Review Article

Neurologic Emergencies in Sports Vernon B. Williams, MD ABSTRACT Purpose of Review: Sports neurology is an emerging area of subspecialty. Neurologists and non-neurologists evaluating and managing individuals participating in sports will encounter emergencies that directly or indirectly involve the nervous system. Since the primary specialty of sports medicine physicians and other practitioners involved in the delivery of medical care to athletes in emergency situations varies significantly, experience in recognition and management of neurologic emergencies in sports will vary as well. This article provides a review of information and elements essential to neurologic emergencies in sports for the practicing neurologist, although content may be of benefit to readers of varying background and expertise. Recent Findings: Both common neurologic emergencies and less common but noteworthy neurologic emergencies are reviewed in this article. Issues that are fairly unique to sports participation are highlighted in this review. General concepts and principles related to treatment of neurologic emergencies that are often encountered unrelated to sports (eg, recognition and treatment of status epilepticus, increased intracranial pressure) are discussed but are not the focus of this article. Neurologic emergencies can involve any region of the nervous system (eg, brain, spine/spinal cord, peripheral nerves, muscles). In addition to neurologic emergencies that represent direct sports-related neurologic complications, indirect (systemic and generalized) sportsrelated emergencies with significant neurologic consequences can occur and are also discussed in this article. Summary: Neurologists and others involved in the care of athletes should consider neurologic emergencies in sports when planning and providing medical care.

Address correspondence to Dr Vernon Williams, Kerlan-Jobe Orthopaedic Clinic, 6801 Park Terrace, Los Angeles, CA 90045-1543, [email protected] Relationship Disclosure: Dr Williams is the founding director of the Center for Sports Neurology at Kerlan-Jobe Orthopaedic Clinic, serves as chief medical officer of the Sports Concussion Institute and on the Board of Directors of the Kerlan-Jobe Orthopaedic Foundation and Team HEAL (Helping Enrich Athletes Lives), and has received personal compensation for providing expert legal testimony. Unlabeled Use of Product/Investigational Use Disclosure: Dr Williams reports no disclosure. * 2014, American Academy of Neurology.

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INTRODUCTION The neurologist’s role in the evaluation and management of neurologic emergencies in sports varies with the practice environment. Neurologists serving as team physicians, emergency department consultants, hospitalists or neurologic intensive care unit staff, or clinic-based consultants will have very different responsibilities in the continuum of care of an athlete. No matter the specific role or practice environment, all neurologists should be aware of basic principles and both commonly encountered and less common but noteworthy neurologic emergencies in Continuum (Minneap Minn) 2014;20(6):1629–1644

sports. For the team physician, participation in the development of a specific and documented plan of action for how emergencies should be handled, and establishment of specific responsibilities of participating staff, is critical. Another critical recommendation for managing neurologic emergencies is preparation for a potential emergency event, including formal rehearsal or practice run (Table 6-1). Emergency activation plans for catastrophic head and neck injuries and plans to reduce risk or prevent potential emergencies such as lightning strikes are examples.1 Team physicians covering games must be aware of, and www.ContinuumJournal.com

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Neurologic Emergencies KEY POINTS

h A critical recommendation for managing neurologic emergencies is preparation for a potential emergency event, including formal rehearsal or practice run.

TABLE 6-1 Neurologic Emergency Planning Considerations for the Team Physician b Player Down Practice airway, breathing, circulation (ABCs) Practice on-field neurologic assessment

h Emergency activation

Practice spine precautions (eg, positioning, neutral spine, spine board)

plans for catastrophic head and neck injuries and plans to reduce risk or prevent potential emergencies such as lightning strikes are examples of preparation for a potential emergency event.

Emergency medical technician access and replacement if player sent to emergency department b Environment Strategy for determining unsafe environment for exertion (eg, risk of heatstroke) Strategy for removing players to safety from lightning risk b Equipment Well-maintained player safety equipment

h Team physicians covering

Access to water and oxygen for athletes

games must be aware of, and proficient in, examination of the nervous system during a potential emergency at athletic event sites. The neurologic examination in the athletic environment may be very different from an examination conducted in the emergency department, hospital, or clinic.

Access to bag-valve-mask, pulse oximetry, spine board Access to rectal thermometer or gastrointestinal thermometer Portable serum sodium analyzer for endurance athletes b Positioning Practice and competition event placement allowing vantage point from which to directly view and survey for injury in real time b Transfer Knowledge of area resources in case of need for transfer Trauma centers Intensive care units Neurosurgical consultants

h The New Orleans Criteria and the Canadian CT Head Rule outline decision rules for detecting clinically important brain injury and the need for neurosurgical intervention in individuals presenting with a minor head injury and Glasgow Coma Scale score of 13 to 15.

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Hyperbaric chambers

proficient in, examination of the nervous system during a potential emergency at athletic event sites. The neurologic examination in the athletic environment may be very different from an examination conducted in the emergency department, hospital, or clinic. Early and accurate recognition of neurologic emergencies as well as appropriate first-responder management techniques and disposition are potential lifesaving skills when addressing an athlete ‘‘down on the field’’ (unconscious or with possible neurologic symptoms such as a potential cervical spine injury).2

For neurologists consulting in the emergency department, the ability to treat status epilepticus and to analyze the presence or absence of red flags supporting the need for imaging or emergent neurosurgical consultation is required. The New Orleans Criteria and the Canadian CT Head Rule outline decision rules for detecting clinically important brain injury and the need for neurosurgical intervention in individuals presenting with a minor head injury and Glasgow Coma Scale score of 13 to 15 (Table 6-23 and Table 6-34).5 Intensive care unit and hospitalbased neurologists may be called on

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a TABLE 6-2 New Orleans Criteria

CT is needed if the patient meets one or more of the following criteria b Headache b Vomiting b Older than 60 years of age b Drug or alcohol intoxication b Persistent anterograde amnesia (deficits in short-term memory) b Visible trauma above the clavicle b Seizure CT = computed tomography. a Data from Haydel MJ, et al, N Engl J Med.3 www.nejm.org/doi/full/10.1056/nejm200007133430204.

