首页> 中文期刊> 《中国神经免疫学和神经病学杂志》 >脑梗死性共济失调患者手指运动的 BOLD-fM RI 定量研究

脑梗死性共济失调患者手指运动的 BOLD-fM RI 定量研究

         

摘要

目的:运用全脑血氧水平依赖性磁共振脑功能成像(BOLD‐fMRI)技术,定量研究脑梗死所致共济失调患者手共济运动中枢的脑功能情况。方法健康右利手志愿者(对照组)和脑梗死所致共济失调患者(脑梗死组)进行主动与被动复杂对指运动,同时行全脑BOLD‐fM RI检查比较两组相应脑运动功能区对侧感觉运动区(SMC)和同侧小脑的激活体积和强度。结果对照组主动和被动对指运动时右手激活对侧 SMC 体积(1373.7±509.6 vs .726.8±299.2,t=3.482, P=0.002;1531.2±455.3 vs .539.2±272.7, t=3.761, P=0.001)和强度(9.8±3.2 vs .7.9±6.1,t=2.132,P=0.041;11.3±5.1 vs .10.1±9.7,t=2.256,P=0.032)均大于左手;脑梗死组右手为患手时主动及被动对指运动时激活对侧SMC的体积(605.8±408.2 vs .452.7±213.5,t=2.491,P=0.020;397.2±248.7 vs .311.2±158.3,t=2.681,P=0.013)、强度(9.5±2.7 vs .7.6±5.0,t=2.372,P=0.031;7.9±6.1 vs .5.0±4.7,t=2.482,P=0.023)均低于对照组;脑梗死组左手为患手时主动及被动对指运动时激活对侧SMC的体积(1399.7±209.6 vs .689.5±422.7,t=2.846,P=0.010;3551.2±495.3 vs .413.6±264.2,t=3.072,P=0.007)、强度(11.3±5.1 vs .7.2±3.1,t=2.279,P=0.032;10.1±9.7 vs .6.1±3.9,t=2.811,P=0.016)亦均低于对照组;脑梗死组患手主动运动及被动运动激活同侧小脑的体积(932.5±2016.2 vs .61.8±214.0,t=2.441,P=0.021;197.6±297.4 vs .37.2±19.0,t=3.124,P=0.004)、强度(15.0±3.2 vs .6.7±1.8,t=3.001,P=0.005;13.8±2.9 vs .6.3±1.7,t=2.121,P=0.032)均小于对照组。结论脑梗死所致共济失调患者主要以对侧SMC及同侧小脑的功能受损为主。%Objective BOLD fMRI was used to make a quantitative analysis of brain function of hand coordination movement center among cerebral infarction patients with ataxia .Methods Healthy volunteers of right‐handed (the control group) and cerebral infarction patients with ataxia (the cerebral infarction group) were respectively selected to scan the mode of whole‐brain BOLD‐fMRI while they were performing complex active and passive finger to finger movement . The corresponding motor cortex ’ s active volume and intensity were recorded .Results In the control group ,contralateral sensorimotor area (SMC ) volume (1373.7 ± 509.6 vs . 726.8 ± 299.2 , t=3.482 ,P=0.002 ;1531.2 ± 455.3 vs .539.2 ± 272.7 ,t=3.761 ,P=0.001) and intensity (9.8 ± 3.2 vs .7.9 ± 6.1 , t=2.132 , P=0.041 ;11.3 ± 5.1 vs .10.1 ± 9.7 , t=2.256 , P=0.032 ) activated by left hand (non dominant hand) and right hand (dominant hand) when performing active and passive finger to finger movement were statistically significantly different. In the cerebral infarction group ,when the right hand was involved ,SMC volume (605.8 ± 408.2 vs .452.7 ± 213.5 , t=2.491 , P=0.020 ;397.2 ± 248.7 vs .311.2 ± 158.3 , t=2.681 , P=0.013) and intensity (9.5 ± 2.7 vs .7.6 ± 5.0 , t=2.372 , P=0.031 ;7.9 ± 6.1 vs . 5.0 ± 4.7 ,t=2.482 , P=0.023) activated by active and passive finger to finger movement were lower than the control group. In the cerebral infarction group ,when the left hand was involved ,SMC volume (1399.7 ± 209.6 vs .689.5 ± 422.7 , t= 2.846 , P= 0.010 ;3551.2 ± 495.3 vs .413.6 ± 264.2 , t= 3.072 , P= 0.007 ) and intensity (11.3 ± 5.1 vs .7.2 ± 3.1 , t=2.279 , P=0.032 ;10.1 ± 9.7 vs .6.1 ± 3.9 , t=2.811 , P=0.016 ) activated by active and passive finger to finger movement were lower than the control group .In the cerebral infarction group ,ipsilateral cerebellum volume (932.5 ± 2016.2 vs .61.8 ± 214.0 , t=2.441 , P=0.021 ;197.6 ± 297.4 vs .37.2 ± 19.0 , t= 3.124 , P= 0.004 ) and intensity (15.0 ± 3.2 vs .6.7 ± 1.8 , t= 3.001 , P=0.005 ;13.8 ± 2.9 vs . 6.3 ± 1.7 , t= 2.121 , P= 0.032 ) activated by active and passive finger to finger movement were lower than the control group . Conclusions The influenced area was mainly located in contralateral SMC and ipsilateral cerebellum in cerebral infarction patients with ataxia .

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