• T Lescot, C Marchand-Verrecchia, and L Puybasset.
• Département d'anesthésie-réanimation, université Pierre et Marie-Curie, CHU de la Pitié-Salpêtrière, APHP, 47-83, boulevard de l'Hôpital, 75651 Paris cedex 13, France.
• Ann Fr Anesth Reanim. 2006 Jul 1; 25 (7): 755-60.

AbstractTraumatic brain injury leads to primary and secondary brain injuries. Primary brain injury results from mechanical forces applied to the head at the time of impact. Secondary brain injury occurs at some time after the primary impact. Numerous pathophysiological mechanisms have been postulated to explain the progressive tissue damage produced by secondary injuries. The endogenous neuroinflammatory response after traumatic brain injury contributes to the development of blood-brain barrier breakdown, cerebral oedema and neuronal cell death and this has led to various pharmacological therapies to try to limit this type of damage. Studies employing glutamate receptor antagonist for cerebral protection have yielded promising results in laboratory animals but failed to produce clinically significant improvements. The present review will summarize the mechanisms of post traumatic cerebral inflammation with a special focus on the anti-inflammatory drug targets.

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