Vertebral artery dissection

Vertebral artery dissection, like arterial dissection elsewhere, is a result of blood entering the media through a tear in the intima of the vertebral artery. It is potentially lethal and can be difficult to diagnose clinically and radiologically.

Epidemiology

Vertebral artery dissections have an incidence of 1-5 per 100,000 ^10,11. They are typically encountered in a somewhat younger cohort than internal carotid artery dissections ¹⁵. 

The link between chiropractic neck manipulation and cervical artery dissection (both the carotid artery and vertebral artery) has been long suspected and has been the source of much litigation and heated debates. Although as yet there is no conclusive evidence of a direct causal link between the two ¹⁶, an increased association between patients who present with cervical dissections and preceding neck manipulations has been established ¹⁸ which has led some medical associations to suggest a cautionary link ¹⁷ based on plausibility and limited established benefits of neck manipulation ¹⁹. Chiropractors have dismissed this association, perhaps correctly, on the grounds that dissection causes neck pain and results in patients seeking out chiropractic manipulation ^ref135. 

Clinical presentation

Patients present with a variety of signs and symptoms, most frequently with neck pain and headache (typically occipital) as well as posterior fossa ischaemic events (e.g. TIA or stroke) manifesting as nausea, ataxia, dysarthria, lateral medullary syndrome, or even collapse and coma ^11,15,13. Intradural extension is quite common, with a high frequency of subarachnoid haemorrhage (SAH) ¹⁵¹³. Other presentations include spinal cord infarction and even cervical nerve root 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. The vertebral arteries, like the ICA, have a differing distribution of elastic fibres compared to similar-sized vessels elsewhere (this has been disputed by FT Merei ¹⁴).  Although the tunica media and tunica adventitiaare present, they are only a third as thick as their extracranial counterparts, with the vast majority of elastic fibres located in a subendothelial elastic lamina. This fundamental difference accounts for the markedly different natural history of intracranial arterial dissections compared to their extracranial counterparts. When a tear breaches the aforementioned subendothelial elastic layer, then there is little tissue preventing extension into the subarachnoid space, thus accounting for the very high rate of subarachnoid haemorrhage.

Aetiology

• blunt trauma (most common)
• antecedent neck manipulation or other sudden 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% ^2-3,3,11. 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 PICA ³.

Vertebral artery dissections can be divided into two groups:

1. extracranial dissection(with or without intracranial extension)
2. intracranial dissection

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 saturatedsuppressed T1 axial images (without contrast) through the neck are beststandard for detecting cervical arterial intramural hematoma, demonstrating a sickle-shapedcrescent sign of hyperintensity in the wall of the affected vessel. Flow-suppressed T1-weighted MPRAGE) sequence has been suggested as a more reliable alternative ¹².

Angiography (DSA)

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

Complications

Recognised complications include:

• arterial thrombosis and occlusion
• 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

Differential diagnosis

It mayExtensive, regular luminal narrowing can be difficultdue to differentiate between a developmental vertebral artery dissection and a hypoplastic vertebral arteryhypoplasia in a trauma setting.