Carotid Dissection

Epidemiology

· Carotid and vertebral dissections are more common than you might think: they are the most common cause of stroke in persons younger than 45 yrs, accounting for 20% of strikes in this age group

 

 

Pathophysiology

· The pathologic lesion is intramural hemorrhage within the media of the arterial wallàhematoma can extend circumferentially along the length of the vessel, causing partial or complete occlusion

· Platelet aggregation and thrombus formation also occur, which can contribute to distal embolization

· timing of these events is variable, symptoms of cerebral ischemia can occur days to years after dissection

Clinical Presentation

· typical presentation is the abrupt onset of pain in the neck or face--neurologic findings usually occur within the first few hours, but can occur months later

· The classic triad of symptoms (for unilateral) carotid dissection include: unilateral headache, ipsilateral Horner's syndrome (sympathetic hypofunction may be due to interference with the sympathetic fibers around the internal carotid artery), and contralateral hemispheric findings (ie. aphasia, neglect, visual disturbances, or hemiparesis)

· Acute severe retro-orbital pain in a previously healthy person with no history of cluster headaches is particularly suggestive of carotid dissection

· Early symptoms and signs are often subtle, and in the absence of neurologic findings delays in diagnosis are common

 

 

Etiology

· Collagen vascular disease or other intrinsic factors can predispose to dissection, including fibromuscular dysplasia, Marfan's syndrome and Ehlers-Danlos syndrome

· Most commonly associated with trauma to the neck; reported mechanisms include neck torsion, chiropractic manipulation, coughing, minor falls, and MVA (potentially superimposed on structurally abnormal arteries)

· Bilateral carotid dissections are at the case report level (ie. someone better write this up!)

 

 

Diagnosis

· MRI/MRA or CTA usually confirms the diagnosis

· Carotid ultrasound may not be sufficient if dissection is intracranial

· Gold standard is digital subtraction angiography

 

 

Treatment

· Medical therapy generally includes antiplatelet agents; until recently, anticoagulation with heparin/coumadin had been used, but recent meta-analyses suggest that there is no additional benefit for full dose anticoagulation

· IV tPA can be used in the acute window (<3 hrs, possibly up to 4.5hrs), esp if evidence of embolic dz

· Endovascular treatment (including stenting, angioplasty, intra-arterial tPA) has been used, but often not pursued unless there is an associated aneurysm, as most dissections do heal on their own

 

 

(Victoria Kelly MD, 3/11/11)