Sports-related cervical spine injuries, while relatively uncommon, can be season ending, career ending, life altering, or even life ending.

The majority of neck injuries are ligament sprains, muscle strains, or contusions (2).

The sports medicine physician can take steps to help prevent catastrophic neck injuries in athletes. The training of physicians who wish to care for athletes, therefore, should impart an understanding of the mechanisms and management of cervical spine injuries.

The majority of athletic cervical spine injuries in the United States occur in football players, partly related to the large numbers of participants in the sport. As a result, most of the sports literature has examined the epidemiology and pathomechanics of cervical spine injuries in football players. Regardless of the sport, the principles for management of athletic cervical spine injuries remain constant.

Athletes sustain 10% of the 10,000 cervical spinal cord injuries that occur each year.

Sports with a greater risk of cervical spine injuries include diving, football, rugby, surfing, skiing, boxing, ice hockey, wrestling, and gymnastics (16).

While the prevalence of sports-related cervical spine injuries has not been adequately researched, it is estimated that 10%-15% of football players may experience a soft tissue or neurologic injury of the cervical spine that results in time loss from sport (10).

In football, those most at risk play defensive positions, that is defensive backs, linemen, and linebackers (4,5).

The prevalence of the stinger or burner (i.e., neurapraxic injury to the nerve root or brachial plexus) is reported to be ≥ 50% in football players (7).

Helmets have decreased fatalities but may have increased the risk of nonfatal cervical spine injury due to the emergence of spear tackling and by imparting a sense of invincibility to the athlete in his “armor” (15).

There are seven cervical vertebrae and eight exiting nerve roots.

The cranium articulates with C1 at the atlantooccipital joint, where approximately 50% of all flexion and extension occur (the “yes” joint). The first and second cervical vertebrae form the atlantoaxial joint and are uniquely designed to allow for 50% of all cervical rotatory motion (the “no” joint).

Lateral bending occurs coupled with rotation via motion from C3 to C7.

Intervertebral discs between C2 and C7 serve to dissipate and transmit compressive or axial loads.

The discs are thicker anteriorly and this design contributes to the normal cervical lordosis.

Normal sagittal diameter of the cervical spinal canal between C3 and C7 is ≥ 15 mm, and spinal stenosis is suggested and may be present below 13 mm. Functional spinal stenosis refers to the loss of protective cushioning from cerebrospinal fluid around the spinal cord as documented on magnetic resonance imaging (MRI), computed tomography (CT), or myelography (3).

Each nerve root occupies between 25% and 33% of the neural foramen, which is bordered by the uncovertebral joints anteromedially, the intervertebral disc medially, the zygapophyseal or facet joints posterolaterally, and superiorly/inferiorly by the pedicles of adjoining vertebrae. Degenerative arthritic changes of any of the structures that form or border the foramina may contribute to nerve root compression.

From C2 to C7, the nerve roots exit above their corresponding numbered vertebral body, whereas C1 exits between the occiput and atlas, and C8 exits between the C7 and T1 vertebrae (8).

The cervical spine depends on both static (i.e., osseocartilaginous and ligamentous) and dynamic (i.e., musculotendinous) stabilizing factors to absorb and/or dissipate forces.

Pain in the cervical spine is mediated by free nerve endings in the outer one-third of the annulus fibrosus of each intervertebral disc, in the zygapophyseal (facet) joints, in the ligaments (i.e., posterior longitudinal ligament, ligamentum flavum, interspinous and supraspinous ligaments), and in the supporting musculature.

The cervical spine is normally able to absorb significant multidirectional external forces by virtue of several supportive mechanisms.

The cervical lordosis aids in dissipating axial loads through the intervertebral discs, facet joints, interspinous ligaments, and paraspinal muscles. Tucking the chin during a tackle or before an impact can lead to reversal of the normal lordosis and impairs the mechanism for dissipating axial loads.

Axial loading has been shown to be the mechanism of catastrophic cervical spine injury in all National Football League cases that were documented well enough to allow detailed analysis (13).

Hyperflexion or hyperextension of the cervical spine in an athlete with a congenitally or developmentally narrowed canal may cause neurologic injury by a pincer mechanism (12).

External forces that cause a combination of lateral bending and extension may lead to neuroforaminal compression and the neurologic injury commonly called a stinger or burner.

A second proposed mechanism for the stinger or burner is flexion or extension combined with lateral bending and ipsilateral shoulder depression resulting in a traction injury to the cervical nerve roots.

Acceleration/deceleration forces, such as those that occur in whiplash injuries, occur commonly in contact/collision sports and commonly cause injury to the muscular or ligamentous supports (cervical strain/sprain) or the cervical facet joints.