Spontaneous Bilateral Vertebral Artery Dissection Secondary to PAI-1, MTHFR C677T and ACE Gene Mutations in a Young Man

Discussion Stroke in young adults is no longer a rare phenomenon. One third occur in patients younger than 65 years [3] . Etiologies include atrial fibrillation with embolization [3] , hypertension, diabetes mellitus, cervicocerebral stenosis [1, 2, 4] , cerebral venous thrombosis [5] and a hypercoaguable state [4–9] . Carotid stenosis and strokes are associated with PAI-1 mutation [4] . Venous thrombosis has been associated with factor V Leiden, prothrombin II G20210A and MTHFR C677T gene mutations [5, 6] . The prothrombin II G20210A mutant gene is associated with a 5.1-fold increase in ischemia [7] . The most frequent candidate polymorphism associated with the risk of cerebral stroke include ACE, factor V Leiden, MTHFR, prothrombin G20210A and apolipoprotein E [8] . The thrombogenic risk factor increases with the cumulative existence of the variant mutations: the gene-dose effect [6, 9] . Vertebral artery dissections (VAD) present with posterior neck pain, suboccipital headache and posterior circulation ischemia [1] . The annual incidence is 1–1.5 per 100,000 [1] . Causes include trauma, respiratory infection, hypertension, oral contraceptive drugs, inherited connective tissue disorders [2] and genetic mutations. We report bilateral spontaneous VAD in a healthy young man in association with MTHFR C677T, PAI-1 and ACE gene mutations.