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Clin Sports Med 24 (2005) 637–662

CLINICS IN SPORTS MEDICINE

Management of Common NeurologicConditions in SportsElliot L. Dimberg, MD, Ted M. Burns, MD*Department of Neurology, University of Virginia, Box 800394 Charlottesville, VA 22908, USA

eurological conditions are common in athletes. Trauma can cause directcentral (eg, concussion or hemorrhage) or peripheral (eg, stinger)injury. Also, as neurological conditions in athletes become better under-

stood, more people who have pre-existing conditions are becoming involvedin organized sports. This article reviews assessment and initial managementof head injury, stingers, seizures, and headaches. Return-to-play criteria arealso discussed.

CONCUSSION AND CATASTROPHIC INJURYThe American Academy of Neurology (AAN) has defined concussion as “atrauma-induced alteration in mental status that may or may not involve lossof consciousness” [1]. This definition underscores that the injury may notnecessarily involve a direct blow to the head, nor loss of consciousness. TheCenter for Disease Control has reported that approximately 300,000 sportsrelated concussions occur annually [2]. Actual incidence may be higher becauseof potential underreporting of concussion symptoms by athletes [3]. Concus-sions may occur in sports and situations not typically thought to put the athleteat risk, and not necessarily during games [4]. Such information should put theathletic trainer and physician at high suspicion for such an injury. The sportsmedicine practitioner must be able to recognize, assess, and manage the acutesetting, determine appropriate return-to-play (RTP) time frames, and under-stand the long-term sequelae of this injury.

Preinjury Education and AssessmentConcussion management begins with preinjury education. It is importantthat the athlete be educated on symptoms of concussion, because recent reportshave shown that athletes often are not aware that they have suffered a concus-sion [3]. The potential long-term and cumulative sequelae should be emphasized[5], because disregard for the seriousness of concussion can also lead to athlete

* Corresponding author. E-mail address: tmb8r@virginia.edu (T.M. Burns).

0278-5919/05/$ – see front matter © 2005 Elsevier Inc. All rights reserved.doi:10.1016/j.csm.2005.04.002 sportsmed.theclinics.com

638 DIMBERG, BURNS

underreporting [3]. The AAN has released a “Patient Page” on concussion atwww.neurology.org/cgi/reprint/63/8/E15 that can assist with the education ofathletes at any level and their parents.A total concussion history should be taken after concussion education.

Previously concussed athletes have been shown to be at significantly higherrisk for repeat concussions than teammates who have no prior concussions [6].Previous concussions may have already caused neurocognitive and neuro-psychological consequences that can affect postinjury assessment accuracy;this underscores the need for preinjury testing [7]. Previously concussed athleteshave also been shown to report fewer symptoms at 2 hours postinjury, al-though they report more symptoms at baseline and at 1 week postinjury [8].This also has implications for postinjury assessment and RTP decisions.Practitioners should decide which assessment tool will be used once contact

begins, and athletes should undergo baseline testing for accurate comparisonpostinjury. Baseline testing establishes accurate preinjury level of functioningand allows for effective correction for confounding factors such as learningdisabilities, behavioral disorders, education level, and intelligence. Learning

1) ORIENTATION:

Month: ______________________________________

Date: _______________________________________

Day of week: _________________________________

Year: _______________________________________

Time (within 1 hr): _____________________________

Orientation Total Score ________________________

2) IMMEDIATE MEMORY: (all 3 trials are completed regardless of score on trial 1 & 2; total score equals sum across all 3 trials)

Immediate Memory Total Score __________ / 15(Note: Subject is not informed of delayed recall testing of memory)

List

Word 1

Word 2

Word 3

Word 4

Word 5

Total

Trial 1

0 1

0 1

0 1

0 1

0 1

Trial 2

0 1

0 1

0 1

0 1

0 1

Trial 3

0 1

0 1

0 1

0 1

0 1

EXERTIONAL MANEUVERS(when appropriate):

5 jumping jacks5 sit-ups

5 push-ups5 knee-bends

NEUROLOGIC SCREENING:

Loss of Consciousness: (occurrence, duration)

Retrograde & Posttraumatic Amnesia:(recollection of events pre- and post-injury)

Strength:

Sensation:

Coordination:

4) DELAYED RECALL:

Word 1

Word 2

Word 3

Word 4

Word 5

Delayed Recall Total Score

0 1

0 1

0 1

0 1

0 1

/ 5

SUMMARY OF TOTAL SCORES:

ORIENTATION

IMMEDIATE MEMORY

CONCENTRATION

DELAYED RECALL

OVERALL TOTAL SCORE

/ 5

/ 15

/ 5

/ 5

/ 30

3) CONCENTRATION:

Digits Backward (If correct, go to next string length. If incorrect, read

trial 2. Stop after incorrect on both trials.)

4-9-3

3-8-1-4

6-2-9-7-1

7-1-8-4-6-2

Months in Reverse Order: (entire sequence correct for 1 point)

Dec-Nov-Oct-Sep-Aug-Jul

Jun-May-Apr-Mar-Feb-Jan

Concentration Total Score

6-2-9

3-2-7-9

1-5-2-8-6

5-3-9-1-4-8

0 1

0 1

0 1

0 1

0 1

/ 5

0 1

0 1

0 1

0 1

0 1

/ 5

Fig. 1. Standardized Assessment of Concussion (SAC). (From McCrea M. Standardized men-tal status testing on the sideline after sport-related concussion. J Athl Train 2001;36(3):276;with permission.)

639MANAGEMENT OF COMMON NEUROLOGIC CONDITIONS

disability in itself is associated with lower baseline neuropsychological function-ing, but also may be associated with significantly worse long-term neurocog-nitive sequelae in conjunction with multiple concussions [7]. The NationalAthletic Trainer’s Association (NATA) Position Statement [9] currently recom-mends that sideline screening measures, such as the Standardized Assessmentof Concussion (SAC) [10,11] (Fig. 1), the Balance Error Scoring System(BESS) [12] (described in Box 1 below) or symptom checklists [9] (Table 1),be used in conjunction with more extensive neuropsychological testingor vestibular balance testing. The use of computerized neuropsychologicaltesting is gaining acceptance by some for these purposes due to time,cost, and ease of testing [13]. Should these or like measures be used, base-line testing should be obtained. If they are not used, RTP may be delayed, orworse, premature.

