皮质下缺血性血管性认知损害患者注意功能障碍的临床研究

目的:观察皮质下缺血性血管性认知功能损害(SIVCI)患者注意亚型障碍的特征。方法:对30例非痴呆型SIVCI(SIVCIND)患者(SIVCIND组)、15例皮质下缺血性血管性痴呆(SIVD)患者(SIVD组)和15名健康志愿者(对照组)采用计算机上持续操作任务(CPT)、Stroop试验及双任务测试法测试持续注意、选择注意和分散注意功能。结果:与对照组比较,SIVD组CPT反应时延长,漏报率增加(P<0.05);SIVCIND组漏报率与对照组比较显著增加,差异有显著统计学意义(P<0.01)。SIVD患者冲突及中性条件下,反应时与错误率及干扰量均增加;SIVCIND患者Stroop试验冲突条件反应时延长(P<0.01)、双任务法耗时差无明显增加(P>0.05);SIVD患者耗时差增加(P<0.01)。结论:SIVCIND早期主要以持续:注意及选择注意功能损害为主,晚期则持续注意、选择注意和分散注意功能普遍受累。     

皮质下缺血性血管性认知损害的特点

目的 观察皮质下缺血性血管性认知损害(subcortical ischemic vascular cognitive impairment,SIVCI)患者各阶段认知损害特点,研究其神经心理学损害特征及可能的病理生理机制.方法 对45例SIVCI患者(其中30例非痴呆型皮质下缺血性认知损害患者、15例皮质下缺血性痴呆患者)和15名年龄、性别和教育程度匹配的正常对照,运用蒙特利尔认知测评量表和简易精神状态检查量表检测总体认知功能.结果 与对照组比较,非痴呆型皮质下缺血性认知损害组患者仅执行(2.70±1.34 vs 4.53±0.75)、注意(3.47±1.22 vs 5.07±0.78)和延迟回忆(3.00±1.11 vs 4.53±0.64)等认知功能水平降低 (P<0.05),抽象(1.33±0.72 vs 1.73±0.46)、定向(4.33±1.27 vs 5.20±0.77)、命名能力(2.10±0.80 vs 2.33±0.72)、语言重复及流畅性(2.07±0.69 vs 2.47±0.74)等认知功能水平无明显降低(P>0.05);皮质下缺血性痴呆组执行(1.87±1.06 vs 4.53±0.75)、注意(2.33±1.05 vs 5.07±0.78)、延迟回忆(1.80±1.27 vs 4.53±0.64)、抽象(0.93±0.88 vs 1.73±0.46)和定向(2.00±1.20 vs 5.20±0.77)等认知功能水平均降低(P<0.05),命名能力(1.87±1.74 vs 2.33±0.72)、语言重复及流畅性(1.93±0.70 vs 2.47±0.74)等认知功能水平无明显改变(P>0.05).结论 SICVI患者执行、注意、延迟回忆等皮质下认知功能较早受累且受损害程度较重,可能与缺血性小血管病变损害脑深部白质中认知纤维环路有关.     

皮质下缺血性脑血管病认知功能障碍研究

目的应用系列神经心理学测试分析皮质下缺血性脑血管病(SIVD)患者的认知损害特征。方法入选SIVD患者53例,年龄及性别相当的健康老年人25例为正常对照组。SIVD患者按照认知损害的诊断标准分为血管性痴呆(VaD)组27例和血管性认知障碍非痴呆(VCIND)组26例。进行MMSE及血管性痴呆包括记忆力、注意力、语言、视空间结构及执行功能5个认知域在内的神经心理学测试,确定VCIND患者受损的认知域。结果①与正常对照组比较,VaD组患者各项量表测试均严重受损,具有统计学差异(P﹤0.05);②VCIND组患者MMSE、数字倒背评分下降,连线测验时间延长,差异有统计学意义(P﹤0.05);③VaD组与VCIND组相比,上述各项均受损严重,其中单词回忆、连线测验、画钟测验、数字广度测验评分差异有统计学意义(P﹤0.05)。结论①SIVD患者同时存在多个认知域损害,以执行功能、注意力损害较为突出,记忆、语言受累相对较轻;②VCIND患者表现为执行功能、注意力受损,程度均低于VaD组,晚期VaD患者全面认知功能明显下降。     

