Chronic Traumatic Encephalopathy

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It was homecoming, 1988. I stood stunned on the sidelines with the other cheerleaders, praying that he would wake up. It had been 20 minutes and he still wasn’t moving. The crowd was silent as the ambulance pulled away. He would be pronounced dead upon arrival at the hospital. Keith, our star linebacker, was 17 years-old, and our hearts were broken. His family was religiously opposed to an autopsy, but we were told he had likely died from a congenital cerebral aneurysm. 25 years later, almost to the day, I sat watching an ESPN discussion about an Arizona high school football player who had died after a game sustained concussion, likely from second impact syndrome. Suddenly I was back on that sideline. “Keith,” I said aloud to nobody in the room. Thus began my thirst for knowledge about traumatic brain injury and the possible resulting pathologies such as chronic traumatic encephalopathy.
Pathophysiology
Nearly 86 years ago, Dr. Harrison Martland penned the first clinical delineations of what he termed “punch drunk”; a pattern of neurologic sequelae found in boxers (Martland, 1928). The condition would later become know as pugilistic dementia and then chronic progressive traumatic encephalopathy of boxers (Critchley, 1957; Millspaugh, 1937). Today this condition is called chronic traumatic encephalopathy or CTE and includes a wide array of clinical manifestations, ranging from mild cognitive, motor and behavioral dysfunction, to complete dementia with Parkinson's-like tremors (McKee et al., 2013). Those battling CTE often struggle with aggression towards others and are at high risk for suicidal behavior.
CTE occurs in patients with a history of blunt force, closed-head trauma. Although highly associated with groups prone to rep...

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