10 – Modulation of Immune Response by Head Injury

Publisher Summary This chapter highlights the controversies concerning the role of brain inflammation elicited after brain trauma. In clinical practice, classification of primary brain injury is determined by neuroimaging scans that reveal specific types of damage, including skull fractures, tissue lacerations, subdural or epidural hemorrhages, and contusions, which constitute the hallmarks of focal Traumatic brain injury (TBI). The pathological alterations resulting from brain injury trigger multiple biochemical cascades that lead to the release of neurotoxic substances that ultimately exacerbate neuronal cell death. Much research effort has been dedicated to establishing the roles of excitotoxicity, the oxidative pathway, and cerebral inflammation after brain injury. Cellular and molecular responses to TBI, including inflammation, may vary according to genetic patterns, use of animal strains, and the methods used to produce brain injuries. It is clear that cryolesion can hardly be compared to fluid percussion injury or diffuse axonal damage. Also, individual laboratories use distinctly different behavioral tests to assess outcomes, making the comparison of studies almost impossible. Despite this experimental variability, the common consensus today remains: Inflammation possesses both beneficial and detrimental properties, as complete ablation of cytokines and cytokine receptors generates exacerbated tissue and neurological damage after TBI.