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。     

健康老年人脑白质病变体积与认知障碍的关系

目的通过利用半自动化分析软件对脑白质病变患者不同区域白质损伤(f MRI序列上的高信号)进行定量,并对其与认知功能评分进行分析,探讨脑白质病变体积与认知障碍的关系。方法选取承德市中心医院门诊"健康"人群75例。采用简易智能状态检查量表(MMSE)及蒙特利尔认知评价量表(MoCA)对其进行认知功能评价。基于FLAIR定量计算全脑、侧脑室旁及深部皮质下脑白质受损体积,将认知功能评分与以上白质受损体积进行偏相关分析。将脑白质病变患者分为轻度认知障碍组和对照组,比较两组认知障碍特点。结果控制年龄、性别、文化程度后,全脑白质体积与认知功能评分MoCA有偏相关性(r=-0. 541,P=0. 001),尤其是侧脑室旁白质体积(r=-0. 518,P=0. 000),与深部白质也存在偏相关性(r=-0. 312,P=0. 025);全脑白质体积与认知功能评分MMSE(r=-0. 303,P=0. 033),侧脑室旁体积与认知功能评分MMSE (r=-0. 330,P=0. 019)及深部白质损伤体积(r=-0. 257,P=0. 039)。脑白质病变体积认知障碍组与对照组在执行功能及视空间(P=0. 003)、注意力(P=0. 041)、语言(P=0. 040)及记忆力(P=0. 000)方面评分差异具有明显统计学意义(P 0. 05)。结论全脑、侧脑室旁、皮质下脑白质损伤体积增大,认知功能评分随之下降;全脑白质体积与MoCA的相关性比与MMSE相关性大;而且,侧脑室旁体积与深部白质损伤体积相比,与认知功能的相关性更大。脑白质病变体积引起轻度认知障碍主要表现在执行功能、注意力、视空间及记忆力方面。     

皮质下缺血性脑血管病白质改变与认知损害初探

目的:对皮质下缺血性脑血管病(SIVD)的临床特征、认知和MRI白质改变进行分析,初步探讨SIVD患者认知损害与MRI白质改变的关系。方法:经过访谈和详细查体,记录患者症状和体征,进行神经心理学评估并行头MRI扫描。依据Erkinjuntti提出MRI诊断标准确定SIVD患者29例。结果:认知正常者、血管性CIND患者和VaD患者的MMSE得分分别为(27.5±1.84)、(23.7±2.06)和(18±1.58)。随着认知功能损害程度的加重,其白质改变的评分增加,具有统计学显著差异。结论:SIVD患者的认知功能损害与其白质改变程度有关。     

缺血性脑白质病变与认知功能障碍的相关性研究

目的探缺血性脑白质病变与认知障碍的关系，为血管性痴呆的预防、早期诊断和治疗提供理论依据。方法选择138例经颅脑MRI证实的脑白质病变患者，并分为缺血性脑白质病变组和非缺血性脑白质病变组，分别进行简易智能状态检查量表（MMSE）评估比较，并对白质病变进行分级，进行组内及两组患者认知功能严重程度比较。结果缺血性白质病变组认知功能障碍发生率及Ⅱ、Ⅲ段白质病变者的认识功能障碍的严重程度明显高于非缺血性白质病变组；组内比较缺血性白质病变组和非缺血性白质病变组认知功能障碍与白质病变严重分级呈正相关，而二者无明显关系。结论缺血性白质病及其严重程度对认知功能障碍的发生及严重程度有显著影响，而非缺血性白质病则对认知功能障碍影响较小。     

CADASIL的临床、影像学特征及其诊断策略(附2例报道)

目的 探讨常染色体显性遗传性脑动脉病伴皮质下梗死和白质脑病(CADASIL)的临床表现及影像学特征和确诊的要素。方法 系统回顾分析经皮肤及肌肉活检或基因检测确诊的2例CADASIL的临床及影像学资料。结果 例1临床表现为进行性记忆障碍,例2临床表现为脑缺血性卒中样发作,2例均无通常的脑血管疾病的危险因素,脑MRI T₂W及FLAIR序列均显示两侧脑室周围及深部脑白质、外囊及前颞区对称性分布的高信号,例1皮肤活检发现在血管壁平滑肌细胞基膜层有嗜锇颗粒(GOM)沉积; 例2基因检测显示Notch3基因外显因子4,c.544C>T位点突变。结论 如若患者具有进行性认知损害、反复缺血性脑卒中样发作等临床表现,且无通常的脑血管病的危险因素,磁共振检查显示两侧脑白质对称性异常信号时,应考虑CADASIL的可能,此时进行皮肤或肌肉活检及/或基因检测有助确诊。     

