Cervical Disc Disease 

Updated: Apr 16, 2020
Author: Michael B Furman, MD, MS; Chief Editor: Dean H Hommer, MD 

Overview

Practice Essentials

Cervical disc disorders encountered in physiatric practice include herniated nucleus pulposus (HNP), degenerative disc disease (DDD), and internal disc disruption (IDD). HNP (seen in the image below) is defined as localized displacement of nucleus, cartilage, fragmented apophyseal bone, or fragmented anular tissue beyond the intervertebral disc space.[1] Most of the herniation is made up of the annulus fibrosus. DDD involves degenerative annular tears, loss of disc height, and nuclear degradation. IDD describes annular fissuring of the disc without external disc deformation. Cervical radiculopathy can result from nerve root injury in the presence of disc herniation or stenosis, most commonly foraminal stenosis, leading to sensory, motor, or reflex abnormalities in the affected nerve root distribution.[2, 3]

Plain cervical spine radiographs are used to evaluate chronic degenerative changes, metastatic disease, infection, spinal deformity, and stability, while magnetic resonance imaging (MRI) remains the imaging modality of choice to assess cervical HNP. For most cervical disc disorders, studies support conservative treatment, such as the McKenzie approach and cervicothoracic stabilization programs, combined with aerobic conditioning.

Sagittal magnetic resonance imaging (MRI) scan dem Sagittal magnetic resonance imaging (MRI) scan demonstrating cervical intervertebral disc protrusions at C3-C4 and C7-T1.

Understanding cervical disc disease requires basic knowledge of anatomy and biomechanics. The intervertebral disc is a functional unit connecting 2 vertebral bodies of the spine. The disc absorbs shock, accommodates movement, provides support, and separates vertebral bodies to lend height to intervertebral foramina. The disc consists of 3 structural components; an eccentrically located nucleus pulposus, a surrounding lamellar annulus fibrosus, and 2 cartilaginous endplates, separating each segmental level between the C2-T1 vertebrae. No disc exists between C1 and C2, and only ligaments and joint capsules resist excessive motion. Disc degeneration and/or herniation can injure the spinal cord or nerve roots and result in stenosis[4] and/or myofascial pain.

Symptoms of cervical disc disease

Discogenic pain without nerve root involvement is typically vague, diffuse and distributed axially. Depending on whether primarily motor or sensory involvement is present, radicular pain is deep, dull, and achy or sharp, burning, and electric. Such radicular pain follows a dermatomal or myotomal pattern into the upper limb. Cervical radicular pain most commonly radiates to the interscapular region, although pain can be referred to the occiput, shoulder, or arm as well. Neck pain does not necessarily accompany radiculopathy and frequently is absent.

Diagnosis of cervical disc disease

Consider performing rheumatologic workup to evaluate for possible rheumatoid arthritis, ankylosing spondylitis, Reiter syndrome, and polymyalgia rheumatica. In addition, consider performing infection workup to evaluate for possible discitis, epidural abscess, and vertebral osteomyelitis.

Plain cervical spine radiographs are used to evaluate chronic degenerative changes, metastatic disease, infection, spinal deformity, and stability.

Computed tomography (CT) scans delineate cervical spine fracture and are used extensively in trauma cases.

A myelogram followed by a CT scan may be obtained prior to cervical decompressive spinal cord or nerve root surgery. This study evaluates the spinal canal, its relationship to the spinal cord, and nerve root impingement from disc, spur, or foraminal encroachment.

Magnetic resonance imaging (MRI) remains the imaging modality of choice to evaluate cervical HNP, due to its low morbidity.[5, 6] Advantages include soft-tissue definition (eg, cervical discs, spinal cord), cerebrospinal fluid visualization, noninvasiveness, and lack of patient radiation exposure.

Provocative discography is the only procedure that can determine whether a disc serves as the pain generator. Discomfort and invasiveness render this procedure less desirable than cervical MRI, which provides much of the anatomical information that provocative discography does.

