How To Treat A Concussion

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1 Concussion: Definition, Diagnosis, and Management Guy Monteleone, M.D. Division of Sports Medicine Dept of Family Medicine West Virginia University School of Medicine Clinical Case You are the physician are covering the High School State football semi-finals. Near the end of the game, you notice a wide receiver being driven head first into the turf after catching the ball. You immediately go out on the field, and the athlete is conscious, Glasgow Coma Scale of 14, and confused. He is not alert to his name, place, date, score. He is unable to perform serial 7 s or serial 3 s. His gross neurological exam including cranial nerves is nonfocal and he moves all extremities. He complains of pain at his right parietal/occipital area and cervical paraspinal musculature on the right He is able to get up with assistance and is pronounced winner by default. You escort him to the training room to finish your motor, sensory, and cerebellar examination and find them normal. Your serial exams at 5, 10, and 15 minutes are unchanged. Finally, at 20 minutes he turns the corner, being able to recite the above and complains only of a headache. By this time, you realize that the team has won the game and is going to the state championships next week. * How do you manage him? When can he compete again? A. Introduction At the turn of the century in 1904, approximately 19 athletes were either killed or paralyzed from playing football. President Theodore Roosevelt became so infuriated that he initiated the formation of the National Collegiate Athletic Association in hopes of developing a governing body which would set rules up in athletics for safer competition. Despite the many years and hard work of the NCAA, fatalities at all levels in football peaked in 1964 at 30, most related to head and neck injuries. Since then, there s been a downward trend in those injuries mainly due to the implementation of rule changes, protective-equipment improvements, and coaching techniques. B. Definitions There are many definitions proposed for concussion. One that has gained some degree of acceptance was put forth by the Committee on Head Injury Nomenclature of the Neurological Surgeons in 1966: A concussion is a clinical syndrome characterized by immediate and transient post-traumatic impairment of neural functions, such as alterations of consciousness, disturbance of vision, equilibrium, etc. due to brain stem involvement. The hallmarks are confusion and amnesia. It represents an interruption of neurochemical and electrical function of the cortex and brainstem. It is a diffuse injury in contrast to hematomas (subdural, epidural or intracerebral).

2 C. Epidemiology Approximately 1.5 million HS and college FB players/year. General incidence is 300,00/year in the US Generally occurs in American Football during tackling or blocking: o Making tackle 45% o Being tackled 25 o Blocking 20 o Being blocked 10 There is some data to suggest that athletes who suffer a second concussion demonstrate significant and sustained changes on neuropsych tests. These effects may be cumulative. Sports specific incidence o Ice hockey 12% o Football 8 o Soccer 5 o Boxing Professional 6.5; Amateur 5% Many contact sports make the athlete susceptible to head injuries such as high impact like football, hockey, boxing as well as other sports like snow skiing, basketball, and baseball. D. Pathophysiology The most common head injury is the mild variety also known as a concussion. The athlete will display very brief periods of neurologic dysfunction such as confusion and posttraumatic amnesia. The usual mechanism for a closed head injury is a sudden acceleration or deceleration of the head from a blow that deforms the skull. These can result in a sudden dysfunction in the neurons of the brainstem s reticular activating system. Some experimental concussion modules have shown transient cerebral ischemia, edema, widespread depolarization from the release of acetylcholine, and shearing of neurons and nerve fibers. Also, scattered capillary damage can be seen in the various parts of the brain including the reticular activating system and the superficial portion of the cerebral cortex. E. Classification/Grading Many proposed classification systems (more than 17 in the literature). The Boards will usually give a clinical case and ask according to a specific classification system, what the treatment, return to play issues, etc would be. The American Academy of Neurology (AAN) submitted their classification system 1997, hoping to have one universally accepted scheme which according to them, is essential to the advancement of research into the incidence and complications associated with concussions. Since no gross pathological changes are consistently demonstrated in experimental concussion, the classifications used are primarily on the basis of clinical presentation, namely the degree of confusion present, duration of amnesia, and the presence/absence of loss of consciousness. Three of the most commonly used classification systems are listed below:

