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Extracranial Carotid and Vertebral Artery Dissection: A Review

  • Gary John Redekop (a1)


Dissection of the extracranial carotid and vertebral arteries is increasingly recognized as a cause of transient ischemic attacks and stroke. The annual incidence of spontaneous carotid artery dissection is 2.5 to 3 per 100,000, while the annual incidence of spontaneous vertebral artery dissection is 1 to 1.5 per 100,000. Traumatic dissection occurs in approximately 1% of all patients with blunt injury mechanisms, and is frequently initially unrecognized. Overall, dissections are estimated to account for only 2% of all ischemic strokes, but they are an important factor in the young, and account for approximately 20% of strokes in patients less than 45 years of age. Arterial dissection can cause ischemic stroke either by thromboemboli forming at the site of injury or as a result of hemodynamic insufficiency due to severe stenosis or occlusion. Available evidence strongly favors embolism as the most common cause. Both anticoagulation and antiplatelet agents have been advocated as treatment methods, but there is limited evidence on which to base these recommendations. A Cochrane review on the topic of antithrombotic drugs for carotid dissection did not identify any randomized trials, and did not find that anticoagulants were superior to antiplatelet agents for the primary outcomes of death and disability. Healing of arterial dissections occurs within three to six months, with resolution of stenosis seen in 90%, and recanalization of occlusions in as many as 50%. Dissecting aneurysms resolve on follow-up imaging in 5- 40%, decrease in size in 15-30%, and remain unchanged in 50-65%. Resolution is more common in vertebral dissections than in carotid dissections. Aneurysm enlargement occurs rarely. The uncommon patient presenting with acute hemodynamic insufficiency should be managed with measures to increase cerebral blood flow, and in this setting emergency stent placement to restore cerebral perfusion may be considered, provided that irreversible infarction has not already occurred.

<span class='bold'>RÉSUMÉ</span>:

On reconnaît de plus en plus que la dissection de la portion extracrânienne de la carotide et de l’artère vertébrale peut être une cause d’ischémie cérébrale transitoire (ICT) et d’accident vasculaire cérébral (AVC). L’incidence annuelle de la dissection spontanée de la carotide est de 2,5 à 3 par 100,000 alors qu’elle est de 1 à 1,5 par 100,000 pour la dissection spontanée de l’artère vertébrale. La dissection traumatique survient chez à peu près 1% de tous les patients qui subissent une contusion et passe souvent inaperçue lors de l’évaluation initiale. On estime que les dissections sont responsables de seulement 2% de tous les accidents ischémiques, mais elles constituent un facteur important chez les jeunes et elles sont la cause d’à peu près 20% des accidents vasculaires chez les patients de moins de 45 ans. La dissection artérielle peut causer un accident ischémique soit par thromboembolie à l’endroit du traumatisme ou à cause de l’insuffisance hémodynamique due à une sténose sévère ou à une occlusion. Selon les données actuelles, la cause la plus fréquente serait l’embolie. Les anticoagulants et les antiplaquettaires ont été proposés comme traitement, mais il existe peu de données pour étayer ces recommandations. Une revue systématique (Cochrane Library) portant sur l’administration d’antithrombotiques dans la dissection carotidienne n’a pas identifié d’essai randomisé et n’a pas déterminé si les anticoagulants étaient supérieurs aux agents antiplaquettaires quand le critère d’évaluation principal était le décès et l’invalidité. Une dissection artérielle guérit en 3 à 6 mois, avec résolution de la sténose dans 90% des cas et recanalisation de l’occlusion dans 50% des cas. Le suivi par imagerie des anévrismes disséquant démontre une résolution dans 5 à 40% des cas, une diminution de la taille de l’anévrisme dans 15 à 30% des cas et aucun changement dans 50 à 65% des cas. La résolution est plus fréquente dans les dissections vertébrales que dans les dissections carotidiennes. On observe rarement une augmentation de la taille de l’anévrisme. Chez les rares patients qui présentent une insuffisance hémodynamique aiguë, le traitement en phase aiguë vise à augmenter la perfusion cérébrale et on peut envisager la mise en place d’un stent d’urgence en l’absence d’infarctus irréversible.

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