皮质下缺血性脑血管病患者额叶白质病变对认知领域的损害研究

目的探讨皮质下缺血性血管病(SIVD)患者的额叶的白质病变(WML)累及的认知功能域。方法将50例SIVD患者,根据额叶WML评分的严重程度,分为严重WML组(视觉评分3分)27例和轻度WML组(视觉评分≤3分)23例。另以7例无SIVD的人群作为对照。对所有受试者进行全套的认知心理学测查并对结果进行对比分析。结果 3组间一般资料的差异无统计学意义。与轻度WML组和对照组相比,严重WML组的非额叶白质评分、额叶腔隙灶数目明显增多(均P=0.000);与轻度WML组相比,严重WML组的蒙特利尔认知评估量表评分明显降低(P=0.047);且执行功能相关的认知评分明显降低(P=0.006),在调整了额叶的腔隙灶数量后,该差异仍有统计学意义(P=0.038)。多元回归分析发现,对注意执行Z分显著影响的因素为额叶WML评分(P=0.000)。结论在SIVD患者中,额叶的WML主要累及执行功能。     

皮质下缺血性脑血管病的临床特点和危险因素

目的 研究皮质下缺血性脑血管病（SIVD）在缺血性卒中患者中的发病率、临床特点和危险因素。方法 门诊连续登记的526例发病3个月后的卒中患者入选该研究。对入选患者进行多种神经心理学和功能量表评定以及神经影像学评估,并记录人口学资料、卒中临床特点和血管危险因素。结果 526例患者中,SIVD患者110例（20.9%）,其中男性占61.8%,平均年龄66.8±10.5岁。高血压是最常见的危险因素（80.0%）,其次是血脂异常和吸烟史,分别为52.7%和40.9%,有57.3%的患者有2个以上的危险因素。32.7%的患者有抑郁障碍。用Lawton FAQ量表评定显示工具性日常生活能力下降的SIVD患者53人（48.0%）,用Barthel 指数（BI）测定显示日常生活能力下降者14人（12.8%）。49例（44.5%）有血管性认知功能损害,其中26例（23.6%）符合血管性痴呆标准。结论 缺血性卒中患者中,SIVD约占1/5,SIVD患者认知损害、抑郁、工具性日常生活能力受累较常见,并伴有多种危险因素。     

皮质下缺血性脑血管病的神经心理学改变

概述皮质下缺血性脑血管病(subcortical ischemic vascular diseases,SIVD)是造成血管性认知功能损害(vascular cognitive impairment,VCI)的重要原因,它所导致的认知损害是VCI中具有同质性和最为常见的亚型(皮质下型VCI)。VCI覆盖了从轻微的     

缺血性额叶白质病变的认知功能损害研究

目的探讨皮质下缺血性血管病患者额叶白质病变对认知功能的影响。方法回顾性收集2013年1月至2015年1月期间我科住院诊断为皮质下缺血性脑血管病患者121例,根据额叶白质病变程度,将皮质下缺血性脑血管病患者分为轻度(67例)和重度(54例)脑白质病变组。同时选择同年龄段60例健康、无认知障碍者为对照组;所有受试者均为右利手,且母语均为中文。对三组受试者进行神经心理量表测定,评估其认知功能、记忆功能及执行功能,并对额叶白质病变的程度与认知功能进行非参数等级相关分析。结果与轻度脑白质病变组和对照组相比,重度脑白质病变组的MMSE评分、AVLT评分、ROCF评分及Stroop评分明显降低,P值均0.05。患者MMSE评分与脑白质病变损害严重程度呈正相关(R=0.933,P=0.013),即脑白质病变的严重程度与认知障碍程度呈正相关。结论皮质下缺血性脑血管病患者,额叶的脑白质主要累及认知功能、记忆功能及执行功能,且脑白质病变的严重程度与认知障碍程度呈正相关。     

