current controversies and issues in the assessment and management of sports-related concussion

Current Controversies and Issues in

the Assessment and Management

of

Sports-related ConcussionPhilip Schatz, PhD Department of Psychology

Saint Joseph’s University, Philadelphia PA

Ruben J. Echemendia, PhDPsychological and Neurobehavioral

Associates, Inc.State College, PA

National Academy Of Neuropsychology - November 2007

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 neuroimaging

CISG, Vienna (2001); Prague (2004)

However: There is Controversy

• Defining concussion & LOC

• Metabolic cascade/SIS

• Pathophysiology of injury

• Long-term/cumulative effects

• Depression

QuickTime™ and aTIFF (Uncompressed) decompressor

are needed to see this picture.

Head Games Chris Nowinski

Lots of Controversy

• Symptom Validity/Effort Testing

• Value Added of Neuropsych • Conflict Of Interest

• Full disclosure

• What have we learned from NFL

Defining Concussion-Symptoms

“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 w/LOC?

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


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)


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)

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)



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)


LOC is not required for diagnosis

LOC 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)

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?

“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.



“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.



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)


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)


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=LOC?

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

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

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


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


It appears that metabolic alterations can be correlated with periods of post-concussion vulnerability and with neurobehavioral abnormalities.

What of Second Impact Syndrome?

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

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)

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.

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


Vagnozzi et al. Neurosurg 2007:

Methodology:


mTBI1 mTBI2Wait 1-5days

Wait 2days Look at Brains

mTBI1 mTBI2Wait 3days

Wait 5 or7 days Look at Brains

(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.



Post-mTBIMetabolic Changes:

Energy metabolism impairment peaks at 3-day interval

(Vagnozzi et al. Neurosurg

2007)


Post-mTBIMetabolic Changes:

Variations in cerebral genetic expression (dim=no change)

(Vagnozzi et al. Neurosurg

2007)

• 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)


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)


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.


• 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)


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


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

Mechanism of Injury

• Reconstruction of Game FootageFrame-by-frame video/laboratory reconstruction

Mechanism of Injury

Patho.

LaboratoryReconstructionAllows for a highLevel of Precision

Mechanism of Injury

(SI=Severity Index; 300=normal tolerance levels, 1200=NOCSE peak)

Mechanism of InjuryLocation and Direction of Helmet Impacts (Part 2) Neurosurg 2003

(Part 2, Neurosurg, 2003)

Mechanism of Injury

Location and Direction of Helmet Impacts (Part 2) Neurosurg 2003

A, 0- to 45-degree, Q3 to Q1 FM, Q2 to Q3 H; B, 45- to 90-degree, Q2 to Q1 FM,Q2 to Q3 H; C, 90- to 135-degree, Q1 to Q4 levels;D, 135- to 180-degree, Q1 to Q4 levels.

E and F:striking players: E, 0- to 45-degree, Q2 to Q4 levels; F, 45- to 90-degree quadrant, Q3 to Q4 levels.


Mechanism of Injury


Highest impact from Q1Lowest from Q4(Part 2, Neurosurg, 2003)

Striking players sameImpact velocity

Mechanism of Injury


Highest accel from Q4Despite lowest vel(Part 2, Neurosurg, 2003)

Striking players lowerHead acceleration

Mechanism of Injury


Highest delta V from Q4Despite lowest velocity(Part 2, Neurosurg, 2003)

Non-concussed players Lower delta V

Striking same as struckFor non-concussed

TranslationalAcceleration(Part 2, Neurosurg, 2003)

RotationalAcceleration(Part 2, Neurosurg, 2003)

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.

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,

Mechanism of Injury

Mechanism of Injury


Biomechanical investigations of head impacts in football

• Elbow: linear g of 21.3 • Forearm: linear g of 20.4, • Head: linear g of 35-80 (front/side vs. forehead-rear)

• NFL: linear g of 98

Mechanism of Injury


Biomechanical investigations off head impacts in football

• Elbow: impact velocity of 3.0 m/s (7 mph), • Forearm: imp. velocity of 7.7 m/s (17.2 mph), • Head: impact velocity of 2.3 m/s (5 mph)

• NFL: impact velocity of 9.3 m/s (20.8 mph)

What about Helmets?

Performance of “Newer Helmets” (Part 13, Neurosurg, 2006)

10 collisions:• helmet-helmet (8) • helmet-ground (2)

5 Helmets (blind)

What about Helmets?