Electrodiagnostic studies continue to be standard for evaluating neurologic function of the cervical spine. Advantages of these tests include limited expense and low morbidity.

Management

For most cervical disc disorders, studies support conservative treatment, such as the McKenzie approach and cervicothoracic stabilization programs, combined with aerobic conditioning.

Physical modalities should be used to reduce pain only in the acute phase. Once past the acute phase, modalities are used sparingly on an as-needed basis.

Cervical traction may relieve radicular pain from nerve root compression. Traction does not improve soft-tissue injury pain. Hot packs, massage, and/or electrical stimulation should be applied prior to traction to relieve pain and relax muscles.

A soft cervical collar is recommended only for acute soft-tissue neck injuries and for short periods of time (ie, not to exceed 3-4 days' continuous use).

Spinal manipulation and mobilization may restore normal range of motion (ROM) and decrease pain; however, no clear therapeutic mechanism of action is known.

Cervical epidural, spinal nerve (or root), Z-joint, and sympathetic injections serve diagnostic and therapeutic roles. These procedures can be instrumental in determining the anatomic pain generator (eg, nerve root, facet) and providing aggressive, conservative treatment.

An anesthetic and corticosteroid mixture may be injected into the epidural space (interlaminar) or along the nerve root (transforaminal) after precise radiologic, contrast-enhanced fluoroscopic localization.[7]

Studies indicate that cervical HNP with radiculopathy can be managed conservatively. Surgery is warranted when neurogenic bowel or bladder dysfunction, deteriorating neurologic function, or intractable radicular or discogenic neck pain exists. Specifically, cervical spine surgical outcomes are most favorable for radicular pain, spinal instability, progressive myelopathy, or upper extremity weakness.

Surgical outcomes for patients with myelopathy have been shown to be significantly greater with regard to motor recovery if surgical intervention is performed less than 1 year after the onset of symptoms.[8]

The literature has demonstrated favorable cervical spine fusion outcomes for chronic discogenic axial neck pain when the presurgical evaluation has incorporated provocative cervical discography. However, fusion can increase intradiscal pressure and other stress at adjacent unfused levels, thereby accelerating postsurgical spinal degeneration.[9, 10, 11, 12, 13]

The possibility of obtaining the goals of anterior cervical decompression and fusion (ACDF) while maintaining adjacent segment motion led to the advent of total disk replacement (TDR).

Pathophysiology

Manifestations of HNP are divided into subcategories by type (ie, protrusion, extrusion, sequestration). Disc bulge, is not a true herniation, per se. It is described as generalized symmetrical or asymmetrical circumferential extension of the disc margin beyond the margins of the adjacent vertebral endplates.

Disc protrusion describes herniation of nuclear material through a defect in the annulus, producing a focal extension of the disc margin; it can further be defined if the greatest distance, in any plane, between the edges of the disc material beyond the disc space is less than the distance between the edges of the base, in the same plane.

Extrusion applies to herniation of nuclear material when, in at least one plane, any one distance between the edges of the disc material beyond the disc space is greater than the distance between the edges of the base, or when no continuity exists between the disc material beyond the disc space and that within the disc space. Extrusion may be further specified as sequestration, if the displaced disc material has lost completely any continuity with the parent disc.

The term migration may be used to signify displacement of disc material away from the site of extrusion, regardless of whether sequestrated or not. Examples of disc herniation are seen in the images below.

Disc herniation classification. A: Normal disc ana Disc herniation classification. A: Normal disc anatomy demonstrating nucleus pulposus (NP) and annular margin (AM). B: Disc protrusion, with NP penetrating asymmetrically through annular fibers but confined within the AM. C: Disc extrusion with NP extending beyond the AM. D: Disc sequestration, with nuclear fragment separated from extruded disc.
Axial magnetic resonance imaging (MRI) scan (C3-C4 Axial magnetic resonance imaging (MRI) scan (C3-C4) demonstrating left-sided posterolateral protrusion of the nucleus pulposus with compression of the cerebrospinal fluid.
Sagittal magnetic resonance imaging (MRI) scan dem Sagittal magnetic resonance imaging (MRI) scan demonstrating cervical intervertebral disc protrusions at C3-C4 and C7-T1.
Postdiscography axial computed tomography (CT) sca Postdiscography axial computed tomography (CT) scan demonstrating right posterolateral subligamentous protrusion.

