Brian Tsang, Maryam Gulzar, Rajab Khan, Noreen Rasheed, Katherine Harries, Harita Sivashankar, Imran SyedPatient
47 years, male
A 47-year-old male presented with sudden onset right eye vision loss, right-sided weakness and vomiting lasting 5 minutes with no past medical history. Arriving at the hospital 30 minutes later, his symptoms appeared to have resolved. He never smoked, worked in a supply chain and is independently mobile.
The CT head was unremarkable. MRI head with diffusion-weighted imaging showed a linear acute infarction involving the superior vermis of the cerebellum. CT angiography (CTA) of the carotids showed a left and right vertebral artery stenosis of 40% and 50% respectively, but no vasculitis or aneurysm.
Magnetic resonance angiography (MRA) of the neck including T1-weighted fat-saturated axial sequences was obtained within 72 hours. At the C5 level, the left vertebral artery diameter was increased and the lumen was eccentrically attenuated. However, the arterial wall did not enhance.
At the C5 level involving the right vertebral artery, the lumen was attenuated and became crescentic. The external diameter increased at the site of luminal attenuation, due to thickened wall secondary to intramural hematoma.
MRA maximum intensity projection sequences confirmed narrowing of bilateral vertebral arteries corresponding to the site of bilateral intramural haematomas, and therefore findings are suggestive of bilateral vertebral artery dissection.
Vertebral artery dissection (VAD) is a rare cause of stroke.  In a younger patient (ages 30-45), VAD may cause up to 10-25% of ischaemic strokes and incidence is reported at 2.5-3/100,000.1-2 Most VAD occurs intracranially. 
Risk factors of vertebral artery dissection are typically divided into traumatic versus spontaneous (atraumatic).  A history of trauma, such as sudden neck or cervical spine rotation, may be associated with VAD.  Spontaneous VAD may be caused by fibromuscular dysplasia, or connective tissue diseases including Ehler-Danlos and Marfan’s, or vasculitis. 
CTA can be used in the diagnosis of VAD. Bony structures, soft tissues and blood vessels are better delineated on CT.  CTA has been found to have similar sensitivity and specificity compared to MRI.  Limitations of CTA include exposure to radiation and contrast, and decreased sensitivity in detecting ischaemic injury. 
Magnetic resonance angiography (MRA) has been found to identify dissection in 88-97% of patients.  Compared to CT, MRI can better detect ischaemic injury, although there may be limited interpretation in VAD due to the presence of blood varying in appearance depending on the onset of injury.  MRA pathognomonic features of dissection include vessel wall hyperintensity on T1 images, an intimal flap and luminal thrombosis. 
T1 appearances of haemorrhage depend on time of onset. If the onset of injury is between 0-3 days, blood is isointense on T1.5 Between 3-7 days, T1 signal gradually increases to become hyperintense.  After 14 days, blood is once again isointense.  Breakdown of blood into its proteins causes the hyperintense signal on T1.5
The patient was thrombolysed on admission. Bloods were normal and vasculitis screen negative. His symptoms improved quickly and was discharged on dual antiplatelets. Follow-up at 3 and 6 months revealed some mild dizziness and unsteadiness remaining.
Vertebral artery dissection is an important cause of stroke in younger patients. MRA pathognomonic features of dissection include vessel wall hyperintensity on T1 images, an intimal flap and luminal thrombosis.
Written informed patient consent for publication has been obtained.
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