Journal
PHYSIOLOGICAL REVIEWS
Volume 95, Issue 3, Pages 953-993Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/physrev.00027.2014
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Funding
- National Institutes of Health [NS061505, NS055104, NS35611]
- Fondation Leducq
- Heitman Foundation
- Ellison Foundation
- Lundbeck Foundation
- NOVO-Nordisk Foundation
- Nordea Foundation for the Center for Healthy Aging
- Foundation Leducq
- Danish Medical Research Council
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Spreading depression (SD) is a transient wave of near-complete neuronal and glial depolarization associated with massive transmembrane ionic and water shifts. It is evolutionarily conserved in the central nervous systems of a wide variety of species from locust to human. The depolarization spreads slowly at a rate of only millimeters per minute by way of grey matter contiguity, irrespective of functional or vascular divisions, and lasts up to a minute in otherwise normal tissue. As such, SD is a radically different breed of electrophysiological activity compared with everyday neural activity, such as action potentials and synaptic transmission. Seventy years after its discovery by Leao, the mechanisms of SD and its profound metabolic and hemodynamic effects are still debated. What we did learn of consequence, however, is that SD plays a central role in the pathophysiology of a number of diseases including migraine, ischemic stroke, intracranial hemorrhage, and traumatic brain injury. An intriguing overlap among them is that they are all neurovascular disorders. Therefore, the interplay between neurons and vascular elements is critical for our understanding of the impact of this homeostatic breakdown in patients. The challenges of translating experimental data into human pathophysiology notwithstanding, this review provides a detailed account of bidirectional interactions between brain parenchyma and the cerebral vasculature during SD and puts this in the context of neurovascular diseases.
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