Spinal Injuries in Sports

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Chapter 71 Spinal Injuries in Sports

Injury to the spine and surrounding structures are common occurrences in athletes with a wide spectrum of consequences ranging from an annoyance to a life-altering event. Although injuries that require minimal intervention are exponentially more common, it is the fear of permanent spinal cord injury (SCI) that causes the trepidation associated with this subject, and the differentiation between minor and serious injuries is the foundation of treatment of the athlete.

This chapter discusses spinal injuries that are unique to the athlete and addresses the spectrum of injury from simple strains/sprains to those resulting in gross instability and permanent neurologic deficits. An optimal response to the athlete with suspected or proven neck injuries has unique facets, which are detailed in this chapter. In addition, the current evidence and expert opinion on return to play following spinal injuries, as well as surgery, is summarized. Section One details the epidemiology of sports-related spinal injuries, broken down by discussion of individual sports with a higher risk of injury. Section Two focuses on the cervical spine, and also covers the on-site management of catastrophic SCI. Section Three deals with the thoracic spine, and Section Four with the lumbosacral complex.

Section One

Sports-Specific Epidemiology

Each year, approximately 10,000 cases of SCI occur in the United States.1 Participation in sporting activities accounts for nearly 10% of these and is the fourth most common cause of SCI (after motor vehicle accidents, violence, and falls).2,3 Sports-related SCIs also occur at a younger mean age of 24 and are the second most common cause of SCI in the first three decades of life.4,5

Spinal injuries are more common in nonorganized sports such as diving and surfing than in organized sports.1,6 The challenge in this population is that rules, supervision, and training are limited. These limitations make it difficult to improve injury patterns by enforcing safety guidelines and manufacturer standards. Although less frequent, spinal injury in organized sports have a much higher public profile. Several organized sports, including football, ice hockey, rugby, skiing, snowboarding, and equestrian sports, have been identified as placing the participant at high risk for SCI.710

Sport-Specific Risks to the Spine

American Football

American football involves approximately 1.4 million athletes at the junior/senior high school level, 75,000 in college, and 1000 in professional play.11 This total contrasts roughly with 60,000 rugby players in the United States. With the innumerable high-velocity collisions incurred during practice and games, it is the most dangerous sport for SCI in terms of exposure and is responsible for the highest risk of cervical spine trauma among organized sports participants. Although American football has a lower per participant rate of catastrophic cervical spine injuries than ice hockey or gymnastics, the huge number of participants translates into the largest overall number with catastrophic cervical spine injuries.11

High school participants are at the highest risk, accounting for over 80% of cervical injuries, largely due to the wide discrepancies in player size, age, maturity, and speed at this level. At the other end of the injury risk spectrum is the preadolescent and early adolescent participant. In this group, disabling spinal injuries are almost nonexistent, a result of the players’ small size and the relative lack of high-velocity collisions.

Notably, a significant increase in catastrophic cervical trauma coincided with the development of the modern football helmet. However, rule changes in 1976 prohibiting playing techniques that used the top of the helmet as the initial point of contact for blocking and tackling (spearing) have significantly reduced this trend. From 1976 to 1987, the rate of cervical injuries decreased 70%, from 7.72 per 100,000 to 2.31 per 100,000 at the high school level.12 Traumatic quadriplegia decreased approximately 82% over the same period.13 Since most football players are injured during tackling, defensive players (defensive backs, members of the kickoff teams, and linebackers) are at the highest risk of injury. Almost all cervical spine injuries occur when a player strikes an opponent with high velocity using the vertex of the helmet or with the head down. This action results in a significant axial load, often with a degree of flexion. The cervical musculature that is responsible for maintaining extension is much stronger than that used in maintaining flexion. Thus, a player who lowers his head in blocking or tackling increases his vulnerability to cervical injury by placing his cervical spine in a position that is less able to absorb the consequent energy.

Basketball

Basketball involves rapid changes in direction and explosive movements, causing repeated stresses to the spinal vertebrae. Thus, it is not surprising that the most common neurologic risk in basketball is to the player’s spine. A variety of acute back injuries, such as lumbosacral sprains, contusions, and facet joint and pars interarticularis injuries, are common.15,16 In addition, this sport is a leading cause of sports-related disc disease and has been reported to be the second most common cause of disc herniation among athletes.17 Herniated discs usually arise dorsally or dorsolaterally and occur as a consequence of numerous microtraumas to the intervertebral disc compounded by chronic overstraining. Cervical cord neurapraxia has also been reported in basketball players.

Equestrian Sports

Approximately 20% of the injuries sustained by an equestrian involve the CNS. One study found that 13% of the patients had injury to the spinal cord, with the cervical region most commonly involved.19 There does not seem to be any correlation between risk of injury and the participant’s age, gender, or experience.20 Equipment failure has been shown to be a common cause of injury. Although jumping events have garnered the majority of attention in the past decade due to catastrophic injuries to celebrities such as Christopher Reeves, the particular type of equestrian activity with the most risk to the spinal cord is unequivocally rodeo rough-stock riding (bull, bareback bronco, and saddle bronco riding).21 Common spinal injuries include cervical and lumbar sprain, acute torticollis secondary to being thrown, and cervicothoracic strain secondary to missing the animal in the steer wrestling competition.

Ice Hockey

The sport of ice hockey has experienced a marked increase in the occurrence of cervical spine injuries through its history.24 Major vertebral column injury occurred at an increased rate between 1982 and 1993, with a mean of 16.8 fracture-dislocations per year during that period. Checking an opponent from behind, which typically produces a headfirst collision of the checked player with the boards, has been identified as an important causative factor in cervical spine trauma in hockey. Changes in the rules that prohibit checking from behind and checking of an opponent who is no longer controlling the puck seem to be decreasing the incidence of these injuries, and data suggest that fewer cases of complete quadriplegia have been caused by these playing techniques since the rule changes have been instituted.24

Mixed Martial Arts

Mixed martial arts (MMA) is a full-contact sport combining elements of boxing, kickboxing, and wrestling. It has evolved since 2001 to become a mainstream sport with improved regulations to minimize injury.25 Most competitions now forbid head butting; stomping or kneeing on an opponent on the ground; and striking the throat, spine, or back of the head. Also, athletes must fight within a predetermined weight class. Despite the dramatic impacts that a participant receives during competition, the overall injury rate in MMA competitions has been determined to be similar to other combat sports, including boxing.25,26 While no catastrophic spinal injury has been reported during competition in the past decade, many of the maneuvers seem to be particularly risky.

Maneuvers known as “spinal locks” are often employed in competition. A spinal lock is performed by forcing the spine beyond its normal ranges of motion and is typically accomplished by bending or twisting the opponent’s head or upper body into abnormal positions. These maneuvers can be separated into two categories based on their primary area of effect on the spinal column: spinal locks on the neck are called neck cranks, and locks on the lower parts of the spine are called spine cranks. Spine cranks are less commonly performed in competition than neck cranks because they are more difficult to apply. These can commonly strain the spinal soft tissue and musculature and if forcefully and/or suddenly applied could theoretically result in ligament damage, bony fracture or displacement, and SCI.

Four of the most commonly utilized maneuvers in the sport are the O goshi (judo), in which the fighter uses his shoulders to swing the opponent over his hips; the suplex (jujitsu), in which the fighter grabs the opponent around the waist and lifts him up over his shoulder to fall forward onto his face; the souplesse, a variant of the suplex, in which the opponent is rotated and slammed down onto his back; and the guillotine drop (a choke hold). A detailed kinematic and biomechanical analysis of these maneuvers showed that the forces involved are of the same order as those involved in whiplash injuries and of the same magnitude as compression injuries of the cervical spine.27

Rugby

Spinal injuries, especially to the cervical region, are common in the traditional tackle games of rugby union, rugby league, and Australian rules football. A retrospective study of SCIs in rugby from 1960 through 1989 identified 117 catastrophic neck injuries. It was also reported that for every serious rugby-associated SCI, 10 severe neck injuries occurred that did not involve the cord.28

Three specific activities during the game of rugby—the tackle, tight scrum, and loose play (ruck and maul)—result in the majority of injuries to the cervical spine.29 Cervical spine injury often results from impact between the tackler’s head and the ground or the body of the opponent (usually the thigh). The immediate halt of the head’s forward progress results in compression fractures of the vertebral bodies from axial forces transmitted down the spine. These forces are increased significantly if the player’s neck is flexed, which eliminates the normal lordosis of the cervical spine. An injury during a high tackle from behind often results from hyperextension secondary to the head being pulled back and down. If the tackle is from the side, hyperflexion injury often results. Rotational forces are also a factor in these injuries, especially if the tackle is performed with only one arm. Double tackles, often referred to as “sandwich” or high-low tackles, are more common near the goal with a concentration of defenders merging on the ball carrier. They can cause injury to both the offensive and defensive player. If the defensive players miss their target, they can collide into each other with considerable force at unexpected angles. If the tackle is successful, the offensive player’s body is forced in two directions. This inhibits the player from moving with either force completely, increasing rotational and shearing stresses to the spine.

