2002, Vol.21, Issues 1, The Spine and Sports

THE SPINE AND SPORTS

PREFACE

WILLIAM C. LAUERMAN, MDGuest Editor

It was indeed my pleasure to accept Dr. Millers invitation to put togetheran issue of Clinics in Sports Medicine dealing with spinal disorders and injury inathletes. I hope the reader will be pleased with the variety of topics presented,all dealing with either common or potentially very serious injuries or conditionsinvolving athletes.

The issue leads off with Dr. Robert McAlindon reviewing appropriate initialevaluation and treatment of athletes who have sustained a head and/or neckinjury during competition. This is an up-to-date review dealing with one of thefew times that orthopaedic surgeons come into contact with potentially life-threatening injuries. Drs. Allen and Kang have contributed a manuscript ontransient quadriparesis in the athlete. This overview brings us up to date oncurrent thinking in terms of etiology, treatment, and return-to-play considera-tions. Drs. Brian Shannon and Klimkiewicz have contributed a very thoroughreview dealing with the subjunctive cervical burners in athletes. This is a com-mon condition, relatively poorly understood and claried greatly, I believe, bythis article.

Drs. Greg Sassmannshausen and Smith have helped out with a discussionof what I believe to be one of the most difcult patient populations to treat, theyoung athlete with back pain. Their common sense approach to evaluation andmanagement, I am quite sure, will be extremely helpful. Dr. R. Lane Wimberlyand I have reviewed the all too common cause of back pain, spondylolisthesisin the athlete.

We are then fortunate enough to have Dr. Kirkham Wood from the Univer-sity of Minnesota and the Twin City Spine Center, who has reviewed the topicof spinal deformity, both scoliosis and kyphosis in the adolescent athlete.

Dr. Robert Watkins has provided an overview of lumbar disc injuries inathletes and Dr. Anthony Delitto discusses for us the subject of low backrehabilitation in the athlete. Finally, Drs. Trainor and Wiesel review the epidemi-ology of low back pain in the athlete.

Hopefully, this collection of articles will prove both entertaining and educa-tional. There is much new information regarding etiology, evaluation, and treat-ment for many of these conditions and I hope that this issue of Clinic in Sports

ix

Medicine will provide a valuable reference for physicians treating both adolescentand adult athletes.

WILLIAM C. LAUERMAN, MDGuest Editor

Georgetown University Hospital3800 Reservoir Rd., NWWashington, DC 20007

x PREFACE

THE SPINE AND SPORTS 02785919/02 $15.00 .00

ON FIELD EVALUATION ANDMANAGEMENT OF HEAD AND

NECK INJURED ATHLETES

Robert J. McAlindon, MD

All physicians who care for athletes must be able to recognize,evaluate, treat, and help to prevent recurrent head and neck trauma.The return of the injured athlete to collision sports is a complex issue.Careful evaluation of all injuries should be done on an individual basis.

HEAD INJURIES

The scalp, skull, meninges, and cerebral spinal uid form a multilay-ered barrier that protects the brain from injury. The brain in competitiveathletics is injured in one of two ways. In one type of injury, an objectstrikes the resting, but movable, head, causing injury at the site of theimpact. This is called a coup lesion. In another type, the moving headstrikes a nonmoving object and produces an injury to the brain in anarea opposite to the site of the impact. This is the so-called contrecouplesion. Each mechanism is capable of generating rotational (angular) ortranslational (linear) forces through the brain tissue. Rotational forcesproduce a shearing mechanism across the nerve bers, commonly lead-ing to a loss of consciousness. Translational forces lead to compressionthat can cause a skull fracture, hematoma, or cerebral contusion, but lessfrequently to a loss of consciousness. The brain tolerates compressivestresses better than shearing stresses. Cerebral spinal uid and the elasticproperties of the brain tissue make the brain somewhat able to becompressed and therefore resistant to translational forces. Shear force

From the The Hughston Clinic, PC, Auburn, Alabama

CLINICS IN SPORTS MEDICINE

VOLUME 21 NUMBER 1 JANUARY 2002 1

2 McALINDON

travels parallel to the surface of the brain and imparts a linear zone ofinjury. The degree of head injury is related to the position and motionof the head at the time of impact.

Classication of Head InjuriesHead injuries can be broadly classied as focal or diffuse. Focal

brain injuries are cerebral contusions or hematomas that result fromtranslational energy. A diffuse brain injury, especially a concussion,occurs as the result of rotational energy and is associated with globaldisruption of neurologic function. A diffuse brain injury often is notassociated with visible or objective brain lesions.

Focal Brain InjuriesFocal brain injuries include cerebral contusions, in which a small, ill-

dened area of hemorrhage or edema is noted, and often are the resultof a contrecoup-type lesion (Fig. 1). Intracerebral hematomas occur withinthe brain. The site and location of the hematoma determine symptoms.

Figure 1. Types of focal brain injury: subdural hematoma, hemorrhage in the subduralspace between the dura and arachnoid membrane; epidural hematoma, accumulation ofblood in the epidural space owing to damage in the middle meningeal artery; and intracere-bral hematoma, hemorrhage in to the cerebrum. (Adapted from Jacko JG: Head injuries.In Baker CL [ed]: The Hughston Sports Medicine Book. Philadelphia, Williams & Wilkins,1995, pp 112117; with permission.)

ON FIELD EVALUATION AND MANAGEMENT OF INJURED ATHLETES 3

Epidural hematomas result from a tear commonly of the middle meningealartery. A rapidly expanding hematoma may prove to be life threateningby causing brain herniation. Subdural hematomas occur when the bridgingveins between the brain and dura are torn. Nausea, vomiting, andseizures may ensue as an enlarging hematoma causes a slowly enlargingmass and pressure on the brain.

Diffuse Brain InjuriesOf all head injuries, a concussion is the most common. Sometimes, it

is the most difcult to recognize. It is estimated that 250,000 concussionsoccur in the United States in football alone each year.5 Twenty percentof high school football players suffer concussions each year, and thechance of sustaining a second concussion is ve times higher than thatof sustaining the rst. Contact with articial turf appears to be associatedwith more serious concussions. Only approximately 9% of concussionsinvolve loss of consciousness. Eighty-six percent involve headaches.Thirty percent of football players who sustain concussions return to playthe same day.12

The complexity of the brain and the lack of objective signs andsymptoms in some patients make injury assessment difcult. Signs andsymptoms present at the time of injury may quickly resolve, but theinjury may be life threatening.

Despite the use of protective equipment, the head and brain aresusceptible to injury during athletic competition. Attempts to character-ize and classify concussions have been difcult. Early detection byrecognizing the signs and symptoms of concussion is critical to manag-ing the head-injured athlete.

Neural BiologyConcussion is dened as a clinical syndrome characterized by im-

mediate and transient post-traumatic impairment of neural function,such as alteration of consciousness, and disturbance of vision or equilib-rium, because of brain stem involvement. However, we continue to lacka complete understanding of the pathology of a concussion. No objectiveneural, anatomic, or physiologic measurements can be used to assessthe severity of a concussion. The athlete can remain in a state of viabilityafter a concussion and therefore is susceptible to second-impact syn-drome during this variable time period.7, 19, 23 In addition, the cumulativeeffects of injury remain a concern.11

It is now known that a metabolic disturbance arises in the damagedbrain tissue.3 There is a notable increase in demand for glucose and areduction in blood ow. This results in inability of the brain tissue torespond to increasing demands for energy. Neural tissue demands morefuel but is limited in its capacity to obtain it. The duration of thisdisturbance may be related to the duration of symptoms and, moreimportantly, the period of vulnerability to second impact. Calcium, he-

4 McALINDON

mostasis, or regulation may play a role in the posttraumatic cerebralblood ow, as well, with vasoconstriction present with high-calciumvalues.29

On-Field Evaluation

Being prepared for head injuries is the key to on-eld management.In the event of an injury, the equipment needed to evaluate and, ifnecessary, to transport the injured athlete must be available. The mostimportant objective of on-eld management is to prevent further injury.

First, an accurate and complete diagnosis of the level of conscious-ness and evaluation of associated injuries, such as cervical spine injuries,must be obtained. When approaching an injured player, the examinershould observe the posture of the athlete and note any spontaneousmotion or verbalization. Total lack of movement may alert the medicalteam to a potential spine injury. Incoherent or confused speech suggestsa signicant concussion. Athletes with closed head injuries frequentlyhave a blank expression and may appear confused or demonstrateinappropriate verbiage. The Glascow coma scale can provide insight intothe level of consciousness (Table 1).29 A grade of 11 or higher on the comascale is generally associated with an excellent prognosis for recovery. A

Table 1. GLASGOW COMA SCALE*

Response Point/s ActionEye openingSpontaneously 4 Reticular activity system is intact; patient may

not be awareTo verbal command 3 Opens eyes when told to do soTo pain 2 Opens eyes in response to painNone 1 Does not open eyes to any stimuli

VerbalOriented, converses 5 Relatively intact central nervous system; aware

of self and environmentDisoriented, converses 4 Well articulated and organized, but disorientedInappropriate words 3 Random, exclamatory wordsIncomprehensible 2 Moaning; no recognizable wordsNo response 1 No response or intubated

MotorObeys verbal commands 6 Readily moves limbs when told toLocalizes to painful stimuli 6 Moves limb in an effort to avoid painFlexion withdrawal 4 Pulls away from pain in exionAbnormal exion 3 Decorticate rigidityExtension 2 Decerebrate rigidityNo response 1 Hypotonic, accid; suggests loss of medullary

function or concomitant cord injury

*Normal, 15.From Wojtys EM, Hovda D, Landry G, et al: Concussion in sports. Am J Sports Med 27:676686,

1999; with permission.


score of 7 or less is, of course, considered serious. The eye motions,verbal cues, and motor competency can be used to rapidly determinethe initial severity of an injury. Retrograde amnesia is an importantfactor to test for. The presence of a headache, dizziness, and blurredvision should also be determined.

