January 2, 2013 13:00 — 1 Comment
Second Concussion Can Be Devastating, Even After Normal CT Scan
Student-athlete Cody Lehe still was having headaches from a concussion sustained several days earlier at a high school football game. But when his CT scan came back normal, the 17-year-old thought it was OK to play. Five days after the helmet-to-helmet collision that the Brookston, Ind., teen described as “the hardest I’ve been hit in my whole life,” he was back on the field practicing with his teammates. The Frontier High School Falcons were heading to the 2006 sectional finals and, as team captain, Lehe intended to be there.
But in the fourth drill of the day, Lehe was hit and knocked to the ground. As he slowly pulled himself back onto his feet, he told a teammate that his head hurt, but he was OK. However, several plays later, Lehe dropped to one knee, dizzy, his legs numb. Then he collapsed, his body shaking with seizures. He was rushed to the emergency room, where doctors found that the pressure in his brain was dangerously high. They reduced the pressure, but the damage was already done. 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 suggest 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 or subsequent injuries. With full microglial activation neurotoxic levels of proinflammatory cytokines and glutamate are released simultaneously. 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 the prognosis is directly linked to the degree of elevation and length of elevation.
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