to manage increased intracranial pressure with appropriate use of head elevation, hyperventilation (using updated indications and parameters), and mannitol in conjunction with intracranial pressure monitoring. The clinic- or office-based neurologist may contribute through recognition of certain signs and symptoms as sentinel events in relation to neurologic emergencies; through primary and secondary prevention; and through management of subacute, subchronic, and long-term neurologic symptoms and consequences related to a survived neurologic emergency. Review of neurologic emergencies in sports can be categorized based on

diagnosis (eg, stroke, status epilepticus, spinal fracture), sport (eg, football, hockey, soccer, equestrian sports), or presenting symptom (eg, headache, altered mental status/loss of consciousness, weakness). This article briefly reviews basic principles of emergency medical management in sports in the context of neurologic injuries. The article also discusses approaching neurologic emergencies from the anatomic perspective of injuries involving the brain, spine and spinal cord, peripheral nerves, and muscles and reviews neurologic emergencies in sports. Common and less common but noteworthy

a TABLE 6-3 Canadian CT Head Rule

b Glasgow Coma Scale score lower than 15, 2 hours after injury b Suspected open or depressed skull fracture b Any sign of basal skull fracture (eg, hemotympanum, ‘‘raccoon eyes,’’ CSF otorrhea or rhinorrhea, Battle sign [bluish discoloration of the postauricular region]) b Two or more episodes of vomiting b Aged 65 years or older b Amnesia before impact of 30 minutes or more b Dangerous mechanism (eg, pedestrian struck by motor vehicle, occupant ejected from motor vehicle, or a fall from a height of at least 3 feet or five stairs) CT = computed tomography; CSF = cerebrospinal fluid. a Modified with permission from Stiell IG, et al, Lancet.4 B 2001 Elsevier. www.sciencedirect.com/ science/article/pii/S014067360004561X.

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Neurologic Emergencies KEY POINTS

h Airway, breathing, and circulation assessments (the A, B, and C associated with the ABCs of emergency medical care) are tenets in the management of neurologic emergencies.

h Jaw thrust is the preferred technique for ensuring an open airway if cervical spine injury is suspected or has not been ruled out. Alternative techniques such as chin lift or head tilt could negatively affect an unstable cervical spine.

h Equipment, padding, and pain causing reduction in chest wall excursion can impair assessment of breathing in an emergently injured athlete.

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emergencies affecting the nervous system are discussed in the context of the sports and athletic activities in which they are most frequently encountered. BASIC PRINCIPLES The basic principles of evaluation and management of neurologic emergencies in sports are no different than those of medical emergencies encountered in other scenarios. Airway, breathing, and circulation assessments (the A, B, and C associated with the ABCs of emergency medical care) are tenets in the management of neurologic emergencies as well. However, some sportsrelated considerations are worth noting. For example, the unique circumstances of airway control in an athlete (often wearing a helmet and face mask) down on the field dictate jaw thrust as the preferred technique for ensuring an open airway. Alternative techniques such as chin lift or head tilt could negatively affect an unstable cervical spine. If an airway is not maintainable with simple maneuvers, procedural intervention is indicated. This requires removal of face mask, if present, which is not a trivial consideration. Appropriate tools must be readily available and equipment maintained in good condition to facilitate removal when necessary. Spinal cord injury at levels affecting muscle activity can certainly impair breathing. Equipment, padding, and pain causing reduction in chest wall excursion can impair assessment of breathing in an emergently injured athlete. Measures should be taken to quickly distinguish between the two possibilities. Circulatory abnormalities are rare and typically occur in the setting of cardiac arrest (more often associated with sudden collapse rather than a witnessed physical trauma or impact). A team physician acting as a first responder attending to an athlete down on the field is at an advantage if activity immediately preceding the emergency was witnessed.

Vantage point and constant vigilant observation of athletic participants during game coverage is crucial. Immediately following an assessment of the ABCs is an evaluation of the level of consciousness and neurologic function. A commonly used system is the Glasgow Coma Scale (based on eye opening, verbal function, and motor function). Its value is greatest when used as a means of serial evaluation and to facilitate communication between practitioners. It does not substitute for a neurologic examination. Standardized assessment of the consciousness of an injured athlete may be accomplished using the AVPU (alert, verbal stimulus response, painful stimulus response, unresponsive) scale. Based on these initial, first-responder assessments, critical next steps must be determined. Cervical spine immobilization (with determination as to whether or not to remove equipment) and activation of an emergency plan are among the most important decisions to make (Case 6-1). Execution of these activities should be practiced on a regular basis so they can be carried out as smoothly as possible at the time of an emergency. When an emergency plan with transport is not deemed necessary, a more detailed assessment of the nervous system can be carried out after the player has been removed from the playing surface to the sideline. The presence of concerning signs or symptoms from subsequent assessments may yet trigger transfer to an emergency department. Surveillance for deterioration should be carried out at frequent intervals. Epidural hematomas and other traumatic injuries are often recognized in the setting of deterioration signaling a neurologic emergency.2 TRAUMATIC BRAIN INJURY AND VASCULAR EMERGENCIES Neurologic emergencies in sports may involve injury to the skull, brain tissue,

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Case 6-1 A 24-year-old professional football player was injured while making a tackle. He was down on the field, was motionless and semiprone, and was emergently assessed by medical staff while game officials controlled the other players. He was conscious, alert, communicating appropriately, and moving all four extremities, but reported right arm pain and paresthesia and neck pain. The team physician repositioned the player, maintaining neutral spine, removed his face mask, and prepared for cervical spine stabilization. Emergency medical services reported to the field and discussed whether or not to remove his shoulder pads and helmet. The team physician assumed primary control and decided (against emergency medical services’ recommendation) not to remove helmet and shoulder pads, to prevent kyphosis or lordosis by maintaining neutral spine. The player was logrolled onto a spine board and transported to the emergency department by ambulance. The head team trainer traveled with the player to ensure appropriate transfer of information. A CT scan of the cervical spine was performed and showed a stable C6 lamina fracture (as reported to the team physician). Instructions were given to carefully remove his helmet and shoulder pads, then to place the athlete in a cervical collar. When the team physician arrived at the emergency department and reviewed the CT scan, he found a fracture of the C6 pedicle as well as the lamina (Figure 6-1). A spine surgeon was consulted, but the player was treated nonsurgically with occipital-cervicalthoracic orthosis. The fracture healed without the need for surgical intervention. His neck stiffness and mild radiculopathy improved. The player was officially cleared to return to play, but chose instead to transition to a different career. Comment. This case illustrates several important aspects of managing a player down on the field. Field-related issues including immediate/emergency stabilization (ABCs) were encountered, and the need for and activation of emergency medical services on-site was demonstrated. Decisions regarding FIGURE 6-1 CT scan of spine showing C6 lamina (red arrows) and pedicle (blue arrow) fractures. who was in charge were necessary and had a significant effect on patient positioning, management, and potential iatrogenic complications of transfer. Appropriate measures were taken to ensure cervical immobilization and safe removal of the player from the field. Decisions were made regarding which team medical personnel traveled with the player to the hospital and which personnel stayed to continue medical services for the remaining athletes. A replacement emergency medical services team was called to be on-site for the rest of the game. This case also demonstrates the importance of careful review of diagnostic imaging, appropriate consultation, and medical decision making.

