4.5 Article

Edema and brain trauma

Journal

NEUROSCIENCE
Volume 129, Issue 4, Pages 1021-1029

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2004.06.046

Keywords

blood brain barrier; brain edema; traumatic brain injury; cerebral perfusion pressure; intracranial pressure; aquaporin

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Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortality following traumatic brain injury (TBI) as it increases intracranial pressure, impairs cerebral perfusion and oxygenation, and contributes to additional ischemic injuries. Classically, two major types of traumatic brain edema exist: vasogenic due to blood-brain barrier (BBB) disruption resulting in extracellular water accumulation and cytotoxic/cellular due to sustained intracellular water collection. A third type, osmotic brain edema is caused by osmotic imbalances between blood and tissue. Rarely after TBI do we encounter a hydrocephalic edema/interstitial brain edema related to an obstruction of cerebrospinal fluid outflow. Following TBI, various mediators are released which enhance vasogenic and/or cytotoxic brain edema. These include glutamate, lactate, H+, K+, Ca2+, nitric oxide, arachidonic acid and its metabolites, free oxygen radicals, histamine, and kinins. Thus, avoiding cerebral anaerobic metabolism and acidosis is beneficial to control lactate and H+, but no compound inhibiting mediators/mediator channels showed beneficial results in conducted clinical trials, despite successful experimental studies. Hence, antiedematous therapy in TBI patients is still symptomatic and rather non-specific (e.g. mannitol infusion, controlled hyperventilation). For many years, vasogenic brain edema was accepted as the prevalent edema type following TBI. The development of mechanical TBI models (weight drop, fluid percussion injury, and controlled cortical impact injury) and the use of magnetic resonance imaging, however, revealed that cytotoxic edema is of decisive pathophysiological importance following TBI as it develops early and persists while BBB integrity is gradually restored. These findings suggest that cytotoxic and vasogenic brain edema are two entities which can be targeted simultaneously or according to their temporal prevalence. (C) 2004 IBRO. Published by Elsevier Ltd. All rights reserved.

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