Box 1: Balance error scoring system (BESS)

Test procedure

• Test in three different stances (both feet, nondominant foot, tandem), two timeseach (once on firm surface, once on medium-density foam 45 cm2 × 13 cmthick, density 60 kg/m3, load deflection 80–90 kg).

• Place hands on iliac crests, close eyes.• Once eyes are closed, test for 20 seconds.• On one foot, elevated leg is maintained at 20° to 30° hip flexion and 40° to

50° knee flexion.• Stand as quietly as possible in position.• If balance is lost, make any necessary adjustments to return to position.• One error point for each error committed• Incomplete test if unable to maintain stance for more than 5 seconds.• Maximum score of 10.

Scoring system

• Errors• Hands lifted off iliac crest• Opening eyes• Step, stumble, or fall• Moving hip into more than 30° of flexion or abduction• Lifting forefoot or heel• Remaining out of testing position for more than 5 seconds• Add 1 point for each error during a 20-second trial

Modified from Guskiewicz KM. Postural stability assessment following concussion:one piece of the puzzle. Clin J Sport Med 2001;11(3):186–7.

Table 1NATA graded symptoms checklist (GSC)

SymptomTime ofinjury

2–3 hourspostinjury

24 hourspostinjury

48 hourspostinjury

72 hourspostinjury

Blurred visionDizzinessDrowsinessExcess sleepEasily distractedFatigueFeel “in a fog”Feel “slowed down”HeadacheInappropriate emotionsIrritabilityLoss of consciousnessLoss or orientationMemory problemsNauseaNervousnessPersonality changePoor balance/coordinationPoor concentrationRinging in earsSadnessSeeing starsSensitivity to lightSensitivity to noiseSleep disturbanceVacant stare/glassy eyedVomiting

The GSC should be used not only for the initial evaluation but for each subsequent follow-upassessment until all signs and symptoms have cleared at rest and during physical exertion. Inlieu of simply checking each symptom present, the ATC can ask the athlete to grade or score theseverity of the symptom on a scale of 0–6, where 0 = not present, 1 = mild, 3 = moderate, and6 = most severe.

From Guskiewicz KM, Bruce SL, Cantu RC, et al. National Athletic Trainer’s Associationposition statement: management of sport-related concussion. J Athl Train 2004;39(3):296;with permission.

640 DIMBERG, BURNS

Finally, a thorough neurological examination should be performed. Thisshould include assessment of mental status, cranial nerves, motor and sensorysystems, coordination, deep tendon reflexes, and gait. This not only serves as abaseline examination, but also alerts the practitioner to potential pre-existingconditions that may warrant further specialist investigation and may preventinclusion in competition.

Clinical ManifestationsThe clinical manifestations of concussion, either as witnessed by the observer orreported by the athlete, are highly varied. As noted in the AAN definition of

641MANAGEMENT OF COMMON NEUROLOGIC CONDITIONS

concussion, loss of consciousness is not a necessary manifestation [1], and itspresence as a benchmark for concussion severity and prognosis has come intoquestion [14,15]. The most common symptoms, in decreasing frequency, are:headache, dizziness, confusion and disorientation, nausea, loss of consciousness,retrograde amnesia, and vomiting [16] (Table 2). The athlete may be unable toanswer questions relating to contest specifics, date, place or time. He or she maysuffer from imbalance or transient visual phenomena, including photophobia.Amnesia may also be anterograde. Observers may note a vacant stare, latentresponse times, poor focus of attention, difficulties of speech, incoordination, oremotional lability. If an athlete presents any signs or symptoms consistent withconcussion, then he or she has almost certainly suffered a concussion and shouldbe treated as such.

Postinjury AssessmentThere is no universally accepted standard for concussion assessment, but basicguidelines are definable. Initial on-field care should focus on assessing level of

Table 2Frequency of symptoms observed at the sideline evaluation and observed or reported at theinitial follow-up examination

Symptoms of injured athletes Percentage

Sideline evaluationHeadache 93.6Dizziness 85.1Confusion/disorientation 83.0Nausea 53.2LOC 25.5Retrograde amnesia 13.0Vomiting 4.3

Initial follow-up examinationHeadache 57.4Cognitive impairment 55.3Fatigue 44.0Memory problems 37.2Nausea 31.9Concentration problems 29.8Dizziness 23.4Weakness 17.0Irritability 17.0Impaired vision 14.9Sleep problems 14.9Sensitivity to light 12.8Depression 10.6Nervousness 8.5Vomiting 0.0Other sensory problems 0.0

Abbreviation: LOC, loss of consciousness.From Erlanger D, Kaushik T, Cantu R, et al. Symptom-based assessment of the severity of

concussion. J Neurosurg 2003;98(3):480; with permission.

642 DIMBERG, BURNS

consciousness and other parameters appropriate for traumatic injury. If at anytime there is concern for a more immediately serious cerebral or spinal injury,the athlete should be removed from the playing environment in a stable mannerby qualified personnel and transported immediately to a facility capable ofappropriate neurological and neurosurgical evaluation and treatment. Onceother potential or real injuries have been evaluated and managed, the athleteshould be removed from the contest and evaluated immediately and at regular(ie, 5-minute) intervals for improvement or deterioration. Assessment shouldinclude mental status testing for orientation, concentration, and perhaps mostimportant, memory, because amnesia has been reported to be an importantprognostic factor [14,15]. Sample sideline questions are listed in Box 2.Neurological testing should include that of pupillary reflexes, extraocular

movements, cranial nerves, strength, sensation, coordination, and gait. Ab-

Box 2: Sample mental status assessment questions

Orientation

• What is your name?• What are you doing?• Where are you/where are you playing?• Who are you playing for?• Who are you playing against?• What year is it?• What month is it?• What day is it?

Concentration

• Spell “world.”• Spell “world” backwards.• What do a penny, a nickel, a dime and a quarter make?• Subtract 7 from 100 (with serial subtractions to 65).• Recite the months of the year in reverse, starting with December.

Memory/amnesia

• Repeat these three words (list three simple unrelated words).• What just happened to you?• What were you doing just before it happened?• Were you winning or losing just before it happened?• What was the score?• What is the last thing you remember?• Repeat the same three words again.

