Brain Arteriovenous Malformation Pathogenesis: A Response-to-Injury Paradigm

Kim, Helen; Su, Hua; Weinsheimer, Shantel; Pawlikowska, Ludmila; Young, William L.

doi:10.1007/978-3-7091-0693-8_14

Cited by 121 publications

(94 citation statements)

References 64 publications

(78 reference statements)

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“…The congenital nature of brain AVMs has been previously questioned by others, 20,21,27 and as we have discussed, there is compelling evidence suggesting the postnatal development of many of these lesions. However, the exact mechanism of AVM formation has yet to be elucidated, and it may involve an interaction between genetic susceptibility and environmental (acquired) factors.…”

Section: Putative Mechanisms Of Avm Formationmentioning

confidence: 60%

“…35 In addition, a variety of candidate gene studies in patients with sporadic AVMs have identified single-nucleotide polymorphisms (SNPs) associated with a susceptibility to develop AVMs and with their progression to intracerebral hemorrhage. 20,34 Most of the studied genes code for essential proteins in the angiogenic and inflammatory cascades. A recent systematic review included all the studies reporting SNPs associated with sporadic brain AVMs, and after a joint analysis of the risk estimates described in the different reports, a statistically significant association was found between an SNP in the ALK1 gene (intervening sequence 3-35A>G) and a susceptibility to develop a brain AVM (OR 2.19, 95% CI 1.25-3.83).…”

mentioning

confidence: 99%

“…19,20,22 Studies of AVM tissue have shown increased endothelial cell proliferation and increased expression of angiopoietin-2 and vascular endothelial growth factor, which promote vascular destabilization and proliferation, respectively. 17 However, the exact triggering event that leads to increased and disorganized angiogenesis ultimately leading to AVM formation has not been identified.…”

mentioning

confidence: 99%

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Are parenchymal AVMs congenital lesions?

Morales-Valero

Bortolotti

Sturiale

et al. 2014

FOC

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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.

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Section: Putative Mechanisms Of Avm Formationmentioning

confidence: 60%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Are parenchymal AVMs congenital lesions?

Morales-Valero

Bortolotti

Sturiale

et al. 2014

FOC

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“…A combination of SRS, embolization, and microsurgery may be used in the palliative management of Spetzler-Ponce Class C lesions. 15,22,36,41 Given that the large majority of high-grade lesions cannot be treated without relatively high morbidity and mortality using current surgical and radiosurgical paradigms, new cellular and molecular biological therapies are under development aiming toward radiosensitization, vascular targeting, and remodeling therapies. 27,43 The current AVM treatment paradigm does not take into consideration any special factors related to the genetics or molecular constitution of the specific patient who has an AVM.…”

Section: Current Managementmentioning

confidence: 99%

Molecular and cellular biology of cerebral arteriovenous malformations: a review of current concepts and future trends in treatment

Rangel-Castilla¹,

Russin²,

Martinez-del-Campo³

et al. 2014

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Object Arteriovenous malformations (AVMs) are classically described as congenital static lesions. However, in addition to rupturing, AVMs can undergo growth, remodeling, and regression. These phenomena are directly related to cellular, molecular, and physiological processes. Understanding these relationships is essential to direct future diagnostic and therapeutic strategies. The authors performed a search of the contemporary literature to review current information regarding the molecular and cellular biology of AVMs and how this biology will impact their potential future management. Methods A PubMed search was performed using the key words “genetic,” “molecular,” “brain,” “cerebral,” “arteriovenous,” “malformation,” “rupture,” “management,” “embolization,” and “radiosurgery.” Only English-language papers were considered. The reference lists of all papers selected for full-text assessment were reviewed. Results Current concepts in genetic polymorphisms, growth factors, angiopoietins, apoptosis, endothelial cells, pathophysiology, clinical syndromes, medical treatment (including tetracycline and microRNA-18a), radiation therapy, endovascular embolization, and surgical treatment as they apply to AVMs are discussed. Conclusions Understanding the complex cellular biology, physiology, hemodynamics, and flow-related phenomena of AVMs is critical for defining and predicting their behavior, developing novel drug treatments, and improving endovascular and surgical therapies.

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“…AVMs are dynamic lesions that show evidence of active angiogenesis, inflammatory responses, and adaptive structural changes to its components over time. 31 AV shunting results in feeding artery dilatation and draining vein arterialization. 9,30 Histologically, the arterial elastic and muscular layers are altered.…”

Section: Pathophysiologymentioning

confidence: 99%