[The Physician and Sportsmedicine]

[CASE REPORT]

Managing Successive Minor Head Injuries: Which Tests Guide Return to Play?

Margot Putukian, MD; Ruben J. Echemendia, PhD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 24 - NO. 11 - NOVEMBER 96

In Brief: This case report describes a female college basketball player who experienced brief loss of consciousness with hemiparesis after being struck in the jaw during a game. When she returned to play a month later, she sustained a second mild head injury, which resulted in persistent headache, cognitive difficulties, and reversal in hand dominance. She has since recovered fully. This case addresses return-to-play issues for the head-injured athlete, especially the risk of recurrent injury. It also illustrates the utility of neuropsychological testing when standard medical tests fail to detect any abnormalities.

A well-prepared protocol is key to the successful initial management and evaluation of an athlete who suffers a head injury. Head injury accounts for 19% of nonfatal injuries in football (1) and 4.5% of all high school sports injuries (2). Data on college athletes from 1984 through 1991 (National Collegiate Athletic Association Injury Surveillance System, Overland Park, Kansas) demonstrate that head concussions account for 1.8% to 4.5% of all injuries, with an injury rate of from 0.11 to 0.27 per 1,000 athlete exposures. Close follow-up of an athlete who sustains a head injury is crucial for proper management and, especially, the return-to-play decision.

The Initial Head Injury

Courtside evaluation. A 21-year-old right-handed college basketball player was struck during a game on the right side of her jaw as she was turning from left to right. She fell backwards, striking the ground with the back of her head. She was unconscious for about 20 seconds. Her pulse was regular; blood pressure and respiration were normal. Once conscious, she complained of occipital head pain. She had no neck pain, and no seizure activity was noted.

Gross exam on the court revealed mild anisocoria (right pupil larger than left), with an intact direct and consensual light response bilaterally. She had pain at the base of her occiput, but no pain along the cervical spine. She was unable to move her left upper extremity, but moved all other extremities; she did not have numbness, tingling, or weakness. Her airway and head were secured in the neutral position. She was placed on a backboard with cervical spine stabilization and taken to the emergency department via ambulance.

Her medical history was notable for a grade 1 concussion 2 years previously (no loss of consciousness, no retrograde or posttraumatic amnesia), which did not result in residual symptoms. After that concussion, she missed 3 days of play. She had no history of seizure disorder or migraine headaches. Family history was noncontributory. She said she did not use recreational drugs or drink alcohol. Her only medication was naproxen sodium for patellar tendinitis.

Emergency department testing. In the emergency department, her vital signs were stable. She was responsive with a Glasgow coma scale of 15. Though she had exact recall of how and where she had been struck, and she knew she was at the hospital, she did not remember the events in between. Her memory of specific events at the game, what she had eaten before the game, colors of the opponents' jerseys, and specific team plays was fragmentary. She recognized her team physician, could name other players on her team, and recalled certain pregame rituals. She could not perform calculations, but confessed that she usually "couldn't anyway." Questions such as "how many dimes in a dollar?" revealed that her factual knowledge was impaired. Her past and remote memory was intact using traditional assessment techniques, though she was slow to answer questions.

Battle's sign was negative. Her extraocular movements were intact, yet she continued to have very mild anisocoria (which, by her report, represents her baseline but had not been previously documented). Her funduscopic exam was normal. She did not have hematotympanum, "raccoon eyes," or cerebrospinal fluid rhinorrhea. Her cervical spine was not tender. She could not move her left upper extremity and had weakness with resisted left hip flexion and left knee extension. Otherwise, her strength testing was 5/5.

Her sensory examination was normal to light touch and pin prick except in the left upper extremity. Her deep tendon reflexes were 3+, symmetrical throughout. Babinski's reflexes were downgoing; she had minimal clonus. Cerebellar examination (finger to nose on the right, heel to shin bilaterally) was intact.

Hospital observation. She was admitted to the hospital for observation as well as additional diagnostic testing. Plain films of her head and cervical spine and emergent computed tomography (CT) scan of her head and cervical spine were all normal without evidence of fracture, instability, or central nervous system bleeding.

Five hours after her injury, her strength and sensory exam returned to normal, though she said her left arm "didn't feel right." Her deep tendon reflexes returned to 2+ symmetrically, and clonus resolved.

