Are parenchymal AVMs congenital lesions?

Abstract

<jats:p>A long-held dogma in neurosurgery is that parenchymal arteriovenous malformations (AVMs) are congenital. However, there is no strong evidence supporting this theory. An increasing number of documented cases of de novo formation of parenchymal AVMs cast doubt on their congenital nature and suggest that indeed the majority of these lesions may form after birth. Further evidence suggesting the postnatal development of parenchymal AVMs comes from the exceedingly rare diagnosis of these lesions in utero despite the widespread availability of high-resolution imaging modalities such as ultrasound and fetal MRI. The exact mechanism of AVM formation has yet to be elucidated, but most likely involves genetic susceptibility and environmental triggering factors. In this review, the authors report 2 cases of de novo AVM formation and analyze the evidence suggesting that they represent an acquired condition.</jats:p>

Superficial middle cerebral vein connection to the cavernous sinus is not infrequent in brain arteriovenous malformations: an argument against their congenital origin?

“…Further work comparing general venous anatomy between brain AVM patients and controls is needed to clarify this point. Finally, the result of this study does not directly contradict the congenital origin of brain AVM but instead only challenge a frequently reported argument for congenital origin [3,[17][18][19].…”

“…Although having been published about 20 years ago, the original report by Mullan et al [5] has never been contradicted and continues to be regularly cited as an argument for the congenital origin of brain AVM [3,[17][18][19]. The aim of our study was to test Mullan's statement that the SMCV is frequently absent or fails to connect with the CS in presence of brain AVM.…”

De Novo Arteriovenous Malformation Growth Secondary to Implantation of Genetically Modified Allogeneic Mesenchymal Stem Cells in the Brain

“…16 The development of an AVM within 3 years after implantation of the GLP-1-secreting CellBeads suggests a possible relationship. Possible pathomechanisms include a local response to potentially angiogenetic peptides secreted by the MSCs or the GLP-1 itself, which may promote endothelial cell proliferation and angiogenesis.…”

“…The diagnosis of the de novo AVM was confirmed after an interval ranging from 2 to 17 years, and patients were 6 to 68 years old at the time of de novo AVM diagnosis (mean, 26.4 years). 16 The pathogenesis of AVMs is not sufficiently understood. It may involve an interaction between genetic susceptibility and environmental (acquired) factors.…”

The relationship of cortical folding and brain arteriovenous malformations

“…Our study raises several points essential to AVM pathogenesis. Although classically described as congenital malformations, there now exist many case reports of de novo AVM formation [42] on serial cerebral angiography. Our study represents a single point in time for each patient, and any structural differences seen in our population could be a result of a disordered cerebral circulation.…”