Sport Related Concussion Michael Pleacher MD FAAP FACSM

Sport Related Concussion Michael Pleacher, MD, FAAP, FACSM OA Centers for Orthopaedics April 28, 2017

Goals/Objectives o o o Understand definition of concussion Identify common signs/symptoms of concussion Gain familiarity with evaluation tools used in concussion Understand current concussion management strategies Gain familiarity with return to learn

Sport Related Concussion Mc. Crory P et al, BJSM, 2013

Definition o Complex pathophysiologic process affecting the brain induced by biomechanical forces n n May be caused by direct or indirect blow Rapid onset temporary neurologic dysfunction Functional rather than structural injury Clinical presentation involving cognitive and physical symptoms is variable Mc. Crory P et al, BJSM, 2013

Epidemiology o CDC Data: n n o 1. 1 million TBIs treated in ERs 235 K TBIs hospitalized Sport related concussion n Estimated 207 K / yr treated in ERs between 2001 -2005 135 K were kids aged 5 -18 5. 1% of all sport-related ER visits MMWR July 27, 2007: 56(29); 733737

Epidemiology o o Most sport-related concussion is not evaluated in ER Best estimate: 1. 6 -3. 8 million sport related concussions annually (Langlois 2006) n o Still likely an underestimate Concussions represent 8. 9% of all high school athletic injuries and 5. 8% of all collegiate athletic injuries. (Gessel, et. al. , 2007)

Gessel L et al. JATA 2007

Youth, HS, and College Football: Incidence Data o Concussions account for: n n n 9. 6% of youth football injuries 4% of HS football injuries 8% of NCAA football injuries Dompier TP et al, JAMA Pediatr, 2015

Risk Factors for Concussion o o Male Gender Participation in high-risk sports n o o o Boxing, Football, Ice Hockey, Soccer, Rugby, Aussie Rules Football Aggressive style of play Prior concussion (RR = 5. 8) Position played Zemper ED, Am. J. Phys. Med Rehab. , 2003, 82: 653 -659

Risks of Concussion o o Second Impact Syndrome Long term neurologic deficits due to recurrent concussions

Second Impact Syndrome o o Identified by Schneider in 1973 Term coined by Saunders, 1984 Football player with a mild concussion returned to play 4 days post injury and sustained a second minor concussion He developed “malignant cerebral edema” and died despite maximal medical and surgical intervention Saunders et al. , JAMA 252: 4, July 1984.

Second Impact Syndrome o o o Cantu reported 17 cases of probable second impact syndrome The US National Center for Catastrophic Sport Injury Research reports another 35 probable cases Most cases of SIS have occurred in adolescent males

Second Impact Syndrome o o Each occurred in an athlete incompletely recovered from prior injury who then sustained another head injury Presumed due to widespread death of vulnerable neurons leading to massive cerebral edema & brainstem herniation Cantu et al. , Physician and Sportsmedicine, 1995

Second Impact Syndrome: Is it real? o Mc. Crory reviewed cases of suspected SIS- found only 5 cases of the original 17 reported that were “highly likely” to be SIS Mc. Crory PR, Neurology 1998; 50: 677 -683.

Risk of Recurrent Concussions: Chronic Traumatic Encephalopathy o o o “Punch Drunk” boxers identified in 1928 Cognitive, motor and behavioral impairments which become evident after repetitive head trauma Dementia puglistica, CTBI Rabadi MH, Clinical Journal of Sports Med. , 2001, 194 -198.

Risk of Recurrent Concussions o o o CTE most often associated with boxing CTE may occur in frequently concussed soccer, football, and hockey players as well Athletes with the Apolipoprotein E 4 allele are at higher risk for CTE Jordan BD et al. JAMA 1997.

Recurrent Sub-concussive blows and cognitive impairment o Matser JT et al. Neurology, 1997: n o Pro soccer players have impairments in memory, planning, visual processing compared to noncontact controls Matser JT et al. JAMA, 1999: n Amateur soccer players had impaired memory and planning skills compared to controls

Concussion: Risk of Depression o Guskiewicz KM et al. MSSE 2007 n n Surveyed retired NFL players Players with concussions at increased risk for depression when compared to players with no concussion history: o o >= 3 concussions, 3 x more likely 1 -2 concussions, 1. 5 x more likely

Concussion Mechanism of Injury Biomechanics of concussion Pathophysiology

Mechanism of Injury

Magnitude of Forces o o Concussion research center at Virginia Tech uses sensors in helmets to record forces (HIT system) Early data shows average football player sustains 30 -50 blows to the head each game >50% of hits had a force measured at 30 Gs or more, the hardest hits were measured at >130 Gs Rotational forces also induce concussion Duma S, CJSM, 2005

