Vertebral artery dissection
Citation, DOI & article data
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.
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 135.
Patients present with a variety of signs and symptoms, most frequently with neck pain and headache (typically occipital) as well as posterior fossa ischemic events (e.g. TIA or stroke) manifesting as nausea, ataxia, dysarthria, lateral medullary syndrome, or even collapse and coma 11,13. Intradural extension is quite common, with a high frequency of subarachnoid hemorrhage (SAH) 13. Other presentations include spinal cord infarction and even cervical nerve root impairment 1.
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 hemorrhage (up to 50% for vertebrobasilar dissections 3) on account of the anatomy of intracranial arteries. Although the tunica media and tunica adventitia are present, they are only a third as thick as their extracranial counterparts, with the vast majority of elastic fibers 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 hemorrhage.
blunt trauma (most common)
antecedent neck manipulation or other sudden movements 5,10
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, an increased association between patients who present with cervical dissections and preceding neck manipulations has been established, which has led some medical associations to suggest a cautionary link based on plausibility and limited established benefits of neck manipulation 14-17. Chiropractors have dismissed this association on the grounds that dissection causes neck pain and results in patients seeking out chiropractic manipulation ref.
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 PICA 3.
Vertebral artery dissections can be divided into two groups:
extracranial dissection (with or without intracranial extension)
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 and CT angiography (CTA) are often the first investigations obtained. Other than demonstrating posterior fossa ischemia or subarachnoid hemorrhage, 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.
In addition to far greater sensitivity to small foci of ischemia (using DWI), and the ability to image the vessel lumen (MRA), MRI is also more sensitive at imaging intramural hemorrhage.
Fat suppressed T1 axial images (without contrast) through the neck are standard for detecting cervical arterial intramural hematoma, demonstrating a crescent 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.
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 hemorrhage, usually with a disastrous outcome.
Factors predicting outcome include:
intracranial extension: subarachnoid hemorrhage
size of the contralateral vertebral artery
size of posterior fossa ischemia
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 embolization and posterior circulation infarcts 3.
Patients with intracranial extension are not treated with anticoagulation or antiplatelet agents on account of the risk of subarachnoid hemorrhage 3. Provided there is adequate collateral flow (i.e. large contralateral vertebral artery, intact circle of Willis), and especially in cases of subarachnoid hemorrhage, 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 ischemia is variable.
Recognized 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
extensive, regular luminal narrowing can be due to developmental vertebral artery hypoplasia ref
T1 hyperintensity around the V3 segment on spin-echo-based images can be due to the perivascular venous plexus rather than intramural hematoma 12
vertebral artery fenestration
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