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。     

线性法测量皮质下缺血性血管病患者脑萎缩及其与认知损害的相关性分析

目的通过线性法测量皮质下缺血性血管病(SIVD)患者脑萎缩,分析其与认知功能损害的相关性。方法共纳入SIVD组50例,健康对照组50例。所有入组对象均完成一般情况评定、Mo CA量表评估认知功能、头颅MRI检查,线性法进行脑萎缩测量。结果 SIVD组代表脑室系统横径的测量值及脑沟测量值,除桥池宽度外,均较对照组显著增大(P 0. 05)。SIVD组的脑萎缩测量相对值除脑干指数外,均显著高于对照组(P 0. 05)。SIVD组双侧侧脑室两额角间最宽距离、双侧侧脑室额角两侧尾状核头间最小距离、第三脑室宽度、双侧侧脑室腰部外侧壁最小距离与Mo CA评分呈显著负相关(P 0. 05)。SIVD组脑萎缩测量相对值中的额角指数、尾状核指数、哈氏值、第三脑室宽度与视空间能力、计算力、延迟记忆和定向力均呈负相关(P 0. 05)。结论 SIVD患者存在明显的皮质和皮质下萎缩,并与认知功能损害相关。哈氏值、额角指数、尾状核指数、第三脑室宽度可作为SIVD患者脑萎缩的预测指标,提示执行功能/视空间及计算力、记忆力的损害。     

脑萎缩对皮质下缺血性血管病患者认知损害的影响

皮质下缺血性血管病(SIVD)是最常见、最具有特征性的血管性认知功能损害的亚型之一。近年来,越来越多的研究提示脑萎缩与SIVD患者的认知损害相关,且脑萎缩可能成为SIVD结构影像学诊断依据之一。本文就脑萎缩对SIVD患者认知损害的影响进行综述。     

半自动MRI定量方法测定脑白质高信号体积与病变定性评分的相关性

背景：在磁共振T2加权像和液体衰减反转恢复像中脑白质病变表现为白质高信号,目前对脑白质高信号体积、部位与认知功能损害的关系仍存在争议。 目的：以头颅磁共振对皮质下缺血性脑血管病患者白质高信号进行定量和定性测定,分析高信号体积和部位与认知损害的关系。 设计、时间及地点：于2007-12/2008-09在河北省人民医院神经内科完成。 对象：依据影像学诊断标准确定皮质下缺血性脑血管病53例,记录症状和体征,并进行神经心理学评估。 方法：采用美国GE公司生产的半自动1.5T MRI机对患者行头MRI扫描,定量测定脑白质高信号体积,并结合脑白质病变定性评分。 主要观察指标：分析皮质下缺血性脑血管病患者脑白质高信号体积与评分的相关性,以及白质病变与认知损害的关系。 结果：脑白质高信号体积和评分高度相关（rs=0.989, P < 0.001）,两者呈曲线关系。分层多元线性回归分析显示,白质高信号体积、白质高信号总评分的变化可以分别解释简明精神状态检查评分改变的10.5%和6.8%,前者较后者能更敏感地预测简明精神状态检查评分变化。不同区域脑白质病变中,仅基底核区白质高信号评分与简明精神状态检查评分有关（t=-2.126, P=0.039）,其他各区域白质高信号评分均非简明精神状态检查评分独立预测指标。 结论：脑白质高信号体积与评分均可应用于脑白质病变的测定,前者测定较脑白质高信号评分更敏感;皮质下缺血性脑血管病患者认知功能损害随着脑白质病变的增多,尤其是基底核区白质病变的增多而加重。     

THE PREVALENCE OF DEMENTIA AND COGNITIVE IMPAIRMENT INCHINA

Early studies of the prevalence of dementia and cognitive impairment in China indicated low rates, but more recently rates have been rising to the levels shown in other countries. Reasons for these changes are discussed.     

血管性认知功能障碍患者经颅多普勒超声血流动力学变化与认知功能的关系

目的探讨轻度血管性认知功能障碍(m VCI)患者TCD血流动力学变化与认知功能的关系。方法依据Erkinjuntti的MRI诊断标准入选的皮质下缺血性血管病(SIVD)患者115例,根据神经心理学评估分为血管性认知障碍(VCI)组和认知正常组。使用经颅多普勒超声(TCD)进行颅内血流动力学检查。最后分析患者的Mo CA评分与大脑中大动脉(MCA)和大脑前动脉(ACA)的搏动指数(PI)、平均血流(Vm)的相关性。结果对于两组患者的MCA-PI和ACA-PI进行比较,差异具有统计学意义(P0.05);而两组患者之间的MCA-Vm和ACA-Vm比较,差异无统计学意义(P0.05)。MCA-PI和SIVD患者的认知损害呈线性相关,回归方程Y=38.783-7.823 X_1,差异有统计学意义(P0.01)。结论 MCA-PI与SIVD患者Mo CA评分线性相关。SIVD患者的PI越高,相对应其认知障碍程度越严重。     

