January 3, 2013 8:00 — 1 Comment
Researchers Use Imaging Study to Chronicle Second Impact Syndrome in High School Football Player
In the January 2013 issue of the Journal of Neurosurgery: Pediatrics, physicians at the Indiana University School of Medicine and the Northwest Radiology Network (Indianapolis) report on the case of a 17-year-old high school football player with second impact syndrome (SIS). A rare and devastating traumatic brain injury (TBI), SIS occurs when a person — most often a teenager —sustains a second head injury before recovery from an earlier head injury is complete. To the best of the authors’ knowledge, this is the first reported case in which imaging studies were performed after both injuries, adding new insight and knowledge about the event. Findings in this case are reported and discussed in “Second impact syndrome in football: new imaging and insights into a rare and devastating condition. Case report,” by Elizabeth Weinstein, MD, and colleagues. For more information, click here to read the full release.
This is an interesting case — a little more complicated than a recurrent concussion since there was a space-occupying lesion involved. Yet, compelling evidence suggests that the central mechanism in all of these cases, even with space-occupying lesions, is initial microglial priming with the first injury and full microglial activation with the second. With full microglial activation, neurotoxic levels of proinflammatory cytokines and glutamate are released together from the microglia. Studies have shown that microglial activation can persist over a decade following concussive injuries (Ramlackhansingh AF et al. Ann Neurol 2011:70:374-383). This has been also demonstrated in a number of experimental TBI studies. I proposed a mechanism for this phenomenon as well as CTE in an article appearing in Surgical Neurology International (Blaylock RL, Maroon J SNI 2011;2:107). Basically, the mechanism involves traumatic microglial activation with an interaction between the proinflammatory cytokines and AMPA glutamate receptors, which enhances excitotoxic sensitivity tremendously by a number of mechanisms. Special involvement is seen between TNFR1 and trafficking of AMPA receptors, which can produce prolonged sensitivity to neurotoxic factors, especially glutamate. A number of studies have shown significantly elevated glutamate levels in TBIs, and that prognosis is directly linked to the degree of elevation and length of elevation.
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