Ischemic stroke and tissue hypodensity on computed tomography

Ischemic Stroke and Tissue Hypodensity on Computed Tomography To the Editor: Clinical experience and experimental data have shown that early identification of patients with a large ischemic brain edema and subsequent hemicraniectomy can decrease mortality and morbidity.1,2 I read with great interest the article by Haring and colleagues3 and appreciate the efforts of the authors to find CT criteria that could early and reliably discriminate acute stroke patients with a malignant course and the potential benefit from craniectomy for those with a more favorable prognosis. I am afraid, however, that the authors did not really meet this goal. The authors used a case-control design and defined the patients with malignant course by their vascular findings (occlusion of the internal carotid artery or middle cerebral artery [MCA] trunk) and by tentorial herniation caused by brain edema within 24 to 96 hours after admission. The authors did not reveal whether the matched controls had the same type of arterial occlusion or why they chose older patients (median age 71 versus 64 years). They found that an attenuated corticomedullary contrast covering at least the entire MCA territory is the only radiological feature that yields both high specificity and sensitivity for a malignant course compared with other CT findings, such as parenchymal hypodensity and signs of focal brain swelling. They correctly stated that the attenuation of the corticomedullary contrast is caused by cortical hypodensity. In their cohort of 31 patients with malignant course, 27 patients showed a hypodensity of the entire MCA territory cortex. They found, however, only 18 patients with a parenchymal hypodensity in .50% of the MCA territory and only 14 patients with hypodensity .67% of the MCA territory. I cannot imagine patients with hypodensity of the entire MCA cortex—which means a total MCA infarction—but hypodensity in ,50% or even 67% of the MCA territory. Unfortunately, the authors did not present an image of one of those 9 patients with parenchymal hypodensity in ,50% of MCA territory but with hypodensity of the entire MCA cortex. They showed a patient (Figure A1) without compression of the subarachnoid space (according to the legend) and with malignant course, although they stated in Table 3 that all these patients had a compressed subarachnoid space. It is my experience with CT that tissue hypodensity is best depicted in gray matter like the basal ganglia or the cortex. Isolated cortical involvement occurs after cerebral hypoxia. With arterial occlusion, however, almost always the cortex and subcortical tissue are affected. Therefore, I think that “attenuated corticomedullary contrast” is not a CT sign after ischemic stroke but an artifact without a pathophysiological meaning. The study confirmed our hypothesis that parenchymal hypodensity exceeding 50% of the MCA territory is a highly specific finding for a malignant course.4