643MANAGEMENT OF COMMON NEUROLOGIC CONDITIONS

normalities in any of these domains of the neurological examination mayherald the signs of a concussive injury. There are many standardized toolsthat exist for acute detection and assessment of concussion, but none supplant athorough neurological examination, although many may be used adjunctively[9–12,17]. Repeated evaluation should continue until there is clinical improve-ment and stabilization. Off-field assessment should include formal neuro-psychological and postural stability evaluation [9,17,18] Neuroimaging maybe reserved for athletes in whom structural lesions (ie, subdural hematoma)are considered. If a grading system such as that provided by the AAN [1] is usedto rate severity of concussion, the particular system should be named andcriteria met should be specified. The circumstances surrounding the injury,including time and place, type and direction of impact, reported symptoms,physical examination, and results of repeat testing and any provocative mea-sures used should be documented.

Return to Play and Follow-UpThere is at present no universally accepted algorithm for follow-up evalua-tion and RTP decision-making. It is clear, however, that RTP decisions shouldbe made upon an individual basis and should follow a standardized assess-ment, with reintroduction of physical exertion to evaluate persistence of symp-toms [1,9,17,18]. Some groups advocate removal of the athlete from competition,with no RTP for the current contest [18]. Others allow for RTP if concussion isvery mild and completely resolves at rest, as long as the athlete is assessed andgradually introduced to RTP by exertional provocative maneuvers over at least10 to 15 minutes [1,9]. Otherwise, the athlete should be removed from thecontest with no same-day RTP. Loss of consciousness (LOC) or amnesia shouldabsolutely disqualify the athlete from same-day RTP; LOC and amnesia signifymore severe concussion and longer symptom duration [14,15]. The practitionershould be comfortable removing an athlete from competition after any severityof concussion. If there is same-day RTP, the athlete should be frequently re-evaluated during the contest and for the next several days.Athletes’ reported symptoms have been demonstrated to be accurate indica-

tors of concussion severity [16] and have become the mainstay of RTP decision-making in many guidelines [1,9,18]. The Concussion in Sports (CIS) Groupreleased its “Return to Play Protocol” in 2002 [18]. It entails a six-step process,described in Box 3, each step taking 1 day at a minimum. Athletes may progressa step once asymptomatic at the current level. Once asymptomatic with noactivity, light aerobic exercise may be undertaken, then sport-specific training,then noncontact training, then contact, then game play. Elicitation of symp-toms at any level necessitates a drop in step with reattempts to progress after24 hours.If possible, athletes should undergo formal neuropsychological evaluations as

well, because this may unmask subtle continued deficits when compared withbaseline testing. Such deficits have been shown to correlate with duration ofsymptoms [16]. This has become an increasingly important tool in concussion

Box 3: CIS group return-to-play protocol

1. No activity, assessment at rest; proceed to step 2 once asymptomatic2. Light aerobic exercise (walking, cycling)3. Sport-specific training (running, ice skating)4. Noncontact training drills5. Full-contact training with medical clearance6. Game play

Adapted from Aubry M, Cantu R, Dvorak J, et al. Summary and agreementstatement of the first international symposium on concussion in sport. Clin J SportMed 2002;12(1):9; with permission.

644 DIMBERG, BURNS

evaluation. Postural stability testing may also be undertaken for adjunctive datain determination of concussion severity.Symptoms, cognitive impairment, and postural impairment tend to resolve by

day 7 postinjury [19,20], lending support for the 7-day sitting-out periodnecessitated by adhering to the CIS group RTP Protocol [18]. Previouslyconcussed athletes tend to report fewer symptoms early after a concussionbut more after 1 week, complicating their assessment [8]. There should be avery low threshold to withhold previously concussed athletes from play if thereis suspicion for a new concussion. Ultimately, the decision to RTP is anindividual one based on initial concussion severity, duration of symptoms,and repeated examinations, and assisted by formal neuropsychological testingand postural testing.

Long-Term SequelaeAlthough cognitive impairment has been shown to resolve within about 7 daysfor most concussions [19,20], cognitive impairment has been shown to persist,particularly for athletes suffering multiple concussions. In one study, a singleconcussion did not correlate with long-term neuropsychological or cognitivecomplications, but multiple concussions resulted in long-term neuropsycho-logical abnormalities, particularly in executive functioning and information-processing speed [7]. Moreover, athletes who have had previous concussionsare more likely to have future concussions, and are more likely to have a longerrecovery time per concussion [5]. Athletes who have a history of concussionshould be treated more carefully; the NATA has recommended that athleteswho have a history of more than two concussions and prolonged recoverytime should consider retiring from contact sports either temporarily or perma-nently [9].

Emergent and Catastrophic InjuryCatastrophic injury has been defined in some epidemiologic studies as an injuryoccurring while participating in high school- or college-sponsored sport, andmay lead to fatality, severe disability, or involve a severe injury but result in no

645MANAGEMENT OF COMMON NEUROLOGIC CONDITIONS

permanent disability [21,22]. Injuries may cause epidural hematoma (EDH),subdural hematoma (SDH), intracerebral hematoma (ICH), cerebral contusion,subarachnoid hemorrhage (SAH), or diffuse axonal injury (DAI). In highschool and college football, 69% of reported fatalities between 1945 and 1999were due to head injuries, with a further 16.3% attributed to cervical spineinjuries [22]. Of fatal head injuries, 74.5% were caused by subdural hematomas[22]. Catastrophic head injuries have been reported in a number of sports,including track and field, baseball, cheerleading, gymnastics, softball, fieldhockey, volleyball, soccer, basketball, boxing, during weight training, andfollowing aerobic and anaerobic exercise [22–28]. This is clearly a partial list,and the sports medicine practitioner must be prepared to evaluate and recognizepotentially catastrophic injuries so as to properly triage the athlete, regardless ofthe sport.Epidural hematomas frequently result from skull fractures with subsequent

laceration of the middle meningeal artery. Classically, EDH leads to an initialloss of consciousness, which is followed by recovery of consciousness and alucid period. The athlete then progressively deteriorates neurologically, withdevelopment of headache, a decline in mental status, and focal neurologicalfindings such as contralateral weakness or numbness, pupillary reflex abnor-malities, or facial asymmetry. Seizures may occur. The classic clinical progres-sion, however, has been reported to develop in only one third of observed cases[29]. Diagnosis is usually made by CT scanning of the head.SDH is thought to result from tearing of bridging veins running between