What about Helmets?

Baseline condition: Original VSR-4 Helmet

What about Helmets?

…Helmets?

New helmets provide approximately a 10% reduction in concussion risks consistent with severity index and translational acceleration

And approximately a 19% reduction based on rotational acceleration findings.


What about Helmets?

Represents a small percentage of 787 total NFL concussions that were studied over a 6-year period.

10 cases from a subset of 25 cases were there the necessary camera angles and on-field yard markers in view on the video tape, so that the theoretical calculations of forces sustained could be made.

These 25 concussions were all somewhat unique: involved WR or QB in the open field sustaining a hit to the side of the helmet that they did not see coming from an individual who essentially made a helmet to helmet collision. (Cantu, Neurosurg, 2006)

What about Helmets?

Analysis of “newer” helmet technology

2141 High School Football players• Riddell Revolution (N=1173)• Standard Helmets (N=968)

Three-year prospective cohort study

(Collins, et al., Neurosurg, 2006)

What about Helmets?

What about Helmets?

What about Helmets?

• The rate of concussion in athletes wearing the Revolution helmet (5.3%) was significantly lower than the rate in athletes wearing traditional helmets (7.6%).

•The two helmet groups did not differ significantly on the average number of days to recover and return to play following concussion.


What about Helmets?

• The relative risk reduction associated with wearing the newer helmet was 31%, and the absolute risk reduction was 2.3%.

• In context:• if 1.5 mil. HS students participate each year• the concussion rate is approx. 4 to 10%, • the relative risk reduction means that 18,600 to 46,500 fewer high school football players would sustain concussion.


What about Helmets?

(Cantu, in response to: Collins, et al., Neurosurg, 2006) This article, in my opinion, suffers from a serious, if not fatal, methodological flaw… that flaw is that we do not know the age of the helmets that comprised the non-Riddell group.

We assume the Riddell helmets were either new or nearly new because the product is new.

However, the helmets that the Riddell helmets were being compared against are of indeterminate age and were very likely significantly older than the Riddell group

What about Helmets?

(Day, in response to: Collins, et al., Neurosurg, 2006) The study has several limitations in its design which may influence the results:• Helmet selection was neither randomized nor controlled• It is not entirely clear what factors led an athlete to be included in the new helmet design group or the standard group• Younger patients tended to use the older helmet type, and that group may be more susceptible to concussions.• Each of the authors has a business relationship with either the computerized neurocognitive testing equipment company or the helmet manufacturer that were being evaluated.

What about Mouthguards?

(Takeda, et al., Dental Traumology, 2005)•pendulum impact equipment and an artificial skull model •strain gages and accelerometers•simulate and measure the surface distortions related to bone deformation or fractures •acceleration of the head related to concussions.

Parietal acceleration without and with mouthguard:


(Takeda, et al., Dental Traumology, 2005)

Distortion of the mandible:


(Takeda, et al., Dental Traumology, 2005)

Head acceleration:


(Wisniewski, et al., Dental Traumology, 2004)

Effectiveness of “boil and bite” versus custom mouthguards

•15-week study: 2001 season

•NCAA Division I

•Trainers

Repeat Injuries

Repeat Injuries (Part 4, Neurosurg, 2004)

Repeat Injuries - NP Testing

Pellman et al (Part 8: Neurosurg, 2005):

Players who are concussed and return to the same game have fewer initial signs and symptoms than those removed from play.

Return to play does not involve a significant risk of a second injury either in the same game or during the season.


• Guskiewicz (2003): NCAA study of 2,905 college football players found those who have suffered concussions are more susceptible to further head trauma for seven to 10 days after the injury.


Cantu (reviewer: Neurosurg 2005) “I caution all readers to read very carefully the nearly two pages of limitations of the study that the authors, to their credit, candidly cite.

…one needs to ask oneself, I believe, are we dealing with a unique population and situation in these articles?

Is it correct to extrapolate these data to the many previous concussion articles and consensus statements involving the high school and college scholar-athlete?


Pellmen, et al (Part 6: Neurosurg 2004)

NFL players did not demonstrate evidence of neurocognitive decline after multiple (three or more) MTBIs or in those players out 7 days.


Bailes (reviewer: Neurosurg 2004)

I do not believe that this study, with correlation between clinical and neuropsychological evaluation, proves that there are no widespread permanent or cumulative effects of single or multiple MTBI in NFL players.


