Vertebral artery dissection

Vertebral artery dissection, likearterial dissection elsewhere, is a result of blood entering themedia through a tear in theintima. It is is potentially lethal and can be difficult to diagnose clinically and radiologically. 

Epidemiology

Vertebral artery dissections occur have an incidence of 1-1.5-5 per 100,000 ^10-11. 

Clinical presentation

Patients present variably variably, most frequently with neck pain and headache as well as posterior fossa ischaemic events (e.g. TIA or stroke)¹¹. Other presentations include spinal cord infarction, subarachnoid haemorrhage (SAH) and even cervical nerve root impairment impairment) ¹. 

Pathology

As with other arterial dissections, blood enters the wall of the artery through a tear in the intima, and dissects along the intima-media plane. As the blood expands the wall, it compromises the lumen resulting in stenosis or occlusion. 

In intracranial dissection, there is a high risk of subarachnoid haemorrhage (up to 50% for vertebrobasilar dissections ³) on account of the anatomy of intracranial arteries. 

Aetiology

• blunt trauma (most common)
• antecedent neck manipulation or other sudden movement movements ^5,10
• spontaneous
  • fibromuscular dysplasia (FMD)
  • connective tissue diseases ²
    • Ehlers-Danlos disease
    • Marfan's disease
    • pseudoxanthoma elasticum

Radiographic features

Dissections are mostly located in the pars transversaria segment (V2) ~35% or in the atlas loop segment (V3) ~34% ^2-3,11. It is important to note that, in addition to the identification of the dissections, the next most important feature is to assess whether or not the dissection involves the intradural portion of the vertebral artery (V4), and thus the origin of the PICA³. 

Vertebral artery dissections can thus be divided into two groups:

1. Extracranial dissection
   • with(with or without intracranial extension)
   • typically occur at the C1/2 level (V3) ^2-3
2. Intracranial dissection
   • typically arise at the origin of the PICA³

CTA, MRI and catheter angiography can all be used to detect vertebral artery dissection, and each has pros and cons. Unfortunately, the vertebral arteries cannot always be satisfactorily imaged using ultrasound, and the diagnosis relies more on indirect Doppler hemodynamic signs than on direct identification of the dissection ¹⁰.

CT

CT and CT angiography (CTA) are often the first investigations obtained. Other than demonstrating posterior fossa ischaemia or subarachnoid haemorrhage, CT may identify an occluded vertebral (hyperdense) or mural thrombus (thickened wall, often with some surrounding stranding). CT may sometimes show a characteristic "double lumen" appearance ⁵.

CTA additionally can, especially with coronal and sagittal reformats, demonstrate irregularity of the lumen, as well as make thickening of the arterial wall more easily appreciable. 

MRI

In addition to far greater sensitivity to small foci of ischaemia (using DWI), and the ability to image the vessel lumen (MRA), MRI is also more sensitive at imaging intramural haemorrhage.

Fat saturated T1 axial images through the neck are best, demonstrating a sickle shaped-shaped hyperintensity in the wall of the affected vessel (crescent sign). 

Angiography (DSA)

Conventional angiography is traditionally considered the gold standard. It may demonstrate focal focal dilatation, proximal or distal stenosis, or fusiform fusiform aneurysmal dilatation ⁹.

Treatment and prognosis

Both treatment and prognosis are strongly affected by whether or not the dissection extends into the intracranial compartment. If the latter is true, then there is a high rate of subarachnoid haemorrhage, usually with disastrous outcome a disastrous outcome. 

Factors predicting outcome include:

• intracranial extension: subarachnoid haemorrhage
• size of the contralateral vertebral artery
• presence and size of posterior communicating arteries and P1 segment of the posterior cerebral artery: collateral flow
• size of posterior fossa ischaemia

Treatment is also largely influenced by the location of the dissection. In dissections limited to limited to the extracranial extracranial vertebral artery then antiplatelet agents are the mainstay of treatment, aimed at preventing artery-to-artery embolisation and posterior circulation infarcts ³.  

Patients with intracranial extension are not treated with anticoagulation or antiplatelet agents on account of the risk of subarachnoid haemorrhage ³. Provided there is adequate collateral flow (i.e. large contralateral vertebral artery, intact circle of Willis), and especially in cases of subarachnoid haemorrhage, consideration should be given to operative or endovascular trapping or coiling of the dissected artery ⁴. Depending on the arterial anatomy, the risk or resulting posterior fossa ischaemia is ischaemia is variable. 

Complications

Recognised complications include:

• arterial thrombosis and occlusion
• embolic infarcts
• dissection-induced stenosis^8,10
  • dissection promotes compression over the true lumen of the artery
• pseudoaneurysm formation^8,10
  • dissection extends toward the adventitia forming a pseudoaneurysm
• thromboembolic infarcts ¹⁰
  • a dissecting aneurysm may become a nidus for distal thromboembolism