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(Stroke. 2004;35:1659.)
© 2004 American Heart Association, Inc.
Original Contributions |
From the University of Cambridge Department of Medicine (C.J.S.P.) and Anaesthesia Section (D.K.M.), Addenbrookes Hospital, Cambridge, UK; Department of Nuclear Medicine (A.M.P., J.R.B., R.W.B., K.K.B.), and Department of Clinical Neurosciences (E.A.W.), Cambridge University Teaching Hospitals Trust, Cambridge, UK; Centre for Applied Medical Statistics (A.L.), Department of Pathology (J.H.X.), Wolfson Brain Imaging Centre (T.F.), and Department of Neurology (J.V.G.), University of Cambridge, UK.
Correspondence to Dr Christopher J.S. Price, MRC Training Fellow in Stroke Medicine, Box 83, R3 Neurosciences, Addenbrookes Hospital, Cambridge CB22QQ, UK. E-mail cp252{at}medschl.cam.ac.uk
Background and Purpose Evidence now exists for a pathogenic role for neutrophils in acute cerebral ischemia. We have studied the patterns and temporal profile of cerebral neutrophil recruitment to areas of acute ischemic stroke (IS) and have attempted to correlate this with neurological status and outcome.
Methods Patients with cortical middle cerebral artery (MCA) IS were recruited within 24 hours of clinical onset. Neutrophil recruitment was studied using indium-111 (111In) troponolate-labeled neutrophils, planar imaging, and single-photon emission computed tomography (SPECT). Volume of brain infarction was calculated from concurrent computed tomography (CT). Hematoxylin and eosin sections were obtained postmortem (n=2). Outcome was measured using Barthel, Rankin, and National Institute of Health Stroke (NIHSS) scales.
Results Fifteen patients were studied. Significant 111Inneutrophil recruitment to ipsilateral hemisphere, as measured by asymmetry index (AI), was demonstrated within 24 hours of onset in 9 patients; this response was heterogenous between patients and on repeated measurement attenuated over time. Histologically, recruitment was confirmed within intravascular, intramural, and intraparenchymal compartments. Interindividual heterogeneity in neutrophil response did not correlate with infarct volume or outcome. In an exploratory analysis, neutrophil accumulation appeared to correlate significantly with infarct expansion (Spearman rho=0.66; P=0.03, n=12).
Conclusions Neutrophils recruit to areas of ischemic brain within 24 hours of symptom onset. This recruitment attenuates over time and is confirmed histologically. While neutrophil accumulation may be associated with either the magnitude or the rate of infarct growth, these results require confirmation in future studies.
Key Words: stroke ischemia neutrophils SPECT histology
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