Kelly (reviewer: Neurosurg 2004)

The findings are somewhat surprising… and should be interpreted with caution.

…a major shortcoming of this study is that a relatively small sample size of concussed athletes, only 22%, actually underwent neuropsychological testing, and participation was voluntary. Why did 78% of concussed players choose not to participate?


Blieberg (reviewer: Neurosurg 2004)

It is perplexing that the authors chose to include athletes 1 to 10 days after injury in their MTBI group

…methodological choices that decrease the likelihood of obtaining statistically significant differences are worrisome

The authors’ choice to dilute their experimental sample by including outliers weakens the impact of their findings, conclusions, and recommendations.


Guskiewicz (reviewer: Neurosurg 2004)

My understanding is that while nearly all teams “participate” in the program, not all players on every team choose to participate.

It is unfortunate that only 22% of the concussed players (16% of the overall concussions sustained) are represented because of incomplete data…. thus, a major limitation of the study is that it could involve a biased sample.

Repeat Injuries - Depression

(Part 4, Neurosurg, 2004) "no evidence of worsening injury or chronic cumulative effects of multiple MTBIs in NFL players."

Center for the Study of Retired Athletes at the University of North Carolina (2003) found a link between multiple concussions and depression among former pro players with histories of concussions.

2005 follow-up study at the Center showed a connection between concussions and both brain impairment and Alzheimer's disease among retired NFL players.


(Guskiewicz, et al., Neurosurg, 2005)

2,500 former N.F.L. players• Higher prevalence of

Alzheimer’s disease among retired NFL players (1.36:1)

• Of 768 withMemory problems:


2,500+ former NFL players (Center for the Study of Retired Athletes)

Evidence of • cognitive impairment, • Alzheimer’s-like symptoms• depression

(Guskiewicz, et al., Med Sci Sport Exer, 2007)


2,500+ former NFL players (Center for the Study of Retired Athletes)

• Depression rose proportionately with the number of concussions they had sustained:– players who sustained three+ concussions were three

times more likely to experience “significant memory problems” and five times more likely to develop earlier onset of Alzheimer’s disease.

(Guskiewicz, et al., Med Sci Sport Exer, 2007)


Of 595 players who recalled sustaining three or more concussions on the football field:

• 20.2 percent said they have depression

• Players with one or two concussions were found to have depression 9.7% of the time, and those with none, 6.6%.

• Average age=54, 2+ seasons in NFL(Guskiewicz, et al., Med Sci Sport Exer, 2007)


Criticism: Bias • Self-report of memory of on-field concussions• 69% return rate• Casson: Survey studies are the weakest type of

research study — they’re subject to all kinds of error and misinterpretation and miscalculation… no objective determination

(NYTimes 5/31/07, response to Guskiewicz, et al., Med Sci Sport Exer, 2007)


Defense:Best (OSU): “We learned that there’s a correlation between the

number of concussions sustained and depression they experience later in life.”

Whyte: “Response rate was good and not a relevant issue to the findings. We have some pretty solid data that multiple concussions caused cumulative brain damage and increased risk of depression, and that is not in conflict with the growing literature.”

(NYTimes 5/31/07, response to Guskiewicz, et al., Med Sci Sport Exer, 2007)


• Guskiewicz (NYTimes 1/18/07):

“I think that some of the folks within the N.F.L. have chosen to ignore some of these earlier findings, and I question how many more, be it a large study like ours, or single-case studies like Terry Long, Mike Webster, whomever it may be, it will take for them to wake up.”


• Cantu (Neurosurgery, 2007)

Findings of chronic traumatic encephalopathy (CTE) in Waters, Webster, Long are similar to dementia pugilistica (cite: Corsellis, 1973)


Omalu: the damage was either caused or drastically expedited by successive concussions sustained playing football

Cantu: while not all PCS players have CTE (e.g., Carson, Toon, Hodge, Aikman, Young, Johnson, Chrebet, not surprised to see this in NFL, need independent evaluation of brain tissue,prospective study of active players by independent researchers outside of NFL

Repeat Injuries: Youth Athletes?

