Concussion Management

Transcription

1 Concussion Management Bill Meehan, MD Director, Micheli Center for Sports Injury Prevention Co-Director, Football Players Health Study at Harvard Division of Sports Medicine, Boston Children s Hospital

2 Financial Disclosures: ABC-Clio Publishing company Royalties for the sale of, Kids, Sports, and Concussion: A guide for coaches and parents and Concussions. Wolters-Kluwer Royalties for writing for UpToDate, Sport-Related Concussion and Chronic Exertional Compartment Syndrome. Springer International Publishing Royalties for the sale of the book, Head and Neck Injuries in Young Athletes. Possible or Possibly Perceived Conflicts of Interest: Grant funding from the National Football League Players Association Philanthropic support from the National Hockey League Alumni Association through the Corey C. Griffin Pro-Am Tournament.

3 Abstract: We investigated gray (GM) and white matter (WM) volumes, fractional anisotropy (FA), and mean diffusivity (MD) using magnetic resonancebased morphometry and diffusion tensor imaging in 10 professional American Football players compared with 10 swimmers. In football players compared with swimmers, decreased GM volumes were observed in the left premotor cortex, SMA, putamen, and superior frontal gyrus, and decreased WM volumes in both corticospinal tracts, both internal capsules, corpus callosum, and left anterior cingulum. Hum Brain Mapp 31: , 2010

4 Definition Working definition Characteristics Trauma Impulse Immediate Self-resolves Functional

5 Biomechanics Biomechanics Rotational acceleration Slaughterhouses free to move, accelerate Denny-Brown 1941 medicine, acceleration Holburn 1943 thought experiment, rotational Ommaya and Genarelli definitive

6 Normal Physiology

7 Normal Physiology

8 Normal Physiology

9 Normal Physiology

10 Pathophysiology Biomechanical injury Ion flux, K+, Na+ Excitatory neurotransmitters NMDA Ca++ influx, further EAA release Exacerbates efflux of K+ Depolarization spreading depression Glyolysis -pump restoration Decreased flow

11 Signs and Symptoms Loss of Consciousness Amnesia, retrograde or antegrade Disorientation Appearing dazed Acting confused Forgetting game rules or play assignments Inability to recall score or opponent Inappropriate emotionality Physical incoordination Imbalance Seizure Slow verbal responses Personality changes Headache Dizziness Nausea or vomiting Difficulty balancing Vision changes Photophobia Phonophobia Feeling out of it Difficulty concentrating Tinnitus Drowsiness Sadness Hallucinations

12 Specific Assessment Tools Assessment Symptoms - PCSS Balance - BESS Neurocognitive: computerized vs. neuropsychological

13 Post Concussion Symptom Scale None Mild Moderate Severe Headache Pressure in head Neck Pain Balance problems or dizzy Nausea or vomiting Vision problems Hearing problems / ringing Don t feel right Feeling dinged or dazed Confusion Feeling slowed down Feeling like "in a fog" Drowsiness Fatigue or low energy More emotional than usual Irritability Difficulty concentrating Difficulty remembering Sadness Nervous or Anxious Trouble falling asleep Sleeping more than usual Sensitivity to light Sensitivity to noise Other:

14 Balance Error Scoring System 1. Double Leg Stance Feet together, hands on hips, eyes closed for 20 seconds. 2. Single Leg Stance Non-dominant foot, 30 degrees hip flexion, 45 degrees knee flexion, hands on hips, eyes closed for 20 seconds. 3. Tandem Stance Non-dominant foot in back, hands on hips, eyes closed for 20 seconds.

15 BESS Errors 1. Hands off iliac crest 2. Opening eyes 3. Step, stumble or fall 4. Moving hip into >30 degrees abduction 5. Lifting forefoot or heel 6. Remaining out of position > 5 seconds Errors counted.

16 Neurocognitive Testing Percentile Verbal Memory Visual Memory Processing Speed Reaction Time Baseline Post Injury 1 Post Injury 2 Post Injury 3 6 Days Post 16 Days Post 23 Days Post

17 Management Management Physical rest (24-48 hours)* Cognitive rest (24-48 hours)* RTP stages Contact only after Sx-free at rest, with exertion Caught up in school, sx-free with full cognitive exertion Pre-injury data back to baseline

18 Step Level of activity 1. No activity, complete rest. Once asymptomatic, proceed to level Light aerobic exercise such as walking or stationary cycling, no resistance training. 3. Sport specific exercise - for example, skating in hockey, running in soccer; progressive addition of resistance training at steps 3 or Non-contact training drills. 5. Full contact training after medical clearance. 6. Game play.

