Hyperdense vertebral artery sign with medullary and cerebellar infarctions

Case contributed by Ibraheem Mohammad AL-Boany
Diagnosis almost certain

Presentation

Patient presented with vertigo, frequent choking and difficulty in swallowing.

Patient Data

Age: 60 years
Gender: Male

Non-enhanced CT study shows multiple hypoattenuated foci involving both cerebellar hemispheres, more on the left side, associated with mild oedema and mass effect. The examined distal left vertebral artery, including its intracranial segment, appears hyperattenuated, giving a picture impressive of hyperdense artery sign suggestive of embolic infarctions.

Questionable hypodensity is also seen in the left posterior aspect of the medulla oblongata which raises concern for infarction.

A Follow-up MRI study was taken 5 days later confirming the presence of multiple acute infarctions involving the cerebellar hemispheres which appear with restricted diffusion pattern on DWI sequence. The study also shows focal acute infarction involving the left posterior aspect of the medulla oblongata, which is suggestive of lateral medullary syndrome.

Case Discussion

The hyperdense artery sign indicates occlusion of the involved artery, which usually precedes the classic radiological findings of acute ischaemic stroke, such as hypodensity and loss of gray-white matter differentiation. The intraluminal thromboembolic material is responsible for the high vessel attenuation. Although CT is not sensitive for detection of this sign, the high specificity (90%) makes this sign helpful for early detection of acute thromboembolic infarction.

Embolic occlusion of the intracranial segment of the vertebral artery can result in ischaemic infarctions involving the medulla oblongata as well as the cerebellum. Ischaemic damage of the lateral medulla, posterior to the inferior olivary nucleus, often leads to Wallenberg syndrome (also called lateral medullary syndrome), which can present with dysphagia, ipsilateral limb ataxia and ipsilateral Horner syndrome such as in this case.

The patient was hospitalised for one week under observation, received anti-platelet therapy and started feeding with a nasogastric tube.

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