Common Spine Injuries in Football: Management and Operative Treatment

Introduction

The 7% of spine-related National Football League (NFL) injuries reported in an 11-year period ranged from the mundane to the catastrophic [10]. For any spine injury, a thorough assessment of the injured area will include range of motion testing, provocative tests, manual strength of spine segments, and a neurologic examination that assesses deep tendon reflexes, presence or absence of pathological reflexes, motor strength, and sensory testing.

All injuries have mechanical and chemical/inflammatory consequences, and treatment options begin in a tiered manner. Initially, spine injuries are iced and immobilized. In the cervical spine, this may mean wearing a cervical collar; in a severe lumbar spine injury, this may mean 1 to 2 days of relative bed rest for self-immobilization of the spine. Appropriate use of anti-inflammatories begins with nonsteroidals and progresses through corticosteroids, depending on injury severity. Judicious use of analgesics and muscle relaxants can also help break the cycle of pain, spasm, and inflammation. When appropriate, image-guided corticosteroid injections help control the inflammation. To address the mechanical aspects of injuries, athletic training modalities can be used, including muscle activation therapy, massage, physical therapy, and rehabilitation of core musculature.

As with other sport-related injuries, after treatment for a spine injury, decisions are made about return to play. The baseline qualifications include pain-free range of motion, full strength of the lumbar or cervical spine against resistance, and a normal neurological examination. At times these requirements are met but the return-to-play decision is altered because of abnormalities identified through magnetic resonance imaging (MRI) or computed tomography (CT) scanning.

This article reviews the most common spine injuries in American football, illustrated by cases detailing diagnostic workups, treatment options, and return-to-play decisions.

Lumbar Disk Herniation

Lumbar disk herniations occur in football slightly more often during weight training than during play. During training, they commonly occur when performing squats, deadlifts, or power cleans. During play, they often occur when a player is engaged with an opponent with significant rotational and flexion forces applied, in both blocking and tackling maneuvers.

Players present with back pain that radiates down to the upper gluteus region and through the leg in a dermatomal pattern. On physical examination, there may be trunk shift upon standing that is accentuated with flexion and normalized in extension. A thorough neurologic examination should be done to make sure there is no significant motor weakness or sensory deficit. Additional key motor examination testing includes a side-lying hip abduction strength test (L5 myotome) as well as single-leg plantarflexion against gravity (S1 myotome), with the noninvolved leg doing 10 repetitions and then the involved leg doing 10 repetitions to determine strength loss and fatigue with comparison.

Diagnostic workup includes plain films followed by MRI. Once a disk herniation has been identified on MRI, treatment is geared toward making the player comfortable with an anti-inflammatory regimen. For pain relief, oral methylprednisolone to start is preferred, followed by nonsteroidal options, although some may begin with nonsteroidal treatments. For severe symptoms, patients may also receive an analgesic and a muscle relaxer as needed.

Other treatment options include transforaminal epidural steroid injections (TFESI) to the affected nerve. If the patient has an L4-L5 disk herniation and a concomitant L5 radiculopathy, the recommendation would be TFESI at L5-S1, which targets the L5 nerve root [11]. The injection flows cranially to best cover the area of injury and decrease the inflammatory response to the injury. While TFESI does not decrease the size of the herniation, it does take the chemical event of inflammation out of play. Steroid injections are beneficial for pain relief but are less helpful with sensory and motor changes.

As symptoms resolve and there is no significant neurological deficit, a comprehensive rehabilitation program may begin. For mechanical symptoms, a simple plan is to restore normal motion by going in the opposite direction of pain caused by the physical examination. For example, if the player has no pain with extension but pain with flexion, he should be started initially in the McKenzie extension program. Conversely, if he has pain with extension but not with flexion, the Williams flexion program can be implemented. Once mechanics have improved, the player can graduate to a program with core stability and aerobic conditioning. Return to play is usually between 6 and 8 weeks; Mall et al [10] found an average of 49.6 days lost to a combined nerve and disk injury in the lumbar spine.

Surgery is recommended only if there is refractory pain or significant motor loss on clinical examination. The recommended procedure is a microscopic lumbar discectomy, a minimally invasive procedure with a proven track record. Return to play in the best of conditions is approximately 3 months after this procedure [19]. Given the game’s high-impact nature, earlier return to play increases risk of re-herniation [4].

