Cervical spondylosis is a progressive degenerative cascade that occurs with aging. Annular tears and biochemical changes in the cervical disc can lead to decreased water content, shrinking or herniation of nuclear pulposus tissue, and disc collapse. This places increased stress on associated facet and uncovertebral joints, causing them to degenerate, eventually leading to axial neck pain and stiffness. In addition, this can lead to the formation of bony spurs and disc herniations that may encroach on the neuroforamina, resulting in radiculopathy.1

The clinical presentation of cervical spondylosis can vary and must be distinguished from referred shoulder or visceral pain. A careful history and physical examination must be done to determine the exact cause of the neck pain. Nonmechanical neck pain is less likely to be related to disc disease, and other sources including tumor and infection must be considered. Radicular symptom neck pain will often be exacerbated by neck extension and rotation to the affected side (Spurling sign). In contrast, muscular neck pain is often exacerbated by neck flexion and rotation away from the more painful side. In cases of lower cervical degenerative disease, the pain often radiates to the shoulder, upper arm, or infrascapular areas, and upper cervical disease may present as temporal pain and retroorbital headaches.²

Cervical radiculopathy typically presents as pain and paresthesia in a single or multiple nerve root distribution. Spurling sign is a reproduction of radicular pain caused by extending the neck and rotating the head to the symptomatic side, which leads to narrowing of the neuroforamina. Axial compression and the Valsalva maneuver may also reproduce symptoms. The “shoulder abduction sign” is the reduction of radicular symptoms caused by placing the hand of the affected arm on top of the head, which decreases tension on the nerve roots.³

Cervical myelopathy typically has gait abnormalities, hyperreflexia, and loss of fine motor skills, which result from mechanical compression of the spinal cord in the cervical region. Motor weakness and muscle wasting may be present, as well as sensory abnormalities. Patients may also complain of neck pain and/or radicular symptoms, so careful evaluation must be done to determine the exact cause of symptoms. Typical examination findings include upper motor neuron signs and hyperreflexia manifested as a positive Hoffman reflex, clonus of deep tendon reflexes, and an upgoing Babinski reflex.

History and physical examination remain the most important processes in the diagnostic workup. Imaging and electromyography or nerve conduction studies can be used to supplement the diagnostic workup. Plain radiographs, including anteroposterior, lateral, oblique, and lateral flexion and extension views, can demonstrate developmental stenosis, disc space narrowing, abnormal alignment, dynamic instability, and osteophyte formation. Radiographic findings may occur with normal age-related degenerative changes, so radiographic findings must be correlated with clinical findings.⁴ Magnetic resonance imaging (MRI) is commonly used and is the most sensitive modality for demonstrating spinal cord morphology in relation to the surrounding bony and soft-tissue structures (Fig. 14-3). Computed tomography myelography is highly sensitive for detecting foraminal stenosis, but it is invasive and does have a risk of complications.⁵ Electromyography and nerve conduction studies can help distinguish between nerve root compression and a peripheral neuropathy and are useful in patients with unclear diagnose. In cases of mechanical neck pain without radiculopathy, several studies support the use of provocative discography to confirm discogenic origin of the pain and to clarify which disc levels are appropriate to treat.^6,7

The majority of patients with axial neck pain experience acceptable resolution of symptoms without surgical intervention. Cervical radiculopathy responds well to conservative treatment, but many patients progress to experience recurrent or persistent symptoms.8 Initially, activity modification and a brief soft collar immobilization are often recommended, but prolonged inactivity may lead to deconditioning. Early pharmacologic treatment is initiated with nonsteroidal antiinflammatory drugs or acetaminophen. With severe acute pain, narcotic analgesics may be used. Paraspinal muscle spasm may be relieved with muscle relaxants but is often improved with a soft collar immobilization alone. Some patients also may respond to oral corticosteroids.⁹ All medications should be prescribed only with careful regard for the potential adverse reactions and interactions with other medications that the patient is taking. Physical therapy is an essential component of conservative treatment and includes modalities, such as traction and heat or cold therapy, as well as an isometric neck and shoulder-stabilizing exercise program. The specifics of a physical therapy program are often left up to the discretion of the particular therapist.

