Postcarotid Endarterectomy Improvement in Cognition Is Associated with Resolution of Crossed Cerebellar Hypoperfusion and Increase in 123I-Iomazenil Uptake in the Cerebral Cortex: A SPECT Study

Background: The purpose of the present study was to investigate whether resolution of crossed cerebellar hypoperfusion (CCH) and increase in 123 I-iomazenil (IMZ) uptake in the ipsilateral cerebral cortex after carotid endarterectomy (CEA) are associated with postoperative improvement of cognitive function. Methods: Neuropsychological testing was performed preoperatively and after 1 postoperative month in 79 patients undergoing CEA for ipsilateral internal carotid artery stenosis (≧70%). Brain perfusion single photon emission computed tomography (SPECT) using N-isopropyl-p- 123 I-iodoamphetamine and 123 I-IMZ SPECT were also performed before and after surgery. Data were analyzed using a three-dimensional stereotaxic region of interest template. Results: Seven patients (9%) showed improvement in postoperative cognitive function. All the 7 patients exhibited both postoperative increase in blood flow in the ipsilateral cerebral cortex and resolution of CCH. Five patients (6%) had a postoperative hemispheric increase in 123 I-IMZ uptake, and cognitive function improved in all of these 5 patients. Analysis by a receiver operating characteristic (ROC) curve was used to estimate the ability to discriminate between patients with and without postoperative cognitive improvement. The area under the ROC curve was significantly greater when analyzing the magnitude of postoperative resolution of CCH (0.991; 95% CI 0.984–1.001) or postoperative hemispheric increase in 123 I-IMZ uptake (0.981; 95% CI 0.972–0.999) when compared with the magnitude of postoperative increase in cerebral blood flow (0.929; 95% CI 0.886–0.971) (p < 0.05). Conclusions: Resolution of CCH and increase in 123 I-IMZ uptake in the ipsilateral cerebral cortex after CEA is associated with postoperative improvement in cognitive function. These results may indicate that cognitive impairment is related to a state of potentially reversible central benzodiazepine receptor downregulation in the cortex in response to transient ischemic attack or minor stroke.