====== Intracranial aneurysm pathophysiology ======

see also [[Intracranial aneurysm hemodynamics]].


Alterations in the internal elastic membrane (lamina elastica interna) of cerebral arteries are thought to weaken vessel walls and render them less resistant to changes in intraluminal pressure
((Selman WR, Tarr RW, Ratcheson RA. Intracranial aneurysms and subarachnoid hemorrhage. In: Bradley WG, et al., eds. Neurology in clinical practice. 3d ed. Boston: Butterworth-Heinemann,2000:1188–90.)).

These changes most frequently develop at sites of vessel bifurcation, where blood flow is most turbulent and shear forces against the arterial wall are greatest
((Inci S, Spetzler RF. Intracranial aneurysms and arterial hypertension: a review and hypothesis. Surg Neurol. 2000;53:530–40.)).

This can be because of acquired disease or hereditary factors. The repeated trauma of blood flow against the vessel wall presses against the point of weakness and causes the aneurysm to enlarge.
As described by the Law of Young-Laplace, the increasing area increases tension against the aneurysmal walls, leading to enlargement.

Despite evidence for a potential role of [[angiotensin]] in the pathophysiology, angiotensin-receptor blockers have shown little-to-no efficacy in preventing aneurysm formation and growth
((Chalouhi N, Ali MS, Jabbour PM, Tjoumakaris SI, Gonzalez LF, Rosenwasser RH, et al. Biology of intracranial aneurysms: role of inflammation. J Cereb Blood Flow Metab. 2012;32:1659–1676.)).

Despite technical and diagnostic progress there are still open questions in the understanding of the pathophysiology of intracranial aneurysms.

Assuming a preexisting reduced resistibility of the vessel wall to pressure changes and an area of permanently low [[wall shear stress]] WSS, an increase in pressure induces geometrical changes. These cause changes of intravascular flow distribution, lowering the already low WSS in specific locations. This leads to endothelial damage in this area and to a decreasing stability of the vessel wall, causing aneurysm development, growth, and rupture
((Doenitz C, Schebesch KM, Zoephel R, Brawanski A. A mechanism for the rapid
development of intracranial aneurysms: a case study. Neurosurgery. 2010
Nov;67(5):1213-21; discussion 1221. doi: 10.1227/NEU.0b013e3181f34def. PubMed
PMID: 20948398.
)).