Extracranial Arterial Dissection
Anticoagulation Is the Treatment of Choice
One of the most frustrating experiences we have as stroke clinicians is the lack of high level evidence for the management of patients with symptomatic and asymptomatic extracranial arterial dissection. Interestingly, this has become even more pressing since the introduction of magnetic resonance angiography (MRA) and computerized tomography angiography (CTA), where we are more frequently identifying dissections, typically in young adults and often with minimal symptoms. Moreover, with increased vascular screening of patients presenting with head and neck trauma, or postchiropractic manipulation,1 even the numbers currently detected may be the tip of the iceberg. Indeed, in 1978, Fisher et al stated that “spontaneous dissection is more common than the literature indicates.”2 What do we do in these circumstances and how should the dilemma be resolved?
Given the absence of a definitive clinical trial, it seems reasonable to use a pathophysiological basis for the decision-making process. Both our protagonists have presented very adequate evidence that there is usually a thromboembolic basis for recurrent cerebral ischemic events, although hemodynamic factors may also be relevant. In fact, both recommend antithrombotic therapy, but the main debate is the use of anticoagulants versus antiplatelet agents.
Interestingly, those who have been avidly reading the Controversies Section of this Journal for the past 3 years will have noted that we generally agree on stroke management strategies, even in controversial areas. However, in some instances, this collegial approach cannot be maintained! This is one such example. One of us (G.A.D.) routinely uses antiplatelet agents alone in cases of extracranial arterial dissection (symptomatic and asymptomatic) and reserves the use of heparin for those cases where recurrent symptoms occur. However, the other (S.M.D.) would routinely use anticoagulation, especially for symptomatic cases, provided that there is no evidence of either large acute infarction or intracranial extension. This is despite the fact that both co-editors were once stroke fellows at the MGH –“Must Give Heparin”!
Apart from the issues we asked our protagonists to address, there are many other interesting questions surrounding arterial dissection and stroke, all of which need to be addressed. For example, the use of tPA in patients with dissection and acute ischemic stroke is feasible, but remains somewhat uncertain.3 Also, optimal management, and particularly the role of endovascular treatment of intracranial arterial dissection, with and without subarachnoid hemorrhage, is uncertain.4
Where does this leave us concerning the central question of the role of anticoagulation in the management of patients with extracranial arterial dissection? Both protagonists are in accord, as are we, that a clinical trial is a priority. This would need to be large, investigator-driven trial, probably involving an international collaboration. A call to arms!
- Received April 3, 2005.
- Accepted April 21, 2005.
Smith WS, Johnston SC, Skalabrin EJ, Weaver M, Azari P, Albers G, Gress DR. Spinal manipulative therapy is an independent risk factor for vertebral artery dissection. Neurology. 2003; 60: 1424–1428.
Derex L, Nighoghossian N, Turjman F, Hermier M, Honnorat J, Neuschwander P, Froment JC, Trouillas P. Intravenous tPA in acute ischemic stroke related to internal carotid artery dissection. Neurology. 2000; 54: 2159–2161.
Anxionnat R, de Melo Neto JF, Bracard S, Lacour JC, Pinelli C, Civit T, Picard L. Treatment of hemorrhagic intracranial dissections. Neurosurgery. 2003; 53: 289–300;discussion 300–301.