Stroke after cranial radiation in glioma: Phenotypic differences by concurrent bevacizumab exposure

Patients with glioma undergoing radiation therapy have been found to have elevated cerebrovascular risk. Bevacizumab, commonly used in this population for radiation necrosis, tumor recurrence, and cerebral edema, has prothrombotic and hemorrhagic effects, though its influence on stroke presentation in this population remains poorly characterized.

We performed a retrospective analysis of patients with glioma who developed stroke following cranial radiation therapy within the PRoGREss institutional registry. Bevacizumab exposure was ascertained at the time of the stroke event. Stroke subtype, severity, antithrombotic use, and discharge functional status were compared between patients with and without concurrent bevacizumab exposure.

Of 910 registry patients, 91 (10.0%) developed stroke following cranial radiation. At the time of stroke, 59 (64.8%) were receiving bevacizumab and 32 (35.2%) were not. Intraparenchymal hemorrhage occurred numerically more often in bevacizumab-exposed patients (32.2% vs. 15.6%), though this difference was not statistically significant (Fisher's Exact p = 0.13). Among patients with IPH, concurrent therapeutic anticoagulation was substantially more prevalent in the bevacizumab-exposed group (31.6% vs. 0.0%, Fisher's Exact p = 0.28).

In this exploratory cohort of 91 patients with stroke after cranial radiation, bevacizumab exposure at the time of stroke was not independently associated with intraparenchymal hemorrhage. The observed numerical difference was not statistically significant and was substantially confounded by higher rates of concurrent therapeutic anticoagulation in the bevacizumab-exposed group. The primary hypothesis generated by these data is that concurrent bevacizumab and therapeutic anticoagulation may together confer meaningful hemorrhagic risk in this population, warranting dedicated prospective investigation.