Objective and importance: It has been suggested that impaired venous drainage of normal brain after surgical removal of an arteriovenous malformation (AVM) may cause perinidal edema and hemorrhage. The term occlusive hyperemia has been proposed for this phenomenon. There is evidence that occlusive hyperemia also may occur after radiosurgical treatment of AVMs. The purpose of this article is to lend further support to the concept that venous occlusion may be responsible for some complications observed after AVM radiosurgery.
Clinical presentation: We report two patients with unusual radiosurgery-associated complications, and we examine the evidence for venous occlusion as the mechanism underlying the observed clinical sequelae in each patient.
Intervention: Patient 1 had a large parietal venous infarct remote from her frontal AVM site 11 months after radiosurgery. At that time, the AVM was confirmed by angiography to have been obliterated. During the next 4 years, the patient experienced persistent posterior hemispheric edema with recurrent focal hemorrhages until the patient's death from massive swelling and uncal herniation. During this period, radiographic studies, including repeat angiography, demonstrated sequential cortical venous occlusions and findings most consistent with venous insufficiency. Postmortem examination revealed no evidence of radionecrosis. Patient 2 exhibited a biphasic pattern of neurological deterioration at 3 and 6 years after radiosurgery. Associated with this unusual phenomenon, there was radiographic evidence of venous outflow obstruction of her thalamic AVM with prominent perinidal edema and progressive occlusion of the nidus.
Conclusion: We conclude that occlusive hyperemia is responsible for some cases of neurological deterioration after AVM radiosurgery, especially in a setting for which the time course or other clinical features are not as might be expected from a radiobiological perspective. The two patients we describe in this report suggest that manifestations may vary.