the brain and dural sinuses. In the young, the classic large subdural fluid col-lection with local mass effect on underlying brain causing neurological dete-rioration is less common than in the elderly. More often, there is a smallamount of subdural blood, but it is associated with underlying contusion,edema, and elevated intracranial pressure [29]. These patients may or maynot have exhibited a lucid interval, frequently lose consciousness at the time ofinjury, and often exhibit focal neurological signs. Diagnosis is again usuallymade by CT scanning of the head.ICH involves blood and hematoma formation within the substance of the

brain parenchyma. A hemorrhagic contusion is similar, but is associated withmore significant edema rather than localized hematoma formation. Loss ofconsciousness is reportedly rare; common clinical features include worseningheadache, confusion, and persistent amnesia [29]. Diagnosis is usually made byCT scanning of the head.SAH can result from trauma or intracerebral aneurysm rupture. Either can

occur in the athlete. Traumatic SAH is related to direct arterial injury, whereasaneurysmal SAH may be spontaneous, but has been reported to result fromvarying forms of exercise, usually those associated with significant Valsalvamaneuvers, such as weight lifting [27]. Diagnosis is made by CT scanning of thehead or by lumbar puncture.DAI is a severe form of closed head injury associated with acceleration-

deceleration or rotational injuries that result in diffuse shearing injury to

646 DIMBERG, BURNS

neuronal axons. When severe, it is associated with focal abnormalities in thecorpus callosum, dorsolateral rostral brainstem, and throughout the cerebralwhite matter, and may include intraventricular hemorrhage [30]. Diagnosis issuggested by CT scanning of the head, but may require MRI of the brain andlonger-term observation.On-field assessment should focus on recognition of the potential for cata-

strophic injury. It needs to be remembered that apparently significant initialneurological impairment, even with loss of consciousness, may be the conse-quence of a concussion, but more severe head injury may present withabnormalities that initially appear mild. Any athlete who suffers any kind ofhead trauma or acceleration-deceleration injury should initially be suspected tohave suffered a closed head injury, and the possibility of cervical spine injuryshould be entertained as well, because the two are closely pathomechanicallyrelated. The athlete should be evaluated for level of consciousness and men-tal status and, if there is concern for cervical spine injury, undergo cervical spinestabilization with a hard cervical collar and spine board until cervical spineclearance can be obtained [31]. If the athlete is unconscious or exhibits analtered level of consciousness, cervical spine injury should be presumed and thecervical spine stabilized [30]. The athlete should be managed according toadvanced trauma life support and advanced cardiac life support guidelines[30,31]. Once severe head or neck injury is considered to be a possibility, theathlete should be removed from the field of play after appropriate stabilizationby qualified personnel, and transported immediately to a facility capable ofappropriate neurological and neurosurgical evaluation and treatment.

CERVICAL NEURAPRAXIA (“STINGER”)The stinger, or “burner,” was initially described in 1965 [32] and was eventuallygiven the name “cervical nerve pinch syndrome” [33]. Incidence is reportedlynear 50% in college contact football players [34], and has been shown to be themost common symptomatic upper extremity nerve injury in athletes [35]. Themechanism of injury may involve trauma to the brachial plexus or cervical nerveroots; it is not a cervical cord injury. Although most signs and symptoms aretransient, some athletes may suffer prolonged symptoms or recurrent injury.

Injury Type, Pathomechanics, Symptoms and SignsA stinger may be precipitated by a blow to the head, neck, or shoulder caus-ing downward pressure on the shoulder on the affected side, with contralateralneck flexion or neck extension, such as in tackling or blocking in football.Although common in football, stingers can occur in other sports [32]. Site ofinjury has been localized to the upper trunk of the brachial plexus or the fifthand sixth cervical nerve roots. Proposed mechanisms of injury include tractioninjury to the upper trunk of the brachial plexus [34,36], compressive injury tothe upper trunk of the brachial plexus [36–38], traction injury to the cervicalnerve root [32,36,40], and compressive injury to the cervical nerve root in theneural foramen [39–42]. Brachial plexus injuries are more common in high

647MANAGEMENT OF COMMON NEUROLOGIC CONDITIONS

school athletes [40,43] and are more likely to result from lateral neck flexionwith shoulder depression. Cervical nerve-root compression is more common incollege and professional football players [40,43], particularly those who haverecurrent or chronic stingers. It may be associated with cervical disk disease,cervical canal stenosis, and neural foraminal stenosis [40–42], and mayresult from neck extension or forceful lateral neck flexion. It is possible thatany or all of these mechanisms may account for a particular athlete’s symptoms.Symptoms involve a single upper extremity; bilateral or lower extremity

symptoms should raise the possibility of a cervical spinal cord injury ratherthan a stinger syndrome. There may be rapid onset of burning pain in theshoulder [34,39], or from the neck [32] or supraclavicular area [33] down thearm to the hand [32,33,37,43] or fingers [39,44,45]. Paresthesias or anesthesiamay occur throughout the upper extremity [32,33,39], but more commonlyoccurs in a C5/C6 dermatomal distribution [43]. Alternatively, there may beno sensory deficit, only pain [37,38]. The athlete may shake the arm [33] orexhibit a dropped shoulder [37,38]. Weakness following a stinger is variable,ranging from mild weakness in a myotomal pattern [43–45] to inability tomove the entire arm [32,33], and the athlete may exit the contest supportingthe affected arm with the contralateral arm [33,45,46]. There may be noevidence of weakness immediately after the injury, only to develop later[33,37]. Muscles commonly involved include the deltoid, biceps, supraspinatus,and infraspinatus [43,45], causing weakness of shoulder abduction, elbowflexion, and upper arm external rotation. Symptoms are usually transient,lasting only seconds to minutes. There is usually no associated neck pain orlimitation of neck movement.