The following morning her left upper extremity felt normal, and her only complaint was general fatigue and a dull occipital headache. An electroencephalogram (EEG) and magnetic resonance imaging (MRI) of the head and cervical spine were normal. Her neurologic examination was normal, including full motor and sensory function of her upper and lower extremities. She was unsteady with tandem gait testing and could not stand with eyes closed without losing her balance. She continued to have some posttraumatic and retrograde amnesia. Two days after the initial injury, a magnetic resonance angiogram of the circle of Willis was normal. She was discharged 2 days after her injury.

Outpatient follow-up. She was seen daily and, after several days, her physical examination returned to normal. She returned to classes and had no significant physical difficulties. For approximately 1 week, she complained of a persistent headache (2/10 in intensity) that was frontal, dull, constant, without radiation or precipitants, and occasionally associated with mild nausea. She was able, however, to continue with activities of daily living, including attending classes.

About 2 1/2 weeks after her initial injury (after being asymptomatic for 1 1/2 weeks), she was allowed gentle cardiovascular activity as an "exercise challenge." This permitted an evaluation as to whether increasing heart rate and blood pressure alone would reproduce or provoke symptoms. After exercising on a stationary bicycle for 20 minutes, she had no adverse exertional symptoms; thus, the following day she was allowed to increase the intensity and duration of this noncontact activity. She was then allowed to participate in noncontact sport-specific activities such as shooting and dribbling. She complained that she felt "out of shape," but reported no headache and overall felt well. At 3 1/2 weeks she participated in contact practice activity, and then after 1 month, full competitive play.

Emergency Management

The athlete's immediate hemiparesis can be explained by the direct blow and trauma to the right motor and premotor cortex. Because of her anisocoria and left upper-extremity flaccidity, initial concern was for intracranial bleeding, with or without skull fracture, or cervical spine injury. Her lower-extremity findings of weakness made cervical plexopathy a less likely cause of her symptoms. The differential diagnosis also included rupture of a cerebral aneurysm or subarachnoid hemorrhage. These concerns were addressed by following the protocol for transporting a patient with a possible cervical spine injury.

Emergency studies excluded both an aneurysm and an occipital fracture associated with subdural or epidural hematoma. Despite significant physical findings, follow-up studies confirmed the lack of significant bleeding or fracture. With these test findings, we felt sure that our patient did not have a predisposition to injury due to a vascular malformation, or a contraindication to return to sport based on a structural problem such as a subdural or epidural hematoma. Her working diagnosis was a grade 3 concussion.

Determining the severity of memory deficit can be challenging, but it is very important in assessing the severity of injury in head concussions. The use of standard measures of memory such as the date, athlete's name, and location are helpful. The presence of a teammate or coach who knows specific plays or personal information can be very useful and may allow for a more sensitive measure of information-handling deficits.

Return to Play?

The many factors to consider in return-to-play decisions begin with the physical examination and subjective complaints. The injury to this young basketball player was considered severe given the loss of consciousness and coexisting deficits in memory and left upper-extremity strength. At the time the athlete first returned to cardiovascular activity, she had been asymptomatic for 1 1/2 weeks and had a normal physical examination. In addition, a history of head injury and temporal relation are important. Our athlete had sustained one minor head injury 2 years earlier with no sequelae. Finally, the athlete's own feeling regarding return to play needs to be considered. Our athlete had no apprehension about returning to play.

The patient was kept out of competition for a full 4 weeks on the basis of the injury severity, her medical history, her physical examination, and return-to-play guidelines. Once she had successfully progressed through increased activity levels, she was allowed to return to play.

There are several classification systems for head injury; most also include return-to-play guidelines (3-6). Most classification systems use loss of consciousness, presence of retrograde and/or posttraumatic amnesia, and symptoms or other physical findings as a way to grade an injury. Given her presentation and symptoms, this athlete's head injury would be classified as a Torg grade 4, a Nelson 3, a Cantu 1, or Colorado Medical Society 3.

Though return-to-play guidelines are not based on long-term prospective data, and thus remain guidelines, they are useful (see "Guidelines for Managing Concussion in Sports: A Persistent Headache," October 1996). No matter what classification system is embraced, the physician needs to make sure that athletic trainers and other medical staff understand the grading system being used. While each system is different and each has its own merit, the choice of a particular system is not as important as using one system consistently and not interchanging systems. Given the variations among these systems, the use of descriptive terms such as loss of consciousness and retrograde or posttraumatic amnesia along with a description of specific symptoms or physical findings is often more helpful than a grade.

