Elsevier

World Neurosurgery

Volume 96, December 2016, Pages 608.e5-608.e12
World Neurosurgery

Case Report
Development of De Novo Arteriovenous Malformation Following Ischemic Stroke: Case Report and Review of Current Literature

https://doi.org/10.1016/j.wneu.2016.09.062Get rights and content

Background

Arteriovenous 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 Description

A 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.

Conclusions

We 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.

Introduction

Intracranial arteriovenous malformations (AVMs) are unique vascular lesions of the brain that consist of arterial feeders, venous drainage, and an intervening nidus that does not contain capillary bed or functional neuronal tissue. Traditionally, AVMs are thought to arise between weeks 4 and 8 of embryonic life secondary to disordered embryogenesis.1 However, despite frequent use of prenatal ultrasound, there is remarkably little evidence to show that AVMs are congenital lesions arising during embryonic development and in utero diagnosis of AVM is rarely reported.2, 3, 4 Only a handful of reports have surfaced in the past 3 decades that mention discovery of de novo AVMs in patients in whom prior cerebrovascular imaging studies did not reveal vascular malformation (Table 1). We present a case of a 52-year-old who presented with a ruptured left frontal AVM that was not found on detailed neuroimaging evaluation when she had presented 8 years earlier with ischemic stroke.

Section snippets

Case Report

Patient data were gathered from our electronic medical records after obtaining approval from the Henry Ford Institutional Review Board (IRB #8179). Our patient is a 52-year-old female who had initially presented 9 years ago in the summer of 2007 with acute-onset right hemiplegia and severe dysarthria; her National Institutes of Health Stroke Scale score on presentation was 22. She was found to have a hyperdense left middle cerebral artery sign on computed tomography (CT) of her head and a left

Methods

A MEDLINE (PubMed and Ovid) and Google Scholar search of the literature was performed from 1992 to January 2016. The databases were queried using key words “arteriovenous malformation,” “AVM,” and “de novo.” This resulted in 116 articles, of which full-text copies of the articles were obtained.

The results were then assessed by 2 independent reviewers (A.P. and R.R.) for articles detailing the occurrence of new AVMs on imaging with prior studies demonstrating negative findings. Those articles

Results

In the 22 studies noted in the literature since 1991, 26 patients were reported to have de novo AVMs after imaging confirmed no presence of a vascular malformation (Table 1). All articles were composed of case reports and case series. No case control, prospective cohort, or randomized control studies met criteria.

Characteristics of patients presenting with de novo AVMs are presented in Table 2. The median age of the patients at time of diagnosis was 15.5 years (±18.4 years). The median duration

Discussion

Multiple hypotheses have been put forward to plausibly explain the etiopathogenesis of brain AVMs and include genetic, molecular, environmental, and biologic factors. However, the long-held dogma of AVMs being static, congenital lesions is being repeatedly questioned as de novo AVMs are being reported with increasing frequency in patients not suffering from neurovascular syndromes such as Osler-Weber-Rendu disease, Wyburn-Mason syndrome, or Sturge-Weber syndrome5, 6, 7, 8, 9, 10, 11, 12, 14, 15

Conclusion

This is the first reported case of development of de novo AVM after ischemic stroke and highlights the role of various molecular markers possibly responsible for development and growth of AVMs. There is a need to explore new paradigms in brain AVM pathogenesis, including the possibility that AVMs might represent benign, slow-growing vascular tumors rather than static congenital lesions that could result from acquired somatic mutations and may represent aberrant adult vasculogenesis.

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    Conflict of interest statement: The authors declare that the article content was composed in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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