Perfusion-CT assessment of the cerebrovascular reserve: A revisit to the acetazolamide challenges

Abstract

Imaging techniques utilizing acetazolamide challenges classically measure cerebral blood flow (CBF). In addition to measuring CBF, Perfusion-CT (PCT) can also assess cerebral blood volume (CBV) and mean transit time (MTT), expanding but also complicating the results of acetazolamide challenges performed using PCT. The goal of this study is to clarify the interpretation of PCT studies obtained during acetazolamide challenges. Four consecutive patients were referred for evaluation of their cerebrovascular reserve because of suspected or known large vessel stenosis or occlusion. In one patient, the potential stenosis was found to be artifactual, and this subject was considered as a normal control. The remaining three patients had clinical histories clearly suggestive of a worsening in cerebrovascular reserve (no.1 with a single transient ischemic attack (TIA), no.2 with several TIAs, no.3 with multiple, prolonged TIAs). All patients underwent a baseline PCT scan, followed by intravenous injection of 1g acetazolamide and, 20 min postinjection, by a second PCT scan at exactly the same locations as the first. PCT cerebral blood flow, volume, and mean transit time values were measured in regions of interest (ROIs) encompassing the brain tissue at-risk and the normal brain tissue, defined based on the site of occlusion and the anatomy of the Circle of Willis. Changes in PCT parameters were calculated in corresponding ROIs on pre- and postacetazolamide PCT maps. As compared to the normal control patient, baseline CBF values in the at-risk regions were similar in patients nos.1 and 2, and lower in patient no.3. After acetazolamide administration, CBF increased by 32% in the normal patient and decreased by 11, 11, and 9% in the at-risk regions in patients nos.1, 2, and 3, respectively; CBV was stable for all patients except no.3, who showed a 36% increase; MTT was the PCT parameter whose change best differentiated the four patients (-17% in the normal patient, +9% in patient no.1, +24% in patient no.2, +48% in patient no.3). Interestingly, the baseline MTT values, measured before acetazolamide injection, showed a similar, gradual increase in the four patients, ranging from 4.5 to 8.1s. The degree of impairment in cerebrovascular reserve, as assessed by clinical history, correlated most closely with the change in MTT in response to acetazolamide. Increased baseline MTT values may be a static, quantitative indicator of compromised cerebrovascular reserve in at-risk territories.