A 43-year-old Caucasian man was admitted to the emergency department of our hospital for headache associated with weakness of the left limbs. He had no medical history, he denied even slight trauma of the neck, and his only cardiovascular risk factor was tobacco smoking for 10 years. Neurological examination revealed verbal aphasia and left hemiparesis.\nDuring CT angiography (TK–64-row MDCT scanner, LightSpeed VCT, GE, Waukesha, WI) of the neck and head, segmental dissections of the right internal carotid artery (ICA) at the level of the cranial basis were discovered (Fig. a). The lumen of the ICA was decreased to 4 × 2.5 mm (60 % of normal flow). Cerebral CT showed a recent infarction involving the medial part of the right temporal lobe and deep structures of the right hemisphere including the thalamus, the genu and the posterior limb of the internal capsule (Fig. b).\nCT angiography of the neck and head also showed a duplication of the left vertebral artery (LVA) with two origins, both from the left subclavian artery (Figs. , ). The duplicated segments were fused at level of the C5–6 vertebrae into a single vertebral artery, which then entered the transverse foramen of C5 (Fig. ). All measurements were taken on an Advantage Workstation (GE).\nThe first LVA originated from the left subclavian artery at a distance of 7 mm from the aortic arch. It measured 2.9 and 2.8 mm in diameter at the points of origin and just before fusion, respectively (Fig. ). The course of the artery was 101 mm. The second LVA arose from the left subclavian artery 37 mm distal to the first (44 mm from the aortic arch). It measured 2.4 and 2.2 mm in diameter at the points of origin and just before fusion, respectively (Fig. ), and its course was 89 mm. Both vertebral arteries possessed a regular lumen. The diameter of the LVA after fusion was 3.3 mm (at level C5–6) (Fig. ).\nThe right VA arose as the first branch from the left subclavian artery, 43 mm from the aortic arch. Its course was normal. The diameters of the right VA were 4 mm at the points of origin and 3.8 mm at the C5–C6 vertebrae (Fig. ). Both thyrocervical trunks were seen to originate separately from the subclavian arteries.\nAdditionally, complementary but independent to CT angiography Doppler Sonography B-flow mode (Vivid 7 Pro, GE) of the vertebral arteries also revealed a duplicated LVA (Fig. ).\nAfter all procedures were completed, Ehlers–Danlos syndrome type IV was diagnosed.
A 63-year-old woman presented with sudden onset vertigo and was diagnosed with an acute infarction in the left cerebellum on October 17, 2015. On the brain magnetic resonance imaging (MRI), an acute infarction was observed in the territory of the left superior cerebellar artery (SCA) (). Magnetic resonance angiography showed a mild irregularity in both proximal VAs and an occlusion in the left SCA (). For further evaluation, we performed a diagnostic cerebral angiography. The SCA was completely recanalized, and there was no definite abnormality in both VAs. Incidentally, we observed an unopacified streaming at the level of C5 during the selective catheter angiography of the left VA originated from the left subclavian artery (). And the medial limb of the left VA arising from the aortic arch could be found on the selective catheter angiography, which was not observed on the MRA. The dominant, lateral limb of the left VA was originated from the left subclavian artery () and the small, medial limb was originated directly from the aortic arch between the left common carotid artery and the left subclavian artery (). They joined at the transverse foramen of the fifth cervical vertebra.\nA right-to-left shunt was suspected on the transcranial doppler using an agitated saline solution with blood. A pulmonary arteriovenous malformation (AVM) in the right lung was detected by transesophageal echocardiography and chest computed tomography. With an elevated level of D-dimer with 421 ng/ml, the pulmonary AVM was suspected as a source of embolus causing an acute cerebellar infarction.