Magnitude of Forces o Schnebel B et al. Neurosurgery, 2007 n n Measured magnitude in HS and College football players Skill players sustained higher magnitude forces compared to lineman Lineman sustained lower magnitude forces, but had more impacts Impacts measuring >98 g occur 1 out of every 70 hits

Magnitude of Forces o o 254 college football players (3 teams) 184, 358 head impacts n n n o 330 practices, 82 games 4. 8 -7. 5 impacts per player practice 12. 1 – 16. 3 impacts per player per game Peak linear acceleration and peak rotational acceleration measured n n n Data heavily skewed to lower values 50%ile LA =20 G, 95%ile = 62 G 50%ile RA =1392 Rad/s, 95%ile = 4289 rad/s Crisco JJ et al. J Appl Biomech, 2012

Magnitude of Forces: Youth o 50 players, age 11 years, 3 teams n o o 1 team had fewer practices and limited contact in those practices, skewing data 11, 978 head impacts over 1 season 240 +/- 147 impacts /player/year 95%ile peak LA = 43 G 95%ile peak RA = 2034 rad/s Cobb BR, et al, Annals of Biomed Eng, 2013

Pathophysiology o o Complex ion shifts and metabolic changes result in increased glycolysis and altered cerebral blood flow The combination of metabolic changes and altered cerebral blood flow may not induce cell death, but may produce a period of cell vulnerability to re-injury

Neurometabolic Cascade Following Cerebral Concussion 500 Calcium % of normal 400 K+ 300 Glucose 200 Glutamate 100 50 0 2 6 12 20 minutes Cerebral Blood Flow 30 6 24 hours 3 6 days (Giza & Hovda, 2001) UCLA Brain Injury Research Center 10

Concussion Clinical Presentation Sideline Evaluation Detection

Common Symptoms

Common Physical Findings o Cognitive changes n n n o o Disorientation or confusion Amnesia Slow response time Poor concentration Disturbance of new learning and short-term memory Reduced attention and information processing Balance impairment / gait alteration Brief LOC, seizures – rare

Vestibulo-Ocular Reflex (VOR) Reflex eye movement triggered by the vestibular system o Stabilizes visual images during head movement by producing eye movement in the opposite direction of head movement o Following concussion VOR can be compromised, resulting in altered VOR function. o

Concussion Eval/Management: Overview o Multi-disciplinary multi-modal evaluation n n Sideline evaluation by AT or MD Possible ED evaluation and/or hospital admission with serial evaluations Neuroimaging Follow up care Monitoring/treatment for long term effects

Evaluation: ED o Emergency Room Evaluation for: n n n Prolonged loss of consciousness Seizure like activity Focal findings on detailed neuro exam Progressively worsening symptoms Decline in mental status over time

Evaluation: Imaging o o o Usually not necessary CT Scan – used acutely (1 st 48 hours) to rule out intracranial hemorrhage MRI Scan: n n n Not used acutely Used to evaluate prolonged symptoms Usually done 10 -30 days after injury

Evaluation: Sideline Assessment o Sideline eval with AT-C / Physician: n n n n o o ABC’s, C-spine eval. Neuro exam *SCAT-3 Maddocks questions Balance Errors Scoring System (BESS) Standard Assessment of Concussion King-Devick test Suspected concussion = remove from play Serial exams on sideline Mc. Crory P, et al. BJSM, 2013

Sport Concussion Assessment Tool o o Symptom checklist Mental status exam – n n n o GCS, Orientation, Maddocks questions Reverse digit span, MOY reverse order Immediate and 5 min recall Physical Exam n n n Neuro Neck Balance / postural stability Mc. Crory P, et al, BJSM 2013

Balance Errors Scoring System Guskiewicz K, et al, J Ath Training, 2001

BESS o Errors: n n n Hands lifted off iliac crests Opening eyes Step/stumble/fall Hip flexion >30 degrees of flexion/abduction Lifting forefoot or heel Out of test position for > 5 seconds Guskiewicz K, et al, J Ath Training, 2001

BESS Guskiewicz K, et al, J Ath Training, 2001

King Devick Test o o o Test of rapid saccadic eye movements May be used on the sideline to identify concussed athletes Slowing >1 s more than baseline correlates with concussion Galetta KM et al, J Neurol Sci 2011

King Devick Test

VOMS Test Vestibular/Ocular Motor Screen o o Brief test of eye movements which triggers symptoms in concussed athletes VOMS screen positive if exacerbates or elicits concussion symptoms Mucha A et al, Am J Sports Med, 2014

