A 57-Year-Old Man With Hemiparesis After Coughing

Francesco Brigo, MD; Giampaolo Tomelleri, MD

Disclosures

November 27, 2017

The treatment of internal carotid artery dissection consists of anticoagulation with intravenous heparin followed by oral anticoagulation for 3-6 months.[13] However, no randomized controlled trials support such a therapeutic approach, and the validity of such treatment has never been definitively proven. A Cochrane review also reported that no randomized controlled trials have been conducted that directly compare the efficacy of anticoagulants and antiplatelet drugs; nonrandomized trials have shown no evidence of a significant difference between the two.[14]

Intravenous thrombolysis with recombinant tissue plasminogen activator has become a standard therapy for ischemic stroke; however, its use in patients with ischemic stroke due to internal carotid artery dissection may potentially worsen intramural hematoma. Nevertheless, studies indicate that the risks for intracranial bleeding and recurrent stroke after thrombolysis in patients with carotid artery dissection appear to be similar to those in patients without carotid artery dissection.[15,16]

Endovascular stenting is another emerging treatment for carotid artery dissection. In a systematic review of the literature, the technical success rate for stenting was 99%, and the procedural complication rate was 2%. Over a mean angiographic follow-up period of 12.8 months, 2% of patients had stent stenosis or occlusion; over a mean clinical follow-up period of 17.7 months, 1.4% of patients had a neurologic event.[17] Randomized, prospective clinical trials are needed to further elucidate the role of endovascular stenting in the management of internal carotid artery dissection.

The patient in this case was first treated with intravenous heparin followed by oral anticoagulation in order to prevent distal embolization. He continued anticoagulant therapy for 3 months. The patient's Horner syndrome completely resolved after 3 days, but the left-sided sensorimotor deficits persisted at discharge.

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