Figure 5.

This cartoon summarizes the main steps of the establishment of inflammation in intracranial aneurysms. Going anti-clockwise: increased mechanical stress in aneurysm-prone regions is believed to trigger events that culminate in vascular dysfunctional, leaving the endothelium nude from anti-thrombotic protection. The inflammatory cascade then begins, with the expression of chemoattractants, pro-inflammatory cytokines and burgeoning of cell adhesion molecules at the surface of ECs, which attract peripheral blood mononuclear cells, including monocytes and T-cells. The complement is also activated through the classical pathway. Monocytes are able to adhere and transmigrate into the endothelium, which they would not do under normal conditions. They subsequently differentiate into macrophages, as observed in morphological studies of IA wall. The level of proteases in aneurysmal wall is increased and given literature knowledge about macrophages, there is good evidence that macrophages are responsible for the imbalance of proteases. During remodeling, the medial layer is destroyed, so is the internal elastic lamina, leading to lower mechanical properties and finally ballooning of the wall.