or blood supply to the brain. A number of clinical presentations are possible, ranging from subtle but persistent headache to immediate catastrophic consequences, depending on the size and location of the injury. The clinical findings may represent direct physical injury to neural tissue, external compression, or ischemic damage from loss of blood flow. Subdural hematoma is classically associated with tearing of bridging veins Continuum (Minneap Minn) 2014;20(6):1629–1644

coursing between the cortex and venous sinuses. A number of potential mechanisms and conditions may predispose athletes to subdural hematoma. Trauma in athletes participating in contact and collision sports (whether helmeted or not) is a common cause. Spontaneous subdural hematoma has been described in association with anabolic steroid use in weightlifters.6 Vigorous Valsalva maneuvers (with attendant fluctuations in www.ContinuumJournal.com

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Neurologic Emergencies KEY POINTS

h Subdural hematoma is associated with more severe injury and more deaths in high school and college football athletes than other head injuries.

h Epidural hematoma may require urgent neurosurgical evacuation as a lifesaving maneuver.

h Even minor and seemingly trivial trauma can result in focal neurologic deficits from vascular injury, as evidenced by reports of ischemic stroke in pediatric populations participating in sports.

h Neurologic emergencies involving the bony spine and spinal cord have the potential for catastrophic and tragic outcome. This is particularly true in cases of injury above C5 because of the effect on respiratory function.

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venous and intracranial pressures), dehydration (with loss of circulating volume), and preexisting coagulopathy (abnormality of platelet count, platelet function, or other bleeding diathesis) are other potential contributors to development of subdural hematoma in athletes. Subdural hematoma is associated with more severe injury and more deaths in high school and college football athletes than other head injuries.7,8 The greatest number of these injuries occur while tackling or being tackled in football activities.8 Epidural hematoma may require urgent neurosurgical evacuation as a lifesaving maneuver. Epidural hematoma may involve the so-called lucid interval after a brief initial loss of consciousness, only to be followed by rapid and severe deterioration in neurologic status. Vigilance for the clinical presentation of this type of traumatic brain injury should be a high priority. Of course, intracranial hematomas and contusions may be neurologic emergencies, particularly if they involve critical regions of the brain or result in a significant increase in intracranial pressure. Cerebral edema and increased intracranial pressure related to sports is a potential consequence of trauma, but this type of brain injury may also be related to athletes participating at high altitude. High-altitude cerebral edema has been reported in association with acute mountain sickness and pulmonary edema.9,10 Physicians managing athletes with signs and symptoms of increasing intracranial pressure should be familiar with the clinical presentation of herniation syndromes (cerebellar tonsil, transtentorial, uncal, and subfalcine) as well as indications for and appropriate execution of treatment measures including hyperventilation, head elevation, intracranial pressure monitoring, osmotic diuretics and hypertonic saline, use of barbiturate coma, and surgical intervention, if necessary.11

Injury to vascular structures in the neck is another risk of participation in sport. Common carotid artery laceration by a teammate’s skate in a hockey player has been reported and represents an uncommon but potentially fatal injury. Pulsatile bleeding must be controlled with direct pressure and emergency surgical repair.12 Carotid artery dissection and vertebral artery dissection have been reported during participation in sports such as hockey, springboard diving, and golf.13Y16 Vigorous head rotation and mechanical forces are suspected to have resulted in vascular injury in these cases. However, even minor and seemingly trivial trauma can result in focal neurologic deficits from vascular injury, as evidenced by reports of ischemic stroke in pediatric populations participating in sports.13,17 Diagnosis may require a high index of suspicion and appropriate diagnostic imaging, and possible subsequent anticoagulation therapy for dissection, if present. A workup to assess for a hypercoagulable state should be performed as well. For further information on sports-related cervical artery dissections, refer to the article ‘‘Some Unusual Sports-Related Neurologic Conditions’’ by Frank Conidi, DO, MS, in this . issue of SPINE AND SPINAL CORD EMERGENCIES Neurologic emergencies involving the bony spine and spinal cord have the potential for catastrophic and tragic outcomes. This is particularly true in cases of injury above C5 because of the effect on respiratory function. Fatal and nonfatal catastrophic injuries to the spine in sports occur most commonly in the cervical region, but thoracic and lumbar injuries can be devastating as well. Contact and collision sports (eg, football, hockey) as well as diving and high-speed activities with fall risks (eg, skiing, snowboarding) have high risk of

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spinal cord injury.18 Cheerleading activities have a low overall risk of injury, but a high risk of catastrophic injury. In 2000, there were an estimated 1814 neck injuries in cheerleaders of all ages, with 76 cervical fractures, according to US Consumer Product Safety Commission estimates.19 The National Center for Catastrophic Sports Injury Research data show a 1.7% risk of cervical fracture resulting in fatality in high school and college athletes over a period from July 1990 to June 2010. All of the cervical fractures were in athletes who played football, and all of the cervical fractures leading to fatality occurred at the high school level.7 It is critically important for emergency action plans to be in place to handle cervical spine injuries, particularly when managing athletes participating in sports that place them at risk. Management of a cervical spine injury begins with recognition. Vigilant observation of athletes at the time of participation can help with identification of axial compression in a neutral, flexed (highly unstable and susceptible to injury), or extended position. ‘‘Spear’’ or head-down tackling can be a significant source of cervical spine injury. The same mechanism of injury results in a small number of thoracic spine injuries.

Observed activity, impact, or injury consistent with potential spinal damage should be managed with spinal precautions. In athletes who experience a loss of consciousness, a spinal injury is presumed until the spine is cleared or injury is proven absent. Until then, spinal precautions should be implemented and observed. Alternatively, the immediate postinjury history and examination might result in description of pain of such location or character that it suggests spinal injury (radiating, electric, bilateral extremity pain). Other neurologic symptoms (eg, numbness, tingling) or signs (eg, weakness, loss of bowel/bladder control, axial guarding/stiffness) may signal spinal injury and the need for spinal precautions. The principles of spinal precautions are to maintain spinal alignment, stabilization, and immobilization until such time as appropriate diagnostic imaging and medical management can be achieved in a controlled fashion at a medical facility. Techniques should be planned and practiced by medical staff covering athletic events (Table 6-4). Spinal injuries occur in sports other than football. Professional soccer teams tracked in 14 Fe´ de ´ ration Internationale de Football Association (FIFA) tournaments during 2001, 2002,

KEY POINTS

h Contact and collision sports (eg, football, hockey) as well as diving and high-speed activities with fall risks (eg, skiing, snowboarding) have high risk of spinal cord injury. Cheerleading activities have a low overall risk of injury, but a high risk of catastrophic injury.

h In athletes who experience a loss of consciousness, a spinal injury is presumed until the spine is cleared or injury is proven absent. Until then, spinal precautions should be implemented and observed.