Surgical treatment depends on the clinical entity treated and success of nonoperative treatment. Conservative treatment is the mainstay of initial treatment for cervical radiculopathy and degenerative disc disease with acceptable results.¹⁰ Surgical intervention for patients with cervical radiculopathy is indicated when the symptoms are persistent or recurrent or they are severe or debilitating enough to merit surgery.¹¹ A prolonged conservative course is recommended for treatment of axial neck pain. If surgery is being considered for axial neck pain and diagnostic evaluation has failed, a discogram is obtained to identify the exact correct level(s) responsible for discogenic pain. As with any elective surgical procedure, appropriate patient expectations and selection must be considered before any surgical intervention (Box 14-1). In general, workers’ compensation patients and those involved in litigation can be expected to have worse outcomes even after successful fusion surgery.^12,13 Cervical myelopathy must be considered separately, however, because clinical progression usually occurs even with conservative treatment. Classically, patients with cervical myelopathy have periods of clinical stability interspersed with “stepwise degeneration” and careful follow-up must be used to monitor disease progression.¹⁴

Once the appropriate level is confirmed, the longus colli muscles are dissected off of the bone laterally and a self-retaining retractor is placed, exposing the disc space to the uncovertebral joints. The operating microscope, sterilely draped, is then brought into the field (Fig. 14-4). Under direct visualization using the microscope, the disc is incised with a scalpel and the anterior portion is removed using a pituitary forceps and an angled curette. A high-speed drill may be used to complete the discectomy and expose the posterior longitudinal ligament (PLL). After exposure, the PLL is elevated off of the posterior aspect of the vertebral bodies using a small 4-0 forward-angled curette; it is then excised using 1 mm and 2 mm Kerrison rongeurs. The PLL does not need to be routinely removed if no nuclear protrusion or extrusion is found, but this has to be carefully explored. The foramina can be probed with the 90° angled nerve hook to confirm adequate decompression or any remaining loose disc fragments. When the discectomy and foraminotomies are complete, the disc space is measured and an appropriately sized graft is chosen. While increased traction is applied on the halter traction device, the graft is gently impacted into position. When it is adequately positioned, all traction is removed. An appropriate-sized plate is then chosen and applied on the anterior aspect of the cervical spine. Care is taken when drilling screw holes to choose a length that will be contained in the vertebral body and be parallel with the endplate of the disc space. When the plate is in position, a lateral radiograph is obtained and graft and hardware positioning is checked (Figs. 14-5 and 14-6).

After instrumentation is complete, the wound is copiously irrigated and thoroughly checked for hemostasis. Often a drain is used even if the wound appears very dry, because a postoperative hematoma may cause significant morbidity. The platysma muscle and subcutaneous tissue are then closed with interrupted absorbable sutures. A running subcuticular layer of suture may follow this closure, followed by a sterile dressing. The patient is then placed into a rigid cervical orthosis before extubation.

Postoperatively, the head of the patient’s bed is maintained in an elevated position to decrease swelling in the neck. The patient should be able to walk, void, swallow liquids, and tolerate a diet before discharge. Most patients are discharged the day after surgery. Patients commonly complain of a sore throat and pain with swallowing a few days after surgery. If these complaints seem more severe than usual, then a single dose or short course of oral corticosteroids may be given in an attempt to minimize swelling.

Postoperatively, patients with radicular symptoms will often note immediate relief of pain after surgery. Most patients report a change in the quality of their axial neck pain to one more typical of postoperative pain. Generally, patients treated for radicular symptoms achieve excellent clinical results (up to 90% satisfactory results), whereas those treated for axial neck pain achieve good results.15,16 One concern in the postoperative period is overactivity before fusion is achieved. Solid consolidation of fusion often requires 6 to 12 weeks, so excessive motion and loading are discouraged during this period. Often patients are maintained in a rigid cervical collar for 6 to 12 weeks to restrict their activities, but patients frequently recover from surgery much sooner and desire to remove the orthosis and resume normal activities. This relative immobilization can result in significant patient deconditioning, which can be a challenge to the therapist. In the early period of return to activity and therapy, it is important to avoid injury caused by an overly strenuous exercise program or an overzealous patient.

ACDF is a generally well-tolerated and successful procedure; however, recent data has shown that cervical fusion may lead to less satisfying results than previously thought.17 Concerns about adjacent segment disease has led to the development of cervical total disc replacement.¹⁸ Recently, results of a multicenter, randomized, prospective Federal Drug Administration clinical trial of cervical disc replacement (Synthes Prodisc-C) versus ACDF has shown clinical equivalence or superiority of cervical disc replacement over fusion.¹⁹ Other clinical studies have demonstrated similar consistent evidence with other cervical disc prosthese.^20,21 These treatments have the potential of offering shorter recovery times and more rapid return to activity and may help prevent the progression of adjacent-level degeneration. Our view is that cervical disc replacement is superior to fusion.

