Cervical Spondylosis

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Chapter 82 Cervical Spondylosis

Cervical spondylosis is a ubiquitous degenerative process of aging that can lead to both pain and neurologic impairment. Radiographically, it is observed in about 10% of people by age 25 and in nearly 95% by age 65.^1,² Multiple authors near the end of the 19th century initially described it as an inflammatory process, possibly infectious in origin, and, therefore, referred to it as cervical spondylitis³ It was not until 1952 that Brain identified this as a degenerative process of aging and coined the term cervical spondylosis. British neurosurgeon Victor Horsley provided the first description of an operation—a C6 laminectomy—for a patient with progressive spastic quadriparesis with presumed cervical spondylotic myelopathy (CSM).^4,⁵

Pathology of Cervical Spondylosis and Myelopathy

Degeneration associated with spondylosis begins at the intervertebral disc, unlike degenerative arthritis, which is associated with inflammation of the synovial lining of joints.¹ The nucleus pulposus consists of proteoglycan aggregates that have hydrophilic hyaluronic chains with side chains containing chondroitin sulfate and keratin sulfate. Repeated stress and aging of the nucleus pulposus lead to several changes.^1,⁶^–¹⁰ Histologically, there are loss of hydrophilic mucopolysaccharides, increase in keratin sulfate, and loss of water, which lead to disc shrinkage, loss of elasticity, and inequitable distribution of hydrostatic pressure on the anulus with compressive forces. As the disc weakens, surrounding structures are required to bear a greater burden of weight-bearing load and dynamic stresses. As surrounding structures bear greater weight, they undergo reactive changes. End plates, uncovertebral joints, and facet joints form osteophytes as a biomechanical mechanism to increase the weight-bearing surface area.¹⁰^–¹⁴ The ligamentum flavum and PLL undergo hypertrophy.¹⁵^–¹⁷ Dorsally, the ligamentum flavum can buckle into the spinal canal as the discs collapse. Ventrally, the anulus bulges into the spinal canal and dissects the PLL of the bone, and the PLL itself hypertrophies. Degenerative changes in the disc occur ventrally first, leading to kyphosis.

Cervical spondylotic changes can lead to spinal canal and intervertebral foramen narrowing that can impinge on the spinal cord centrally or on the exiting nerve roots laterally. Autopsy studies have described histologic changes that are seen in CSM, including white matter demyelination, particularly in lateral corticospinal tracts, gray matter neuronal loss, necrosis, and cavitation.^18,¹⁹ Ogino et al. demonstrated that pathologic changes worsened with smaller anteroposterior canal diameter: reduction to 40% to 44% of normal led to mild white matter demyelination; reduction to 22% to 39% correlated with diffuse white matter demyelination and gray matter cavitation; and reduction to 12% to 19% led to white matter gliosis and diffuse gray matter necrosis.¹⁹

Pathologic changes found in CSM are due to factors that are often divided into static, dynamic, and vascular processes.¹ Static processes are the reactive changes already described stemming from disc desiccation. Dynamic movement in cervical spondylosis may further lead to CSM. During flexion, the spinal cord elongates and may become trapped along ventral osteophytic spurs. With extension, ligamentum buckling may cause dorsal impingement.^1,^16,²⁰ An MRI flexion-extension study by Muhle et al. demonstrated increasing spinal stenosis on average during extension compared to flexion.²¹ Finally, animal studies demonstrate that the changes that are observed in CSM mimic changes seen in ischemic cord models.^18,^22,²³ Some authors hypothesize that this occurs because spinal cord compression leads to ischemia at the microcirculation level.²² Demyelination may also be due to increased susceptibility to ischemia seen in oligodendrocytes.^20,²⁴ While cervical spondylotic changes are seen throughout the subaxial spine, involvement at C5-6 is the most common, followed by C6-7.²⁵ That this is likely due to the fact that motion is more common at C5-6 and C6-7, where most of flexion and extension in the subaxial spine occur, and motion leads to greater reactive changes.^1,²⁶ Spinal cord compression symptoms may be exacerbated by the fact that C5-7 is a watershed area in the cervical cord, with reduced blood flow and greater potential for spinal cord ischemia.^27,²⁸

