gms | German Medical Science

60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit den Benelux-Ländern und Bulgarien

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

24. - 27.05.2009, Münster

A mechanism for the rapid development of intracranial aneurysms

Meeting Abstract

  • C. Doenitz - Klinik für Neurochirurgie, Universitätsklinikum Regensburg
  • K.-M. Schebesch - Klinik für Neurochirurgie, Universitätsklinikum Regensburg
  • R. Zoephel - Klinik für Neurochirurgie, Universitätsklinikum Regensburg
  • A. Brawanski - Klinik für Neurochirurgie, Universitätsklinikum Regensburg

Deutsche Gesellschaft für Neurochirurgie. 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien. Münster, 24.-27.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocP05-04

DOI: 10.3205/09dgnc296, URN: urn:nbn:de:0183-09dgnc2968

Veröffentlicht: 20. Mai 2009

© 2009 Doenitz et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: We had the chance to observe the rapid development and rupture of an aneurysm of the basilar artery within 44 days in one of our patients. Initially the patient suffered from subarachnoid hemorrhage (SAH) due to an aneurysm of the anterior communicating artery. Forty-four days after the initial SAH, the patient experienced a second SAH. Re-angiography now showed a newly grown aneurysm of the basilar tip. Between the two hemorrhages transcranial Doppler sonography (TCD) revealed generalized vasospasm. We performed computational fluid dynamics (CFD) on the models of the initial and ruptured aneurysm state with and focused on wall pressure, impingement point, wall shear stress and asymmetric outflow conditions. In the end we suggest a coherent mechanism for the fast development of aneurysms based on our findings and discuss the current literature.

Methods: Two 3D mesh-models of the initial and ruptured aneurysm state were built using CT-angiography slices. They were generated and smoothed with a 3D modeling software ('AMIRA', TGS Inc., USA). Surface and volume meshes were generated (ICEM 10.0, Ansys Corp., USA). 'AMIRA' and 'ANSYS' software was used for CFD. We assumed rigid walls, pulsatile flow and modeled blood as a non-Newtonian fluid and a shear-dependent dynamic viscosity following a Power Law model. Flow velocity profiles from TCD data were used as input function. We investigated flow velocity, wall pressure, impingement point, wall shear stress, asymmetric and pulsatile flow.

Results: Wall pressure and impingement point did not reveal the site of actual aneurysm growth. Our findings show fading of the impingement point during development, corresponding to the expansion of the basilar head, caused by elevated pressure due to vasospasm of distal arteries, which was measured by TCD. In our case, aneurysm growth starts in the region of steady low wall shear stress (WSS), exposing the site of bleb formation and revealing the site of later rupture. Furthermore, region of permanent low WSS was not affected by pulsatile or asymmetric flow.

Conclusions: Based on our findings, we suggest a coherent mechanism for the fast development of intracranial aneurysms. Locally enhanced blood pressure, e.g. due to peripheral vasospasm or chronic hypertension, results in geometrical changes causing specific alterations of flow patterns. Hereby areas of permanent low WSS do appear, leading to wall degeneration and finally ending in bleb formation and rupture.