Water Sports

The water sport with the most risk for spinal injury is by far recreational diving. Mishaps have been reported to account for up to 75% of all recreation-related spinal cord injuries.3032 These injuries tend to occur in teenage males involved in unsupervised activities during the summer months. The most common cause of injury is the participant striking his head on the bottom of a pool, lake, or ocean after having miscalculated the depth of the water. Diving injuries occur almost exclusively to the cervical spine and often result in quadriplegia. Forward flexion, often with axial compression, is the usual mechanism of injury. The C5 level is most commonly involved, likely attributable to the wide range of motion and the relatively smaller size of the vertebral canal at this level.33

A second water sport with a significant risk of cervical spine injury is surfing. These injuries are usually related to a variety of impact positions, as surfers are propelled by falls or tidal action, striking their heads and necks on the ocean bottom.

Wrestling

The sport of wrestling has been associated with spinal injury, most commonly in the cervical region.34 Although the intervertebral discs, joints, and ligaments are somewhat resistant to compression stresses, they are very susceptible to injury by rotational and shearing forces. Most injuries result from landing with the body twisted on the head and neck and occur during takedowns and sparring. Various combinations of thoracolumbar spine abnormalities, such as spondylolysis, are also prevalent in this population of athletes.

Section Two

Cervical Spine and Brachial Plexus

A dramatic range of symptomatology may result from trauma to the cervical spine and brachial plexus. Although injuries in this area are almost always transient, the large contribution of this part of the nervous system to normal function predicates that they be taken very seriously.

Cervical Sprains, Strains, and Contusions

One of the most common causes of neck pain in the athlete is the constellation of cervical strain, sprain, and contusion. A strain is defined as a stretch injury at the musculotendinous junction or within the muscle itself. If the ligamentous structures of the spine are more involved, it is termed a sprain. Contusions are blunt-force injuries to soft tissue. Injuries in this group most often occur when a force is applied to a contracting muscle. This creates an eccentric contraction resulting in some degree of tensile failure. The most vulnerable area for this injury is at the myotendinous junction as well as areas of greater type II (fast-twitch muscle fibers) concentration.35 Most injuries involve an overlap of all three components, with the severity of injury being a consequence of the magnitude and direction of the applied forces.

The natural course of these injuries is a gradual resolution of pain and muscle spasm with conservative treatment. Obviously, an athlete who presents with pain and limited cervical range of motion should undergo a complete clinical and radiographic examination. At a minimum, this imaging should include dynamic (flexion-extension) plain radiographs in at least two orthogonal planes of the entire cervical spine (occiput to C7-T1 junction). If the injury only appears to be a strain, sprain, or contusion, a cervical collar may be continued until any severe muscle spasm has resolved, which usually takes 7 to 10 days. Use of a cervical collar for longer than this length of time has been demonstrated to result in significant deconditioning and weakening of the cervical musculature.35 Repeat dynamic radiographs can then be taken to ensure that the athlete does not have any delayed instability that could present after the splinting effect of muscle spasm has resolved. If these tests are negative, the collar can be discontinued and physical therapy begun. This should include gentle range-of-motion and isometric strengthening exercises, followed by a more sport-specific regimen.

The athlete may return to play when he or she is asymptomatic, has full range of motion, and has baseline sport-specific neck function. After returning to competition, the athlete should continue stretching and strengthening exercises in an attempt to reduce the incidence and severity of any future injury. The use of a sport-specific protective orthosis (e.g., a “horse collar” in American football) to prevent further injury may be employed, although significant data on their actual benefit are limited. Such orthoses used in American football have been shown to limit hyperextension of the cervical spine while allowing enough extension to prevent axial loading injury.36

Brachial Plexus Neurapraxia

Brachial plexus neurapraxia (also known as stinger-burner or transient brachial plexopathy or nerve root neurapraxia) is a transient neurologic event characterized by pain and paresthesia in a single upper extremity following a blow to the head or shoulder. This condition is one of the most common occurrences in collision sport participation and is not the result of an SCI. It was first described in 1965 by Chrisman et al.37 Because the mechanism was thought to be direct force applied to the shoulder with the neck flexed laterally away from the point of contact, the condition has also been referred to as “cervical pinch syndrome.”38 The symptoms most commonly involve the C5 and C6 spinal roots. The affected athlete can experience burning, tingling, or numbness in a circumferential or dermatomal distribution.38 The symptoms may radiate to the hand or remain localized in the neck. These athletes often maintain a slightly flexed cervical spine posture to reduce pressure on the affected nerve root at the neural foramen or may hold or elevate the affected limb in an attempt to decrease tension on the upper cervical nerve roots.

Weakness in shoulder abduction, external rotation, and arm flexion is a reliable indicator of the injury.39 If weakness is a component, it usually involves the C5-6 neurotome. The radiating arm pain tends to resolve first (within minutes), followed by a return of motor function (within 24–48 hours). Although the condition is usually self-limiting and permanent sensorimotor deficits are rare, a variable degree of muscle weakness can last up to 6 weeks in a small percentage of cases.

As mentioned previously, this injury is most commonly the result of downward displacement of the shoulder with concomitant lateral flexion of the neck toward the contralateral shoulder. This is thought to result in a traction injury to the brachial plexus. The condition may also result from ipsilateral head rotation with axial loading resulting in neural foramen narrowing and compression-impaction of the exiting nerve root within the foramen.40,41 Direct blunt trauma at the Erb point, located superficially in the supraclavicular region, has also been reported to be a cause.42 This can occur when an opponent’s shoulder or helmet drives the affected athlete’s shoulder pad directly into this area.

This injury has been graded using the Seddon criteria. A grade 1 injury is essentially a neurapraxia defined as transient motor or sensory deficit without structural axonal disruption. This type of injury usually completely resolves, and full recovery can be expected within 2 weeks. Grade 2 injuries are equivalent to axonotmesis and involve axonal disruption with an intact outer supporting epineurium. This results in a neurologic deficit for at least 2 weeks, and axonal injury may be demonstrated on electromyographic studies 2 to 3 weeks following the injury. Grade 3 injuries are considered neurotmesis, or total destruction of the axon and all supporting tissue. These injuries persist for at least 1 year and show little clinical improvement.

Stingers with prolonged neurologic symptoms are the most common reason for high school and college athlete cervical spine evaluations in an emergency department.4345 The athlete commonly demonstrates a full, pain-free arc of neck motion with no midline palpation tenderness on examination. If tenderness is present or unilateral neurologic symptoms persist, a paracentral disc herniation with associated nerve root compression should be considered. This is usually accompanied by the sudden onset of dorsal neck pain and spasm. Monoradiculopathy characterized by radiating pain, paresthesias, and/or weakness in the upper extremity also occurs secondary to compression and inflammation of the cervical root.

Although this injury is usually considered benign, an athlete that suffers an episode of brachial plexus neurapraxia should be immediately removed from competition until symptoms have fully resolved. On-field evaluation should include palpation of the cervical spine to determine any points of tenderness or deformity. Sensation and muscle strength should be evaluated using the unaffected limb as a point of reference. Weakness in the muscles innervated by the upper trunk of the brachial plexus is often observed. These include the deltoid (C5), biceps (C5-6), supraspinatus (C5-6), and infraspinatus (C5-6) muscles.46,47 The shoulder of the affected limb should also be evaluated, paying particular attention to the clavicle, acromioclavicular joint, and supraclavicular and glenohumeral regions. Percussion of the Erb point can be performed in an attempt to elicit radiating symptoms. Obviously, the athlete should be evaluated for other serious injuries such as cervical spine fractures and dislocations. It is unusual to find lower brachial trunk injury patterns involving the C7 or C8 nerve roots. It is also uncommon to see persistent sensory deficits involving either the lower or upper extremities. This condition is always unilateral and has never been reported to involve the lower extremities. If bilateral upper extremity deficits are present, SCI should be at the top of the differential diagnosis. Localized neck stiffness or tenderness with apprehension to active cervical movement should alert the examiner to a potentially serious injury and the subsequent initiation of full spinal precautions, including spine board immobilization and transport for imaging.

If the player does not complain of neck pain, decreased range of motion, or residual symptoms, he or she can usually return to competition. If symptoms do not resolve or there is persistent pain, prompt imaging of the brachial plexus via MRI is recommended. If the symptoms persist for over 2 weeks, electromyography can be performed to establish the distribution and degree of injury.48 Residual muscle weakness, cervical anomalies, or abnormal electromyographic studies are exclusion criteria from return to play.44

By definition, brachial plexus neurapraxia is a transient phenomenon. It usually does not require formal treatment. The athlete should be followed closely with repeat neurologic examinations since although the condition usually resolves in minutes, motor weakness may develop hours to days following the injury.39,45 Repeated injury may result in long-term muscle weakness with persistent paresthesias, resulting in permanent removal from competition.49 Options in participants to decrease the risk of future occurrences are to change their field positions or modify their playing techniques.

Cervical Cord Neurapraxia and Transient Quadriplegia

Neurapraxia of the cervical spinal cord (CCN) resulting in transient quadriplegia has been estimated to occur in 7 per 10,000 football players.53 This alarming injury is characterized by a temporary loss of motor or sensory function and is thought to be the result of a physiologic conduction block without true anatomic disruption of neuronal tissue. The affected athlete may complain of pain, tingling, or loss of sensation bilaterally in the upper and/or lower extremities. A spectrum of muscle weakness is possible, varying from mild quadriparesis to complete quadriplegia. The athlete has a full, pain-free range of cervical motion and does not complain of neck pain. Hemiparesis or hemisensory loss is also possible.