After an associated spine injury has been ruled out and the level ofconsciousness is appropriate, the athlete may then be assisted into asitting position. It is believed that a seated or standing position will helpdiminish intracranial pressure and help alleviate some symptoms. Oncestable and seated, the athlete may be assisted to a standing position andhelped off the eld.

Bench Evaluation

After the player is removed from the eld of play, a more thoroughexamination is begun.29 Dizziness, vertigo, double or blurred vision,photophobia, ringing in the ears, headache, and nausea can then beassessed. Vomiting is rare but may be present and should be a causefor concern. Careful inspection and palpation of the head should beundertaken at this time. A visual acuity examination should be done,and the presence of nystagmus should be noted. Nystagmus can indicatea rotational brain injury. A baseline neurologic examination with sensa-tion and strength testing of the extremities must also be done.

If initial ndings are abnormal, frequent re-examinations must bedone to document progression of symptoms. Initially the player mustbe observed for 15 minutes on the sidelines. If any symptoms persist,return to play on the same day is not recommended. Maneuvers, suchas a 40-yard dash, sit-ups, or deep squats, that increase intracranialpressure may help elicit some symptoms. If symptoms are present dur-ing these maneuvers, the player should not return to competition. If aplayer who is asymptomatic and has no difculty with maneuvers thatincrease intracranial pressure subsequently returns to play, he or shemust be re-evaluated during the contest to detect any clinical changes.An athlete who develops seizures, focal neurologic signs, or deteriora-tion in mental status should be transported to an appropriate medical fa-cility.

Concussion Grading

The traditional concussion grading scale was introduced by Cantu.5The grade of concussion represents severity of the brain injury and isbased on the level of consciousness and duration of memory loss. Pa-tients with grade 1 concussions have no loss of consciousness andmemory loss of less than 30 minutes. Patients with grade 2 concussionshave loss of consciousness of less than 5 minutes and memory losslasting up to 24 hours. Patients with grade 3 concussions have loss of

6 McALINDON

consciousness of more than 5 minutes and memory loss exceeding 24hours. In 1991, The Colorado Medical Society developed a gradingsystem.8 According to its system, patients with mild concussions exhibitconfusion but no amnesia and no loss of consciousness. Moderate con-cussions are characterized by amnesia as well as confusion. Loss ofconsciousness characterizes a severe concussion.10

In a recent study by Guskiewicz, 59% of collegiate and high schoolathletes with head injuries demonstrated mental confusion.13 Ninety-sixpercent had headaches. Thirty-two percent of these athletes had confu-sion lasting more than 10 minutes. Nine percent of their series demon-strated loss of consciousness. Disorientation and visual changes occurredmuch more frequently than amnesia. For athletes who had had multipleconcussions, the injury severity increased with the number of recurrentinjuries. In 1983, Gerberich found that an athletes risk for suffering asecond concussion injury was four times greater than an athletes withno history of concussion.10

Return to Play

Determining when an athlete can return safely to competition afteran injury is one of the most controversial issues in sports medicine. Itshould be recognized that some symptoms, such as amnesia and head-ache, are sometimes delayed. In general, if the athlete has any symptomson the eld that are related to the concussion, he or she should not beallowed to return to play. The sport itself should not be a determiningfactor with respect to return-to-play issues. All concussions warrantmonitoring for at least 15 minutes.

If, after 15 minutes, if there has been no loss of consciousness andall signs and symptoms are normal, participation may resume. If residualsymptoms remain, the athlete should be disqualied for that dayscompetition. Only after the athlete has become asymptomatic, has passedmemory testing, and has no symptoms with provocative testing, can heor she be returned to play. The injured athlete must be continuallymonitored throughout the remainder of the event. The stress of thecompetition can produce signs and symptoms not seen off the eld. Anyepisodes of loss of consciousness, no matter how brief, should precludereturn to play at that time.

Reportedly, 30% of high school and collegiate football players returnto participation on the same day of injury.13 Of these players, 14 hadgrade 2, or moderate, concussions. The players who returned to play onthe same day were held out for only an average of 13 minutes. Theremaining 70% of football players with concussions were held out anaverage of four days for a mild grade 1 concussion, and those withgrade 2 injuries returned to play 8 days after injury. Twenty percent ofplayers with concussions do not leave the game because the symptomswere either not reported or not identied until after the competitionended.


Many authors have warned against the dangers involved in re-turning to athletics too early,5, 8, 9, 16, 17, 27 but many times these warningsare ignored. If an athlete returns to play on the same day, he or shemust be asymptomatic for at least 15 minutes both at rest and duringexertion. He or she must have a normal neurologic examination, andcertainly have had no loss of consciousness at any time. Delayed returnto play is reserved for athletes who are not asymptomatic within 15minutes or who develop symptoms or worsening signs on exertion. Anyloss of consciousness precludes play on the same day. Ninety-six percentof athletes have a headache at some point after the concussion. Any newheadache after 48 hours or a change in the character of the headachewarrants further medical evaluation. Dizziness, slowing of response,difculty concentrating, or memory loss precludes participation at anytime. An athlete who feels ne is not necessarily normal. It is not knownhow quickly brain healing occurs after neural function returns to normal.The absence of neural cognitive decit is used to judge return-to-playcriteria but does not necessarily relate to the brain-healing process.Symptoms that last more than 15 minutes preclude same-day play, butexact guidelines regarding play after a longer period of symptoms arenot yet dened. Five to 7 days of rest may benet some athletes, whereasothers may be able to play much sooner. Our current medical knowledgedoes not address this situation.

CERVICAL SPINE INJURIES

Each year, more than 1,000,000 students participate in high schoolfootball and 200,000 in collegiate and professional football. Cervicalspine injuries occur in 10% to 15% of football players.1, 2 Most of theseinjuries are self-limiting, and a full recovery can be expected. In 1976,Albright found that 50% of incoming freshman football players with aprevious neck injury had radiographic changes in their cervical spinethat indicated instability, compression fracture, or neural arch derange-ment.1 Although relatively uncommon, a neck injury can be devastating.Proper and prompt management is absolutely essential. The spacial andgeometric orientation of the cervical facet joints allows a high degree ofmobility, and this mobility allows for a high degree of injury. Soft-tissueinjuries including muscle, ligament, and tendon injuries occur frequentlyas well.

The cervical spine comprises the rst seven vertebrae of the spinalcolumn. C1, or the atlas, is essentially a ring without a vertebral body.It articulates with the base of the skull by means of two synovial jointsformed with the occipital condyles. C2, or the axis, includes a truevertebral body and an upward projection, the dens, that articulates withC1. A strong ligamentous component maintains structural integrity andalignment between C1 and C2. This anatomy allows a high degree ofmobility and rotation. Fifty percent of cervical spine rotation occurs atthe C1-C2 articulation. The remaining 50% of rotation occurs over the

8 McALINDON

inferior ve segments, C3 through C7. The spinal cord is protectedwithin the spinal canal. Paired laminae provide the roof of the canal.There are two facet articulations at each level oriented obliquely toprovide stability in the anterior-posterior direction. Each vertebral bodyis separated from the adjacent body by an intervertebral disc made upof a semisolid nucleus pulposus contained within a brous annulus.

Anterior and posterior ligaments connect the vertebral bodies andprovide structural support to the cervical spine (Fig. 2). The musclesmay be broadly grouped into those of the posterior cervical spine thatextend the head and neck, those of the lateral cervical spine that functionin rotation and lateral exion, and those of the anterior cervical spinethat ex the head and neck. The spinal cord is a continuation of thecentral nervous system and is widest in the midcervical region.

The cervical spine injury that occurs most frequently in footballplayers is neurapraxia of the nerve roots or brachial plexus. As many as50% of linemen, linebackers, and defensive ends have one or moreepisodes per season.26 Stingers or burners are caused by compressive ortraction injuries to the multiple roots or the brachial plexus itself. Theupper roots or trunk are stretched by a shoulder depression and lateralhead exion away from the involved side. Neurapraxia can also becaused by direct compression of the brachial plexus. Athletes may com-plain of a multitude of ndings. Careful examination is required toprevent attribution of a burning or stinging sensation to a benign condi-tion when, in fact, it may be the result of a much more serious problem.

Figure 2. The ligaments of the upper cervical spine (Adapted from Kelley LA: Functionalanatomy of the spine. In Baker CL [ed]: The Hughston Sports Medicine Book. Philadelphia,Williams & Wilkins, 1995, pp 17383; with permission.)


Most often, stingers or burners are unilateral in nature. The presenceof symptoms in both upper extremities suggests a spinal cord ratherthan a nerve root or plexus injury. The athlete may complain of a deadarm with shoulder or arm pain and unilateral muscle paresis. Symptomsare generally self-limiting, and strength usually returns within 24 to 48hours. A variable degree of weakness in the muscles innervated by thespecic portion of plexus or trunk that is irritated can last up to 6 weeks,and certainly permanent changes may be seen as well in severe cases.Examination of the cervical spine should be free of any painful palpation.There should be no midline tenderness over the bony architecture. Rangeof motion should be basically normal with the exception of some musclespasm that may cause some tightness to rotation as well as exion andextension, but overall the arc of motion should be quite normal. Ifsymptoms resolve quickly and the neurologic examination is otherwisenormal, once full motor strength returns the patient may be allowed toreturn to play.

