Current Controversies and Issues in the Assessment and Management of Sports-related Concussion

1. Current Controversies and Issues in the Assessment and Management of Sports-related Concussion Philip Schatz, PhDDepartment of Psychology Saint Joseph’s University, Philadelphia PA Ruben J. Echemendia, PhD Psychological and Neurobehavioral Associates, Inc. State College, PA National Academy Of Neuropsychology - November 2007

2. Defining Concussion-Seems Simple • Mild traumatic brain injury • Alteration in consciousness due to a blow to the head or acceleration/deceleration/rotational force • Does NOT imply or require loss of consciousness. • Usually temporary changes in mental status • Temporary changes in somatic functioning • May produce a wide range of symptoms • Normal structural neuroimagingCISG, Vienna (2001); Prague (2004)

3. However: There is Controversy • Defining concussion & LOC • Metabolic cascade/SIS • Pathophysiology of injury • Long-term/cumulative effects • Depression Head Games Chris Nowinski

4. Lots of Controversy • Symptom Validity/Effort Testing • Value Added of Neuropsych • Conflict Of Interest • Full disclosure • What have we learned from NFL

5. “Physical”: Pressure in head Headache Balance troubles Visual Disturbance Numbness Tingling Feeling slow Sensitivity to light/noise “Psychological”: Feeling like in a “fog” Difficulty concentrating Difficulty remembering Irritability Sadness Nervousness Defining Concussion-Symptoms

6. Cantu (2001) Colorado (1991) AAN (1997) Grade 1 No LOC No LOC No LOC Mild PTA<30min Confusion SX<15 min No Amnesia Grade 2 LOC<5min No LOC No LOC Moderate or Confusion Sx>15 min PTA>30min Amnesia Grade 3 LOC>5min LOC Any LOC Severe or Brief vs PTA>24hr Prolonged Defining Concussion w/LOC?

7. On the bright side:…More than 60% of coaches correctly identified amnesia, confusion, dizziness, headache, and loss of consciousness (LOC) as concussion-related symptoms (McCloud, Swartz, Bay, Sport-Related Concussion Misunderstandings Among Youth Coaches, Clin J Sports Med, 2007) Defining Concussion w/LOC?

8. LOC is not required for diagnosis: No significant differences found between the LOC, no LOC, or uncertain LOC groups for any of the neuropsychological measures used (WMS, TMT, WCST, HVLT, COWAT, GOAT). (Lovell, et al Clin J Sports Med, 1999) Defining Concussion w/LOC?

9. LOC is not required for diagnosis: Concussion may cause a gradient of clinical syndromes that may or may not involve LOC. (CISG-Vienna, Br J Sports Med. 2002) The 2 most recognizable signs of a concussion are LOC and amnesia; yet, neither is required for an injury to be classified as a concussion. (NATA Position Stmt, Guskiewicz, et al.,J Ath Train 2004) Defining Concussion w/LOC?

10. LOC is not required for diagnosisSAC scores immediately after concussion were significantly lower than baseline scores, even for injured subjects without LOC or PTA. Subjects with LOC were most severely impaired immediately after injury, whereas those without LOC or PTA were least impaired. (McCrea, et al Neurosurg, 2002) Defining Concussion w/LOC?

11. LOC is not required for diagnosisLOC was a useful indicator of the initial severity of the injury; LOC did not correlate with other indices of concussion severity, including duration of symptoms. (Erlanger, et al, J Neurosurg, 2003) Defining Concussion w/LOC?

12. Is LOC required for diagnosis?…the presence of loss of consciousness as a symptom would not necessarily classify the concussion as complex (Prague, Br J Sports Med, 2005) Defining Concussion: Complexity?

13. “Simple Concussions”:In simple concussion, an athlete suffers an injury that progressively resolves without complication over 7–10 days. In such cases, apart from limiting playing or training while symptomatic, no further intervention is required during the period of recovery, and the athlete typically resumes sport without further problem. Formal neuropsychological screening does not play a role in these circumstances, although mental status screening should be a part of the assessment of all concussed athletes. Simple concussion represents the most common form of this injury and can be appropriately managed by primary care physicians or by certified athletic trainers working under medical supervision. (Prague, Br J Sports Med, 2005) Defining Concussion: Complexity?

14. “Complex Concussions”:Complex concussion encompasses cases where athletes suffer persistent symptoms (including persistent symptom recurrence with exertion), specific sequelae… prolonged loss of consciousness (more than one minute) or prolonged cognitive impairment after the injury. This group may also include athletes who suffer multiple concussions over time or where repeated concussions occur with progressively less impact force. (Prague, Br J Sports Med, 2005) Defining Concussion: Complexity?