The condition is thought to result from a pincer-type mechanism of compression of the cord between the dorsocaudal portion of one vertebral body and the lamina of the vertebra below.54 Although this can also occur during hyperflexion, it is more commonly the sequela of extension movements with infolding of the ligamentum flavum, which can result in a 30% or more reduction of the anteroposterior diameter of the spinal canal.55 The spinal cord axons become unresponsive to stimulation for a variable period of time, essentially creating a “postconcussive” effect.56

CCN is described by the neurologic deficit, the duration of symptoms, and the anatomic distribution. A continuum of neurologic deficits that range from sensory only, sensory disturbance with motor weakness, or episodes of complete paralysis may occur. These may be described as paresthesia, paresis, or plegia. An injury is defined as grade 1 if the CCN symptoms do not persist for longer than 15 minutes. Grade 2 injuries are defined as lasting from 15 minutes to 24 hours. Grade 3 injuries persist for 24 to 48 hours. All four extremities may be involved; this is considered a “quad” pattern. Upper- and lower-extremity patterns may also be observed.57

By definition, CCN is transient, and complete resolution generally occurs within 15 minutes but may take up to 48 hours. Steroid administration in accordance with the Bracken protocol58 in this population is controversial. No controlled studies have reported that the administration of steroids has altered the natural history of athletes with CCN.44 In players who return to football, the rate of recurrence has been reported to be as high as 56%.57

A considerable amount of controversy exists regarding whether the presence of cervical stenosis makes an athlete more prone to sustaining CCN and even permanent neurologic injury.59,60 This controversy is compounded by the imprecise methods of objectifying whether an individual suffers from stenosis. The anteroposterior diameter of the spinal canal (measured from the dorsal aspect of the vertebral body to the most ventral point on the spinal laminar line) determined from lateral cervical spine radiographs is considered normal if there is more than 15 mm between C3 and C7. Cervical stenosis is considered to be present if the canal diameter is less than 13 mm. However, this measurement varies widely secondary to variations in landmarks used for measurement, changes in target distances for making the radiographs, patient positioning, differences in the triangular cross-sectional shape of the canal, and magnification of the canal because of a patient’s large body habitus. In an effort to eliminate this variability, Torg and Pavlov designed a ratio method for determining the presence of cervical stenosis, comparing the sagittal diameter of the spinal canal with the sagittal midbody diameter of the vertebral body at the same level.61 A ratio of 1:1 was considered normal, and less than 0.8 was indicative of significant cervical stenosis. This ratio was found to mislabel many athletes with adequately sized canals but large vertebral bodies as being stenotic. This observation, as well as an unprecedented ability to image the vertebral column, intervertebral discs, spinal canal, cerebrospinal fluid (CSF), and spinal cord directly, have made MRI, and not boney landmarks, the currently preferred method of choice for assessing “functional spinal stenosis.” MRI assessment of CSF signal around the spinal cord, termed the functional reserve, can be determined, and the visualization of the CSF signal, its attenuation in areas of stenosis, and changes on dynamic sagittal flexion-extension MRI studies are now the standard in diagnosing this condition. An absent CSF pattern on axial and, particularly, sagittal MRI is diagnostic of functional stenosis.

It had been previously accepted that young athletes who suffered an episode of CCN were not predisposed to permanent neurologic injury.60,62 This assumption has recently been called into question now that a player who experienced a CCN subsequently sustained a quadriplegic injury.63

Traumatic Intervertebral Disc Herniation

Acute herniation of an intervertebral disc can occur during participation in sports and in the athletic population. Those involving the cervical spine are less common than lumbar disc injuries and usually involve the older athlete. Compared with the overall incidence of disc herniation in the general public, the incidence is likely increased in the high-performance athlete competing in contact sports such as football and wrestling.64,65 Conversely, participation in noncontact sports might actually be protective against the development of cervical or lumbar disc herniation. This is likely the result of improved muscular conditioning protecting the disc from stresses transmitted to the spine.66

There are two types of disc herniation: hard and soft. Soft disc herniation is a more sudden phenomenon during which the soft nucleus populsus comes through the dorsal anulus. Hard disc herniations, on the other hand, are more of a chronic degenerative issue that likely begins much earlier in life than when the patient becomes symptomatic. This population often demonstrates a diminished disc height, marginal osteophytes, and degenerative disc material bulge and herniation.

Athletes with symptomatic cervical disc herniations most often present with varying degrees of neck or arm pain. Although the types of symptoms are similar in athletes and nonathletes, they may seem to be more severe in the competing athlete due to the demands of the specific sport. A traumatic central disc herniation typically presents with the sudden onset of dorsal neck pain and paraspinous muscle spasm as well as true radicular arm pain or referred pain to the periscapular area.67 Extrusion of disc material into the central spinal canal can result in acute cord compression and injury. Clinically, the athlete may present with acute paralysis of all four extremities and a loss of pain and temperature sensation.

In almost all cases except for those involving acute neurologic deficit, the initial 6 to 8 weeks of treatment should be nonoperative. This is especially important for an athlete who wishes to return to competition since this will be easier to accomplish without an operative intervention in most circumstances. As in the nonathlete, treatment options include rest, activity modification, anti-inflammatory medication, immobilization, cervical traction, and occasionally therapeutic injections.35 In most cases, the symptoms slowly resolve with these modalities, and a gradually increasing intensity of exercises can be initiated. These should at first emphasize isometric strengthening and cervical range of motion, followed by more sport-specific exercises. The athlete can return to competition when asymptomatic and after he or she has regained full strength and painless range of motion.

In some cases, radicular symptoms may persist despite conservative interventions or the athlete may develop myelopathy or a progressive neurologic deficit. In these situations, surgical intervention is considered. Although either a traditional ventral or dorsal approach can be performed, minimal disruption of normal anatomy is critical. Anecdotal evidence has suggested that an athlete may achieve a faster recovery following laminoforaminotomy without fusion, but a direct comparison between athletes undergoing the two types of surgery remains to be performed. This nonfusion procedure also has the advantage of preserving the majority of the disc involved, which theoretically decreases the forces that will be received by the adjacent segments when competition is resumed.

Following a dorsal disc procedure, the athlete can generally return to play when he or she is asymptomatic and has regained full strength and mobility. Following anterior discectomy and fusion at up to two levels, return to play can be considered once a successful bone fusion has been documented and the patient is pain free. Obviously, patients with longer fusions are generally considered to be at risk when returning to contact sports, and therefore the participation of these athletes must be individualized. The stability of disc arthroplasty devices in sports has yet to be determined, and, given the risk of extrusion, athletes who undergo an artificial disc placement are generally barred from a return to contact sports.

Minor Cervical Fractures

Spinous Process Fractures

Fractures of the spinous processes most commonly involve the lower cervical and upper thoracic area, occur as isolated injuries, and are stable. They occur via three mechanisms. The most common involves a strenuous contraction of the trapezius and rhomboid muscles, which avulses the spinous process. The C7 level is the most commonly involved, and this injury was previously termed clay-shoveler’s fracture. A second mechanism of injury is a hyperflexion or hyperextension injury to the neck, resulting in avulsion of the spinous process by the supraspinous and interspinous ligaments. This mechanism of injury is most commonly associated with a high-energy trauma, such as from a motor vehicle accident, but can also occur during contact sports such as football, gymnastics, and hockey.68 A less common mechanism described in the literature entails a direct blow to the spinous process.

Although spinous process fractures often occur as isolated stable injuries, vigilance should be maintained for an accompanying unstable injury. As mentioned earlier, isolated injuries are stable and usually heal with no long-term sequelae. The core of management is rest and symptom control. The athlete is usually placed in a semirigid collar to help control pain as well as to guard against delayed instability. Once the fractured area becomes nontender, dynamic radiographs (flexion-extension) can be obtained and, if negative, strengthening and range-of-motion exercises begun. This process can commonly take 1 to 2 months.

Catastrophic Cervical Spine Injury

A structural distortion of the cervical spinal column associated with actual or potential damage to the spinal cord is classified as a catastrophic cervical spine injury.67 Sports-related cervical spine injuries are divided into three groups that provide useful information when deciding when an athlete is ready to return to play.1,6,69 Type 1 injuries are those in which the athlete sustains permanent SCI. This category includes both immediate, complete paralysis and incomplete SCI syndromes. The incomplete injuries are of basically four types: Brown-Séquard syndrome, anterior spinal syndrome, central cord syndrome, and mixed types. Mixed types include the finding of crossed motor and sensory deficits with more prominent involvement of the upper extremities, which is considered to be a central cord/Brown-Séquard variant. There are, in addition, a few individuals in whom the neurologic deficit is relatively minor but who demonstrate an associated spinal cord pathology on imaging studies. For example, a high-intensity lesion within the spinal cord seen on MRI documents a spinal cord contusion. Type 2 injuries occur in individuals with normal radiographic studies. These deficits completely resolve within minutes to hours, and eventually the athlete has a normal neurologic examination. An example of the type 2 injury is the burning hands syndrome discussed earlier, which is a variant of central cord syndrome characterized by burning dysesthesias of the hands and associated weakness in the upper extremities.50 Most of these patients have normal radiographic studies, and their symptoms completely resolve within about 24 hours. Although certainly dramatic, these injuries are usually not considered catastrophic. Type 3 injuries comprise those with radiographic abnormality without neurologic deficit. This category includes fractures, fracture-dislocations, ligamentous and soft tissue injuries, and herniated intervertebral discs.

