Chaves C J, Silver B, Schlaug G, Dashe J, Caplan L R, Warach S
Stroke Division, Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.
Stroke. 2000 May;31(5):1090-6. doi: 10.1161/01.str.31.5.1090.
The pathophysiology of borderzone infarcts is not well understood. We investigated whether combined diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) could identify pathophysiologically meaningful categories of borderzone infarcts.
Seventeen patients with borderzone infarcts were identified from the Beth Israel Deaconess Medical Center Stroke Database. All patients had DWI and PWI, the majority of them within the first 24 hours of symptom onset.
Three patterns of perfusion abnormalities were associated with the diffusion lesions: 1, normal perfusion (5 patients); 2, localized perfusion deficits matching the area of restricted diffusion (5 patients); and 3, extensive perfusion deficits involving 1 or more vascular territories (7 patients). All but 1 patient with pattern 1 had transient peri-infarct hypotension as the presumed stroke mechanism. Two patients with pattern 2 had cardiac or aortic embolic sources; none had large-artery disease or arterial hypotension. Reperfusion was detected in all patients with this pattern who submitted to a follow-up study. All patients with pattern 3 had severe stenosis or occlusion of a large artery: the internal carotid, anterior cerebral, or middle cerebral.
We postulate that the perfusion abnormality varies according to the mechanism of the borderzone infarction. Transient perfusion deficits occurring with hypotension in the absence of significant large-artery disease may not be revealed by PWI. Embolism may cause some cases of small borderzone perfusion deficits. Critical large-artery disease may cause large territorial perfusion deficits and predispose to borderzone infarction.
边缘带梗死的病理生理学尚未完全明确。我们研究了联合扩散加权成像(DWI)和灌注加权成像(PWI)能否识别具有病理生理学意义的边缘带梗死类别。
从贝斯以色列女执事医疗中心卒中数据库中识别出17例边缘带梗死患者。所有患者均接受了DWI和PWI检查,其中大多数在症状发作后的24小时内进行。
三种灌注异常模式与扩散病变相关:1. 正常灌注(5例患者);2. 局部灌注缺损与扩散受限区域匹配(5例患者);3. 广泛灌注缺损累及1个或更多血管区域(7例患者)。除1例模式1患者外,其他患者均有短暂性梗死周围低血压,推测为卒中机制。2例模式2患者有心脏或主动脉栓子来源;均无大动脉疾病或动脉低血压。接受随访研究的该模式所有患者均检测到再灌注。模式3的所有患者均有颈内动脉、大脑前动脉或大脑中动脉等大动脉的严重狭窄或闭塞。
我们推测灌注异常因边缘带梗死的机制而异。在无明显大动脉疾病的情况下,低血压伴发的短暂灌注缺损可能无法通过PWI显示。栓塞可能导致一些小的边缘带灌注缺损病例。严重的大动脉疾病可能导致大面积的区域灌注缺损并易发生边缘带梗死。