Case

This injury is illustrated by the case of a 22-year-old intercollegiate offensive lineman with a large left-sided L4-L5 disk herniation (Figs. 1 and 2). He presented with severe pain, motor weakness, and sensory changes that were refractory to conservative measures. He underwent a microscopic lumbar discectomy uneventfully and returned to full activity 3 months postoperatively. He has since played an intercollegiate season.

Fig. 1.

Sagittal T2 MRI showing L4-L5 disk herniation. HNP herniation of the nucleus pulposus, MRI magnetic resonance imaging.

Fig. 2.

Axial T2 MRI showing L4-L5 disk herniation. HNP herniation of the nucleus pulposus, MRI magnetic resonance imaging

Lumbar Stress Reactions and Pars Defects

The treatment of acute pars injuries and chronic pars injuries is vastly different. Chronic pars interarticularis defects in an athlete without a history of significant lumbar symptoms should be considered developmental in nature, whereas acute stress reactions are fatigue fractures typically associated with overtraining.

Pars defects seen on plain radiographs should be considered chronic. These typically occur between ages 6 and 14 and usually are due to genetic inheritance rather than trauma [6]. On examination, players with chronic defects often have pain while performing extension due to stress on the pseudoarthrosis created by the pars defect. In fact, on histology of pars defect tissue, there are free nerve endings to suggest that the defect is the source of the patient’s back pain [13]. The player may also present with mild-to-moderate radicular findings. The most common finding with L5 pars injury, for example, is hip abduction weakness, consistent with the L5 myotome.

The preferred treatment is a flexion bias core stability program with a trial of anti-inflammatories. If symptoms are refractory, corticosteroid injections under fluoroscopic guidance into the pars defects often control pain. Recurrent symptoms can be treated with radiofrequency ablation of the pars defect.

However, in some patients, chronic pars defects identified on plain film and imaging will not clinically correlate to a new onset of sharp back pain. The use of MRI under these circumstances is an excellent option as it can identify edema within the posterior elements at a different level, signaling the location of the acute stress reaction.

Players with acute pars injuries present with sharp mechanical back pain that often intensifies over time and renders them unable to play. It usually has a predilection to 1 side and may be accompanied by referred radicular pain. The physical examination shows pain in extension maneuvers, particularly Jackson’s maneuver (Stork test). The radicular pain is caused by the exiting nerve root underneath the pars injury. For example, the L4 nerve may be irritated by L4 pars injury and have concomitant neurological findings on physical examination.

For an acute pars stress reaction or fracture, the best treatment is rest from activity for at least 3 months. Nonsteroidal anti-inflammatories are not recommended as they have been identified as a risk factor for delayed bone healing [1]. If the stress reaction or fracture is at L3 or above, bracing with a lumbar-sacral orthosis (LSO) can help to immobilize the spine and offer lumbar support. If the injury is at L4 or L5, the senior author does not brace as the literature suggests a thigh cuff is needed to properly immobilize the spine and patient compliance is exceptionally low [9].

When assessing for return to activity, the patient’s Jackson’s maneuver (Stork test) and neurologic examination must be negative before rehabilitation begins [8]. These criteria are typically met at the 6-week follow-up visit, at which time the patient can start a non-impact aerobic conditioning program and an isometric core stability program that avoids extension and flexion. At 3 months, if the examination remains normal, the patient can move to a dynamic core stability program and subsequent reintegration into sport-specific training. Repeat imaging is not required, especially for teenage patients, as a failure to unite in 3 months is indicative that the fracture is unlikely to heal and does not change treatment.

Pedicle stress fractures are rarer, and the senior author has not seen one in football players (only in baseball players and Olympic gymnasts). However, they are more difficult to manage, and the time to start rehabilitation can often be prolonged by an additional 3 months. It is the same rehabilitation protocol, but instead of 6 weeks and 12 weeks, it is changed to 3 months and 6 months.

Although several surgical techniques can address pars defects [15], rest and rehabilitation are usually sufficient, and the senior author has never recommended them.

Case

Chronic pars defect with edema is illustrated by the case of an 18-year-old center and long snapper for a high school football team who presented with right-sided paralumbar pain that was worse on extension. Radiographs showed chronic appearing fractures, and subsequent MRI short T1 inversion recovery (STIR) sequences showed edema in his right L4 pars defect (Figs. 3 and 4). After conservative measures failed, he underwent a pars corticosteroid injection that resolved his symptoms. He was able to play the last 8 games of his senior year.

