1. ¹MR Technology, Institute for Biodiagnostics (West), National Research Council, Calgary, Alberta, Canada
2. ²Experimental Imaging Center and Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada
3. ³Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada

Correspondence: Dr UI Tuor, Institute for Biodiagnostics (West), National Research Council of Canada, B153, 3330 Hospital Dr N.W., Calgary, Alberta T2N 4N1, Canada. E-mail: ursula.tuor@nrc-cnrc.gc.ca

Received 21 April 2006; Revised 18 January 2007; Accepted 18 January 2007; Published online 21 March 2007.

Abstract

Although functional magnetic resonance imaging (fMRI) is gaining use as a tool to assess cerebral recovery following various insults, the effects of potential confounders such as hypertension are poorly defined. We hypothesized that after stroke, transient hypertension during an fMRI study could produce a detected activation unrelated to neuronal activity within the infarct. Thus, the effect of norepinephrine induced increases in blood pressure (BP) on the fMRI response to forepaw stimulation were investigated in controls or 1 week after transient middle cerebral artery occlusion in rats. Images were smoothed spatially and voxels correlating to either forepaw stimulation or the change in BP time courses were analyzed. Transient hypertension increased the signal intensity and numbers of voxels correlating to the BP time courses within and adjacent to the ischemic infarct and these exceeded the response in the contralateral hemisphere or in controls. With left paw stimulation at normotension, there was a loss of activation in right sensory-motor cortex—a region with necrosis and disruption of cerebral vessels. As BP increased left paw stimulation also resulted in the detection of activation in the infarcted sensory–motor cortex and peri-infarct regions. Thus, BP changes synchronous with tasks in fMRI studies can result in MR signal changes consistent with a loss of cerebral blood flow (CBF) autoregulation rather than neuronal activation in necrotic brain. After stroke, the use of stressful tasks associated with BP changes in fMRI studies should be limited or the BP change should be considered as a potential source of MR signal changes.