INTRODUCTION — An overview of cervical spinal cord injuries and cervical peripheral nerve injuries in the young athlete will be presented here. The anatomy of the cervical spine, the diagnostic approach to the athlete with neck pain or injury, the management of the athlete with an acute neck injury, musculoskeletal injuries of the neck and the evaluation of cervical spine injuries in children and adolescents are discussed separately:
CERVICAL SPINAL CORD INJURIES — The annual incidence of traumatic spinal cord injury is estimated to be between 30 and 46 cases per million populations in the United States and Canada [1-3]. The majority of injuries occur in young adults: 57 percent of cases occur in people 16 to 30 years of age . Most injuries (>80 percent) occur in males. Motor vehicle crash is the most common mechanism of injury and accounts for approximately 35 percent of cases. The next most common mechanisms (in descending order) are gunshot wounds, falls, and recreational sporting activities, particularly diving and in the United States, American football [5,6].
In a retrospective study of 1016 cases of traumatic spinal cord injury in Germany, 14 percent were caused in sport or diving accidents . The sporting activities during which the injuries were sustained included downhill skiing, horseback riding, air sports (eg, hang-gliding, paragliding), gymnastics, and trampolining. Spinal cord injuries can also occur in ice hockey, where the typical mechanism involves being body-checked from behind and falling head-first into the boards .
Spinal cord injuries may be complete or partial. Partial spinal cord injuries include the central cord syndrome, anterior cord syndrome, Brown-Séquard syndrome, cervical cord neurapraxia, and spinal cord injury without radiographic abnormality (SCIWORA).
SCIWORA is discussed in detail separately. (See "Spinal cord injury without radiographic abnormality (SCIWORA) in children".)
The management of athletes with cervical spinal cord injuries should be directed by a neurosurgeon. The use of methylprednisolone in patients with spinal cord injury is discussed separately. (See "Acute traumatic spinal cord injury", section on 'Glucocorticoids'.)
Complete cord syndrome — Trauma is the most common cause of complete transection of the spinal cord. Other causes include infarction, hemorrhage, and acute disc herniation.
Transection of the spinal cord results in complete loss of motor, sensory and autonomic function below the level of the lesion (table 1 and figure 1 and figure 2). Acute spinal cord transections can cause spinal shock via the removal of ascending and descending cerebral impulses. Spinal shock is manifested by flaccid paralysis with absent deep tendon reflexes in the first day or two after injury. This period of flaccid paralysis is followed by spasticity with hyperactive reflexes. Transection at or above the C3-C5 level can result in diaphragmatic paralysis and respiratory failure. (See "Respiratory complications in the adult patient with chronic spinal cord injury".)
Sympathetic interruption in complete spinal cord interruption can cause neurogenic shock. The sudden loss of sympathetic tone leads to decreased systemic vascular resistance and increased vagal tone, which result in hypotension with paradoxical bradycardia . Other symptoms of neurogenic shock include gastrointestinal dysmotility, bowel and bladder dysfunction, and problems with temperature regulation . (See "Pathophysiology and classification of shock in children", section on 'Distributive shock'.)
The treatment of the athlete with an acute cervical spine injury involves cervical spine immobilization and transport to an emergency medical facility for specialty care. The prognosis for functional improvement in patients with complete cervical spinal cord transection is poor. (See "Pediatric cervical spinal motion restriction" and "Field care and evaluation of the child or adolescent athlete with acute neck injury".)
Central cord syndrome — The central cord syndrome is the most common of the partial cord syndromes. It is typically seen in older patients with degenerative spine disease and cervical spondylosis. In athletes, the central cord syndrome is usually caused by hyperextension injury during which the ligamentum flavum is thought to buckle, resulting in increased pressure on the central cord [11,12]. It may also occur after traumatic disc herniation, trivial trauma, or in hyperflexion injuries [11,13-15].