Assessment and ManagementOn-field evaluation begins with establishment of the mechanism of injury—either lateral flexion/shoulder depression or extension/compression. The athleteshould describe the location of symptoms and their duration if they haveresolved. Otherwise the athlete should be monitored for resolution of symp-toms. The cervical spine should be evaluated by palpation for tenderness,edema, evidence of structural damage, or muscle spasm. The supraclavicularfossa should also be examined in like fashion. If there is no concern for cervicalfracture, active range of motion within the limitation of pain should be assessedto include rotation, lateral flexion, anteroflexion, and extension. A full neuro-logical examination should be performed, with specific attention to strengthtesting in all muscle groups, full sensory examination, and muscle stretch reflextesting. The contralateral extremity should serve as a normal control.If symptoms or deficits involve the bilateral upper extremities or include one

or both lower extremities, or if there is concern for other serious structuraldamage, the cervical spine should be immobilized and spine precautions insti-tuted. The athlete should then be transported in a stable fashion by qualifiedpersonnel to a facility capable of appropriate neurological and neurosurgicalevaluation and treatment.

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If symptoms persist past several minutes, there is limitation of neck rangeof motion, or there is neck pain, the athlete should undergo MRI of the cer-vical spine [33,43,44] before any consideration of RTP. A high incidence ofcervical disk disease or neural foraminal narrowing has been reported inathletes who have chronic or recurrent stingers [40]. Also, some authors havereported a correlation between cervical canal and neural foraminal stenosisand stinger occurrence [41,42], although its significance remains unclear [46].Cervical spine MRI may reveal other pathology contraindicating return tosport [44,45], but these are more likely to cause transient quadriplegia than astinger syndrome.Electromyography (EMG) may be undertaken if abnormalities persist be-

yond 2 or 3 weeks [33,43,46]. Weakness persisting past 72 hours has correlatedto positive EMG findings [36]. EMG assists with injury localization (nerve rootversus brachial plexus), and determination of extent and severity.

Return to Play and PreventionRTP decisions are somewhat controversial, although many authors relyupon clinical and electrodiagnostic criteria in the absence of clear radiographicabnormalities or contraindications [33,43,45–47]. If symptoms resolve withinminutes, the athlete has returned to full strength and sensation, and there isno limitation of neck range of motion or increase in neck pain, the athlete mayreturn to play in the same contest. In this situation, the athlete should be re-examined at least once during the current contest, then during each of the next2 weeks [33] to assess for delayed onset of weakness necessitating furtherevaluation with neuroimaging or electrodiagnostics. In the event of persistentsymptoms, EMG may play a role in RTP decision-making, but this is alsocontroversial. Some recommend that fibrillation potentials in the setting ofclinical weakness necessitate withdrawal from play [44–46]. If weakness persists,repeated studies are recommended. If there is resolution of fibrillation poten-tials or presence of only scattered positive waves and polyphasic motor unitpotentials, the athlete may return to play [46]. This should, however, only occurif the athlete has attained full strength and sensation, with full neck range ofmotion and no neck pain [44,45]. Others have noted that clinical weaknessand EMG abnormalities have not correlated [36], and recommend that thenormalization of the physical examination and lack of contraindications to playon neuroimaging dictate RTP timing. The authors recommend that regardlessof EMG findings, the athlete only return to play after clinical return to baseline,and after an evaluation that may include appropriate neuroimaging in thesetting of prolonged symptoms. EMG is most helpful in the setting of a stingerto assist in localization and to assess changes over time, and to assess forchanges in the setting of repeated injury.One or two stingers, even in the same season, are not an absolute contra-

indication to RTP. Three or more stingers, especially within the same season orafter implementation of equipment adjustment and blocking/tackling techniqueadjustment, should lead to a consideration of cessation of play.

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Following a stinger, a comprehensive rehabilitation program to include neckand shoulder strengthening should be instituted [33,46,47]. High-ridingshoulder pads and neck rolls with or without chest orthosis can be added tofootball uniforms to offer protection against all proposed pathomechanisms[33,38,43,47]. Furthermore, blocking and tackling techniques should be exam-ined and proper technique taught to avoid dropping the head and shoulder[43,46,47]. Because athletes who have suffered a stinger have been shown to bemore likely to experience another stinger [41,48], and repeated stingers maylead to long-term weakness and discomfort [36], prevention is essential aftereven a single injury.

SEIZURES AND EPILEPSYSeizures and epilepsy have long been an area of debate concerning athleticparticipation. Historically, people who have epilepsy, particularly children, havebeen discouraged from sports participation or exercise on the basis that it maylead to seizure-related injuries, precipitate seizures, or worsen the person’sepilepsy [49–52]. Considering the long medical history of epilepsy, it is onlyrelatively recently that restrictions on participation in certain sports have beeneased explicitly [50,53–56]. There are reports of seizures associated with exer-cise [57–61], but as evidence grows that not only are exercise and sportsparticipation rarely harmful to people who have epilepsy, but in many instancesbeneficial [52,58,60–66], it is likely that increasing numbers of people who haveepilepsy will be active participants in sports, including organized sports. Accord-ingly, the sports medicine practitioner should have a basic understanding ofseizures, epilepsy, seizure first aid, the relationship of exercise and sports toseizures and epilepsy, and participation recommendations.

Seizures, Epilepsy, and ClassificationA seizure is a paroxysmal stereotyped event of acute onset resulting fromhypersynchronous, rhythmic, neuronal discharges. A seizure may occur as aresult of a specific insult to the brain, such as an electrolyte abnormality, alcoholwithdrawal, or hemorrhage. A seizure may also occur due to an intrinsiccharacteristic of the brain that may or may not be immediately identifiable.Seizures have been systematically classified by the International League AgainstEpilepsy (ILAE) into partial, or focal, seizures and generalized seizures [67].Partial seizures originate in a relatively small part of the brain, rather thaninvolving both hemispheres at the outset as in generalized seizures. Partialseizures are classified according to clinical manifestations and whether or notthere is an impairment of consciousness. Simple partial seizures do not alterconsciousness, and may be motor, somatosensory/special-sensory (ie, hallucina-tions or smells), autonomic (ie, piloerection), or psychic (ie, déjà-vu). Complexpartial seizures may or may not begin as simple partial seizures, but they doinvolve alteration, but not loss, of consciousness, either eventually or at theoutset. They are usually followed by a short period of “post-ictal confusion,”after which the person returns to normal cognition, although with no memory

