Subarachnoid haemorrhage (SAH) occurs as a result of rupture of intracranial aneurysms. SAH causes significant morbidity and mortality. In addition, SAH leads to significant financial burden. In this chapter, we will look into the association between raised serum homocysteine and intracranial aneurysms. In a study on the Han Chinese patients with intracranial aneurysm who were admitted to the hospital, the mean serum total homocysteine level in the patient group with intracranial aneurysm was significantly higher than those in the control group. In the same study, the patients with raised serum homocysteine had 2.196 higher risk of developing intracranial aneurysms. Ren et al. proposed that homocysteine should be seen as an indicator of the risk of intracranial aneurysm and not a direct cause of intracranial aneurysm. In another study, homocysteine increases the development of intracranial aneurysms in rats. Endothelial damage is an early change in the walls of intracranial aneurysms. Polymorphisms of the genes coding for the various components of the vessel walls may be associated with the formation of intracranial aneurysms. In a previous animal study, the size of intracranial aneurysms is significantly smaller in the mice with inducible nitric oxide synthase (iNOS) compared with the mice without iNOS.
Part of the book: New Insight into Cerebrovascular Diseases