The role of glutamate antagonists for the treatment of CNS injury.
Ischemic damage, chiefly of the focal type, and axonal disruption (diffuse axonal injury) are the major factors causing brain damage after human head injury. About one third of this damage may be delayed hours or days after the injury. Evidence from four animal models, each relevant to different aspects of human head injury, has shown that excitatory amino acid-induced changes are responsible for a proportion of the posttraumatic sequelae and that these effects can be blocked by EAA antagonists. This evidence is reviewed, and the implications for the conduct of human trials with EAA antagonists are discussed.
Bullock
R
R
Department of Neurosurgery, University of Glasgow, Scotland.
Fujisawa
H
H
D000818:Animals; D001925:Brain Damage, Chronic / Q000209:etiology / Q000517:prevention & control; D001930:Brain Injuries / Q000188:drug therapy*; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D002492:Central Nervous System Depressants / Q000627:therapeutic use*; D016291:Dizocilpine Maleate / Q000627:therapeutic use; D018691:Excitatory Amino Acid Antagonists; D006801:Humans; D002546:Ischemic Attack, Transient / Q000188:drug therapy / Q000517:prevention & control; D013119:Spinal Cord Injuries / Q000188:drug therapy*
D002492:Central Nervous System Depressants; D018691:Excitatory Amino Acid Antagonists; D016291:Dizocilpine Maleate