Persistence of symptoms or lack of pain-free range of motion withpalpable pain over the bony architecture requires further evaluation andcervical spine radiographs. The player should be restricted from furtherplay until he or she has recovered full muscle strength. Stingers andburners may be preventable by working on tackling technique. Certainly,the head up position must be maintained. Cervical collars or shoulderpad orthotics can also help with prevention of burners and stingers.

Intervertebral Disc Lesions

Acute traumatic herniation of a disc with resultant cord compressioncan result in transient quadriplegia or permanent quadriparesis or quad-riplegia. Affected athletes experience bilateral pain, numbness, and tin-gling in the extremities. In severe cases, paralysis may be noted. Immedi-ate transport to an appropriate medical facility, radiographs, and furtherimaging, such as computed tomography or magnetic resonance imaging,may be warranted. Decompression by discectomy and interbody fusionmay be warranted in patients with symptoms of persistent radiculopathyor myelopathy.

Transient Quadriplegia

Transient quadriplegia is caused by neurapraxia of the cervicalcord.25 The symptoms include bilateral burning pain, tingling, and lossof sensation in the arms or legs. Motor symptoms vary from mildweakness to complete paralysis. Episodes are transient, and completerecovery usually occurs within 10 to 15 minutes, but it can take as longas 48 hours. Radiographs are negative for fractures or dislocations butfrequently reveal congenital stenosis.

Cord compression without residual radiographic abnormality may

10 McALINDON

occur by means of a pincer-like mechanism. When the cervical spine ishyperextended, the cord is compressed between the inferior margin ofthe superior vertebra and the anterior and superior laminae of thesubjacent vertebra. The posterior longitudinal ligament and ligamentumavum may become infolded and contribute to the central canal nar-rowing. Athletes with congenital or acquired cervical stenosis are predis-posed to cord neurapraxia with hyperextension or hyperexion loading.

Stenosis is dened on the basis of a diameter in which the cervicalcanal is believed to be narrow.21 To assess for narrowing, the canaldiameter is measured on a lateral radiograph from the midpoint of theposterior aspect of the vertebral body to the nearest point along thespinolaminar line. The normal midsagittal diameter should be between14 mm and 23 mm. Stenosis is dened on the basis of a diameter of lessthan 13 mm. Variations and technique as well as lm distances andanatomy often contribute to inaccurate measurements. To minimize theseareas, Torg and Pavlov proposed using a ratio of the segmental sagittaldiameter of the canal to the width of the vertebral body (Fig. 3).24 Aratio of less than 0.8 has been used to dene canal stenosis. It hasbeen found that 93% of players with transient quadriplegia, 12% ofasymptomatic nonathletes, and 48% of asymptomatic football playershave spinal stenosis. A threefold increase in the incidence of stingershas also been noted in athletes with spinal stenosis.4

Unstable Cervical FracturesMost patients with football-related spinal cord injuries have had

concomitant unstable fractures and dislocations. Through the late 1960s

Figure 3. The Torg ratio is calculated by dividing the shortest distance between theposterior vertebral body and the spinolaminar line (a) by the vertebral body width (b).(Adapted from Torg JS, Pavlov H: Cervical spinal stenosis with cord neurapraxia andtransient quadriplegia. Clin Sports Med 6:115133, 1987; with permission.)


and early 1970s, the incidence of severe head injuries decreased, whereasthe incidence of severe cervical spine injuries increased.27 The act oftackling by defensive players was associated with the greatest risk ofinjuries that resulted in quadriplegia.27 Most catastrophic events resultedfrom either a combined fracture dislocation or anterior compressionfracture. Improvements in helmet design and construction have de-creased head injuries, but as athletes have become stronger, faster, andmore agile, the cervical spine has been placed at substantial risk ofinjury. Tackling techniques such as using the head as a spear alsoincrease the risk of catastrophic cervical spine injury.6

Axial loading of the cervical spine is the primary mechanism forsevere neck injuries.26 The cervical spine can absorb much of the energyof collision by dissipation through the paravertebral musculature, theintervertebral discs, and the normal lordotic curve of the cervical spine.When the neck is exed beyond 30 degrees, the normal lordotic curve isattened and forces applied along the top of the head are now directedinto a straight column (Fig. 4).28 In this position, the cervical spine ismuch less able to disperse the forces that are being exerted. With contin-uing load, compression forces occur within the vertebral disc causingirregular deformation and buckling. Intervertebral disc pathology mayoccur. Eventually, should the force continue, the spine fails in exionwith a resultant fracture or dislocation. Although axial loading accountsfor most fracture dislocations, it does not account for all patterns. A

Figure 4. A, When the neck is in a normal, upright, anatomical position, the cervical spineis slightly extended because of the natural cervical lordosis. B, When the neck is slightlyexed to approximately 30, the cervical spine is straightened and converted into a seg-mented column. (Adapted from Torg JS, Vegso JJ, ONeill MJ, et al: The epidemiologic,pathologic, biomechanical, and cinematographic analysis of football-induced cervical spinetrauma. Am J Sports Med 18:5057, 1990; with permission.)

12 McALINDON

combination of rotation and compression can produce a variety of recog-nized spinal injuries. A couple of motions can lead to extensive injury.Flexion, extension, rotational, and shear forces within adjacent regionsof the cervical spine can place the cervical spinal cord at risk.

Field Evaluation And Early Treatment

Initial involvement of the sports medicine physician in the care ofan athlete with a cervical spine injury begins on the eld. Essentialsideline equipment should include a stretcher, tools necessary to removea face mask, a spine board, and airway protective equipment. Prepared-ness is paramount to timely management.

It is necessary to remove the face mask for airway control of theunconscious athlete while simultaneously protecting the cervical spine.20In general, newer cage-type masks are removed by cutting the plasticattachment loops with a scalpel or utility knife. Most of these masks arealso held on with a series of screws that can easily be removed by usingPhillips head screwdrivers. The chin strap and helmet are best left inplace. Spinal malalignment is noted when the shoulder pads are left inplace and the football helmet is removed. Recent studies have alsoshown that hockey helmets that are removed while leaving the shoulderpads in place also cause spinal malalignment.18 In general, it is probablysafest to leave the helmet in place while protecting the airway after face-mask removal. The jaw-thrust technique is probably safe as well inproviding and maintaining good airway alignment. Transportation to amedical facility is necessary for any athlete with mental status changes,neck pain or tenderness, limited cervical motion, and symptoms refer-able to a cord injury. The patient must be fully immobilized on a spineboard with the helmet and shoulder pads remaining in place. The helmetshould be removed only when permanent mobilization in a controlledsetting can be instituted after lateral cervical spine radiographs havebeen taken. Only at that time should the chin strap be removed, the earaps of the helmet spread, and the helmet gently pulled in line with thecervical spine while the head is supported under the occiput.

Return To Play

Sideline evaluations are often a difcult matter. The player must beexamined to determine the specic location of pain, the presence ofnumbness, tingling, or weakness, and the duration of symptoms. Again,a complete motor and sensory neurologic evaluation of the upper andlower extremities should be performed. Mental status should also beevaluated at this time.

An athlete with tenderness over bony prominences must have radio-graphic documentation of normality before returning to play. Any signsor symptoms of neurologic decit on both sides of the body should


preclude return to play for the same day as well. Transient unilateralmild numbness and tingling that resolves quickly, as in the situation ofa stinger or burner, may not preclude a players return to play. Ingeneral, when normal pain-free motor strength and normal sensationreturn, these athletes can be allowed to return to competition.

The return of the injured athlete to collision sports is a complexissue. Each athlete must be evaluated carefully on an individual basis.Frequent serial examinations are necessary to help guide the physicianin his or her treatment regimen. Although the decision to allow anathlete to return to play after some injuries can be complicated andequivocal, the medical sequelae of certain cervical spine injuries areabsolute contraindications to a return to contact sports. Neck injuriesthat result in permanent central nervous system dysfunction, permanentand signicant peripheral nerve dysfunction, and spinal fusion at theC4 level or above are examples of such contraindications. Anatomicabnormalities such as spinal stenosis are relative contraindications to anathletes to return to play even after a full clinical recovery.

References

1. Albright JP, McAuley E, Martin RK, et al: Head and neck injuries in college football:An eight-year analysis. Am J Sports Med 13:147152, 1985

2. Albright JP, Moses JM, Feldick HG, et al: Nonfatal cervical spine injuries in interscho-lastic football. JAMA 236:12431245, 1976

3. Bergsneider M, Hovda DA, Shalmon E, et al: Cerebral hyperglycolysis following severetraumatic brain injury in humans: A position emission tomography study. J Neurosurg86:241251, 1997

4. Bruce D, Schut L, Sutton L: Brain and cervical spine injuries occurring during orga-nized sports activities in children and adolescent. Clin Sports Med 1:495514, 1982

5. Cantu RC: Guidelines for return to contact sports after cerebral concussion. PhysicianSportsmed 14:7583, 1986

6. Cantu RC, Mueller FO: Catastrophic spine injuries in football (19771989). J SpinalDisord 3:227231, 1990

7. Cantu RC, Voy R: Second impact syndrome: A risk in any contact sport. PhysicianSportsmed 23:172177, 1995

8. Colorado Medical Society. Report of the Sports Medicine Committee: Guidelines for theManagement of Concussion in Sports (revised). Denver, Colorado Medical Society, 1991

9. Evans RW: The postconcussion syndrome: 130 years of controversy. Semin Neurol 14:3239, 1994

10. Gerberich SG, Priest JD, Boen JR, et al: Concussion incidences and severity in secondaryschool varsity football players. Am J Public Health 73:13701375, 1983

11. Gronwall D, Wrightson P: Cumulative effects of concussion. Lancet 2:995997, 197512. Guskiewicz KM, Perrin DH, Gansneder BM: Effect of mild head injury on postural

stability in athletes. J Athl Train 31:300306, 199613. Guskiewicz K, Weaver NL, Padua DA: Epidemiology of concussion in collegiate and

high school football players. Am J Sports Med 28:643650, 200014. Jacko JG: Head injuries. In Baker CL (ed): The Hughston Sports Medicine Book.