Clinical Syndromes

Axial Pain

Neck pain is a common presenting chief complaint seen by the general practitioner. Contributing anatomic sources of neck pain are multiple and include neck musculature, tendons, ligaments, facet joints, intervertebral discs, craniovertebral junction, and cervical vasculature. Referred pain can be seen with shoulder and temporomandibular joint pathology as well. The intervertebral disc is innervated ventrally by branches from the sympathetic plexus and dorsally by the sinuvertebral nerve, which arises from the ventral nerve root.²⁹^–³¹ The sinuvertebral nerve also innervates the PLL, the dura, and a substantial portion of the vertebral body periosteum.^1,²⁸ Cervical facet joints are innervated by branches arising from the dorsal ramus.¹

Axial pain can occur alone or in conjunction with radiculopathy and/or myelopathy. When pain occurs alone, the traditional dictum advocates nonoperative management. However, experience shows that when axial pain accompanies radiculopathy or myelopathy, surgery to ameliorate the latter frequently relieves the former.²⁹ The most common cause of nondegenerative isolated neck pain is cervical strain resulting from injury to neck muscles, tendons, and ligaments that is frequently seen with whiplash injury.²⁹ Beliefs about the anatomic source of isolated neck pain in patients with cervical spondylosis vary. The intervertebral disc is commonly cited as the source of axial pain.³² Tears in the anulus may stimulate the sinuvertebral nerve.^33,³⁴ Additionally, injection of local anesthetic in the disc space can temporarily relieve pain in some patients.³⁵ The facet joints are another potential source of axial pain.^36,³⁷ Stimulation of subaxial facet joints generates reproducible neck pain patterns in normal volunteers.³⁸ However, facet steroid injections³⁹ and percutaneous radiofrequency neurotomy have demonstrated mediocre results.^40,⁴¹

Isolated axial pain that fails to respond to initial conservative therapy can be further evaluated with cervical radiographs. Cervical spondylotic changes on radiograph are ubiquitous in the aging population and include loss of disc height, osteophyte formation, kyphosis, and subluxation.^1,⁴² Flexion-extension cervical films greatly help in ruling out instability or motion that may be a source of significant pain.

In appropriately selected patients, several studies have demonstrated good results in operative management of axial pain.^31,⁴³^–⁴⁵ These studies utilized provocative discography to localize the level(s) of axial pain and treat symptomatic levels with anterior cervical decompression and fusion (ACDF). Neck pain is common in rheumatoid arthritis and can be secondary to instability or from basilar invagination, and surgery is commonly employed in this population. One must always be alert to the possibility of a C3-4 radiculopathy as a source of axial pain. Unilateral pain should alert the practitioner to look for sensory alterations, ask about paresthesias in this distribution, and look for a positive Spurling sign. C3-4 radiculopathy that causes axial pain generally responds very well to surgical decompression.⁴⁶ Pseudarthrosis from previously attempted fusion can also lead to significant axial pain with or without radiculopathy and is a condition that also responds well to reoperation.

Isolated axial pain can be disabling to patients and presents a significant diagnostic and management challenge to the practitioner. The source of neck pain varies from person to person and in many patients is likely multifactorial. Acute neck pain deserves a trial of NSAIDs and short-term muscle relaxants if needed.⁴⁷ A temporary soft neck collar can provide comfort as well. Chronic neck pain can be managed with analgesia and physical therapy exercises to strengthen the cervical musculature. Surgery should be reserved for patients with well-accepted indications. Although controversial, surgery may be considered in certain cases of disabling neck pain with positive properly performed discography.

Radiculopathy

Cervical radiculopathy results from compression of an exiting cervical nerve root. This often results from uncovertebral and facet osteophyte formation extending into the neural foramen. Patients often describe a sharp or burning radiating pain in a dermatomal distribution. Nerve compression can also result in paresthesias or impaired sensation in a dermatomal distribution or weakness in the respective myotome. Physical examination is often significant for a positive Spurling sign: Axial compression with lateral bending to the ipsilateral side reproduces the radicular pain. The abduction relief sign—relief of radicular pain by abducting the ipsilateral arm and putting the hand on the head—can help to differentiate radiculopathy from thoracic outlet syndrome or shoulder pathology.^4,⁴⁸ One must carefully evaluate the radiculopathic complaint and consider alternative etiologies such as peripheral entrapment syndromes, thoracic outlet syndrome, brachial neuritis, shoulder pathology, reflex sympathetic dystrophy, and even angina.¹

MRI has become the standard for evaluating the neural foramina for radiculopathy. On T2 imaging, individual neural foramina can be evaluated for significant stenosis. With existing hardware, CT myelography is more useful. Dynamic flexion-extension radiographs are invaluable in additionally evaluating for instability to plan operative strategy. In attempting to sort out radiculopathy from peripheral syndromes, electrodiagnostic studies such as electromyography and nerve conduction studies are routinely used.