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of the event itself. Partial seizures may also secondarily generalize when the fo-cal neuronal discharge spreads to involve both hemispheres.Generalized seizures originate in both hemispheres and necessarily lead to

alteration and loss of consciousness. They may be absence seizures (ie, briefrelatively motionless staring spells immediately followed by a return to normalcognition, usually occurring in children), myoclonic (ie, small isolated jerks),tonic-clonic (ie, generalized convulsions), tonic (ie, tonic limb muscle contrac-tion), clonic (ie, jerking movements), or atonic (ie, sudden loss of muscle tonewith falls) [67]. In all but absence and myoclonic seizures, the post-ictal recoveryperiod may be more pronounced and prolonged than after a complex partialseizure. It is simple to see how various manifestations of seizures hold verydifferent implications for different activities, particularly depending uponeffects on level of consciousness and the ability to protect oneself and reactto the environment.A person who has a seizure does not necessarily have epilepsy. Epilepsy

is a disease manifested as the tendency toward recurrent seizures. The ILAEhas also classified the epilepsies according to syndrome type [68]. Epilepsysyndromes vary according to clinical and electrographic characteristics, as wellas according to potential etiology. A full discussion of the epilepsy syndromes isbeyond the scope of this article; please see the ILAE’s published classificationfor details [68].

Assessment and ManagementBefore an athlete who has epilepsy participates in sports, the sports medicinepractitioner should become familiar with the athlete’s seizure history. The typi-cal seizure type, clinical manifestations, frequency, duration, and post-ictalrecovery characteristics should be known. Any history of the athlete havingbeen in status epilepticus (ie, a seizure or series of seizures that did not stop)should be clearly understood. There should be some understanding of theadequacy of seizure control, use of anticonvulsant medications, and theathlete’s compliance with those medications. Many people who have epilepsyhave known precipitants [69], and these should be known so as to be avoidedif possible. The more knowledge held about an athlete’s seizures, the betterequipped the practitioner will be if the athlete seizes.If an athlete has a seizure, basic seizure first aid applies, regardless of whether

the athlete is known to have epilepsy or not. Most importantly, medicalpersonnel should stay calm and urge those around them to do so as well.As with any potentially unstable situation, attention should be given to basiclife support principles—ensure adequacy of airway, breathing, and circulation.During a seizure, respiration can be compromised, and this should be monitoredand treated appropriately. The athlete should be assisted to the ground in theevent of a generalized convulsion, potentially harmful objects should be movedaway, the head cushioned if possible, and restrictive clothing, uniforms, orequipment should be loosened or, if necessary, removed. The athlete shouldnot be actively restrained. The athlete should only be moved if in a potentially

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dangerous place (ie, at the top of a staircase or at the side of a pool of water).Always prevent injury. Never place anything in the mouth or between the teethof an athlete having a seizure—the tongue will not be “swallowed,” but teeth caneasily be broken off by an object placed in the mouth and swallowed oraspirated. If the seizure is complex partial, the athlete should be attended to,but not forcibly interfered with unless entering into potentially harmful activity.With an absence seizure, the athlete may persist in the activity he or she wasengaged in at the onset of the seizure, and should be gently guided away fromdangerous situations. Several characteristics of the seizure should be at leastmentally recorded if possible. Seizure characteristics are listed in Box 4. Mostseizures stop without intervention. Once the seizure has stopped, the athleteshould be rolled to the side in case there is post-ictal vomiting. Nothing should begiven by mouth until the athlete is fully alert. The athlete should be attended tofor the duration of the seizure and recovery.There are several situations that should prompt activation of emergency

medical services and subsequent stable transport to a facility capable of neuro-logical or neurosurgical evaluation. If it is the athlete’s first seizure of life, itneeds to be evaluated for etiology and possible treatment. If the seizure isprolonged—lasting for more than 2 to 5 minutes—depending upon the athlete’stypical seizure duration if known, or if there are repeated seizures withoutrecovery to baseline mental status, this meets criteria for status epilepticus and isa medical emergency requiring prompt treatment. If the athlete has been injuredby the seizure or circumstances surrounding it, if there is any evidence ofrespiratory compromise following the seizure, or if anything is unusual about aseizure occurring in an athlete who has epilepsy, he or she should be evaluatedmore extensively. This is not an exhaustive list; if in any circumstance thesports medicine practitioner is uncomfortable or concerned, the athlete should

Box 4: Seizure characteristics to note

Activity at the time of the seizure onsetAthlete premonition, aura, or warning of seizure onsetTime of seizure onsetInitial clinical manifestation of seizure (ie, focal twitching of the right arm versus

generalized convulsion)Changes in clinical manifestation during seizure evolutionAbsence or presence of alteration of consciousnessPresence of cyanosisAutomatic activities (ie, lip smacking, playing with clothing)Seizure durationPresence of tongue biting or incontinenceMental state after seizure cessationDuration and character of post-ictal state

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be evaluated by a physician knowledgeable and experienced in seizure manage-ment and epilepsy.Special note should be made regarding the head-injured athlete and sei-

zures. Despite some evidence that head injury causes seizures, particularly insevere head injury, there is little to support the notion that sport-related headtrauma (such as concussion) predictably leads to seizure onset or epilepsy [52,70–72]. Nonetheless, there is evidence that the occurrence of a seizure up toa week after even mild head injury (ie, resulting in a Glasgow Coma Scale of13 to 15) may herald intracranial pathology, including that requiring neuro-surgical intervention, albeit in a low percentage of patients [73–75]. Fol-lowing even mild head injury, new onset of seizures should lead to promptevaluation and neuroimaging via CT scan or MRI to rule out catastrophic,treatable conditions.

Exercise, Seizure Exacerbation and Improvement, and ParticipationRecommendationsAs stated above, there are reports of exercise exacerbating seizures and generat-ing epileptiform electroencephalographic (EEG) activity [57–61]. In most series,however, these patients represent the minority of those studied [58,60,61]. Otherstudies have revealed a higher proportion of patients who experienced anattenuation of seizure frequency or epileptiform EEG changes with regularexercise [58,60–64,66]. It has even been shown that hyperventilation fol-lowing muscular exercise does not lead to the induction of absence seizures as

Table 3Sport specific recommendations for athletic participation in epilepsy

Sport Recommendation

Water sports Generally permitted with precautions—visual supervision of personqualified to rescue and resuscitate, clear water; children supervised bylifeguard or trained adult; no swimming in open water or swimmingallowed with flotation device; boating or fishing with flotation device,but avoid if frequent seizures; scuba diving, competitive underwaterswimming, or diving prohibited if active epilepsy

Sports at heights Pilot’s license prohibited; sky diving, hang gliding, free climbingdiscouraged; gymnastics discouraged for parallel bars and acrobatics forsome athletes; equestrian sports avoided except as closely supervisedtherapy for children

Motor sports Discouraged in active epilepsyShooting sports Dependent upon seizure frequency and type, occurrence pattern,

weapon usedContact sports No restriction, except possibly in new diagnosis with unclear courseAerobic sports No restriction; appropriate headgear and safety for skiing and ice skatingWheeled sports No restrictions except if frequent seizures or unclear frequency;

appropriate safety equipmentOther sports Exclusion more likely harmful than a seizure during the activity

Adapted from Fountain NB, May AC. Epilepsy and athletics. Clin Sports Med 2003;22(3):611–3; with permission.