Philadelphia, Williams & Wilkins, 1995, pp 11211715. Kelley LA: Functional anatomy of the spine. In Baker CL (ed): The Hughston Sports

Medicine Book. Baltimore, Williams & Wilkins, 1995, pp 1738316. Kelly JP, Nichols JS, Filley CM, et al: Concussion in sports: Guidelines for the preven-

tion of catastrophic outcome. JAMA 266:28672869, 1991

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17. Kelly JP, Rosenberg J: Diagnosis and management of concussion in sports. Neurology48:575580, 1997

18. LaPrade RF, Schnetzler KA, Broxterman RJ, et al: Cervical spine alignment in theimmobilized ice hockey player. A computed tomographic analysis of the effects ofhelmet removal. Am J Sports Med 28:800803, 2000

19. McCrory PR, Berkovic SF: Second impact syndrome. Neurology 50:677683, 199820. Palumbo MA, Hulstyn MJ, Fadale PD, et al: The effect of protective football equipment

on alignment of the injured cervical spine: Radiographic analysis in a cadaveric model.Am J Sports Med 24:446453, 1996

21. Pavlov H, Torg JS, Robie B, Jahre C: Cervical spinal stenosis: Determination withvertebral body ratio method. Radiology 164:771775, 1987

22A. Robertson WC Jr, Eichman PL, Clancy WG: Upper trunk brachial plexopathy infootball players. JAMA 241:14801482, 1979

23. Saunders RL, Harbaugh RE: The second impact in catastrophic contact sports headtrauma. JAMA 252:538539, 1984

24. Torg JS, Pavlov H: Cervical spinal stenosis with cord neurapraxia and transient quadri-plegia. Clin Sports Med 6:115133, 1987

25. Torg JS, Pavlov H, Genuario SE, et al: Neurapraxia of the cervical spinal cord withtransient quadriplegia. J Bone Joint Surg Am 68:13541370, 1986

26. Torg JS, Sennett B, Vegso JJ, et al: Axial loading injuries to the middle cervical spinesegment: An analysis and classication of twenty-ve cases. Am J Sports Med 19:620, 1991

27. Torg JS, Truex R Jr., Quedenfeld TC: The national football head and neck injuryregistry: Report and conclusions 1978. JAMA 241:14771479, 1979

28. Torg JS, Vegso JJ, ONeill MJ, et al: The epidemiologic, pathologic, biomechanical, andcinematographic analysis of football-induced cervical spine trauma. Am J Sports Med18:5057, 1990

29. Wojtys EM, Hovda D, Landry G, et al: Concussion in sports: Am J Sports Med 27:676686, 1999

Address reprint requests to

Dr. McAlindon at The Hughston Clinic, PC161 E. University Drive

Auburn, AL 36832

e-mail: [email protected]


TRANSIENT QUADRIPARESISIN THE ATHLETE

Christina R. Allen, MD, and James D. Kang, MD

SYNOPSIS

Transient quadriparesis is a rare cervical spine injury caused byaxial loading of the neck in extension or exion. Transient quadriparesisis associated with sensory or motor functional changes or a combinedsensorimotor decit. The athlete may complain of total body numbnessand moderate to severe weakness in all four extremities. The episodes,by denition, are not permanent, and complete sensory and motorrecovery occurs in 10 minutes to 48 hours. In all cases of the abovephenomenon, radiographs are negative for fractures and dislocations butfrequently demonstrate evidence of congenital spinal stenosis, acquiredstenosis, cervical instability, or congenital abnormalities such as Klippel-Feil syndrome. A considerable amount of controversy exists regardingreturn-to-play criteria and the risk for more severe injury after an athleteexperiences an episode of transient quadriparesis.

Introduction

One of the most disturbing and dramatic clinical syndromes associ-ated with cervical spine injury in athletics is transient quadriparesis.Also referred to as transient neurapraxia and cervical cord neurapraxia,transient quadriparesis may be considered a concussion of the cervicalspinal cord. It was perhaps rst described in 1879 by Obersteiner when

From the Division of Sports Medicine (CRA), Division of Spine Surgery (JDK), Departmentof Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsyl-vania



16 ALLEN & KANG

he used the term spinal cord concussion to describe spinal cordinjuries that resulted in complete neurologic recovery in 24 to 48 hours.17The phenomenon, although rare in incidence, has been noted to occurmost frequently in football athletes, but also has been documentedin athletes participating in boxing, hockey, basketball, and wrestling,21generally as the result of axial loading of the neck in extension or exion.Transient quadriparesis is associated with sensory or motor functionalchanges, or a combined sensorimotor decit. Sensory changes includeburning pain, numbness, tingling, and sensory losses. Motor changesrange from weakness to complete paralysis of both the upper and lowerextremities. The athlete may complain of total body numbness andmoderate to severe weakness in all four extremities. The episodes, bydenition, are not permanent, and complete sensory and motor recoveryoccurs in 10 minutes to 48 hours.5, 20, 21 Except for burning paresthesias,neck pain is not present at the time of injury, and there is completereturn of full, pain-free cervical motion.

A variant of this phenomenon, described by Maroon, is burninghands syndrome. Thought to be a mild form of central cord syndrome,burning hands syndrome causes burning dysesthesias and weakness ofthe hands and arms. An anteroposterior compressive force causes aninjury to the corticospinal and spinothalamic tracts. Most symptomsresolve within 24 hours, but the athlete may demonstrate reversibleabnormalities on magnetic resonance imaging and electrophysiologicstudies.10, 11

In all cases of the above phenomenon, radiographs are negativefor fractures and dislocations, but frequently demonstrate evidence ofcongenital spinal stenosis, acquired stenosis, cervical instability, or con-genital abnormalities such as Klippel-Feil syndrome. As a result of anNCAA football study performed by Torg in 1984, the incidence oftransient quadriparesis has been estimated at 1.3 episodes of transientweakness with paresthesias per 10,000 athletes, with an additional esti-mated incidence of 6 episodes of transient paresthesias alone per 10,000athletes.21

MECHANISM AND PATHOPHYSIOLOGYThe pathophysiology of transient quadriparesis is not entirely un-

derstood. It is believed to be a neurapraxia, implying that the injury iscaused by a physiologic conduction block that causes peripheral nerveaxon dysfunction without anatomic disruption. This conduction block isusually caused by compression or contusion, resulting in segmentaldemyelination and prolongation of the absolute refractory periods oflong-tract axons. This increases the time during which axons are unre-sponsive to subsequent stimulation, resulting in a postconcussive ef-fect.8, 31 Torg has postulated that disruption of cord function is a resultof the effects of local cord anoxia and the increased concentration ofintracellular calcium. He performed experiments involving the mechani-cal deformation of squid axons and determined that recovery of neuro-

TRANSIENT QUADRIPARESIS IN THE ATHLETE 17

logic function is directly proportional to the intracellular calcium concen-tration, which is directly proportional to the amount and rate of tensionapplied to the axon.25

The spinal cord is narrower in the anterior-posterior direction thanin the transverse plane and is most susceptible to congenital narrowingbetween the third and fth cervical vertebrae. As previously mentioned,the mechanism of injury in transient quadriparesis has been documentedto be an axial load applied to the cervical spine while held in extensionor exion. The greatest dynamic compression of the spinal cord occurswith hyperextension because it is known to produce maximal narrowing(up to an additional 2 mm) of the anterior-posterior diameter of thespinal canal,4 thereby placing athletes with acquired or congenital cervi-cal stenosis at increased risk for cord injury. Penning has described thepincer mechanism effect of hyperextension on the cervical spinalcord.13, 25 During hyperextension, the distance decreases between theposterior-inferior aspect of the superior vertebral body and the anterior-superior aspect of the spinal laminar line of the subjacent vertebra (Fig.1). The cord is therefore pinched between the processes of the twoopposing bodies, with the degree of compression dependent of thesagittal diameter of the canal, the degree of extension, the presence ofspondylitic degenerative spurs, and the infolding of soft tissues such asthe ligamentum avum and posterior-longitudinal ligaments. In fact,Taylor reported that infolding of the laminar ligaments during hyperex-tension might decrease canal size an additional 30%.3, 4, 18 Conversely, inhyperexion, the distance decreases between the spinal laminar line ofthe superior vertebra and the posterior superior aspect of the body of

Figure 1. Hyperextension pincer mechanism, as described by Penning. During hyperex-tension, the distance decreases between the posterior inferior aspect of the superiorvertebral body and the anterior superior aspect of the spinal laminar line of the subjacentvertebra (double-headed arrow). The cord is, therefore, pinched between the processes ofthe two opposing bodies.

