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Published Online
on June 11, 2009

Stroke. 2009
Published online before print June 11, 2009, doi: 10.1161/STROKEAHA.109.549303
A more recent version of this article appeared on August 1, 2009
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Submitted on February 28, 2009
Revised on April 25, 2009
Accepted on May 1, 2009

Preliminary Evidence That Ketamine Inhibits Spreading Depolarizations in Acute Human Brain Injury

Oliver W. Sakowitz MD*; Karl L. Kiening MD; Kara L. Krajewski BA; Asita S. Sarrafzadeh MD; Martin Fabricius MD; Anthony J. Strong MD; Andreas W. Unterberg MD; and Jens P. Dreier MD

From the Department of Neurosurgery (O.W.S., K.L.K., K.L.K., A.W.U.), University of Heidelberg, Heidelberg, Germany; the Department of Neurosurgery (A.S.S.), Charité University Medicine Berlin, Berlin, Germany; the Department of Clinical Neurophysiology (M.F.), Glostrup Hospital, University of Copenhagen, Copenhagen, Denmark; the Department of Clinical Neurosciences (A.J.S.), King's College London, London, UK; and the Department of Neurology and Center for Stroke Research (J.P.D.), Charité University Medicine Berlin, Berlin, Germany.

* To whom correspondence should be addressed. E-mail: oliver.sakowitz{at}med.uni-heidelberg.de.

Background and Purpose—Spreading depolarizations, characterized by large propagating, slow potential changes, have been demonstrated with electrocorticography in patients with cerebral hemorrhage and ischemic stroke. Whereas spreading depolarizations are harmless under normal conditions in animals, they cause or augment damage in the ischemic brain. A fraction of spreading depolarizations is abolished by N-methyl-D-aspartate receptor antagonists.

Summary of Case—In 2 patients with severe acute brain injury (traumatic and spontaneous intracranial hemorrhage), spreading depolarizations were inhibited by the noncompetitive N-methyl-D-aspartate receptor antagonist ketamine. This restored electrocorticographic activity.

Conclusions—These anecdotal electrocorticographic findings suggest that ketamine has an inhibitory effect on spreading depolarizations in humans. This is of potential interest for future neuroprotective trials.
Key words: electrocorticography • intracerebral hemorrhage • NMDA receptor antagonists • spreading depression • traumatic brain injury






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