• Nicola Biasca and William L Maxwell.
• Clinic of Orthopaedic, Sports Medicine and Traumatology, Department of Surgery, Spital Oberengadin, CH-7503 Samedan/St. Moritz, Switzerland. Biasca@medicmotion.com
• Prog. Brain Res. 2007 Jan 1; 161: 263-91.

AbstractMinor traumatic brain injury (mTBI) is caused by inertial effects, which induce sudden rotation and acceleration forces to and within the brain. At less severe levels of injury, for example in mTBI, there is probably only transient disturbance of ionic homeostasis with short-term, temporary disturbance of brain function. With increased levels of severity, however, studies in animal models of TBI and in humans have demonstrated focal intra-axonal alterations within the subaxolemmal, neurofilament and microtubular cytoskeletal network together with impairment of axoplasmic transport. These changes have, until very recently, been thought to lead to progressive axonal swelling, axonal detachment or even cell death over a period of hours or days, the so-called process of "secondary axotomy". However, recent evidence has suggested that there may be two discrete pathologies that may develop in injured nerve fibers. In the TBI scenario, disturbances of ionic homeostasis, acute metabolic changes and alterations in cerebral blood flow compromise the ability of neurons to function and render cells of the brain increasingly vulnerable to the development of pathology. In ice hockey, current return-to-play guidelines do not take into account these new findings appropriately, for example allow returning to play in the same game. It has recently been hypothesized that the processes summarized above may predispose brain cells to assume a vulnerable state for an unknown period after mild injury (mTBI). Therefore, we recommend that any confused player with or without amnesia should be taken off the ice and not be permitted to play again for at least 72h.

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