15. Recovery in Simple vs. Complex Concussions Athletes were classified retrospectively (using Prague criteria) as having sustained a simple (n = 55) or complex (n = 59) concussion on the basis of their recovery times only and not on the basis of whether they had a previous concussion. (Iverson, Clin J Sports Med, 2007) Defining Concussion: Complexity?

16. Recovery in Simple vs. Complex Concussions Within 72 hours after injury, athletes with complex concussions performed more poorly on neuropsychological testing and reported more symptoms than those with simple concussions. Athletes with complex concussions who were slow to recover were 18 times more likely to have 3 unusually low neuropsychological test scores than those with simple concussions. Athletes with previous concussions did not recover more slowly (Iverson, Clin J Sports Med, 2007) Defining Concussion: Complexity?

17. Recovery in Simple vs. Complex Concussions Athletes with past concussion history are classified as having sustained complex concussions (without waiting to see if they recover within 10 days) Concussion history did not influence recovery time in either simple or complex concussion groups (Iverson, Clin J Sports Med, 2007) Defining Concussion: Complexity?

18. Summary Results cast doubt on the importance of LOC as a predictor of neuropsych test performance during the acute phase of recovery from mild traumatic brain injury. Measurable neurocognitive abnormalities are evident immediately after injury without PTA or LOC. Neither a brief LOC nor a history of concussion was a useful predictor of the duration of postconcussion symptoms. Classification of simple vs. complex may have limited clinical utility Defining Concussion=LOC?

19. Physiological Changes • Shearing or strain injury of axons • Diffuse microscopic changes to axons • Microscopic tearing of small blood vessels • Metabolic cascade resulting in imbalance between glucose demands and regional CBF supply (vulnerable to SIS)Giza & Hovda, JAT, 36(3), 228-35

20. Neurometabolic Changes

21. Neurometabolic Changes • The primary elements of the pathophysiologic cascade following concussive brain injury include • abrupt neuronal depolarization, • release of excitatory neurotransmitters, • ionic shifts, • changes in glucose metabolism, • altered cerebral blood flow, • and impaired axonal function. Giza & Hovda, JAT, 2001

22. Neurometabolic Changes K, potassium; Ca2, calcium; CMRgluc, oxidative glucose metabolism; CBF, cerebral blood flow. Giza CC, Hovda DA. In: Cantu RC, Cantu RI. Neurologic Athletic and Spine Injuries, 2001

23. Neurometabolic Changes It appears that metabolic alterations can be correlated with periods of post-concussion vulnerability and with neurobehavioral abnormalities.What of Second Impact Syndrome?

24. Second Impact Syndrome: Characterized by • pre-existing head injury, • persistent concussive-type symptoms (often under-recognized) • a "second impact" to the head or torso of the athlete. • cerebral edema precipitates a loss in the ability of the brain to auto-regulate intracranial and cerebral per-fusion pressure. • subsequent massive cerebral hyperemia and cerebral edema

25. Second Impact Syndrome: Incidence unclear: • 712 football fatalities from 1945-1999, 491 head-related, 75% subdural; high school-professional (Meuller, JAT, 2001) • 69 catastrophic football head injuries from1984-1999: 6 college, 63 high school (Meuller, JAT, 2001) • CDC: more than 20 people have died from SIS. • Nat’l Center for Catastrophic Sports Injury Research identified 35 probable cases from 1980-1993: 17 confirmed,18 suspected (Meuller & Deihl; Meuller & Cantu, 2000) • Only 5 of 17 documented cases of suspected cases were found to be SIS. (McCrory & Berkovic, Neurology, 1998)

26. Neurometabolic Changes & SIS Vagnozzi et al. Neurosurg 2007: Temporal window of metabolic brain vulnerability to concussions: Mitochondrial-related impairment-Part I • Shows the existence of a temporal window of brain vulnerability after mTBI. • A second concussive event falling within specific post-mTBI time range had profound consequences on mitochondrial-related metabolism.

27. Neurometabolic Changes & SIS Vagnozzi et al. Neurosurg 2007: Rats were subjected to two diffuse mTBIs (450 g/1 m height) with the second mTBI delivered after 1, 2, 3, 4, or 5 days; sacrificed 2 days later 2 more groups received a second mTBI after 3 days, and sacrificed 5 and 7 days later

28. Neurometabolic Changes & SIS Vagnozzi et al. Neurosurg 2007: Methodology: Wait 1-5 days Wait 2 days mTBI1 mTBI2 Look at Brains Wait 3 days Wait 5 or 7 days mTBI1 mTBI2 Look at Brains

29. Neurometabolic Changes & SIS (Vagnozzi et al. Neurosurg 2007) Vulnerability 24 hours after the first injury, Maximal changes when mTBIs spaced by 3 days Postinjury Day 3 is when the brain exhibits its greatest degree of vulnerability.

