Vertebral Artery Dissection
- What is vertebral artery dissection
- What does it do and clinical effects of damage
- What is the management
Vertebral artery dissection
Cervical artery dissection is a generic term for dissections of the vertebral and carotid and accounts for 10-20% of all strokes in young adults. It is a relatively new diagnosis as the first report of a spontaneous internal carotid artery (ICA) dissection appeared in 1959 . Spontaneous dissections are the leading cause of stroke in patients younger than 45 years of age. It is a diagnosis that must be constantly sought and can easily be missed if the correct imaging tests are not done or delayed. Dissection occurs when there is a tear in the intimal layer of a blood vessel with bleeding and haematoma within the vessel wall. The diagnosis needs to show the presence of a mural haematoma located in the arterial wall. The haematoma may be due to an intimal tear and entry of luminal blood or from vasa vasorum or both. This can lead to overlying thrombus or vessel stenosis or occlusion. The clot can cause complete or subtotal occlusion of the carotid artery or vertebral artery. Damage to the endothelium means that the vessel loses its natural "non-stick-surface" and so clot can form on the luminal intimal surface and cause an artery to artery embolisation which is the rationale for anticoagulation/antithrombotic therapy.
This as above is a disease predominantly of younger adults but can happen at any age. 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 infarcts 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.
Intracranial artery dissection differs from extracranial dissection as it is less common and there is an increased risk specifically of SAH. It is also reportedly more common in children and in Asian populations. The diagnosis can be more challenging because characteristic imaging features can be difficult detect in view of the small size of intracranial arteries. Intracranial artery dissections tends to favour the posterior circulation more frequently than the anterior circulation which contrasts with cervical dissection. Multimodal imaging e.g. CTA/MRA/ and DSA may be needed. A good review is found below.
|Possible risk factors for dissection|
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|Presentations of Vertebral Dissection|
- Bloods FBC, U&E, LFTs, ESR, CRP
- OthersECG for AF. CXR may be needed.
- DuplexCarotid/Vertebral duplex: may show altered flow in vertebral vessels.
- Imaging 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. Aneurysm formation may also be seen.
The patient may simply present with dissection and posterior circulation stroke symptoms which may be mild and neck pain and in this case the treatment of choice is anti-platelets or antithrombtics. The MRI will confirm stroke and dissection. 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. Interesting question on how to manage dissection alone with no evidence of infarction and in these most would at least give antiplatelets to try and prevent intimal thrombus formation. It is quite possible that dissection without stroke is much more common than we think.
- 1. Debette S et al. Epidemiology, pathophysiology, diagnosis, and management of intracranial artery dissection. Lancet Neurol 2015; 14: 640-54
- 2. Debette S, Leys D. Cervical-artery dissections: predisposing factors, diagnosis, and outcome Lancet Neurol 2009; 8: 668-78
- 3. Rabinov JD, Hellinger FR, Morris PP, Ogilvy CS, Putman CM. Endovascular management of vertebrobasilar dissecting aneurysms. AJNR Am J Neuroradiol. 2003;24(7):1421-1428.