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voluntary hyperventilation does [62,64]. Furthermore, positive psychological,social, and physical effects of exercise and participation in sports for patients whohave epilepsy have been asserted and demonstrated [49,50,53–56,58,65,66].Other than true exercise-induced seizures, exercise seems to have an overall

positive effect for people who have epilepsy. Any decision to participate insport, however, must be individualized. Age of the athlete, seizure type, seizurefrequency, predictable seizure timing, anticonvulsant compliance, and sport ofchoice all factor into the decision to participate [50]. The ILAE publishedrecommendations for the restriction of activities in children who have epilepsyin 1997 [50], and the only “activities that should be avoided” are scuba divingand sky diving. In their excellent review of current data, Fountain and May [52]outline several recommendations that are specific to particular sports andrecreational activities. Full details can be found in the original article. Asummary of their recommendations can be found in Table 3.

HEADACHEHeadache remains an extremely prevalent condition in the general population.One-year prevalence of all headache has been reported to be as high as 46%in women and 30% in men [76], with frequent headache of at least 180 headachesper year occurring in up to 4.1% of randomly selected people in one study [77].Migraine headache alone has been estimated to have a 1-year prevalence of6.0% in men and 17.2% in women in one survey [78], but up to 38.8% in womenand 19.6% in men when pooling patients including criteria for both strict mi-graine and probable migraine [79] as defined under the revised InternationalClassification of Headache Disorders (ICHD-2) [80]. Sport- and exercise-relatedheadache has been reported in 35% of university student respondents [81].Although the epidemiology of sport- and exercise-related headaches is less welldefined, athletes are susceptible to the same maladies that affect the generalpopulation. Athletes also suffer from exacerbations of underlying headachedisorders due to exercise, and are susceptible to headaches due to sports-relatedcauses such as trauma and high altitude. Although it is not necessary for thesports medicine practitioner to be able to treat and prevent many of the primaryheadache disorders, it is necessary that the practitioner is able to assess the athletewho has headache, is able to recognize “red flags” indicating a potentially moreserious condition, is familiar with some of the more common headache syn-dromes as classified in the ICHD-2, and knows when to refer an athlete to aspecialist for evaluation, treatment, and prophylaxis.

AssessmentA complete history and physical examination, both systemic and neurological,begin the assessment of the athlete who has headache. The focus is not only ondetermining headache characteristics to aid in diagnosis, but also on delineatingsigns of possible secondary headaches, such as those caused by intracranialhemorrhage or other mass lesion, infection or inflammation, or substance abuseor withdrawal. Important headache history notes can be found in Box 5. The

Box 5: Headache history

Current headache• Time of onset• Acuity of onset• Pain severity• Pain location• Pain character• Preceding injury• Associated symptoms• Exacerbating and alleviating maneuvers• Treatment attempts/medication use/drug use

Past history• History of prior headaches• Age of onset of prior headaches• Characteristics of prior headaches (as above)• Changes in headaches• Past medical history• Family history of headaches

Screen for red flags (see Box 6, below)

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physical examination should include, but not be limited, to: inspection for rashesor other signs of infection; cranial and cervical palpation for tenderness, triggerpoints, evidence of structural abnormality, and cervical range of motion; mentalstatus, including assessment of level of consciousness and speech and languageabilities; all cranial nerves, including ophthalmoscopy for fundoscopic examina-tion; motor and sensory testing; muscle stretch reflexes; and coordination andgait. If at any time the sports medicine practitioner is concerned about anypotential abnormalities in an athlete’s history or examination, a referral to aneurological specialist is warranted.Of particular import are certain signs and symptoms that may denote seri-

ous underlying pathology as the etiology of an athlete’s headache. There havebeen few studies validating these red flags, but they stand as important warningsigns. In one study investigating certain clinical features as predictors ofabnormal neuroimaging, only paralysis, papilledema, and the symptom com-plex of drowsiness, confusion, memory impairment, or loss of consciousnesswere statistically significant predictors, although asymmetrical pupillaryresponse and progressive visual or neurological changes also correlated. Pres-ence of three or more red flags also showed a strong correlation to abnormalimaging [82]. Such indicators, however, do not only indicate the possibility ofabnormal imaging; the presence of any red flag warrants not only neuroimag-ing, but also prompt neurological evaluation to assess for conditions that may

Box 6: Partial list of headache red flags

First or worst headache of life, particularly in adulthoodChange in stable headache patterns or characteristicsFocal neurological symptoms and signs (ie, pupillary asymmetry, visual loss,

paralysis, sensory deficits, incoordination, ataxia)PapilledemaNausea or vomiting, particularly unassociated with headachesPain maximal at onset or out of sleepAlteration in mental status or level of consciousnessAmnesiaMeningismus or other sign of infectionIncrease with straining, coughing, sneezingSeizures

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or may not be found on neuroimaging studies. A partial list of these red flagwarning signs can be found in Box 6.

