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CTE Dr. Pete Biglin, DO May 14, 2106. DR. PETE BIGLIN, DO Board Certified: 1. Physical Medicine & Rehabilitation 2. Pain Management 3. Sports Medicine.

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Presentation on theme: "CTE Dr. Pete Biglin, DO May 14, 2106. DR. PETE BIGLIN, DO Board Certified: 1. Physical Medicine & Rehabilitation 2. Pain Management 3. Sports Medicine."— Presentation transcript:

1 CTE Dr. Pete Biglin, DO May 14, 2106

2 DR. PETE BIGLIN, DO Board Certified: 1. Physical Medicine & Rehabilitation 2. Pain Management 3. Sports Medicine 4. Electrodiagnosis-EMG Training: 1. Wayne State University- PM&R 2. Michigan State University Fellowship- Sports Medicine

3 Question: Will you let your son play football?

4 CONCUSSION SUMMARY ARTICLE Consensus statement on concussion in sport: the 4 th International Conference in Sport held in Zurich, November 2012 – (CSC 2012) Breaking News!......... Consensus statement on concussion: 5 th international conference to be held in Berlin, Germany October 2016

5 CONCUSSION review facts: When in doubt, sit them out* Removal from activity once suspected concussion is sustained is THE STANDARD OF CARE! TREATMENT = Cognitive Rest* Possibly stay home from school 1-2 days Limit homework NO TV, computer usage, video games, texting TREATMENT = Physical Rest* No return to activity until no symptoms at rest and with cognitive exertion

6 Risk factors for prolonged concussion recovery Previous history of concussion Once an individual has sustained a concussion, he/she is FOUR TIMES as likely to sustain another injury. It will take less of a blow each time and symptoms will take longer to resolve Diagnosis of ADD/ADHD History of headaches or migraines treated by a physician

7 Other possible factors for prolonged concussion recovery Females LOC > 1 min Amnesia Seizure disorder Anxiety or Depression  *Note: LOC < 1 minute & duration of post traumatic amnesia do NOT reliably predict outcomes

8 CTE : Chronic Traumatic Encephalopathy

9 What is CTE?  “Chronic traumatic encephalopathy”  Progressive degenerative disease of the brain  History of repetitive brain trauma- concussions and sub-concussive trauma to the head that may not cause symptoms  Buildup of tau protein  Occurs in athletes as well as military veterans

10 How do you get CTE?  Repetitive brain trauma (concussive and sub-concussive)  Number of hits unknown  Other factors-genetics….. Not everyone with a history of repeated brain trauma develops the disease!

11 CTE  CT E is a neuropathologically distinct, slowly progressive Taupathy (Tau protein) with a clear environmental cause.  Estimated incidence - 17% of patients with repetitive concussion can develop CTE

12 CTE  First called “punch drunk” 1920s in boxers. Original medical term “Dementia Pugilistica”  49 cases described in all medical literature between 1928 and 2009. 39 cases were boxers. One case was Australian circus performer- “dwarf-throwing”  Who is affected? –boxing, football, ice hockey, soccer, wrestling and military veterans. Victims of domestic violence and “head-bangers”

13 How is CTE diagnosed?  Postmortem autopsy ONLY- neuropathological analysis- Tau protein in the form of neurofibrillary tangles- which eventually lead to brain cell death.  Right now there is no diagnostic methods for patients that are living

14 Stages of CTE I. Headaches, diminished attention & concentration, possible dizziness II. Depression, social instability, erratic behavior short-term memory impairment III. Cognitive impairment, problems with executive functions specifically planning, organization and multitasking IV. Full blown dementia, bradykinesia, tremor, vertigo, deafness and suicidality

15 CTE DIAGNOSIS-AUTOPSY

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17 CTE Gross Brain Pathology  Decreased brain weight  Atrophy of frontal and temporal cortex  Enlarged third ventricle, and lateral ventricle  Pallor of the Substantia Nigra  Atrophy of all factory, thalamus brainstem and cerebellum

18 CTE microscopic brain pathology  Neuron cell loss (cell death)  TAU protein deposition forming as dense neuro-fibrillatory tangles (NFT)  Beta amyloid deposition uncommon

