| Literature DB >> 27317657 |
Jens P Dreier1,2,3, Martin Fabricius4, Cenk Ayata5,6, Oliver W Sakowitz7,8, C William Shuttleworth9, Christian Dohmen10,11, Rudolf Graf11, Peter Vajkoczy1,12, Raimund Helbok13, Michiyasu Suzuki14, Alois J Schiefecker13, Sebastian Major1,2,3, Maren Kl Winkler1, Eun-Jeung Kang1,3, Denny Milakara1, Ana I Oliveira-Ferreira1,3, Clemens Reiffurth1,3, Gajanan S Revankar1, Kazutaka Sugimoto14, Nora F Dengler1,12, Nils Hecht1,12, Brandon Foreman15, Bart Feyen16, Daniel Kondziella17, Christian K Friberg4, Henning Piilgaard4, Eric S Rosenthal6, M Brandon Westover6, Anna Maslarova18, Edgar Santos8, Daniel Hertle8, Renán Sánchez-Porras8, Sharon L Jewell19, Baptiste Balança20,21, Johannes Platz22, Jason M Hinzman23, Janos Lückl1, Karl Schoknecht1,3,24, Michael Schöll8,25, Christoph Drenckhahn1,26, Delphine Feuerstein11, Nina Eriksen27,28, Viktor Horst1,29, Julia S Bretz1,29, Paul Jahnke29, Michael Scheel29, Georg Bohner29, Egill Rostrup27, Bente Pakkenberg28,30, Uwe Heinemann1,24, Jan Claassen31, Andrew P Carlson32, Christina M Kowoll10,11, Svetlana Lublinsky33,34, Yoash Chassidim33,34, Ilan Shelef34, Alon Friedman33,35, Gerrit Brinker36, Michael Reiner36, Sergei A Kirov37, R David Andrew38, Eszter Farkas39, Erdem Güresir18, Hartmut Vatter18, Lee S Chung40, K C Brennan40, Thomas Lieutaud20,21, Stephane Marinesco20,41, Andrew Ir Maas16, Juan Sahuquillo42, Markus A Dahlem43, Frank Richter44, Oscar Herreras45, Martyn G Boutelle46, David O Okonkwo47, M Ross Bullock48, Otto W Witte49, Peter Martus50, Arn Mjm van den Maagdenberg51,52, Michel D Ferrari52, Rick M Dijkhuizen53, Lori A Shutter47,54, Norberto Andaluz23,55, André P Schulte56, Brian MacVicar57, Tomas Watanabe58, Johannes Woitzik1,12, Martin Lauritzen4,59, Anthony J Strong19, Jed A Hartings23,55.
Abstract
Spreading depolarizations (SD) are waves of abrupt, near-complete breakdown of neuronal transmembrane ion gradients, are the largest possible pathophysiologic disruption of viable cerebral gray matter, and are a crucial mechanism of lesion development. Spreading depolarizations are increasingly recorded during multimodal neuromonitoring in neurocritical care as a causal biomarker providing a diagnostic summary measure of metabolic failure and excitotoxic injury. Focal ischemia causes spreading depolarization within minutes. Further spreading depolarizations arise for hours to days due to energy supply-demand mismatch in viable tissue. Spreading depolarizations exacerbate neuronal injury through prolonged ionic breakdown and spreading depolarization-related hypoperfusion (spreading ischemia). Local duration of the depolarization indicates local tissue energy status and risk of injury. Regional electrocorticographic monitoring affords even remote detection of injury because spreading depolarizations propagate widely from ischemic or metabolically stressed zones; characteristic patterns, including temporal clusters of spreading depolarizations and persistent depression of spontaneous cortical activity, can be recognized and quantified. Here, we describe the experimental basis for interpreting these patterns and illustrate their translation to human disease. We further provide consensus recommendations for electrocorticographic methods to record, classify, and score spreading depolarizations and associated spreading depressions. These methods offer distinct advantages over other neuromonitoring modalities and allow for future refinement through less invasive and more automated approaches.Entities:
Keywords: Spreading depolarization; anoxic depolarization; asphyxial depolarization; brain edema; brain trauma; cerebral blood flow; epilepsy; epileptogenesis; focal ischemia; global ischemia; intracerebral hemorrhage; neurocritical care; neuroprotection; neurovascular coupling; peri-infarct depolarization; spreading depression; spreading ischemia; subarachnoid hemorrhage; vasospasm
Mesh:
Year: 2016 PMID: 27317657 PMCID: PMC5435289 DOI: 10.1177/0271678X16654496
Source DB: PubMed Journal: J Cereb Blood Flow Metab ISSN: 0271-678X Impact factor: 6.200