丘脑梗死后丘脑放射纤维继发变性的磁共振弥散张量成像

The secondary degeneration of the thalamic radiation fibers after thalamus infarction detected with diffusion tensor imaging

目的应用磁共振弥散张量(diffusion tensor imaging,DTI)技术动态观察局灶性丘脑梗死后丘脑放射纤维的弥散变化,探讨丘脑梗死后,病灶上方的丘脑放射纤维继发性损害的发生发展规律。方法连续收录首次发病、单侧丘脑梗死患者17例为实验组,选择健康志愿者17例作对照研究。患者分别在发病的第1周(W1)、第4周(W4)和第12周(W12)进行1次DTI检测,对照组进行1次DTI检测。每次DTI检测之前进行美国国立卫生研究院卒中评分(national institute health stroke scale,NIHSS)和Barthel生活指数(BI)以及自订的感觉障碍分级评分(Sensory disturbance rating,SDR)评定。结果梗死灶上方的半卵圆中心部分异向(fractional anisotropy,FA)值随时间延长逐渐减少(W1:0.42±0.02,W2:0.38±0.02,W12:0.34±0.03,P<0.01),而平均弥散量(mean diffu-sion,MD)却无明显变化。梗死灶上方的半卵圆中心FA值的变化百分数与NIHSS、和BI的变化百分数无明显相关(P>0.05),与SDR变化的百分数呈负相关(r=-0.246,P<0.05)。结论局灶性丘脑梗死可以引起丘脑放射纤维继发性损害,在12周内这种继发性损害逐渐加重,而且还可能阻碍患者感觉功能的恢复。

Objective To investigate the secondary degeneration of the thalamic radiation fibers and its regular pattern ＇after the thalamus infarction using diffusion tensor imaging （DTI）. Methods Seventeen patients with a recent thalamic infarct underwent DTI and evaluations with the NIH Stroke Scale （NIHSS） and the barthel index （BI） and Sensory disturbance rating （SDR） 3 times at the first （W1）, the fourth （W4） and twelfth weeks （W12） after onset of stroke, respectively. Seventeen gender and age matched healthy volunteers underwent DTI once as controls. The DTI parameters of Mean diffusivity （MD） and fractional anisotropy （ FA value） were measured at the region of interest （ROI） of the thalamic radiation at the eentrum semiovale level. Results The FA values of the thalamic radiation at the centrnm semiovale level ispilateral to the primary infarction significantly decreased over time from W1 to W12 （ W1 ： 0. 42 ± 0. 02 , W2 ： 0. 38 ± 0. 02, W12：0. 34 ±0.03, P 〈0. 01 ） . However, its MD remained unchanged. The percent changes of FA values of the thalamic radiation at the centrnm semiovale level ispilateral to the primary infarction did not correlated with percent changes of NIHSS, and BI （P 〉 0. 05 ）, but correlated negatively with percent changes of SDR （ r = - 0. 246, P 〈 0. 05 ）. Conclusions Our data suggest that focal thalamus infarction may cause the secondary degeneration in the ispilateral thalamic radiation fibers, which further deteriorates over time within observed three months and thus hinders sensory recovery.