18 ALLEN & KANG

the subjacent vertebra. In each hyperextension or hyperexion scenario,a rapid decrease in sagittal diameter occurs, with resultant compressionof the spinal cord.13

CERVICAL STENOSIS

The sagittal diameter of the cervical spinal canal is cited as asignicant predictor of acute and chronic neurologic dysfunction.2, 4, 7, 29However, a considerable amount of controversy and opinion existsregarding whether the presence of cervical stenosis makes an athletemore prone to sustaining permanent neurologic injury or transient quad-riparesis.2, 15, 16, 20, 22, 23

Traditionally, the anteroposterior diameter of the spinal canal (mea-sured from the posterior aspect of the vertebral body to the most anteriorpoint on the spinal laminar line) was determined from lateral cervicalspine radiographs and used to determine the presence of spinal stenosis(measurement A in Fig. 2A, 13 mm in Fig. 2B ). The accepted opinion isthat between C3 and C7, anteroposterior canal dimensions of more than

Figure 2. A, Lateral cervical spine radiograph. The space between the midpoint of theposterior cortex of the vertebral body anteriorly and the spinolaminar line posteriorly (A) isthe sagittal width of the spinal canal. The Pavlov ratio represents the ratio of the width ofthe spinal canal (A) to the width of the vertebral body (B, or A:B). B, Lateral cervical spineradiograph demonstrating a 13 mm width of the spinal canal at C6, and a correspondingPavlovs ratio of 13:22 or 0.59. Additionally, the lms demonstrate evidence of absolutestenosis at the C5 level, with a canal diameter of 12 millimeters.


15 mm are normal, whereas cervical stenosis is present if the canaldiameter is less than 13 mm.7, 21, 30

The variability of technique used and the structural anatomy of thesubject can signicantly affect the quality of measurement of cervicalspine canal dimensions determined from lateral cervical spine radio-graphs. Variations in landmarks used for measurement, changes in targetdistances for making the radiographs, positioning of the neck while theradiograph was taken, differences in the triangular cross-sectional shapeof the canal, and magnication of the canal because of a patients largebody habitus all may affect canal measurements. Herzog demonstratedthat athletes with large shoulders might have a magnication factor ofup to 21% (versus the standard 10%15% in the general population) onlateral radiographs of the cervical spine.6 In an effort to eliminate thevariability in absolute measurements caused by confounders such asbody habitus, Torg and Pavlov designed a ratio method for determiningthe presence of cervical stenosis. They compared the sagittal diameterof the spinal canal to the sagittal midbody diameter of the vertebralbody at the same level, designating a normal Pavlov ratio as 1:1 (Fig. 2).Torg and Pavlov further asserted that a Pavlov ratio of less than 0.8indicates signicant cervical stenosis.12, 21

In contrast, Herzog actually demonstrated a high correlation coef-cient when comparing plain lm sagittal measurements adjusted formagnication to those measured from a midline sagittal computed to-mography image. The plain lm canal size measurements were moreaccurate than those obtained from magnetic resonance images. He alsomade note of the high sensitivity but low positive predictive value ofthe Pavlov ratio in predicting the true presence of spinal stenosis.6 In hisstudy, 41% of the professional football players tested had a Pavlov ratio0.80 but a normal developmental sagittal diameter of the cervicalspinal canal. Herzog proposed that screening players with the Pavlovratio might result in labeling many athletes as stenotic when they haveadequately sized canals but large vertebral bodies. He stated that thePavlov ratio should be utilized as a screening tool for spinal stenosiswhen one does not have knowledge of the magnication factors neededto determine the true developmental sagittal diameter.

Many authors have pointed out the utility of computed tomographymyelograms, plain lm myelography, and magnetic resonance imagingin determining the hidden impact of ligamentous hypertrophy and diskprotrusion on spinal canal size, what some authors refer to as functionalspinal stenosis (Fig. 3).3, 14 Although more accurate and indicative of allpotentially compressive structures and effects within the spinal canal,these studies are more costly and difcult to institute as potential screen-ing tools.

RISK OF INJURYIn 1996, Torg published his results on the evaluation of 45 athletes

who experienced transient quadriparesis during athletic participation.

20 ALLEN & KANG

Figure 3. MR image demonstrating the presence of critical cervical stenosis in a 25-year-old patient. The coexistence of bulging/herniating disks at C3-4, C4-5, and C5-6 would beconsidered a relative contraindication to participating in contact sports by Torgs standards.

By his criteria, 42 of 45 athletes (93%) had cervical stenosis at one spinallevel or more or a Pavlov ratio of 0.80 or less.20 Of note, these sameathletes had a mean anteroposterior canal diameter of 15.3 mm, consid-ered to be a low-normal dimension by current standards, but not ste-notic. In contrast, 41% and 42% of asymptomatic college and professionalfootball athletes tested met Pavlovs criteria for cervical stenosis, andtheir average canal sagittal diameters were greater than 18 millimetersat each level. The incidence of stenosis by absolute criteria and thePavlov ratio in Torgs control non-athlete group was not delineated, butthe average canal sagittal diameter was greater than 18 mm at eachlevel, and the average Pavlov ratio was well over 0.95 at each cervicallevel. In Torgs previous study published in 1986, only two of 49 controlsubjects had a Pavlov ratio of 0.80, in contrast to 17 of 24 athletesshowing radiographic evidence of stenosis who experienced an episodeof transient quadriparesis.21 Applying his 1996 data to the results of his1984 study that demonstrated an incidence of transient neurapraxia(sensory and/or motor changes) of 7.3 per 10,000 athletes who playedfootball, Torg estimated that the positive predictive value of having aTorg ratio less than 0.80 and subsequently experiencing an episode of


transient neurapraxia is 0.2%.20, 21 Torg concluded that a Pavlov ratio of0.80 in an asymptomatic athlete should not preclude participationin contact sports, and he recommended against screening with plainradiographs to assess for stenosis and suitability for play in contactsports.

Torgs 1996 study also involved interviews and radiographic exami-nation of 77 individuals who were permanently quadriplegic as a resultof an injury while playing high school or college football. Interestingly,this cohort demonstrated a mean Pavlov ratio of more than 0.90, andan average canal size of 18.9 mm. Torg argued that a smaller meananteroposterior diameter would be an expected nding in this group ofpermanently quadriplegic patients if developmental narrowing of thespinal canal played an important role in the etiology of their permanentneurologic decits.20 In fact, data collected revealed that the anteropost-erior dimensions of the vertebral bodies in this group were signicantlysmaller than those of the asymptomatic athletes and those athleteswho experienced an episode of transient neurapraxia, indicating thatcatastrophic neurologic injury may result from collapse or fracture of aproportionally smaller vertebral body that fails during axial loading. Healso noted that none of the 77 individuals interviewed recalled havingan episode of transient neurapraxia before their catastrophic injury, andnone of the 45 athletes who experienced transient neurapraxia episodesever became quadriplegic. Given all of these factors combined, Torg feltthat developmental narrowing of the cervical canal in a spine that hasno evidence of instability is neither a predictor of nor a contributor topermanent neurologic injury.

In further support of his research, Torg has more recently publishedstatistics on 110 cases of cervical cord neurapraxia caused by a sports-related injury. In this study, 36% of athletes experienced transient paraly-sis, 26% transient weakness, and 38% experienced sensory changes only.Symptoms tended to last less than 15 minutes (73% of athletes), butsome lasted more than 24 hours (10%). The average Pavlov ratio was0.69, with an average canal diameter measured by magnetic resonanceimaging of 9.6 millimeters.19 Of the 65% of athletes who returned totheir sport, 56% experienced a recurrent episode of transient quadripar-esis. The risk of recurrence increased with a smaller Pavlov ratio, asmaller disk-level canal diameter, and less space available for the cord.Cervical cord neurapraxia was not associated with permanent neurologicinjury, and no permanent morbidity occurred in patients who returnedto contact sports. He therefore reiterated that individuals with cervicalstenosis who experience an episode of uncomplicated cervical cord neu-rapraxia could be allowed to return to play without an increased risk ofpermanent injury, but they may have recurrent episodes of neura-praxia.19, 23

Although Torg believes that cervical stenosis in the absence ofinstability or degenerative changes is not a rm contraindication tocontinued participation in contact sports, there are others with an oppos-ing viewpoint. Specic details are not available on his series of patients,

22 ALLEN & KANG

but Schneider asserted that he had treated a large group of athletes whosustained neck injuries resulting in permanent neurologic decits andwere later found to have cervical stenosis.15, 16 Cantu also strongly assertsthat athletes with documented spinal stenosis should not participate incollision sports, citing the works and recommendations of Penning,Eismont, Wolfe, and Ladd and Scranton.2, 4, 9, 39 Cantu reports that, unlikeTorg, he has seen permanent quadriplegia occur in a stenotic patientafter an initial episode of transient quadriplegia without fracture ordislocation.2 Additionally, Cantu states that in the data from the NationalCenter for Catastrophic Sports Injury, cases of quadriplegia withoutspine fracture have been seen only when functional spinal stenosis ispresent and that the complete neurologic recovery rate after cervicalspine fracture/dislocation is 0% when cervical stenosis is present, com-pared to 21% in the absence of stenosis.2, 3

EVALUATION

An evaluation of athletes who have experienced an episode oftransient quadriparesis includes obtaining a complete history and physi-cal. The history may be helpful in delineating the occurrence of previousneck injuries or episodes of transient quadriparesis, as well as clarifyingthe mechanism of injury. A complete and thoroughly documented neuro-logic exam is mandatory because it will be used to document theprogress of neurologic recovery and serve a role in determining whenan athlete may return to play.

