Abstract 1122‐000050: Arterial Steal in AVM: An Etiology of Ischemic Stroke

Introduction : Arteriovenous malformations (AVM) are rare congenital malformations in the brain, often presenting with cerebral hemorrhage. Unruptured AVMs usually remain asymptomatic, or they can present with headache, seizure, or focal neurological deficits. “Arterial steal” is one of the mechanisms which can lead to focal neurological deficits. The idea of vascular steal through high flow shunting within brain AVMs is not a new concept. There is, however, debate about whether the vascular steal phenomenon indeed exists empirically. In a study focused on vascular reserve in patients with cerebral AVMs (utilizing acetazolamide augmentation and perfusion CT methods), decreased hemodynamic reserve was noted in 27% of parenchymal regions of interest close to the AVM and in 17% of parenchymal regions of interest far from the AVM. Other imaging modalities have shown abnormal blood regulation around AVM however there exists a level of discordance between various modalities which questions whether vascular steal exists in vivo. We present an ischemic stroke caused by “arterial steal” phenomenon. Methods : Case report Results : 63‐year‐old male with past medical history of seizure, hypertension presented with confusion and dysarthria for 3 weeks. On exam he was found to have right upper quadrantanopia. CT head without contrast and MRI of brain revealed an evolving infarct in the left posterior cerebral artery (PCA) territory. CT angiogram showed possible occlusion in the left PCA P2 segment which correlated to the previously described stroke and in addition showed evidence of left thalamic AVM. Evaluation for cardioembolic or atheroembolic sources was unrevealing. A diagnostic cerebral angiogram showed a 1.3 mm AVM fed through anterior choroidal branches as well as posterior choroidal branches through left posterior communicating artery. There was delayed filling in the left PCA territory likely due to steal phenomenon which might be the etiology of the stroke. Conclusions : In our case, as demonstrated on angiogram, vascular steal phenomenon through high flow shunting of AVM is the likely explanation for the ischemic stroke.

Large vascular malformation in a child presenting with vascular steal phenomenon managed with pial synangiosis

The management of large and giant arteriovenous malformations (AVMs) in patients presenting with nonhemorrhagic neurological deficits secondary to vascular steal phenomenon is challenging and controversial. In many cases, large AVMs cannot be completely excised or cured, leaving patients with residual or partially treated AVMs, the natural history of which is unknown. Additionally, large, diffuse vascular malformations with multiple, small feeders, slow flow, or so-called cerebral proliferative angiopathy represent a related but distinct clinical and angiographic entity that may require a different therapeutic approach than traditional brain AVMs. The current management of children with other conditions of chronic cerebral hypoperfusion, such as moyamoya disease, involves consideration of surgical revascularization to enhance blood flow to the compromised hemisphere. Here, the authors present the case of a young child with a large thalamic vascular malformation who presented with clinical and radiological features of vascular steal and ischemia. In an effort to augment flow to the hypoperfused brain and protect against future ischemia, the authors treated the child with unilateral pial synangiosis. At 12 months, postoperative angiography demonstrated robust neovascularization, and the child has not sustained any further ischemic events. The authors discuss concept of vascular malformation–related hypoperfusion and the utility of indirect revascularization for inoperable vascular malformations presenting with ischemic symptoms.