Sports-related traumatic brain injury
Rules exist within each sport to help prevent cerebral contusions and traumatic brain injuries. However, individual athletes are the best prevention against their own injuries. In a game, athletes notice when they have the symptoms of a cerebral contusion and should take themselves out of the game. It may be hard for medical personnel or coaches to notice when a player has a traumatic brain injury, so it is in the player’s best interest to be removed from play. In hockey, traumatic brain injuries constitute 10%-15% of all head injuries. With the high percent of injuries being traumatic, extensive design improvements have been made to helmets. These improvements reduce the risk of cerebral contusions by providing more padding around the skull and a chin strap that keeps the helmet snug. In baseball, major improvements to helmets have been made to protect batters from the impact a baseball can have when hitting their head. Helmets, before this major improvement, were designed to withstand a velocity of 70 mph from a pitch or foul ball. Since the company Rawlings’ new design, helmets can withstand a velocity of 100 mph and have further padding around the softer parts on the side of the skull.
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.