VOMS

Concussion Diagnosed: NOW WHAT? ? ? Management Neuropsychological Evaluation Return to Play Return to Learn

Concussion Management: Overview o o o Remove from play Cognitive rest Abstinence from Physical Exertion Neuropsychological evaluation Serial symptom checklist Gradual return to physical activity

Cognitive Rest: Key to recovery Brown NJ et al, Pediatrics 2014

Cognitive Rest o NJ Brown et al, Pediatrics 2014 n n n Cohort of 335 teenagers with concussion High levels of cognitive activity correlated with prolonged symptom recovery Also found that high symptom score at initial visit correlates with longer recovery

Cognitive rest: Dose? o Thomas DG et al, Pediatrics, 2015 n Strict rest (5 d) vs. Usual Care (2 d) o o n Resultso o n Strict rest = no school, no physical activity UC = no school x 2 d, then graded increase Higher total symptom scores, longer duration of symptoms in SR group No difference on cognitive testing (Impact) Conclude that SR for 5 days less beneficial than UC recommendations

Physical Rest o Majerske et al, J Ath Training, 2008 n n High levels of physical activity correlate with prolonged recovery on neuropsych test battery Moderate levels of physical activity had quickest time to recovery

Neuropsychological Testing

Neuropsychological Evaluation o o o Neuropsychological testing of the athlete via computerized screening test = one tool in the tool box Assesses verbal memory, visual memory, processing speed, reaction time Not a stand alone test to diagnose concussion, nor to deem recovery

Timeline for Neuropsych Tests o Common use of NP test: n n Preseason baseline testing Retesting at 24 -48 hours after injury Once asymptomatic and progressing physical activity, retest If athlete has not returned to baseline, repeat evaluations weekly until at baseline

Results of Neuropsych Testing o o Among college athletes, significant decline in function 48 hours after injury Majority return to baseline by 7 days post-injury Echemendia RJ, Clin J. of Sports Med. , 2001, 11: 23 -31.

Neuropsych Impairment of High School Athletes o o Injured HS athletes had prolonged memory dysfunction when compared to college athletes with similar or more severe injury Injured HS athletes still had memory impairment at 7 days post-injury Field M, Journal of Pediatrics, 2003, pp 546 -553

Neuropsych Impairment of High School Athletes o 2003 study by Lovell and Collins n n n HS athletes had resolution of symptoms by an average of 4 days post-injury However, HS athletes had abnormal tests of memory that persisted beyond 7 days This subgroup of athletes may require more cautious return to play advice Lovell MR, Journal of Neurosurgery, 2003, 98: 296 -301.

Summary of Neuropsych Testing o o o Short computerized batteries of tests are now available Most useful if each player has both preseason and post-injury testing Deficits on neuropsych testing for college athletes correspond with symptom resolution Neuropsych deficits for HS athletes persist after symptom resolution Neuropsych testing is useful tool to help guide safe return-to-play when combined with other measures of recovery Only one tool in the toolbox; prudent to use MULTIPLE measures of recovery

Physical Activity Advance o o 24 hours at each level If symptoms recur, rest x 24 hrs, restart at last successfully completed level Mc. Crory P, BJSM, 2013

Concussion Management: Return to Learn o o o Recent attention in medical literature Programmatic opportunity School staff / family / physician roles Halstead ME et al, Pediatrics, 2013 Mc. Grath N, J Ath Training, 2010 Again, “dose” and effect of classroom accommodations unknown

REAP Program o http: //rockymountainhospitalforchildr en. com/service/concussionmanagement-reap-guidelines

Classroom Accommodations Mc. Grath N, J Ath Training, 2010

Concussion Management Models for Management of Concussion

Concussion Management Model: Bowdoin College o Athlete identified with concussion by AT-C or Physician (SCAT card) n n Removed from play / physical activity Brain Rest x 48 hours Complete Physical Rest Within 48 hours of injury: o o n Health center eval Impact, BESS, KD Daily symptom score with AT-C

Concussion Management Model: Bowdoin College o Once asymptomatic x 24 hours n o Repeat BESS, Impact, KD prior to full clearance n o Gradual activity advance Only necessary to repeat tests that were abnormal at post-injury visit If BESS/Impact/KD are at baseline and if athlete has remained asymptomatic during activity advance, return to full sport participation

Concussion Management Model: Bowdoin College o Academic affairs n Work with Dean’s office to: o o Adjust schedules Create classroom accommodations Incomplete classes / make up work Potentially coordinate medical leave