A Second Head Injury

On her second day back in competitive play, the athlete was again struck on the right side of her head. She held her head, then stumbled to the ground. She did not lose consciousness, but immediately complained of right-sided tinnitus, headache, dizziness, and nausea, which increased over the next hour. She did not have retrograde or posttraumatic amnesia. Because of increasing tinnitus, nausea, and headache, she was transferred to a hospital, where an emergency CT scan was normal. Over the next several hours, all her symptoms except mild headache slowly resolved.

Over the subsequent week, the patient's mild headache persisted. She expressed concern about the risk of reinjury: "Each time I got hit I lost something, and though I get it all back, I'm afraid that if I get hit again, it might not all come back." Given the athlete's recurrent injury, medical history, persistent symptoms, and apprehension regarding return to activity, a decision was made to pursue a medical waiver for the rest of the season.

She continued to have persistent headaches for about a month. She complained of slow reading, general "slowness," "zoning out" in class, and difficulty naming familiar faces and objects. She also reported unusual use of her nondominant hand: carrying objects and reaching with her left hand for doors and for chalk to write on the chalkboard.

Shortly after her second injury (2 1/2 months after her initial injury), she underwent neuropsychological testing, which evaluated her concentration, intellectual functioning, memory, attention, and learning (table 1). With her permission, previous Scholastic Aptitude Test (SAT) scores and intelligence tests were obtained, which provided the only available baseline neuropsychological information. Her initial battery of neuropsychological testing reflected a modest decrease from her premorbid functioning. Her retention of verbal and visual information was significantly below average, and she had significant word-finding difficulties based on the Boston Naming Test. Tests that assessed higher-order cognitive skills (Category, Wisconsin Card Sort, Tactual Performance Test, Trails B) were essentially normal. Motor tests revealed a reversal in expected hand dominance: Her left hand was superior in speed, strength, and agility.


Table 1. Tests and Variables Measured in the Neuropsychological Assessment Battery for a 21-Year-Old Female Basketball Player Who Sustained Two Head Injuries

Initial Battery (2 1/2 Mo After First Injury, Shortly After Second Injury)

Test Variable(s) Measured

Boston Naming Test Word finding
Category Test Hypothesis testing, problem solving
Finger tapping Finger speed
Grooved pegboard Fine motor (digital) coordination/speed
Hand dynamometer Upper-extremity strength
Memory Assessment Scale (list acquisition, recall, delayed recall) Broad memory assessment
Sensory-Perceptual Exam Sensory stimulation/suppression
Tactual Performance Test Complex visual/spatial problem solving, visual/spatial memory
Trail Making Test (Trails A and B) Simple and complex visual sequencing, visual scanning
Visual Search and Attention Task (VSAT) Visual attention, visual scanning
Wechsler Adult Intelligence Scale-Revised (WAIS-R) General intellectual functioning
Wisconsin Card Sort Cognitive flexibility, perseveration, problem solving

Follow-up Battery (9 Mo after First Injury)

Test Variable(s) Measured

List learning Verbal learning
Paced Auditory Serial Attention Test Complex test of auditory attention/concentration
VIGIL/W Continuous Performance Test Reaction time
Symbol Digit Modalities Test Complex scanning and visual tracking
Boston Naming Test
Category Test
Finger tapping
Grooved pegboard
Hand dynamometer
Memory Assessment Scale
Tactual Performance Test
Trail Making Test
VSAT
WAIS-R

About 7 months after her initial injury, she started cardiovascular training. She developed occasional headaches similar to her previous postinjury headaches, which exertion often exacerbated. Initial treatment was symptomatic: She was given naproxen and/or acetaminophen and decreased her exercise intensity when the headaches were severe. When they became almost daily, she was placed on nortriptyline hydrochloride, which prevented the headaches, but made her somewhat sleepy and was eventually discontinued. She had no other significant complications. She returned to competitive off-season basketball 7 1/2 months after her initial injury. Her headaches eventually decreased in frequency and severity, occurring only about once every 3 weeks.

On return to campus 9 months after her injury, neuropsychological tests were repeated, and she demonstrated improvement. Her general fund of knowledge remained below average, but did improve. Moderate-to-severe impairment remained in long-term memory of visually presented stimuli (Boston Naming Test). All higher-order cognitive tests improved. Right-hand dominance was apparent on repeat testing.

The player is currently back playing competitive Division I basketball and doing very well. She has not had any recurrent injury, and has not been bothered by significant headaches. She prefers to "play through" occasional headaches she does have, rather than take medication.