TABLE 6-4 Principles of Cervical Spine Precautions in Football Players b Cervical spine immobilization and spine boarding should be practiced. b Immobilize the head to the shoulders as one unit, grasping the shoulders while supporting the head with the forearms from a position above the head. b Maintain neutral spine. If athlete is wearing helmet and shoulder pads, do not remove either. Removal of the helmet can result in lordosis; removal of the shoulder pads can result in kyphosis. b If a face mask is present, it should be removed by the quickest and safest method to maintain airway access. Cut plastic face mask clips if possible. Electric screwdrivers are not always reliable and should not be depended upon. Maintain equipment and change hardware frequently. b Remove helmet only if unable to access airway and only under safest conditions. Remove side cheek pads and deflate air bladders, if present. Rotate back to front to remove. Do not spread the sides of the helmet.

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Neurologic Emergencies KEY POINT

h The risk of spinal cord injury exists in noncontact sports as well, documented in the example of surfer’s myelopathy.

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2009, and 2010 showed that, out of all injuries recorded, head and neck injuries constituted 2.2%. Of these injuries, 20.6% were specific to the cervical spine, including contusions, hematomas, disc herniation, nerve root compression, facet joint pain, muscular strain, and ligamentous strain.20 Spinal injuries appear to be increasing in skiers over the past 20 years, particularly among young male participants.19 Participation in other contact sports, such as rugby and ice hockey, diving, and even noncontact sports such as baseball (eg, from base runner/fielder or fielder/fielder collisions), may also result in catastrophic spine injury causing a neurologic emergency. Cervical contusion is a less catastrophic injury to the spinal cord. Transient pain, paresthesia, or motor weakness in more than one extremity that resolves completely in 10 minutes to 48 hours is similar to a stinger, but involves the spinal cord. Also called spinal cord concussion or transient neurapraxia, cervical contusions have been reported in football players and appear to be related to a combination of preexisting cervical stenosis, hypermobility of the cervical spine (particularly at the C3-C4 level), and an extension mechanism of injury.21 Controversy exists over whether or not these athletes should return to collision sports, but some have returned to play, even after surgical intervention. Some have advocated for restriction from return to play in the setting of structural radiographic or neurologic abnormalities.22 The risk of spinal cord injury exists in noncontact sports as well, documented in the form of surfer’s myelopathy.23,24 In a review of clinical cases, patients presented with acute myelopathic symptoms of urinary retention and progressive paraparesis after surfing, without specific acute trauma or premorbid neurologic conditions. The activity common to all of the patients appeared to be prolonged periods of lying prone on

a surfboard, punctuated with periodic rapid change of position to standing on the surfboard. These patients felt back discomfort or pain followed by relatively rapid onset of weakness and paresthesia on walking out of the surf. The proposed mechanism of injury was likely a dynamic vascular compression, vasospasm, or thrombosis of the great anterior radicular artery of Adamkiewicz. Overall, the severity of spinal cord injury at the time of admission seemed to be the predictive factor in clinical outcome. Treatment of the acute phase of injury with methylprednisolone or increase in mean arterial pressure with vasopressors did not seem to influence outcome in this series.24 For further information on surfer’s myelopathy, refer to the article ‘‘Some Unusual Sports-Related Neurologic Conditions’’ by Frank Conidi, DO, . MS, in this issue of Recent guidelines from the American Association of Neurological Surgeons and the Congress of Neurological Surgeons (2013) on clinical management of acute spinal cord injuries document Level I evidence that administration of methylprednisolone for the treatment of acute spinal cord injury is not recommended. Class I, II, and III evidence exists that high-dose steroids are associated with harmful side effects, including death.25 The same guidelines indicate that hypothermia has not been sufficiently shown to be of clear benefit in the treatment of spinal cord injury based on currently available evidence. ROOT, PLEXUS, PERIPHERAL NERVE, AND MUSCLE RELATED EMERGENCIES Trauma involving the neck, shoulder, chest, or upper arm may result in injury to nerve roots or the brachial plexus during sports activities. Lumbosacral plexus injuries are less common (Table 6-5). Athletes may present with acute injuries, such as the acute burning pain and

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TABLE 6-5 Common Brachial Plexus Injuries in Sports Stingers

Thoracic Outlet Syndrome

Onset

Sudden

Insidious

Most Common Distribution

Upper trunk

Lower trunk

Anatomic Involvement

Neural (nerve/plexus)

Neurovascular

Typical Sport/Athletic Activity

Football, cycling falls

Overhead (baseball, swimming)

Typical Clinical Course

Self-limited

Requires intervention

temporary/self-limited weakness of neurapraxia associated with stingers in football. More chronic presentations, such as the vague and subtle thoracic outlet syndrome symptoms of increase in fatigue, decreased velocity, and poor control described by baseball pitchers with neurovascular compression, also occur. Stingers (also called burners) derive their name from the electric, burning, and radiating pain in the affected upper extremity after contact or collision, resulting in stretch or compression of the brachial plexus. Numbness and weakness are usually associated with the pain. Symptoms are typically transient and variably resolve over the course of minutes to days. Stingers are very common in collegiate football, occurring in 50% to 65% of players over the course of a 4-year collegiate career. A key characteristic is that the burning pain is unilateral. (Bilateral upper extremity symptoms should prompt evaluation to rule out cervical spine injury.)22 Stingers in sports are not, however, limited to collegiate football players, and not all injuries result in reversible neurapraxia. Brachial plexus injuries occur in 4% of severe winter sports injuries.26 Cycling accident victims with brachial plexus avulsions are more likely to experience involvement of the upper trunk (89% of the time) than lower trunk injury (which is more often seen in motor vehicle accidents and in nonYsports-related brachial Continuum (Minneap Minn) 2014;20(6):1629–1644

