磁共振扩散峰度成像诊断亚急性脑梗死进展性的价值

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目的利用MR扩散峰度成像(DKI)研究亚急性期进展性脑梗死责任病灶,并结合NIHSS评分探讨其影像征象与临床相关性。方法前瞻性研究发病时间>72 h且在本影像中心行MRI扫描的亚急性期脑梗死病人79例,其中男45例,女34例,年龄43~88岁,平均(64.75±11.05)岁。根据NIHSS评分和病灶数目将其分为4组:单发脑梗死进展阴性组、多发脑梗死进展阴性组、单发脑梗死进展阳性组、多发脑梗死进展阳性组。对所有病人进行颅脑DKI及常规MRI扫描,获取MD和MK参数图,并于相应的参数图测量相应的参数值及病灶面积。多发性脑梗死病例在MD和MK图同一层面选取同一供血区内的2个独立病灶,分别将兴趣区设置于该缺血区的核心区(ROI 1)和周边区(ROI 2)。采用配对样本Wilcoxon符号秩检验比较MD图和MK图中病灶面积和信号的差异,采用散点图和信号变化百分比描述缺血灶的时间-信号变化。结果 (1)病灶面积。进展阴性组病人MD图与MK图中不同梗死灶的面积大小均相仿,其差异均无统计学意义(均P>0.05);进展阳性组MD图中不同梗死灶的面积均大于MK图(均P<0.05)。进展阴性组和阳性组的MD/MK不匹配区面积(显著的MD/MK不匹配区)百分比分别为0.2%和9.7%。(2)时间-信号散点图。a单发脑梗死组:与正常脑区相比,不同进展程度的单发脑梗死病人的病灶区均表现为MD值显著下降、MK值显著上升。进展阳性组病灶的信号恢复延迟,且MD、MK值偏离正常值的幅度大于进展阴性组。两组的MK值偏离正常值的幅度均大于MD值的变化幅度。b多发脑梗死组:多发性脑梗死进展阴性组病灶的MD和MK的时间-信号散点图与单发脑梗死进展阴性组相仿,ROI 1和ROI 2的时间-信号变化趋向一致性良好。多发性脑梗死进展阳性组ROI 1的MD和MK的时间-信号散点图与单发脑梗死进展阳性组相仿,而ROI 2的MD和MK的时间-信号散点图则呈无规律的杂乱曲线,表现出多病灶的异质性。结论脑梗死灶MK值恢复的延迟或多病灶的异质性均提示原发脑梗死病灶扩大及新发脑梗死,是亚急性脑梗死进展性诊断的重要征象。 Objective To investigate the responsible lesion of subacute progressive cerebral infarction by using MR diffusion kurtosis imaging (DKI) and to explore the relationship between its imaging features and clinical features by NIHSS score. Methods A prospective study of 79 patients with subacute cerebral infarction with a onset time> 72 h and MRI scans in this imaging center included 45 males and 34 females, ranging in age from 43 to 88 years with an average of (64.75 ± 11.05) years. According to the NIHSS score and the number of lesions, it was divided into four groups: negative progressing solitary cerebral infarction, multiple cerebral infarction negative progressing group, single cerebral infarction positive progressing group and multiple cerebral infarction positive progressing group. All patients were subjected to brain DKI and conventional MRI scans, MD and MK parameter maps were obtained, and corresponding parameter values ​​and lesion areas were measured in the corresponding parameter maps. Multiple cerebral infarction patients selected two independent lesions in the same donor area at the same level in the MD and MK maps, and set the ROI in the core area (ROI 1) and the peripheral area (ROI 2) of the ischemic area respectively. Wilcoxon signed-rank test was used to compare the difference of lesion area and signal between MD and MK images. Scatter plot and percent change of signal were used to describe the time-signal changes of ischemic focus. Results (1) Lesion area. The area of ​​different infarct size in patients with negative progressing group was similar to that in patients with age-related adverse events (all P> 0.05). The area of ​​different infarct size in MD with positive progressing group was larger than that of MK P <0.05). The percentages of MD / MK mismatch area (significant MD / MK mismatch area) in progression-negative and positive groups were 0.2% and 9.7%, respectively. (2) time - signal scatter plot. Single-infarct group: Compared with the normal brain area, single-infarction patients with different degrees of progression of the lesion showed a significant decline in MD values, MK increased significantly. The progress of the positive group was delayed in signal recovery, and the amplitude of MD and MK deviated from the normal range was greater than that of the negative group. The magnitude of deviation of MK value from normal value in both groups was greater than that of MD value. b Multiple cerebral infarction group: The time-signal scatter plots of MD and MK in lesions of patients with progressive cerebral infarction were similar to those of negative patients with progressive cerebral infarction. The time-signal changes of ROI 1 and ROI 2 tended to be consistent. The time-versus-signal scatter plots of MD and MK in ROI-1 positive patients with progressive cerebral infarction were similar to those of positive patients with single cerebral infarction, whereas the time-signal scatter plots of MD and MK in ROI 2 were irregular Curves, showing the heterogeneity of multiple lesions. Conclusions The delayed recovery of the MK value of cerebral infarction or the heterogeneity of multiple lesions suggest that the enlargement of primary infarction and new-onset cerebral infarction are important signs of progressive diagnosis of subacute cerebral infarction.
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