Fig. 3.

Plain radiograph showing chronic defect of pars.

Fig. 4.

Magnetic resonance imaging STIR sequence showing edema in right L4 pars defect. STIR short T1 inversion recovery.

Lumbar Spine Fractures

The 2 most common lumbar spine fractures are transverse process fractures and vertebral compression fractures. Transverse process fractures often occur on direct impact when a player is being tackled. They are more common in the upper lumbar spine transverse processes (L1-L3). Concomitant renal injury should be ruled out. Almost universally, the player will finish the game, miss the next one, and return for the following game.

Vertebral compression fractures are secondary to significant flexion motion while under load. On history, the player will describe a significant pop or crack consistent with a fracture. Compression fractures will have edema present without the loss of structural integrity. These are essentially bone bruise injuries with trabecular edema. Most players can be managed symptomatically, and when standard return-to-play criteria are met, they may resume. Fractures with loss of structural integrity require 2 to 3 months of healing before return to play, depending on fracture severity. Compression fractures at L3 or above are treated in a LSO.

Case 1

An NFL quarterback sustained direct contact injury to his right flank with severe pain, sustaining L2 and L3 transverse process fractures (Figs. 5 and 6). He finished the game, missed the next game, and return the following week. Renal workup was negative.

Fig. 5.

L2 transverse process fracture.

Fig. 6.

L3 transverse process fracture.

Case 2

A 29-year-old NFL linebacker was injured while tackling with a compression and flexion force. The player felt a deep pop and had a feeling of fracture. MRI indicated an L1 compression fracture with approximately 5 to 7 mm of height loss (Fig. 7). He was treated in a thoracic- LSO for 3 months and returned to play that season without incident.

Fig. 7.

L1 compression fracture on MRI with 5 to 7 mm of collapse. MRI magnetic resonance imaging

Cervical Disk Herniation

Cervical disk herniations occur more commonly while playing (blocking) than while training. In comparison, lumbar disk herniation is more common with weight training and less so on the football field. This typically presents with unilateral neck pain that radiates to the parascapular boundary and then down the arm in a dermatomal fashion. On clinical examination, there will be a painful range of motion and a positive Spurling’s maneuver. In addition, a trigger point may be located along the medial aspect of the scapula. The location of this trigger point can help to identify specific nerve root involvement. For example, if the trigger point is over the trapezius, it is commonly associated with C5 nerve involvement, whereas a trigger point over the levator scapulae or the inferior medial boundary of the scapula would be more indicative of a C6 or C7 nerve injury, respectively.

Initial treatment includes immobilization of the neck with a soft collar and either an oral nonsteroidal anti-inflammatory or methylprednisolone regimen. For significant pain, an oral corticosteroid is preferred. Other analgesics and muscle relaxers can be used as needed. After thorough evaluation, if there is significant motor weakness or severe pain, a diagnostic workup with plain films and an MRI should be initiated. If there is persistent pain and disability, a targeted steroid injection under fluoroscopic guidance (cervical epidural) is recommended. While this intervention often relieves pain, the injection does not improve the sensory and motor aspects of the radiculopathy.

If the patient has radicular pain without significant motor or sensory changes, conservative management consisting of oral analgesics, targeted injections, and physical therapy is initiated. Return to play is usually 10 to 12 weeks [16].

If the motor impairment is significant (less than 4/5 strength on examination), early operative intervention should be considered. If persistent motor deficit is noted greater than 3 weeks, operative intervention should be a strong consideration as there is a higher likelihood of nerve recovery with decompressive surgery [5].

There are 2 options for decompressive surgery. If the disk herniation is lateral to spinal cord or in the neuroforamen, a posterior microsurgical discectomy can be done. In contrast, if there is substantial portion of the disk herniation underneath the spinal cord, then the preferred method is an anterior cervical discectomy fusion utilizing autogenous structural iliac crest autograft and plate. Iliac crest autografts have been shown to have greater durability and a quicker speed to union [7]. Autograft remains the gold standard, particularly in a sometimes-noncompliant population. For both decompressive surgery options, the return to play is approximately 3 to 6 months, with the caveat that the CT scan shows complete healing of the interbody fusion.

