Brain Advance Access published online on April 3, 2009
Brain, doi:10.1093/brain/awp010
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Early brain temperature elevation and anaerobic metabolism in human acute ischaemic stroke
1 Division of Clinical Neurosciences, University of Edinburgh, Western General Hospital, Crewe Rd, Edinburgh, EH4 2XU, UK 2 Department of Neurology of Adults, Medical University of Gdansk, ul. Debinki 7, 80-211 Gdansk, Poland 3 Medical Physics, Division of Medical and Radiological Sciences, University of Edinburgh, Western General Hospital, Crewe Rd, Edinburgh, EH4 2XU, UK 4 Oxford Centre For Functional Magnetic Resonance Imaging of the Brain, Department of Clinical Neurology, University of Oxford, Oxford, UK
Correspondence to:
Prof. Joanna M. Wardlaw, Division of Clinical Neurosciences, Western General Hospital, Crewe Rd, Edinburgh, EH4 2XU, UK E-mail: joanna.wardlaw{at}ed.ac.uk
Early after acute ischaemic stroke, elevation of brain temperature might augment tissue metabolic rate and conversion of ischaemic but viable tissue to infarction. This might explain the observed link between pyrexia, severe stroke and poor outcome. We tested this hypothesis by measuring brain temperature and lactate concentration with multi-voxel magnetic resonance spectroscopic imaging across the acute ischaemic stroke lesion and normal brain as determined on diffusion imaging. We compared patterns of lactate concentration (reported in ‘institutional units’) and temperature elevation in diffusion lesion core, potential penumbra, ipsilateral and contralateral normal brain and with stroke severity. Amongst 40 patients with moderate to severe acute stroke imaged up to 26 h after onset, lactate concentration was highest in the ischaemic lesion core (42 versus 26 units in potential penumbra, P < 0.05), whereas temperature was highest in the potential penumbra (37.7 versus 37.3°C in lesion core, P < 0.05). Neither sub-regional temperature nor lactate concentration correlated with stroke severity. With increasing time after stroke, ipsilateral brain temperature did not change, but contralateral hemisphere temperature was higher in patients scanned at later times; lactate remained elevated in the lesion core, but declined in potential penumbral and ipsilateral normal tissue at later times. We conclude that early brain temperature elevation after stroke is not directly related to lactate concentration, therefore augmented metabolism is unlikely to explain the relationship between early pyrexia, severe stroke and poor outcome. Early brain temperature elevation may result from different mechanisms to those which raise body temperature after stroke. Further studies are required to determine why early brain temperature elevation is highest in potential penumbral tissue.
Key Words: ischaemic stroke; lactate metabolism; brain temperature; MR spectroscopy; pyrexia
Abbreviations: FID, free induction decay; MRSI, magnetic resonance spectroscopic imaging; OCSP, Oxfordshire Community Stroke Project; PRESS, Point Resolved Spectroscopy; T2W, T2-weighted; UCP-2, uncoupling protein 2
Received July 12, 2008. Revised December 12, 2008. Accepted January 5, 2009.