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(Stroke. 2009;40:e519.)
© 2009 American Heart Association, Inc.
Case Report |
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.), Kings College London, London, UK; and the Department of Neurology and Center for Stroke Research (J.P.D.), Charité University Medicine Berlin, Berlin, Germany.
Correspondence to Oliver W. Sakowitz, MD, Department of Neurosurgery, University of Heidelberg, Im Neuenheimer Feld 400, D-69120 Heidelberg, Germany. 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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