Cervical spondylosis refers to the age-related degeneration of the cervical spine, primarily involving the intervertebral disks, facet joints, and uncovertebral joints. Disk degeneration occurs as a result of aging and repetitive loading, as hydrostatic pressures and disk heights are reduced over time (Figure 1). Cervical intervertebral disks support load distribution and proper head motion, and the degeneration of these disks redistributes physiologic loads, resulting in structural degeneration of the disk (tearing, bulging, or herniation), ligament hypertrophy and calcification, and the formation of osteophytes.¹ This process may result in chronic neck pain and disability, although many patients are asymptomatic.² Loss of intervertebral disk height along with bony and ligamentous hypertrophy may cause foraminal stenosis compressing the exiting spinal nerve roots leading to symptoms of radiculopathy. Central stenosis also results from degenerative changes typically located within the subaxial spine, which may lead to symptoms of myelopathy. Progressive degeneration of the spinal column, including atrophy of the surrounding musculature and attenuation of spinal ligaments, may also lead to structural deformity.

Axial neck pain may result from a simple cervical sprain or strain, or from cervical disk degeneration in the absence of radiculopathy or myelopathy. History and physical exam for patients with axial neck pain is difficult, as pain is often chronic, nonspecific, and insidious in nature.³ In patients presenting with radiculopathy or myelopathy and concomitant axial neck pain, cervical disk disease may be a large contributor to their pain.³

Atlantoaxial osteoarthritis has a prevalence of 4% and may be a contributor to axial neck pain, especially in spondylotic elderly patients.⁴ Atlantoaxial osteoarthritis is frequently unrecognized, as its presentation varies with symptoms including radiating and nonradiating pain in the posterior neck and occiput, pain with axial rotation and lateral bending, and pain with palpation of the C1-C2 facet joints. Because the differential diagnosis for posterior neck pain is wide ranging, atlantoaxial osteoarthritis is sometimes misdiagnosed as migraines, cluster headaches, or occipital neuralgia.⁴

Cervical radiculopathy occurs from compression or irritation of spinal nerve roots. Patients with radiculopathy present with radiating pain as the prominent feature; however, they may also present with concomitant ipsilateral neck and shoulder pain.⁵ Traditionally, radiculopathy was thought to follow a dermatomal distribution based on the cervical levels involved. However, nonstandard localization of symptoms is common at all cervical levels, affecting up to 46% of patients with single-level disease.⁵ This may be due to variations in brachial plexus anatomy or intradural connections of
spinal roots. Accordingly, advanced imaging is required to confirm the level of disease. Given the possibility of peripheral nerve compression and shoulder pathology resembling symptoms of cervical radiculopathy, a careful history and physical examination must be performed to determine if a patient’s pain is cervical in origin. The Spurling test, in conjunction with other nerve tension tests such as the Phalen test for median nerve compression, can help differentiate between central and peripheral etiologies of radicular-type pain. Cervical radiculopathy may also occur because of a tortuous vertebral artery, a rare type of vascular anomaly in which the artery loops around the exiting nerve root, and it is important for spine surgeons to be aware of this possibility when reviewing preoperative imaging.⁶

Nonsurgical treatment should be attempted prior to surgical intervention. Three major surgical treatment options for cervical radiculopathy include anterior cervical diskectomy and fusion (ACDF), cervical disk arthroplasty, and posterior cervical foraminotomy. Based on a 2020 meta-analysis of 21 randomized controlled trials, there is no superior surgical treatment option.⁷ ACDF continues to be the most common treatment option for single-level radiculopathy, whereas posterior cervical foraminotomy has been decreasing in prevalence with the advent of cervical disk arthroplasty.⁸ Further discussion of surgical and nonsurgical management for cervical radiculopathy is presented later in the chapter.

