title: Adaptive changes of autoregulation in chronic cerebral hypotension with arteriovenous malformations: an acetazolamide-enhanced single-photon emission CT study.
abstract: OBJECTIVE
  To evaluate the relationship among feeding arterial pressure, lesion size, and perfusion in cerebral cortex adjacent to cerebral arteriovenous malformations (AVMs).
  
  
  METHODS
  Eleven patients with hemispheric AVMs underwent 99mTc hexamethyl-propyleneamine oxime single-photon emission CT before and after 1 g of acetazolamide was administered intravenously. AVM volume was estimated from MR dimensions and measured according to the method described by Pasqualin. Pressure measurements were obtained in arteries feeding the cortex adjacent to AVMs. Single-photon emission CT regions of interest were defined in cortex adjacent to the AVM and compared with contralateral regions using the Mountz method to estimate a baseline and dynamic (acetazolamide-challenged) perfusion defect volume.
  
  
  RESULTS
  Eight of 11 patients had baseline perfusion defects, but these defects were unrelated to feeding artery pressures (y = -.06x + 9.92, r2 = .04) or the dynamic change in defect volume after acetazolamide administration (y = .01x + .02, r2 = .002). However, there was a correlation between AVM volume and the baseline defect volume (y = .75x - 1.9, r2 = .76). Five patients had increased defect volume after acetazolamide administration; 5 patients had either no change in or improvement of perfusion. Dynamic changes in defect volume were related to feeding artery pressures.
  
  
  CONCLUSIONS
  Perilesional baseline perfusion defects appear to be related to lesion size and not to local arterial pressure. Cerebrovascular reserve generally was preserved, and perfusion defects appeared to be more pronounced with lower arterial pressures in feeding vessels. Although vasodilatory testing can unmask hemodynamic failure with severe local hypotension, baseline perfusion defects near the lesion and distant perfusion changes are more likely attributable to other causes such as mass-related or neurogenic changes.
authors.affiliation: Department of Radiology, College of Physicians and Surgeons, Columbia University, New York, NY, USA.
authors.forename: L
authors.initials: L
authors.lastname: Hacein-Bey
authors.forename: R
authors.initials: R
authors.lastname: Nour
authors.forename: J
authors.initials: J
authors.lastname: Pile-Spellman
authors.forename: R
authors.initials: R
authors.lastname: Van Heertum
authors.forename: P D
authors.initials: PD
authors.lastname: Esser
authors.forename: W L
authors.initials: WL
authors.lastname: Young
mesh_terms: D000086:Acetazolamide / Q000494:pharmacology*; D000222:Adaptation, Physiological; D000293:Adolescent; D000328:Adult; D001794:Blood Pressure; D002257:Carbonic Anhydrase Inhibitors / Q000494:pharmacology*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D002908:Chronic Disease; D005260:Female; D006706:Homeostasis; D006801:Humans; D002538:Intracranial Arteriovenous Malformations / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D015609:Organotechnetium Compounds; D010091:Oximes; D019690:Technetium Tc 99m Exametazime; D015899:Tomography, Emission-Computed, Single-Photon; D014664:Vasodilation / Q000187:drug effects
chemical_list: D002257:Carbonic Anhydrase Inhibitors; D015609:Organotechnetium Compounds; D010091:Oximes; D019690:Technetium Tc 99m Exametazime; D000086:Acetazolamide