Chronic Traumatic Encephalopathy Flashcards
What is Chronic Traumatic Encephalopathy (CTE)?
CTE is a progressive neurodegenerative disease that develops in individuals with a history of concussive head impacts.
Who first described a condition now known as CTE and what was it called?
Dr. H. Maitland in 1928 coined the term “dementia pugilistica” or “punch drunk syndrome,” referring to what he saw in some boxers/fighters.
Who wrote about CTE in 2005 and which football player was discussed?
Dr. Bennet Omalu wrote about the case of pro football player Mike Webster.
When was the term “Chronic Traumatic Encephalopathy” officially used in a paper and by whom?
In 2009 by Dr. Ann McKee.
Who is the current acknowledged leader in the CTE research field and what institution is associated with her team?
Dr. Ann McKee leads the team at Boston University. They operate the VA-BU-CLF Brain Bank (Veterans Affairs—Boston University—Concussion Legacy Foundation).
What types of individuals are most likely to develop CTE?
Professional athletes (especially football players, boxers, hockey players, rugby and soccer players, wrestlers), military personnel, victims of domestic abuse or prolonged bullying, some epileptics, and psychiatric patients who “head bang.”
Is it possible to develop CTE from a single concussion?
No, there is no known case of someone developing CTE from only one concussion.
What is a sub-concussion and why is it important in understanding
A sub-concussion is a lower-grade, possibly asymptomatic head or whiplash event that happens repeatedly and plays a significant role in CTE development.
What percentage chance of developing CTE is predicted for football players with 10–20 year careers?
Studies predict an 80–100% chance.
When do the first signs and symptoms of CTE typically appear?
3–5 years or more after the last impact injury.
What is the primary lesion found in the brains of those with CTE?
Tau protein tangles, similar to Alzheimer’s Disease.
How do tau protein tangles differ in CTE compared to Alzheimer’s Disease (AD)?
In AD, they appear mostly in white matter; in CTE, they are prominent in the cortex, midbrain, and around blood vessels, initially appearing as small brown spots.
What role do lesions around blood vessels play in CTE?
They reduce perfusion and drainage, making it harder for the brain to repair itself and manage dysfunction.
What is the progression pattern of tauopathy in CTE?
Damage may seem minor at first but becomes devastating as tau protein tangles spread through the brain.
What are common symptoms of Stage 1 CTE?
May be asymptomatic; or symptoms may include headaches, recent memory changes, mood disorders (anxiety/depression), impulsivity, and aggressive behaviors—often hidden well.
What are the characteristics of Stage 2 CTE?
Headaches, confusion, memory loss, poor judgment, social instability, mood swings, major depression, impulsivity, personality change, possible rage, paranoia, aggression, and executive dysfunction.
What symptoms define Stage 3 CTE?
Obvious cognitive deficits, severe memory impairments, aphasias, executive dysfunction, psychosis/hallucinations, visuospatial issues, and motor symptoms like dysphagia, ptosis, tremor, bradykinesia, festination, dystaxia, vertigo, and possible hearing loss.
What happens in Stage 4 CTE?
Full-blown dementia, severely impaired communication, psychosis, paranoia, parkinsonism-type motor dysfunction, and a need for constant care.
Does everyone with CTE progress through the stages the same way?
No, there is considerable variation in symptom onset, pattern, and severity.
What mental health and behavioral risks are associated with CTE?
High incidence of suicidal ideation, suicide attempts, successful suicides, and risk of violent aggression and murder/suicide.
Can CTE be diagnosed while a person is alive?
No, confirmation is only possible at autopsy, though diagnosis can be suspected through history and symptoms.
Is there a cure or specific treatment for CTE?
No, there is currently no cure. Treatment is symptom-based using medications and supportive care.
