Prevalence and volume of internal border zone lesions in patients with impaired cerebral carbon dioxide vasomotor reactivity: a follow-up study.
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.
Bisschops
Robertus H C
RH
Department of Radiology, University Medical Center, Utrecht, the Netherlands. r.h.c.bisschops@azu.nl
Klijn
Catharina J M
CJ
Kappelle
L Jaap
LJ
van Huffelen
Alexander C
AC
van der Grond
Jeroen
J
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
D002245:Carbon Dioxide