19 Recent Concern Risk Cumulative Second Impact Syndrome Chronic Traumatic Encephalopathy

20 Chronic Traumatic Encephalopathy: What We See and Hear CTE is common in Football Time

21 Chronic Traumatic Encephalopathy: What We See and Hear CTE is common in Football Time CTE causes aggression

22 Chronic Traumatic Encephalopathy: What We See and Hear CTE is common in Football Time CTE causes aggression CTE causes suicide

23 What We Are Saying Risk of neurodegenerative disease unclear/unlikely Association between trauma and pathology unclear Suicide less common Association between pathology and symptoms unclear

24 Why It Maters? Goals End football Get some attention Athletes Truth Treatment Prevention

25 Chronic Traumatic Encephalopathy Controversial Defined pathologically Repeated concussions Possible role of sub-concussive blows Possible agent of later life symptoms

26 Chronic Traumatic Encephalopathy Harrison Martland 1928 Punch Drunk Syndrome Sluggers, 2 nd rate fighters, used for training Unsteady gait, mental confusion, slowed muscular response, foot drag, Parkinsonism Corsellis 1973 Cerebral atrophy, enlargement of ventricles, cavum with fenestrations, loss of pigment substantia nigra Roberts Β-Amyloid plaques

27 Chronic Traumatic Encephalopathy Bennet Omalu First cases of former NFL players Grossly normal, β-amyloid Ann McKee Cerebral atrophy Ventricular dilation Fenestrated septum pellucidum Tau-positive neurofibrillary tangles; β-amyloid inconsistent

28 Current Hypothesis 1. People exposed to head trauma during American football are more likely to have hyperphosphorylated tau within certain regions of the brain than those not exposed to head trauma during football. 2. People exposed to head trauma during American football who have this hyperphosphorylated tau within these regions are more likely to experience the symptoms attributed to CTE than those people exposed to head trauma during American football who do not have hyperphosphorylated tau within these regions.

29 Epidemiology Largely unknown Boston University Largest sample 111 former NFL players studied; 110 with CTE 110/111 = 99% of those studied; 110/ ~24,000 = ~0.5% MINIMUM Small proportion Selection bias

30 More Recent Information 35% of bodies in routine neuropathology service 48% of those with h/o head trauma 42% of those with h/o substance abuse 55% of those with h/o both 20% of those with no h/o of either Noy et al. Chronic Traumatic Encephalopathy-Like Abnormalities in a Routine Neuropathology Service. J Neuropathol Exp Neurol. 2016

31 Need For an Animal Model What we don t know Does the Cis-tau result from trauma? Is Cis-tau causative of the signs/symptoms? Are there other risk factors in addition to trauma? Can you prevent it?

32 Cis-tau after trauma

33 Need For an Animal Model What we don t know Does the Cis-tau result from trauma? YES Is Cis-tau causative of the signs/symptoms? Are there other risk factors in addition to trauma? Can you prevent it?

34 Tau proliferates after trauma Cortex Hippocampus

35 Cis tau leads to neuronal degeneration Axonal Microtubules TBI SHAM

36 Cis tau associated with neurobehavioral outcomes (risk taking)

37 Need For an Animal Model What we don t know Does the Cis-tau result from trauma? Yes Is Cis-tau causative of signs/symptoms? Maybe some Are there other risk factors in addition to trauma? Can you prevent it?

38 Ab Blocks cis-tau prevents degeneration

39 Ab Blocks cis-tau spares neurobehavioral function

40 Need For an Animal Model What we don t know Does the Cis-tau result from trauma? Yes Is Cis-tau causative of signs/symptoms? Maybe some Are there other risk factors in addition to trauma? Can you prevent it? Maybe some of it

41 Cis P-tau is disease driver, linking TBI to CTE, can be neutralized by antibody

42 Conclusions 1. Trauma leads to cis-tau formation 2. It does so in the absence of other factors 3. Cis tau causes neurodegeneration 4. Cis Tau results in neurobehavioral sequelae

43 Acknowledgements Rebekah Mannix, MD, MPH Kun Ping Lu, MD, PhD Xiao Zhou, MD Mike Whalen, MD Jianhua Qiu, PhD Dody Robinson, MD Alvaro Pascual-Leone, MD, PhD Lauren Jantzie, PhD Ann McKee, MD

44 Children s Sports Medicine Foundation Dedicated to encouraging sports and exercise, especially among children and young adults, while simultaneously preventing sports injuries.

45 Injury Risk Profile and Prescription for Prevention Physical Assessment Historical Assessment Training Prevention RX

46 Other Services Running Program Concussion Preparation and Prevention ACL Injury Prevention Class Coaching and Community Clinics Activity for Sedentary Kids Dance Program Training (Independent and 1 on 1) Scholarships for Underserved Athletes

47 Other Services Running Program Concussion Preparation and Prevention ACL Injury Prevention Class Coaching and Community Clinics Activity for Sedentary Kids Dance Program Training (Independent and 1 on 1) Scholarships for Underserved Athletes

48 Further Reading McCrory et al. Consensus statement on concussion in sport, 5th international conf. on concussion in sport, Berlin. Br J Sports Med 2017 [Epub ahead of print] Shaw. The neurophysiology of concussion. ProgNeurobiol 2002;67: Meehan and Bachur. Sport-related concussion. Pediatrics 2009;123(1): Kondo, et al. Antibody against early driver of neurodegeneration cis P-tau blocks brain injury and tauopathy. Nature 2015;523(7561):431-6 McKee AC, et al. Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury. J Neuropathol Exp Neurol 2009;68: Meehan WP, et al. Chronic Traumatic Encephalopathy and Athletes. Neurology 2015;85(17): Noy S, Krawitz S, Del Bigio MR. Chronic Traumatic Encephalopathy-Like Abnormalities in a Routine Neuropathology Service. J Neuropathol Exp Neurol. Epub ahead of print 2016.

49 Questions?