Preliminary evidence that ketamine inhibits spreading depolarizations in acute human brain injury

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 d...

Full description

Saved in:
Bibliographic Details
Published in:Stroke (1970) 2009-08, Vol.40 (8), p.e519-e522
Main Authors: Sakowitz, Oliver W, Kiening, Karl L, Krajewski, Kara L, Sarrafzadeh, Asita S, Fabricius, Martin, Strong, Anthony J, Unterberg, Andreas W, Dreier, Jens P
Format: Article
Language:English
Subjects:
Adult
Brain Injuries - drug therapy
Brain Injuries - physiopathology
Brain Injuries - surgery
Cortical Spreading Depression - drug effects
Cortical Spreading Depression - physiology
Humans
Ketamine - pharmacology
Ketamine - therapeutic use
Male
Middle Aged
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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. 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.
ISSN:0039-2499
1524-4628
DOI:10.1161/STROKEAHA.109.549303