Case

A 23-year-old NFL wide receiver presented with persistent right C6 radicular pain refractory to conservative measures. Preoperative MRI showed left-sided herniation of the nucleus pulposus (HNP) at the C5-C6 level (Fig. 8). A CT scan 3.5 months postoperatively showed a solid fusion (Fig. 9). Following postoperative CT and normal physical examination, he was cleared for full participation.

Fig. 8.

Preoperative MRI showing left-sided HNP at the C5-C6 level. MRI magnetic resonance imaging, HNP herniation of the nucleus pulposus.

Fig. 9.

Computed tomography scan 3.5 months postoperatively showing a solid fusion.

The Cervical “Stinger”

A “stinger” or “burner” is a common word football players use to describe a lancinating, burning pain that radiates down the arm. Often presenting as a pins-and-needles sensation down the arm with associated weakness, a stinger is a type of root neuropraxia that represents a reversal peripheral nerve injury [16], although some players use the term to describe a sharp pain in the neck and trapezial region, without concurrent paresthesia.

There are 2 known mechanisms for the generation of stinger injury. The first, seen in young players, typically at the high school level, involves an athlete creating contact with shoulder depression, and the head is flexed or abducted away from the side of the impact. This causes the brachial plexus stretch injury leading to the typical unilateral burning pain that radiates from the neck to the hand. On examination, a player with this stretch mechanism of injury will typically have tenderness in the trapezial region and deltoid or bicep weakness. However, any of the nerves that affect the upper extremity can be implicated in this type of injury, and it is not uncommon to see triceps, forearm, or intrinsic hand muscle weakness with associated sensory deficits.

The second mechanism of stinger injury occurs due to entrapment of a single nerve within a narrowed neuroforamen. When the neck is hyperextended and flexed laterally, the intervertebral foramen reduces in diameter and can compress an isolated cervical nerve root [12]. These are usually extension and rotation injuries that often occur with more experienced players at the college and professional level.

Players often have recurrent stingers secondary to multiple injuries over several years. The injury repair mechanism that occurs at the level of the disk and uncovertebral joint can create mild to moderate neuroforaminal narrowing that allows easier compression with subsequent impacts.

Unlike a brachial plexus stretch injury, injury to a cervical nerve root causes unilateral neck pain, point tenderness over the affected facet joint, and a positive Spurling’s test on physical examination. The neurologic examination will usually be within a discrete cervical myotome and dermatome, as well.

Differentiating brachial plexus injuries from cervical nerve root injuries is critical for determining treatment. If the burning pain is recreated by shoulder depression and head abduction, a brachial plexus injury can be suspected. Assuming there is no concurrent axial neck pain, plain films are not necessary. Instead, treatment should focus on adequate recovery to allow return of normal sensation and strength. Prior to the player’s return to play, the shoulder compression and head abduction maneuver should not elicit any symptoms. Furthermore, modifications to equipment can be made including adding either lifters, a cowboy collar, or a horseshoe pad. Coaches and players should also ensure that the shoulder pads and helmets are appropriately fitted. Off the field, players should work on neck strength, trapezial strength, and shoulder strength and be instructed in appropriate tackling and blocking techniques.

Despite these modifications, injury recurrence in the same season is frequent. After the first injury, it takes much less trauma for the second injury to occur. The same guidelines to return to play following reinjury apply, as the player must return to baseline strength and sensation and have no pain when recreating the injury mechanism on examination. Time is the single greatest factor in recovery from this injury. If significant weakness persists 3 weeks after injury, an electromyography nerve conduction study should be considered for prognostic purposes.

The nerve root stinger is usually seen in older, more mature players with excellent blocking and tackling technique. Typically, because the head is up when they receive the blow, extension, rotation, and sometimes compression dynamically narrow the neuroforamen. Once again, in an older player this has happened multiple times, and through injury repair mechanisms, a player may develop some mild to moderate neuroforaminal narrowing that precipitates the onset of the symptoms during the latter part of their career. These injuries also cause damage to the facet joint and uncovertebral joint. On examination, the most specific test is Spurling’s maneuver, where the hyperextension of the neck reproduces symptoms [18]. If positive, there is a high likelihood that there is cervical root compression. In addition, athletes with this injury will usually have significant tenderness over the affected facet joint and pain with deep palpation. With these injuries, cervical spine films are recommended to assess for spondylosis and potential fracture. Recurrent symptoms should be worked up with an MRI and potentially a CT scan.