3 Cantu 1992, 2001 Colorado Medical Society NCAA endorsed American Academy of Neurology 1997 Grade I (mild) No LOC, PTA<30 min No LOC, Confusion without amnesia Grade II (moderate) LOC < 5 min or PTA >30 min No LOC, Confusion with amnesia No LOC, transient confusion, duration of mental status abnormalities <15 min No LOC, transient confusion, duration of mental status abnormalities > 15 min Grade III (severe) LOC >5 min or PTA >24 hours LOC LOC, brief (sec) or prolonged (min) LOC: loss of consciousness, PTA: post-traumatic amnesia F. Evaluation/Management Any athlete who receives a blow to the head or any significant acceleration-deceleration type force should be evaluated for a possible head injury. If an on-the-field evaluation is required on an athlete that doesn t awaken readily after a blow to the head, the physician should be suspicious of a serious head injury. In that case the initial assessment involves the ABC s of cardiopulmonary resuscitation while immobilizing the cervical spine. The differential diagnosis includes spinal cord injury, cerebral contusion, intracranial hemorrhage, epidural hematoma, subdural hematoma, and intracerebral hematoma. The evaluation should be brief but thorough. The first thing to establish is whether the athlete is conscious or unconscious. Remember, it s not recommended to remove the athlete s helmet or shoulder pads. An airway can be obtained by removing the face mask. The best way to secure the airway if needed is by the jaw-thrust maneuver. Any athlete unconscious should be suspected for c-spine injury. All athletes suspicious for c-spine injuries should be placed on a backboard with the c-spine immobilized. If the player is face down, he must be brought face-up by a log-roll technique. The conscious athlete can be evaluated with a cursory neurological exam on the field. The conscious athlete who is breathing spontaneously, but complains of focal neck pain, paralysis or paresis of bilateral extremities, one should suspect a c-spine injury. Initial questioning should be looking for those symptoms suggestive of a concussion (headache, dizziness/vertigo, nausea, confusion, disorientation, blurred/double vision, photophobia, tinnitus). The typical exam includes the orientation (place-school, name, date), memory (immediate: object recall, score, pre-game meal; short-term: repeat three words; long-term: place/date of birth), concentration (months of year in reverse, serial 7's), gross neuro including cerebellar ( cranial nerves, motor strength, reflexes, sensory:: finger-to-nose, heel-toe walking, Romberg). A concussed athlete will typically display that glassy-eyed dazed and confused look. The athlete should be monitored on the sidelines and serially evaluated every 15 minutes looking for any worsening of the neurological status. The guidelines on return to play will be discussed later. G. Imaging

4 An athlete that is suspected for a serious head injury (Grade III concussion, c-spine injury, intracranial bleed) or one with a mild/moderate concussion with signs of neurological insult should be transported to an emergency facility immediately. These signs may include impairment of consciousness as shown by a change in mental status, decreased motor activity, change in vital signs i.e. ventilation pattern, increased blood pressure, or decreasing pulse rate, seizures, and pupil inequality. The neuro imaging studies that are most likely to define neuroanatomic changes are MRI and CT of the brain. CT is useful for documenting bleeding and swelling, especially in the acute situation. MRI is more sensitive to traumatic brain injuries detecting hemorrhagic and non hemorrhagic lesions (especially in the inferior frontal lobe and temporal lobe), anatomical abnormalities, and any lesion that has persisted for more than 10 days. Either way imaging should be considered when: a) worsening subjective symptoms (headache, nausea, tinnitus, etc) b) progression of focal neurological deficits c) any initial grade 3 concussion d) recurrent grade 2 or grade 3 concussions H. Return to Play Colorado Medical Society Severity Signs/Sx 1 st Concussion 2 nd Concussion 3 rd Concussion Grade 1 (mild) Confusion, No LOC RTP if no sx at least 20 min Terminate game, RTP if no sx for 1 week 3 months if no sx Grade 2 (moderate) Confusion with amnesia, No LOC Terminate game, RTP if ASx for 1 week Consider terminate season, but consider RTP if no sx for 1 month next season if no sx Grade 3 (severe) LOC Terminate game, transport to ER, RTP 1 month after 2 weeks with no sx, ok to condition after 1 ASx week next season if no sx Terminate season, highly recommend avoidance of contact/collision sports Cantu Severity Signs/Sx 1 st Concussion 2 nd Concussion 3 rd Concussion Grade 1 (mild) No LOC, PTA <30 min RTP if no sx RTP in 2 weeks if no sx for 1 week next season if no sx Grade 2 (moderate) LOC < 5 min or PTA > 30 min RTP if no sx for 1 week 1 month restriction, RTP if no sx for 1 week, consider terminating season Terminate season, may RTP next year if no sx Grade 3 (severe) LOC > 5 min or PTA 1 month restriction, RTP if no sx for 1 week next year if no sx

