Arterial Dissections Dissections of the carotid and vertebral arteries are relatively common causes of TIA and stroke, particularly among young patients. Dissections may occur as a result of significant head and neck trauma, but approximately half occur spontaneously or after a trivial injury.588 A number of underlying connective tissue disorders appear to be risk factors for spontaneous dissection, including fibromuscular dysplasia, Marfan syndrome, Ehlers-Danlos syndrome (type IV), osteogenesis imperfecta, and genetic conditions in which collagen is abnormally formed. At present, none of these underlying conditions are amenable to disease-specific modifying treatment. Ischemic stroke related to dissection may be a result of thromboembolism or hemodynamic compromise, although the former appears to be the dominant mechanism.589–591 In some cases, dissections can lead to formation of a dissecting aneurysm, which can also serve as a source of thrombus formation. Intracranial dissections, particularly in the vertebrobasilar territory, pose a risk of subarachnoid hemorrhage, particularly if treated with acute anticoagulation, as well as cerebral infarction.592 The optimal strategy for prevention of stroke in patients with arterial dissection is controversial. Options include anticoagulation, antiplatelet therapy, angioplasty with or without stenting, or conservative observation without specific medical therapy. Surgical approaches are unconventional. Early anticoagulation with heparin or LMWH had been classically advocated at the time of diagnosis,593–595 particularly because the risk of stroke is greatest in the first few days after the initial vascular injury.593,595–598 However, there have been no controlled trials supporting the use of any particular antithrombotic regimen, and observational data are conflicting. A Cochrane systematic review of 1262 patients with carotid dissection in 36 observational studies found no statistically significant difference in subsequent ischemic stroke when antiplatelet agents were compared with anticoagulants (OR, 0.63; 95% CI, 0.21–1.86).599 Recurrent stroke was seen in 1.9% of cases with anticoagulation and 2.0% with antiplatelet therapy. Another systematic review that included 762 patients with carotid or vertebral artery dissection from 34 case series similarly showed no significant difference in risk of stroke, which occurred in 1.9% of patients given antiplatelet agents and 2.0% given anticoagulants.600 These studies pooled data from many smaller studies and likely suffer from substantial heterogeneity, as well as publication bias. Two large cohorts, including a retrospective cohort of 432 patients with carotid or vertebral artery dissection601 and a prospective cohort of 298 subjects with only carotid dissection,602 reported a much lower risk of subsequent stroke, 0.3% over the 3- to 12-month period after dissection. In contrast, a cohort study of 250 patients with acute stroke or TIA caused by cervical dissection found a cumulative risk of subsequent stroke of 10.7% at 1 year, with significantly fewer strokes among those treated with anticoagulants than among those given antiplatelet agents (2.0% versus 16.7%; HR, 0.11; 95% CI, 0.02–0.69).603 Some of the inconsistencies among studies may be related to the study populations. Specifically, a clinical presentation of ischemic symptoms (ie, TIA or stroke) may be associated with an increased risk of subsequent stroke compared with a presentation with only local symptoms (eg, Horner syndrome, head or neck pain, or cranial nerve palsy) or no symptoms. In addition, the timing and acuity of symptoms may be important, because most subsequent strokes occur early after presentation. Overall, existing observational data suggest that antiplatelet therapy and anticoagulation are associated with a similar risk of subsequent stroke but that the former is likely safer. A randomized trial comparing these strategies is under way.604 Dissections usually heal over time, and an antithrombotic therapeutic regimen is commonly maintained in such patients for at least 3 to 6 months. This duration of therapy is arbitrary, and some authors suggest that imaging studies be repeated to confirm recanalization of the dissected vessel before a change in therapy.597,605,606 Anatomic healing of the dissection with recanalization occurs in the majority of patients.607 Those dissections that do not fully heal do not appear to be associated with an increased risk of recurrent strokes.601,608 A dissecting aneurysm may also persist, but these appear to pose a low risk for subsequent stroke or rupture and therefore do not usually warrant aggressive intervention.608 Although most ischemic strokes caused by dissection are a result of early thromboembolism, a minority are attributed to hemodynamic compromise.609,610 The prognosis may be worse in these cases, and revascularization procedures such as stenting or bypass surgery have been proposed in this setting,609,611–614 although prospective studies do not currently exist. Arterial Dissection Recommendations 1. For patients with ischemic stroke or TIA and extracranial carotid or vertebral arterial dissection, antithrombotic treatment with either antiplatelet or anticoagulant therapy for at least 3 to 6 months is reasonable (Class IIa; Level of Evidence B). 2. The relative efficacy of antiplatelet therapy compared with anticoagulation is unknown for patients with ischemic stroke or TIA and extracranial carotid or vertebral arterial dissection (Class IIb; Level of Evidence B). 3. For patients with stroke or TIA and extracranial carotid or vertebral arterial dissection who have definite recurrent cerebral ischemic events despite medical therapy, endovascular therapy (stenting) may be considered (Class IIb; Level of Evidence C). 4. Patients with stroke or TIA and extracranial carotid or vertebral arterial dissection who have definite recurrent cerebral ischemic events despite medical therapy and also fail or are not candidates for endovascular therapy may be considered for surg