SCIs can also be divided into upper (occiput, atlas, and axis) and lower (C3-T1) cervical spine injuries. A thorough understanding of the normal anatomy and unique motion of the spine at various segments is mandatory when treating these injuries.

Unstable fractures and/or dislocations are the most common cause of catastrophic cervical spine trauma. The most common primary injury vector is axial loading with flexion occurring in football and hockey.70,71 Eighty percent of injuries to the cervical spine result from the accelerating head and body striking a stationary object or another player.72,73 The cervical spine is compressed between the instantly decelerated head and the mass of the continuing body when an axial force is applied to the vertex of the helmet. In neutral alignment, the cervical spinal column is slightly extended as a result of its normal lordotic posture, and it is believed that compressive forces can be effectively dissipated by the paravertebral musculature and vertebral ligaments. This buffering cervical lordosis is eliminated when the cervical spinal column is straightened and large amounts of energy are transferred directly along the spine’s longitudinal axis.71 Under high enough loads, the cervical spine can respond to this compressive force by buckling.

Two major patterns of spinal column injury result from the compression injury vector. Compression-flexion injury is the most common variant that results from the combination of axial loading and flexion. It results in shortening of the anterior column because of compressive failure of the vertebral body and lengthening of the posterior column because of tensile failure of the spinal ligaments.74 If the cervical vertebra is subjected to a relatively pure compression force, both the anterior column and posterior column shorten, resulting in a vertical compression (burst) fracture. The vertebral body essentially explodes, during which disc material extrudes through the fractured end plate, and osseous material retropulses into the spinal canal, resulting in possible cord damage.75 Alternatively, a significant SCI may occur without major disruption of the spinal column’s integrity. This type of injury is the result of transient spinal column distortion with energy transfer to the spinal cord.

Catastrophic cervical trauma caused by the primary disruptive vector flexion generally results from either a direct blow to the occipital region or rapid deceleration of the torso. The flexion-distraction injury most likely to result in spinal cord dysfunction is a bilateral facet dislocation.76,77 Unilateral facet dislocation, associated with cord injury in up to 25% of cases, can occur with the addition of axial rotation to the distractive force.78 It should be recognized that unstable cervical fracture-dislocations do not always result in upper motor neuron dysfunction. A unilateral facet dislocation can cause a monoradiculopathy due to foraminal compression of a nerve root on the side of the dislocated articular process. In other cases, major osseous or ligamentous damage produces no neurologic impairment. SCI potential in these scenarios is based on the amount of lost structural integrity of the vertebral column.67

Upper Cervical Spine Injury

For the purposes of sports-related injuries, the upper cervical spine is considered to include the occiput, atlas (C1), and axis (C2). The major function of the atlanto-occipital joint is motion in the sagittal plane, which accounts for 40% of normal flexion and extension of the spine and 5 to 10 degrees of lateral bending. The midline atlantodens articulation is stabilized by the transverse atlantal ligament, which prevents forward translation of the atlas. This specialized osseoligamentous anatomy allows the atlas to rotate in a highly unconstrained manner. The atlantoaxial complex is responsible for 40% to 60% of all cervical rotation.79 This rotation is limited by the alar ligaments extending from the odontoid process to the inner borders of the occipital condyles. The apical ligaments attach the odontoid centrally to the ventral foramen magnum. Atlantoaxial joint strength is provided by the transverse ligament and the lateral joint capsules.48

Spinal cord damage due to fractures or dislocations involving the upper cervical spine is rare because proportionately greater space exists within the spinal canal than with the lower cervical segments. Injuries that destabilize the atlantoaxial complex (fracture of the odontoid or rupture of the transverse atlantal ligament) are most likely to result in spinal cord dysfunction. Flexion is the most common cause of injury at the atlantoaxial joint. Odontoid fractures can also result from extension injuries. Unilateral rotary dislocations are usually the result of rotational forces. Cord compression is unusual with a burst fracture of the atlas or traumatic spondylolisthesis of the axis because these osseous injuries further expand the dimensions of the spinal canal. If anteroposterior radiographs demonstrate spreading of the lateral masses of greater than 7 mm, the transverse ligament is likely torn. Bilateral pedicle fractures of the axis may occur from extension of the occiput on the cervical spine. Importantly, although these injuries can result in instability, they usually do not cause neurologic deficits due to the anatomically wide spinal canal that is also present at this level.48 If an upper cervical cord injury does occur, diaphragmatic paralysis with acute respiratory insufficiency can occur along with quadriplegia since the phrenic nerve arises from three cervical nerve roots (C3-5).

Lower Cervical Spine Injury

The lower cervical spine encompasses the C3 through C7 vertebrae. This area accounts for the remaining arcs of neck flexion, extension, lateral bending, and rotation and has several important anatomic differences with respect to the upper cervical spine. The spinal canal is not as wide at this level, and the facet joints are oriented at a 45-degree angle. Because of this angulation, axial rotation is somewhat limited.

Each motion segment can be separated into an anterior and a posterior column. Stability of a cervical segment is derived mainly from the ventral spinal elements. Compression of the spinal column is primarily resisted by the vertebral bodies and intervertebral disc, whereas shearing forces are opposed primarily by paraspinal musculature and ligamentous support. Instability of the lower cervical spine has been defined radiographically as translational displacement of two adjacent vertebrae greater than 3.5 mm or angulation of greater than 11 degrees between adjacent vertebrae.80

The majority of fractures and dislocations occur in the lower cervical region. Lower cervical spine injuries are defined by the forces acting on the area (i.e., flexion, extension, lateral rotation, axial loading). Dislocated joints are usually the result of a flexion mechanism with either distraction or rotation. The ligamentous structures are the primary restraints to distraction of the spine.79 Compression of the dorsal structures as well as damage to the ventral structures is usually the result of extension or whiplash injuries. This mechanism of injury commonly results in tearing or the anterior longitudinal ligament and fractures of the dorsal elements.48

Compressive forces usually result in vertebral body fractures. These are commonly seen in spear tackling, a tackle in football in which a player’s entire body is launched head first—spear-like—against an opponent, resulting in significant axial loading on the cervical spine because the top of the head is the “spear point” of contact.81 This population commonly has a flexed posture to the head and a loss of the protective cervical lordosis.48 Large axial loads can result in protrusion of disc material or fractured bone into the spinal canal. This is the most common mechanism for sports-related quadriplegia.82,83 The C3-4 level is most commonly involved in cases of quadriplegia secondary to cervical dislocations.84,85

On-Site Evaluation and Management of Spinal Cord Injury

Participation in contact and collision sports carries an inherent risk of injury, for which injuries to the nervous system have the greatest potential for significant morbidity and mortality. Neurologic injuries suffered during athletic competition must be treated promptly and correctly to optimize outcome, and differentiating between minor and serious injuries is crucial to their management. Catastrophic injuries to the head or spinal cord are usually easy to identify, as are those that develop an immediate neurologic deficit. More challenging is the diagnosis of an injury with minimal initial symptomatology. This section is a guide to identifying and managing serious sports-related spinal injuries.

Primum non Nocere

The most important rule in dealing with potentially injured athletes is that an unstable spine injury can be easily converted into an injury with permanent neurologic deficit if mishandled. Because severe athletic-related injuries are relatively rare, the experience of the on-site medical staff is usually limited. Thus, everyone who shares responsibility for treating spine-injured athletes should be adequately trained and receive frequent refresher courses in the care of possible injury situations. The Inter-Association Task Force for Appropriate Care of the Spine-Injured Athlete was formed in 1998 and developed guidelines for the treatment of the catastrophically injured athlete.86 The five categories of on-field management are (1) preparation for any neurologic injury, (2) suspicion and recognition, (3) stabilization and safety, (4) immediate treatment and possible secondary treatment, and (5) evaluation for return to play.

Prior preparation should ensure that all of the proper equipment (e.g., spine boards, cervical collars or immobilization devices, cardiopulmonary resuscitation equipment, and stretchers) is available on site and easily accessible during a sporting event. Additionally, specific equipment for protective gear removal (e.g., football face mask) should also be readily available. There should be a clear hierarchy among the medical staff, indicating one member as the “captain” who directs the efforts of the team. In addition, arrangements should be made in advance to have ambulance services on site or close at hand. Preparation allays discomfort among providers and fosters efficiency and good decision making in the event of injury.72 It should also be mentioned that those who would treat injured athletes are legally responsibile for their actions, and precedent exists for legal action against team physicians and trainers who fail to properly care for those players.80

On-Site Management

The prevailing goal among the medical team members should be the prevention of secondary neurologic injury as a result of improper handling of the fallen athlete. Cervical spine injury should be suspected, and the athlete treated as if the injury were present whenever the mechanism of injury involves forced movement of the head and neck, even in the absence of neurologic deficit. The head and neck of the player should be immediately immobilized in a neutral position.