Like the brachial plexus injury, those with a nerve root compression injury need to have a normal sensory and motor examination to be cleared to return to play. One component of the manual examination includes players having full, active, pain-free range of motion of the cervical spine and excellent isometric strength in all planes, particularly with flexion. Recreation of the pain in flexion, causing the athlete to retract, is the most common examination finding that disqualifies them for return to play as they must be able to protect their cervical column with their musculature to play collision sports.

Elite players can also consider a selective nerve root corticosteroid injection with a concomitant facet joint injection to decrease the inflammatory aspect of the injury. This should be done only after careful neurological evaluation and imaging that correlates with the patient’s clinical presentation. This modality should be used sparingly, and the player should be held from contact activities for 72 hours post-injection.

Last, recurrent stingers that occur from the same pathology can be treated surgically. Two procedures are currently available for the treatment of foraminal stenosis that cause recurrent stingers. If the pathology is more on the facet side, a lamina foraminotomy can be done through a posterior approach to decompress the nerve and enlarge the neuroforamen. Return to play after such a procedure is approximately 3 months.

If the recurrent injuries and neuroforaminal stenosis are due to spondylosis and uncovertebral hypertrophy, the recommended surgical procedure is an anterior cervical discectomy and fusion with tricortical iliac crest autograft and plating. Return to play after this procedure is between 3 and 6 months and is typically dictated by healing of the interbody graft, which is best seen on CT scan.

Case

A 29-year-old professional left offensive tackle for several years experienced recurring stingers that were temporarily relieved with C4 nerve root steroid injections. Further nonoperative interventions were unsuccessful. Magnetic resonance imaging revealed severe foraminal stenosis C3-C4 on the left and concomitant C3-C4 facet hypertrophy (Fig. 10). A laminoforaminotomy at C3-C4 on the left completely relieved symptoms. The player has since played 2 professional seasons without incident.

Fig. 10.

Magnetic resonance imaging revealing severe left C3-C4 foraminal stenosis and facet hypertrophy.

Transient Quadriplegia and Cervical Cord Neuropraxia

Cervical cord neuropraxia is a transient concussive injury to the spinal cord with temporary loss of motor and/or sensory function that gives symptoms in either the upper extremities, lower extremities, or both. These symptoms may be fleeting to months in duration. Most times neck pain is minimal or not present.

Typically, this injury occurs from an axial load to the vertex of the helmet with combination forces of compression, flexion, and extension creating a pincer mechanism compressing the spinal cord. It is more likely to occur with a stenotic canal, whether it be congenital stenosis, degenerative stenosis, or a combination. It can also occur in normal size canals under significant load, although this occurs less often.

Clinical presentation of cervical cord neuropraxia can vary widely. Some players have fleeting symptoms and continue to play, only to discuss it with their athletic trainer or physician while on the sidelines. Others may present motionless on the field. All players who have cervical cord neuropraxia/transient quadriplegia symptoms should be removed from the game. This is a solid “no go” decision. Spine boarding should be strongly considered for the player who is motionless on the field. If there is significant neck pain potentially indicating a fracture, they absolutely should be boarded. There are several excellent resources for the preparation and implementation of these plans during athletic contests, namely for collision sports [2].

Subsequent evaluation includes radiographs and MRI to evaluate for spinal canal dimensions, signal in the cord, ligamentous and capsular injuries, and disk herniation. If there is significant neck pain, a CT scan should be done to rule out fracture [14]. If the diagnostic testing is negative, the patient must meet the return-to-play criteria before being released.

More likely, there will be an abnormality noted on imaging consistent with either congenital stenosis or a combination of congenital stenosis with degenerative stenosis. It is not uncommon for football players in their early 20 s to have disk degeneration noted on the cervical spine films [17]. At this juncture, return-to-play criteria are less definitive. The nuances of risk/benefit with different anatomic considerations are beyond the scope of this article, but it must be noted that there are clear-cut indicators for disqualification. Among these are os odontoideum, Klippel-Feil congenital fusions with adjacent level stenosis, ligamentous instability, 1-level cervical fusion with adjacent segment stenosis and history of quadriparesis, cervical stenosis with cord signal, and what the senior author calls “-tics disease”: kyphotic, stenotic, and spondylotic abnormalities.

Surgical treatment of quadriparetic episodes with successful return to play includes anterior cervical discectomy and fusion for large central disk prolapses, degenerative stenosis with recurring symptoms, and facet fracture dislocations. When they meet return-to-play criteria, and a solid fusion has been documented, then there is no contraindication to play.