plexopathy.)26 The mechanism of violent stretch when the head and neck are displaced away from the shoulder places the upper trunk at risk, exposing it to injury. In football, the injury rarely results in nerve root avulsion, but it has been reported.27 MRI of the cervical spine and plexus are typically revealing, but CT myelogram (not MRI) may be more valuable in demonstrating avulsion injury if clinically suspected. The thoracic outlet syndrome presentation is typically (but not always) more gradual in onset and more often involves the lower trunk distribution. External compression of elements at the scalene triangle, costoclavicular space, or pectoralis minor space may affect any combination of vascular structures (subclavian artery or vein) or neural structures (brachial plexus). Occasional emergency/acute presentation occurs from repetitive positional compression causing subclavian vein thrombosis or axillary artery injury, requiring surgical intervention to prevent distal embolism. These injuries most typically occur in elite athletes with vigorous overhead arm motion (eg, pitchers, swimmers).28,29 High-quality MRI of the brachial plexus as well as diagnostic ultrasound and vascular testing (venogram, angiogram) should be considered in athletes who fit this profile. Prompt recognition and appropriate treatment frequently allow return to sport with preservation of function and performance.

KEY POINT

h Stingers are very common in collegiate football, occurring in 50% to 65% of players over the course of a 4-year collegiate career. The burning pain is unilateral. (Bilateral upper extremity symptoms should prompt evaluation to rule out cervical spine injury.)

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Neurologic Emergencies KEY POINTS

h In acute compartment syndrome, soft tissue necrosis with nerve damage, rhabdomyolysis, and renal failure are possible from unrecognized and untreated elevations in tissue pressure above 40 mm Hg.

h Therapeutic hypothermia is supported as a neuroprotective mechanism after cardiac arrest with Level 1/Class1 support in the 2010 ACLS Guidelines. Cooling to 32-C to 34-C via induction through surface, core, or regional mechanisms is beneficial.

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Acute compartment syndrome may result from prolonged external pressure (eg, from bandages, wraps, pads, or casts), soft tissue vascular injury, trauma (fracture or dislocation), or dramatic increase in exercise intensity.30Y34 The increase in tissue pressure within a fascia-bound enclosed space may lead to increase in venous pressure, changes in the arteriovenous gradient, and subsequent reduction in arterial flow. Without urgent reduction in tissue pressure (removal of dressings or other external contributions to increased pressure, repositioning, and possibly surgical fasciotomy), severe complications, such as soft tissue necrosis with nerve damage, rhabdomyolysis, and renal failure, are possible. Normal intramuscular compartment pressure at rest is 0 mm Hg to 10 mm Hg. Resting pressure above 40 mm Hg is consistent with acute compartment syndrome. Criteria for chronic exertional compartment syndrome diagnosis are more elusive, and while intramuscular compartment measurements before and after exercise may provide guidance, the diagnosis emphasizes history over measurement criteria.35 In addition to the complications of acute compartment syndrome outlined above, rhabdomyolysis may occur as a neurologic emergency in sports as a result of hereditary metabolic myopathy with exercise intolerance or as a result of extreme exertion.36Y39 McArdle disease has occasionally been diagnosed in athletes who have developed muscle necrosis and extreme elevations in serum creatine kinase in association with exercise. Athletes with dark discoloration of the urine (a manifestation of myoglobin, not blood, in the urine) may require aggressive hydration and maintenance of high urine volume to address potential acute renal failure. When an obvious trigger from aggressive exercise, trauma, or drug toxicity is not present in an athlete with rhabdomyolysis,

evaluation to rule out metabolic myopathy is indicated.36,38,39 For further information about sportsrelated peripheral nerve injuries, refer to the article ‘‘Peripheral Nerve Injury in Sports’’ by Brian W. Hainline, MD, FAAN, . in this issue of INDIRECT NEUROLOGIC EMERGENCIES IN SPORTS Cardiac Arrest Cardiac arrest is an unfortunate but real risk of participation in sports activities. Sudden cardiac death is often associated with hypertrophic cardiomyopathy. Arrhythmias in various forms may be successfully treated with advanced cardiac life support (ACLS) protocols, but postcardiac arrest syndromes are frequently debilitating. The overwhelming majority of individuals who survive cardiac arrest are admitted to the intensive care unit. Many do not survive. The most significant complication of survival is brain damage. Cortical structures are more susceptible to hypoxia than the relatively more refractory brainstem. This selective susceptibility to hypoxic injury may lead to a persistent vegetative state. Therapeutic hypothermia is endorsed as a neuroprotective mechanism with Level 1/Class 1 support in the 2010 ACLS Guidelines.40Y42 Cooling to 32-C to 34-C via induction through surface, core, or regional mechanisms is beneficial. Evidence shows that longerduration therapeutic hypothermia confers more benefit with more preservation of brain tissue.43 Readers should review any future updates to these guidelines. Heat-Related Illnesses Heat-related illnesses vary in scope and severity, but have the potential of progressing to a neurologic emergency in sports. Less-severe manifestations may involve extremity edema, spasm or cramps, rash (miliaria rubra, or prickly heat), or syncope. More significant/severe

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December 2014

heat exhaustion produces more severe neurologic manifestations, such as disorientation, dizziness, imbalance, delirium, loss of consciousness, or coma. Despite the technical distinctions between heat exhaustion (representing symptoms with core body temperature less than 40-C as per rectal thermometer or swallowed gastrointestinal temperature probe) and exertional heatstroke (equal to or greater than 40-C), emergencies requiring urgent treatment may develop at any point along the spectrum in either technical category. Severity and duration of hyperthermia are critical factors in morbidity (neurologic and multiorgan failure) and mortality. The earlier the symptoms are recognized and the more quickly the temperature is reduced, the better the outcome. Acclimatization (60 to 90 minutes of exposure to high-heat environment at moderate-intensity exercise) is an important strategy in risk reduction and takes 1 to 2 weeks to achieve. Every attempt should be made to maintain normal hydration status through aggressive replacement of fluids lost to sweat, evaporation, and urinary loss. Athletes should be encouraged to drink and replace fluids at any time, not just during designated breaks. Extreme exertion in environments with combinations of high ambient temperature, low breeze, high humidity, and insufficient cloud cover should increase vigilance. Clothing and garments that impede evaporation of sweat may contribute as well. Athletes developing symptoms of hypotension, tachycardia, nausea/ vomiting, encephalopathy, or other signs and symptoms must be rapidly cooled. Submerging the body in ice water is the preferred method. Rotating wet, ice-cold towels is an option when ice bath submersion is not possible. It is preferable to initiate this type of cooling procedure immediately (even prior to transport to a medical facility and initiation of rehydration, if necessary).1,7 Continuum (Minneap Minn) 2014;20(6):1629–1644

