title: Prevalence and volume of internal border zone lesions in patients with impaired cerebral carbon dioxide vasomotor reactivity: a follow-up study.
abstract: BACKGROUND
  The precise etiology of border zone infarcts is controversial. Hemodynamic impairment due to obstructive disease of the internal carotid artery (ICA) is suggested as a cause of border zone infarcts.
  
  
  OBJECTIVE
  To investigate changes in prevalence and volume of ischemic border zone lesions over time in patients with occlusive disease of the ICA after 1 year of follow-up.
  
  
  METHODS
  Follow-up study.
  
  
  METHODS
  Referral center.
  
  
  METHODS
  Fifty-eight patients with an occlusion of the ICA were included. At baseline, ischemic lesions were classified on magnetic resonance imaging, and vasomotor reactivity was assessed with transcranial Doppler ultrasonography with carbon dioxide challenge.
  
  
  METHODS
  Changes in prevalence and volume of ischemic lesions were monitored and were correlated with carbon dioxide reactivity at baseline.
  
  
  RESULTS
  No significant changes in the prevalence of any infarct types were observed after 1 year of follow-up in the hemispheres ipsilateral or contralateral to the ICA occlusion. However, in hemispheres ipsilateral to an occluded ICA, we found an increase in mean volume of internal border zone infarcts (P =.002). In hemispheres with a low carbon dioxide reactivity, we found an increase in mean volume of internal border zone lesions after 1 year (carbon dioxide reactivity, <or=18%, P =.02 and 19%-35%, P =.02). These changes were not observed for external border zone lesions.
  
  
  CONCLUSIONS
  The association between impaired vasomotor reactivity and an increase in ischemic lesion volume in the internal border zone suggests a hemodynamic component.
authors.affiliation: Department of Radiology, University Medical Center, Utrecht, the Netherlands. r.h.c.bisschops@azu.nl
authors.forename: Robertus H C
authors.initials: RH
authors.lastname: Bisschops
authors.forename: Catharina J M
authors.initials: CJ
authors.lastname: Klijn
authors.forename: L Jaap
authors.initials: LJ
authors.lastname: Kappelle
authors.forename: Alexander C
authors.initials: AC
authors.lastname: van Huffelen
authors.forename: Jeroen
authors.initials: J
authors.lastname: van der Grond
mesh_terms: D000328:Adult; D000368:Aged; D001921:Brain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002545:Brain Ischemia / Q000175:diagnosis / Q000378:metabolism* / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000378:metabolism* / Q000494:pharmacology*; D002343:Carotid Artery, Internal / Q000187:drug effects* / Q000378:metabolism*; D004453:Echoencephalography; D005260:Female; D005500:Follow-Up Studies; D007839:Functional Laterality / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D017585:Ultrasonography, Doppler, Transcranial; D014666:Vasomotor System / Q000187:drug effects* / Q000378:metabolism
chemical_list: D002245:Carbon Dioxide