Radiographic evaluation includes anteroposterior, lateral, oblique,and open-mouth odontoid views. Because the superior endplate of T1 isoften difcult to see radiographically in this patient population, axialcomputed tomography scanning with 3-mm cuts may be necessary toevaluate any areas not adequately visualized on plain radiographs.Dynamic exion-extension radiographs may be helpful in evaluatingcases of suspected ligamentous instability but should be obtained onlywhen the patient can actively perform the maneuvers while supervisedby a physician. Instability is dened as radiographic evidence of morethan 3.4 millimeters of translation in the anteroposterior direction or 11degrees of angulation in the sagittal plane between two adjacent verte-brae.21, 28 The radiographs are closely inspected for evidence or fracture,instability, congenital or developmental stenosis, spondylosis, or congen-ital abnormalities (Klippel-Feil syndrome, odontoid agenesis or hypopla-sia, developmental os odontoidium, spina bida occulta). Radiographicevaluation frequently leads to the discovery of one of these abnormalitiesin the patient who has experienced an episode of transient quadripar-esis.21

Any athlete with a documented history of transient quadriparesisor an abnormal neurologic exam after a suspected episode is evaluatedwith magnetic resonance imaging to rule out ongoing extrinsic cord or


nerve root compression (herniated disk), intrinsic cord abnormalities, orevidence of ligamentous injury.

Electromyographic or nerve conduction studies may be helpful insome cases to differentiate a brachial plexus traction injury from radicu-lopathy. Somatosensory-evoked potentials may be useful in document-ing physiologic cord dysfunction, which may preclude a return tosports.2

Herzog designed an algorithm for assessment of symptomatic ath-letes with cervical stenosis as determined by their developmental sagittaldiameter. He believed that the symptomatic athlete with a develop-mental sagittal diameter 12.5 mm should be further evaluated with afunctional magnetic resonance imaging study to determine the size ofthe spinal cord and to assess the functional reserve of the spinal canal.Additionally, exion-extension radiographs should be obtained on allsymptomatic athletes (whether or not they meet the criteria for stenosis)to assess spinal stability. If horizontal translation exceeded 3 mm, afunctional magnetic resonance imaging study should also be performed.The main aim of testing is to determine the impact of a small develop-mental sagittal diameter or instability on the functional reserve of thespinal canal.6, 13

RETURN-TO-PLAY CRITERIA

There is a general consensus that an athlete should be completelyasymptomatic with a normal sensory and motor neurologic examinationand a full, painless range of motion of the cervical spine before returningto his or her sport. The main controversy involves the disposition of theathlete with imaging abnormalities such as evidence of instability, diskherniation, congenital or developmental stenosis, congenital abnormali-ties (Klippel-Feil syndrome, odontoid agenesis or hypoplasia, os odon-toidium, spina bida occulta), or spear tacklers spine.

Torg recently recommended guidelines for the management of ath-letes with documented spinal stenosis who participate in contact sports.23He stated that an asymptomatic athlete with a Pavlov ratio of 0.8 or lesshas no contraindications to play. However, in slight contrast to hiscomments in earlier publications, Torg considered a Pavlov ratio of0.8 or less with one episode of cervical cord neurapraxia a relativecontraindication to return to play. Documented episodes of cervicalcord neurapraxia associated with intervertebral disk disease and/ordegenerative changes was also considered a relative contraindication toreturning to play. A single documented episode of cervical cord neura-praxia associated with magnetic resonance imaging evidence of a cervi-cal cord defect or cord edema was considered a relative or absolutecontraindication to return to play, evaluated on a case-by-case basis.Finally, cervical cord neurapraxia associated with ligamentous instability,neurologic ndings or symptoms lasting more than 36 hours, or multiple

24 ALLEN & KANG

episodes of neurapraxia are considered to be absolute contraindicationsto return to sport.

As delineated in a previous section, Cantu believes that the athleteswith documented cervical stenosis should not engage in collision sportssuch as football because he feels they are predisposed to both transientquadriparesis and permanent neurologic injury. If a patient withoutdocumented evidence of cervical stenosis experiences an episode oftransient quadriparesis, Cantu states that return to play is probably safein the absence of spinal stenosis, bony or ligamentous injury, and if noevidence of spinal cord injury exists. A second incident of transientquadriparesis should initiate a repeat full evaluation including radio-graphs and magnetic resonance imaging. If tests are all normal, theplayer may return to sport, with full consideration given to limitingparticipation in contact sports, given the recurrence of symptoms.2

Watkins created a scoring system to determine whether athletesexperiencing an episode of transient quadriparesis should be allowed toreturn to play.27 Points are assigned based on the athletes symptoms ormeasurements in three categories: extent of neurologic decit, durationof symptoms, and severity of cervical stenosis. The sum of points isutilized to determine the players risk for cervical spine injury.

Bailes has categorized sports-related cervical spine injuries intothree groups, which provides useful information when making return-to-play decisions.1, 11, 26 Type I injuries involve a permanent spinal cordinjury (major decits), or a minor neurologic injury associated withspinal cord hemorrhage, cord contusion or swelling as demonstrated onmagnetic resonance imaging. Athletes with Type I injuries should notbe allowed to return to contact sports. Type II injuries, specicallytransient quadriparesis or burning hands syndrome, are transient neuro-logic decits. As dened previously, radiographic studies show no evi-dence of fracture or instability. Magnetic resonance imaging studiesshow no evidence of cord lesion. Return to play is permissable if neuro-logic symptoms fully resolve and there is truly no evidence of radio-graphic abnormality, including instability, stenosis, fracture, or congeni-tal abnormalities. Patients with recurrent episodes of transientquadriparesis should be restricted from participation in contact sports.Individuals with type III injuries comprise a heterogeneous group ofathletes with solely radiographic or imaging abnormalities, includingfractures, fracture-dislocations, pure ligamentous and soft-tissue injuries,and herniated disks. The neurologic exam of the athlete is normal.Because of the variety of injury types or abnormalities in this group, thedecision about whether an athlete can return to play must be determinedon a case-by-case basis, primarily by considering how stable the injurywill be when the athlete is subjected to large forces during contactplay. Those with signicant bony or ligamentous injury or spinal cordcontusion should be advised not to return to contact sports. Disruptionof the anterior and posterior elements or evidence of ligamentous insta-bility prohibits further participation.28 Players with stable healed frac-tures (lamina fractures, spinous process fractures, minor vertebral bodyfractures) should be evaluated for stability using exion-extension radio-


graphs before return to play. Any individual requiring atlantoaxial fu-sion caused by fracture or ligamentous instability should be restrictedfrom contact sports. Relative contraindications to return to sport includehealed non-displaced Jefferson fractures, type I and II odontoid fractures,and asymptomatic lateral mass fractures.23

There are several congenital anomalies of the cervical spine that areabsolute contraindications to continued participation in contact sports.The presence of odontoid agenesis, odontoid hypoplasia, or os odontoi-dium is an absolute contraindication to participation in collision sportsbecause small injury to weakened or compromised structures may resultin marked C1-2 instability and neurologic injury. Additionally, the pres-ence of a congenital atlantooccipital fusion is an absolute contraindica-tion to participation in contact sports.22, 24 Torg has subdivided congenitalKlippel-Feil deformities into two types. A type I Klippel-Feil deformityis a mass fusion of the cervical or upper thoracic vertebrae. It constitutesan absolute contraindication to participation in contact sports becausespinal mechanics are altered, predisposing the patient to injury. A typeII Klippel-Feil deformity is a fusion of only one or two interspaces. Inthis group, if a player has signs of limited cervical spine motion, instabil-ity, disk disease, or spondylosis, contact sports participation should beprecluded. In contrast, there is no contraindication to participation of anasymptomatic athlete with a type II Klippel-Feil deformity involvinginterspaces at C3 and below with an absence of other cervical spineabnormalities.22

SPEAR TACKLERS SPINE

There is one special subset of football players who merit specialdiscussion. Torg in 199324 identied a group of athletes who are at highrisk for cervical quadriplegic injury because of their habits when playingfootball. He identied 15 athletes from the National Football Headand Neck Injury Registry who sustained a cervical spine injury anddemonstrated ndings of congenital cervical stenosis (Pavlov ratio of 0.8or less), persistent straightening or reversal of the normal cervical lor-dotic curve on radiographs, radiographic evidence of pre-existing post-traumatic cervical spine abnormalities, and a history of using spear-tackling techniques. These athletes chronically employed the techniqueof spearing while performing tackles (using the top of the helmet toram the opponent in the chest or back). This method of applying repeti-tive axial loads to a straightened cervical spine can result in develop-mental stenosis, loss or even reversal of the normal lordotic curve of thecervical spine, compression fractures, disk bulging or herniation, orligamentous instability. Dubbed by Torg spear tacklers spine, it is anabsolute contraindication to continued participation in contact sports.

Four of the 15 athletes examined sustained permanent neurologicalinjury.24 Torg determined that axial loading applied to the straightenedcervical spine resulted in permanent spinal cord injury in these athletes.With the neck slightly exed and its lordotic curve straightened, the

26 ALLEN & KANG

cervical spine becomes a segmented column. Axial loads (spearing)impair bending, and the energy of impact is directly transmitted to thespinal structures, to the point that the spine may buckle in exion withlarge enough axial loads. Fractures, dislocations, and neurologic injurymay result if the axial load is not absorbed by controlled motion in thespinal segments.24

As mentioned previously, because of the potential for sustainingcatastrophic neurologic injury, Torg recommended that athletes with thesyndrome of spear tacklers spine be withheld from participation incontact sports. However, Torg recognized that return to play could beconsidered if the loss of cervical lordosis was reversible and if the athletecould be trained to employ proper and safe tackling techniques.24

SUMMARY

A considerable amount of controversy persists regarding return-to-play criteria and the risk for more severe injury after an athlete experi-ences an episode of transient quadriparesis. Similarly, the implication ofthe presence of congenital stenosis in an athlete participating in contactsports elicits great debate in the literature in terms of the athletes riskfor neurologic injury. The relatively infrequent occurrence rate of bothtransient quadriparesis and permanent cervical cord injury make it dif-cult to predict with certainty whether or not an episode of transientquadriparesis is a risk factor for permanent neurologic injury.