• Relying on symptoms Relying on symptoms alone may be dangerousalone may be dangerous

• Attentional processes, Attentional processes, memory, and cognitive memory, and cognitive

• speed are key speed are key elements of testingelements of testing

• Younger athletes deserve Younger athletes deserve particular attentionparticular attention

238 youth athlete volunteers ... divided into four independent groups on the basis of concussion history.

• No Concussion: 82 healthy volunteers with no history of concussion.

• One Previous Concussion: 56 youth athletes who had sustained one previous concussion (not within the past six months).

• Two+ Previous Concussions: 51 youth athletes who had sustained two or more previous concussions (not within the past six months).

• Recent Concussion: 49 youth athletes who had sustained a recent concussion, with no identified medical or neuropsychological difficulties related to concussion within one week of testing. (Moser, Schatz & Jordan, Neurosurgery 2005)


3.05

3.1

3.15

3.2

3.25

3.3

3.35

3.4

3.45

3.5

3.55

No Concussion: (82) One Previous: (56) Two+ Previous: (51) Recent: (49)

Concussion Group

GPA by Concussion Group


(Moser, Schatz & Jordan, Neurosurgery 2005)

• Multivariate Analysis of Variance (MANOVA) revealed a significant overall effect of concussion history on cognition [F(21,672)=1.8; p=.015].

• Univariate F-tests revealed significant main effects of concussion history on Attention [F(3,228)=4.72; p=.003] and GPA [F(3,228 =5.76; p=.001].


(Collins, et al., JAMA, 1999)

• MANOVA: significant main effects for LD (p<.001) resulting in lowered baseline neuropsychological performance.

• Sig. interaction was between LD and history of multiple concussions and LD Trails B (p=.007) and SDMT (p=.009); poorer performance for the group with LD and multiple concussions compared with other groups.


• Health non-concussed youth athletes with a history of concussion often show deficits at baseline assessment.

• These enduring effects of previous cerebral concussions can be detected using traditional measures.

•A more vulnerable and susceptible youth brain

•Participation in multiple sports over a long period of years.


What about Effort?

Effort: (Green, et al., Brain Injury, 2001)• >50% of variance in scores was due to

poor effort

• Education = 11%

• Age = 4%

Symptom Validity Testing (Bush, et al NAN, ACN),:

“it is necessary to evaluate symptom validity objectively in any neuropsychological assessment”

QuickTime™ and aTIFF (Uncompressed) decompressor

are needed to see this picture.

• Little data on effort at time of assessment:– “…speculation that athletes are often motivated to underreport

symptoms so they can return to competition” (Echemendia & Cantu, 2003)

– “…motivated to underreport subjective symptoms to hasten the return to competition.” (Erlanger, et al., 2003)

– “An athlete’s apparent fear of removal from a game or of losing his or her position on the team may tempt some athletes to deny or underreport postconcussive symptoms.” (Lovell, 1998)

– “Ostensibly, symptom minimization occurs in hopes of a faster return to the playing field, court or ice.” (Lovell, et al., 2002)

– “it is more likely that suspicion regarding the use of the test results and/or general disinterest and apathy could impact the accurate measurement of cognitive ability at baseline” (Echemendia & Cantu, 2003)

What about Effort?

• Bailey, Echemendia, Arnett (2006), JINS– Assigned to High Motivation at Baseline (HMB) and

Suspect Motivation at Baseline (SMB) groups based on whether baseline performance fell one or more standard deviations from the mean of the given measure

– N=26 to 33, Pre, Post-Mild TBI, Trails, Dig Span, Stroop

– In repeated measures ANCOVA (that removed achievement performance), the SMB groups demonstrated greater improvement than the HMB groups for the Trail Making Test A & B ( TMT-A & B), Digit Span, and Stroop-Color Word (Stroop-CW) tests.

What about Effort?

Effort & Motivation Among Athletes(Bailey & Echemendia, JINS, 2006)

• It is assumed that athletes are motivated to perform well on cognitive testing.

• Clinical experience suggests that effort and motivation may vary across athletes and test sequence.

• Virtually all athletes are motivated to perform well after concussion because of RTP.


• At baseline athlete performance may vary due to:

• Feeling threatened by testing • Feeling inconvenienced by the

testing• Apathetic or hostile to testing • May realize that lower baseline

performance MAY hasten RTP post injury.

