Rupture of a cerebral artery aneurysm ➠ blood ejected into the subarachnoid space ➠ acute increase of intracranial pressure ➠ reduction of cerebral perfusion pressure ➠ reduced cerebral blood flow ➠ initial loss of consciousness ➠ Cushing reflex➠ possible recovery of consciousness.
The mechanisms responsible for creating a cerebral artery aneurysm are not fully understood. They often develop where there is a weakness in the thin smooth muscle layer (intima) of a cerebral vessel. Such a weakness is more likely to occur near the bifurcation of a vessel where hemodynamic turbulence, shear forces and vessel remodeling act to alter the integrity of vessel wall. Inflammatory mediators such as activated B cells, tumor necrosis factors, oxidative species, and macrophages are also thought to influence the development of cerebral aneurysms (Aoki & Nishimura, 2010; Lucke-Wold, et al., 2016).
In areas of vessel injury or intimal weakness, arterial blood pressure forces the remaining layer to expand outward, forming a thin walled balloon. The thin adventitia can rupture, allowing blood to be ejected under pressure into the subarachnoid space, cisterns, ventricles, sulci and spinal subarachnoid space.
Non-Modifiable risk factors (Bor, Koffijberg, Wermer & Rinkel, 2010; Broderick, et al., 2009; Connolly et al., 2010) include:
- Female gender (XX)
- Presence of unruptured cerebral aneurysm
- History of previous aSAH
- Autosomal dominant polycystic kidney disease
- Ehlers-Danlos Syndrome Type IV
- Family history of aSAH
Modifiable risk factors (Etminan, Beseoglu, Steiger & Hanggi, 2011; Clarke, 2008; Feigin, et al., 2005) include:
- Alcohol or illicit drug abuse
- Use of sympathomimetic drugs (cocaine)
- Low body mass index (BMI)
- Significant stressful life events