Ruptured Cerebral Arteriovenous Malformation Presenting as Intraventricular Hemorrhage

Abstract

A 64-year-old woman with a history of ovarian carcinoma and cerebrovascular accident presented with the acute onset of a severe throbbing headache with associated nausea and vomiting. The patient described intermittent headaches over the preceding month with associated vision changes during these episodes. She was found to have intraventricular hemorrhage on an initial head computed tomography (CT) scan. Follow-up CT angiography and digital subtraction cerebral catheter angiography were performed. The initial unenhanced head CT (Figure ​(Figure11) reveals hyperdense hemorrhage layering in the frontal horns and atria of the lateral ventricles in addition to suspicious punctuate atrial calcifications. Such calcifications often herald the presence of an arteriovenous malformation (AVM). The CT angiogram (Figure ​(Figure22) and catheter angiogram (Figure ​(Figure33) demonstrate an enhancing nidus of blood vessels located in the medial temporal-occipital lobe and atrium of the right lateral ventricle consistent with an AVM. The vascular malformation is fed predominantly through an enlarged posterior communicating and posterior cerebral artery with drainage through both an enlarged basal vein of Rosenthal and enlarged superficial cortical veins. No intranidal aneurysm was detected. Figure 1 (a, b) Initial unenhanced axial CT images with diffuse intraventricular hemorrhage (arrows) and punctuate AVM calcifications (arrowheads). Figure 2 (a) Axial CT angiogram demonstrates the AVM nidus in the atrium of the lateral ventricle (arrows). (b) Axial reconstructed CT angiogram reveals enlargement of the posterior cerebral and posterior communicating arteries (arrowheads) in addition to an enlarged ... Figure 3 (a) Anteroposterior and (b) lateral catheter angiogram images show the AVM nidus (arrowheads) with enlargement of the right posterior cerebral and posterior communicating arteries (arrows). True AVMs contain one or more enlarged feeding arteries, a nidus, and enlarged early draining veins with no intervening capillary bed. They are considered a congenital anomaly but typically do not become symptomatic until beyond the third or fourth decade of life. AVMs are classified using the Spetzler-Martin grading system (grades 1 through 5) on the basis of size, location, and venous drainage patterns; higher numbers indicate less favorable surgical and treatment outcomes. The presented case meets criteria for a grade 2 AVM in this system. Treatment options for AVMs include endovascular embolization, surgical resection, and radiosurgery alone or in combination. In AVMs <3 cm in diameter, particularly those that are deeply situated in the brain, stereotactic radiosurgery is the therapy of choice, achieving cure rates of 80% to 90% at 2 to 3 years after treatment.