temporal lobe atrophy. Eighty-two of the 85 patients completed the assessment for dementia conversion at a 1-year follow-up assessment. Multivariate logistic regression analyses were conducted to examine independent clinical and MRI variables associated with dementia conversion. Twenty-four patients（29.3%） had converted to dementia at the 1-year follow-up, and these individuals had significantly more CMBs in the fronto-subcortical circuits. Multivariate logistic regression analyses revealed that the patients with CMBs in the fronto-subcortical circuits（odds ratio = 4.4; 95% confidence interval： 1.602-12.081, P = 0.004） and 5 or more CMBs overall（odds ratio = 17.6, 95% confidence interval： 3.23-95.84, P = 0.001） had a significantly increased risk of dementia at the 1-year follow-up. These findings indicate that CMBs in the fronto-subcortical circuits may be predictive of dementia conversion in CSVD patients with V-CIND, and thus extend the clinical significance of CMBs.
文摘目的探讨原发性高血压并腔隙性脑梗死(lacunar infarction,LI)患者认知功能障碍的相关危险因素。方法选择2016年10月-2017年6月在新疆医科大学第一附属医院高血压科住院的原发性高血压患者292例,根据是否合并腔隙性脑梗死分为2组,高血压并LI患者186例(高血压并LI组),高血压非LI组(高血压组)106例。检测所有受试者的血脂、同型半胱氨酸,行颈部血管B超、头颅多普勒、头颅CT或MRI、动态血压检查,同时采集病史,采用简易精神评估量表(mini-mental state examination,MMSE)进行认知功能测定,依据MMSE评分及相关评估结果分为认知正常患者及认知障碍患者,对认知功能障碍组行单因素差异性分析(P<0.05),对相关危险因素进行二元Logistic回归分析。结果认知正常患者174例,认知障碍患者118例,高血压并LI组MMSE评分[(25.55±3.86)分]低于高血压组[(27.28±2.66)分](P<0.01);高血压并LI组认知功能障碍的比例(47.31%)高于高血压组(28.30%)(P<0.05);二元Logistic回归分析显示:年龄、受教育年限、合并冠心病、颈部血管斑块阳性、夜间收缩压为原发性高血压合并LI患者发生认知功能障碍的独立危险因素。颈部血管斑块阳性的原发性高血压合并LI患者发生认知功能障碍的风险为斑块阴性患者的2.59倍。患有冠心病的原发性高血压合并LI患者发生认知功能障碍的风险为无冠心病患者的2.87倍。结论年龄、受教育年限、夜间收缩压、合并冠心病、颈部血管斑块阳性是原发性高血压并LI患者发生认知功能障碍的重要危险因素。
文摘目的研究初次发病的腔隙性脑梗死(lacunar infarction,LI)患者认知功能障碍的发病率及相关危险因素。方法前瞻性选取首次发病、病程<2周的LI患者,发病72h内应用简易智力状态检查量表(mini-mental state examination,MMSE)对LI患者进行认知功能评定。结果60例患者中21例(35%)出现了不同程度的认知功能障碍。Logistic回归分析显示LI患者认知功能障碍的出现与高血压、糖尿病、高脂血症及高同型半胱氨酸(HHcy)有关(P<0.05)。结论首次发病的LI常可出现认知功能障碍,高血压、糖尿病、高脂血症及HHcy与认知功能障碍的关系密切。
文摘目的探讨老年腔隙性脑梗死部位与认知功能障碍的关系及随时间发展的趋势。方法选择98例老年腔隙性脑梗死患者，另选同期健康体检的老年人60例为对照组。分别对患者急性期（脑梗死发生3～4周）、12个月、24个月以及对照组采用中文版蒙特利尔认知评估量表（MoCA）进行认知功能评估，观察腔隙性脑梗死部位与认知功能障碍的关系及随时间发展的趋势。结果各部位腔隙性脑梗死患者注意力集中、执行功能得分均显著低于对照组，病变部位在小脑区的患者记忆得分显著低于其他各组，病变部位在大脑皮层的患者命名得分显著低于其他各组，病变部位在小脑区和脑干区的患者定向力得分显著低于其他各组。病变部位在内囊及基底节区、脑干区、大脑皮层区与小脑区的患者抽象思维和语言得分显著低于病变部位在丘脑区的患者和对照组。随访结果发现，各病变部位的患者在24个月随访的 MoCA 得分总分均显著低于急性期的得分。差异均有统计学意义（ P ﹤0.05）。结论老年腔隙性脑梗死患者存在认知功能障碍，其认知功能障碍与梗死的部位相关，且随着病变进展出现缓慢恶化的趋势。
文摘目的探讨非高密度脂蛋白(non-HDL-C)与腔隙性脑梗死(LI)认知障碍的关系。方法回顾性分析2017年1月~2018年11月就诊于我院神经内科符合LI诊断标准的患者171例,参照MoCA量表进行评分,分为认知障碍组和非认知障碍组,测量总胆固醇及高密度脂蛋白,并计算non-HDL-C水平。对non-HDL-C与LI认知障碍之间的关系进行Logistic多因素回归分析。结果调整潜在混杂因素后,与non-HDL-C最低四分位组相比,non-HDL-C最高四分位组患者认知障碍患病率较高[OR=3.806(95%CI):1.475~9.822,P=0.006]。随着non-HDL-C的增高,患者认知障碍可能进一步增加(P for trend=0.004)。结论Non-HDL-C与认知障碍呈现正相关,且随着non-HDL-C水平增高,认知障碍可能会出现增加的趋势。
