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Head injuries have become an increasingly contentious topic in American sports. Contact sports, especially American football, are more popular than ever, but the games may be fundamentally changing because of public concern over chronic traumatic encephalopathy.
What Is Chronic Encephalopathy?
Encephalopathy is gradual degeneration of brain tissue. Chronic traumatic encephalopathy, also known as CTE, is a process of ongoing destruction of brain cells that continues months, years, or even decades after a traumatic head injury. Before the twenty-first century, CTE was more common among boxers than in any other sport, and the condition was known as dementia pugilistica. Since about 2005, neurologists and brain researchers have been noting more cases among football players, so the condition is now described with a broader term.
CTE has come to public attention through a series of tragedies. In December of 2012, NFL linebacker Tiaina Baul "Junior" Seau Jr. committed suicide at the age of 43. He didn't leave a suicide note, but he scribbled a reference to the country song "Who I Ain't," in which a man expresses regret for the person he has become. Two years earlier, another NFL play, David Duerson, had committed suicide by shooting himself in the chest, leaving a note requesting that his brain should be donated to science for study of head injury. Examination of Duerson's brain did not reveal any signs of large-scale brain injury, but the fact that he had suffered insomnia for seven years and he had exhibited changes in personality suggested he had some kind of undetected brain injury.
Brain Injury Symptoms May Be Subtle
Further studies, many of them involving veterans of the Iraq wars who had suffered concussion or brain injury, revealed the consequenes of traumatic brain injury don't occur all at once. Sometimes head trauma causes ischemic injury to the brain. The trauma injures the brain in ways that cause a clearly identifiable loss of circulation to some part or parts of the brain. Sometimes, however, head trauma causes hypoxic injury to the brain. In a hypoxic injury, the visible blood vessels conduct blood normally, but oxygen still doesn't reach some parts of the brain.
Chronic inflammation of brain cells around tiny capillaries may impede the flow of blood in the brain. This inflammation may or may not occur where there is visible injury to brain tissue. It is possible to suffer a blow to one part of the brain that causes inflammation and hypoxia in a different part of the brain. When the medical profession realized that this problem is common, research went into high gear for developing a test for hypoxia.
Fast and Slow Measurements of Brain Injury
Scientists at the United States Uniformed Services University have been looking at differences in two biomarkers that are generated by brain injury, glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase L1 (UCH-L1). GFAP is an indicator that brain cells have begun to break down. It peaks about 20 hours after an injury, but it may still be detectable after seven days. UCH-L1 is an indicator that neurons have been injured. It peaks about 8 hours after injury and is only detectable during the first 48 hours.