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Sports Injuries

Summer  2000
Volume 11, Number 1

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The Concussed Athlete

Alan H. Weintraub, MD

Sports related brain injuries represent approximately 20% of the 1.5 million brain injuries estimated annually in the United States. Concussion, a term synonymous with “Mild Traumatic Brain Injury” (MTBI), is an alteration in mental status due to biomechanical forces affecting the brain which may or may not cause loss of consciousness. This article will provide an overview of the challenging problems facing clinicians responsible for the health of athletes in recognizing and appropriately managing concussion.

Definition and Neurobiology. “Mild” traumatic brain injury (MTBI) or concussion is becoming an increasingly recognized injury resulting from both contact and in some circumstances, non-contact sports.1, 2 The most widely accepted definition of concussion was originally proposed by the Congress of Neurological Surgeons in 1964. This stated “concussion is a clinical syndrome characterized by the immediate and transient post-traumatic impairment of neural function.” Therefore, trauma which leads to mental status alteration without a clear-cut loss of consciousness was considered a form of concussion.3 The distinction between these “milder” forms of brain injury and more serious injury is based on the absence or presence of disturbed consciousness including post-traumatic amnesia and other post-traumatic historical and physical findings. While MTBI can occur with direct trauma to the head during contact sports, it can also occur as a result of collisions or falls from all forms of athletic activity.4 This even includes events whereby sufficient force is applied in a so-called “whiplash mechanism.”5 In 1974, Gennarelli and Ommaya created an animal model of TBI. In this model, 3 of the 6 grades of concussion did not involve loss of consciousness. They demonstrated that brain injury can occur from angular or linear forces applied to the brain. Frequently, in human experiences both forces act together with a rotational component and are more likely to cause diffuse axonal injury associated with shearing forces affecting brain tissue. Most recently, it has been noted that axonal swelling and metabolic changes occur following these forces.

Following concussion, frequently there may be no objective neuroanatomic or physiologic measure which can be used to determine injury severity. Studies are under way to further define the pathophysiologic basis for why a seemingly mild insult may lead to an “injury – induced vulnerability and clinical symptomatology.” Experimental studies have demonstrated that for up to 3 days following a concussion or more severe cerebral insult, there is a reduction in cerebral blood flow which would normally be well-tolerated, but renders the brain susceptible to physiologic and anatomical neuronal cell loss.8

Although not entirely understood in terms of its underlying cellular mechanisms, experimental studies have identified following acute injury, a period of enhanced metabolic vulnerability.8 This consists of an increase in glucose metabolism and the relative reduction in cerebral blood flow rendering the brain in a state of metabolic induced cellular vulnerability. In experimental MTBI, this metabolic dysregulation may play a role in prognostication. Therefore, the “mis-match” between glucose demand and fuel availability is the key to future research correlating those cellular changes with clinical manifestations the athlete may be experiencing.

Medical Management of Concussion. There are a number of health concerns which need to be addressed at the time of a suspected concussion.9, 10 These include:

  1. Appropriate management of the injured athlete at the time of the injury to identify potential neurosurgical emergencies, ie, subdural, epidural, and intracerebral hemorrhages.
  2. Prevention of catastrophic outcomes related to a loss of central vascular auto-regulation from repeated concussion occurring over a short span of time – Second Impact Syndrome.
  3. Avoidance of cumulative cognitive deficits and chronic post-concussive somatic, behavioral and emotional symptomatology.
  4. Clinical decisions regarding return to play.
  5. Treatment considerations

Recognition and Acute Management. The early signs and symptoms of concussion (seconds to minutes) may include a brief disturbance of consciousness or a lack of awareness of surroundings, nausea, vomiting, headache, dizziness, or vertigo. Athletes on the field or sideline may display impaired attention manifested as a vacant stare, delays in response time, or the inability to focus. Additional deficits may include slurred or incoherent speech, uncoordination, disorientation, memory impairments, or emotional reactions out of proportion to the situation. Any observable or documented loss of consciousness should also be noted and may represent a more serious injury. Later signs of concussion (hours to days) may include persistent headache, dizziness/vertigo, diminished attention, concentration and memory, nausea or vomiting, fatigue, irritability, intolerance of loud noises or bright lights, anxiety and/or depression, and sleep disturbance. The “post-concussive syndrome” is when somatic, cognitive, and/or emotional deficits persist for weeks or months following injury.