Factors in a Second Return to Play

The athlete's persistent deficits are most likely explained by a contrecoup injury to the left hemisphere, in which the brain rebounded against the inner surface of the skull opposite where her head had been hit. Because standard medical tests didn't define any abnormality, this is based on her injury mechanism as well as the abnormalities seen and her neuropsychological testing. Probably the most important factors in the decision to keep her out for the remainder of the season were the successive nature and severity of her injuries and her apprehension regarding return to play.

The risk of recurrent head injury and second impact syndrome (7) is very important to discuss with the athlete, coach, and parents. An athlete who has had a concussion is at a greater risk of incurring a second concussion than an athlete who has not had such a previous injury (1). This risk for recurrent head injury is difficult to estimate; however, as time passes, the risk does diminish.

In second impact syndrome, an individual who sustains a mild head injury when symptoms from a prior concussion are still present can incur fatal brain swelling. Return-to-play guidelines attempt to diminish these risks by taking into account injury severity, and not allowing an athlete to return to competition if symptoms are present. If a cardiovascular challenge alone can reproduce symptoms, return to contact play should not be permitted.

Neuropsychological tests demonstrated deficits that, for the most part, improved after 9 months. Despite persisting abnormalities on some of these tests, the athlete was allowed to return to activities. Because we did not have baseline neuropsychological tests, we were not sure if her testing could justifiably be used to exclude participation. We chose to follow standard guidelines and, after a lengthy discussion with her, allowed her to return.

Postconcussion Issues

Headaches are a common sequela of mild head injury (1,8-12). They can be difficult to treat, especially if they become severe or daily, and can interfere not only with competition, but also with daily functioning. Unfortunately, postconcussive headache is often difficult to differentiate from trauma-induced migraine, though the presence or absence of neurologic impairment can provide a clue. Trauma-induced migraine, or "footballer's migraine," is a typical migrainelike headache that occurs after subtle head trauma and is associated with no other neurologic symptoms. Whether exertional headaches are a form of postconcussive syndrome is uncertain.

Choosing appropriate medication for an athlete who has postconcussive headaches is also difficult: Beta blockers or calcium channel blockers can be difficult to use because they may impair cardiovascular performance. Interestingly, whether or not they demonstrably harm performance, the potential effect was enough in our situation to preclude their use. Our athlete did not want to try any medication that might blunt her cardiovascular response.

Fortunately, our athlete did not display other complications of minor head injury, such as posttraumatic seizures, skull fracture, or associated cervical spine injury. These often accompany head injury and should be looked for. She did, however, demonstrate symptoms of postconcussive syndrome, which include not only headaches, but also an inability to concentrate, easy fatigue, and irritability. Neuropsychological assessment has shown that as many as half of individuals who sustain head injury have such difficulties 3 months or more after their injury (12-14). Attention to such complications is extremely important, especially in a student-athlete or working person.

The patient's apparent reversal in hand dominance during the initial battery of neuropsychological testing was an unexpected finding. Without baseline testing, it at first appeared possible that she might have been equally strong and quick with both hands as a result of her basketball training. The change to right-hand dominance on the second evaluation suggests that the patient did indeed experience a reversal of handedness because of the central nervous system injury.

Though CT scanning, MRI, and EEG reveal abnormalities with head injuries (11,15-19), they may not always detect deficits associated with the mild head injuries that are typical in athletic competition. Neuropsychological tests, however, can be very useful in the assessment and recovery phases of sports head injuries when the patient has any suspected cognitive changes (12,20-24). In this case, the areas of abnormality on neuropsychological testing corresponded well to the patient's injury and to her self-reported difficulties. They were useful not only in detecting subtle deficits, but in demonstrating a slow but steady improvement in functioning back to a predicted baseline level.

Having baseline neuropsychological data available with which to make comparisons could have helped clarify whether persistent deficits in word finding had been present premorbidly or represented postconcussive sequelae. As neuropsychological test batteries become more streamlined and specific to athletic competition, their usefulness for preparticipation physical examinations will be established (25).

More Sensitive Testing

This case demonstrates the complexity of assessing and following the head-injured athlete. Close follow-up and evaluation of the athlete are essential, and decisions regarding return to play are difficult. The use of traditional diagnostic testing, such as CT, EEG, or MRI, is useful in ruling out significant structural injury such as skull fracture or intracranial bleeding but may not reveal subtle abnormalities in neurologic functioning. Neuropsychological testing can provide a sensitive assessment of neurologic function as well as demonstrate improvement over time. These tests may also provide additional prognostic information to the physician and may become more useful in the future for assessment of athletes who sustain head injuries.

