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Lecture 17

KIN354 Lecture Notes - Lecture 17: Gene Tunney, Myelin, Incubation Period


Department
Kinesiology
Course Code
KIN354
Professor
Peter Hall
Lecture
17

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Lecture 17: CTE
Chronic traumatic encephaolopathy long term progressive disease that results from injury and diffused
effects on the brain
- Has to do with accumulative effect over many, many incidences of concussions
- Latency period usually decade period long made it harder to track and detect as problem
- People forget about the link of whatever comes 15 years later, to what came before. Not linked
back to the occurrence in sport.
- Acute syndrome is immediate, clear of what the cause was
Boxing - Rotational force in twisting of head and linear force are thought to result in damage of neurons
that comprise the brains. Damage to axons/nerve cells and disrupt myelin sheath which reduces impulse
and cause cutting of axons (axonal injury).
Sluggers are type of fighters only going for the knock out.
Gene tunney heavyweight champion in 1926
- Physique differences. Not as bulky back then. Anxious of possible long term damage from
repeatedly exposing himself to head trauma. Was criticized a lot for having a wimpy way out.
Very intellectual and thought to be very right individual. One of the first heavyweight boxer to
study films of his own fights and other peoples fights in order to learn from them and improve
by looking at what went right/wrong.
To document CTE, what evidence do we need?
Steroid use and substance use are the main explanations to alternations of CTE.
You need sample of brain damage and see if there are characteristics in abnormalities in older people
that have dementia. The case studies referred to in documentary were looking at post-mortem brain
tissue in those who died and examine for the presenance of abnormalities. The older the athlete, the
less clear it is to find out if abnormalities are truly caused by sport injury
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