Most of the sports medicine and spine literature has focused on acute cervical spine injuries in collegiate and professional sports, especially American football and rugby. However, there is a relative paucity of studies looking at older athletes who have developed degeneration of the cervical spine. Degenerative changes throughout the spine, termed spondylosis, become more prevalent with increasing age and create conditions that do not typically affect younger athletes.

Although the development of cervical spondylosis is accepted as a natural consequence of aging, the possible contributory effects and long-term sequelae from repetitive loads and demands placed on a young athlete’s neck are less clearly understood. On the one hand, Mundt and colleagues examined weightlifters and other athletes involved in noncollision sports (e.g., baseball, swimming, racquet sports) and found that these activities did not put players at increased risk for developing cervical or lumbar disk herniations.¹ On the other hand, there is literature suggesting that athletes who participate in contact sports hasten the development of cervical degeneration, possibly because of repetitive loads or undiagnosed injuries they may experience.^2,3,4,5 Several studies on American football and rugby players have found that the risk of developing low back pain, degenerative disk disease, and facet degeneration increase with the number of years they participate in their sport.^2,6,7 Soccer players have also been shown to be at increased risk of developing early cervical degenerative changes caused by recurrent trauma from heading the ball.⁸ Other sports with established risk for cervical spine injuries include rugby, ice hockey, wrestling, skiing, gymnastics, diving, pole vaulting, and cheerleading.⁹

No matter if it is in a previously elite athlete or an individual who is just getting into a new sport, degenerative changes in the cervical spine accumulate over time even if they are initially asymptomatic. Most of the research on cervical spondylosis is in middle-aged or elderly individuals because this is the population in which degenerative changes tend to become symptomatic. By age 65 years, spondylosis is seen in 95% of the population.¹⁰ Boden and colleagues, in their classic study, evaluated 67 individuals who had never had any back pain, sciatica, or neurogenic claudication and found that degenerative changes on lumbar spine MRI scans were present in about 25% of people younger than 60 years old and in about 60% of people older than 60 years.¹¹ Matsumoto et al performed a similar MRI study involving asymptomatic volunteers but focused specifically on the cervical spine and found that degenerative changes increased linearly with age and was present in nearly 90% of people older than 60 years.¹² Other similar studies have confirmed the pervasiveness of cervical spondylosis on both plain radiographs and MRI.^13,14

As the human body ages, structural components of the spine naturally wear down. This degenerative process
starts with the intervertebral disk, resulting in a loss of disk height that may lead to a bulging annulus, infolding of the ligamentum flavum, arthrosis of the uncovertebral and facet joints, and even loss of normal cervical lordosis and motion.^15,16,17,18 These degenerative changes can manifest as axial neck pain, radiculopathy, myelopathy, or a combination of the three. Axial neck pain refers to nonradiating neck pain involving the axial cervical spine or paraspinal region (or both). In addition to being caused by cervical sprains and strains, axial neck pain has been attributed to pathology within cervical disks (innervated by the sinuvertebral nerve) and facet joints (innervated by the medial branches of the cervical dorsal rami).^19,20

Radiculopathy describes radiating pain that typically begins in the neck and travels into the arm and may be accompanied by sensory or motor deficits in the distribution of the involved nerve root. Radiculopathy is caused by nerve root compression, which can occur with lateral or foraminal stenosis from bulging disks, inflammation of the facet capsule, or osteophyte formation at the facet or uncovertebral joints.

Finally, cervical spondylotic myelopathy (CSM) describes the phenomenon of central cervical stenosis caused by age-related degenerative changes leading to spinal cord compression and dysfunction.²¹ When present, developmental stenosis (also known as congenital stenosis) is a critical predisposing condition for developing CSM.^22,23 The normal midsagittal anteroposterior (AP) diameter of the spinal canal from C3 to C7 measures 17 to 18 mm in adults, with the cervical spinal cord itself measuring 10 mm in the same dimension.^24,25 Individuals with a midsagittal canal diameter of less than 13 mm are considered to have developmental cervical stenosis.²⁶ These individuals have less space available for the spinal cord and thus are more susceptible to the cumulative degenerative factors that further narrow the spinal canal.²⁷ These contributory degenerative factors can include static elements, such as bulging degenerative disks, osteophytes, and infolded or thickened ligamentum flavum, as well as dynamic factors. Abnormal cervical motion in the setting of a stenotic canal can lead to chronic, repetitive spinal cord trauma from impingement against bony spurs or pathologically subluxed vertebral bodies.²² It has also been postulated that developmental stenosis reduces the cushioning effect of cerebrospinal fluid during minor trauma, increasing the risk for cord injury.²⁸

Cervical stenosis has been quantified using the Torg ratio, which is calculated from plain lateral radiographs by dividing the canal diameter (measured from the anterior aspect of the lamina to the mid-portion of the posterior cortex of the vertebral body) by the AP width of the vertebral body at its midsection.²⁹ A normal ratio is approximately 1.0, and anything 0.8 or less is indicative of cervical stenosis. However, some studies have called into question how applicable the Torg ratio is for collision sport athletes who have larger vertebral bodies, which can lead to a high false-positive rate and thus poor predictive value.^30,31 Moreover, Torg et al published on the use of the ratio in predicting the likelihood and severity of an athlete’s spinal cord injury (SCI) after a fracture or ligamentous instability.²⁹ This ratio did not predict cases of devastating neurologic injury or quadriplegia. It has mistakenly been thought to be a screening measure for cervical canal stenosis. In fact, Blackley et al demonstrated how poorly the Torg ratio correlated to the actual canal diameter as measured on a CT scan.³² With the wide availability of MRI today and its ability to directly visualize the neural elements, this is currently the modality of choice for imaging a patient with suspected cervical stenosis.³³

Stenosis of the cervical spine is thought to be a risk factor for cervical cord neurapraxia (CCN) and SCI.^34,35 CCN results from a compressive or concussive injury to the cervical spinal cord in the absence of a cervical fracture or dislocation and results in a transient complete or partial loss of motor or sensation bilaterally that can last anywhere from a few seconds to 36 hours. The mechanism of CCN is thought to be cord compression between the posteroinferior margin of the vertebral body and the anterosuperior edge of the subjacent lamina,³⁶ especially with neck extension because this decreases the sagittal diameter of the spinal canal by 2 mm.³⁷ Therefore, athletes with smaller canal diameters may be at increased risk for sustaining an episode of CCN with trauma, especially if this involves neck hyperextension. A retrospective study consisting of American football players who experienced CCN revealed that all participants had evidence of developmental or acquired spinal stenosis as determined by the Torg ratio.²⁹

Although cervical stenosis can place an asymptomatic athlete at risk for CCN, if spinal cord compression is severe enough and present for a long enough time, the individual can develop myelopathy. When the myelopathy is a result of stenosis from cervical spondylosis, it is termed CSM. The clinical findings in early myelopathy are typically subtle, and the insidious onset of symptoms is responsible for lengthy delays in diagnosis. One study reported a 6.3-year average delay in diagnosing myelopathy, with gait abnormalities presenting as the earliest
consistent symptom in their cohort.³⁸ In addition to gait disturbances, patients with myelopathy often complain of hand clumsiness and a decline in their manual dexterity or fine motor skills. Depending on the specific spinal cord tracts that are affected, patients may complain of a constellation of upper extremity weakness or sensory disturbances (or both).