Falsely normal CT perfusion ischemic core readings are common and often associated with deep infarcts.

ABSTRACT

BACKGROUND: Proper identification of infarct extent is crucial for thrombectomy and prognostication. We sought to study the frequency and topographic aspects of those cases in which CT perfusion (CTP) misses a core lesion that is present on initial non-contrast CT (NCCT). METHODS: A review was carried out of a prospectively collected database of endovascular patients with anterior circulation large vessel occlusion strokes from January 2014 to November 2018. Patients with an e-ASPECTS <10 and adequate CTP maps were included. Total missed ischemic core (TMC) was defined as a CTP core lesion (relative cerebral blood flow <30%) <1 mL with a visualized hypodensity on NCCT. RESULTS: In total, 629 patients were analyzed of which 161 (25.6%) had a TMC. On univariate analysis, TMC was associated with isolated deep middle cerebral artery (MCA) strokes (77.6% vs 56.6%, p<0.001), lower National Institutes of Health Stroke Scale (NIHSS) score (9 (15-20) vs 17 (13-21), p=0.007) and longer times to treatment (452 (288-652) min vs 355 (236-655) min, p=0.03). After adjusting for identifiable confounders, isolated deep MCA stroke was an independent predictor of TMC (OR 2.49 (95% CI 1.63 to 3.8), p<0.001). There were no differences between patients presenting with a TMC and those not with good outcomes (modified Rankin Scale 0-2) (50.8% vs 47.6%, p=0.53) or 90-day mortality (23% vs 17.6%, p=0.17). However, TMC was associated with lower rates of any parenchymal hematomas (5.2% vs 14.6%, p=0.02; aOR 0.11 (95% CI 0.01 to 0.91), p=0.04) and smaller final infarct volumes (20.5 (11.3-42.9) mL vs 47.5 (20.3-85) mL, p<0.001). CONCLUSIONS: CTP may completely fail to detect ischemic core in as many as 25% of cases, especially in isolated deep MCA strokes. Technical refinements of the post-processing algorithms are therefore warranted. TMC infarcts may have a lower risk of reperfusion hemorrhage, potentially due to greater preservation of the neurovascular unit structure in face of delayed recovery of cerebral blood flow.