Currently, there are no uniform return-to-play considerations for recurrent transient quadriplegia/cervical cord neuropraxia. They need to be taken on a case-by-case basis depending on the severity of symptoms, number of recurrences, and anatomical findings. Suffice it to say that increasing magnitude of symptoms and frequency of occurrences should lead to disqualification.

Case 1

A 14-year-old 8th-grade football player with a quadriparetic episode had a C4 sensory loss in a cape-like distribution for 1 month. The player sat out the remainder of the year but met return-to-play criteria the following year and played throughout his high school career without incident. His MRI did not show evidence of canal stenosis; in fact, it was capacious (Fig. 11). Notably, the patient is the senior author’s son.

Fig. 11.

Magnetic resonance imaging following quadriparetic episode without evidence of spinal stenosis.

Case 2

A 17-year-old high school linebacker with recurrent transient quadriplegia had plain films that identified Klippel-Feil anomalies (Fig. 12). Subsequent MRI showed cervical stenosis with signal in the cord at the level above the congenital fusion (Fig. 13). The player was disqualified.

Fig. 12.

Plain film depicting Klippel-Feil anomaly.

Fig. 13.

Magnetic resonance imaging showing the congenital fusion with associated cervical spine stenosis.

Cervical Spine Fractures

Cervical spine fractures are rare in football, but when they occur, they can cause devastating spinal cord injuries. Fractures and fracture dislocations are responsible for 79% of the spinal cord injuries seen in football [3], most often from tackling and blocking, placing defensive backs and other defense players at an increased risk [17]. Players with severe neck pain and neurological injury should be treated as though they have a cervical fracture until proven otherwise. Most players will feel a deep pop/crack in the neck, indicative of structural failure. Simply ask the player, “Did you feel a pop or a crack in your neck?”

Nondisplaced facet fractures may be treated in a cervical collar. Once a player has healed and met return-to-play criteria, there is only a minimal increased risk of recurrent injury. Patients with facet fractures and dislocations should undergo operative management. They can return to play after a successful 1-level anterior cervical or posterior cervical fusion.

Stable compression fractures may be treated in a collar until the fracture is healed. Burst fractures usually require operative intervention, as the rate of neurological injury is high.

There are some fractures that are less consequential and may be managed with an early return to play. Isolated transverse process fractures and spinous process fractures may be treated in a cervical collar until the player is comfortable and meets return-to-play criteria.

Overall, providers should have a high index of suspicion for spinal fractures when players present with severe neck pain. The surgical treatment is fairly algorithmic but return to play requires careful consideration based on individual patient circumstances.

Case 1

A 26-year-old NFL fullback suffered a lateral blow to the neck and presented with severe cervical pain. Plain films and subsequent CT showed a C7 transverse process fracture (Fig. 14). The patient was immobilized intermittently in a soft collar for 5 days and treated with standard athletic training modalities. He returned to play without incident.

Fig. 14.

C7 transverse process fracture on coronal CT. CT computed tomography.

Case 2

A 17-year-old high school linebacker injured his neck during a game and had pain and stiffness for the ensuing 5 games. After the season, he was evaluated and noted to have a perched facet at C5-C6 and an anterolisthesis (Figs. 15 and 16). He was reduced and treated with an anterior cervical fusion with autograft and plate (Fig. 17). He played 4 years of college football without incident.

Fig. 15.

Perched facet at C5-C6 on plain film.

Fig. 16.

Perched facet at C5-C6 on computed tomography.

Fig. 17.

Resolution of perched facet following anterior cervical discectomy and fusion of C5-C6.

In summary, the injuries common to training and playing football require a physical examination and a thorough history including a description of the mechanism of injury. Prompt attention to and treatment of the inflammatory component of these injuries is critical. The physical examination should assess both mechanical and neurological function; it will guide appropriate treatment. Cervical spine injuries with significant neck pain should be treated with a high index of suspicion for fracture. Superficially, return-to-play criteria are straightforward. A normal, pain-free range of motion with good strength in the affected area and a normal neurological examination with normal imaging provide a clear path to return to competition. However, the same situation but with abnormal imaging is less straightforward. There are several congenital anomalies that render the player disqualified. At present, there is no consensus about disqualification after serial cervical cord neuropraxia. Return to play after a 1-level cervical fusion is widely accepted.