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The mystery of intracranial aneurysm formation

O mistério da formação de aneurismas intracranianos

EDITORIAL

The mystery of intracranial aneurysm formation

O mistério da formação de aneurismas intracranianos

Jamary Oliveira-Filho

Federal University of Bahia, Salvador BA, Brazil

Correspondence Correspondence: Jamary Oliveira-Filho Rua Waldemar Falcão 2106 / apto 201 40296-710 Salvador BA - Brasil E-mail: jamaryof@ufba.br

Intracranial aneurysms are a common and potentially devastating condition. They are found in approximately 1% of autopsies and 7% of patients referred for catheter angiography for indications other than subarachnoid hemorrhage1. Pathogenesis is not completely understood, but it is generally accepted that both genetic and hemodynamic factors play a role. As a group, a number of known heritable disorders account for only 5% of aneurysm cases, such as Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, Marfan syndrome and others2. A series of recent genome-wide association studies have identified candidate genes related to increased risk of aneurysm formation3,4. While some of these genes are related to wall structure, others are related to hemodynamic wall stress5. Thus, hemodynamic factors are still thought to play the dominant role in aneurysm formation, justifying their preferential location in arterial bifurcations.

In this issue of Arquivos de Neuro-Psiquiatria, Silva Neto et al.6 shed further light into the pathophysiology of aneurysm formation. In this angiographic case series, 169 patients diagnosed with intracranial aneurysms were compared with 256 patients referred for multiple reasons to catheter angiography without intracranial aneurysms. A series of common anatomic variants of the circle of Willis were found to be related to different aneurysm locations. Aneurysms in the posterior communicating artery (PComA) were associated with fetal-type PComA; and anterior communicating artery (AComA) aneurysms were associated with A1 hypoplasia. Both variants increase flow to arterial bifurcations, theoretically increasing the odds of aneurysm formation. Moreover, a careful analysis of the carotid syphon was performed, measuring the angle between the intracavernous and supraclinoid segments of the carotid artery. A lower angle (which also increased local blood flow distally) was associated with higher occurrence of aneurysm.

Some emphatic points in Silva Neto's work are the large sample size and biological plausibility of the findings. As in any single-center case series, authors must recognize that their findings may not generalize to other unselected samples. The authors do not explain their criteria for excluding 57 cases (from a sample of 512 patients, 30 did not have reports, 169 had aneurysms and 256 were controls, leaving 57 unaccounted patients). Calculation of the syphon angle is subject to an unknown measure of inter-rater variability and some bias may be expected from raters, as they were not blind to aneurysm status or location. Still, the authors are to be congratulated for their efforts in studying a significant population and for increasing our knowledge on the origin of intracranial aneurysms in a Brazilian population.

Received 30 October 2012

Accepted 06 November 2012

Conflict of interest: There is no conflict of interest to declare.

  • 1. Nakagawa T, Hashi K. The incidence and treatment of asymptomatic, unruptured cerebral aneurysms. J Neurosurg 1994;80:217-223.
  • 2. Schievink WI. Genetics of intracranial aneurysms. Neurosurgery 1997;40:651-662.
  • 3. Foroud T, Koller DL, Lai D, et al. Genome-Wide Association Study of Intracranial Aneurysms Confirms Role of Anril and SOX17 in Disease Risk. Stroke 2012;43:2846-2852.
  • 4. Low SK, Takahashi A, Cha PC, et al. Genome-wide association study for intracranial aneurysm in the Japanese population identifies three candidate susceptible loci and a functional genetic variant at EDNRA. Hum Mol Genet 2012;21:2102-2010.
  • 5. Gaál EI, Salo P, Kristiansson K, et al. Intracranial aneurysm risk locus 5q23.2 is associated with elevated systolic blood pressure. PLoS Genet 2012;8:e1002563.
  • 6. Silva Neto AR, Câmara RLB, Valença MM. Carotid siphon geometry and variants of the circle of Willis in the origin of carotid aneurysms. Arq Neuropsiquiatr 2012;12:917-921.
  • Correspondence:

    Jamary Oliveira-Filho
    Rua Waldemar Falcão 2106 / apto 201
    40296-710 Salvador BA - Brasil
    E-mail:
  • Publication Dates

    • Publication in this collection
      03 Jan 2013
    • Date of issue
      Dec 2012
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