@entity131 is a major health problem in all developed countries. The main aim of this review is to provide a short update on the most recent advances in our knowledge of the brains response to mechanical injuries, focusing on metabolic, cellular, subcellular, and molecular events that take place in severe @entity542 . Knowledge of these events is essential for a better understanding of new pharmacological avenues and non-pharmacological strategies, such as moderate @entity2332 , which are being developed to improve the outcome of this silent epidemic. We will focus on several topics that we consider to be the most significant: @entity21 , @entity63 and the cascades it generates, metabolic derangements, excitotoxicity, oxidative stress, and other phenomena that have been included in the term tertiary injuries. Recent evidence has clearly demonstrated that traumatic @entity75 are highly dynamic and that the different lesions observed after @entity6075 are not single events but processes set in motion by the mechanical impact. These processes are not finished until an unpredictable time after injury. We will discuss recent evidence showing that in @entity21 , primary immediate damage can coexist with axons that, although initially intact, may be evolving towards secondary disconnection. The concept of ischemic penumbra and the more recent concept of traumatic penumbra are discussed, together with recent experimental and clinical data that shed light on the non-ischemic forms of @entity12807 . The role of excitotoxicity in mechanically-induced cell death and the molecular events that excessive release of @entity2227 induce, including apoptosis and delayed inflammatory processes, are reviewed. Finally, new knowledge on how central nervous system cells regulate their volume, the new family of channel water molecules known as aquaporins and their possible role in the physiopathology of the swollen brain are discussed. Basic and clinical investigations are still needed to translate the huge amount of pathophysiological knowledge acquired in the last decade into effective treatments for these @entity1 .

Current aspects of pathophysiology and cell dysfunction after severe XXXX .

@entity1 :: ('9606', 'Species') :: ['patients'] @entity12807 :: ('MESH:D002534', 'Disease') :: ['brain hypoxia'] @entity131 :: ('MESH:D001930', 'Disease') :: ['Traumatic brain injury'] @entity2227 :: ('CHEBI:29987', 'Chemical') :: ['glutamate'] @entity63 :: ('MESH:D007511', 'Disease') :: ['ischemia'] @entity75 :: ('MESH:D001927', 'Disease') :: ['brain lesions'] @entity542 :: ('MESH:D006259', 'Disease') :: ['head injuries'] @entity6075 :: ('MESH:D016489', 'Disease') :: ['closed head injury'] @entity21 :: ('MESH:D001480', 'Disease') :: ['diffuse axonal injury'] @entity2332 :: ('MESH:D007035', 'Disease') :: ['hypothermia']
@entity542 :: (MESH:D006259,Disease) :: ['head injury']