The decision-making process in determining player eligibility in theface of congenital stenosis or after a documented spinal injury is difcultand at times confusing. Every injury and athlete should be evaluated onan individual basis in terms of cause, symptoms, radiographic ndings,and previous history. It is hoped that the guidelines for return-to-playdelineated in this article will help the physician and the athlete make aninformed and rational decision regarding the criteria for and relativerisks of returning to participation in a contact sport.

References

1. Bailes JE, Hadley MN, Quigley MR, et al.: Management of athletic injuries of thecervical spine and spinal cord. Neurosurgery 29:491497, 1991

2. Cantu RC: Stingers, transient quadriplegia, and cervical spinal stenosis: Return to playcriteria. Med Sci Sports Exerc 29(suppl):S233S235, 1997

3. Cantu RC, Bailes JE, Wilberger JE: Neurologic athletic head and neck injuries: Guide-lines for return to contact or collision sport after a cervical spine injury. Clin SportMed 17:137146, 1998

4. Eismont FJ, Clifford S, Goldberg M: Cervical sagittal spinal canal size in spinal injury.Spine 9:663666, 1984

5. Engle CA, Kang JD, Lauerman WC: Cervical stenosis in the athlete. Op TechniquesOrthopaed 5:218222, 1995

6. Herzog RJ, Wiens JJ, Dillingham MF, et al: Normal cervical spine morphometryand cervical spinal stenosis in asymptomatic professional football players: Plain lm


radiography, multiplanar computed tomography, and magnetic resonance imaging.Spine 16(suppl 6):S178S186, 1991

7. Kang JD, Figgie MP, Bohlman HB: Sagittal measurements of the cervical spine insubaxial fractures and dislocations. An analysis of 288 patients with and withoutneurological decits. J Bone Joint Surg Am 76:16171628, 1994

8. Kline DG, Hudson AR: Acute injuries of peripheral nerves. In Youmans (ed): Neurolog-ical Surgery. Philadelphia, WB Saunders, 1990, pp 24232510

9. Ladd AL, Scranton PE: Congenital cervical stenosis presenting as transient quadriple-gia in athletes: Report of two cases. J Bone Joint Surg Am 68:13711374, 1986

10. Maroon JC: Burning hands in football spinal cord injuries. JAMA 238:20492051, 197711. Maroon JC, Bailes JE: Athletes with cervical spine injury. Spine 21:22942299, 199612. Pavlov H, Torg JS, Robie B, et al: Cervical spinal stenosis: Determination with vertebral

body ratio method. Radiology 164:771775, 198713. Penning L: Some aspects of plain radiography of the cervical spine in chronic myelopa-

thy. Neurology 12:513519, 196214. Resnick D: Degenerative disease of the spine. In Diagnosis of Bone and Joint Disorders.

Philadelphia, WB Saunders, 1981, pp 1408141515. Schneider RS: Serious and fatal neurological football injuries. Clin Neurosurg 12:

226236, 196616. Schneider RS, Reifel E, Grisler H: Serious and fatal football injuries involving the head

and spinal cord. JAMA 177:362367, 196117. Sonntag VKH, Hadley MN: Nonoperative management of cervical spine injuries. Clin

Neurosurg 34:630649, 198818. Taylor AR: The mechanism of injury to the spinal cord in the neck without damage to

the vertebral column. J Bone Joint Surg Br 33B:543547, 195119. Torg JS, Corcoran TA, Thibault LE, et al: Cervical cord neurapraxia: Classication,

pathomechanics, morbidity, and management guidelines. J Neurosurg 89:687690, 199720. Torg JS, Naranja RJ, Pavlov H, et al: The relationship of developmental narrowing of

the cervical spinal canal to reversible and irreversible injury of the cervical spinal cordin football players: An epidemiological study. J Bone Joint Surg Am 78:13081314, 1996

21. Torg JS, Pavlov H, Genuario SE, et al: Neurapraxia of the cervical spinal cord withtransient quadriplegia. J Bone Joint Surg Am 68:13541370, 1986

22. Torg JS, Ramsey-Emrhein JA: Management guidelines for participation in collisionactivities with congenital, developmental, or post-injury lesions involving the cervicalspine. Clin Sport Med 16:501530, 1997

23. Torg JS, Ramsey-Emrhein JA: Suggested management guidelines for participation incollision activities with congenital, developmental, or postinjury lesions involving thecervical spine. Med Sci Sports Exerc 29(suppl):S256S272, 1997

24. Torg JS, Sennett B, Pavlov H, et al: Spear tacklers spine: An entity precluding participa-tion in tackle football and collision activities that expose the cervical spine to axialenergy inputs. Am J Sports Med 21:640649, 1993

25. Torg JS, Thibault L, Sennett B, et al: The pathomechanics and pathophysiology ofcervical spinal cord injury. Clin Orthop 321:259269, 1995

26. Warren WL, Bailes JE: Neurologic athletic head and neck injuries: On the eld evalua-tion of athletic neck injury. Clin Sport Med 17:99110, 1998

27. Watkins RG, Dillin WH, Maxwell J: Cervical spine injuries in football players. SpineState Art Rev 4:391408, 1990

28. White AA, Johnson RM, Panjabi MM, et al: Biomechanical analysis of clinical stabilityin the cervical spine. Clin Orthop 109:8596, 1975

29. Williams JP: Biomechanical factors in spinal injury. Br J Sports Med 14:14, 199030. Wolfe BS, Khilnani M, Malis L: The sagittal diameter of the bony cervical spinal canal

and its signicance in cervical spondylosis. J Mount Sinai Hosp 23:283292, 195631. Zwimpfer TJ, Bernstein M: Spinal cord concussion. J Neurosurg 72:894900, 1990

Address reprint requests toJames D. Kang, MD

Associate Professor, Department of Orthopaedic SurgeryUniversity of Pittsburgh Medical Center

3471 Fifth Avenue Suite 1010Pittsburgh, PA 15213


CERVICAL BURNERSIN THE ATHLETE

Brian Shannon, MD, and John J. Klimkiewicz, MD

Approximately 1.2 million high school athletes and 200,000 collegeand professional athletes participate in American football each year.13For the thousands of physicians responsible for the medical care of theseathletes, no situation is fraught with more danger or elicits more anxietythan that of the injured player who demonstrates symptoms consistentwith spinal cord dysfunction. Neck injuries have been perennial prob-lems in American football. Nineteen instances of death or paraplegia in1904 prompted Theodore Roosevelt to demand either an end to thebrutality involved in football or elimination of the game. Rooseveltsdemands resulted in the formation of the National Collegiate AthleticAssociation.1 Since that time, safety of the athlete has continued to be ofprimary importance in the evolution of American football. In 1973,Schneider stated that The football elds of our nation have been a vastproving ground or laboratory for the study of the tragic neurologicsequelae of head and neck trauma in man. These concerns were takento heart, and at the conclusion of the 1975 football season, governingbodies at both the interscholastic and the intercollegiate levels outlawedthe use of the helmet or facemask in blocking and tackling (NCAA rule99-1-2-N and 0-1-2-1 and National Federation of High School AthleticAssociation rule 9-3-2-k and 9-3-1). Furthermore, in 1977 and 1980 addi-tional rule changes were implemented, allowing offensive players to usetheir hands and arms to block. These changes appear to have beenfollowed by a reduced incidence of catastrophic injuries because therehave been less than 10 catastrophic spinal injuries reported since theimplementation of these changes in the years 19771990.1, 6

From the Department of Orthopaedic Surgery, Division of Sports Medicine, GeorgetownUniversity Medical Center-MedStar Health, Washington, DC



30 SHANNON & KLIMKIEWICZ

Statistics of catastrophic injury, however, are not reective of themore common stingers and neck sprains. The stinger syndrome repre-sents one of the most common injuries seen in tackle football. The stingersyndrome or burner is thought to be caused by trauma to the brachialplexus and/or nerve roots. The injury most typically is characterized byunilateral shoulder and/or arm pain with burning dysesthesias and oftenmuscle weakness involving the biceps, deltoid, and spinatus muscles.Because the pain, paresthesias, and weakness typically last only a fewseconds or minutes, these injuries often go unreported to medical staff.The transient nature of these symptoms have classied these neurologicinjuries into the category of a neuropraxia.18 The actual incidence ofthese injuries may in fact approach 50% to 65% of college football playersthroughout a 4-year collegiate career.17 Persistent sensory changes arerare with these injuries. The subjective manifestations are usually shortlived, but in some instances weakness may persist for days to weeks.Prolonged weakness, when present, is generally found in the deltoid,biceps, and spinatus muscles. Overall, 5% to 10% of these injuries aremore serious, presenting with a neurologic decit lasting several hoursor longer.2, 19 Those injuries with neurologic disturbances lasting morethan 2 weeks represent examples of greater stretch to the brachial plexusresulting in axonotmesis as described by Seddon.18 The differential diag-nosis for these athletes include cervical radiculopathy, cord contusion,and brachial plexus injury.

When considering these other possibilities, a variant injury de-scribed by Torg and colleagues known as transient quadriplegia repre-sents a neurapraxia at the level of the cervical spinal cord.20 This syn-drome differs from cervical burners in that it represents injury to theactual spinal cord. It often involves bilateral upper extremity and lowerextremity neurologic involvement with no associated fracture or disloca-tion, and usually resolves within 36 hours. The incidence of transientquadriplegia, or cervical cord neuropraxia, has been estimated to be 7.3per 10,000 football participants.