脑白质高信号伴认知功能障碍患者胆碱能通路损伤与皮质结构改变的关系研究

目的探讨脑白质高信号伴不同程度认知损害患者的胆碱能通路损伤与大脑皮质结构改变之间的关系。方法以2016年3月至2018年12月80例脑白质高信号患者为研究对象,根据蒙特利尔认知评价量表(MoCA)和临床痴呆评价量表(CDR)分为脑白质高信号不伴认知损害组(WMH-CN组,43例)、脑白质高信号伴非痴呆型血管性认知损害组(WMH-VCIND组,21例)和脑白质高信号伴血管性痴呆组(WMH-VaD组,16例),胆碱能通路高信号量表(CHIPS)评价胆碱能通路中白质损害程度;MRI标记胆碱能通路中34个大脑皮质兴趣区(ROI),测量层厚和体积。Spearman秩相关分析和偏相关分析探讨左侧和右侧大脑半球CHIPS总评分与同侧皮质兴趣区层厚和体积的相关性。结果 (1)WMH-CN组、WMH-VCIND组和WMH-VaD组患者全脑(P=0.023)、左侧大脑半球(P=0.039)和右侧大脑半球(P=0.004)CHIPS评分差异有统计学意义,其中,WMH-VCIND组(P=0.002,0.000,0.001)和WMH-VaD组(P=0.000,0.003,0.000)3个脑区CHIPS评分均高于WMH-CN组,WMH-VaD组3个脑区CHIPS评分亦高于WMH-VCIND组(P=0.008,0.013,0.020)。(2)脑白质高信号患者与正常对照者左侧大脑半球皮质兴趣区层厚(P=0.000)和体积(P=0.000)、右侧大脑半球皮质兴趣区层厚(P=0.000)差异均有统计学意义,其中,WMH-CN组、WMH-VCIND组和WMH-VaD组左侧兴趣区层厚(均P=0.000)和体积(均P=0.000)、右侧兴趣区层厚(均P=0.000)均低于正常对照组;WMH-VaD组左侧兴趣区层厚高于WMH-CN组(P=0.000)和WMH-VCIND组(P=0.036),WMH-CN组左侧兴趣区体积高于WMH-VCIND组(P=0.033)、低于WMH-VaD组(P=0.025),WMH-VCIND组(P=0.001)和WMH-VaD组(P=0.000)右侧兴趣区层厚均高于WMH-CN组。(3)相关分析仅WMH-VCIND组患者左侧大脑半球CHIPS评分与同侧皮质兴趣区层厚呈正相关(r=0.439,P=0.047)。结论脑白质高信号伴认知功能障碍患者随着认知功能障碍的加重,左侧大脑半球胆碱能通路中34个大脑皮质兴趣区体积和层厚均有一定程度的下降,且皮质结构改变与左侧大脑半球胆碱能通路损害程度呈正相关,但上述结构改变在右侧大脑半球并不明显。     

脑梗死相关白质疏松患者磁共振波谱与认知功能关系的研究

目的研究脑梗死患者白质疏松的磁共振波谱表现特点,以及白质疏松的磁共振波谱与认知功能的关系,为血管性认知功能障碍的早期识别及防治提供依据。方法选择51例脑梗死伴白质疏松患者及21例非白质疏松者进行简易智能状态测验(MMSE)、画钟试验测试、Fuld物体记忆测验(FOM)、快速词汇测验(RVR)及WAIS数字广度测验;同时行头颅磁共振成像(MRI)及双侧额叶白质的磁共振波谱(MRS)检查,测定N-乙酰天门冬氨酸(NAA)、肌酸(Cr)及胆碱(Cho)的浓度。分析白质疏松的MRS表现特点及其与认知功能障碍的关系。结果重度脑白质疏松组Cho/Cr值明显高于无、轻及中度疏松组;Cho/Cr值与白质疏松程度呈正相关;左侧额叶白质NAA/Cr值与MMSE评分及画钟试验评分正相关;右侧Cho/Cr值与WAIS数字广度测验评分负相关。结论双侧额叶白质区MRS改变主要为Cho/Cr值升高,并且与白质疏松程度正相关。血管性认知障碍与双额叶白质区神经纤维损害不一定完全一致。     

伴皮质下梗死和白质脑病的常染色体显性遗传性脑动脉病的临床特点(附1家系报告)

目的 探讨伴皮质下梗死和白质脑病的常染色体显性遗传性脑动脉病(CADASIL)的临床特点.方法 对1例CADASIL患者及其家系的临床资料进行回顾性分析.结果 先证者以大脑皮质下梗死起病,伴有渐进性认知功能障碍.头颅MRI示皮质下多发梗死灶,脑白质疏松.NOTHC3基因检测为第3号外显子Arg110Cys突变,家系调查显示为常染色体显性遗传.结论 CADASIL临床表现主要为缺血性卒中、认知障碍、偏头痛及精神症状.MRI特征性改变是颞极白质T2的异常高信号.NOTCH3基因检查发现突变.     

