Response to Letter by Menon and Norris
Norris and Menon suspect that both patients whom we reported to have recurrent vasospasms of the internal carotid artery1 were likely to have carotid artery dissection (CAD). In fact, CAD had been the initial diagnosis in both patients. There were, however, several findings which could not be explained in the context of CAD and led us to the assumption of internal carotid artery vasospasm.
We agree that MRI with MR angiography is sensitive in the diagnosis of CAD. Ultrasound detects dissection mainly by its hemodynamic sequelae than by depiction of the vessel wall hematoma itself, particularly in submandibular dissection. It may thus not consistently differentiate between vasospasm and dissection in case of poor insonation conditions. In both of our patients, T1-fat–suppressed MRI (several times in patient 1, once during the course of repeated high-grade stenoses in patient 2) had been performed. However, no wall hematoma was detected in MRI2 or in repeated sonographic examinations with insonation conditions allowing clear depiction of the vessel wall. The possibility to perform repeated sonographic examinations as a noninvasive monitoring with detection of recurrent high-grade stenoses gave the ultrasound method a high impact during the clinical course of our patients.
In both patients we observed repeated changes in severity and side of stenosis within days. A resolution of CAD within 2 days from high-grade stenosis to no stenosis, which implies the rapid reabsorption of a considerable carotid wall hematoma, is not very plausible. Moreover, recurrence of arterial dissection in the same vessel is rare.3 In addition, we documented a regression of a high-grade internal carotid artery stenosis during intraarterial infusion of papaverine which cannot be explained by CAD.
Migraine is a moderate risk factor for CAD.4 On the other hand, migraine is known to go along with vasospasms.5 In 1 of our 2 patients, migrainous headaches had occurred for several years. They were clearly associated with the recurrent vasospasms. We therefore suggest that in this patient recurrent vasospasms had regularly occurred long before the ischemic event. We do not know whether vasospasms occurred during a migraine attack or whether the pulsatile headaches were secondary to vasospasm.
In both patients we observed no stabilization of the vascular situation for several weeks, and the patients were repeatedly at high risk for new ischemic events. Both patients received antithrombotic therapy to prevent thromboembolic complications—the same rationale is used to justify antithrombotic treatment in CAD. This modus operandi in CAD has not yet been investigated in a randomized trial.6 Assuming that the observed high-grade stenoses of internal carotid artery were caused by vasospasms, we additionally initiated an antivasospastic treatment as well as, in patient 2, an antiphlogistic treatment.
Janzarik WG, Ringleb PA, Reinhard M, Rauer S. Recurrent extracranial carotid artery vasospasms: report of 2 cases. Stroke. 2006; 37: 2170–2173.
Pezzini A, Granella F, Grassi M, Bertolino C, Del Zotto E, Immovilli P, Bazzoli E, Padovani A, Zanferrari C. History of migraine and the risk of spontaneous cervical artery dissection. Cephalalgia. 2005; 25: 575–580.
Lyrer P, Engelter S. Antithrombotic drugs for carotid artery dissection. Stroke. 2004; 35: 613–614.