The characteristic physical findings of central cord syndrome are bilateral motor paresis greater in the upper than in the lower extremities, bladder dysfunction, and variable sensory loss below the level of injury (figure 2). This pattern occurs because the most central portions of the spinal tracts contain fibers from the upper extremities (figure 3). (See "Anatomy and localization of spinal cord disorders", section on 'Central cord syndromes'.)
Anterior cord syndrome — The anterior cord syndrome is caused by direct or indirect injury to the anterior spinal cord. Direct injury may occur secondary to a crush injury or compression from a hematoma; indirect injury result from ischemia secondary to compression of the anterior spinal artery . In athletes, anterior cord syndrome is typically seen after hyperflexion injuries with bony instability, acute disc herniation, or hematoma formation.
The anterior cord syndrome, which involves injury to the spinothalamic tract, is characterized by loss of motor, pain, light touch, and temperature sensation (figure 2). Because the posterior columns are preserved, the patient retains fine touch, vibration, pressure, and proprioception sensation distal to the injury (figure 3). (See "Evaluation of the child or adolescent athlete with neck pain or injury", section on 'Anatomy'.)
In addition to the usual care for spinal cord injury, treatment of the anterior cord syndrome involves stabilization or removal of any structure that exerts increased pressure on the anterior aspect of spinal cord. Laminectomy may be necessary to decompress the spinal cord.
Brown-Séquard syndrome — The Brown-Séquard syndrome is a rare spinal injury that results in hemisection of the spinal cord. It is usually caused by penetrating trauma; other causes include blunt trauma , disc or bone herniation, hematoma, and tumor. The Brown-Séquard syndrome can also occur as a complication of decompression sickness [17,18].
The Brown-Séquard syndrome is characterized by ipsilateral loss of motor function, vibration, and proprioception below the level of the lesion with contralateral loss of pain and temperature sensation beginning approximately two levels below the lesion (figure 2 and figure 3). This pattern of deficits occurs because the spinothalamic tract travels on the ipsilateral side of the cord before crossing over to the contralateral side. In addition, ipsilateral loss of pain and temperature sensation may occur at one or two levels below the lesion. Most cases of Brown-Séquard syndrome are partial cases with varying degrees of paresis and analgesia . The Brown-Séquard syndrome also may be associated with Horner syndrome (ptosis, miosis, and anhydrosis) if there is coexistent injury to the cervical paravertebral sympathetic chain and inferior cervical (stellate) ganglion [19,20]. (See "Horner syndrome".)
Cervical cord neurapraxia — Cervical cord neurapraxia (CCN), also known as transient quadriparesis or transient neurapraxia, is a rare cervical spine injury that is often considered a "concussion" of the cervical spinal cord . It is thought to be caused by axial loading of the neck in flexion or extension. CCN occurs most commonly in football players who lead with their heads when hitting an opposing player. In the National Collegiate Athletic Association (NCAA), the incidence is 1.3 per 10,000 athletes per season .
Clinical features — The affected athlete has sudden posttraumatic onset of bilateral sensory, motor, or combined neurologic deficit. Sensory findings include burning, numbness, tingling, or loss of sensation; motor findings include weakness or complete paralysis [23,24]. Burning hands syndrome, a variant of this central cord injury, consists only of upper-extremity symptoms, most notably temporary burning dysesthesias and weakness of the arms and hands [25-27]. By definition, the symptoms of CCN are transient and completely resolve within 10 minutes to 48 hours. CCN should be distinguished from cervical "burners" (unilateral paresis of an upper extremity, often associated with neck pain) . (See 'Cervical burners' below.)
Mechanism of injury — The pathophysiology and mechanism of injury in CCN are incompletely understood. CCN is thought to result from compression and/or contusion of the spinal cord. One hypothesis is that the cervical cord is compressed between the posterior margin of one vertebral body and the anterior margin of the spinous process of the vertebra below it (the pincer mechanism, (figure 4)) . Such compression is most likely to occur in a hyperextension injury with axial loading. Compression of the spinal cord is postulated to cause prolongation of the absolute refractory period of the long tract axons . Reversible magnetic resonance imaging (MRI) and electrophysiologic abnormalities have been documented in patients with burning hands syndrome .
