[Neurochemical changes and current pharmacological approaches in craniocerebral trauma].
In recent years, our knowledge concerning pathophysiological changes in brain metabolism after traumatic brain injury (TBI) has greatly expanded. This, in turn, has enabled the development of specific pharmacological strategies for the supplementary treatment of brain-injured patients with the aim of reducing secondary brain damage. The present article focuses on the pathophysiology of TBI and the possibilities for pharmacological intervention. While some of the substances reviewed and presently used in the treatment of TBI, others are under experimental and clinical evaluation at different stages.
Kossmann
T
T
Klinik für Unfallchirurgie, Departement Chirurgie, Universitätsspital Zürich.
Lenzlinger
P M
PM
Stover
J F
JF
Stocker
R
R
Morganti-Kossmann
M C
MC
Trentz
O
O
D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use; D016718:Arachidonic Acid / Q000037:antagonists & inhibitors / Q000502:physiology; D001930:Brain Injuries / Q000188:drug therapy / Q000503:physiopathology*; D002118:Calcium / Q000502:physiology; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology*; D018691:Excitatory Amino Acid Antagonists / Q000627:therapeutic use; D018846:Excitatory Amino Acids / Q000502:physiology; D016489:Head Injuries, Closed / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D017382:Reactive Oxygen Species / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*
D000975:Antioxidants; D002121:Calcium Channel Blockers; D018691:Excitatory Amino Acid Antagonists; D018846:Excitatory Amino Acids; D017382:Reactive Oxygen Species; D016718:Arachidonic Acid; D002118:Calcium