Abstract
PurposeLittle is known about the long-term course of arterial stenosis after spontaneous cervical artery dissection (sCAD). We analyzed changes over time and evaluated factors potentially associated with these changes and recurring sCAD.Materials and MethodsAdult patients with sCAD, admitted to our neurological department between 2004 and 2018, were included. All patients underwent initial and follow-up repetitive neurovascular ultrasound for a mean duration of 15.3 ± 21 months. Clinical and imaging data were registered for each patient.ResultsA total of 259 sCADs were diagnosed in 224 patients. Either internal carotid arteries (n = 133, 59.4%), vertebral arteries (n = 58, 25.9%), or multiple arteries (n = 33, 14.7%) were affected. In 93 out of 183 patients (51%), and in 117 out of 210 arteries under investigation (55.7%), vascular stenosis decreased over time. Occluded arteries recanalized early in 34 (54%) and stayed occluded in 29 patients (46.0%). Of 145 initially hemodynamically relevant stenosis, 77 (53.1%) improved over time. Overall, 12 patients (5.4 %) had a recurring sCAD during follow-up. Pseudoaneurysms were found in 19 patients.ConclusionThe sonographical course of sCAD is highly dynamic within the first year after disease onset and should be monitored carefully. Decreasing degrees of stenosis and recanalization of occluded arteries occurred in half of all patients. Recurrent sCAD was a rare event in our cohort.
Highlights
In spontaneous cervical artery dissection, the outer arterial wall is primarily affected
The pathophysiological mechanism of spontaneous cervical artery dissection (sCAD) is the formation of an intramural hematoma along the medial/adventitial border due to rupture of vasa vasorum and neoangiogenetic capillaries (1)
The intramural hematoma can be visualized by neurovascular ultrasound as an echolucent wall thickening leading to a non-atherosclerotic stenosis
Summary
In spontaneous cervical artery dissection (sCAD), the outer arterial wall is primarily affected. The pathophysiological mechanism of sCAD is the formation of an intramural hematoma along the medial/adventitial border due to rupture of vasa vasorum and neoangiogenetic capillaries (1). The intramural hematoma can be visualized by neurovascular ultrasound as an echolucent wall thickening leading to a non-atherosclerotic stenosis. Previous studies showed a tendency of decreasing degrees of stenosis caused by sCAD, primarily in the first 6 months after disease onset (3–5). Other investigators reported some degree of recanalization in 58.8% of patients, being more frequent in women, in a larger restrospective case series (n = 177) (6). Arauz et al (7) (n = 130) found better clinical outcomes in sCAD of the vertebral artery (VA) compared to cases of affected internal carotid artery (ICA), in patients with demonstrated complete recanalization, in a Mexican cohort
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