One large randomized controlled trial (12,737 patients) showed a reduction in mortality in patients with mild-to-moderate head injury (baseline GCS 9-15) who were treated with tranexamic acid (an antifibrinolytic agent) within three hours of injury, compared with those who were not. Although neuropsychological tests are an important component of concussion assessment, they should not be the only benchmark in making decisions about recovery from a concussion. The clinician should ensure that an appropriate amount of time has passed between testing sessions to guard against practice effects and uphold test validity. It is also of value with regard to postconcussion syndrome and is useful as an objective measure of subjective complaints following cognitive recovery/decline (e.g., in order to determine if a concussed patient is being truthful about symptom resolution or embellishing on perceived cognitive dysfunction). Neuropsychological testing may also be helpful in making return-to-play decisions for athletes, and return to school or work for nonathletes. Neuropsychological testing can be used to diagnose the effects of concussion as well as to monitor recovery. Neuropsychological tests have been shown to be of clinical value and continue to contribute significant information in concussion evaluation and management. Cognitive performance can be affected by stress, fatigue, effort, and medications and therefore, neuropsychological evaluations should be carried out by trained neuropsychologists who can disentangle the effects of these factors from the consequences of concussion. Neuropsychological testing involves paper-and-pencil or computerized tests assessing attention, memory, and executive functions, as well as reaction times. The disparity in energy balance and the tendency to restore ionic balance is met with decrease in blood flow, creating a cellular energy crisis that is suspected to be the mechanism for postconcussive vulnerability, leaving the brain more vulnerable to a second injury and potentially longer-lasting, more severe deficits. This hypermetabolic state co-occurs with diminished cerebral blood flow. Acutely, the sodium-potassium pump works overtime to restore a homeostatic balance, requiring increasing amounts of adenosine triphosphate and a corresponding increase in glucose metabolism. These ionic shifts lead to acute and subacute changes in cellular metabolism and physiology. Excitatory neurotransmitters, such as glutamate, bind to N-methyl-D-aspartate receptors leading to further neuronal depolarization with the influx of calcium and the efflux of potassium. The biochemical cascade of concussion is marked by an initial period of indiscriminate neurotransmitter release and unchecked ionic fluxes.
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