The decision to operate on the cervical spine may be driven by localized tissue damage and subsequent focal pain, but the majority of spinal surgeries are initiated because of damage to (or threat of damage to) the neural network of the body. Myelographic computed tomography and MRI studies have all demonstrated that 20% to 30% of people who have disc herniation and stenosis do not have radicular symptoms, and many of these people do not have neck pain.22 It has also been shown that under anesthesia, only nerves that are inflamed will produce radicular symptoms when compressed or placed under traction. Therefore, although the intervertebral disc or stenosis can be the source of neck pain, it is generally injury to the nerve that drives the decision to undergo surgery. Protecting the nervous system from further damage and providing an environment in which the nerve can heal are primary goals of the surgery and rehabilitation thereafter.

Within the spine, injury or damage to the nerve often occurs at the spinal nerve root or the dorsal root ganglia. Anatomically, differences in the nerve root make it more susceptible to injury than at other regions of the peripheral nerve. The nerve root is not as well protected, less able to withstand deformation, and less able to repair itself than the remainder of the peripheral nerve. The other structure within the intervertebral foramen that is susceptible to damage is the dorsal root ganglia. The position of the dorsal root ganglia is not constant and can be found inside the foramen, outside the foramen, or in the spinal canal, which can increase the likelihood that it will be injured. In addition, unlike the spinal nerve root and peripheral nerve, the dorsal root ganglia do not have a blood-nerve barrier, which is necessary to prevent foreign substances from invading the nerve. These anatomic differences predispose the dorsal root ganglia to edema and mechanical compression.^22–24

Nerves must also be able to move and glide within the tissue. For this to occur, some slack in the system must exist. The spinal cord changes length by 7 cm from flexion to extension. Studies in the arm show that a 7-mm excursion occurs in the nerves with movement. In addition to compression, increased tension of the nerve can result in nerve damage.

More specifically, tension in nerves causing a 20% to 30% increase in length will cause the nerve to break. Boyd and associates²⁵ demonstrated that as little as 6% strain decreases the amplitude of action potentials by 70%, and 10% to 12% strain causes complete conduction block. They have also shown that nerve stretch of as little as 8% greater than the resting length will cause a 50% decrease in blood flow to the nerve and stretch of 15% will cause 80% to 100% reduction in blood flow. Therefore, exercises that place undue stress and tension on the nerves should be avoided.²⁶

Neurons are incapable of dividing and migrating; therefore regeneration occurs only through existing neurons. If the connective tissue sheathing remains intact, then a potential for nerve regrowth exists. If the sheath is disrupted, then the potential for regrowth diminishes. Initially, like any tissue, an inflammatory process is seen within the nerve. Within hours after injury, the nerves start to grow back from the distal stump at 1 to 2 mm per day. In addition to transmitting nerve impulses, the axon of the nerve functions to transmit nutrients and chemicals down its lumen. These axons are filled with axoplasm, which is necessary for nerve health and survival. Axoplasm is a viscous substance and is thixotropic, which means that it needs constant agitation or it will gel.^22–24 Thus care must be taken to encourage movement and gliding of the nerve, but at the same time, positions that place tension on the nerve should be avoided.

ACDF surgery affects the sternocleidomastoid, platysma, anterior scalene, middle scalene, and the longus colli muscles. It also requires the resection of the anterior longitudinal ligament, PLL, joint capsule, and synovium.^27–30 After the trauma incurred during surgery, the body is only capable of repairing small muscle lesions with regeneration of muscle tissue. Large lesions will fill in with dense connective scar tissue. Although dense connective scar tissue can function to reestablish tissue continuity, it lacks the contractile elements of normal muscle tissue and the tensile strength of normal ligament and tendon tissue. Therefore the ability to generate contractile forces or resist tensile loading through the region of repair is compromised.^31–34

Bone grafts from the iliac crest or from bone donors are often used within the disc space, between two vertebral bodies, to aid in the mineralization and fixation of the region. The iliac crest is used as the primary source of graft material because of its cancellous bone composition. Cancellous bone has a greater potential for revascularization and osteogenesis than grafts from denser cortical bone sources. Healing after a cortical bone graft can take up to two times longer than its cancellous bone graft counterpart.^31,32 As will become apparent later in the chapter, the healing and mineralization of bone at the site of fusion is a major factor driving progression through the rehabilitation process.