Hypothetical example: Motivated vs. Unmotivated at Baseline

0

20

40

60

80

100

120

Motivated Unmotivated

Baseline2 hour48 hour1 Week

• 360 college athletes with MTBI• Baseline and one week post injury eval• Divided into two groups for each

measure: Suspect Motivation at Baseline (SMB)/High Motivation at Baseline (HMB)

• SMB 1 or more SD Below group mean on measure

• HMB 1 or more SD Above group mean


• True Score Adjustment was used to control for regression to the mean.

• RCI’s calculated using 80% CI• Groups divided into Improved, Declined &

No change from baseline.• Groups did not differ on baseline

demographic or concussion hx except that HMB had sig. higher SAT scores, which were then covaried.

• 2 (Motivation) x 2 (Evaluation) repeated measures ANCOVA (-SAT)


SDMT SMB 0 47 53

HMB 9 36 55

TMT-A*** SMB 0 13 87

HMB 0 81 19

TMT-B** SMB 0 39 61

HMB 0 87 13

COWA SMB 0 73 27

HMB 0 77 23

DST SMB 0 54 46

HMB 7 73 20

STROOP-W* SMB 56 31 13

HMB 14 86 0

STRP-CW* SMB 7 21 72

HMB 6 65 29

VIGIL* SMB 27 27 46

HMB 33 67 0

% Decline No Change Improve

Trail Making: Motivation by Test

Sequence

0

5

10

15

20

25

30

35

TSABaseline

1 Week

SMBHMB

0

10

20

30

40

50

60

70

TSABaseline

1 Week

SMBHMB

TMT-A TMT-B

CONCLUSIONS(Bailey & Echemendia, JINS, 2006)

• Athlete motivation is variable at baseline.

• Suggests improvement where none has occurred

• Some tests may be less susceptible to variable motivation than others. (e.g. Stroop-W).

• Clear need to develop and refine approaches to detect suspect motivation at baseline.

WHY ALL THE FUSS?

• 155 Participants: 77 athletes, 78 from human subjects pool

• Administered Word Memory Test (WMT) and ImPACT

• Only looked at Baseline performance

– (Schatz & Sucharski, ACN, 2006 [abstract])

What about Effort?

• Incidence of Poor Effort

Good (>95%) Poor (<95%) Athletes 48 (62.3%) 29 (37.7%) Non-athletes 43 (55.1%) 35 (44.9%) [X^2(1, N=155)=.831; p=.36]

What about Effort?

Good (>95%) Poor (<95%) F Sig. F SYMPTOM TOTA L 6.97 10.73 4.148 .043 (9.642) (13.394) VERBAL MEMORY .892 .831 15.689 .000 (.081) (.110) VISUAL MEMORY .767 .701 10.327 .002 (.127) (.126) PROCESS SPEED 42.676 38.128 17.063 .000 (5.871) (7.834) REACTION TIME .537 .562 4.120 .044 (.077) (.075) IMPULSE CTRL 8.912 10.922 .631 .428 (14.238) (17.151)

What about Effort?

• Given the wide-spread use of computer-based tests for the purpose of documenting baseline cognitive function in athletes, neuro-psychologists and sports-medicine professionals should utilize external measures of athletes' effort.

• Further, employing normal controls from human subjects pools may provide less accurate comparisons than desired.

What about Effort?

On Field Markers and Concussion Symptoms

• Echemendia et al (2001): NP testing better predictor of injury status at 24 hours.

• Collins et al. (2003): Amnesia, not LOC most predictive of severity at 3 days post MTBI

• Erlanger et al. (2003): Athletes w/ memory probs had more sxs, longer duration of sxs, and sig. dec in NP functioning.

• Collins et al. (2003): any HA sx at 1 week assoc w poor NP functioning and greater sx reporting. MTBI w HA at 7 days had many more PCS and dec NP functioning.

Does neuropsychological testing add any information over and

above self-reported symptoms?

Symptom Reporting

• McCrea et al. (2004): 47% of players did not report sxs assoc. w/ a blow because they did not think it sig., did not want to leave game, lack of awareness about MTBI.

• Guskiewicz et al. (2003) 1/3 of athletes who were not symptomatic during game developed sxs 3 hours afterward.

Participants

• 435 males at Penn State participating in football, hockey, soccer, baseball, basketball, and rugby.

• 280 athletes reported no history of mTBI.

• 155 athletes reported a history of at least one previous mTBI

Symptom reporting at the 2 hour, 48 hour, and 1 week assessments for concussed athletes with

and without a history of previous concussion (* = <. 05).

