ADAPTIVE-CHANGES OF AUTOREGULATION IN CHRONIC CEREBRAL HYPOTENSION WITH ARTERIOVENOUS-MALFORMATIONS - AN ACETAZOLAMIDE-ENHANCED SINGLE-PHOTON EMISSION CT STUDY

Citation
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
ISSN journal
01956108
Volume
16
Issue
9
Year of publication
1995
Pages
1865 - 1874
Database
ISI
SICI code
0195-6108(1995)16:9<1865:AOAICC>2.0.ZU;2-C
Abstract
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.