Herniation typically occurs secondary to posterolateral annular stress. There are 2 main types of herniation that are described in the literature: focal and broad-based. Focal herniation involves less than 25% of the disc circumference, whereas broad-based herniations involves between 25-50% of the disc circumference.[1] Herniation rarely results from a single traumatic incident. Acute traumatic cervical HNP serves as a major etiology of central cord syndrome. The C6-C7 disc herniates more frequently than discs at other levels.

Acute disc herniation causes radicular pain through chemical radiculitis in which proteoglycans and phospholipases released from the nucleus pulposus mediate chemical inflammation and/or direct nerve root compression. Interleukin 6 and nitric oxide are also released from the disc and play a role in the inflammatory cascade. Denda et al has also recently showed that chronic compression of the spinal canal can lead to higher than normal levels of nitric oxide (NO) in the cerebrospinal fluid (CSF). Excessive NO levels have been shown to be cytotoxic and can induce neuronal apoptosis.[14] Although high levels of NO have not been correlated to severity of pain or disease, this data may play a role in targets for future interventions.

The chemical radiculitis is a key element in the pain caused by HNP because nerve root compression alone is not always painful unless the dorsal root ganglion is also involved. Herniation may induce nerve demyelination with resulting neurologic symptoms. Cervical HNP maybe resorbed during the acute phase. Indeed, studies documenting frequent herniation resorption and correlating herniation regression with symptom resolution support conservative treatment of cervical radicular pain.

A rare trauma-induced high cervical (C2-C3) HNP syndrome manifests as nonspecific neck and shoulder pain, perioral hypesthesia, more radiculopathy than myelopathy, and more upper limb motor and sensory dysfunction than lower limb symptomatology. Decreased middle and/or lower cervical spine mobility from spondylosis, with consequent overload and hypermobility at higher segments, may precipitate high cervical disc lesions in older patients. A retro-odontoid disc may result from an upwardly migrating C2-C3 HNP. Some case reports describe cervical HNPs causing Brown-Séquard syndrome, as well as atypical nonradicular symptoms in patients with congenital insensitivity to pain. Although spondylosis may affect motion at adjacent levels, isolated disc herniation in the cervical spine does not seem to alter motion of adjacent levels, regardless of the degree of disc degeneration or the size of the disc herniation.[15]

A study by Nam et al indicated that in patients with cervical disc herniation, risk factors for motor weakness include decreased disc height, a percentage of the HNP in the spinal canal, and a signal intensity change in the spinal cord. A disc height cutoff value of 5.8 mm produced a sensitivity and specificity of 39.5% and 94.1%, respectively, while a cutoff value of 28.1% for HNP in the spinal canal produced a sensitivity and specificity of 57.9% and 82.4%, respectively. In addition to motor weakness, signal intensity change in the spinal cord also may predict delayed recovery.[16]

Cervical radiculopathy results from mechanical nerve root compression or intense inflammation (ie, chemical radiculitis). Specifically, nerve root compression may occur at the intervertebral foraminal entrance zone at the narrowest segment of the root sleeve anteriorly by disc protrusion and uncovertebral osteophytes and posteriorly by superior articulating process, ligamentum flavum, and periradicular fibrous tissue.[17] Decreased disc height, as well as age-related foraminal width decrease from inferior Z-joint hypertrophy, may impinge subsequently on nerve roots. The cervical region accounts for 5-36% of all radiculopathies encountered. Incidence of cervical radiculopathies by nerve root level is as follows: C7 (70%), C6 (19-25%), C8 (4-10%), and C5 (2%).