0

5

10

15

20

25

2 hour * 48 hour 1 week

hx prev. mTBIno prev. mTBI

(Bruce & Echemendia, 2005)

Symptom reporting at the 2 hour, 48 hour, and 1 week assessments for concussed athletes and

controls without a history of concussion (* = p < .05).

0

5

10

15

20

25

2 hour * 48 hour * 1 week

mTBIcontrol

(Bruce & Echemendia, 2005)

Initial Data Analyses: Injured vs. Controls(Echemendia, Putukian, Mackin, Julian & Shoss, 2001)

• 29 players who sustained mTBI• 43% football• 33% ice hockey• 10% men’s soccer• 10% men’s basketball• 4% women’s basketball

Initial Data Analyses: Injured vs. Controls(Echemendia, Putukian, Mackin, Julian & Shoss, 2001)

• 20 controls matched by sport, age, ethnicity

• Ethnicity of sample:• 82% Caucasian• 12% African American• 1.6% Latino• 4.4% unidentified

Normalized Scores at 2 hours Post Injury

80

85

90

95

100

105

110

115

120

PCS DSF HLI HDI HPR LLI

mTBIControl

Normalized Scores at 48 hours Post Injury

60

70

80

90

100

110

120

DSB HLI HDI HPR STROOP2

mTBIControl

Normalized Scores at 1 Week Post Injury

80

85

90

95

100

105

110

DSB Vg1AD Vg2O SDMT #C

mTBI

Control

“Value Added” of NP EvaluationVanKampen, Lovell, Pardini, et al., 2006 AJSM

• Pre-Post Design with ImPACT & PCCS

• College and HS athletes (Injured + age/educ Controls)

• Tested 48 hours post injury

• RCI comparisons for significant change

“Value Added” of NP EvaluationVanKampen, Lovell, Pardini, et al., 2006 AJSM

64% concussed had sig increase in PCCS

83% concussed had sig decrease in NP scores

19% increase in sensitivity

93% concussed had ABN NP OR sxs

30% controls had ABN NP or sxs

0% of controls had both ABN sxs and ABN NP

VALUE ADDED OF NEUROPSYCH TESTINGVALUE ADDED OF NEUROPSYCH TESTING

201 concussed High School and collegiate athletes tested with 2 days of injury. Abnormal performance determined by RCI’s (van Kampen, 2004).

NP testing increasesDiagnostic yield to88%

% DECLINEDFROM BL

SYMPTOMS

NEUROPSYCH

EITHER

88

82

65

50556065707580859095

100

“Value Added” of NP EvaluationFazio, Lovell, Pardini, et al., 2007 Neurorehabilitation

College & HS athletesImPACT & PCSS78 concussed & symptomatic, 44 concussed

but not sx, 70 noninjured controlsTested one week post concussion All composite scores (Verbal Memory, Visual

Memory, Proc Speed, Reaction Time) revealed:

Concussed sxs < Concussed not sxs < controls

Conflict of Interest in Sports Neuropsychology

• Financial interest in neuropsychological test products.

• Promotion of neuropsychological evaluations in sports viewed as “lining one’s pocket.”

• Sole presence on committees as the voice of neuropsychology.

• Failure to disclose financial interest in products on research publications or public/professional presentations.


• Implications for neuropsychology as a field• It’s OK to develop products, market them and

make money in the process, but BE CAREFUL.• All journals should require disclosure

statements from all authors.• Journals should require disclosure statements

from reviewers and exclude those where a conflict exists.

• Test developers must be very sensitive to not place themselves in positions where they are the sole representative of neuropsychology on committees, forums, etc. They must require representation by other neuropsychologists.


• Test developers must encourage and facilitate independent research with their product.

• Marketing of products should be independent of clinical interpretation of products.

• Training workshops for products should be conducted in “neutral” professional settings.

• Extensive interpretation guidelines, case examples, and documentation should be readily available.


• Test developers must be responsible in selling their product to qualified persons.

• Should athletic trainers be interpreting neuropsychological tests?

• Test developers must be responsible in dictating appropriate test administration conditions.

• Can athletes take tests unsupervised?

current controversies and issues in the assessment and management of sports-related concussion

Documents

diagnosis loc

injury loc

loc severe

loc mild pta5min loc

loss of consciousness

uncertain loc groups

indices of concussion

clin j sports med