Abstract
Traditionally, surgical clipping was the only available treatment modality for intracranial aneurysms. However, in the last few decades, the endovascular therapy of intracranial aneurysms (IAs) has seen a tremendous evolution and development. From coiling to flow diversion and flow disruptor devices, endovascular treatment modalities have increased in number and received broader indications throughout the years. In this review article, the treatment modalities for the endovascular management of IAs are presented, emphasizing newer devices and technologies.
Highlights
In the last three decades, several treatment modalities for the management of intracranial aneurysms (IA) have been introduced
Multiple genetic loci have been investigated for a potential link with IA formation and/or rupture, including candidate polymorphisms located in the ANRIL, SOX17, EDNRA, COL1A2, COL3A1, ACE, IL-6, SERPINA3 (α1-antichymotrypsin), VCAN, and HSPG2 genomic regions [9]
IAs are more frequently found on the medial cerebral artery (MCA), followed by the internal carotid artery (ICA), anterior cerebral artery (ACA), anterior communicating artery (AComA), posterior communicating artery (PComA), and vertebrobasilar arteries [1]
Summary
In the last three decades, several treatment modalities for the management of intracranial aneurysms (IA) have been introduced. After that, coiling-assistant devices were introduced, namely balloons and stents. At the start of the 21st century, flow diversion devices were introduced in the treatment of IAs, representing a novel stent with enhanced features compared to traditional stents. The present review aims to highlight the main treatment modalities for the management of IAs. recent technological advances in coiling, with the use or absence of either stent or balloon assistance, flow diversion, and flow disruption are discussed. In a population without comorbidities, the prevalence of unruptured intracranial aneurysms (UIAs) is estimated at 3.2%. The prevalence is significantly higher in individuals older than 30 years of age compared to those under 30 years. The prevalence of UIA in patients aged 30 years and older has been reported to vary between 3.6 and 6.5% [2]. Smoking is an independent risk factor, with smokers at a higher risk of IA development and rupture, especially in individuals who started smoking at a young age [6]
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