Clinical significance of subcortical vascular disease in patients with mild cognitive impairment

Patients with mild cognitive impairment (MCI) typically present with memory complaints. Some of these patients have subcortical vascular disease on computed tomography (CT) scan, namely white matter changes and lacunar infarcts, however it is not known whether these findings are associated with more pronounced cognitive deficits. In the present study we compare demographic, clinical and neuropsychological characteristics of MCI patients according to the presence or the absence of subcortical vascular disease. Forty consecutive patients with memory complaints, at least one neuropsychological memory test below 1 SD the normal for age and education, and maintained activities of daily living, were included. Patients with dementia, history of stroke or transient ischemic attack, or other brain disorders, were excluded. Twenty-five (62.5%) patients with MCI had no ischemic lesions on CT scan, and 15 (37.5%) were found to have subcortical vascular changes. MCI patients with subcortical vascular changes were older (77.1 +/- 6.8 vs. 70.8 +/- 7.5 years old), and more often males. The number of vascular risk factors, the frequency of neurological signs, the Hachinski score and the neuropsychological tests scores were not significantly different. The presence of subcortical vascular disease on CT scan is frequent in older patients with MCI, but does not appear to be associated with the severity of cognitive deficits.     

The Gothenburg MCI study: Design and distribution of Alzheimer’s disease and subcortical vascular disease diagnoses from baseline to 6-year follow-up

There is a need for increased nosological knowledge to enable rational trials in Alzheimer’s disease (AD) and related disorders. The ongoing Gothenburg mild cognitive impairment (MCI) study is an attempt to conduct longitudinal in-depth phenotyping of patients with different forms and degrees of cognitive impairment using neuropsychological, neuroimaging, and neurochemical tools. Particular attention is paid to the interplay between AD and subcortical vascular disease, the latter representing a disease entity that may cause or contribute to cognitive impairment with an effect size that may be comparable to AD. Of 664 patients enrolled between 1999 and 2013, 195 were diagnosed with subjective cognitive impairment (SCI), 274 with mild cognitive impairment (MCI), and 195 with dementia, at baseline. Of the 195 (29%) patients with dementia at baseline, 81 (42%) had AD, 27 (14%) SVD, 41 (21%) mixed type dementia (=AD + SVD = MixD), and 46 (23%) other etiologies. After 6 years, 292 SCI/MCI patients were eligible for follow-up. Of these 292, 69 (24%) had converted to dementia (29 (42%) AD, 16 (23%) SVD, 15 (22%) MixD, 9 (13%) other etiologies). The study has shown that it is possible to identify not only AD but also incipient and manifest MixD/SVD in a memory clinic setting. These conditions should be taken into account in clinical trials.     

Modeling subcortical ischemic white matter injury in rodents: unmet need for a breakthrough in translational research

Subcortical ischemic white matter injury(SIWMI), pathological correlate of white matter hyperintensities or leukoaraiosis on magnetic resonance imaging, is a common cause of cognitive decline in elderly. Despite its high prevalence, it remains unknown how various components of the white matter degenerate in response to chronic ischemia.This incomplete knowledge is in part due to a lack of adequate animal model. The current review introduces various SIWMI animal models and aims to scrutinize their advantages and disadvantages primarily in regard to the pathological manifestations of white matter components. The SIWMI animal models are categorized into 1) chemically induced SIWMI models, 2) vascular occlusive SIWMI models, and 3) SIWMI models with comorbid vascular risk factors. Chemically induced models display consistent lesions in predetermined areas of the white matter, but the abrupt evolution of lesions does not appropriately reflect the progressive pathological processes in human white matter hyperintensities. Vascular occlusive SIWMI models often do not exhibit white matter lesions that are sufficiently unequivocal to be quantified. When combined with comorbid vascular risk factors(specifically hypertension), however, they can produce progressive and definitive white matter lesions including diffuse rarefaction, demyelination, loss of oligodendrocytes, and glial activation, which are by far the closest to those found in human white matter hyperintensities lesions. However, considerable surgical mortality and unpredictable natural deaths during a follow-up period would necessitate further refinements in these models. In the meantime, in vitro SIWMI models that recapitulate myelinated white matter track may be utilized to study molecular mechanisms of the ischemic white matter injury. Appropriate in vivo and in vitro SIWMI models will contribute in a complementary manner to making a breakthrough in developing effective treatment to prevent progression of white matter hyperintensities.