2025 Volume 53 Issue 4 Pages 218-223
A 58-year-old man presented with cognitive dysfunction and visual field disturbances and underwent resection of a right temporal lobe glioblastoma. Magnetic resonance imaging (MRI) obtained 4 months after 60 Gy radiation therapy and chemotherapy with temozolomide did not show tumor recurrence or aneurysmal formation. One month later, the patient was transferred to our facility due to sudden-onset headache and nausea. Head computed tomography (CT) and CT angiography revealed an intracerebral hemorrhage in the tumor cavity and an 8 mm aneurysm adjacent to the hematoma at the M2 portion of the right middle cerebral artery. Bypass-assisted parental artery occlusion using the previous craniotomy was performed to prevent rebleeding from the aneurysm. The right Sylvian fissure was opened after harvesting the superficial temporal artery and performing a recraniotomy, securing the M2 portion proximal to the aneurysm. Indocyanine green (ICG) videoangiography under temporary occlusion of the M2 portion precisely detected the target recipient vessel at the surface, and a superficial temporal artery–to–middle cerebral artery bypass was performed. Subsequent removal of the hematoma caused bleeding from the defect of the vessel wall at the aneurysmal neck and demonstrated that the aneurysmal structure was a pseudoaneurysm without a proper aneurysmal wall. The vessel wall defect segment of the M2 portion was trapped using two aneurysmal clips and removed with a pseudoaneurysm. Pathological investigation revealed no vessel structures, such as elastic lamina or endothelial cells, suggesting a pseudoaneurysm. The patient’s postoperative course was uneventful, and he was discharged. In this article, we discuss the pathophysiological mechanisms of de novo aneurysm formation and rupture after the initial treatment of glioblastoma and the validity of surgical intervention when the tumor is well-controlled.
