Figure 4.

The pathogenesis of spontaneous and anticoagulation-associated intracerebral hemorrhage (ICH) involves interaction between an underlying bleeding-prone small vessel disease (e.g., cerebral amyloid angiopathy) and the use of oral anticoagulation treatments. This dynamic interplay is modified at various levels by genetic and ethnic factors and cardiovascular risk factors. Acute trigger factors for example, sudden increases in blood pressure or minor trauma may cause the rupture of these abnormally weak vessels. Anticoagulation may promote ICH by allowing an otherwise innocuous minor and self-limiting vessel leak to expand into a life-threatening hematoma.