MECHANISM OF INJURY

Based on the typical clinical presentation of cervical burners, generalconsensus is that the C5-C6 nerve distributions are the most commonlyaffected, which would implicate either the root level or a brachial plexusupper trunk lesion as a cause for the symptoms. Initially, Clancy et alcharacterized the pathology in cervical burners as occurring at the bra-chial plexus level, secondary to traction mechanisms.7, 17 Although othershave supported this mechanism as the etiology for some cervical burn-ers, controversy has arisen about the potential for a cervical root injurysecondary to compression at this level as an additional explanation forthese injuries.4, 11, 14, 16, 17 In Meyers study of 40 collegiate and professionalplayers with stingers, 34 (85%) had extension-compression mechanismsthought to involve the nerve root, whereas only six (15%) athletes had

CERVICAL BURNERS IN THE ATHLETE 31

brachial plexus stretch mechanisms.14 Similiary, Levitz et al characterizedneck extension combined with ipsilateral-lateral deviation as the mecha-nism in 83% of patients presenting with chronic or recurrent burners. Inthis series, the pathology was thought to occur at the nerve root levelbased on clinical examination and roentgegnographic work-up.11 Finally,a third potential causative mechanism thought to result from directtrauma of the shoulder pads to the brachial plexus has been proposed.12Neither of the previous two reports mentioned this mechanism as anexplanation for the stingers. These somewhat conicting studies concern-ing both the mechanism and point of injury in cervical stingers leavesthree main hypothetic mechanisms to explain stingers or transient neuro-praxia in this population: (1) nerve root compression in the neuralforamen (extension-compression), (2) Brachial plexus stretch (tractioninjuries), and (3) A direct blow to the plexus (Fig. 1).

Cervical hyperextension with or without concomitant lateral exionis thought to compress or pinch the nerve root at the interverteralforamen. Extension-compression burners occur in more mature athleticpopulations (collegiate and professional). They are generally associatedwith pre-existing radiologic evidence of cervical disk disease or arthriticchange. These patients usually exhibit a positive Spurlings test onphysical examination indicating compression at the nerve root level. Astudy conducted by Watkins and Odor focused on 12 professional and

Figure 1. Proposed areas of brachial plexus involvement with different mechanisms ofcervical burners. A, Extension-ipsilateral compression. B, Flexioncontralateral exion (trac-tion) or direct trauma. (Modied from Grants Atlas of Anatomy Williams & Wilkins, 1983,8th Edition.)


several intercollegiate football players who had a mechanism of exten-sion and ipsilateral compression.23 These players had the severest symp-toms of those studied. They attributed the symptoms to injury of thenerve root at the intervertebral foramen.

Brachial plexus stretch or traction injuries occur if the head is forcedaway from the symptomatic side with concomitant ipsilateral shoulderdepression. These injuries occur more commonly in younger athleteswithout cervical stenosis or degenerative changes of the cervical spine.Spurlings test is usually negative. Sallis stated that lateral neck exionwith contralateral shoulder depression was the mechanical stimulus fora traction injury to the plexus most commonly at the C5-C6 level. Thisis the most frequent mechanism cited in the literature as cause of theseinjuries.7, 17, 19

The third mechanism of compression of the xed brachial plexusbetween the shoulder pads and the superior medial scapula that canoccur when the pad is pushed into the area of Erbs point, where thebrachial plexus is most supercial has been described by Markey et al.12

ROLE OF CERVICAL STENOSIS

The signicance of cervical spinal stenosis in this active populationhas long been a topic of debate. Several investigators have noted anassociation of cervical spinal stenosis and burner syndrome. Meyer et alnoted an incidence of 47% of spinal stenosis on the University of Iowafootball team in players who sustained a cervical burner compared toonly 25% in assymtomatic players.14 Players with this condition werethought to have a threefold increased risk of sustaining a stinger thanthose without cervical stenosis. Similarly, Kelley et al reported an associ-ation between cervical stenosis and this syndrome.10 These investigatorshave proposed that a narrowed canal with accompanying shortenedpedicles leads to narrow neural foramina increasing the risk of burnerscaused by nerve root compression.

The actual denition of what constitutes cervical spinal stenosis inthis population and how it is measured continues to evolve as differenttheories about its association with cervical burners continues to develop.The most commonly employed method for determining the sagittaldiameter of the spinal canal is measuring the distance from the middleof the posterior surface of the vertebral body to the nearest point of thecorresponding spinal laminar line on the lateral radiograph. The use ofthe actual measurement in millimeters on the lateral view of the cervicalspine to document spinal stenosis can be misleading, and the dimensionsconsidered to be signicant vary as reported in the literature.5, 9 Thesecond method, designated as the Pavlov ratio or ratio method, comparesthe sagittal spinal canal diameter measured from the posterior surfaceof the vertebral body to the nearest point of the corresponding spinallaminar line, with the sagittal diameter of the corresponding vertebralbody measured at its midpoint.15 When Torg compared actual measure-


ments, as previously described, with the ratio method, the ratio methodwas more then 2.5 times as sensitive as the conventional method withuse of a cutoff value of 0.82 representing signicant stenosis. Therewas a 92% accuracy rate compared with a 62% accuracy rate with theconventional method.21 The Pavlov ratio has proven to be a reliable toolfor determining cervical spinal stenosis and is independent of technicalfactor variables. However, the main criticism of using this method inthis athletic population lies in the fact that these individuals usually arelarger in size than the general population with inordinately larger verte-bral bodies. This may generate falsely low values overstating the signi-cance of spinal stenosis in this population.8, 10

Although the previously mentioned studies have demonstrated apotential for cervical stenosis to contribute to cervical stingers in a classicsense, one should be aware of relationship of this phenomenon withcervical cord neuropraxia. Torg et al compared football players at differ-ent skill levels to a control group of 105 nonathletes to determine therelationship, if any, between a developmentally narrowed cervical canaland reversible and irreversible injury of the cervical cord. A Pavlov ratioof 0.80 or less had a high sensitivity (93%) for transient neurapraxia. Thelow positive predictive value of this ratio (.02%), however, precludes itsuse as a screening mechanism for determining the suitability of anathlete for participation in contact sports.21 These authors concludedfrom this analysis that symptoms may result from a transient reversibledeformation of the spinal cord in a developmentally narrowed osseouscanal, yet developmental narrowing of the cervical canal in a stable spinedid not appear to predispose an individual to permanent catastrophicneurologic injury, and therefore should not preclude an athlete formparticipation in contact sports.

TREATMENT

Treatment issues are often difcult decisions as a result of thetransient nature of the majority of these episodes, yet the substantialpotential risk associated with cervical spine injuries. Criteria involvinga return to play after a cervical burner emphasize a complete andthorough physical examination. In addition to an intact neurologic examfocusing on normal strength and sensation within the upper extremities,the cervical spine exam must be normal. Cervical range of motion, headcompression test, Spurling and Adsons maneuvers, and resistive headpressures should all be within normal limits. Watkins states criteriafor removing a player form a game usually involve two predominantndings.23 First is any radiating arm pain and neurologic decit that canbe an indicator of a more serious problem, and second is a nding ofloss of cervical range of motion, because many times unstable cervicalspine lesions without a neurologic decit may present only with loss ofcervical range of motion.

Any positive ndings as listed above mandate removal from compe-


tition and further evaluation.3, 22, 23 Watkins in his experience with profes-sional, collegiate, and high school football players noted that when thesymptoms persist, the numbness usually settles into the C6 area of theindex nger and thumb, whereas the initial weakness presents in shoul-der abduction and wrist and thumb extension.23 The player classicallyholds himself with a head-forward posture and stiff neck and attemptsto avoid any extension and rotation.

Once the symptoms persist emphasis should be placed on the chest-out posturing and thoracic outlet obstruction exercises. The chest-outposturing produces three effects: (1) it opens the intervertebral foraminato its maximum size, (2) it reduces the effect of the weight of the headas the head is brought back over the body in this position, and (3) itopens the thoracic outlet by changing the alignment of the scalenemuscles and the clavicle relative to the neck. A stoop-shoulder, head-forward posture will cause the symptoms of brachial plexus irritation topersist. Neck strengthening and stretching is also important componentof therapy. Neck isometrics should be done with the head in the midlineposition, and resisting forces should be applied perpendicularly to thehead from every direction. Emphasis has also been placed on midlinestretching through a full range of motion.

Electrodiagnostic studies have been performed on cases in whichthe symptoms have persisted. Continued muscular weakness at 72 hoursafter the actual injury seems to correlate with positive electrodiagnostictesting performed at 4 weeks.19 These ndings at 4 weeks from the timeof injury have been shown to persist at up to 4 years from the time ofthe initial event in up to 80% of the cases studied; however, clinicallythese ndings have not contributed to substantial strength decits orlimitation of function.4, 19

PREVENTION OF BURNERS

The primary equipment needed to prevent burners includes wear-ing properly tting shoulder pads.23 Shoulder pads should accomplishfour basic functions: (1) absorb shock, (2) protect the shoulders, (3) tthe chest, and (4) x the mid cervical spine to the trunk. A propershoulder pad should encompass many of the qualities of a well-ttedcervicothoracic orthosis. Important characteristics of a proper shoulderpad include a modied A-frame shape, rm circumferential xation tothe chest, and xation of the neck to the chest by the t of the shoulderpad at the base of the neck. Thick, comfortable, stiff pads at the base ofthe neck are essential. It is this support laterally at the base of the neckthat offers xation to the cervical spine. A common method of adaptingpads is to add lifters and neck rolls. The lifters provide a pad at the baseof the neck that can provide additional support, whereas the neck rollsattempt to limit compression but are often compromised in their functionby poorly tted shoulder pads.


References

1. Albright JP, McAuley E, Martin RK, et al: Head and neck injuries in colle

Documents

2002, Vol.21, Issues 1, The Spine and Sports