摘要目的 利用CT灌注成像技术(CTP)观察脑出血患者的脑血液动力学变化规律及对临床神经功能缺损评分(SSS)的影响.方法 对41例幕上脑出血患者于发病后5 h～14 d同步行头颅CT平扫和CTP检查,观察时间、血肿体积、水肿范围、发病期间的血糖水平、同步平均动脉压(MBP)对脑出血患者脑血液动力学的影响和这种血液动力学变化与脑出血患者SSS相关性.结果 (1)血肿周围水肿带内、水肿带外(距离水肿边缘1 cm内)、同侧皮层区间不同病理区域脑血流量(分别为CBF1、CBF2、CBF3)差异有统计学意义(P<0.05),且随时间呈波动性变化;CBF1、CBF2呈直线正相关关系(r=0.334,P=0.035),与CBF3无直线相关关系(r=0.027,P=0.870;r=0.142,P=0.383).另外水肿带内CBF1和脑血容量(CBV1)呈直线正相关关系(r=0.803,P=0.000),但与达峰时间(PT1)无相关关系(r=-0.52,P=0.752).(2)CBF1的下降程度与血肿体积、血肿周围水肿范围呈直线负相关关系(r=-0.501,P=0.001;r=-0.589,P=0.000),与发病期间的血糖水平、MBP无相关关系(r=0.141,P=0.386;r=0.014,P=0.930).(3)血肿周围灌注损伤范围(参数图灌注缺损范围-血肿范围,此范围内的CBF<20mL/100 g·min)与血肿体积、血肿周围水肿范围呈直线正相关关系(r=0.449,P=0.003;r=0.645,P=0.000),与发病期间的血糖水平、MBP无相关关系(r=-0.047,P=0.769;r=0.141,P=0.378).(4)脑出血患者同步的SSS与血肿体积、血肿部位、CBF的下降程度、CBV的下降程度呈相关关系(r=-0.418,P=0.007;r=0.542,P=0.000;r=0.376,P=0.017;r=0.312,P=0.051),与血肿最大平面的灌注缺损范围、水肿范围无相关关系(r=-0.283,P=0.073;r=-0.163,P=0.308).结论 (1)脑出血患者血肿周围水肿带内、外及同侧皮层血流减低均降低,但趋势不一致.(2)血肿周围水肿带内存在着缺血性损伤(CBF<20mL/100g·min),其范围和程度均血肿大小、水肿范围有关,随时间波动变化,但未达到统计学差异.(3)出血部位、血肿体积、血肿周围水肿带内脑灌注水平影响脑出血患者的SSS.

abstractsObjective To investigate the hemodynamic changes in patients with intracerebral hemorrhage (ICH) using CT perfusion (CTP) imaging and the relation between cerebral perfusion and the Scandinavian Stroke Scale (SSS) of the patients. Methods Forty-one patients with supratentorial ICH underwent plain CT scanning and CTP imaging at different times after ICH onset (from 5 h to 14 days). The impact of the time after ICH onset, hematoma volume, edema area, mean hlood pressure (MBP) and blood glucose on the hemodynamics of the patients was assessed, and the correlation between the SSS and the hemodynamic changes evaluated. Resnlts The cerebral blood flow in the edema area (CBF1), the peripheral area of the edema (CBF2, within 1 cm to the edema) and the distant cortical area from the hematoma (CBF3) showed significant differences (r=0.027, P=0.870) and fluctuated with time. CBF1 showed a positive linear relation with CBF2 (r=0.334, P=0.035), but neither of them was correlated to CBF3 (r=0.027, P=0.870;r=0.142, P=0.383). CBF1 also showed positive linear relations with relative cerebral blood volume (rCBV1) (r=0.803,P=0.000) and the peak time (PT1) (r=-0.52, P=0.752). The reduction of CBF1 was inversely correlated to the hematoma volume and the edema area (r=-0.501, P=0.001;r=-0.589, P=0.000), but not related with MBP or blood glucose (r=0.141, P=0.386;r=0.014, P=0.930). The area of ischemic injury (the ischemic area defined by CBF parameters-the hematoma area, edema area (r=0.449, P=0.003;r=0.645, P=0.000), but not to the MBP or blood glucose (r=-0.047, P=0.769;r=0.141,P=0.378). SSS was found to correlate to the volume and location of the hematoma and the reduction of CBF and CBV (r=-0.418, P=0.007;r=0.542, P=0.000;r=0.376, P=0.017;r=0.312, P=0.050), but not to the ischemic and edema area (r=-0.283, P=0.073;r=-0.163, P=0.308). Conclusion CBF is reduced in the edema area, peripheral area of the edema and the distant cortical area from the hematoma but showing different patterns of variation. Ischemic injury is present in the edema area around the hemotema, and its scope and severity is related with the hemotoma volume and the size of the edema area and may vary with time. The location and volume of the hematoma as well as the perfusion level in the edema area all affect the SSS of the patients.