The most common cause of cervical radiculopathy is foraminal encroachment (70-75%). The cause is multifactorial, including degeneration of the discs and the uncovertebral joints of Luschka and the zygapophyseal joints. In contrast to lumbar spine disorders, HNP in the cervical spine is responsible for only 20-25% of radiculopathies.

Cervical DDD most commonly is due to age-related changes, but the condition also is affected by lifestyle, genetics, smoking, nutrition, and physical activity. Degenerative disc changes observed on radiographs may reflect simple aging and do not necessarily indicate a symptomatic process.

The disc begins to degenerate in the second decade of life. Degenerative disc disease is essentially a process disrupting homeostasis. This degenerative process of the less hydrated and more fibrous nucleus pulposus fails to withstand the compressive loading, resulting in uneven distribution of forces to the surrounding annulus, which leads to the formation of radial tears. Circumferential tears form in the posterolateral annulus after repetitive use. Several circumferential tears coalesce into radial tears, which progress into radial fissures. The disc then disrupts with tears passing throughout the disc.

Loss of disc height occurs with subsequent peripheral annular bulging. Proteoglycans and water escape through fissures formed from nuclear degradation, resulting in further thinning of the disc space. Changes in the cartilaginous endplates alter nutritional supply to the nucleus that contributes to preexisting dehydration of the disc, compounding the effects of the degenerative cascade. Vertebral sclerosis and osteophytic formation ultimately follow.[5]

IDD describes pathologic annular fissuring within the disc without external disc deformation. This disorder results from trauma-related nuclear degradation, cervical flexion/rotation-induced annular injury, or whiplash.

The intervertebral disc has few pain receptors and little innervation, except in the periphery of the disc. The intervertebral disc may not be irritated until the inflammation process becomes moderate or severe. The nucleus pulposus appears to be the first site of degeneration with the annulus fibrosis being the primary pain generator once injury or degeneration occurs. DDD ultimately may progress to IDD.

Epidemiology

Frequency

United States

HNP may be observed with magnetic resonance imaging (MRI) in 10% of asymptomatic individuals aged younger than 40 years and 5% of those older than 40 years. Degenerative disc disease (DDD) may be observed with MRI in 25% of asymptomatic individuals aged less than 40 years and 60% of those aged more than 40 years. The true incidence and prevalence of cervical radiculopathy is uncertain; however, studies have shown that 51-67% of adults experience neck and arm pain at some time, and 54% report pain present within the last 6 months. In a population-based study in Rochester, Minn published in 1994 the annual incidence of documented cervical radiculopathy for men and women from all causes was 107.3 and 63.5 cases per 100,000 population, respectively.[18] A separate study looking at a population at risk of more than 13,000,000 people in the military found an incidence of 1.79 per 1000 person-years.[19]

International

A study from Italy in 1996 reported a prevalence of cervical spondylotic radiculopathy as 3.5 cases per 1000 people.[20]

Mortality/Morbidity

Occasionally, an acute HNP can herniate centrally and cause a myelopathy. This can manifest as hyperreflexia, positive pathologic reflexes (such as Babinski and Hoffman signs), and sphincter disturbances. If left untreated, the effects can be irreversible.

Sex

Kelley suggests that the male-to-female incidence of cervical disc herniation is approximately 1:1.[21] Marchiori and Henderson cite women as reporting higher disability with increasing levels of DDD than men.[22]

Schoenfeld et al found that female sex was a significant risk factor for developing cervical radiculopathy.[19]

Age

HNP typically affects younger patients (ie, < 40 y). DDD, part of natural aging, typically affects older patients (ie, >40 y).

Those older than 40 years were also found to have the greatest risk of cervical radiculopathy.[19]

 

Presentation

History

Pertinent history should include the following information:

  • Information about pain onset (eg, abrupt onset suggests acute injury)

  • Time since injury

  • Mechanism of injury

  • Percentage of axial versus peripheral pain (eg, 90% neck pain vs 10% upper limb)

  • Review of systems to uncover possible systemic illness (eg, fever suggests infection, weight loss suggests malignancy), as well as any other associated symptoms, including postural changes and pain that primarily occurs at night may also indicate an etiology that warrants further investigation

Discogenic pain without nerve root involvement is typically vague, diffuse and distributed axially.

