Brain Advance Access originally published online on May 5, 2004
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Brain, Vol. 127, No. 7, 1670-1677,
July 2004
© 2004 Guarantors of Brain
doi: 10.1093/brain/awh191
In vivo MRI of brain inflammation in human ischaemic stroke
1 Institute of Diagnostic Radiology and 2 Department of Neurology, University Hospital, Heinrich-Heine-University, Düsseldorf, Germany
Correspondence to: Dr Sebastian Jander, Department of Neurology, University Hospital, Heinrich-Heine-University, Moorenstrasse 5, D-40225 Düsseldorf, Germany. E-mail: jander{at}uni-duesseldorf.de
Inflammation contributes to brain damage caused by ischaemic stroke. Macrophages, as the prevailing inflammatory cell population in stroke lesions, can be visualized using ultrasmall superparamagnetic iron oxide (USPIO) as a cell-specific contrast agent for MRI. In this single-centre open-labelled clinical phase II study we tested the potential of USPIO-enhanced MRI for macrophage imaging in human ischaemic stroke lesions. In a series of 10 consecutive patients, USPIO contrast agent was infused at the end of the first week after symptom onset. Two follow-up MRI scans were performed 24–36 h and 48–72 h after infusion. Two distinct components of USPIO-related signal changes were discernible, one associated with blood vessels and one representing parenchymal enhancement. Vessel-associated changes appeared as signal loss on T2/T2*-weighted images and decreased from the first to second scan after USPIO infusion, most likely reflecting a transient blood pool effect of the contrast agent. Conversely, parenchymal enhancement was mainly evident on T1-weighted images, increased over time, and matched with the expected distribution of macrophages. Importantly, USPIO-induced signal alterations throughout differed from signatures of conventional gadolinium-enhanced MRI, thus being independent from breakdown of the blood–brain barrier. We suggest that increasing USPIO-enhancement on T1-weighted images indicates brain infiltration by USPIO-laden macrophages. Thus, USPIO-enhanced MRI may provide an in vivo surrogate marker of cellular inflammation in stroke and other CNS pathologies.
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