30. Neurometabolic Changes & SIS Post-mTBIMetabolic Changes: Energy metabolism impairment peaks at 3-day interval (Vagnozzi et al. Neurosurg 2007)

31. Neurometabolic Changes & SIS Post-mTBIMetabolic Changes: Variations in cerebral genetic expression (dim=no change) (Vagnozzi et al. Neurosurg 2007)

32. Neurometabolic Changes & SIS • No amelioration was produced by prolonging the time of recovery after the second impact up to 7 days • Indicates that metabolic activities, particularly those related to mitochondrial functions, were still severely altered at that time point in rats in Group 3 (mTBI - 3 days - mTBI). (Vagnozzi et al. Neurosurg 2007)

33. Neurometabolic Changes & SIS Two main findings:1) the lag time between repeat mTBIs is the crucial factor affecting the reversibility of cerebral metabolic alterations; and 2) if a second mTBI takes place within the temporal window of metabolic vulnerability, severe, “difficult-to-reverse” brain damage will occur. (Vagnozzi et al. Neurosurg 2007)

34. Neurometabolic Changes & SIS Hovda, in response to: Vagnozzi et al. Neurosurg 2007: • The greatest effect is seen when these two mild insults are separated by 3 days. • This would suggest that repeated insults on either side of this critical window may not be as devastating • Opens up the possibility that for at least a few hours, the brain may initiate protective mechanisms that are exhausted by 3 days, after which the brain needs at least 2 more days to recover.

35. Neurometabolic Changes & SIS • Extrapolating these animal findings to humans is certainly a challenge and may even be unreasonable to attempt.Vagnozzi et al. Neurosurg 2007: • At this time, there is no existing animal or other experimental model that accurately reflects a sporting concussive injury. Whether similar metabolic changes occur in sports concussion, however, remains speculative at this time. (Prague, Br J Sports Med, 2005)

36. Neurometabolic Changes & SIS While the time course of these changes is well understood in experimental animal models, it is only beginning to be characterized following human concussion. Giza & Hovda, JAT, 2001

37. Mechanism of Injury • Select articles from a series of 14 articles in Neurosurgery on the NFL’s research on concussion in professional football • NFL mTBI Subcommittee - headed by Dr. Elliott Pellman from 1994-2007, and by Drs. Ira Casson and David Viano

38. Mechanism of Injury • Reconstruction of Game FootageFrame-by-frame video/laboratory reconstruction

39. Mechanism of Injury

40. Patho. Laboratory Reconstruction Allows for a high Level of Precision

41. Mechanism of Injury (SI=Severity Index; 300=normal tolerance levels, 1200=NOCSE peak)

42. Mechanism of Injury Location and Direction of Helmet Impacts (Part 2) Neurosurg 2003 (Part 2, Neurosurg, 2003)

43. Mechanism of Injury Location and Direction of Helmet Impacts (Part 2) Neurosurg 2003 A, 0- to 45-degree,Q3 toQ1 FM, Q2 toQ3 H; B, 45- to 90-degree,Q2 toQ1 FM,Q2 toQ3 H; C, 90- to 135-degree,Q1 toQ4 levels; D, 135- to 180-degree,Q1 toQ4 levels. E and F:striking players: E, 0- to 45-degree,Q2 toQ4 levels; F, 45- to 90-degree quadrant,Q3 toQ4 levels.(Part 2, Neurosurg, 2003)

44. Mechanism of Injury Location and Direction of Helmet Impacts (Part 2) Neurosurg 2003 Highest impact from Q1 Lowest from Q4 (Part 2, Neurosurg, 2003) Striking players same Impact velocity

45. Mechanism of Injury Location and Direction of Helmet Impacts (Part 2) Neurosurg 2003 Highest accel from Q4 Despite lowest vel (Part 2, Neurosurg, 2003) Striking players lower Head acceleration

46. Mechanism of Injury Location and Direction of Helmet Impacts (Part 2) Neurosurg 2003 Highest delta V from Q4 Despite lowest velocity (Part 2, Neurosurg, 2003) Non-concussed players Lower delta V Striking same as struck For non-concussed

47. Translational Acceleration(Part 2, Neurosurg, 2003)

48. Rotational Acceleration (Part 2, Neurosurg, 2003)

49. Mechanism of Injury • Reconstruction of Game Impacts • (Part 1, Neurosurg, 2003) • “Striking observations” - concussion in NFL football involves an average: • impact velocity of 9.3 m/s (20.8 mph), • head velocity change of 7.2 m/s (16.1 mph), • head acceleration of 98 g, • duration of 15 milliseconds.

50. Mechanism of Injury • The “other” football • (Withnall, et al., BJSM, 2005) • Biomechanical investigations of head impacts in football • game video of 62 cases of head impact, • 38% upper extremity - human re-enacted, • 30% head-to-head - dummies,