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Biomedical Reviews

Pathobiology of human intracranial saccular aneurysms

Mária Tóth, György L. Nádasy, Tibor Kerényi, István Nyáry, Emil Monos


Intracranial saccular aneurysms develop in the course of life in a few percent of the total population. Usually they grow slowly, remain unnoticed, but their rupture induces subarachnoid bleeding with fatal or devastating consequences. Several theories have been constructed to explain the pathomechanism of aneurysm development and rupture. Here these theories will be reviewed. The very complicated blood flow pattern in arteries at the human cerebral base, instability of collateral circulation as well as blood pressure changes can disturb normal, laminar blood flow at bifurcations. With endothelial damage, integrity of basal lamina and internal elastic lamina will also be affected. Evagination of the thin wall occurs with increasing stresses on medial elements. Any pathological factor affecting molecular structures joining connective tissue components with each other, or with the cellular structures, will promote the evagination process. With further enlargement of the sack, increasing mechanical forces make the presence of smooth muscle cells impossible in the wall. When this happens, the ability to rearrange, reorientate connective tissue fibers with the aid of active forces will be lost. Passive rearrangement of fiber structure governed by distending forces, thinning of the wall will be the result, unavoidably leading to the fatal outcome. We can conclude that current hypotheses of human intracranial saccular aneurysm development are not necessarily contradictory. Probably, they describe different factors promoting separate phases in the aneurysm development.

Biomedical Reviews 2000; 11: 53-61.

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About The Authors

Mária Tóth
Semmelweiss University

György L. Nádasy
Semmelweiss University

Tibor Kerényi
Semmelweiss University

István Nyáry
National Institute of Neurosurgery of Budapest

Emil Monos
Semmelweiss University

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