PET 3097: Health and Wellness
Mr. William Kuminka
December 9, 2013
Chronic Traumatic Encephalopathy
Chronic Traumatic Encephalopathy (CTE) has been a hot topic in the sports world as of the past couple of years with recent findings of the disease in many retired NFL players. Recently a lawsuit has been brought up by the NFLPA against the NFL to cover loss and damages to the former players who have had traumatic brain injuries due to football related incidents during their tenure in the National Football League. What exactly is CTE and what are its effects? What are we doing to stop it?
What is “CTE”? According to McKee (n.d.), “Chronic traumatic encephalopathy is a progressive tauopathy that occurs as a consequence of repetitive mild traumatic brain injury” (13643-16). It is a form of encephalopathy that is a progressive degenerative disease, which can only be definitively diagnosed postmortem, in individuals with a history of multiple concussions and other forms of head injury. The disease was previously called dementia pugilistica (DP), as it was initially found in those with a history of boxing.
CTE is believed to be the cause of repeated injuries to the head/brain, particularly related to sports injuries. According to Yi (2013), “sports-related concussions have gained increased prominence, in part due to media coverage of several well-known athletes who have died from consequences of chronic traumatic encephalopathy (CTE). CTE may result from multiple concussions or sub-concussive blows resulting in a neurodegenerative process that appears in some ways to clinically and histo-pathologically resemble features seen in tau-related dementias and amyotrophic lateral sclerosis (ALS) along with features of parkinsonism and is associated almost invariably with depression” (28-32). According to be a soon to be published survey on the topic of CTE, suggesting “the clinical presentation of CTE is a distinct entity from concussions and post-concussive syndrome (PCS). CTE is not a result of the accumulation of prior injuries but rather progressive neuronal dysfunction and death. Thus, it may arise in patients who had no prior symptomatology. This would explain the manifestation of symptoms years after removal from exposure to repetitive traumatic injury. It also may arise in individuals who had complete resolution of PCS symptoms. Lastly, some cases involve overlap, more specifically subsiding PCS symptoms with progressively worsening CTE symptoms.
The clinical manifestations of CTE have been described numerous times in medical literature since the early 20th century. In 1928, Martland coined the term “punch drunk” to describe the signs and symptoms observed in boxers, especially those who experienced considerable head trauma from repeated blows to the head. Millspaugh used the term “dementia pugilistica” in 1937 for the syndrome consisting of motor deficits and mental confusion also seen in boxers. By the 1960s, “chronic traumatic encephalopathy” had come to encompass both these terms in describing the neurologic deterioration that ensued after repetitive traumatic brain injury.
The classic symptoms of impaired cognition, mood, behavior, and motor skills also have been reported in professional football players, and in 2005, the histo-pathological findings of CTE
were first reported in a former National Football League (NFL) player. These findings were similar to Alzheimer’s disease in some ways but differed in critical areas such as a predominance of tau protein deposition over amyloid. According to Yi (2013), “The pathophysiology is still unknown but involves a history of repeated concussive and sub-concussive blows and then a lag period before CTE symptoms become evident” (28-32).
There was an autopsy performed on a 44 year old ex NFL player who committed suicide by shooting himself in