19 Dr Ann McKee, MD- Boston University

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23 CTE diagnosis in living athletes ******Not available at this time*******  Possibilities and future studies: PET tracers designed to find Tau protein (not specific enough at this time) Functional MRI DTI (DWI) imaging (Diffusion Tensor Imaging) Serum blood testing for auto immune antibodies versus brain tissue

24 Differences CTE and Alzheimer’s  CTE present earlier 40s  Initial symptoms- Alzheimer’s disease and memory problems while CTE involves problems and reasoning, problem solving, impulse control and aggression which is not seen in Alzheimer’s  Different postmortem neuropathological findings

25 CTE Case 1- 45-year-old male  Accidental gunshot wound while cleaning a gun.  Retired NFL player  Possible 12 concussions during college and professional career. Only one medically confirmed  Never diagnosed with post concussive syndrome

26 CTE Case 1- 45-year-old male  Family history negative for dementia or psychiatric illness  At age 40- symptoms noticed by family included short-term memory loss, impaired organization and planning and problem-solving.  He would repeatedly asked the same questions over and over. He would asked to rent a movie that he had already seen.  Towards the end of his life he would become angry and verbally aggressive over insignificant issues  CTE found postmortem

27 CTE Case 2 – 30 year old

28  Died of pneumonia caused by inhaling his vomit while in the wilderness- 2013  CTE found on autopsy - Severity of CTE described as moderate.  Paranoia and anxiety symptoms reported by family up to a year before his death  “ CTE possibly affected his judgment, insight and behavior, but there are other factors including use of oxycodone that most likely contributed to his death”

29 Case 2 – 30 year old  Quote from a family friend: “ He didn’t run out of bounds. He put his head down and got the first down. He wasn’t the guide to through the ball away. He probably took some hits shouldn’t have”  Medical records and # confirmed concussions-not available

30 Case 3- “Possible” CTE  Initially first 8 seasons with the 49ers “mild mannered and hard- working, soft-spoken”  5 arrests in the last year (2015) including 2 in the past month- domestic violence.  Recently released by the Chicago Bears  What could cause the seemingly abrupt change in his behavior?

31 CTE Prevention possibilities  Reduced the number of concussions or mild TBI  Changes in rules to prevent “violence” versus “aggressive play” (e.g. penalizing intentional hits to the head)  Appropriate concussion treatment  Strict return to play guidelines

32 CTE Prevention possibilities Opinion: “In athletes, by instituting and following proper guidelines for return to play after a concussion, it is possible that the frequency of sports related CTE could be dramatically reduced or perhaps, entirely prevented.”

33 CTE History  2012 Junior Seau (CTE confirmed at autopsy after suicide)

34 CTE Fears  Concussion does not equal CTE  Post concussive syndrome does not equal CTE  Football it self does not cause CTE  Suicide is a multi-factorial entity, & does not equal CTE (possible higher frequency in pro football than other sports)

35 CTE History  2010- CTE confirmed in a 17-year-old football player (youngest ever diagnosed)  2011- July: NFL changed Return to Play guidelines and also reduced the number of contact practices allowed  2015 Boston University identified CTE 96% of NFL players examined at autopsy

36 CTE debate  Hypothesis that repeated concussions cause CTE cannot be definitively proven (to date, there is also no evidence to falsify this hypothesis)  However, growing body of evidence and the NFL (by admission) support hypothesis that repeated concussions cause CTE

37 SUMMARY- CTE  There is no available evidence that isolated, & well managed concussions give rise to CTE. This is why our job as medical professionals covering athletic events is so important (preventing long- term disability).  Next GOAL: diagnose in someone alive & define treatment and prevention strategies

38 REFERENCES  Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy following Repetitive Head Injury (J Neuropathol Exp 2009 July; 68(7) 709- 735)  Boston University: Center for the Study of Traumatic Encephalopathy (CSTE)  Consensus statement on concussion in sport: the 4 th International Conference in Sport held in Zurich, November 2012 –(CSC 2012)


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