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1. Cortical spreading depression is a non-physiological global depolarisation of neurones and astrocytes that can be initiated with varying degrees of difficulty in the normally perfused cerebral cortex in the experimental laboratory. Induction is typically with electrical stimulation, needling of the cerebral cortex, or superfusion of isotonic or more concentrated potassium chloride solution. The phenomenon propagates across the cerebral cortex at a rate of 2-5 mm per minute, and is accompanied by marked but transient increases in cerebral blood flow, in local tissue oxygen tension, and most probably in metabolic rate.

2. Peri-infarct depolarisation is also a depolarisation event affecting neurones and glia, with an electrophysiological basis similar or identical to CSD, but occurring spontaneously in the ischaemic penumbra or boundary zone in focal cerebral cortical ischaemia. Most such events arise from the edge of the ischaemic core, and propagate throughout the penumbra, at a rate similar to that of cortical spreading depression.

3. Cortical spreading depression in the normally perfused cortex does not result in histological damage whereas peri-infarct depolarisations augment neuronal damage in the penumbra, and are believed by many authors to constitute an important, or the principal, mechanism by which electrophysiological penumbra progressively deteriorates, ultimately undergoing terminal depolarisation and thus recruitment into an expanded core lesion.

4. There is some experimental evidence to suggest that under some circumstances induction of episodes of cortical spreading depression can confer protection against subsequent ischaemic insults.

5. Although cortical spreading depression and peri-infarct depolarisations have been extensively studied in the experimental in vivo models, there is now clear evidence that depolarisations also occur and propagate in the human brain in areas surrounding a focus of traumatic contusion.

6. Whether such events in the injured human brain represent cortical spreading depression or peri-infarct depolarisation is unclear. However, invasive and probably non-invasive monitoring methods are available which may serve to distinguish which event has occurred.

7. Much further work will be needed to examine the relationship of depolarisation events in the injured brain with outcome from cerebral ischaemia or head injury, to examine the factors which influence the frequency of depolarisation events, and to determine which depolarisation events in the human brain augment the injury and should be prevented.

Acknowledgements

We thank the Medical Research Council, the Wellcome Trust, the National Lottery Charities Board (Community Fund), HeadFirst, the Golden Charitable Trust, the Patrick Berthoud Trust and GlaxoSmithkline for their support over the period covered by this review.

We are very grateful to Drs Sue Robertson and George Somjen for helpful comments on the manuscript.

Key Original Papers and Reviews

Busch E, Gyngell ML, Eis M, Hoehn Berlage M, Hossmann KA (1996) Potassium-induced cortical spreading depressions during focal cerebral ischemia in rats: contribution to lesion growth assessed by diffusion-weighted NMR and biochemical imaging. J Cereb Blood Flow Metab 16:1090-1099 Grafstein B (1956) Mechanism of spreading cortical depression. J Neurophysiol 19:154-171

Hadjikhani N, Sanchez DR, Wu O, Schwartz D, Bakker D, Fischl B et al (2001) Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Proceedings of the National Academy of Sciences of the United States of America 98:4687-4692 Hossmann KA (1996) Periinfarct depolarizations. [Review] [81 refs]. Cerebrovasc

Brain Metab Rev 8:195-208 Leao AAP (1944) Spreading depression of activity in cerebral cortex. J Neuro-physiol 7:359-390

Somjen GG (2001) Mechanisms of spreading depression and hypoxic spreading depression-like depolarisation. Physiol Rev 81:1065-1096 Strong AJ, Fabricius M, Boutelle MG, Hibbins SJ, Hopwood SE, Jones R et al (2002) Spreading and synchronous depressions of cortical activity in acutely injured human brain. Stroke 33:2738-2743 Tsacopoulos M, Magistretti PJ (1996) Metabolic coupling between glia and neurons. J Neurosci 16:877-885

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