Radiculopathy without significant weakness deserves an appropriate trial of conservative therapy. This includes analgesia, NSAIDs, and possibly anticonvulsant therapy. Although not FDA approved, anticonvulsant therapy with gabapentin or pregabalin, which has demonstrated benefits in diabetic neuropathy, is now frequently used for radiculopathic pain with good anecdotal results. Epidural steroid injection or localized nerve blocks can provide therapeutic relief, and the latter can help to confirm diagnostic hypotheses.

When conservative therapy fails and the diagnosis of cervical root compression is certain, surgical decompression provides good results. When alignment is well maintained, a minimally destabilizing approach includes dorsal laminoforaminotomy. When fusion is needed, either ACDF or dorsal decompression with fusion provides good results in class III evidence. Persson et al. randomized 81 patients with cervical spondylotic radiculopathy to ACDF, physical therapy, or cervical collar immobilization. Evaluation at 3 to 4 months revealed improved pain scores (using a visual analogue scale) and motor and sensory improvements with surgery compared to nonoperative alternatives. This effect dissipated at 12-month follow-up; however, a disability rating index showed improved return to work and dressing ability at 12 months with surgery.^49,⁵⁰

Myelopathy

Patients with myelopathy commonly present with unsteady gait and difficulty with fine motor coordination in the hands.^8,¹¹ Physical examination may demonstrate hyperreflexia below the level of compression, increased muscle tone, clonus, the Babinski sign, the Hoffman sign, and the finger escape sign.^8,⁵¹ Some patients may describe the Lhermitte sign (electric shock sensations traveling down the spine with flexion), which is thought to be due to stimulation of the dorsal columns. Hands may demonstrate intrinsic muscle atrophy, which is a classic sign in myelopathy.^51,⁵² Some patients may complain of urinary retention or spastic detrusor activity leading to frequent urges with or without incontinence. Additional localizing upper motor signs include pectoral muscle reflex, which is suggestive of compression at or above C2-4, and the jaw jerk, which if present suggests a lesion above the foramen magnum.^53,⁵⁴ Patients with severe cervical spondylosis with canal stenosis can experience central cord syndrome with even minor trauma, particularly in hyperextension injury. Greater motor impairment is seen in the upper extremities and is often accompanied by urinary retention.⁵⁵ Burning hands have been described in football injuries and are thought to be a variant of central cord syndrome in patients with congenital canal stenosis.⁵⁶ The differential diagnosis for CSM is broad and includes multiple sclerosis, syringomyelia, atrophic lateral sclerosis, subacute combined degeneration, intraspinal tumor, spinal arteriovenous malformation, epidural abscess, Chiari malformation, ossification of the posterior longitudinal ligament, normal pressure hydrocephalus, tabes dorsalis, hereditary spastic paraplegia, and tropical spastic paraparesis.^1,^11,^57,⁵⁸ Several grading systems have been developed to classify the severity of CSM in an objective, reliable, and valid assessment that can also be used to measure responsiveness to therapeutic interventions. The Japanese Orthopaedic Association (JOA) scale and the modified version by Benzel et al. are the two most widely used systems and have demonstrated good interobserver and intraobserver reliability.⁵⁹^–⁶¹ Other accepted systems include gait analysis and the short form-36 (SF-36).⁶²^–⁶⁵

The gold standard for imaging in CSM has become MRI because it provides the best view of the spinal cord, exiting nerve roots, and CSF signal.⁶⁶ CT myelography may be more useful in cases of previous surgery because it is superior to MRI in viewing residual bony anatomy and produces less artifact with existing hardware. The examiner must be aware that the degree of stenosis on imaging frequently does not correlate with clinical impairment. In one study of asymptomatic elderly patients, 26% had some degree of spinal cord impingement on MRI.^11,⁶⁷ Multiple studies have attempted to correlate spinal cord signal changes on MRI with neurologic recovery after decompression. Several class III studies demonstrate that T2 hyperintensity at a single segment does not predict outcome, but when present at multiple levels or in combination with T1 hypointensity, it does correlate with poor neurologic recovery after surgery.⁶⁸^–⁷² Other studies have attempted to correlate the degree of canal stenosis with neurologic recovery after surgery. Most studies demonstrate poorer neurologic recovery in patients with greater radiographic canal stenosis, with most studies using a canal area of 30 to 45 mm² as the cutoff to dichotomize groups.⁷³^–⁷⁶ One study did not corroborate these findings.⁷⁷