Fig. 1
From: The effect of concomitant peripheral injury on traumatic brain injury pathobiology and outcome
Possible pathways through which extracranial injury may alter TBI pathobiology. Secondary injury processes of TBI include neuroinflammation, excitotoxicity, metabolic disturbances, apoptosis, ischemia, oxidative stress, and BBB disruption. The neuroinflammatory response of TBI is characterized by microglial and astrocyte activation, leukocyte infiltration and elevated levels of pro-inflammatory cytokines. For multitrauma/polytrauma patients, there is potential for the systemic effects of significant extracranial injuries to impact upon secondary injury pathways of TBI, and in particular the neuroinflammatory response. Possible extracranial trauma-induced influences on TBI include elevated circulating inflammatory cytokines, growth factors, reactive oxygen species, and for the patient with bone fracture, potential influence of fat emboli and mobilized mesenchymal stem cells. Polytrauma may produce the added risk of central influences of sepsis, SIRS and hemorrhagic shock