Cervical myelopathy, which occurs from compression of the spinal cord, is the most common cause of spinal cord dysfunction, and commonly presents with symptoms in the upper extremity including weakness, numbness, and loss of dexterity.⁹ However, 1% of patients may report no upper extremity symptoms at all.¹⁰ Clinical diagnosis is frequently supported by MRI, which may aid in determining the nature and severity of cervical degeneration and spinal cord involvement.¹ The severity of spinal cord damage (myelomalacia) can be determined from hyperintensity on T2-weighted sequences and hypointensity on T1-weighted sequences¹¹ (Figure 2). Changes in the spinal cord can be categorized as indistinct, which typically indicates reversible edema and/or Wallerian degeneration (Figure 2, B), or sharp with clear borders that typically indicates irreversible tissue loss and necrosis (Figure 2, A and C).¹¹ The amplitude of low-frequency fluctuations on functional MRI may be a predictive biomarker for postoperative improvement in cervical myelopathy following surgery.¹² CT may be used to evaluate bone quality, and to identify ossification of the posterior longitudinal ligament and/or ligamentum flavum.¹¹ Although the incidence of ossification of the posterior longitudinal ligament is approximately 2% in the general population, it is of particular interest in cervical myelopathy patients, with a reported incidence as high as 11%.¹¹ Standard radiographs, including flexion-extension films, are also useful for surgical planning and the assessment of global alignment, balance, and stability.¹¹

Other symptoms of cervical myelopathy include gait disturbance, imbalance, and weakness. Patients with cervical myelopathy have increased center of mass sway and head sway to maintain standing posture, requiring greater muscle activity and energy expenditure in the trunk and lower extremities.¹³ Physical examination may demonstrate hyperreflexia, positive Hoffman sign, difficulty with rapid alternating movements, positive Babinski sign, and clonus. Many symptoms of cervical myelopathy are nonspecific, and a differential diagnosis should include multiple sclerosis, transverse myelitis, normal-pressure hydrocephalus, and stroke, in addition to spinal cord compression from other etiologies such as trauma, tumor, and infection. Normal-pressure hydrocephalus may be especially difficult to differentiate as
asymptomatic spinal cord compression is also common within this patient population.¹⁴ Although the pathophysiology of cervical myelopathy is presumed to be from spinal cord compression, the severity of cervical myelopathy and level of functional impairment, as measured by the Japanese Orthopaedic Association score, may be further exacerbated by arteriosclerosis of the carotid and vertebral arteries suggesting a vascular contribution to symptomatology.¹⁵

Somatosensory-evoked potentials, a type of neurophysiologic monitoring, may be used to predict the progression of disease severity in cases of mild cervical myelopathy.¹⁶ Somatosensory-evoked potentials used in conjunction with motor-evoked potentials (MEP) are able to identify patients with subtle presentations, differentiate between spinal cord compression and neurodegenerative disorders, and assist in determining postoperative recovery.¹¹ Transcranial electrical motor-evoked potentials have been shown to have superior sensitivity compared to somatosensory-evoked potentials for detecting cervical myelopathy in the early stages of the disease.¹¹

Cervical myelopathy sometimes is associated with fatty infiltration and atrophy of deep paraspinal muscles, particularly the longus capitis, longus colli, and multifidus at the level of spinal cord compression and caudally, which play a role in cervical alignment.¹⁷ The degree of change in sagittal alignment parameters on dynamic radiographs has been noted to be related to the severity of symptoms in patients with cervical myelopathy. For example, in a 2020 study, patients with C2-C7 lordosis in flexion greater than 29° demonstrated better outcomes than patients with lordosis in flexion of up to 29°, regardless of surgical or nonsurgical treatment.¹⁸ Along with muscle atrophy, fragility fractures are a significant contributor to morbidity and mortality in patients with cervical myelopathy, with the incidence decreasing after surgical intervention.¹⁹

Nonsurgical treatment may be initiated for mild myelopathy, although surgical intervention is recommended to prevent progression of myelopathy and the resultant denervation and atrophy of musculature. Although all patients stand to improve following surgery, patients with increased age, symptom duration longer than 1 year, increased baseline symptom severity, history of diabetes and smoking, and psychiatric comorbidities may experience inferior outcomes.¹¹,²⁰ Surgery is recommended for patients with moderate or severe cervical myelopathy as measured by the modified Japanese Orthopaedic Association score.¹