5 American Academy of Neurology Severity Signs/Sx 1 st Concussion 2 nd Concussion 3 rd Concussion Grade 1 (mild) No LOC, confusion, mental status abnl < 15 min Removal from competition, exam q 5 min, RTP same day if post-concussive sx resolve within 15 min Incurring a 2 nd concussion on the same day, RTP when no sx for 1 week Grade 2 (moderate) No LOC, transient confusion, mental status abnl > 15 min Removal from competition, if sx worsen or persist > 1 week, then extensive diagnostic testing. RTP when no sx for 1 week Incurring a Grade 2 concussion subsequent to a Grade 1 concussion on the same day, then restrict from competition until no sx for 2 weeks Grade 3 (severe) LOC, brief (sec) or prolonged (min+) Brief: RTP when ASx for 1 week Prolonged: RTP when ASx for 2 weeks Prolonged LOC or abnormal neurologic signs on initial exam: Transport to ER. No sports activity until ASx for 1 month Any athlete with abnormality on CT or MRI (swelling, contusion, or any other intracranial pathology) no RTP that season and strongly discouraged from future participation in contact sports sx: symptoms, RTP: return to play, LOC: loss of consciousness, PTA: post-traumatic amnesia, abnl: abnormal Key Points: 1) The overwhelming majority (> 90%) of concussions are mild. 2) If an athlete has sustained a concussion, he/she should not return to competition if they are still symptomatic (at rest and with exercise). 3) Monitor the athlete with serial neurological exams on the sidelines, after the game, and by a friend or family member at the home setting. 4) Communicate and educate the player, coaches, and parents about what is a concussion. The phrase head injury can be a scary term and encompass many entities. 5) Most authors agree that all athletes with loss of consciousness should be evaluated at medical center, with consideration of imaging. 6) Evidence-based medicine is changing the way we view concussion evaluation, treatment and return to play issues (McKeag, Lovell and McCrea). Specifically, evidence exists suggesting that brief loss of consciousness may not be the predictor of poor outcomes that

