ADAPTIVE-CHANGES OF AUTOREGULATION IN CHRONIC CEREBRAL HYPOTENSION WITH ARTERIOVENOUS-MALFORMATIONS - AN ACETAZOLAMIDE-ENHANCED SINGLE-PHOTON EMISSION CT STUDY
L. Haceinbey et al., ADAPTIVE-CHANGES OF AUTOREGULATION IN CHRONIC CEREBRAL HYPOTENSION WITH ARTERIOVENOUS-MALFORMATIONS - AN ACETAZOLAMIDE-ENHANCED SINGLE-PHOTON EMISSION CT STUDY, American journal of neuroradiology, 16(9), 1995, pp. 1865-1874
Citations number
41
Categorie Soggetti
Neurosciences,"Radiology,Nuclear Medicine & Medical Imaging
PURPOSE: To evaluate the relationship among feeding arterial pressure,
lesion size, and perfusion in cerebral cortex adjacent to cerebral ar
teriovenous malformations (AVMs). METHODS: Eleven patients with hemisp
heric AVMs underwent Tc-99m hexamethyl-propyleneamine oxime single-pho
ton emission CT before and after 1 g of acetazolamide was administered
intravenously. AVM volume was estimated from MR dimensions and measur
ed according to the method described by Pasqualin, Pressure measuremen
ts were obtained in arteries feeding the cortex adjacent to AVMs, Sing
le-photon emission CT regions of interest were defined in cortex adjac
ent to the AVM and compared with contralateral regions using the Mount
z method to estimate a baseline and dynamic (acetazolamide-challenged)
perfusion defect volume. RESULTS: Eight of 11 patients had baseline p
erfusion defects, but these defects were unrelated to feeding artery p
ressures (y = -.06x + 9.92, r(2) = .04) or the dynamic change in defec
t volume after acetazolamide administration (y = .01x + .02, r(2) = .0
02), However, there was a correlation between AVM volume and the basel
ine defect volume (y = .75x - 1.9, r(2) = .76), Five patients had incr
eased defect volume after acetazolamide administration; 5 patients had
either no change in or improvement of perfusion, Dynamic changes in d
efect volume were related to feeding artery pressures. CONCLUSION: Per
ilesional baseline perfusion defects appear to be related to lesion si
ze and not to local arterial pressure. Cerebrovascular reserve general
ly was preserved, and perfusion defects appeared to be more pronounced
with lower arterial pressures in feeding vessels. Although vasodilato
ry testing can unmask hemodynamic failure with severe local hypotensio
n, baseline perfusion defects near the lesion and distant perfusion ch
anges are more likely attributable to other causes such as mass-relate
d or neurogenic changes.