Exertional Hyponatremia Exertional hyponatremia may cause fatal encephalopathy if undiagnosed and untreated. Excessive, prolonged sweating and fluid replacement with free water (which results in inadequate replacement of sodium losses) can combine to cause nausea and vomiting, dizziness, headache, disorientation, seizures, cerebral edema, and death. Defined as serum sodium concentration less than 130 mEq/L, exertional hyponatremia is most frequently seen in situations of extreme exertion and participation in contests lasting longer than 4 hours (more commonly seen in distance runners and other endurance athletes).44 Treatment involves sodium replacement with hypertonic saline (3% to 5%) in moderate to severe cases. Care should be taken to manage correction of hyponatremia at an appropriate rate to avoid central pontine myelinolysis. Rate calculators are readily available and very helpful in assisting with safe replacement of sodium based on the sex, age, and weight of the patient; sodium concentration; and replacement fluid type. In mild cases, oral rehydration with liquids combined with ingestion of foods with high sodium content is most beneficial. The condition can be prevented with attention to hydration protocols that specifically and accurately address fluid losses related to exertion without dilutional overhydration.1 Handheld and portable serum sodium analyzers are available and able to provide serum sodium concentration within minutes.

KEY POINTS

h Despite the technical distinctions between heat exhaustion (representing symptoms with core body temperature less than 40-C as per rectal thermometer or swallowed gastrointestinal temperature probe) and exertional heatstroke (equal to or greater than 40-C), emergencies requiring urgent treatment may develop at any point along the spectrum in either technical category.

h Severity and duration of hyperthermia are critical factors in morbidity (neurologic and multiorgan failure) and mortality. The earlier symptoms are recognized and the more quickly temperature is reduced, the better the outcome.

h Defined as serum sodium concentration less than 130 mEq/L, exertional hyponatremia is most frequently seen in situations of extreme exertion and participation in contests lasting longer than 4 hours (more commonly seen in distance runners and other endurance athletes).

Scuba Diving Complications Scuba diving complications may cause neurologic emergencies as a result of decompression sickness, air emboli, or barotrauma. Decompression sickness type I (commonly referred to as the bends) occurs due to increased nitrogen and oxygen release from tissues into the bloodstream during rapid ascension. It is www.ContinuumJournal.com

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h Decompression sickness type I (commonly referred to as the bends) occurs due to increased nitrogen and oxygen release from tissues into the bloodstream during rapid ascension.

h Exertional sickling can result in respiratory difficulties, muscle weakness, cramping, pain, and, occasionally, catastrophic complications of rhabdomyolysis or death.

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experienced as deep muscle and joint pain, often associated with rash. In mild cases, symptoms can resolve within 30 minutes of surfacing. Decompression sickness type II is far more severe and often appears after surfacing. It is associated with neurologic symptoms of vestibular dysfunction, headache, visual disturbances, and respiratory difficulties. While type I may improve without treatment, type II requires immediate transport to a compression chamber to simulate depth and dissolve nitrogen. Type II sickness may result in permanent nerve and spinal cord injury (typically at the thoracic level).45 Clinical presentation is varied, as signs and symptoms may include pain, weakness, paresthesia, mental status changes, and a number of other possibilities, depending on which neurologic structures are affected by the bubble emboli. Because the volume of a gas varies inversely with pressure, gas expands as divers ascend. When the gas expansion results in tissue injury (from failure to equalize internal and external pressures of a gas-filled body space), barotrauma results. With pulmonary barotrauma, arterial gas emboli may cause neurologic or cardiac symptoms as bubbles pass into the arterial circulation via right to left shunt. Emboli reaching the brain through cerebral vessels can cause stroke symptoms within minutes of surfacing.46 Barotrauma may affect other tissues, with clinical features occurring based on the body cavity affected. When neurologic manifestations of air emboli and barotrauma are present, on-site treatment with 100% oxygen should be initiated immediately upon surfacing. Hyperbaric oxygen therapy should be initiated via emergency transfer to the nearest hyperbaric facility.47 If evacuation occurs via air transport, it should be done at low altitude to prevent further worsening of injury/illness. Another potential neurologic emergency associated

with diving is nitrogen narcosis. An alcohol intoxicationYlike drowsiness occurs as the partial pressure of nitrogen in the CNS increases with increasing ambient pressure. When recognized, divers should ascend to a depth of less than 100 feet. Sickle Cell Trait Sickle cell trait is classically described as being consistent with a normal lifespan and good general health; however, there may be increased risk of neurologic emergency with extreme exertion. Incidence rates of sickle cell trait are approximately 8% in African Americans, 0.5% in Hispanics, and 0.2% in whites. Exertional sickling can result in respiratory difficulties, muscle weakness, cramping, pain, and, occasionally, catastrophic complications of rhabdomyolysis or death. Predisposing factors may include exertion at high altitude, dehydration, and concomitant illness. Exertional sickling has been associated with extreme exertion in athletes running repetitive wind sprints (‘‘gassers’’) and intense exertions at the ends of practices. It has been associated with intense uphill runs and long-distance runs. However, sickling can occur within minutes of all-out exertion, and there have been episodes of collapse associated with brief sprints early in the course of exercise at the beginning of a sport season.1,48 Some controversy exists as to how strong the association is between sickle cell trait and catastrophic injury from participation in sports based on case control studies and over whether or not mandatory screening for sickle cell trait should be imposed.49 Some sports medicine specialists support universal screening. Others support targeted screening based on race/ethnicity.50,51 A physiologic rationale exists for exertional sickling. Clinical evidence shows that among deaths of National Collegiate

