The Epidemiology of Brain Arteriovenous Malformations

Abstract

The estimates for AVM prevalence that are published in the medical literature are unfounded. Because of the rarity of the disease and the existence of asymptomatic patients, establishing a true prevalence rate is not feasible. Owing to variation in the detection rate of asymptomatic AVMs, the most reliable estimate for the occurrence of the disease is the detection rate for symptomatic lesions: 0.94 per 100,000 person-years (95% confidence interval, 0.57-1.30/100,000 person-years). This figure is derived from a single population-based study, but it is supported by a reanalysis of other data sources. The prevalence of detected, active (at risk) AVM disease is unknown, but it can be inferred from incidence data to be lower than 10.3 per 100,000 population.

Pathogenesis and radiobiology of brain arteriovenous malformations: implications for risk stratification in natural history and posttreatment course

“…For example, HHT is an autosomal dominant genetic disorder with a high prevalence of BAVM, representing an interesting example of genetic influences in the development of BAVM. 6,59 Whereas the incidence of sporadic BAVM in the normal population is estimated to be 0.01%, incidence in HHT2 is 1%, and in HHT1 it is 10%, highlighting the fact that genetic dysfunction in HHT represents a "hyper-risk factor" for development of BAVM. 6,59 The gene involved in HHT1 codes for endoglin, an accessory protein of transforming growth factor-β receptor complexes, whereas HHT2 involves the gene for ALK1, a transmembrane kinase.…”

“…6,59 Whereas the incidence of sporadic BAVM in the normal population is estimated to be 0.01%, incidence in HHT2 is 1%, and in HHT1 it is 10%, highlighting the fact that genetic dysfunction in HHT represents a "hyper-risk factor" for development of BAVM. 6,59 The gene involved in HHT1 codes for endoglin, an accessory protein of transforming growth factor-β receptor complexes, whereas HHT2 involves the gene for ALK1, a transmembrane kinase. 59 The highly elevated risk of BAVM development among HHT patients suggests that germline variants of genes relating to these pathways could exert influence over risk for development of sporadic BAVMs.…”

Durable thrombosis in a rat model of arteriovenous malformation treated with radiosurgery and vascular targeting

“…For each of the 4 time points (1,7,30, and 90 days after treatment), the LPs/sTF+RTX group contained 3 rats (total 12), the LPs/sTF-RTX group contained 3 rats (total 12), and the saline+RTX group contained 2 rats (total 8). At 6 weeks after creation of the AVM model, radiosurgery was administered.…”

“…The prevalence of AVMs is 10-500 AVMs per 100,000 persons (0.01%-0.5% of the population), 1,5,38 yet these lesions are the most common cause of neurological impairment or death among patients younger than 20 years. 42,53 The goal of AVM treatment is to obliterate flow through the abnormal vessels and, therefore, eliminate the threat of intracranial hemorrhage, while maintaining normal circulation and preserving neurological function.…”

Differentiated neurosurgical treatment of cerebral arteriovenous malformations with epileptic seizures

“…Артеріо-венозні мальформації (АВМ) головного мозку -одна з найчастіших вроджених вад судин головного мозку, яка виникає внаслідок порушення ембріогенезу нейрональної та судин-ної систем плода. Це судинне ураження ЦНС має характерні клінічні прояви і потребує специфічного лікування [1]. За даними епідеміологічних дослід-жень, АВМ виявляють приблизно у 0,5% населення [2,3].…”