Cervical Artery Dissections: Etiopathogenesis and Management

Abstract

Cervical Artery Dissection (CeAD) is a frequent stroke etiology for patients younger than 50 years old. The most common immediate complications related to CeAD are headache and neck pain (65-95%), TIA/ischemic stroke (>50%), and partial Horner's syndrome (25%). The prevailing hypothesis regarding the pathogenesis of sCeAD is that the underlying constitutional vessel wall weakness of patients with sCeAD is genetically determined and that environmental factors could act as triggers. The stroke prevention treatment of CeAD remains controversial, involving anticoagulation or antiplatelet therapy and potentially emergent stenting and/or thrombectomy or angioplasty for selected cases of carotid artery dissection with occlusion. The treatment of headache associated with CeAD depends on the headache phenotype and comorbidities. Radiographically, more than 75% of CeAD cases present with occlusion or non-occlusive stenosis. Many patients demonstrate partial and complete healing, more commonly in the carotid arteries. One-fifth of the patients develop dissecting pseudoaneurysm, but this is a benign clinical entity with an extremely low rupture and stroke recurrence risk. Good recovery is achieved in many CeAD cases, and mortality remains low. Family history of CeAD, connective tissue disorders like Ehlers-Danlos syndrome type IV, and fibromuscular dysplasia are risk factors for recurrent CeAD, which can occur in 3-9% of the cases. This review serves as a comprehensive, updated overview of CeAD, emphasizing etiopathogenesis and management.

Keywords: cervical artery dissection; genetics; stroke.

Figure 1

Normal blood vessel structure, flow patterns (depicted with red arrows) and mechanism dissection and related embolism.

Figure 2

Prominent tortuosity of bilateral vertebral (A) and carotid arteries (A and B) in a patient with fibromuscular dysplasia (FMD).

Figure 3

Impingement of internal carotid artery (ICA) due to elongated styloid process (Eagle’s syndrome).

Figure 4

(A) Intramural hematoma in the vessel wall of the left cervical internal carotid artery (ICA) (hyperintense signal on T1w). (B) The dissection with false lumen in the origin of the left vertebral artery. Of note, no dissection in the subclavian or aorta is noted. (C) Dissection flap and double lumen sign of the left cervical ICA. Pathologies are highlighted with red arrows.

Figure 5

Right cervical internal carotid artery (ICA) dissecting pseudoaneurysm (white arrow) (reconstructed images from MRA) (figure on the left) and ipsilateral stroke on the ICA territory.

Figure 6

Headache or neck pain locations with internal carotid (pink) and vertebral artery dissections (green).

Figure 7

Partial Horner’s syndrome of the left eye; ptosis and miosis.

Figure 8

(A) Lower cranial nerves traveling adjacent to the internal carotid artery. (B) Patient presenting with C5 radiculopathy is found to have a prominent left vertebral artery pseudoaneurysm compressing the nerve roots at C5 level (shown by the red arrow).