The effect of head injury upon the immune system

Severe head injuries are characterized by high mortality and morbidity. In spite of guidelines based therapy the treatment is frequently unsuccessful. Extracranial infectious complications are considered to be an important problem during the course of recovery, and possibly immunological changes could explain their occurrence. Head injuries cause an imbalance within the helper cell community, resulting in a T(H)2 dominance. This development is influenced by the soluable agents of the sympathic nervous system and the hypothalamic-pituitary-adrenal axis. The crucial research of damaged cellular immunity concluded Quattrocchi in 1991. Both the activation of microglial cells and the accumulation of T-cells after crossing the BBB indicate production of pro-inflammatory mediators in the CNS after injury. The leaking of pro-inflammatory mediators to the circulation develops to a systemic inflammatory response syndrome (SIRS). On the contrary, an overwhelming of anti-inflammatory substances leads to an anti-inflammatory response syndrome (CARS). It is suggested that an imbalance between these two immune responses is responsible for organ dysfunction and increased susceptibility to infections in polytrauma victims. Concerning mediators, IL-6 draws attention because of its high marker ability. Finally, post-traumatic infections have also been correlated with an altered function of antigenpresenting cells (APC). Concerning the quantity, the humoral part of immune system seems to be stimulated, but its function and phagocyte activity shows several defects. Finally, T(H)2 dominance induces IgE levels accumulation. All these changes are strongly under effect of stress based release of endogenous glucocorticoids and catecholamine, which influence the complex network of cytokines and cell mediators (Fig. 3, Ref 18).