Pain referred from disc to upper limb usually is nondermatomal, and does not follow any predictable course

In a study using provocative discography for symptom mapping, Slipman et al showed that unilateral symptoms were found just as often as bilateral symptoms. Slight variation was noted for referred somatic pain originating from each disc level to the neck, shoulder, and upper thoracic region but with a great amount of overlap.[23]

Activities that increase intradiscal pressure (eg, lifting, Valsalva maneuver) intensify symptoms. Conversely, lying supine provides relief by decreasing intradiscal pressure.

Vibrational stress from driving can also exacerbate discogenic pain. Yates et al showed that vibration and shock loading provided sufficient mechanical injury to exacerbate preexisting herniations, whereas a flexed posture did not influence the distance of nucleus pulposus tracking.[24]

Depending on whether primarily motor or sensory involvement is present, radicular pain is deep, dull, and achy or sharp, burning, and electric. Such radicular pain follows a dermatomal or myotomal pattern into the upper limb. Cervical radicular pain most commonly radiates to the interscapular region, although pain can be referred to the occiput, shoulder, or arm as well. Neck pain does not necessarily accompany radiculopathy and frequently is absent.

Patients may present with distal limb numbness and proximal weakness in addition to pain. Atrophy may be present.

A study has demonstrated cervical HNP-induced thermal changes (ie, thermatomes) in specific upper extremity distributions.

Mechanical stimulation of cervical nerve roots has shown that the distribution of referred radicular symptoms (ie, dynatome) may be different from sensory deficits outlined by traditional dermatomal maps.

Physical

The patient with radicular pain also displays decreased cervical range of motion (ROM). The 3 most common maneuvers to test for cervical radiculopathy are the Spurling maneuver, shoulder abduction (relief) sign, and neck distraction test.

  • Spurling maneuver: The patient's neck is extended, laterally bent, and held down and performed in the seated position. It is designed to elicit radicular symptoms. A positive test finding is reproduction of radicular symptoms distal to the neck. A positive test finding has shown a sensitivity of 40-60% and specificity of 92-100%.[25]

  • Shoulder abduction sign: Active abduction of symptomatic arm, placing the patient’s hand on head, is performed in the seated position. Positive test finding is relief or reduction of ipsilateral cervical radicular symptoms. Sensitivity is 43-50%, and specificity is 80-100%.[25]

  • Neck distraction test: The examiner grasps the patient’s head under occiput and chin and applies an axial traction force. It is performed in the supine position with an approximate traction force of 10-15 Kg. Positive test finding is relief or reduction of cervical radicular symptoms. Sensitivity is 40-43%, and specificity is 100%.[25]

Decreased sensation to pain, light touch, or vibration may be present in the distal upper limb. Proximal limb weakness manifests when significant motor root compromise exists, but this symptom must be differentiated from pain-related weakness.

Diminished or absent reflexes corresponding to the root level may be present. Increased upper and lower limb reflexes or other upper motor neuron signs suggest myelopathy and mandate aggressive diagnostic evaluation as well as differentiation from other causes of upper motor neuron pathology

The patient with discogenic pain without nerve root involvement demonstrates decreased cervical range of motion, normal neurologic examination, and possible pain exacerbation with axial compression and pain alleviation with distraction.

Myofascial tender or trigger points, which may be primary in origin or secondary to other pathologic processes, commonly, are palpable.

Tenderness with posteroanterior mobilization may suggest disc pathology.

Causes

HNP results from repetitive cervical stress or, rarely, from a single traumatic incident. Increased risk may accrue because of vibrational stress, heavy lifting, prolonged sedentary position, whiplash accidents, and frequent acceleration/deceleration.

