Pathophysiology of traumatic injury in the developing brain: an introduction and short update

Current understanding about the main peculiarities in pathophysiology of immature brain traumatic injury involves marked developmental discrepancy of biomechanical properties, aspects of altered features in water and electrolyte homeostasis as well as maturation dependent differences in structural and functional responses of major transmitter systems. Based on the fact that traumatic brain injury (TBI) is one of the major causes of morbidity and mortality in infants and children, the currently available epidemiological data are reviewed in order to gain insights about scope and dimension of health care engagement and derive the requirements for reinforced pathogenetic research. To this end, the main aspects of peculiarities in primary and secondary TBI mechanisms in the immature/developing brain are discussed, including structural and functional conditions resulting in a markedly diminished shear resistance of the immature brain tissue. As such, the immature brain tissue appears to be more susceptible to mechanical alterations, because similar mechanical load induces a more intense brain tissue displacement. Furthermore, available indications for increased incidence of brain swelling in the immature brain after TBI are reviewed, focusing on the interrelationship between the age-dependent differences in extracellular space and aquaporin-4 expression during brain maturation. The developmental differences of TBI induced cerebrovascular response as well as some relevant aspects of altered neurotransmission following TBI of the immature brain in regard to the glutamatergic and dopaminergic transmitter system are assessed. Thus, this mini-review highlights some progress but also an increased necessity for expanded pathogenetic research on a clinical scale in order to develop a solid foundation for adequate therapeutic strategies for the different life-threatening consequences of TBI in infancy and childhood, which mainly have failed up to now.