• Aqueel H Pabaney, Richard A Rammo, Rizwan A Tahir, and Donald Seyfried.
• Department of Neurosurgery, Henry Ford Hospital, Detroit, Michigan, USA. Electronic address: ahpabaney@gmail.com.
• World Neurosurg. 2016 Dec 1; 96: 608.e5-608.e12.

BackgroundArteriovenous malformations (AVMs) are hypothesized to be static, congenital lesions developing as early as 4 weeks of fetal life. New literature has shown that AVMs may represent dynamic and reactive vascular lesions arising from cerebral infarction, inflammation, or trauma. A literature search reveals 17 previously reported cases of new AVM formation after previous negative imaging studies. This reactive development or "second hit" theory suggests that at a molecular level, growth factors may play a vital role in aberrant angiogenesis and maturation of an arteriovenous fistula into an AVM.Case DescriptionA 52-year-old female presented with a ruptured left frontal AVM demonstrated by computed tomography angiography and digital subtraction angiography. The patient had suffered an acute ischemic stroke in the similar cerebral vascular territory 8 years prior due to left internal carotid artery occlusion. Detailed neuroimaging at that time failed to reveal any vascular malformation, suggesting that the AVM might have developed in response to initial vascular insult.ConclusionsWe believe that there might exist a subset of AVMs that display dynamic characteristics and could potentially appear, grow, or resolve spontaneously without intervention, especially in the presence of local growth factors and molecular signaling cascades. When combined with a previous cerebral insult such as stroke, trauma, or inflammation, de novo AVM formation may represent a "second hit" with abnormal angiogenesis and vessel formation.Copyright © 2016 Elsevier Inc. All rights reserved.

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