The immediate treatment of the player who has suffered an SCI should follow standard trauma protocols that address airway, breathing, and circulation. During this assessment, a rapid evaluation of the athlete’s level of consciousness may also be performed. Unless the player is unconscious or airway or breathing considerations exist, he or she should be left in the position in which he or she lies, until safe transfer onto a spine board can occur. If an athlete is wearing protective gear with a face mask, the face mask should be removed. If the player is wearing a helmet, it can usually be left in place until the head and neck can be adequately immobilized.87 The following situations require removal of the helmet: (1) a loose-fitting helmet that does not hold the head securely, thereby allowing the head to remain mobile; (2) an uncontrolled airway or inadequate ventilation provided even after removal of the face mask; (3) a face mask that cannot be removed after a reasonable period of time; and (4) a helmet that prevents immobilization for transport in an appropriate position.86 If necessary, the helmet should be removed with concomitant occipital support or simultaneous removal of shoulder pads (in American football). If left in place following helmet removal, the shoulder pads may cause cervical hyperextension. Obviously, if the helmet is removed, cervical immobilization must be maintained during the procedure.

The initial objective in this primary survey is to assess the athlete for immediately life-threatening conditions and to prevent further injury. During this primary survey, appropriate resuscitation procedures are instituted and the emergency medical system is activated immediately on recognizing a life-threatening problem or serious spinal injury.88

Following the initial survey, one of three clinical scenarios will become apparent: actual or impending cardiopulmonary collapse, altered mental status but no compromise of the cardiovascular or respiratory system, or normal level of consciousness and normal cardiopulmonary function. In a neurologically intact athlete with a normal mental status, once cervical spine involvement has been excluded, the athlete may be assisted to a sitting position and, if stable in this position, to a standing position. If able to stand, the athlete can then be walked off the field for further evaluation.

Unconscious athletes need to be stabilized before any neurologic appraisal. When sudden unconsciousness without preceding craniospinal trauma occurs, a cardiac etiology should be considered. If the athlete is experiencing cardiopulmonary collapse, the use of advanced cardiac life support principles is essential. If the athlete is lying prone, he or she must be carefully log rolled into a supine position on a rigid backboard if available. Any face mask should be rapidly removed to provide adequate airway access. As mentioned earlier, the removal of the helmet or other equipment is not routinely indicated unless they interfere with resuscitation. If still in place, the mouthpiece should be taken out while manual stabilization of the neck in a neutral position is maintained. Airway evaluation should be performed, understanding that obstruction can be secondary to a foreign body, facial fractures, or direct injury to the trachea or larynx. A depressed level of consciousness can also contribute to the inability to maintain an airway.

If breathing is of insufficient depth or rate, assisted ventilation is required. On the field, this usually is performed by using a bag-valve device and face mask. Hypoxia should be rapidly corrected by providing adequate ventilation with protection of the vertebral column at all times. In a patent airway, respiratory collapse could be the result of an upper cervical SCI due to paralysis of the diaphragm and accessory breathing muscles. Indications for definitive airway control by endotracheal intubation include apnea, inability to maintain oxygenation with face mask supplementation, and protection from aspiration. Circulation must also be addressed during the primary survey. Neurogenic shock due to SCI could result in diminished amplitude of the peripheral pulses in combination with bradycardia. If the femoral or carotid pulses are not palpable, cardiopulmonary resuscitation is required. If this is the case, the front of the shoulder pads can be opened to allow for chest compressions and/or defibrillation.86

If the athlete’s mental status is altered without cardiopulmonary compromise, a brief neurologic examination can be performed. The prevention of further injury to the cord is of primary importance, and once initial resuscitation and evaluation are performed, focus should be placed on immobilization. The helmet and shoulder pads should remain in place unless removal is required to access the airway. Neutral axial alignment and occipital support must be maintained. If a player is unconscious, he or she should be log rolled into a supine position and any mouthpiece removed.

If, after completion of the primary survey, the athlete is found to have a normal mental status without cardiopulmonary compromise, a neurologic assessment should be performed. If the athlete exhibits symptoms or signs suggestive of cord damage, a catastrophic cervical cord trauma should be assumed. If the neurologic assessment is normal but the athlete exhibits cervicothoracic pain, focal spinal tenderness, or restricted neck motion, an unstable spinal column injury with potential cord compromise is assumed.

The athlete should be taken from the field while maintaining strict immobilization of the spine. A rigid backboard with cervical collar or bolsters on the sides of the head should be used. It is important to remember that the athlete’s helmet may cause unintended cervical flexion on a rigid spine board. Once the athlete arrives at the hospital, if they are still in place, the helmet and shoulder pads should be removed before radiographic examination.

Off-the-Field Management

The treatment of the various forms of cervical spine injury has been summarized by numerous authors and follows established guidelines.1 The initial caregivers of the spine-injured athlete must be aware of the potential for respiratory failure and hemodynamic instability, as well as associated lesions, such as head injuries, which may affect the timing and order of needed treatments. Because of these concerns, patients with acute neurologic deficit from SCIs usually are initially cared for in an intensive care environment. The neurologic deficits from SCI may be improved by the early administration of steroids, but this method is controversial.78 The early induction of hypothermia has also been anecdotally reported to be beneficial.

After initial resuscitation and radiographic evaluation, informed decisions concerning the management of the injury can be made. Some bony injuries, such as spinous process fractures or unilateral laminar fractures, may require no treatment or only immobilization in a cervical collar. Others, such as the bilateral pars interarticularis fracture of C2 (“hangman’s fracture”) may require immobilization with a cervical collar or halo vest. Unstable injuries should initially be reduced and temporarily stabilized with cervical traction using Gardner-Wells tongs or a halo ring device. Contrast-enhanced CT scan or MRI of the cervical spine should be obtained before fracture reduction to rule out the presence of retropulsed intervertebral disc material, which has been implicated in the sudden neurologic deterioration of patients undergoing reduction of cervical fractures. Severe comminuted vertebral body fractures, unstable dorsal element fractures, type 2 odontoid fractures, incomplete SCIs with canal or cord compromise, and progression of neurologic deficit to higher levels of spinal cord function may require surgical intervention.

Any permanent neurologic injury should disqualify an athlete from further competition. Likewise, those whose fractures require halo vest or surgical stabilization are usually considered to have insufficient spinal strength to safely return to contact sports, although there may be exceptions. Even after the fracture has healed, the altered biomechanics in surrounding spinal segments and loss of normal motion result in a high risk of future sports-related injury. Athletes without cord injury who have stable fractures as evidenced by flexion-extension radiographs may be allowed to return to their previous level of activity. Athletes with burning hands syndrome or brachial plexus injuries may be considered safe for return to play when their neurologic examination returns to normal and they are symptom free.

Managing traumatic spinal injury in athletes presents a unique challenge for the surgeon. The classification scheme previously described is useful in decision making regarding optimal treatment and ultimate playing status of these athletes. Type 1 athletic injuries (those with permanent neurologic injury) preclude the player from further participation in contact sports. In type 2 injuries (transient neurologic disturbances with normal radiographic studies), if the complete workup reveals no injury, the player may return to competition once he or she is symptom free. Players with type 3 injuries (heterogeneous, including all players with radiographic abnormalities) such as bony or ligamentous spinal instability, or spinal cord contusion, are advised not to return to contact sports. Other radiographic abnormalities, such as spear tackler’s spine, dorsal ligamentous injury, congenital fusion or stenosis, herniated discs, or degenerative spondylitic disease, should be evaluated on an individual basis.

Spear tackling puts a group of athletes at high risk for cervical quadriplegic injury and has been considered a relative contraindication for participation in contact sports.81 Affected athletes have (1) developmental cervical canal stenosis, (2) persistent straightening or reversal of the normal cervical spine lordotic curve, (3) evidence of preexisting, posttraumatic radiographic abnormalities of the cervical spine, and (4) documentation of having previously used spear tackling techniques showing predisposal to injury from cervical spine axial energy forces. When a spine with a congenitally narrowed canal is straightened, impact at the top or crown of the helmet causes buckling of the neck because the movement of the head is momentarily stopped while the trunk continues to accelerate forward. This axial loading impact to the persistently straightened cervical spine, which occurs when athletes deliberately engage in frequent head impact, can result in permanent SCI. Occasionally, if no significant bone or ligamentous instability is present, cervical lordosis may be restored through physiotherapy. If the player can be coached against using head vertex impact, a return to competition may be allowed. Otherwise, these individuals should be withheld from participation in contact sports.

Section Three

Thoracic Spine

Injuries involving the thoracic spine are relatively infrequent in athletes, largely because athletic training provides significant stability gains to the rib cage, sternum, and broad paraspinal musculature. The osseous elements of the rib cage alone have been found to increase the stability of the thoracic spine by 20% to 40%. This has been previously referred to as a “fourth column” of stability in reference to the Denis three-column model of instability for thoracolumbar fractures. Despite the protective advantages to the thoracic region, injuries can occur. Most are minor and can be treated as discussed in the previous section. When an unstable injury does happen, there is a theoretically increased risk of injury to the cord due to a higher ratio of spinal cord to spinal canal diameter.

The thoracic spine can be divided into three separate zones each with varying risks of injury: midthoracic zone, cervicothoracic junctional zone, and thoracolumbar junctional zone. The midthoracic zone is the most structurally stable of the three but does have a higher theoretical risk of minor injuries such as contusions due to the prominence at its apex. The junctional areas have an increased vulnerability for unstable injuries. As mentioned previously, the cervicothoracic junction is a common site for spinous process avulsion fractures.