6 clinicians have historically presumed. I. Post-Concussive Syndrome This syndrome usually consists of a variety of symptoms that follow an episode of cerebral concussion. Headache, dizziness, irritability, and impaired memory and concentration are the most common entities. The persistence of symptoms is thought to be due to altered neurotransmitter function. If symptoms persist, a CT or MRI and neuropsychiatric tests can be performed. When to obtain testing is hotly debated. As stated before, return to competition can be allowed when all symptoms have resolved. J. Second-Impact Syndrome (SIS) Originally described by Schneider in 1973 and Saunders and Harbaugh in 1984 as the second-impact syndrome of catastrophic head injury. The syndrome occurs when an athlete sustains a head injury such as a concussion or cerebral contusion, then sustains a second head injury before the symptoms from the first have cleared. The symptoms as already described are headache, visual, auditory, or memory problems. The second head injury can be relatively minor, perhaps a blow to the chest which causes the athlete s head to jerk back and forth. In contrast to a concussion the athlete will remain stunned and may finish the play, but will suddenly collapse to the ground and be semi-conscious with dilating pupils and progressive cardiorespiratory failure. The pathophysiology involves a loss of autoregulation of the vascular system in the brain. This leads to massive cerebral edema and increased intracranial pressure, herniation of the temporal lobe through the foramen magnum, and respiratory failure. The usual time from SIS to respiratory failure is estimated to be 2 to 5 minutes. Animal studies performed by Moody and Ruamsuke showed that brain edema is very difficult to treat. The primary aim of treatment is prevention. From the National Center for Catastrophic Sports Injury Research Foundation, they have reported that from 1980 to 1993, there were 35 cases of SIS among American football players alone. Therefore, following the grading/classification systems as above in addition to education of the coaches, players, and parents may help to prevent future cases of SIS.

7 REFERENCES Alves WM, Polin RS: Sports-Related Head Injury. Narayan RK, Wilberger JE Jr, Povlishcok JT: Neurotrauma. New York, McGraw-Hill, 1996, p913 Buckley WE: Concussions in college football. Am J Sports Med 16:1, 1988 Cantu RC: Second-Impact Syndrome. Clin Sports Med 17:1, 37-44, 1998 Cantu RC: Return to Play Guidelines After a Head Injury. Clin Sports Med 17:1, 45-60, 1998 Clarke KS: Epidemiology of Athletic Head Injury. Clin Sports Med 17:1, 1-12, 1998 Collins MW, Lovell MR, McKeag DB. Current issues in managing sports-related concussion. J Am Med Assoc. 282(24): , 1999 Gentry LR, Godersky JC, Thompson B, et al: Prospective comparative study of intermediate field MR and CT in the evaluation of closed head trauma. Am J Neuroradiol 150: 673, 1988 Guskiewicz KM, McCrea M, Marshall SW, et al. Cumulative effects associated with recurrent concussion in collegiate football players. J Am Med Assoc. 290(19): , Kelly JP, Rosenberg JH: Diagnosis and management of concussion in sports. Neurology 48: , 1997 Kissick J, Johnston KM. Return to play after concussion: principles and practice. Clin J Sports Med. 15(6): 42631, Lehman LB, Ravich SJ. Closed head injuries in athletes. Clin Sports Med 1990; 9(2): Lovell MR, Collins MW, Iverson GL, et al. Grade 1 or ding concussions in high school athletes. Am J Sports Med. 32(1):47-54, 2004 McCrea M, Kelly JP, Kluge J, et al: Standardized Assessment of Concussion in football players. Neurology 48, , 1997 McCrea M, Guskiewicz KM, Marshall SW, et al. Acute effects and recovery time following concussion in collegiate football players. J Am Med Assoc. 290(19): , 2003 McKeag DB. Understanding sports-related concussion. J Am Med Assoc. 290(19):2604-5, 2003 MMWR. Sports-Related Recurrent Brain Injuries- United States.;46: , 1997 Moody RA, Ruamsuke S, Mullen SF: An evaluation of decompression in experimental head injury. J Neurosurg 29:586, Mueller FO, Blyth CS: Fatalities from head and cervical spine injuries occurring in tackle football. Clin Sports Med 6:1, 1987 Povlishock JT, Lontos HA. Continuing axonal and vascular change following experimental brain trauma. J Cent Nerv Syst Trauma 1985; 2: Saunders RL, Harbaugh RE. The second impact in catastrophic contact-sports head trauma. JAMA 1984; 252: Warren Jr WL, Bailes, JE: On the Field Evaluation of Athletic Head Injuries. Clin Sports Med 17:1, 13-26, 1998 Wilberger JE, Maroon JC: Head injuries in athletes. Clinics in Sports Med 15:5, 1993

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