Abstract
Severe brain trauma remains poorly understood, because of its pathophysiological complexity, and this has so far thwarted our attempts to improve outcome by means of drug therapy, although better understanding of the role of ischemic events has led to improved mortality rates, in some centers. With regard to excitatory amino acid antagonists, new mechanistic insights from both animal models, and human monitoring has enabled better trial design, which may allow the tremendous laboratory neuroprotective potency of this group of compounds to be translated to clinical benefit. Key words: excitatory amino acids; brain trauma; glutamate; ion channels