Traumatic brain injury
Since a major cause of TBI are vehicle accidents, their prevention or the amelioration of their consequences can both reduce the incidence and gravity of TBI. In accidents, damage can be reduced by use of seat belts, child safety seats and motorcycle helmets, and presence of roll bars and airbags. Education programs exist to lower the number of crashes. In addition, changes to public policy and safety laws can be made; these include speed limits, seat belt and helmet laws, and road engineering practices.
Changes to common practices in sports have also been discussed. An increase in use of helmets could reduce the incidence of TBI. Due to the possibility that repeatedly "heading" a ball practicing soccer could cause cumulative brain injury, the idea of introducing protective headgear for players has been proposed. Improved equipment design can enhance safety; softer baseballs reduce head injury risk. Rules against dangerous types of contact, such as "spear tackling" in American football, when one player tackles another head first, may also reduce head injury rates.
Falls can be avoided by installing grab bars in bathrooms and handrails on stairways; removing tripping hazards such as throw rugs; or installing window guards and safety gates at the top and bottom of stairs around young children. Playgrounds with shock-absorbing surfaces such as mulch or sand also prevent head injuries. Child abuse prevention is another tactic; programs exist to prevent shaken baby syndrome by educating about the dangers of shaking children. Gun safety, including keeping guns unloaded and locked, is another preventative measure. Studies on the effect of laws that aim to control access to guns in the United States have been insufficient to determine their effectiveness preventing number of deaths or injuries.
Recent clinical and laboratory research by neurosurgeon Julian Bailes, M.D., and his colleagues from West Virginia University, has resulted in papers showing that dietary supplementation with omega-3 DHA offers protection against the biochemical brain damage that occurs after a traumatic injury. Rats given DHA prior to induced brain injuries suffered smaller increases in two key markers for brain damage (APP and caspase-3), as compared with rats given no DHA. “The potential for DHA to provide prophylactic benefit to the brain against traumatic injury appears promising and requires further investigation. The essential concept of daily dietary supplementation with DHA, so that those at significant risk may be preloaded to provide protection against the acute effects of TBI, has tremendous public health implications.”
Axotomy
A traumatic brain injury is defined as a blunt non-missile penetrating or missile injury to the head. It has been shown that the extent of the damage incurred after a head trauma correlates more directly with the amount of deformation incurred by the brain than the amount of stress per area applied to the head. There are two modes of axotomy that can occur as a result of a TBI. Primary axotomy occurs immediately and is characterized as complete mechanical transaction of axons. More often, secondary axotomy occurs, evolving over time and ultimately leading to disconnection. While this type of injury is often irreversible, the axons do occasionally recover. Researchers are currently working towards utilizing this potential for recovery to develop therapies for patients suffering from traumatic brain injuries. These therapies rely on the scientific understanding of the axotomy response. Two mechanisms that aid in the reinnervation process are acute inflammation and the activation of molecules in the extracellular matrix surrounding the synapse. Immediate acute inflammation leads to the removal of the severed axons by activating the local glia. The inflammation response also recruits growth factors that aid in the repopulation of postsynaptic sites. The negative effects of this inflammation may be difficult to detect immediately post injury. Inflammation of the head is often slow to onset after injury, and can lead to a fatal rise in cerebral pressure. A recently discovered and understood cytokine is currently being used to try to treat the axotomy before the rise in pressure occurs. This cytokine, called osteopontin, may be able to aid in axon regeneration by exposing its integrin receptor binding sites. Osteopontin secretion may be able to regulate synaptogenesis and target the necessary neuroglia required for the repair of the axons. A study done by Julie L. Chan proves the functionality of osteopontin in initiating the immune response necessary for synaptic repair and reorganization after injury (axotomy). Though the study effectively proved the functionality of osteopontin in diminishing the intense inflammatory response following a traumatic brain injury, it did not provide evidence of the long-term effects of implanting this as a treatment option. Altering the inflammatory response may unintentional halt the beneficial aspects of inflammation and have devastating effects on the brain’s ability to heal itself.