BACKGROUND AND PURPOSE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND AND PURPOSE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
Authors: Y Kaichi; S Kakeda; J Moriya; N Ohnari; K Saito; Y Tanaka; F Tatsugami; S Date; K Awai; Y Korogi Journal: AJNR Am J Neuroradiol Date: 2013-07-25 Impact factor: 3.825