Traumatic brain injury insults

Matsushita Y., BramlettH. M., Alonso O., and Dietrich W. D. (2001) Posttraumatic hypothermia is neuroprotective in amodel of traumatic brain injury complicated by a secondary hypoxic insult. Crit. Care Med. 29, 2060-2066. 

Cysteine proteases, called calpains, are known to be activated by sustained elevations in intracellular free calcium. Once activated, calpains degrade the cytoskeleton, transmitter and membrane channels, and metabolic enzymes (Hou and MacManus 2002 Mattson 2003 Nicholls 2004). Functionally, calpains have been characterized as pivotal mediators of both active necrotic cell death and PCD (Wang 2000) following cell-damaging stressors and insults such as soman exposure, excitotoxic challenges, toxins, free radicals, UV radiation, acute hypoxia, traumatic brain injury, cytokines, heat, and in chronic neurodegenerative conditions (Fischer et al. 1991 Caner et al. 

In addition to aberrant internal metabolism, external insult such as traumatic brain injury can increase the risk of AD [63-65]. The mechanisms by which head traiuna may augment the risk of AD is unknown. Repetitive head traiuna experienced by professional boxers may lead to punch drunk syndrome or dementia pugifistica later in fife [66]. This syndrome is characterized by progressive dementia and parkinsonism and the presence of senile plaques and neurofibrillary tangles [67,68]. Ap deposition has been detected in the brains of victims of even a single head injury [69]. In preclinical models head trauma can exacerbate the formation of plaques or tangles, induce neu-... 

McHugh, G.S., Engel, D.C., Butcher, I., et al., 2007. Prognostic value of secondary insults in traumatic brain injury results from the IMPACT study. J. Neurotrauma 24, 287—293. 

Like spinal cord trauma, traumatic head injury consists of a primary injury, attributable to the mechanical insult itself, and a secondary injury, attributable to the series of systemic and local neurochemical changes that occur in brain after the initial traumatic insult (Klussmann and Martin-Villalba, 2005). The primary injury causes a rapid deformation of brain tissues, leading to rupture of neural cell membranes, release of intracellular contents, and disruption of blood flow and breakdown of the blood-brain barrier. In contrast, secondary injury to the brain tissue includes many neurochemical alterations such as release of cytokines, glial cell reactions involving both activated microglia and astroglia, and demyelination... 

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