急性皮质下脑梗死后进展性运动功能缺损的预测因素和发生机制：回顾性病例系列研究

Predictors and pathogenesis of progressive motor deficits after acute subcortical cerebral infarction： a retrospective case series study

目的探讨急性皮质下脑梗死后进展性运动功能缺损（progressive motor deficits，PMD）的预测因素和发生机制。方法连续纳入发病24h内的急性皮质下脑梗死患者，根据美国国立卫生研究院卒中量表运动项目评分变化分为PMD组（5d内增加I〉2分）和非PMD组，比较两组间人口统计学、影像学资料和相关危险因素的差异，筛选PMD的早期预测因素。对PMD组和部分非PMD组患者进行弥散加权成像复查，从影像学角度分析PMD的发生机制。结果共纳入117例发病24h内的急性皮质下脑梗死患者，其中PMD组26例，非PMD组91例。单变量分析显示，PMD组既往卒中或短暂性脑缺血发作史的患者构成比显著性低于非PMD组（11．5％对31．9％；X2=4．206，P=0．040），糖基化血红蛋白（6．7％±2．0％对5．9％±1．7％；t=-2．206，P=0．029）和梗死层面数（3．7±1．4对3．0±1．6；t=-2．147，P=0．034）显著性高于非PMD组，放射冠部位梗死（73．1％对25．3％；X^2=20．081，P〈0．001）以及大脑中动脉（middle cerebral artery，MCA）狭窄或闭塞（76．9％对51．6％,X^2=5．279，P=0．022）的患者构成比显著性高于非PMD组。多变量logistic回归分析显示，放射冠梗死[优势比（oddsratio，OR）10．459，95％可信区间（confidence interval，CI）3．091～35．396；P〈0．001]与MCA狭窄或闭塞（OR4．036，95％CI 1．057～15．417；P=0．041）是急性皮质下脑梗死后PMD的独立预测因素。PMD组梗死灶扩大（50．0％对6．5％；X^2=13．830，P〈0．001）和梗死复发（38．5％对3．2％；X^2=11．273，P=0．001）的患者构成比显著性高于非PMD组，无任何改变（23．1％对90．3％扰。=26．566，P〈0．001）的患者构成比显著性低于非PMD组。结论放射冠部位梗死以及MCA狭窄或闭塞是急性皮质下脑梗死后PMD的重要独立预测因素，梗死灶扩大和梗死复发可能是PMD的主要发生机制。

Objective To investigate the predictors and pathogenesis of progressive motor deficits （PMD） after acute subcortical cerebral infarction. Methods Consecutive patients with acute subcortical cerebral infarction admitted to hospital within 24 hours of after onset were enrolled. They were divided into either a PMD group （increase ≥ 2 points within 5 days） or a non-PMD group according to the changes of motor scores of the National Institutes of Heakh Stroke Scale. The differences of demographics, imaging data and related risk factors were compared between two groups in order to screen for the early predictors for PMD. The reexamination of diffusion-weighted imaging （DWI） was conducted for all patients in the PMD group and part of patients in the non-PMD group. The pathogenesis of PMD was analyzed from the radiological point of view. Results A total of 117 patients with acute subcortical cerebral infarction within 24 hours of after onset were enrolled, 26 of them were in the PMD group, and 91 were in the non-PMD group. Univariate analysis showed that the proportions of the histoi＇y of previous stroke or transient ischemic attack of the PMD group were significantly lower than those of the non-PMD group （11.5% vs. 31.9% ; X^2 = 4. 206, P = 0. 040）; glycated hemoglobin （6. 7 % ± 2. 0% vs. 5.9 % ± 1.7 % ; t = - 2. 206, P = 0. 029） and infarction levels （3.7± 1.4vs. 3.0± 1.6, t= -2.147, P= 0.034） of the PMD group were significantly higher than those of the non-PMD group; the proportions of corona radiata infarct （73.1% .vs. 25.3%;X^2= 20. 081, P 〈 0. 001） and middle cerebral artery （MCA） stenosis or occlusion （76. 9% vs. 51.6% ;X2 =5. 279, P =0. 022） of the PMD group were significantly higher than those of the non-PMD group. Multivariate logistic regression analysis showed that corona radiata infarct （odds ratio [ OR] 10. 459, 95% confidence interval [ CI] 3. 091 - 35. 396; P 〈 0. 001） and MCA stenosis or occlusion （OR 4. 036, 95% CI 1. 057- 15. 417; P= 0. 041） were the independent predictors for PMD after acute subcortical cerebral infarction. The proportions of infarct expansion （50. 0% vs. 6. 5% ;X2 = 13. 830, P 〈0. 001） and recurrent infarction （38.5% vs. 3.2%; X2 = 11. 273, P = 0. 001） of the PMD group were significantly higher than those of the non-PMD group. However, the proportion of patients without any change （23.1% vs. 90. 3%; X2 =26. 566, P〈0. 001） was significantly lower than that of the non-PMD group. Conclusions Corona radiata infarct and MCA stenosis or occlusion are the important and independent predictors for PMD after acute subcortical cerebral infarction. Infarct expansion and recurrent infarction may be the main mechanism of PMD.