DDD is part of natural aging, but it is also a consequence of poor nutrition, smoking, atherosclerosis, job-related activities, and genetics.

IDD can result from cervical trauma, including whiplash, cervical flexion/rotation injury, and repetitive use.

Cervical radiculopathy results from nerve root compression secondary to herniated disc material, stenosis, or proteoglycan-mediated chemical inflammation released from discs. Smoking and certain occupational activities also predispose patients to cervical radiculopathy.

A study by Abdalkader et al found that of 100 athletes from the 2016 Olympic Summer Games in Rio de Janeiro who, during the games, underwent spinal MRI, 126 cervical discs fell into one of the Pfirrmann disc degeneration grades, I through V. That included 55 discs (43.6%) with mild degenerative changes, 17 discs (13.5%) with moderate degenerative changes, and 1 disc (0.8%) with severe degenerative changes. Cervical DDD was most prevalent among athletes who competed in athletics, boxing, or swimming.[26]

 

DDx

Diagnostic Considerations

Mechanical etiologies include the following:

  • Cervical stenosis

  • Cervical zygapophyseal (facet) arthropathy

Infectious etiologies include the following:

  • Discitis

  • Epidural, subdural, or intradural abscess

Metabolic etiologies include the following:

  • Osteomalacia

  • Parathyroid disease

Rheumatologic etiologies include the following:

  • Polymyalgia rheumatica

  • Ankylosing spondylitis

  • Reiter syndrome

  • Enteropathic arthritis

  • Diffuse idiopathic skeletal hyperostosis

Differential Diagnoses

 

Workup

Laboratory Studies

See the list below:

  • Consider performing rheumatologic workup to evaluate for possible rheumatoid arthritis, ankylosing spondylitis, Reiter syndrome, and polymyalgia rheumatica. These tests include the following:

    • Rheumatoid factor (elevated in rheumatoid arthritis)

    • HLA-B27 (positive in ankylosing spondylitis)

    • Erythrocyte sedimentation rate (elevated in polymyalgia rheumatica)

  • Consider performing infection workup to evaluate for possible discitis, epidural abscess, and vertebral osteomyelitis, including the following tests:

    • White blood cell count with differential (elevated with a left shift in bacterial infection)

    • Blood cultures (positive for the infecting organism)

    • Erythrocyte sedimentation rate (elevated in infection, but may be a nonspecific finding)

Imaging Studies

Imaging studies evaluate anatomy rather than function and are prone to false positive and negative results. For example, Boden et al's cervical MR study cites abnormalities in nearly 20% of asymptomatic subjects.[27] In a study by Kuijper et al, clinically significant root compression was found in 73% of patients on MR, whereas in 45% of patients, root compression was found that could not be clinically correlated.[28] Consequently, results of imaging studies must be interpreted within the context of each clinical case, as false-positives and false-negative MRI findings occur rather frequently.

Plain radiographs

See the list below:

  • Plain cervical spine radiographs are used to evaluate chronic degenerative changes, metastatic disease, infection, spinal deformity, and stability.

  • Cervical spine trauma films use 7 views, including anteroposterior (AP), lateral, bilateral oblique, open-mouth, flexion, and extension.

  • Flexion-extension views identify subluxations or cervical spine instability.

  • Open-mouth views evaluate the odontoid process and C1-C2 stability.

  • AP views identify tumors, osteophytes, and fractures.

  • Lateral views assess stability and spondylosis (ie, spurring, disc space narrowing).

  • Oblique views reveal DDD, as well as foraminal encroachment by uncovertebral or Z-joint osteophytes.

CT scanning

See the list below:

  • See the image below.

    Postdiscography axial computed tomography (CT) sca Postdiscography axial computed tomography (CT) scan demonstrating right posterolateral subligamentous protrusion.
  • CT scans delineate cervical spine fracture and are used extensively in trauma cases.

  • Helical or spiral CT scanning generates an infinite number of images after data acquisition, providing more information for detailed fracture evaluation than does conventional CT scanning

CT myelography

See the list below:

  • A myelogram followed by a CT scan may be obtained prior to cervical decompressive spinal cord or nerve root surgery.