It is recommended that all athletes suspected of having a concussion undergo an objective and quantifiable initial assessment which includes a mental status exam and neurological screen including exertional provocative measures.10 The Standardized Assessment of Concussion (SAC) (Table 1) was developed to establish a quantitative valid standardized systematic sideline evaluation for the immediate assessment of concussion in athletes.11 The Sideline Concussion Checklist (SCC-B) is a checklist that “provides a systematic and structured format for evaluating physiological, neurological, and cognitive effects associated with concussion.” It includes evaluation of pupil size, orientation, fine motor dexterity, coordination, symptoms, vision, gait, attention, concentration, memory, and exertional symptoms. It takes about 3 minutes to administer. The SCC-B is a checklist, not a scale, and has not been empirically validated. Close observation and serial reliable assessments of the injured athlete are critical to the prevention of serious or catastrophic complications and for the avoidance of cumulative, cognitive, emotional, or behavioral impairments.

Table 1. Sideline Evaluation
Mental Status Testing
Orientation: 
Time, place, person, and situation (circumstances of injury)
Concentration
Digits backward (ie, 3-1-7, 4-6-8-2, 5-3-0-7-4). Months of the year in reverse order.
Memory
Names of teams in prior contest.
Recall of 3 words and 3 objects at 0 and 5 minutes.
Recent newsworthy events.
Details of contest (plays, moves, strategies, etc.)
Exertional Provocative Tests:
40 yard sprint, 5 sit-ups, 5 knee-bends
Neurological Tests:
Strength
Coordination and agility
Sensation
Any appearance of associated symptoms is abnormal, eg, headaches, dizziness, nausea, unsteadiness, photophobia, blurred or double vision, emotional liability, or mental status changes.

The purpose of “concussion” grading systems are that one can reliably assess depth and duration of disturbed consciousness including post-traumatic amnesia in order to differentiate mild, moderate, and severe injuries. There have been more than 15 concussion grading systems utilized to assess the severity of an injury.3, 4, 10, 13, 14 It is the variability of presenting symptoms which complicates any grading system. Most grading systems are based on clinical observations. These grading systems have led to numerous anecdotal guidelines assessing injury severity and subsequent recommendations regarding return and/or exclusion from the sport. These recommendations should be seen as guidelines only rather than scientific fact. Despite concern regarding scientific validation of any specific classification system, the majority of clinicians are familiar with the Cantu Classification System,14 Colorado Guidelines or the Classification System endorsed by the American Academy of Neurology. (Table 2)14, 10 It is hoped that further research and validation of these guidelines will lead to more specific management and return to play recommendations.

Table 2. Concussion severity classifications.  

Grade 
Cantu Guidelines
Colorado Guidelines
AAN Guidelines
Grade 1 (mild) 
No LOC
PTA < 30 min 
Confusion without amnesia
No LOC 
Transient confusion, No LOC
Concussive symptoms resolve < 15 min
Grade 2  
(moderate) 
 
LOC < 5 min
PTA> 30 min  
Confusion with amnesia
No LOC
 Transient confusion, No LOC
Concussive symptoms last > 15 min
Grade 3 (severe) 
LOC > 5 min 
PTA > 24 hours 
LOC 
Any LOC either brief (seconds) or prolonged (minutes)
Table 2.  Adapted from Cantu, RC. Guidelines for return to contact sports after cerebral concussion. Phys Sportsmed. 14:75-83, 1986; Colorado Medical Society. Report of the Sports Medicine Committee: Guidelines for the Management of Concusussions in Sport. (revised). Denver: Colorado Medical Society, 1991; Report of the quality standards subcommittee. Practice Parameter: The management of concussion in sports (summary statement). Neurology, 1997: 48:581-

Prevention of Complications. The differential diagnosis and pathophysiology of concussion requires prompt recognition. It is important to rule out more severe neurosurgical injuries such as skull fracture, subdural or epidural hematoma or intracerebral hemorrhage.

The neuronal insult from concussion causes an acute increased demand for intracellular glucose and subsequently this is believed to alter the regulation of cerebral blood flow. These changes, resulting in a heightened metabolic vulnerability and must be recognized in avoidance of a catastrophic “second impact syndrome.”12 The Second Impact Syndrome (SIS) is felt to be caused by a loss of autoregulation of the vascular components of the brain. This “SIS” occurs when an athlete sustains a second brain or neuronal insult before recovering from the initial insult. This may result in massive cerebral edema over seconds to minutes resulting in permanent damage and/or death. It has been most reported in boxers and football players with the majority of cases reported in children and adolescence.6 The Malignant Brain Edema Syndrome 3,12 is also a poorly understood and rare condition that may occur in young children following a single brain trauma. The pathophysiology of this condition resembles SIS with the loss of vascular autoregulation and resultant diffuse brain hyperemia. In these situations there may be a rapid decline leading to coma and possibly death. Therefore, an athlete that has sustained a concussion should not be allowed to return to practice or competition while symptomatic or displaying ANY signs of concussion.1-3, 9, 10,13, 14