General return to competition guidelines are similar to those already discussed in the cervical spine section. Athletes requiring surgery in this area can usually return to competition once they are pain free and have regained full range of motion. If a fusion procedure was performed, there should also be radiographic evidence of solid bone fusion. Relative contraindications for return to competition are fusions that cross the cervicothoracic or thoracolumbar junction. Absolute contraindications to return to competition are fusions that terminate at a junctional zone.

Section Four

Lumbosacral Spine

Most population-based surveys of back pain report a point prevalence of 15% to 30%, a 1-year prevalence of 50%, and a lifetime prevalence of 60% to 80%.89 Given these numbers, it is not surprising that issues with the lumbosacral portion of the spine are fairly frequent in sports. An incidence of 7% has been reported in college athletes, and approximately 30% of college football players miss games due to lumbar spine problems.90 These injuries become more common as the level of play increases; the majority are simple lumbar strains. Most of these injuries are the result of direct contact causing a significant axial load or repeated hyperextension activities. Fortunately, most are minor and resolve spontaneously or with minimal intervention. This section deals with lumbosacral pathology in athletes, including diagnosis and surgical management. Simple strain, sprain, and contusion management were detailed in the cervical spine discussion.

Disc Herniation

Although lumbar discogenic disease is relatively uncommon in the younger population, its incidence increases with involvement in sporting activity.22 Pain can be axial mechanical, radicular, or both, and injuries range from anular tears to herniation with nerve root compression. Disc herniation in athletes is a consequence of numerous microtraumas to the intervertebral disc, which are further compounded by chronic overstraining. Although symptoms of other common injuries can resemble disc disease or damage, some mimickers are unusual. For example, a fracture of the lumbar lamina with epidural hematoma simulating herniation of a disc has been reported.91

When disc herniations occur in athletes in the teenage years or early twenties, they often present more subtly, with the main symptoms being back pain and muscle spasm. Signs of radiculopathy are less obvious due to the more viscous nature of the younger anulus and the lower likelihood of a free fragment.

Conservative therapies, including limiting participation, activity modification, anti-inflammatory medications, and therapeutic injections, are most commonly the first employed. Although these modalities have an excellent chance of improving symptoms, athletes frequently resist being sidelined and pressure the physician for a “quick fix.” This is especially true in the elite athlete.

Intractable symptoms refractory to conservative treatment and signs of progressive neurologic deficit or cauda equina syndrome are often treated operatively. Although true for most surgeries, minimal tissue disruption is particularly important for the athlete with the goal of return to competition. Either standard microsurgical discectomy or percutaneous microendoscopic discectomy is the technique of choice. Since the anulus of the disc is going to be subjected to considerable and frequent tensile forces when the athlete does return to competition, avoiding wide anular disruptions may decrease the incidence of reherniation. Bilateral laminectomies should be avoided to preserve as much bony and ligamentous structural integrity as possible.

Generally, surgical treatment is well tolerated, and the athlete can return to competition without restriction in as little as 3 weeks. Criteria for return to competition following surgery are a completely healed incision and pain-free activity. If more time can be taken off, postoperative physical therapy including core strengthening should be performed.

Pars Interarticularis Injury

The majority of sporting activities involve rapid changes in direction and explosive movements. A spectrum of injuries, ranging from stress fractures to complete spondylolysis and pars interarticularis defect, may result from such movements. The younger athlete is more prone to these injuries since this small bony connection is not yet fully developed in early adolescence. Because athletes in this population is also beginning a rapid growth phase, they are also more vulnerable to some of the more significant complications of spondylolysis, such as vertebral slippage and spondylolisthesis.93,94 Even without the development of deformities or instability, pars defects can result in chronic back pain.95

Early detection in the adolescent is critical to arresting and possibly reversing damage. If not corrected, spinal stenosis and narrowing of the foramen can result in chronic lower back pain, radiculopathy, and symptoms of neurogenic claudication. Patients with spondylolysis or spondylolisthesis with less than 50% slippage can be treated with rest, but more severe injuries often require bracing of the lumbosacral spine or surgical fusion.9698

Impending Spondylolysis or Impending Pars Defect

Ideally, stress fractures of the pars interarticularis can be discovered and treated before a frank bony separation occurs. This stage of injury is referred to as an impending spondylolysis, spondylolysis in the developmental stage, pars stress fracture, or impending pars defect. The first sign of such an injury is constant axial mechanical lower lumbar pain in an adolescent athlete that worsens with activity. Point tenderness is often evident at the lumbosacral junction, particularly over the L5 vertebra.99

Traditional bone-imaging modalities such as plain radiographs or CT scans are of limited value since no bone displacement has yet occurred, yet several other tests may give objective evidence of this condition.100,101

Generally, impending pars defects appear hypointense on T1-weighted MRI sequences and hyperintense on T2-weighted sequences. The extent of the edema can often be appreciated best on fat-presaturated T2-weighted images. MRI has the advantage of not exposing the athlete to radiation.

Nuclear scanning tests such as a bone scan can reveal bone inflammation indicative of an impending pars defect. Single-photon emission computed tomography (SPECT) can also aid in the diagnosis of an impending pars defect. It is similar to conventional nuclear medicine planar imaging but can provide true three-dimensional information typically presented as cross-sectional slices. The disadvantages to these modalities are the radiation exposure required and their fairly nonspecific results. For example, SPECT cannot distinguish between a pars stress fracture and other causes of increased activity in the pars such as arthritis, osteoid osteoma, or infection. Since these conditions are uncommon in the population that would be evaluated for an impending pars defect, this becomes less of a factor.102,103

In most cases, athletes, especially in their adolescence, with greater than 3 weeks of axial mechanical back pain and no structural abnormalities evident on normal plain radiographs of the lumbar spine (including oblique views) should be evaluated by MRI. If this testing is negative and a high degree of suspicion remains, nuclear imaging modalities may be employed. Once an impending pars interarticularis defect has been discovered, the treatment goals are the relief of pain, prevention of spondylolysis and spondylolisthesis, and eventual return to unrestricted activity. These goals are met by withholding the athlete from participation and practice involving any strenuous activity and possibly bracing. To our knowledge, there is no evidence that bracing has any benefit in healing versus simply restricting activity. Bracing may play a more important role in the noncompliant athlete who will not adhere to activity restrictions. Bone healing generally occurs after 6 to 12 weeks, and the athlete can gradually be reintroduced to activity when pain free. Numerous studies have demonstrated that the early recognition and treatment of an impending pars interarticularis defect is up to 80% successful in preventing progression.103105

Spondylolysis and Spondylolisthesis

Spondylolysis is a defect of the pars interarticularis, typically resulting from repetitive extension activities. It accounts for a much larger percentage of lumbar spine injuries in adolescent athletes than in adults. Pars defects are more common in athletes involved in activities that involve repetitive hyperextension and axial loading. It is present in more than 10% of college football players and gymnasts, in contrast to an incidence of less than 3% in the general population. In American football, participants playing on the line are the most at risk, again because of the repetitive axial loading and extension involved in the position.106,107 Because an actual bony defect is present, these injuries are easily identified using plain lumbar radiographs including obliques or CT imaging.

Once a pars defect has occurred, management goals are to alleviate pain and prevent progression and instability. Because the pars consists primarily of cortical bone with a poor blood supply, defects to it do not heal well. The athlete is restricted from activities until the pain subsides and adequate range of motion is achieved. This is followed by a gradual resumption of sporting activity. Typically, all athletic activity is stopped for at least 2 months or until the patient can achieve painless lumbar extension. Should the pain resume, a period of lordotic bracing may be attempted for 3 to 6 months or until pain once again subsides. The use of an external bone growth stimulator has also been suggested.

Surgical management for pars defects with no associated spondylolisthesis is considered when the patient continues to have disabling pain refractory to conservative therapy. Numerous methods of fixation have been described, including dorsal wiring of the transverse process and spinous processes (Scott wiring), translaminar interfragmentary screws (Buck technique), and various pedicle screw to hook constructs within the same vertebra. The prognosis for return to competition is excellent after surgery. In a retrospective case series of four competitive athletes who underwent direct pars repair for symptomatic spondylolysis, all returned to presymptomatic levels of activity.108 A separate study of 22 similarly treated athletes (13 professional footballers, 4 professional cricketers, 3 hockey players, 1 tennis player, and 1 golfer) also demonstrated the strong likelihood of return to play.109

Spondylolysis that progresses to a spondylolisthesis is first managed conservatively. Athletes with low-grade slips can usually return to competition after an aggressive rehabilitation program. Return to play is based on the individual athlete’s symptoms and treatment. Patients sufficiently treated conservatively may return to full play after adequate pain control and range of motion are achieved. Typically, all athletic activity is stopped for at least 2 months, or until the patient can achieve painless lumbar extension.

Surgical management is reserved for progressing slips, refractory symptoms, neurologic deficits, or high-grade slips. Although no large series of instrumented or noninstrumented lumbar spine fusions in athletes exists to date, it is believed that the extent of tissue disruption, scarring, and stress placed on adjacent structures greatly increases the likelihood of continued postoperative pain with aggressive activity. Nevertheless, when lumbar fusion surgery is performed, either with lateral fusion alone or with interbody fusion, there is no absolute contraindication to the return to competition after complete recovery from surgery. Criteria for release for return to competition should include resolution of pain, no disabling neurologic deficit, and evidence of bone fusion on imaging. A clear understanding between the physician and the athlete about the possibility and consequences of reinjury is crucial.

