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Vertebral Artery Dissection

Vertebral artery dissection

This as above is a disease predominantly of younger adults. Anatomically it most commonly occurs in the V3 segment of the vertebral artery between where it exits the transverse foramen and enters the foramen magnum. Consider and screen for it in any younger person (under 50) with a posterior circulation stroke particularly if there is neck pain or where there is no alternative aetiology found e.g. AF. Dissection leads to endothelial luminal clot formation which can embolise. The clot can also cause occlusion of the vertebral or embolise into basilar and then posterior cerebral arteries in branches such as those to the cerebellum. Brainstem, thalamic, occipital and cerebellar infracts may be seen. Thromboembolism originating at vertebral level may cause infarcts above the basilar artery on either side of the posterior circulation (occipital cortex and thalamus).

There is a predisposition to dissection in those with Ehlers Danlos Type IV or Fibromuscular dysplasia. Dissection may be precipitated by neck trauma e.g. hairdressers, reversing car looking over shoulder. There is a small risk of intracranial dissections bleeding causing SAH (thunderclap headache).

Dissection and vertebral occlusion can cause an ipsilateral lateral medullary syndrome with the interesting presentation of a Horner's syndrome due to disruption of the primary neurone of the oculosympathetic tract. With carotid dissection the Horner's is due to disruption of the tertiary neurone.

Clinical

Presentations of Vertebral Dissection
  • Asymptomatic presenting only as posterior circulation stroke
  • Neck pain, may be post neck manipulation
  • Ipsilateral Horner's syndrome due to lateral medullary syndrome
  • Migrainous type headache
  • Vertebral artery occlusion causing Lateral medullary syndrome
  • Hemianopia due to emboli to Occipital cortex
  • Ataxia due to cerebellar infarction
  • Subarachnoid haemorrhage

Investigations

Investigation of choice is MRI with fat suppression of neck to shows crescent shaped intramural clot. CTA or MRA are also done to show the level of any blockage and to demonstrate infarction. Classically the dissection shows a mild tapering rather than an abrupt stenosis rather than an abrupt occlusion seen with embolism or thrombosis in situ.

Management

The patient may simply present with posterior circulation stroke symptoms which may be mild and neck pain. Management is the same as for carotid dissection. The fact that it has not been shown that anticoagulation is better than anti-platelet therapy makes life simpler when the imaging is equivocal or the presentation is late one can simply treat as ischaemic stroke with either aspirin or clopidogrel or even dual therapy for a short period that theoretically allows the interrupted possibly prothrombotic intima to repair and re-endothelialise.


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