Sport-Specific Risks to the Spine

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. 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. 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 can begin. 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.

Facet Injury

Facet joints contain encapsulated mechanicoreceptors that provide proprioceptive information from the cervical spine. They can also play a significant role in protective muscular contraction (spasm) in response to unexpected external forces. Forced flexion-type forces commonly received by the cervical spine of the athlete may lead to damage of the cartilaginous surfaces of these joints, resulting in chronic pain and premature degenerative changes. Chronic pain experienced by some individuals following a cervical whiplash-type injury can usually be managed with rest, physical therapy, and occasionally injection therapy. If the pain becomes intractable, serious consideration should be given to limiting participation in sports.

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 and colleagues. 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.” 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. 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. 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 to 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. Direct blunt trauma at Erb’s point, located superficially in the supraclavicular region, has also been reported to be a cause. 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 a 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. 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, paresthesia, 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 who 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. 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 Erb’s 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 magnetic resonance imaging (MRI) is recommended. If the symptoms persist for over 2 weeks, electromyography can be performed to establish the distribution and degree of injury. Residual muscle weakness, cervical anomalies, or abnormal electromyographic studies are exclusion criteria from return to play.

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 because although the condition usually resolves in minutes, motor weakness may develop hours to days following the injury. Repeated injury may result in long-term muscle weakness with persistent paresthesias, resulting in permanent removal from competition. Options for participants to decrease the risk of future occurrences are to change their field positions or modify their playing techniques.

Central Cord Syndrome

Injury to the lower cervical cord can result in a spectrum of neurologic dysfunction. Incomplete SCI can occur with partial preservation of sensory or motor function. Central cord syndrome is the most common manifestation, followed in frequency by the anterior cord syndrome.

Burning hand syndrome is considered to be a variant of central cord syndrome. It is characterized by burning dysesthesia in both upper extremities and is likely the result of vascular insufficiency affecting the medial aspect of the somatotopically arranged spinothalamic tracts. The lower extremities may occasionally be involved, and weakness may occasionally be evident. Cervical spine fracture or soft tissue injury is frequently associated with these syndromes, and any athlete exhibiting this condition should be initially treated as having an SCI (see the section titled “ On-Site Evaluation and Management of Spinal Cord Injury ”).

Cervical Cord Neurapraxia and Transient Quadriplegia

Neurapraxia of the cervical spinal cord (cervical cord neurapraxia, or CCN) resulting in transient quadriplegia has been estimated to occur in 7 per 10,000 football players. 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 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. 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. The spinal cord axons become unresponsive to stimulation for a variable period of time, essentially creating a “postconcussive” effect.

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.

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 protocol in this population is controversial. No controlled studies have reported that the administration of steroids has altered the natural history of athletes with CCN. In players who return to football, the rate of recurrence has been reported to be as high as 56%.

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. 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. A ratio of 1 : 1 was considered normal, and less than 0.8 indicated 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—has made MRI, and not bony 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 standard in diagnosing this condition. An absent CSF pattern on axial and, particularly, sagittal MRI is diagnostic of functional stenosis.

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

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. 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.

There are two types of disc herniation: hard and soft. Soft disc herniation is a more sudden phenomenon during which the soft nucleus pulposus 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. 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, as 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. 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

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. 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. 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. 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 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. Eighty percent of injuries to the cervical spine result from the accelerating head and body striking a stationary object or another player. 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. 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. 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. 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. 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. 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.

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.

Off-the-Field Management

The treatment of the various forms of cervical spine injury has been summarized by numerous authors and follows established guidelines. 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. 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 computed tomography (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. 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.