Cervical spinal stenosis is a risk factor that can predispose athletes to CCN , although it is inconsistently present in children with CCN . Functional spinal stenosis is defined as the loss of cerebrospinal fluid from around the spinal cord or deformation of the spinal cord (as seen on contrast-enhanced CT, MRI (image 1), or myelography) [33,34]. The stenosis is most common at the C3-C5 levels and is usually congenital, although it can be acquired (eg, in disk herniation, cervical spine instability, etc).
Evaluation — The majority of athletes with CCN have spinal stenosis or some other cervical spine abnormality. Burning hands syndrome is associated with a bony or ligamentous spinal abnormality in approximately one-half of cases . Thus, the initial evaluation consists of cervical spine radiographs  to evaluate for evidence of spinal canal stenosis, cervical instability, or congenital anomalies, such as Klippel-Feil syndrome (a disorder in which there is congenital fusion of variable numbers of cervical vertebrae and associated defects including scoliosis, renal anomalies, elevated scapula, congenital heart disease, and deafness).
Plain radiographs are usually followed by MRI to better identify and clarify the extent of any associated pathology (eg, congenital spinal stenosis, herniated disk, intrinsic cord abnormalities, or ligamentous injury) [21,36]. If the MRI is inconclusive, contrast-positive computed tomography (CT) or myelogram can be used to better delineate the anatomy.
Return to play — Whether spinal stenosis increases the risk of permanent neurologic injury in the young athlete is controversial [32,37-40]. Some studies indicate that spinal stenosis predisposes to spinal cord injury [39,40], but clear evidence of permanent injury is lacking. Thus, it is difficult to establish guidelines for returning to play.
We do not permit our patients with proven spinal stenosis to participate in contact or collision sports . The decision regarding return to play for athletes who have CCN and no evidence of cervical spine stenosis or abnormality after a thorough evaluation must be individualized for each athlete in consultation with an experienced neurosurgeon.
CERVICAL PERIPHERAL NERVE INJURIES — Peripheral nerve injuries are classified into three categories according to severity [41-45]. Within each grade, and across the categories, there is a spectrum of clinical severity.
●Grade I injury, or neurapraxia, describes a disturbance of physiologic function without significant damage to or degeneration of the nerve . Transient alteration of motor or sensory function usually lasts seconds to minutes, but more severe cases can last up to a few weeks. By definition, electrophysiologic evidence of denervation is absent when tested 18 to 21 days after the injury. The prognosis for full recovery for all grade I injuries is excellent.
●Grade II injury, or axonotmesis, describes an injury resulting in some axonal and myelin degeneration within an intact neurilemmal sheath. Motor or sensory losses persist for at least two weeks. At 18 to 21 days, the electromyogram (EMG) is abnormal, and it may remain so up to one year . Full recovery is often seen, but it may be incomplete and unpredictable.
●Grade III injury, or neurotmesis, is the most severe injury and is rarely seen in athletic competition. Grade III injuries are characterized by complete disruption of the nerve with complete degeneration . EMG changes are permanent. Some motor units may attempt to regenerate, resulting in as much as 30 percent recovery of motor function. However, prognosis for good functional outcome is generally poor.
Cervical burners — The "burner," or "stinger," is a brachial plexus injury resulting from trauma to the neck and shoulder. It is one of the most common injuries among football players, occurring at least once in 50 to 65 percent of football players during a four-year college career. Burners or stingers are seen less commonly in hockey, wrestling, and gymnastics. The incidence is unknown since the injury, unless severe or prolonged, often goes unreported. (See "Burners (stingers): Acute brachial plexus injury in the athlete", section on 'Epidemiology'.)
Mechanism of injury — The burner is a brachial plexopathy caused by injury to the upper brachial plexus or nerve roots, usually affecting the C5-C6 levels (figure 5). Most burners are caused by one of three mechanisms:
●Stretch injuries to the brachial plexus are more common among high-school football players . Stretch injuries occur when the athlete makes a tackle with the shoulder depressed and simultaneous lateral flexion of the neck toward the opposite side, causing traction on the upper trunks of the brachial plexus on the side of the depressed shoulder.
