Cervical Artery Dissection

Clinical Presentation

Carotid dissections may be asymptomatic or present as various combinations of cerebral ischemia (transient ischemic attack [TIA] or stroke), head and neck pain, and cranial neuropathy. Early studies suggested that more than 90% of the time they presented as cerebral or retinal ischemia. However, this was likely because they were rarely diagnosed outside the setting of recent TIA or stroke. Some studies suggest that as few as 50% of dissections have associated ischemic manifestations. Furthermore, nearly 80% of those with strokes due to carotid dissections have preceding transient symptoms that include unilateral head, face, orbit, or neck pain; partial Horner syndrome; pulsatile tinnitus; or cranial nerve palsies (with the hypoglossal nerve being the most commonly affected). Ipsilateral Horner syndrome results from injury of sympathetic fibers that travel with the internal carotid artery in the neck on the way to the orbit. Pain typically occurs first. In a carotid dissection, the pain is often over the carotid artery in the neck but can also present as referred pain around the ipsilateral orbit, forehead, or temple. Median time from onset of pain to neurologic symptoms is 4 days.

The presentation of vertebral artery dissections may be more varied. One case series of 49 posterior circulation dissections showed that 44.9% presented with subarachnoid hemorrhage, whereas only 42.8% presented with ischemic stroke. Early signs of vertebral artery dissections include posterior neck pain and occipital headache. Median time from onset of neck pain to ischemic symptoms in these dissections may be up to 2 weeks. This delay between actual dissection and onset of neurologic symptoms makes early accurate diagnosis imperative.

The most common locations for cervical artery dissections are in the mobile portions of the vessels. Specifically, dissections in the internal carotid artery typically start 2 to 3 cm above the bifurcation and continue for various lengths up into the petrous portion. The V3 segment of the vertebral arteries is the most common site of posterior circulation dissections. It is also the most common site of bilateral dissections, which account for 12% to 15% of all dissections. Vertebral dissections are much more likely than carotid dissections to extend intracranially, leading to potentially catastrophic subarachnoid hemorrhage. It is also thought that intracranial dissections have a higher likelihood of resulting in ischemic stroke. Thus, those with intracranial dissections have permanent disabling deficits in 44% of cases, versus 14% when the dissection is limited to the cervical portion of the vessel.

Prognosis after a cervical artery dissection largely depends on whether the patient presents with a stroke, and on infarct size and location. Although a dissected artery can occlude, patients with good collateral circulation may avoid cerebral ischemia. Strokes are believed to be due to embolization of thrombus that forms at or near the site of dissection, either because of slow blood flow or endothelial disruption. For this reason, the mainstay of treatment has been antithrombotic therapy to prevent embolization (see later discussion). For patients who survive the acute dissection with minimal cerebral ischemia, the prognosis is generally excellent. Recurrent ischemic events are uncommon. Dissecting pseudoaneurysms are discussed later. The lifetime rate of recurrent dissection in another artery is estimated to be between 5% and 10%. Recurrent dissections typically occur within 6 to 12 months. In a study of 282 cervical artery dissection patients at Heidelberg University Hospital, Germany, patients were followed a median of 52 months (range 12–204 months). Late recurrent cervical artery dissections (defined as >1 month from the onset of the initial dissection) occurred in only 17 patients (7.1%), with 5 patients (2.1%) having multiple recurrent dissections over time. Late recurrent dissections resulted in ischemic stroke in only 8.7% of cases and were asymptomatic in 41.3% of cases. The only baseline factor that predicted later recurrent dissection was younger age.

Diagnostic Testing

Angiography is an excellent means for diagnosis, particularly of subtle carotid artery dissections or lesions in the vertebral arteries. Fig. 67.1 illustrates several of the characteristic appearances of dissections, such as a flame-shaped tapering of the lumen and a sudden widening of the lumen distal to the dissection. Occasionally, an intimal flap can be seen with a false lumen. Magnetic resonance and computed tomographic angiography can also detect dissections that cause stenosis or occlusion. However, digital subtraction angiography may be superior for dissections that occur close to the origin of the vessels in the chest, where magnetic resonance or computed tomographic angiography may simply show an absent vessel.

Carotid artery ultrasound may detect a high-resistance flow pattern, but because dissections usually occur distal to the carotid artery bifurcation (typically around the C2 level), the dissection is usually not directly visualized by ultrasound. Waveforms at the carotid artery bifurcation, however, may show a high-resistance pattern in the internal carotid artery because of distal occlusive disease.

Perhaps the gold standard of diagnosis for carotid artery dissection is the use of axial T1- and T2-weighted neck imaging with fat suppression. In acute dissection, the intramural hematoma is visible as a crescent of hyperintense signal in the involved segment of the artery, as shown in Fig. 67.2 . Visualization of the same process in the vertebral artery is possible but less reliable.