Traumatic brain injury pathophysiology

Cerebral ischemia is the key pathophysiologic event triggering secondary neuronal injury following severe traumatic brain injury (TBI). Intracellular accumulation of calcium is postulated to be a central pathophysiologic process in am-plifying and perpetuating secondary neuronal injury via inhibition of cellular respiration and enzyme activation. 

Ray SK, Hogan EL, Banik NL (2003) Calpain in the pathophysiology of spinal cord injury neuroprotection with calpain inhibitors. Brain Res Rev 42 169-185 Ray SK (2006) Currently evaluated calpain and caspase inhibitors for neuroprotection in experimental brain ischemia. Curr Med Chem 13 3425-3440 Rhodes JK, Sharkey J, Andrews PJ (2009) The temporal expression, cellular localization, and inhibition of the chemokines MlP-2 and MCP-1 after traumatic brain injury in the rat. J Neurotrauma 26 507-525... 

Hu, Z., Yu, D., Almeida-Suhett, C., et al., 2012. Expression of miRNAs and their cooperative regulation of the pathophysiology in traumatic brain injury. 

Werner, C., Engelhard, K., 2007. Pathophysiology of traumatic brain injury. Br. 

Related to the post-traumatic microvascular damage is the pathophysiological process of vasogenic brain edema that represents a disruption of blood-brain barrier integrity, resulting in sodium and protein accumulation and osmotic fluid expansion of the brain extracellular space. Clinically, this is reflected by an increase in intracranial pressure which, if unchecked, can cause secondary compressive injury to vital brain structures. 

---