●Nerve compression injuries are more common among college and professional athletes , who typically have preexisting radiological evidence of arthritic changes or degenerative disk disease. Compression of the nerve roots at the intervertebral foramen occurs when the athlete undergoes collision with the neck extended and laterally flexed toward the side with symptoms. Athletes with nerve compression injuries usually have a positive Spurling's test (picture 1). (See "Burners (stingers): Acute brachial plexus injury in the athlete", section on 'Pathophysiology'.)
●Direct blows to the supraclavicular fossa at Erb's point, where the brachial plexus is most superficial, can also result in cervical burners . This type of injury is more common among athletes who wear less protective padding (eg, rugby, as opposed to football, players).
Clinical features — The athlete with a burner usually becomes symptomatic immediately after an injury with the appropriate mechanism. Symptoms are primarily sensory, and include unilateral shoulder and/or arm pain with burning dysesthesias in the C5-C6 nerve root distribution with associated weakness of the deltoid, biceps, and/or the external rotators of the shoulder (table 1 and figure 1). The player is often observed to be shaking or holding the affected arm to his side after the injury. The symptoms usually resolve within minutes of the injury. In some cases, however, the symptoms may develop hours or days later . Severe cases result in more persistent symptoms. (See "Burners (stingers): Acute brachial plexus injury in the athlete", section on 'Examination findings'.)
Evaluation — The sideline management of the patient with a suspected burner begins with a history and physical examination. The focus is to rule out more serious conditions, such as a spinal cord injury. If the athlete remains on the playing field, spinal cord injury must be ruled out before the athlete is permitted to walk. (See "Field care and evaluation of the child or adolescent athlete with acute neck injury" and 'Cervical spinal cord injuries' above.)
A detailed history, including the mechanism of injury, exact symptomatology (distribution and duration of symptoms), and previous history of burners should be noted. Examination of the neck and shoulder should be performed. The examination should include active cervical range of motion within pain tolerance, palpation for muscle spasm and bony tenderness, and a detailed neurologic examination, including special attention to the motor function of the C5-C7 myotomes (table 1). (See "Burners (stingers): Acute brachial plexus injury in the athlete", section on 'Examination findings'.)
The brevity of symptoms and presence of a full, pain-free range of motion are key features in the diagnosis of cervical burners. The presence of neck pain or stiffness, posterior midline neck tenderness, bilateral neurologic symptoms, or symptoms involving a lower extremity are not consistent with a simple burner. (See "Burners (stingers): Acute brachial plexus injury in the athlete", section on 'Differential diagnosis'.)
The athlete with any signs or symptoms of spinal cord injury (table 2) should be assumed to have a cervical spinal cord injury, and must be immobilized and transferred to an appropriate facility for further evaluation and management. (See "Pediatric cervical spinal motion restriction" and "Evaluation and acute management of cervical spine injuries in children and adolescents".)
Management — The athlete with a burner must have serial examinations (initially every 10 to 15 minutes) to evaluate evolution and resolution of symptoms. Most burners last no more than a few minutes, allowing for safe return to play provided the following criteria are met:
●Absence of neck pain and symptoms
●Normal neck examination (no tenderness, normal range of motion, normal strength, and negative axial compression and Spurling tests, (picture 1)) (see "Evaluation of the child or adolescent athlete with neck pain or injury")
Athletes who have persistent symptoms must be held out of competition until symptoms resolve and strength returns to normal. Additional evaluation is indicated if symptoms persist for more than two weeks. (See "Burners (stingers): Acute brachial plexus injury in the athlete", section on 'Follow-up and returning to sport'.)
Depending upon the symptoms and duration of symptoms, the evaluation may include cervical spine radiographs or MRI. EMG and nerve conduction studies should be performed in patients who have symptoms for more than three weeks. These studies can be helpful in differentiating brachial plexus injury from cervical radiculopathy and may also help to qualify the severity of the nerve injury. (See "Burners (stingers): Acute brachial plexus injury in the athlete", section on 'Cervical imaging' and "Burners (stingers): Acute brachial plexus injury in the athlete", section on 'Electrodiagnostic studies'.)
