Isaka Y, Ishida M, Nakayama H, Ashida K, Imaizumi M, Furukawa T
Department of Cardiovascular Medicine and Nuclear Medicine, Osaka National Hospital.
Kaku Igaku. 1991 Jul;28(7):737-42.
In 32 patients with asymptomatic white matter lesions (WMLs), we evaluated the age-related changes in the number of white matter lesions, cerebral blood flow (CBF), cerebrovascular resistance (CVR) and mean arterial blood pressure (MABP). CBF was measured with the intravenous 133Xe injection method. The number of WMLs in whole brain was measured by the magnetic resonance imaging. CBF decreased with advancing age (r = 0.529; p less than 0.01), while the number of WMLs (r = 0.39; p less than 0.05), CVR (r = 0.464; p less than 0.01) and MABP (r = 0.229; ns) increased with advancing age. There was a significantly negative correlation (r = -0.499; p less than 0.01) between CBF and the number of WMLs. While, CVR showed a positive correlation with the number of WMLs (r = 0.468; p less than 0.01). Multivariate regression analysis with stepwise forward selection method indicated that the number of WMLs and age were independent and negative predictors for CBF, while other factors did not. CBF decreased with a concomitant rise in CVR. On the basis of the results listed above, we assumed that ischemic damage of the white matter and/or functional suppression of distant loci due to the primary tissue damage are the best explanation for CBF reduction in asymptomatic individuals with WMLs. High resolution CBF imaging as well as evaluation of structural alterations in cerebrovascular vessels should be required to further define the mechanisms.
在32例无症状性脑白质病变(WMLs)患者中,我们评估了脑白质病变数量、脑血流量(CBF)、脑血管阻力(CVR)和平均动脉血压(MABP)与年龄相关的变化。采用静脉注射133Xe法测量CBF。通过磁共振成像测量全脑WMLs的数量。CBF随年龄增长而降低(r = 0.529;p < 0.01),而WMLs数量(r = 0.39;p < 0.05)、CVR(r = 0.464;p < 0.01)和MABP(r = 0.229;无统计学意义)随年龄增长而增加。CBF与WMLs数量之间存在显著负相关(r = -0.499;p < 0.01)。同时,CVR与WMLs数量呈正相关(r = 0.468;p < 0.01)。采用逐步向前选择法的多变量回归分析表明,WMLs数量和年龄是CBF的独立负性预测因子,而其他因素不是。CBF随着CVR的升高而降低。基于上述结果,我们认为脑白质的缺血性损伤和/或由于原发性组织损伤导致的远处位点功能抑制是无症状性WMLs个体CBF降低的最佳解释。需要高分辨率CBF成像以及脑血管结构改变的评估来进一步明确其机制。