References

1. Bailes J.E., Hadley M.N., Quigley M.R., et al. Management of athletic injuries of the cervical spine and spinal cord. Neurosurgery. 1991;29:491-497.

2. Wilson J.B., Zarzour R., Moorman C.T.3rd. Spinal injuries in contact sports. Curr Sports Med Rep. 2006;5:50-55.

3. Ellis J.L., Gottlieb J.E. Return-to-play decisions after cervical spine injuries. Curr Sports Med Rep. 2007;6:56-61.

4. Nobunga A., Go B., Karunas R. Recent demographic and injury trends in people served by the model spine cord injury care systems. Arch Phys Med Rehabil. 1999;80:1372-1382.

5. DeVivo M.J. Causes and costs of spinal cord injury in the United States. Spinal Cord. 1997;35:809-813.

6. Maroon J.C., Bailes J.E. Athletes with cervical spine injury. Spine. 1996;21:2294-2299.

7. Levy A.S., Smith R.H. Neurologic injuries in skiers and snowboarders. Semin Neurol. 2000;20:233-245.

8. Quarrie K.L., Cantu R.C., Chalmers D.J. Rugby union injuries to the cervical spine and spinal cord. Sports Med. 2002;32:633-653.

9. Schmitt H., Gerner H.J. Paralysis from sport and diving accidents. Clin J Sport Med. 2001;11:17-22.

10. Tator C.H., Carson J.D., Cushman R. Hockey injuries of the spine in Canada, 1966–1996. CMAJ. 2000;162:787-788.

11. Cantu R.C., Mueller F.O. Catastrophic spine injuries in American football, 1977–2001. Neurosurgery. 2003;53:358-362. discussion 362–363

12. Torg J.S., Truex R.Jr., Quedenfeld T.C., et al. The National Football Head and Neck Injury Registry. Report and conclusions 1978. JAMA. 1979;241:1477-1479.

13. Torg J.S., Quedenfeld T.C., Burstein A., et al. National football head and neck injury registry: report on cervical quadriplegia, 1971 to 1975. Am J Sports Med. 1979;7:127-132.

14. Nadeau M.T., Brown T., Boatman J., Houston W.T. The prevention of softball injuries: the experience at Yokota. Mil Med. 1990;155:3-5.

15. Sward L. The thoracolumbar spine in young elite athletes. Current concepts on the effects of physical training. Sports Med. 1992;13:357-364.

16. Jackson D.S., Furman W.K., Berson B.L. Patterns of injuries in college athletes: a retrospective study of injuries sustained in intercollegiate athletics in two colleges over a two-year period. Mt Sinai J Med. 1980;47:423-426.

17. Kovac D., Negovetic L., Vukic M., et al. [Surgical treatment of lumbar disc hernias in athletes. Reumatizam. 1998;46:35-41.

18. Wilber C.A., Holland G.J., Madison R.E., Loy S.F. An epidemiological analysis of overuse injuries among recreational cyclists. Int J Sports Med. 1995;16:201-206.

19. Hamilton A.J. Cowboy care. Emerg Med Serv. 24, 1995. 24–28, 30

20. Grossman J.A., Kulund D.N., Miller C.W., et al. Equestrian injuries. Results of a prospective study. JAMA. 1978;240:1881-1882.

21. Sinclair A.J., Smidt C. Analysis of 10 years of injury in high school rodeo. Clin J Sport Med. 2009;19:383-387.

22. Clark J.E. Apophyseal fracture of the lumbar spine in adolescence. Orthop Rev. 1991;20:512-516.

23. Kolt G.S., Kirkby R.J. Epidemiology of injury in elite and subelite female gymnasts: a comparison of retrospective and prospective findings. Br J Sports Med. 1999;33:312-318.

24. Tator C.H., Provvidenza C.F., Lapczak L., et al. Spinal injuries in Canadian ice hockey: documentation of injuries sustained from 1943–1999. Can J Neurol Sci. 2004;31:460-466.

25. Bledsoe G.H.H., Edbert B., Grabowski, et al. Incidence of injury in professional mixed martial arts competitions. J Sports Sci Med. 2006:136-142. (Combat Sports Special Issue)

26. Ngai K.M., Levy F., Hsu E.B. Injury trends in sanctioned mixed martial arts competition: a 5-year review from 2002 to 2007. Br J Sports Med. 2008;42:686-689.

27. Kochhar T., Back D.L., Mann B., Skinner J. Risk of cervical injuries in mixed martial arts. Br J Sports Med. 2005;39:444-447.

28. Kew T., Noakes T.D., Kettles A.N., et al. A retrospective study of spinal cord injuries in Cape Province rugby players, 1963–1989. Incidence, mechanisms and prevention. S Afr Med J. 1991;80:127-133.

29. Scher A.T. Rugby injuries of the spine and spinal cord. Clin Sports Med. 1987;6:87-99.

30. Kewalramani L.S., Kraus J.F. Acute spinal-cord lesions from diving—epidemiological and clinical features. West J Med. 1977;126:353-361.

31. Good R.P., Nickel V.L. Cervical spine injuries resulting from water sports. Spine. 1980;5:502-506.

32. Frankel H.L., Montero F.A., Penny P.T. Spinal cord injuries due to diving. Paraplegia. 1980;18:118-122.

33. Bailes J.E., Herman J.M., Quigley M.R., et al. Diving injuries of the cervical spine. Surg Neurol. 1990;34:155-158.

34. Jarret G.J., Orwin J.F., Dick R.W. Injuries in collegiate wrestling. Am J Sports Med. 1998;26:674-680.

35. Zmurko M.G., Tannoury T.Y., Tannoury C.A., Anderson D.G. Cervical sprains, disc herniations, minor fractures, and other cervical injuries in the athlete. Clin Sports Med. 2003;22:513-521.

36. Hovis W.D., Limbird T.J. An evaluation of cervical orthoses in limiting hyperextension and lateral flexion in football. Med Sci Sports Exerc. 1994;26:872-876.

37. Chrisman O.D., Snook G.A., Stanitis J.M., Keedy V.A. Lateral-flexion neck injuries in athletic competition. JAMA. 1965;192:613-615.

38. Hershman E.B. Brachial plexus injuries. Clin Sports Med. 1990;9:311-329.

39. Weinberg J., Rokito S., Silber J.S. Etiology, treatment, and prevention of athletic “stingers.”. Clin Sports Med. 2003;22:493-500. viii

40. Clancy W.G.Jr., Brand R.L., Bergfield J.A. Upper trunk brachial plexus injuries in contact sports. Am J Sports Med. 1977;5:209-216.

41. Robertson W.C.Jr., Eichman P.L., Clancy W.G. Upper trunk brachial plexopathy in football players. JAMA. 1979;241:1480-1482.

42. Markey K.L., Di Benedetto M., Curl W.W. Upper trunk brachial plexopathy. The stinger syndrome. Am J Sports Med. 1993;21:650-655.

43. Castro F.P.Jr., Ricciardi J., Brunet M.E., et al. Stingers, the Torg ratio, and the cervical spine. Am J Sports Med. 1997;25:603-608.

44. Castro F.P.Jr. Stingers, cervical cord neurapraxia, and stenosis. Clin Sports Med. 2003;22:483-492.

45. Meyer S.A., Schulte K.R., Callaghan J.J., et al. Cervical spinal stenosis and stingers in collegiate football players. Am J Sports Med. 1994;22:158-166.

46. Vaccaro A.R., Klein G.R., Ciccoti M., et al. Return to play criteria for the athlete with cervical spine injuries resulting in stinger and transient quadriplegia/paresis. Spine J. 2002;2:351-356.

47. Vaccaro A.R., Watkins B., Albert T.J., et al. Cervical spine injuries in athletes: current return-to-play criteria. Orthopedics. 2001;24:699-703. quiz 704–705

48. Ghiselli G., Schaadt G., McAllister D.R. On-the-field evaluation of an athlete with a head or neck injury. Clin Sports Med. 2003;22:445-465.

49. Speer K.P., Bassett F.H.3rd. The prolonged burner syndrome. Am J Sports Med. 1990;18:591-594.

50. Maroon J.C., Abla A.A., Wilberger J.I., et al. Central cord syndrome. Clin Neurosurg. 1991;37:612-621.

51. Wilberger J.E., Abla A., Maroon J.C. Burning hands syndrome revisited. Neurosurgery. 1986;19:1038-1040.

52. Kim D.H., Vaccaro A.R., Berta S.C. Acute sports-related spinal cord injury: contemporary management principles. Clin Sports Med. 2003;22:501-512.

53. Torg J.S., Guille J.T., Jaffe S. Injuries to the cervical spine in American football players. J Bone Joint Surg [Am]. 2002;84:112-122.

54. Penning L. Some aspects of plain radiography of the cervical spine in chronic myelopathy. Neurology. 1962;12:513-519.

55. Moiel R.H., Raso E., Waltz T.A. Central cord syndrome resulting from congenital narrowness of the cervical spinal canal. J Trauma. 1970;10:502-510.

56. Zwimpfer T.J., Bernstein M. Spinal cord concussion. J Neurosurg. 1990;72:894-900.

57. Torg J.S., Corcoran T.A., Thibault L.E., et al. Cervical cord neurapraxia: classification, pathomechanics, morbidity, and management guidelines. J Neurosurg. 1997;87:843-850.