Migraine HeadacheMigraine headache is common generally, and the same is true in athletes. Thereare many types of migraine classified by the ICHD-2 that may commonly occur inthe athlete, such as migraine without aura, migraine with aura and its variants,and retinal migraine. Diagnostic criteria for migraine include at least five attackslasting 4 to 72 hours (without successful treatment) with at least two of the fourcharacteristics of unilaterality, pulsatile quality, moderate to severe pain, andaggravation with routine activity. Nausea with or without vomiting, or photo-phobia and phonophobia must be present. An aura is a reversible, focal, oftenvisual neurological abnormality that occurs before or during the headache. Theheadache may not be attributable to another disorder. A retinal migraine consistsof monocular vision changes followed by a typical migraine headache [80].Migraine headache has many potential triggers, including menstruation,

tannins, chocolate, aspartame, and stress [83,84], to name a few. Migraineshave also been associated with exertion and trauma [84,85]. If known triggersexist, prevention focuses on avoidance or reduction, although this may not berealistically possible for the athlete who has exertion-exacerbated migraines.Certain nutritional adjustments or supplementations such as magnesium andriboflavin may be helpful [84,86]. Pharmacologic prophylaxis should be con-sidered when headaches are interfering with activities, when two headaches perweek require abortive therapy, when at least two headaches per month are noteffectively aborted, or when abortive therapy cannot be used [87]. In the UnitedStates, common prophylactic medications include tricyclic antidepressants,beta-blockers, and certain anticonvulsants. Alternative regimens may includecalcium channel blockers, selective serotonin reuptake inhibitors, and indo-methacin [84]. Medications given to abort acute migraines include anti-

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inflammatories, ergot derivatives, and triptans; some have reported utility ofoxygen, lidocaine nasal drops, and isometheptene [84].

Tension-Type HeadacheTension-type headache (TTH) is probably the single most common primaryheadache type. Episodic TTH (ETTH) has been shown to have a 1-yearprevalence of 38.3% in the United States, with chronic TTH (CTTH) havinga 1-year prevalence of 2.2% [88], although some studies have rated it muchhigher. It may or may not be associated with pericranial tenderness. TTH maylast from minutes to days, is generally bilateral, has a tight nonpulsatile quality,is mild to moderate in intensity, and is usually not exacerbated by routineactivity. ICHD-2 criteria do not allow for nausea or vomiting, and allowphotophobia or phonophobia, but not both [80]. In practice, TTH can be fairlysevere and may involve nausea, photophobia, or phonophobia. Musculartenderness to palpation over the head and neck is common. Non-narcotic,over-the-counter analgesics such as aspirin and acetaminophen have beenshown to be effective in the acute setting [89,90], as have nonsteroidal anti-inflammatory drugs [91–93], which have also been shown to be equivalent to[94,95] or superior to [96,97] acetaminophen. Physiotherapy [98–101] andcertain antidepressants [101–105] are useful in TTH prophylaxis. A recentwell-constructed trial of botulinum toxin A, the first of its kind, did not find asignificant effect on TTH [106], but this remains a controversial issue.

Post-Traumatic HeadacheHeadache is a common sequela of even mild head or neck injury, and a verycommon manifestation of concussion [16]. In a study of 443 high school andcollege football players, 85% reported experiencing a headache at some time as aresult of hitting, 21% in the preceding contest; and only 16% of those experienc-ing headache overall informed a coach, physician, or trainer [107]. The trueincidence of acute post-traumatic headache (PTH) is difficult to determine forthis reason. The ICHD-2 indicates that for a headache to be considered acutePTH, it must have an onset within 7 days of any severity of head trauma (or ofregaining consciousness), and must resolve within 3 months (or it is known aschronic PTH), but PTH has no typical characteristics [80]. Almost any headachetype may result from head injury, but TTH is most common, occurring in up to85% of patients [108]. The single most important consideration in acute PTH isto exclude other more serious pathology. This may require neuroimaging orneurological or neurosurgical evaluation. Treatment is focused on addressingany underlying pathology, and PTH is treated generally with prophylacticmedication and abortive medication appropriate to the primary headache syn-drome of which the PTH is reminiscent. Treatment may involve physiotherapyor biofeedback [108,109].

Primary Exertional HeadachePreviously known as benign exertional headache, this headache has been de-scribed as being the most common type of exercise-related headache in athletes,

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although not with strict criteria applied [85]. It is considered exclusive ofmigraine induced by exercise. It is precipitated by exercise, described as throb-bing, and lasts 5 minutes to 48 hours. Upon first occurrence of such a headache,subarachnoid hemorrhage must be excluded [80] by CT of the head or cere-brospinal fluid analysis. When benign, it usually occurs in the young, typicallyin men, is less explosive, and is often bilateral. When associated with under-lying pathology (usually due to subarachnoid hemorrhage), age of occurrence isolder, there is no gender predominance, and the headache is explosive andpersistent and is more reliably bilateral [110]. Indomethacin has been describedas beneficial for the benign exertional form [111,112].

Cautions and WarningsHeadaches are extremely variable in presentation, characteristics, evaluation,and management. There is a vast array of headache syndromes, far beyondwhat can be addressed in this article. In addition to the few relatively commontypes described here, other headache syndromes may result from neuralgiformpain, vascular etiologies, inflammatory disorders, or structural abnormalities.Concern has even been raised that dietary supplements, herbal preparations, andsports energy drinks may lead to headache, sometimes as a symptom of intra-cranial hemorrhage (Bradford Worrall, MD, Charlottesville, Virginia, personalcommunication, January 2005).Treatment can be complex, particularly in the athlete. A number of com-

mon headache abortive regimens and prophylactic medications can be foundon the World Anti-Doping Agency’s Prohibited List for 2005 [113], althoughthere is a process for therapeutic exemptions. Many headache medicationshave the potential for overuse as well, and this can lead to analgesic overuse,or rebound, headache, which can be quite difficult to manage and treat.Newer recommendations regarding the safety of certain nonsteroidal anti-inflammatory medications have only served to make treatment of the patientwho has headache more difficult. Anyone treating athletes who have headachesshould have familiarity with the medications being used, knowledge of theindications, effects, maximal doses, potential complications, and contraindica-tions to usage. If at any time the sports medicine practitioner is not comfort-able with the evaluation or management of an athlete who has headache, itis appropriate to refer the athlete to a specialist with experience in the field ofheadache management.

SUMMARYNeurological conditions are relatively common in sports, either as a result ofinjury suffered during play (eg, head injury, stingers, or post-traumatic head-ache), or as a pre-existing condition such as epilepsy or common headachesyndromes. Sports medicine practitioners need to be prepared to assess theinjured athlete, appropriately triage the athlete according to possible severityof injury, and be aware of RTP issues. Moreover, they need to be sufficientlyaware of the appropriateness of referral to a neurological specialist for evalua-

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tion and management of certain conditions, and be comfortable with certainmodes of management that such specialists may implement.

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