CAJ | 학술논문

目的采用基于体素的分析(VBA)方法研究遗忘型轻度认知障碍(aMCI)患者和轻度阿尔茨海默病(AD)患者全脑白质微观结构改变的特点及其与灰质萎缩模式的关系.方法选取33例aMCI患者(aMCI组)、32例轻度AD患者(轻度AD组)和31名正常老年人(健康对照组),对全脑进行3.0 T DTI及三维快速扰相梯度反转回波(3DFSPGR)脉冲序列扫描.采用统计参数图(SPM)5软件对被试者的结构图像及各向异性(FA)图进行预处理,然后采用t检验对aMCI组、轻度AD组和正常对照组的全脑灰质体积及FA值进行基于体素的统计学比较,计算出有统计学意义的脑区.结果与正常对照组比较,aMCI组的双侧额颞叶和左侧枕叶白质、左侧扣带前部、左侧顶下小叶、右侧脑室三角区外上方白质的FA值减低;轻度AD组的双侧额颞枕叶、海马旁白质、扣带前部、胼胝体、侧脑室三角区旁白质、顶下小叶、左侧颞于、左侧丘脑、右侧楔前叶FA值减低.基于体素的形态测量学(VBM),分析发现,aMCI患者组左侧海马、海马旁回、舌回、颞上回,双侧岛叶、颞中回出现了灰质萎缩;轻度AD患者组双侧海马、海马旁回、杏仁核、丘脑、额叶、颞叶、顶叶、枕叶皮质出现了灰质萎缩.aMCI与轻度AD患者组全脑白质FA值减低的模式与灰质萎缩模式不同.aMCI组与轻度AD组比较未发现具有统计学意义的FA值减低脑区.aMCI、轻度AD患者组全脑白质FA值与简易智能精神状态检查量表(MMSE)评分没有相关性.结论基于体素的MR DTI全脑白质分析能够较全面、客观地揭示aMCI、轻度AD的脑白质损害的模式.aMCI、轻度AD患者白质损害的模式与灰质不同,提示脑白质病变是多种病理机制导致的.aMCI患者向轻度AD进展过程中,脑白质各向异性改变不显著,脑白质FA值的改变可能无法反映患者认知功能障碍的严重程度.
목적 채용기우체소적분석(VBA)방법연구유망형경도인지장애(aMCI)환자화경도아이자해묵병(AD)환자전뇌백질미관결구개변적특점급기여회질위축모식적관계.방법 선취33례aMCI환자(aMCI조)、32례경도AD환자(경도AD조)화31명정상노년인(건강대조조),대전뇌진행3.0 T DTI급삼유쾌속우상제도반전회파(3DFSPGR)맥충서렬소묘.채용통계삼수도(SPM)5연건대피시자적결구도상급각향이성(FA)도진행예처리,연후채용t검험대aMCI조、경도AD조화정상대조조적전뇌회질체적급FA치진행기우체소적통계학비교,계산출유통계학의의적뇌구.결과 여정상대조조비교,aMCI조적쌍측액섭협화좌측침협백질、좌측구대전부、좌측정하소협、우측뇌실삼각구외상방백질적FA치감저;경도AD조적쌍측액섭침협、해마방백질、구대전부、변지체、측뇌실삼각구방백질、정하소협、좌측섭우、좌측구뇌、우측설전협FA치감저.기우체소적형태측량학(VBM),분석발현,aMCI환자조좌측해마、해마방회、설회、섭상회,쌍측도협、섭중회출현료회질위축;경도AD환자조쌍측해마、해마방회、행인핵、구뇌、액협、섭협、정협、침협피질출현료회질위축.aMCI여경도AD환자조전뇌백질FA치감저적모식여회질위축모식불동.aMCI조여경도AD조비교미발현구유통계학의의적FA치감저뇌구.aMCI、경도AD환자조전뇌백질FA치여간역지능정신상태검사량표(MMSE)평분몰유상관성.결론 기우체소적MR DTI전뇌백질분석능구교전면、객관지게시aMCI、경도AD적뇌백질손해적모식.aMCI、경도AD환자백질손해적모식여회질불동,제시뇌백질병변시다충병리궤제도치적.aMCI환자향경도AD진전과정중,뇌백질각향이성개변불현저,뇌백질FA치적개변가능무법반영환자인지공능장애적엄중정도.
Objective To evaluate the microstructural integrity of white matter (WM) in patients with amnestic mild cognitive impairment (aMCI) and mild Alzheimer's disease (AD) using voxel-based analysis (VBA), and investigate the relationship between WM abnormalities and gray matter(GM) atrophy.Methods Thirty-three cases with aMCI, 32 cases with mild AD and 31 normal aging volunteers as control subjects were scanned on a 3.0 T MR system using diffusion tensor imaging (DTI) and three-dimensional spoiled gradient-recalled(3DSPGR) sequences. Fractional anisotropy (FA) maps and morphological images were preprocessed by SPM5 and voxel-based comparisons between the 2 patient groups and the control group were performed by t test. Results Relative to the control group, patients with aMCI showed significantly reduced FA value in bilateral frontal, temporal and left occipital WM, left anterior part of cingulum, left inferior parietal lobule, and the W M adjacent to the triangular part of the right lateral ventricle(k≥20 voxels).In mild AD,significantly reduced FA value was found in bilateral hippocampal,inferior parietal lobular,frontal,temporal,and occipital WM,bilateral corpus callosum,anterior part of cingulums,the WM adjacent to the triaangular part of the bilateral lateral ventricles,left temporal stem,left thalamus,right precuneus(k≥20 voxels).Significantly reduced GM volume was found in left hippocampus,parahippocampal gyrus,lingual gyrus and superior temporal gyrus,bilateral insulae and middle temporal gyri in aMCl group whencompared with control group(k≥50 voxels).In mild AD,significantly reduced GM volume was found in bilateral hippoeampi,parahippocampal gyri,amygdalae,thalami,temporal,parietal,frontal,occipital cortex(k≥50 voxels).The pattern of areas with reduced FA differs;from that of the GM volumetric reduction.No areas with significantlv reduced FA was detected in aMCl compared with mild AD. There was no significant correlation between FA value of WM in patient groups and Mini-Mental State Examination(MMSE)scores.Conclusions Voxel-based MRI DTI analysis of whole brain white matter can objectively reveal widespread white matter abnormalities in early-stage AD.The difierence between WM FA reduction pattern and GM volumetric reduction pattern indicates that the pathological WM changes in earlyslage AD were caused by multiple mechanisms. FA did not vary significantly in patients pr0gressing from aMCI to mild AD and can hardly reflect the severitv of cognitive function damage in these patients.