title: Mechanism of ischemic infarct in spontaneous cervical artery dissection.
abstract: OBJECTIVE
  It is unclear whether strokes in patients with spontaneous cervical artery dissection (CAD) are due to secondary thromboembolism or to a reduction in cerebral blood flow from the primary cervical lesion. The aim of this study was to identify the most likely mechanism of stroke using cervical and cerebral imaging parameters in patients with CAD.
  
  
  METHODS
  The study was approved by the local Ethics Committee. Informed consent was waived. We retrospectively evaluated the cerebrovascular ultrasound, cervical MR angiography, and stroke brain MRI in consecutive patients with CAD. An embolic mechanism was considered in the case of direct visualization of an intracranial embolism as a susceptibility vessel sign on T2* or in the case of pial artery territory infarction on diffusion-weighted imaging. A hemodynamic mechanism was considered in the case of watershed infarction and in the case of an association of watershed infarction and pial artery territory infarction when ≥ 2 of the following were present: severe stenotic or occlusive CAD, reduced intracranial velocity on cerebrovascular ultrasound or signal on MR angiography, or hyperintense vessel sign on fluid-attenuated inversion recovery. The remaining patients were considered to have a mixed mechanism.
  
  
  RESULTS
  Of 172 consecutive patients with CAD, 100 (58%) had acute stroke on diffusion-weighted imaging. Stroke was attributed to a thromboembolic mechanism in 85 of 100 patients, a hemodynamic mechanism in 12 of 100 patients, and a mixed mechanism in 3 of 100 patients.
  
  
  CONCLUSIONS
  Stroke in patients with CAD is most frequently associated with both direct and indirect signs of artery-to-artery embolization on imaging, a finding that should help design future therapeutic trials.
authors.affiliation: Neuroradiology, Hôpital Sainte-Anne, Paris, France.
authors.forename: Audrey
authors.initials: A
authors.lastname: Morel
authors.forename: Olivier
authors.initials: O
authors.lastname: Naggara
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Touzé
authors.forename: Jean
authors.initials: J
authors.lastname: Raymond
authors.forename: Jean-Louis
authors.initials: JL
authors.lastname: Mas
authors.forename: Jean-Francois
authors.initials: JF
authors.lastname: Meder
authors.forename: Catherine
authors.initials: C
authors.lastname: Oppenheim
mesh_terms: D000328:Adult; D000368:Aged; D020520:Brain Infarction / Q000209:etiology* / Q000503:physiopathology*; D002536:Cerebral Arteries / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D038524:Diffusion Magnetic Resonance Imaging; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D020767:Intracranial Thrombosis / Q000150:complications* / Q000503:physiopathology*; D018810:Magnetic Resonance Angiography; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow / Q000502:physiology; D012189:Retrospective Studies; D012422:Rupture, Spontaneous / Q000150:complications / Q000503:physiopathology; D014463:Ultrasonography