Case ReportDevelopment of De Novo Arteriovenous Malformation Following Ischemic Stroke: Case Report and Review of Current Literature
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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Vascular Malformations: A Histopathologic and Conceptual Appraisal
2023, Actas Dermo-SifiliograficasState of the Art and Future Direction in Diagnosis, Molecular Biology, Genetics, and Treatment of Brain Arteriovenous Malformations
2022, World NeurosurgeryCitation Excerpt :However, de novo cases have been reported,35,36 as well as cases of recurrences after surgical resection37-39 and remodeling during follow-up.40,41 These reports suggest that AVMs are dynamic structures guided by genetics and molecular pathways.42 In 1997, Lasjaunias et al.43 suggested that these diseases could be the expression of various diseases rather than a disease itself and could be caused by biological dysfunction of the remodeling process at the capillarovenous junction.
Cerebral Arteriovenous Malformations as Acquired Lesions: Case Reports and Review of the Literature
2020, Journal of Stroke and Cerebrovascular DiseasesCitation Excerpt :Recent advancements in imaging technology coupled with an increasing number of clinical studies have led to a new body of evidence challenging the classic belief that all AVMs develop in the perinatal period and have a long period of clinical silence. In fact, various reports have described cases in which de novo AVM formation occurred.1–35 All of these cases were characterized by an intracranial environmental trigger (“second hit”) in addition to a genetic predisposition for de novo AVM formation.
Infant Fistula-Type Arteriovenous Malformation with Cerebellar Hemorrhage Developed into Nidus-Type in Adolescence
2020, World NeurosurgeryCitation Excerpt :At the initial treatment, the aneurysm was not visualized by feeder occlusion; however, we speculate that the fistula was not occluded completely, leading to its eventual transformation to nidus-type AVM. Recurrent AVM and de novo AVM are reported to occur in pediatric, rather than adult, patients.2,3,6,12-14 Pediatric AVM is immature and remains dynamic via intrinsic molecular factors.3,14
Arteriovenous Malformations: Congenital or Acquired Lesions?
2020, World Neurosurgery
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.