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December 2014

Athletic Association (NCAA) Division I athletes over a 10-year period (all occurring during conditioning, not practice or game activities), 10 of 16 athletes were sickle cell trait positive.48 The NCAA currently requires screening of athletes for sickle cell trait. Athletes with sickle cell trait should be encouraged to rest and recover between conditioning reps, use supplemental oxygen, hydrate appropriately, and consider refraining from exertion during periods of illness. Consideration should be made for excusing athletes with sickle cell trait from performance tests (eg, qualifying runs), particularly in high heat and humidity or at high altitude.1 If signs and symptoms of sickling are present in an athlete, they should be handled as a potential medical emergency, and the athlete should be removed from play. High-flow oxygen should be administered via a nonrebreather mask and vital signs monitored. Any deterioration or collapse should result in emergency transport to a medical facility for further treatment. Lightning Strikes Lightning strikes may occur with outdoor sports and recreational activities. They occur in three different forms, all of which have the potential for resulting in a neurologic emergency. Most commonly, lightning strikes an object first, then takes the path of least resistance by traveling (flashing) to a person standing or situated next to the object that sustained the direct strike. Alternatively, lightning can strike the earth and travel along the ground, affecting an individual standing in the path of electrical current. A voltage difference between right and left feet positioned apart on the ground may cause the current to travel up one leg and down the other, causing what is referred to as a stride potential. Finally, a direct strike is possible. This is typically the most severe form of lightning strike and is Continuum (Minneap Minn) 2014;20(6):1629–1644

usually fatal.52 Lightning strikes can affect any aspect of the neuraxis, often with catastrophic effects. Hypoxic encephalopathy after cardiac arrest is often fatal. Spinal cord injury may result in permanent paralysis. Cranial nerve lesions are relatively uncommon. Peripheral nerve injuries occur and may include localized ballooning of the myelin sheath.52 It should be noted that survival can occur even in situations where victims appear to have died, so aggressive resuscitation is recommended when a lightning strike victim is encountered. Aside from the traditional ABCs of emergency treatment of medical and neurologic emergencies in sports, prevention and reduction in risk represent the mainstays of lightning strike management. Having a plan for monitoring weather events and for retreat to appropriate shelter in the event of dangerous weather is critical. Lightning strikes are of particular concern for hikers and mountaineers. Bicyclists and golfers are also at significant risk as they may be vulnerable in their inability to seek shelter quickly. For mountaineers, specific preventive measures include staying off ridges and summits and away from single trees. If possible, mountaineers should stay close to a wall, but keep a distance of at least 1 meter from the wall. All metal objects (eg, carabiners, ice axes, and ski poles) should be removed and stored away safely. Lightning currents can follow wet ropes. When lightning is present or threatening, climbers are advised to remove any unnecessary wet ropes attached to their person or extended across a mountain face, if possible. To prevent blunt trauma to the head, the helmet should not be removed.53 Cyclists should seek indoor shelter or shelter in a closed vehicle as the rubber on their bicycle tires is insufficient to protect them from a lightning strike. All outdoor athletes

KEY POINT

h Aside from traditional ABCs of emergency treatment of medical and neurologic emergencies in sports, prevention and reduction in risk represent the mainstays of lightning strike management. Having a plan for monitoring weather events and for retreat to appropriate shelter in the event of dangerous weather is critical.

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should seek shelter before a lightning storm and remain indoors until after the storm has passed. It should be noted that lightning can strike as far as 10 miles away from active rainfall. When thunder is heard, athletes should seek shelter. A common rule of thumb is to stay indoors or protected until 30 minutes after the last thunder is heard. CONCLUSION Sports activities can be very rewarding, with a wide range of benefits to the participant. In most cases, the benefits outweigh the risks of participation. Likewise, caring for athletes participating in sports can be a very rewarding experience. Physicians (neurologists and nonneurologists) and other health care practitioners responsible for the safety and management of athletes must be aware of the risk of neurologic emergencies associated with participation. The ability to prepare for, predict, and prevent injury when possible, as well as to respond to neurologic emergencies when they occur, will significantly improve the risk-benefit equation for participants and enhance the satisfaction of those caring for participating athletes. ACKNOWLEDGMENTS The author would like to thank Jose Posas, MD, and Luga Podesta, MD, for their assistance and contributions to the content of this article. REFERENCES 1. Casa DJ, Guskiewicz KM, Anderson SA, et al. National athletic trainers’ association position statement: preventing sudden death in sports. J Athl Train 2012;47(1):96Y118. 2. Casson IR, Pellman EJ, Viano DC. Concussion in athletes: information for team physicians on the neurologic evaluation. Semin Spine Surg 2010;22(4):234Y244. 3. Haydel MJ, Preston CA, Mills TJ, et al. Indications for computed tomography in patients with minor head injury. N Engl J Med 2000;343(2): 100Y105.

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4. Stiell IG, Wells GA, Vandemheen K, et al. The Canadian CT Head Rule for patients with minor head injury. Lancet 2001;357(9266): 1319Y1396. 5. Stiell IG, Clement CM, Rowe BH, et al. Comparison of the Canadian CT Head Rule and the New Orleans Criteria in patients with minor head injury. JAMA 2005;294(12):1511Y1518. 6. Alaraj AM, Chamoun RB, Dahdaleh NS, et al. Spontaneous subdural haematoma in anabolic steroids dependent weight lifters: reports of two cases and review of literature. Acta Neurochir (Wien) 2005;147(1):85Y87. 7. Boden BP, Breit I, Beachler JA, et al. Fatalities in high school and college football players. Am J Sports Med 2013;41(5):1108Y1116. 8. Cantu RC, Mueller FO. Brain injury-related fatalities in American football, 1945-1999. Neurosurgery 2003;52(4):846Y853. 9. Yarnell PR, Heit J, Hackett PH. High-altitude cerebral edema (HACE): the Denver/Front Range experience. Semin Neurol 2000;20(2): 209Y217. 10. Dumont L, Lysakowski C, Kayser B. [High altitude cerebral oedema]. Ann Fr Anesth Reanim 2003;22(4):320Y324. 11. Ling GS, Marshall SA, Moore DF. Diagnosis and management of traumatic brain injury. Continuum (Minneap Minn) 2010; 16(6 Traumatic Brain Injury):27Y40. 12. Bisson LJ, Sanders SM, Noor S, et al. Common carotid artery laceration in a professional hockey player: a case report. Am J Sports Med 2009;37(11):2249Y2251. 13. Payton TF, Siddiqui KM, Sole DP, McKinley DF. Traumatic dissection of the internal carotid artery. Pediatr Emerg Care 2004;20(1):27Y29. 14. Furtner M, Werner P, Felber S, Schmidauer C. Bilateral carotid artery dissection caused by springboard diving. Clin J Sport Med 2006;16(1): 76Y78. 15. Maroon JC, Gardner P, Abla AA, et al. ‘‘Golfer’s stroke’’: golf-induced stroke from vertebral artery dissection. Surg Neurol 2007;67(2):163Y168. 16. Yamada SM, Goto Y, Murakami M, et al. Vertebral artery dissection caused by swinging a golf club: case report and literature review. Clin J Sport Med 2013;24(2):155Y157. 17. Sepelyak K, Gailloud P, Jordan LC. Athletics, minor trauma, and pediatric arterial ischemic stroke. Eur J Pediatr 2010;169(5):557Y562. 18. Boden BP, Jarvis CG. Spinal injuries in sports. Neurol Clin 2008;26(1):63Y78; viii. 19. Boden BP, Prior C. Catastrophic spine injuries in sports. Curr Sports Med Rep 2005;4(1): 45Y49.

