title: Lack of evidence for a poor haemodynamic or metabolic state of the brain in patients with haemodynamic clinical features associated with carotid artery occlusion.
abstract: OBJECTIVE
  To assess whether patients with carotid artery occlusion (CAO) who have clinical features suggesting a haemodynamic origin have a poor haemodynamic or metabolic state of the brain.
  
  
  METHODS
  In 117 patients with ischaemic symptoms of the eye or brain that were transient or at most moderately disabling and associated with a CAO, we compared CO(2) reactivity, quantitative flow measurement by magnetic resonance (MR) angiography, metabolic ratios measured by (1)H-MR spectroscopy, collateral blood flow patterns and the presence of infarcts of the borderzone type between patients grouped by the following clinical features: (1) presence or absence of at least one of the 'classical' haemodynamic symptoms: limb shaking, retinal claudication, precipitation of symptoms by exercise, by rising from a sitting or lying position, by transition from a cold to a warm environment, or by documented hypotension, and (2) symptoms having occurred after demonstration of the CAO or only before the occlusion was documented.
  
  
  RESULTS
  Patients with (n = 16) and without (n = 101) one of the 'classical' haemodynamic symptoms did not differ in any of the measured indices. Patients with recurrent symptoms after documentation of the CAO (n = 56) had lower CO(2) reactivity (difference 8.3%, 95% confidence interval 0.1-16.5) than those with symptoms only before documentation of the occlusion (n = 61), whereas no significant differences were found in any of the other measured indices. The difference in CO(2) reactivity was no longer significant after adjustment for the interval between the patients' last symptoms and the CO(2) reactivity measurement.
  
  
  CONCLUSIONS
  In patients with CAO we could not find an association between symptoms that have been associated with hypoperfusion and a poor haemodynamic or metabolic state of the brain.
authors.affiliation: University Department of Neurology, University Medical Center Utrecht, Utrecht, The Netherlands. c.j.m.klijn@neuro.azu.nl
authors.forename: C J
authors.initials: CJ
authors.lastname: Klijn
authors.forename: L J
authors.initials: LJ
authors.lastname: Kappelle
authors.forename: J
authors.initials: J
authors.lastname: van der Grond
authors.forename: G H
authors.initials: GH
authors.lastname: Visser
authors.forename: A
authors.initials: A
authors.lastname: Algra
authors.forename: C A
authors.initials: CA
authors.lastname: Tulleken
authors.forename: J
authors.initials: J
authors.lastname: van Gijn
mesh_terms: D000328:Adult; D000368:Aged; D001921:Brain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000503:physiopathology; D002341:Carotid Artery Thrombosis / Q000175:diagnosis / Q000378:metabolism* / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D005260:Female; D006801:Humans; D018810:Magnetic Resonance Angiography; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D017585:Ultrasonography, Doppler, Transcranial