TY - JOUR
T1 - How spreading depolarization can be the pathophysiological correlate of both migraine aura and stroke
AU - The COSBID study group
AU - Dreier, Jens P.
AU - Reiffurth, Clemens
AU - Woitzik, Johannes
AU - Hartings, Jed A.
AU - Drenckhahn, Christoph
AU - Windler, Claudia
AU - Friedman, Alon
AU - Macvicar, Brian
AU - Herreras, Oscar
N1 - Funding Information:
This work was supported by grants of the Deutsche Forschungsgemeinschaft (DFG DR 323/6-1) and the Bundesministerium für Bildung und Forschung (Center for Stroke Research Berlin, 01 EO 0801; Bernstein Center for Computational Neuroscience Berlin 01GQ1001C B2) to Dr. Dreier; the German Israeli Foundation (GIF No. 124/2008) to Dr. Friedman and Dr. Dreier; the ERA-NET NEURON (01EW1212) to Dr. MacVicar, Dr. Friedman, and Dr. Dreier; DFG DR 323/5-1 to Dr. Friedman, Dr. Woitzik and Dr. Dreier; DFG WO 1704/1-1 to Dr. Woitzik; and US Army CDMRP PH/TBI research program to Dr. Hartings.
Publisher Copyright:
© Springer International Publishing Switzerland 2015
PY - 2015/1/1
Y1 - 2015/1/1
N2 - The term spreading depolarization describes a mechanism of abrupt, massive ion translocation between neurons and the interstitial space, which leads to a cytotoxic edema in the gray matter of the brain. In energy- compromised tissue, spreading depolarization is preceded by a nonspreading silencing (depression of spontaneous activity) because of a neuronal hyperpolarization. By contrast, in tissue that is not energy compromised, spreading depolarization is accompanied by a spreading silencing (spreading depression) of spontaneous activity caused by a depolarization block. It is assumed that the nonspreading silencing translates into the initial clinical symptoms of ischemic stroke and the spreading silencing (spreading depression) into the symptoms of migraine aura. In energy-compromised tissue, spreading depolarization facilitates neuronal death, whereas, in healthy tissue, it is relatively innocuous. Therapies targeting spreading depolarization in metabolically compromised tissue may potentially treat conditions of acute cerebral injury such as aneurysmal subarachnoid hemorrhage.
AB - The term spreading depolarization describes a mechanism of abrupt, massive ion translocation between neurons and the interstitial space, which leads to a cytotoxic edema in the gray matter of the brain. In energy- compromised tissue, spreading depolarization is preceded by a nonspreading silencing (depression of spontaneous activity) because of a neuronal hyperpolarization. By contrast, in tissue that is not energy compromised, spreading depolarization is accompanied by a spreading silencing (spreading depression) of spontaneous activity caused by a depolarization block. It is assumed that the nonspreading silencing translates into the initial clinical symptoms of ischemic stroke and the spreading silencing (spreading depression) into the symptoms of migraine aura. In energy-compromised tissue, spreading depolarization facilitates neuronal death, whereas, in healthy tissue, it is relatively innocuous. Therapies targeting spreading depolarization in metabolically compromised tissue may potentially treat conditions of acute cerebral injury such as aneurysmal subarachnoid hemorrhage.
KW - Aneurysmal subarachnoid hemorrhage
KW - Delayed cerebral ischemia
KW - Spreading depression
UR - http://www.scopus.com/inward/record.url?scp=84925022510&partnerID=8YFLogxK
U2 - 10.1007/978-3-319-04981-6_23
DO - 10.1007/978-3-319-04981-6_23
M3 - Article
AN - SCOPUS:84925022510
SN - 0065-1419
VL - 120
SP - 137
EP - 140
JO - Acta Neurochirurgica, Supplement
JF - Acta Neurochirurgica, Supplement
ER -