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20. Nilsson M, Ha¨gglund M, Ekstrand J, Walde´n M. Head and neck injuries in professional soccer. Clin J Sport Med 2013;23(4):255Y260. 21. Brigham CD, Capo J. Cervical spinal cord contusion in professional athletes: a case series with implications for return to play. Spine (Phila Pa 1976) 2013;38(4):315Y323. 22. Rihn JA, Anderson DT, Lamb K, et al. Cervical spine injuries in American football. Sports Med 2009;39(9):697Y708. 23. Thompson TP, Pearce J, Chang G, Madamba J. Surfer’s myelopathy. Spine (Phila Pa 1976) 2004;29(16):E353YE356. 24. Chang CW, Donovan DJ, Liem LK, et al. Surfers’ myelopathy: a case series of 19 novice surfers with nontraumatic myelopathy. Neurology 2012;79(22):2171Y2176. 25. Walters, BC, Hadley MN, Hurlbert RJ, et al. Guidelines for the management of acute cervical spine and spinal cord injuries: 2013 update. Neurosurgery 2013;60(suppl 1):82Y91. 26. Kaiser R, Waldauf P, Haninec P. Types and severity of operated supraclavicular brachial plexus injuries caused by traffic accidents. Acta Neurochir (Wien) 2012;154(7):1293Y1297. 27. Saliba S, Saliba EN, Pugh KF, et al. Rehabilitation considerations of a brachial plexus injury with complete avulsion of c5 and c6 nerve roots in a college football player: a case study. Sports Health 2009;1(5): 370Y375. 28. Nitz AJ, Nitz JA. Vascular thoracic outlet in a competitive swimmer: a case report. Int J Sports Phys Ther 2013;8(1):74Y79. 29. Duwayri YM, Emery VB, Driskill MR, et al. Positional compression of the axillary artery causing upper extremity thrombosis and embolism in the elite overhead throwing athlete. J Vasc Surg 2011;53(5):1329Y1340. 30. Schwartz JT Jr, Brumback RJ, Lakatos R, et al. Acute compartment syndrome of the thigh. A spectrum of injury. J Bone Joint Surg Am 1989;71(3):392Y400. 31. Mallo GC, Stanat SJ, Al-Humadi M, Divaris N. Posterior thigh compartment syndrome as a result of a basketball injury. Orthopedics 2009;32(12):923.

34. Sinikumpu JJ, Lepoja¨rvi S, Serlo W, Orava S. Atraumatic compartment syndrome of the foot in a 15-year-old female. J Foot Ankle Surg 2013;52(1):72Y75. 35. Aweid O, Del Buono A, Malliaras P, et al. Systematic review and recommendations for intracompartmental pressure monitoring in diagnosing chronic exertional compartment syndrome of the leg. Clin J Sport Med 2012;22(4):356Y370. 36. Krivickas LS. Recurrent rhabdomyolysis in a collegiate athlete: a case report. Med Sci Sports Exerc 2006;38(3):407Y410. 37. Amezyane T, El Kharras A, Abouzahir A, et al. [McArdle disease revealed by exercise intolerance associated with severe rhabdomyolysis]. Ann Endocrinol (Paris) 2009;70(6):480Y484. 38. Lin AC, Lin CM, Wang TL, Leu JG. Rhabdomyolysis in 119 students after repetitive exercise. Br J Sports Med 2005;39(1):e3. 39. Moeckel-Cole SA, Clarkson PM. Rhabdomyolysis in a collegiate football player. J Strength Cond Res 2009;23(4):1055Y1059. 40. Alexander RE. Summary of the new 2010 American Heart Association Guidelines for Basic Life Support (CPR). Tex Dent J 2011;128(3):279Y288. 41. Field JM, Hazinski MF, Sayre MR, et al. Part 1: executive summary: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122(18 suppl 3): S640YS656. 42. Morris S. 2010 BLS and ACLS guideline changes: post-cardiac arrest syndrome and therapeutic hypothermia. Can J Cardiovasc Nurs 2011;21(3):3Y8. 43. Che D, Li L, Kopil CM, et al. Impact of therapeutic hypothermia onset and duration on survival, neurologic function, and neurodegeneration after cardiac arrest. Crit Care Med 2011;39(6):1423Y1430. 44. Speedy DB, Rogers I, Safih S, Foley B. Hyponatremia and seizures in an ultradistance triathlete. J Emerg Med 2000;18(1):41Y44. 45. Hawes J, Massey EW. Neurologic injuries from scuba diving. Phys Med Rehabil Clin N Am 2009;20(1):263Y272.

32. Wind TC, Saunders SM, Barfield WR, et al. Compartment syndrome after low-energy tibia fractures sustained during athletic competition. J Orthop Trauma 2012;26(1): 33Y36.

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48. Eichner ER. Sickle cell trait in sports. Curr Sports Med Rep 2010;9(6):347Y351. 49. Key NS, Derebail VK. Sickle-cell trait: novel clinical significance. Hematology Am Soc Hematol Educ Program 2010;2010:418Y422. 50. Acharya K, Benjamin HJ, Clayton EW, Ross LF. Attitudes and beliefs of sports medicine providers to sickle cell trait screening of student athletes. Clin J Sport Med 2011;21(6):480Y485. 51. Anderson SA, Doperak J, Chimes GP. Recommendations for routine sickle cell trait screening for NCAA Division I Athletes. PM R 2011;3(2):168Y174.

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52. Cherington M, Yarnell P, Lammereste D. Lightning strikes: nature of neurological damage in patients evaluated in hospital emergency departments. Ann Emerg Med 1992;21(5):575Y578. 53. Zafren K, Durrer B, Herry JP, et al. Lightning injuries: prevention and on-site treatment in mountains and remote areas. Official guidelines of the International Commission for Mountain Emergency Medicine and the Medical Commission of the International Mountaineering and Climbing Federation (ICAR and UIAA MEDCOM). Resuscitation 2005;65(3):369Y372.

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Neurologic emergencies in sports.

Sports neurology is an emerging area of subspecialty. Neurologists and non-neurologists evaluating and managing individuals participating in sports wi...
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