Prevention — Because burners tend to recur, any player who suffers a burner should consider taking steps that may reduce the risk of recurrence. Although suggested, none of these interventions has been proven to reduce the risk of cervical burners .
Potential interventions include:
●An exercise program to improve strength and flexibility of the neck, shoulder, and upper extremity may be helpful, although the efficacy of this intervention has not been established .
●Maintenance of good posture (ie, reduced cervical flexion and extension) can decrease encroachment of the spinal nerves at the intervertebral foramen.
●The athlete should wear properly fitting shoulder pads.
●Several types of protective equipment, including neck rolls, cowboy collars, and custom orthoses, have been developed to limit cervical extension and lateral neck flexion [49,51].
●The athlete's blocking and tackling techniques should be reviewed and changed if indicated .
If recurrences persist, despite the above interventions, consideration may be given to changing the athlete's position and/or discontinuing the causative athletic activity .
Nontraumatic cervical radiculopathy — Nontraumatic cervical radiculopathy is caused by impingement of the nerve root near the intervertebral foramen. The most common causes of nerve root impingement include a bulging disk or degenerative changes at the intervertebral foramen such as osteophytes or local inflammation. Less common causes include tumors and abscesses. Long-term contact/collision athletes may have accelerated degenerative changes that predispose them to nontraumatic cervical radiculopathy at a relatively younger age than individuals who did not participate in these sports.
Characteristic symptoms include sharp arm pain and paresthesias in a dermatomal pattern (figure 1). The pain is exacerbated by neck movements that cause further nerve impingement, such as extension and lateral flexion. There may or may not be associated neck pain or weakness of the associated myotomes(s) with diminished deep tendon reflexes (table 1). The Spurling test (picture 1) or axial compression test may reproduce symptoms. (See "Evaluation of the child or adolescent athlete with neck pain or injury".)
Cervical radiculopathy is a symptom of pathology, not a diagnosis. Management depends on making the correct diagnosis . Radiographs are useful in identifying arthritic changes of the cervical spine or other bony abnormalities. If the diagnosis is in doubt, an MRI should be performed.
Treatment for disk or arthritic nerve root pain consists of techniques to relieve the pressure on the nerve. These include maintenance of proper posture and the use of in-line cervical traction devices. Antiinflammatory and analgesic measures such as nonsteroidal antiinflammatory drugs (NSAIDs), ice, heat, and transcutaneous electric nerve stimulation (TENS) may be a helpful adjunct. Physical therapy for mobilization and improving strength and flexibility may also reduce pain. Surgery remains an option for those who fail to make improvement with conservative measures. The management of cervical disc disease in the young athlete is discussed separately. (See "Overview of musculoskeletal neck injuries in the child or adolescent athlete", section on 'Cervical disc disease'.)
Acute brachial neuropathy — Acute brachial neuropathy (ABN, also called brachial plexus neuritis, shoulder girdle syndrome, and Parsonage-Turner syndrome) is an uncommon cause of shoulder pain that can affect athletes as well as relatively inactive people. The cause is unknown, but it is often preceded by viral infection, radiation or chemotherapy, pregnancy, or strenuous activity . The condition is bilateral in approximately 25 percent of cases and may recur.
Clinical features — Because ABN is uncommon, the clinician must have a high index of suspicion to make the diagnosis. The hallmark clinical presentation is severe, acute, burning pain in the shoulder and upper arm with no apparent cause . The pain can last from several hours to several weeks. It may radiate proximally toward the neck or distally to the elbow and forearm . Weakness of the shoulder usually occurs four to five days after the onset of the pain; the delayed onset of motor deficit distinguishes this disorder from cervical radiculopathy or brachial plexus injury (see above). Cutaneous sensation is often diminished. Multiple nerves of the brachial plexus are usually involved (picture 1), instead of the single nerve root that is typically involved in a cervical radiculopathy.