缺血性脑卒中患者抑郁状态与影像学改变的关系

目的探讨缺血性脑卒中患者抑郁状态与卒中部位、病灶体积及脑白质病变之间的关系。方法对59例缺血性脑卒中患者随访12～18个月(平均13个月),采用24项Hamilton抑郁量表(HAMD)对患者进行评分,得分<8分为无抑郁症状,8～17分为抑郁状态,>17分为抑郁。于入组及随访结束时分别行头颅磁共振成像(MRI)及Hamilton评分检查。结果抑郁的发生与患者脑深部白质病变(DWML)、脑室周围白质病变(PWML)的程度无关及卒中病灶部位无关(P均>0.05),且与随访期间新发病灶无关(P>0.05),与病灶体积亦无关(P>0.05)。结论缺血性脑卒中患者卒中后抑郁的发生与卒中病灶部位及脑白质病变程度无关。     

脑卒中患者白质高信号体积变化与认知功能的相关性

目的 探讨脑卒中患者白质高信号体积变化与认知功能的相关性。方法 2020年7月-2021年1月139例脑卒中患者为研究对象,采用蒙特利尔认知评估量表(MoCA)及MRI评估患者基线认知功能及白质高信号体积,随访1年后,再次收集患者认知功能情况及白质高信号体积,分析脑卒中患者白质高信号体积变化情况及认知功能情况,并根据患者认知功能情况分为正常组和障碍组,探讨白质高信号体积变化与患者认知功能降低的相关性。结果 139例患者随访1年后,共9例失访,最终纳入130例脑卒中患者,46.15%(60/130)的脑卒中患者白质高信号体积进展,23.85%(31/130)患者白质高信号体积改善,30.00%(39/130)白质高信号体积保持稳定。其中53例患者出现认知功能障碍为障碍组,77例为认知功能正常组。两组患者年龄、性别等一般资料比较差异无统计学意义(P> 0.05),白质高信号体积变化障碍组高于正常组(P<0.05),Pearson相关性分析显示,脑卒中患者白质高信号体积变化与患者认知功能评分呈负相关(P<0.05)。结论 脑卒中后患者白质高信号体积变化多呈进展趋势,并与患者...     

Diffusion tensor quantification of the relations between microstructural and macrostructural indices of white matter and reading

Few researchers agree about the relationship between fronto–temporo–parietal white matter microstructure and reading skills. Unlike many previous reports, which only measured fractional anisotropy, we have also measured macroscopic volume (regional white matter tract volume) and three microstructural indices (axial, radial, and mean diffusivity) to increase interpretability of our findings. We examined the reading‐related skills and white matter structure in 10 adolescents and adults with a history of poor reading and 20 age‐matched typical readers. We applied a diffusion tensor imaging atlas‐based algorithm to major white matter pathways. The relation of white matter structural indices to reading group, hemisphere, and reading‐related skill was analyzed using linear models. White matter microstructural indices were related to performance on a sublexical decoding task, but the relations between particular microstructural indices and sublexical decoding ability and reading group were different for association (i.e., cortical–cortical) and projection (i.e., subcortical–cortical) white matter pathways. Changes in projection pathways were consistent with alterations in white matter organization and axonal size, whereas changes in association pathways were consistent with alternations in pathway complexity. Changes in macrostructure paralleled changes in microstructure. We conclude that the relations between several microstructural indices and factors related to reading ability are different for association and projection pathways. Hum Brain Mapp, 2011. © 2010 Wiley‐Liss, Inc.     

脑白质病变临床特点与白质传导束关系研究进展

脑白质病变(WML)是脑小血管病的一种,与年龄、高血压等血管危险因素相关。WML与脑卒中、记忆、语言、步态及情绪等有密切联系,而且其进展预示着临床预后较差。利用MR微细结构成像技术了解到脑白质传导束的病变与其多样化的临床表现相关。MRI技术为WML的病理生理机制提供了依据,为进一步了解WML多样化临床表现提供了新视角。     

缺血性脑白质病变的研究进展

缺血性脑白质病变是最常见的白质脑病类型之一。文章就其危险因素、发病机制、遗传学、临床表现、影像学、治疗等方面的进展做一综述。     

Brain maps 4.0—Structure of the rat brain: An open access atlas with global nervous system nomenclature ontology and flatmaps

