Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

Journal of Cerebral Blood Flow and Metabolism - Tập 31 Số 1 - Trang 17-35 - 2011
Martin Lauritzen1,2, Jens P. Dreier3,4,5, Martin Fabricius2, Jed A. Hartings6, Rudolf Graf7, Anthony J. Strong8
1Center for Healthy Aging and Institute for Neuroscience and Pharmacology, University of Copenhagen, Glostrup, Denmark
2Department of Clinical Neurophysiology, Glostrup Hospital, Glostrup, Denmark
3Center for Stroke Research Berlin, Charité University Medicine Berlin, Berlin, Germany
4Department of Experimental Neurology, Charité University Medicine Berlin, Berlin, Germany
5Department of Neurology, Charité, University Medicine Berlin, Berlin, Germany
6Department of Neurosurgery, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA
7Max Planck Institute for Neurological Research, Cologne, Germany
8Department of Clinical Neuroscience, King's College, London, UK

Tóm tắt

Cortical spreading depression (CSD) and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine, stroke, subarachnoid hemorrhage and traumatic brain injury. The implications of these findings are widespread and suggest that intrinsic brain mechanisms have the potential to worsen the outcome of cerebrovascular episodes or brain trauma. The consequences of these intrinsic mechanisms are intimately linked to the composition of the brain extracellular microenvironment and to the level of brain perfusion and in consequence brain energy supply. This paper summarizes the evidence provided by novel invasive techniques, which implicates CSD as a pathophysiological mechanism for this group of acute neurological disorders. The findings have implications for monitoring and treatment of patients with acute brain disorders in the intensive care unit. Drawing on the large body of experimental findings from animal studies of CSD obtained during decades we suggest treatment strategies, which may be used to prevent or attenuate secondary neuronal damage in acutely injured human brain cortex caused by depolarization waves.

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