Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 37, Issue 5, Pages 1571-1594Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/0271678X16654495
Keywords
Spreading depression; brain trauma; cerebral blood flow; electrophysiology; focal ischemia; brain edema; subarachnoid hemorrhage; vasospasm; two photon microscopy; system biology; stroke; selective neuronal death; neurovascular coupling; neuroprotection; neurocritical care; global ischemia; diffusion weighted MRI; cerebrovascular disease; cardiac arrest; brain ischemia
Categories
Funding
- Mayfield Education and Research Foundation
- Deutsche Forschungsgemeinschaft [DFG DR 323/6-1, DFG DR 323/5-1]
- Bundesministerium fur Bildung und Forschung (Center for Stroke Research Berlin) [01 EO 0801, BCCN 01GQ1001C B2]
- Era-Net Neuron [01EW1212]
- Hungarian Scientific Research Fund [K111923]
- Bolyai Janos Research Scholarship of the Hungarian Academy of Sciences [BO/00327/14/5]
- U.S. Department of Defense [CDMRP PR130373]
- National Institutes of Health [NS085413, NS083858, NS055104, NS061505]
- Wellcome Trust [HICF 0510-080]
- Fondation Leducq
- Heitman Foundation
- Ellison Foundation
- Novo Nordisk Fonden [NNF15OC0017366] Funding Source: researchfish
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A modern understanding of how cerebral cortical lesions develop after acute brain injury is based on Aristides Le (a) over tilde $o's historic discoveries of spreading depression and asphyxial/anoxic depolarization. Treated as separate entities for decades, we now appreciate that these events define a continuum of spreading mass depolarizations, a concept that is central to understanding their pathologic effects. Within minutes of acute severe ischemia, the onset of persistent depolarization triggers the breakdown of ion homeostasis and development of cytotoxic edema. These persistent changes are diagnosed as diffusion restriction in magnetic resonance imaging and define the ischemic core. In delayed lesion growth, transient spreading depolarizations arise spontaneously in the ischemic penumbra and induce further persistent depolarization and excitotoxic damage, progressively expanding the ischemic core. The causal role of these waves in lesion development has been proven by real-time monitoring of electrophysiology, blood flow, and cytotoxic edema. The spreading depolarization continuum further applies to other models of acute cortical lesions, suggesting that it is a universal principle of cortical lesion development. These pathophysiologic concepts establish a working hypothesis for translation to human disease, where complex patterns of depolarizations are observed in acute brain injury and appear to mediate and signal ongoing secondary damage.
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