We report a case of a patient who developed glioblastoma in the territory of a previous infarction. Two years after an ischemic stroke, the patient presented with a cystic, necrotic, and heterogeneously enhancing mass. Open biopsy and debulking of the mass with histological analysis revealed the mass to be glioblastoma. Though several cases of posttraumatic GBM have been reported, this is the first proposed case of GBM after an ischemic stroke. From this case, we suggest that the ischemic stroke, like other forms of cortical injury, may predispose to glioblastoma formation. 1. Introduction Previous reports have suggested that glioblastoma (GBM) may arise from areas of gliosis resulting from traumatic brain injury, chronic abscess, or surgical resection [1–4]. The process of reactive gliosis that follows such injuries may increase the chance of malignant transformation. The mechanisms underlying this process remain unclear. Here, we present a patient who developed GBM two years after an ischemic infarction. We propose that this GBM developed in the region of previous infarction and review the existing evidence of posttraumatic tumorigenesis. 2. Case Report 2.1. Initial Presentation A 73-year-old woman with a history of mechanical aortic valve replacement and atrial fibrillation, maintained on warfarin, initially presented with acute left-sided hemiparesis and a right gaze deviation in the setting of a subtherapeutic prothrombin time/international normalized ratio (PT/INR). Head computed tomography (CT) revealed loss of differentiation of the grey-white junction in the right insula and lateral basal ganglia with densities in the right middle cerebral artery (MCA) and right internal carotid artery (ICA) (Figure 1(a)). Concurrent CT angiography (CTA) revealed an occlusion of the supraclinoid segment of the right ICA extending to the M1 segment of the MCA (Figure 1(b)). Despite intravenous tissue plasminogen activator (tPa), intra-arterial urokinase, and attempted mechanical thrombectomy, her occlusion remained. Figure 1: Imaging of initial ischemic stroke. (a) CT without contrast, showing dense right MCA (white solid arrow) and loss of differentiation of the grey-white junction on the right. (b) CT angiography, revealing occlusion of the right MCA (white solid arrow). (c) CT without contrast, showing subsequent hemorrhagic transformation of the infarct. Serial head CT scans obtained over the next several days revealed an evolving right MCA territory infarction extending to the right temporal pole, frontal operculum, and basal ganglia, as well as a
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