Concussion Management Model: Boston Children’s Hospital

Concussion Management Model: Boston Children’s Hospital

Concussion Management Model: Boston Children’s Hospital

Post-Concussion Management Medications Physical Therapy Neuropsychological testing

Medications o o Target medical therapy based on symptom cluster All medications used in management of concussion are off-label

Amantadine o o Amantadine 100 mg BID x 30 days Cognitive symptom cluster, symptoms lasting >21 days Reddy CC et al, J Head Trauma Rehab, 2012

Other commonly used medications o Cognitive Cluster: n n n o o Amantadine 100 mg BID Methylphenidate Donepezil 5 mg QHS n n Physical Cluster: n n Mood Cluster: n Nortriptyline 25 mg QHS Gabapentin 300 mg TID o Nortriptyline 25 mg QHS Sertraline 25 -50 mg QD Counseling! Sleep Cluster: n n n Meehan W, CJSM 2012 Nortriptyline 25 mg QHS Zolpidem 10 mg QHS Trazodone 50 mg QHS

Physical Therapy o o o Evolving treatment adjunct for prolonged Post-Concussion Symptoms Vestibular therapy Graded sub-symptom threshold exercise

Vestibular therapy o o VOR Habituation Balance retraining Dix-Hallpike and Epley’s Maneuver https: //www. youtube. com/watch? v=v XTsf_Zv 5 i 4

Graded Subsymptom Threshold Exercise o Balke Protocol n n n o o 1 min, 3. 3 mph, 0% incline 1 min, 3. 3 mph, 2% incline Each min thereafter, 3. 3 mph +1% incline Protocol stops at 1 st sign of symptom exacerbation Monitor RPE and HR Exercise prescribed at 80% of threshold HR Bike, walk, row, 20 min 1 -2 x/day at 80%HR

Exercise Therapy: Safety and Efficacy o Leddy JJ et al, CJSM 2010; 20: 21 -27 n n o Balke protocol exercise assessment Exercise prescription, 5 -6 days/week Improvement in PCS over time No adverse events Gagnon I et al, Brain Inj, 2009 Case series of PT / exercise in peds pts with PCS n Exercise associated with hastened recovery, reduction in symptoms n

Other Adjunct Treatments o Osteopathic / Chiropractic evaluation and treatment n o Neuro-optometric rehabilitation n o Cervicogenic headaches Convergence disorders Counseling n n n Mood disorders Prolonged recovery, retirement from sport Sleep hygiene (self hypnosis)

Neuropsychological Testing o Full Battery traditional NP testing for patients w/ refractory cognitive sx n n 3 mo of cognitive dysfunction Guides IEP/504 plan Targeted neuropsychological / cognitive rehabilitation (unproven) VERY limited resource in Maine, insurance coverage variable

Additional Issues Detection Prevention Policy

Detection o Helmets n Impact sensors (Shockbox, Shok. Spot. R, Heads-up Stabilizer™)

Detection o Impact monitoring system on chin strap n o o o Light flashes above ~70 g impact Not a proven technology Not 100% accurate Flashing lights are NOT a sign or symptom of concussion and will not diagnose a concussion.

Prevention o Mouth guards n n o No proven benefit in reducing concussion risk Prevents peri-oral and dental injury Helmets n n n Designed to prevent skull fractures – not concussions. PROPER FIT most important aspect Virginia Tech STAR study helmet ranking o Should not be considered accurate – too many limitations

Prevention o Soccer “Full 90” n n o Ineffective at reducing risk of concussion Reduces rate of scalp lacs / facial trauma Rugby headgear n n Does not reduce rate of concussion Reduces rate of scalp lacs / facial trauma

Prevention o Cumulative effect of subconcussive blows n n o Interest in limited contact practices “Hit Counts” Rugby tackling technique, helmetless practices at UNH n http: //usafootball. com/headsup

Policy: Concussion Laws o o Since 2009, every state in US has enacted legislation regarding concussion Most call for education of coaches, mandate evaluation for suspected concussion, etc None are particularly enforceable http: //www. mainelegislature. org/legis/bills/ bills_124 th/billpdfs/HP 090301. pdf

Summary o o o Concussion is a complex disorder requiring skillful management by a coordinated group of diverse caregivers Multiple tools aid in diagnosis of concussion Multiple measures of recovery should be used to determine readiness for return to play

Summary o o Medications and adjunct therapies can be useful in management of prolonged PCS Reduction in risk in future will likely be accomplished by technique changes and exposure reduction rather than protective equipment

Thanks!