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|Title:||Mechanisms of cerebral edema in traumatic brain injury: Therapeutic developments|
|Citation:||Current Opinion in Neurology, 2010; 23(3):293-299|
|Publisher:||Lippincott Williams & Wilkins|
|James J. Donkin and Robert Vink|
|Abstract:||<h4>Purpose of review</h4>Although a number of factors contribute to the high mortality and morbidity associated with traumatic brain injury (TBI), the development of cerebral edema with brain swelling remains the most significant predictor of outcome. The present review summarizes the most recent advances in the understanding of mechanisms associated with development of posttraumatic cerebral edema, and highlights areas of therapeutic promise.<h4>Recent findings</h4>Despite the predominance of cytotoxic (or cellular) edema in the first week after traumatic brain injury, brain swelling can only occur with addition of water to the cranial vault from the vasculature. As such, regulation of blood-brain barrier permeability has become a focus of recent research seeking to manage brain edema. Aquaporins, matrix metalloproteinases and vasoactive inflammatory agents have emerged as potential mediators of cerebral edema following traumatic brain injury. In particular, kinins (bradykinins) and tachykinins (substance P) seem to play an active physiological role in modulating blood-brain barrier permeability after trauma. Substance P neurokinin-1 receptor antagonists show particular promise as novel therapeutic agents.<h4>Summary</h4>Attenuating blood-brain barrier permeability has become a promising approach to managing brain edema and associated swelling given that increases in cranial water content can only be derived from the vasculature. Inflammation, both classical and neurogenic, offers a number of attractive targets.|
|Keywords:||Aquaporins; cytotoxic edema; neurogenic inflammation; neurotrauma, neurovascular unit; trauma; vasogenic edema|
|Rights:||Copyright 2010 Wolters Kluwer Health. Lippincott Williams & Wilkins|
|Appears in Collections:||Anatomical Sciences publications|
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