58. Bracken M.B., Shepard M.J., Holford T.R., et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA. 1997;277:1597-1604.

59. Thomas B.E., McCullen G.M., Yuan H.A. Cervical spine injuries in football players. J Am Acad Orthop Surg. 1999;7:338-347.

60. Torg J.S., Naranja R.J.Jr., Palov H., et al. The relationship of developmental narrowing of the cervical spinal canal to reversible and irreversible injury of the cervical spinal cord in football players. J Bone Joint Surg [Am]. 1996;78:1308-1314.

61. Torg J.S., Pavlov H. Cervical spinal stenosis with cord neurapraxia and transient quadriplegia. Clin Sports Med. 1987;6:115-133.

62. Torg J.S., Pavlov H., Genuario S.E., et al. Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg [Am]. 1986;68:1354-1370.

63. Cantu R.C. Cervical spine injuries in the athlete. Semin Neurol. 2000;20:173-178.

64. Albright J.P., McAuley E., Martin R.K., et al. Head and neck injuries in college football: an eight-year analysis. Am J Sports Med. 1985;13:147-152.

65. Albright J.A. Cervical spine injuries in football. Conn Med. 1976;40:677-679.

66. Mundt D.J., Kelsey J.L., Golden A.L., et al. An epidemiologic study of sports and weight lifting as possible risk factors for herniated lumbar and cervical discs. The Northeast Collaborative Group on Low Back Pain. Am J Sports Med. 1993;21:854-860.

67. Banerjee R., Palumbo M.A., Fadale P.D. Catastrophic cervical spine injuries in the collision sport athlete, part 1: epidemiology, functional anatomy, and diagnosis. Am J Sports Med. 2004;32:1077-1087.

68. Mazur M.L. Derek Shockro saving lives. Diabetes Forecast. 2002;55:50-54.

69. Warren W.L.Jr., Bailes J.E. On the field evaluation of athletic neck injury. Clin Sports Med. 1998;17:99-110.

70. Tator C.H., Carson J.D., Edmonds V.E. Spinal injuries in ice hockey. Clin Sports Med. 1998;17:183-194.

71. Torg J.S., Vegso J.J., O’Neill M.J., Sennett B. The epidemiologic, pathologic, biomechanical, and cinematographic analysis of football-induced cervical spine trauma. Am J Sports Med. 1990;18:50-57.

72. Bohlman H.H. Acute fractures and dislocations of the cervical spine. An analysis of three hundred hospitalized patients and review of the literature. J Bone Joint Surg [Am]. 1979;61:1119-1142.

73. Davis D., Bohlman H., Walker A.E., et al. The pathological findings in fatal craniospinal injuries. J Neurosurg. 1971;34:603-613.

74. Torg J.S., Pavlov H., O’Neill M.J., et al. The axial load teardrop fracture. A biomechanical, clinical and roentgenographic analysis. Am J Sports Med. 1991;19:355-364.

75. Allen B.L.Jr., Ferguson R.L., Lehmann T.R., O’Brien R.P. A mechanistic classification of closed, indirect fractures and dislocations of the lower cervical spine. Spine (Phila Pa 1976). 1982;7:1-27.

76. Razack N., Green B.A., Levi A.D. The management of traumatic cervical bilateral facet fracture-dislocations with unicortical anterior plates. J Spinal Disord. 2000;13:374-381.

77. Wolf A., Levi L., Mirvis S., et al. Operative management of bilateral facet dislocation. J Neurosurg. 1991;75:883-890.

78. Coelho D.G., Brasil A.V., Ferreira N.P. Risk factors of neurological lesions in low cervical spine fractures and dislocations. Arq Neuropsiquiatr. 2000;58:1030-1034.

79. Ghanayem A., Zdeblich T., Dvorak J. Functional anatomy of joints, ligaments, and discs. In: Society C.S.R., editor. The cervical spine. Philadelphia: Lippincott-Raven; 1998:45-52.

80. White A.A.3rd, Johnson R.M., Panjabi M.M., Southwick W.O. Biomechanical analysis of clinical stability in the cervical spine. Clin Orthop Relat Res. 1975;109:85-96.

81. Torg J.S., Sennett B., Pavlov H., et al. Spear tackler’s spine. An entity precluding participation in tackle football and collision activities that expose the cervical spine to axial energy inputs. Am J Sports Med. 1993;21:640-649.

82. Torg J.S. Epidemiology, pathomechanics, and prevention of athletic injuries to the cervical spine. Med Sci Sports Exerc. 1985;17:295-303.

83. Tator C.H., Edmonds V.E. National survey of spinal injuries in hockey players. Can Med Assoc J. 1984;130:875-880.

84. Torg J.S., Sennett B., Vegso J.J. Spinal injury at the level of the third and fourth cervical vertebrae resulting from the axial loading mechanism: an analysis and classification. Clin Sports Med. 1987;6:159-183.

85. Kang J.D., Figgie M.P., Bohlman H.H. Sagittal measurements of the cervical spine in subaxial fractures and dislocations. An analysis of two hundred and eighty-eight patients with and without neurological deficits. J Bone Joint Surg [Am]. 1994;76:1617-1628.

86. Kleiner DM, Almquist JL, Bailes J, et al: Prehospital care of the spine-injured athlete. Paper from the Inter-Association Task Force for Appropriate Care of the Spine-Injured Athlete, National Trainers’ Association, Dallas, Tx, March 2001

87. Waninger K.N. On-field management of potential cervical spine injury in helmeted football players: leave the helmet on!. Clin J Sport Med. 1998;8:124-129.

88. Banerjee R., Palumbo M.A., Fadale P.D. Catastrophic cervical spine injuries in the collision sport athlete, part 2: principles of emergency care. Am J Sports Med. 2004;32:1760-1764.

89. Nachemson A.L., Waddell G., Norlund A.I. Epidemiology of neck and back pain. In: Nachemson A.L., Jonsson E., editors. Neck and back pain: the scientific evidence of causes, diagnosis and treatment. Philadelphia: Lippincott Williams & Wilkins; 2000:165-188.

90. Smith C.F. Physical management of muscular low back pain in the athlete. Can Med Assoc J. 1977;117:632-635.

91. Garth W.P.Jr., Van Patten P.K. Fractures of the lumbar lamina with epidural hematoma simulating herniation of a disc. A case report. J Bone Joint Surg [Am]. 1989;71:771-772.

92. Mooney V., Robertson J. The facet syndrome. Clin Orthop Relat Res. 1976;115:149-156.

93. Micheli L.J., Curtis C. Stress fractures in the spine and sacrum. Clin Sports Med. 2006;25:75-88. ix

94. Micheli L.J. Overuse injuries in children’s sports: the growth factor. Orthop Clin North Am. 1983;14:337-360.

95. Jackson D.W., Wiltse L.L., Dingeman R.D., Hayes M. Stress reactions involving the pars interarticularis in young athletes. Am J Sports Med. 1981;9:304-312.

96. Micheli L.J., Hall J.E., Miller M.E. Use of modified Boston brace for back injuries in athletes. Am J Sports Med. 1980;8:351-356.

97. Micheli L.J. Back injuries in dancers. Clin Sports Med. 1983;2:473-484.

98. Micheli L.J. Back injuries in gymnastics. Clin Sports Med. 1985;4:85-93.

99. Kruse D., Lemmen B. Spine injuries in the sport of gymnastics. Curr Sports Med Rep. 2009;8:20-28.

100. Cohen E., Stuecker R.D. Magnetic resonance imaging in diagnosis and follow-up of impending spondylolysis in children and adolescents: early treatment may prevent pars defects. J Pediatr Orthop B. 2005;14:63-67.

101. van den Oever M., Merrick M.V., Scott J.H. Bone scintigraphy in symptomatic spondylolysis. J Bone Joint Surg [Br]. 1987;69:453-456.

102. Zukotynski K., Curtis C., Grant F.D., et al. The value of SPECT in the detection of stress injury to the pars interarticularis in patients with low back pain. J Orthop Surg Res. 5(13), 2010.

103. Tallarico R.A., Madom I.A., Palumbo M.A. Spondylolysis and spondylolisthesis in the athlete. Sports Med Arthrosc. 2008;16:32-38.

104. Sairyo K., Sakai T., Yasui N. Minimally invasive technique for direct repair of pars interarticularis defects in adults using a percutaneous pedicle screw and hook-rod system. J Neurosurg Spine. 2009;10:492-495.

105. Radcliff K.E., Kalantar S.B., Reitman C.A. Surgical management of spondylolysis and spondylolisthesis in athletes: indications and return to play. Curr Sports Med Rep. 2009;8:35-40.

106. Fredrickson B.E., Baker D., McHolick W.J., et al. The natural history of spondylolysis and spondylolisthesis. J Bone Joint Surg [Am]. 1984;66:699-707.

107. Beutler W.J., Fredrickson B.E., Murtland A., et al. The natural history of spondylolysis and spondylolisthesis: 45-year follow-up evaluation. Spine (Phila Pa 1976). 2003;28:1027-1035. discussion 1035

108. Reitman C.A., Esses S.I. Direct repair of spondylolytic defects in young competitive athletes. Spine J. 2002;2:142-144.

109. Debnath U.K., Freeman B.J., Gregory P., et al. Clinical outcome and return to sport after the surgical treatment of spondylolysis in young athletes. J Bone Joint Surg [Br]. 2003;85:244-249.