On examination, any movement of the shoulder exacerbates the pain. The position of maximal comfort is usually with the shoulder adducted and the elbow flexed . In fact, it may be difficult to perform an adequate motor examination because of the patient's pain. Deep tendon reflexes may be diminished depending upon the degree of neuromuscular involvement.
Evaluation — MRI of the clinically weak muscles may reveal high signal intensity of the affected muscles on the T2 study . EMG can differentiate ABN from traumatic upper trunk or other brachial plexus injuries.
Management — Initial treatment involves analgesics and the use of a sling to rest the arm. Corticosteroids have not been shown to be beneficial in treating ABN. After the pain has subsided, the treatment shifts to rehabilitation of the shoulder and arm. Recovery of range of motion, strength, and endurance are the main goals of physical therapy .
The course of ABN is usually one of gradual improvement and recovery of muscle strength in three to four months . Some patients, however, experience several years of motor dysfunction or some permanent residual weakness. In general, a longer duration of pain will result in a longer delay in recovering strength .
Return to play — Return to play for athletes should be based on individual sport needs and the degree of functional limitation.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cervical spine injury".)
SUMMARY AND RECOMMENDATIONS
●Recreational sports are a relatively common cause of cervical spine injury, especially in older adolescents and young adults. Spinal cord injuries may be complete or partial. Partial spinal cord injuries include the central cord syndrome, anterior cord syndrome, Brown-Séquard syndrome, cervical cord neurapraxia, and spinal cord injury without radiographic abnormality (SCIWORA). Once identified, cervical spinal cord injuries warrant emergency consultation with a neurosurgeon. (See 'Cervical spinal cord injuries' above.)
●Cervical cord neurapraxia (CCN), also known as transient quadriparesis or transient neurapraxia, is a rare cervical spine injury that is often considered a "concussion" of the cervical spinal cord. The majority of athletes with CCN have spinal stenosis or some other cervical spine abnormality upon radiologic evaluation. (See 'Cervical cord neurapraxia' above and 'Clinical features' above.)
●Burning hands syndrome, a variant of CCN, consists only of upper-extremity symptoms, most notably temporary burning dysesthesias and weakness of the arms and hands. By definition, the symptoms of CCN are transient and completely resolve within 10 minutes to 48 hours. (See 'Clinical features' above.)
●The cervical burner is a brachial plexopathy caused by injury to the upper brachial plexus or nerve roots, usually affecting the C5-C6 levels (figure 2 and figure 5) and is the most common cervical peripheral nerve injury in athletes, especially American football players. Symptoms are primarily sensory, and include unilateral shoulder and/or arm pain with burning dysesthesias in the C5-C6 nerve root distribution with associated weakness of the deltoid, biceps, and/or the external rotators of the shoulder (table 1 and figure 1). The symptoms usually resolve within minutes of the injury and many players can immediately return to play. (See 'Cervical burners' above.)
●Nontraumatic cervical radiculopathy is caused by impingement of the nerve root near the intervertebral foramen. The most common causes of nerve root impingement include a bulging disk or degenerative changes at the intervertebral foramen such as osteophytes or local inflammation. Characteristic symptoms include sharp arm pain and paresthesias in a dermatomal pattern (figure 1). (See 'Nontraumatic cervical radiculopathy' above.)
●Acute brachial neuropathy (ABN, also called brachial plexus neuritis, shoulder girdle syndrome, and Parsonage-Turner syndrome) is an uncommon cause of shoulder pain that can affect athletes as well as relatively inactive people. The hallmark clinical presentation is severe, acute, burning pain in the shoulder and upper arm with no apparent cause. (See 'Acute brachial neuropathy' above.)
●Careful history, physical examination, and, in patients with persistent or concerning findings, radiologic evaluation help determine the type of peripheral nerve injury, its management, and prevention. Return to play is based upon the underlying etiology and whether symptoms have resolved. (See 'Cervical peripheral nerve injuries' above.)
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