PubMed · 1992 · 109 citations · 0 references
MedicineNeurosciencePharmacologyClinical NeuroscienceNeurochemistryNeuropharmacologyAmino Acid NeurochemistryDiffuse Axonal InjuryGlutamatergic PharmacologyNeuroprotectionNeuroprotective PharmacologyTraumatic Brain InjuryAnimal Disease ModelsGlutamate AntagonistsHuman Subject TrialsTraumatic Axonal InjuryTraumatic Brain Injury ModelsTraumatic Brain Injury PathologyTraumatic Brain Injury PharmacotherapyTraumatic Brain Injury Sequelae
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.