The fourth edition (following editions in 1992, 1998, 2004) of Brain maps: structure of the rat brain is presented here as an open access internet resource for the neuroscience community. One new feature is a set of 10 hierarchical nomenclature tables that define and describe all parts of the rat nervous system within the framework of a strictly topographic system devised previously for the human nervous system. These tables constitute a global ontology for knowledge management systems dealing with neural circuitry. A second new feature is an aligned atlas of bilateral flatmaps illustrating rat nervous system development from the neural plate stage to the adult stage, where most gray matter regions, white matter tracts, ganglia, and nerves listed in the nomenclature tables are illustrated schematically. These flatmaps are convenient for future development of online applications analogous to “Google Maps” for systems neuroscience. The third new feature is a completely revised Atlas of the rat brain in spatially aligned transverse sections that can serve as a framework for 3‐D modeling. Atlas parcellation is little changed from the preceding edition, but the nomenclature for rat is now aligned with an emerging panmammalian neuroanatomical nomenclature. All figures are presented in Adobe Illustrator vector graphics format that can be manipulated, modified, and resized as desired, and freely used with a Creative Commons license.     

Heterogeneity of microglia and their differential roles in white matter pathology

Microglia are resident immune cells that play multiple roles in central nervous system (CNS) development and disease. Although the classical concept of microglia/macrophage activation is based on a biphasic beneficial‐versus‐deleterious polarization, growing evidence now suggests a much more heterogenous profile of microglial activation that underlie their complex roles in the CNS. To date, the majority of data are focused on microglia in gray matter. However, demyelination is a prominent pathologic finding in a wide range of diseases including multiple sclerosis, Alzheimer's disease, and vascular cognitive impairment and dementia. In this mini‐review, we discuss newly discovered functional subsets of microglia that contribute to white matter response in CNS disease onset and progression. Microglia show different molecular patterns and morphologies depending on disease type and brain region, especially in white matter. Moreover, in later stages of disease, microglia demonstrate unconventional immuno‐regulatory activities such as increased phagocytosis of myelin debris and secretion of trophic factors that stimulate oligodendrocyte lineage cells to facilitate remyelination and disease resolution. Further investigations of these multiple microglia subsets may lead to novel therapeutic approaches to treat white matter pathology in CNS injury and disease.     

Topographic correspondence between white matter hyperintensities and brain atrophy

White matter hyperintensities (WMHs) are a common finding in normal elderly persons. We studied the biological damage associated with WMHs by assessing the correspondence between WMH location and regional gray matter loss.Voxel–based morphometry of the gray matter was carried out with statistical parametric mapping on high resolution MR images.Neurologically intact persons with mainly anterior (frontal>parieto–occipital; N = 39) and mainly posterior WMHs (parieto– occipital>frontal; N = 14) were compared with a group devoid of WMHs (N = 80). Subjects with mainly frontal WMHs had bilateral frontal (medial, superior, and inferior gyri) atrophy in gray matter, while subjects with mainly posterior WMHs had more diffuse atrophy, involving mainly the frontal but also the right insular region. Our findings suggest that frontal WMHs are associated with frontal gray matter damage while parietooccipital WMHs seem to have a weaker and more diffuse impact on gray matter.     

Associations between T1 white matter lesion volume and regional white matter microstructure in aging

White matter lesions, typically manifesting as regions of signal intensity abnormality (WMSA) on MRI, increase in frequency with age. However, the role of this damage in cognitive decline and disease is still not clear, as lesion volume has only loosely been associated with clinical status. Diffusion tensor imaging (DTI) has been used to examine the quantitative microstructural integrity of white matter, and has applications in the examination of subtle changes to tissue that appear visually normal on conventional imaging. The primary goal of this study was to determine whether major macrostructural white matter damage, (total WMSA volume), is associated with microstructural integrity of normal appearing white matter, and if these macrostructural changes fully account for microstructural changes. Imaging was performed in 126 nondemented individuals, ages 43–85 years, with no history of cerebrovascular disease. Controlling for age, greater WMSA volume was associated with decreased fractional anisotropy (FA) in widespread brain regions. Patterns were similar for FA and radial diffusivity but in contrast, WMSA was associated with axial diffusivity in fewer areas. Age was associated with FA in several regions, and many of these effects remained even when controlling for WMSA volume, suggesting the etiology of WMSAs does not fully account for all age‐associated white matter deterioration. These results provide evidence that WMSA volume is associated with the integrity of normal‐appearing white matter. In addition, our results suggest that overt lesions may not account for the association of increasing age with decreased white matter tissue integrity. Hum Brain Mapp 35:1085–1100, 2014. © 2013 Wiley Periodicals, Inc.