Seizures or “concussive convulsions” in collision sports are an uncommon but traumatic symptom following concussion.12 These concussive convulsions occur within seconds of impact and are not felt to be associated with structural brain injury. It is speculated that the concussive impact itself creates a transient functional decerebration akin to the cortico-medullary disassociation seen in convulsive syncopy. These players frequently have a good outcome and do not display any evidence of structural cerebral injury or long-term neuropsychological damage. Therefore, it is felt that these events are relatively benign, late seizures do not occur, and anti-epileptic therapy is not indicated. Also, there should not be necessarily a future prohibition from participating in collision sports and the overall management plan should center on the appropriate treatment of the concussion injury itself.3 

Assessment. Following the initial assessment of concussion, utilizing the SAC or SCC-B, a more detailed neuropsychological evaluation may be useful.6 Also a detailed neurological examination may be necessary. Follow-up neuroimaging studies may also be useful. Acutely, CT scans are more readily available and can detect bleeding or swelling that may require neurosurgical intervention. More sensitive MRI techniques may detect subtle anatomical and/or physiologic injury which may correlate with longer lasting post- concussive symptomatology and may help guide treatment.

Return to Play. Theoretically, acute return to play decisions should be based on the assumption that there is neurovascular intracerebral stability with re-establishment of normal chemical and ionic environments within the brain. Therefore, medical consensus is that any athlete who is continuing to experience signs or symptoms of concussion would preclude their ability to return to practice or competition. Controversy exists within the medical community regarding the theoretical or emperical guidelines and return to play decisions.15 The American Academy of Neurology has published “Return to Play Guidelines.”4,10 (Table 3) These guidelines should not be viewed as fixed standards of care and return to play decisions should be made on an individual basis.15

Table 3. Management of concussion in sports 

Grades of Concussion
Grade 1
  1. Transient confusion (inattention, inability to maintain a coherent stream of thought and carry out goal-directed movements)

  2. No loss of consciousness

Grade 2
  1. Transient confusion

  2. No loss of consciousness

  3. Concussion symptoms or mental status abnormalities (including amnesia) on examination last more than 15 minutes

Grade 3
  1.  Any loss of consciousness

a) Brief (seconds)

b) Prolonged (minutes)

Management Recommendations

Grade 1 

  1. Remove from contest

  2. Examine immediately and at 5-minute intervals for the development of mental status abnormalities or post-concussive symptoms at rest and with exertion

Grade 2 
  1. Remove from contest and disallow return that day

  2. Examine on-site frequently for signs of evolving intracranial pathology

  3. A trained person should re-examine the athlete the following day

  4. A physician should perform a neurologic examination to clear the athlete for return to play after one full asymptomatic week at rest and with exertion

Grade 3
  1. Transport the athlete from the field to the nearest emergency department by ambulance if still unconscious or if worrisome signs are detected (with cervical spine immobilization, if indicated)
  2. A thorough neurologic evaluation should be performed emergently, including appropriate neuroimaging procedures when indicated.
  3. Hospital admission is indicated if any signs of pathology are detected, or if the mental status of the athlete remains abnormal.

Treatment Considerations. The natural history of post concussion symptomatology is improvement over time.16 However, a small percentage of injured athletes may continue to complain of somatic, behavioral and/or emotional symptomatology lasting one or more years post injury.15 Repeated concussions can cause cumulative cognitive, emotional, and behavioral impairments.17

This may include impaired attention, concentration, memory, and slurred speech. Even when concussive events are separated by months or years, there may also be a stepwise decline in a person’s abilities. Symptoms may be evident even when no abnormalities are detectable on further detailed neurological exams. Also, an athlete with a history of concussion may also be more likely to suffer subsequent concussions compared to an athlete who has never had one, an area requiring further study.

Recent studies indicate that an early preventative model is effective in the management of MTBI.18 Education focused on the understanding and management of symptoms has been empirically demonstrated to reduce the number and duration of symptoms.17, 19 Early selective neuropsychological evaluation of attention, memory, information processing, and executive functioning provides a framework in the management of symptoms and structuring a gradual resumption of activities.6

It is also helpful to manage neuromedical and somatic symptoms of pain, headaches, cervicogenic and vestibular dysfunction, irritability, sleeplessness, and mood dysfunction. “Rational” pharmacotherapy and a brief program of goal specific rehabilitation services frequently are useful during the early recovery period.18 In our experience, pharmacologically stabilizing sleep induction and maintenance patterns with low dose SSRI’s or sedating tricyclic antidepressants have an immediate positive effect on symptom presentation.