References

  1. Gerberich SG, Priest JD, Boen JR, et al: Concussion incidences and severity in secondary school varsity football players. Am J Public Health 1983;73(12): 1370-1375
  2. Garrick JG, Requa R: Medical care and injury surveillance in the high school setting. Phys Sportsmed 1981;9(2):115-120
  3. Cantu RC, Micheli LJ (eds): American College of Sports Medicine's Guidelines for the Team Physician, Philadelphia, Lea & Febiger, 1991
  4. Colorado Medical Society Sports Medicine Committee: Guidelines for the Management of Concussion in Sports. Denver, Colorado Medical Society, 1991
  5. Nelson WE, Jane JA, Gieck JH: Minor head injury in sports: a new system of classification and management. Phys Sportsmed 1984;12(3):103-107
  6. Torg JS (ed): Athletic Injuries to the Head, Neck, and Face, ed 2. St Louis, Mosby-Year Book, 1991
  7. Saunders RL, Harbaugh RE: The second impact in catastrophic contact-sports head trauma. JAMA 1984;252(4):538-539
  8. Gronwall D, Wrightson P: Delayed recovery of intellectual function after minor head injury. Lancet 1974;2(7881):605-609
  9. Henderson JM, Browning DG: Head trauma in young athletes. Medi Clin North Am 1994;78(2):289-303
  10. Jordan BD, Zimmerman RD: Computed tomography and magnetic resonance imaging comparisons in boxers. JAMA 1990;263(12):1670-1674
  11. Jordan BD: Head injury in sports, in Jordan BD, Tsairis P, Warren RF (eds): Sports Neurology. Rockville, MD, Aspen Publishers, 1989
  12. Rimel RW, Giordani B, Barth JT, et al: Disability caused by minor head injury. Neurosurg 1981;9(3): 221-228
  13. Levin HS, Lippold SC, Goldman A, et al: Neurobehavioral functioning and magnetic resonance imaging findings in young boxers. J Neurosurg 1987: 67(5);657-667
  14. Levin HS, Mattis S, Ruff RM, et al: Neurobehavioral outcome following minor head injury: a three-center study. J Neurosurg 1987;66(2):234-243
  15. Borczuk P: Predictors of intracranial injury in patients with mild head trauma. Ann Emerg Med 1995; 25(6):731-736
  16. Davis RL, Mullen N, Makela M, et al: Cranial computed tomography scans in children after minimal head injury with loss of consciousness. Ann Emerg Med 1994;24(4):640-645
  17. Hoffman JR: CT for head trauma in children. Ann Emerg Med 1994;24(4):713-714
  18. Lampert PW, Hardman JM: Morphological changes in brains of boxers. JAMA 1984;251(20):2676-2679
  19. Tysvaer AT, Storli OV, Bachen NI: Soccer injuries to the brain: a neurologic and electroencephalographic study of former players. Acta Neurol Scand 1989; 80(2):151-156
  20. Abreau F, Templer DI, Schuyler BA, et al: Neuropsychological assessment of soccer players. Neuropsych 1990;4(3):175-181
  21. Alves WM, Rimel RW, Nelson WE: University of Virginia prospective study of football-induced minor head injury: status report. Clin Sports Med 1987;6 (1):211-218
  22. Levin HS, Amparo E, Eisenberg HM, et al: Magnetic resonance imaging and computerized tomography in relation to the neurobehavioral sequelae of mild and moderate head injuries. J Neurosurg 1987;66(5):706-713
  23. Rimel RW, Giordani B, Barth JT, et al: Moderate head injury: completing the clinical spectrum of brain trauma. Neurosurg 1982;11(3):344-351
  24. Tysvaer AT, Lochen EA: Soccer injuries to the brain; a neuropsychologic study of former soccer players. Am J Sports Med 1991;19(1):56-60
  25. Echemendia RJ, Putukian M, Julian L, et al: The Penn State Concussion Program preliminary test data. Read before the annual meeting of the American Psychological Association, Aug 1996, Toronto

Dr Putukian is team physician and assistant professor of internal medicine, orthopedics, and rehabilitation and Dr Echemendia is director of The Psychological Clinic and associate professor of psychology at The Pennsylvania State University in University Park, Pennsylvania. Dr Putukian is a fellow of the American College of Sports Medicine. Address letters to Margot Putukian, MD, Hershey Medical Center for Sports Medicine, 1850 E Park Ave, Suite 112, University Park, PA 16803; e-mail to [email protected]


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