title: Pathophysiology of acute cerebrovascular syndrome in patients with carotid artery stenosis: a magnetic resonance imaging/single-photon emission computed tomography study.
abstract: BACKGROUND
  The mechanisms underlying acute cerebrovascular syndrome in patients with carotid artery stenosis remain unclear.
  
  
  OBJECTIVE
  To assess the relationships among infarct localization, hemodynamics, and plaque components.
  
  
  METHODS
  This prospective study included 38 patients with acute cerebrovascular syndrome resulting from ipsilateral carotid artery stenosis. Cerebral infarct localization was categorized into 3 patterns (cortical, border zone, and mixed pattern). Carotid plaque components were evaluated with T1-weighted magnetic resonance imaging and time-of-flight imaging. Cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) were also quantified.
  
  
  RESULTS
  Infarcts were identified in 38 patients with the use of diffusion-weighted magnetic resonance imaging. On the basis of the assessment of hemodynamics, the cortical pattern was seen in 18 of 21 patients with type 1 ischemia (normal CBF, normal CVR), whereas the mixed pattern was seen in 2 patients with type 2 ischemia (normal CBF, impaired CVR) and 12 of 15 patients with type 3 ischemia (impaired CBF, impaired CVR). The plaque components were categorized into fibrous (4 patients), lipid-rich (14 patients), and intraplaque hemorrhage (IPH; 20 patients). Of the patients with fibrous plaque, 2 had border-zone and 2 had mixed-pattern infarcts. Of the patients with lipid-rich plaque, 7 had cortical and 6 had mixed-pattern infarcts. Of patients with intraplaque hemorrhage, 11 had cortical and 9 had mixed-pattern infarcts.
  
  
  CONCLUSIONS
  Cortical infarction occurs as a result of vulnerable plaque. Reduced cerebral perfusion induces border-zone infarction. Both factors are implicated in mixed-pattern infarction. Developments in noninvasive diagnostic modalities allow us to explore the mechanisms behind acute cerebrovascular syndrome in carotid artery stenosis and to determine the ideal therapies.
authors.affiliation: *Departments of Neurosurgery and ‡Radiology, Graduate School of Medicine and Pharmacological Science, University of Toyama, Toyama, Japan; §Department of Neurology, Toyama University Hospital, Toyama, Japan.
authors.forename: Daina
authors.initials: D
authors.lastname: Kashiwazaki
authors.forename: Naoki
authors.initials: N
authors.lastname: Akioka
authors.forename: Naoya
authors.initials: N
authors.lastname: Kuwayama
authors.forename: Kyo
authors.initials: K
authors.lastname: Noguchi
authors.forename: Kortaro
authors.initials: K
authors.lastname: Tanaka
authors.forename: Satoshi
authors.initials: S
authors.lastname: Kuroda
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D016893:Carotid Stenosis / Q000150:complications* / Q000473:pathology; D002544:Cerebral Infarction / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000502:physiology; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D002546:Ischemic Attack, Transient / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008875:Middle Aged; D058226:Plaque, Atherosclerotic / Q000000981:diagnostic imaging; D011446:Prospective Studies; D011859:Radiography; D013577:Syndrome; D015899:Tomography, Emission-Computed, Single-Photon