For life reintegration issues, such as school and/or work, a program designed to gradually increase tolerance for cognitive demands and organized problem-solving strategies can be helpful.19 Since chronic dysfunction following MTBI is often accompanied by negative emotional sequelae, it is important to address secondary factors by teaching athletes to cope with symptoms, resume activities, and avoid over-dependence on the healthcare system.19

Summary. It is important to identify and educate others about optimal prevention of concussion in sports. Implementing sideline evaluations and treatment recommendations will help to prevent further morbidity and fatal injury including the second impact syndrome and persistent post-concussive symptomatology. Preventative tools include rule changes, and the further development of design changes in helmets and other protective equipment. Ongoing research regarding education, risk factors, and the early detection of concussion using reliable and valid assessment tools, such as the SAC and SCC-B, are crucial to further guideline improvement.

In order to make sports safer and increase awareness about sports related concussion, interdisciplinary efforts of medical personnel, trainers, coaches, officials, parents, and participants are necessary. This will ultimately allow young players to reach their fullest potential beyond sports and in life.

References

1. Wojtysem, Hovda D, Landry G, et al. Concussion in Sports. American Journal of Sports Medicine. 1999;27(5):676-686.
2. Sturmi JE, Smith C, Lombardo JA. Mild brain trauma in sports medicine. Sports Medicine. 1998; 25(6)351-358.
3 McCrory PR.Were you knocked out? A team physicians approach to initial concussion management. Medicine and Science in Sports and Exercise.1997;S207-S212.
4. Clark KS. Epidemiology of athletic head injury. Neurologic Athletic Head and Neck Injuries. 1998;17(1):1-11.
5. Yarnell P, Lynch S. The ‘ding’ amnestic state in football trauma. Neurology. 1973;23:196-197.
6. Erlang DM, Kutner KC, Barth JT, Barnes R. Neuropsychology of sports related head injury: Dementia pugilistica to post concussion syndrome. Clinical Neuropsychologist. 1999;13(2):193-209.
7. Dick RW. A summary of head and neck injuries in collegiate athletics utilizing the NCAA surveillance system. In: Hoerner EF, ed. Head and Neck Injuries in Sports. Philadelphia, PA; 1994.
8. Houda DA, Lehm, Lifshitz J, et al. Long-term changes in metabolic rates for glucose following mild, moderate and severe concussive head injuries in adult rats. J Neurosurg. 376A; 1995.
9. Kelly JP, Rosenberg JH. The development for the management of concussion in sports. J Head Trauma Rehabil. 1998;13(2):53-65.
10. Report of the Quality Standards Subcommittee: Practice Parameter: The Management of Concussion in Sports (Summary Statement). Neurology. 1997;48:581-585.
11. McCrea M, Kelly JP, Kluge J, Ackley B, Randolf C. Standardized Assessment of Concussion in Football Players. Neurology. 1997; 45:586-588.
12. Cantu RC. Second-impact Syndrome. Neurologic Head and Neck Injuries. 1998;17:137-43.
13. Cantu RC. Return to play guidelines after a head injury. Clinic Sports Medicine. 1998;17:45-60.
14. Cantu RC. Return to play guidelines after a head injury. Neurologic Athletic Head and Neck Injuries. 1998;17:145-160.
15. McCrory P. The eighth wonder of the world: The mythology of concussion management. British Journal Sports Medicine. 1999;33(2):136-137.
16. Levin HS, Mattis S, Ruff RM, et al. Neurobehavioral outcome following minor head injury: A three center Study. J Neurosurg. 1987;66:234-243.
17. Gronwall D. Cumulative and persisting effects of concussion on attention and cognition. In: Levin H, Eisenberg H, Benton A, eds. Mild Head Injury. New York, NY: Oxford University. 1989.
18. Wrightson P. Management of disability and rehabilitation services after mild head injury. In: Levin H, Eisenberg H, Benton A, eds. Mild Head Injury. New York, NY: Oxford University. 1989.
19. Gerber D, Berry J, Schraa J. Mild traumatic brain injury: Acute neurobehavioral treatment. CNI Review. 1997;8:23-27.
20. Kutner K, Barth J. Sport related head injury. The Bulletin of the National Academy of Neuropsychology. 1998;14(1):19-23.

 

Alan H. Weintraub, MD Alan H. Weintraub, MD is the Medical Director of the Brain Injury Program at Craig Hospital and Assistant Clinical Professor at the University of Colorado Health Sciences Center. Dr. Weintraub is presently the Medical Director for the Rocky Mountain Regional Brain Injury System, a federally designated Traumatic Brain Injury Model System of Care.
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Alan H. Weintraub, MD
Craig Hospital
3425 S. Clarkson Street
Englewood, CO 80113
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