  • This study evaluates the spinal canal, its relationship to the spinal cord, and nerve root impingement from disc, spur, or foraminal encroachment.

  • CT myelography, still the criterion standard, remains superior to MRI in detecting lateral and foraminal encroachment, despite greater expense and morbidity. Consequently, CT myelography is not the initial imaging study to evaluate cervical spine and is reserved for complicated cases.

MRI

See the list below:

  • MRI remains the imaging modality of choice to evaluate cervical HNP, due to its low morbidity.[5, 6]

  • Advantages include soft-tissue definition (eg, cervical discs, spinal cord), cerebrospinal fluid visualization, noninvasiveness, and lack of patient radiation exposure. (See the images below.)

    Axial magnetic resonance imaging (MRI) scan (C3-C4 Axial magnetic resonance imaging (MRI) scan (C3-C4) demonstrating left-sided posterolateral protrusion of the nucleus pulposus with compression of the cerebrospinal fluid.
    Sagittal magnetic resonance imaging (MRI) scan dem Sagittal magnetic resonance imaging (MRI) scan demonstrating cervical intervertebral disc protrusions at C3-C4 and C7-T1.
  • Newer MRI pulse sequences and higher field magnets provide faster and more detailed imaging.

  • Unfortunately, some sequences (eg, spin echo) depict pathology larger than actual size and obscure other abnormalities. Other disadvantages include expense, inability of claustrophobic patients to tolerate the procedure, dependence on patient cooperation to minimize artifact, high false-positive rate, and insensitivity compared with CT scanning in evaluating bony structures.

  • Furthermore, MRI appears inferior in differentiating cervical disc prolapse (ie, soft cervical disc) from spondylitic osteophytic compression (ie, hard cervical disc).

  • A literature review by Michelini et al indicated that upright MRI can be used to demonstrate spinal problems in symptomatic patients in whom conventional MRI produces negative results, with kinetic MRI allowing patients to be imaged in weight-bearing, flexed, and extended positions.[29]

  • Contraindications to MRI include patients with embedded metallic objects, such as pacemakers, surgical clips, spinal cord stimulators, or prosthetic heart valves that may be dislodged by MRI magnets.

Discography

See the list below:

  • Provocative cervical discography has been controversial since its introduction in 1957 by Smith. (Examples of discography appear below.)

  • This imaging procedure involves sterile-technique placement of spinal needles into cervical intervertebral discs

  • At least 2 different techniques exist for performing this procedure.

    • The paravertebral technique uses digital palpation to retract vital soft-tissue structures (eg, trachea, carotid artery, esophagus).

    • The oblique approach obviates the need for digital palpation. After spinal needles are placed within the center of the nucleus pulposus, contrast is injected to determine internal disc architecture and any pain response provoked.

  • Provocative discography is the only procedure that can determine whether a disc serves as the pain generator.

  • Discomfort and invasiveness render this procedure less desirable than cervical MRI, which provides much of the anatomical information that provocative discography does.

  • Provocative cervical discography identifies symptomatic disc(s), assisting in evaluation of patients with inconclusive diagnostic tests and presurgical fusion planning.

  • Contraindications to provocative discography include large disc herniation and midsagittal spinal canal diameter of less than 12 mm.

  • Complications include discitis, epidural abscess, quadriplegia, stroke, pneumothorax, nerve injury, and spinal cord injury. The reported rate of cervical discitis is 0.37%.

  • Discography should be performed at all accessible cervical levels, given the high frequency of multilevel symptomatic cervical discs.

  • Provocative discography may identify poor surgical candidates, thereby improving fusion outcomes.

  • A systematic review of cervical discography has found that if performed using the International Association for the Study of Pain (ISAP) criteria, cervical discography may be a useful tool for the evaluation of discogenic neck pain without disc herniation or radiculitis. Cervical discography was found to have level II-2 strength of evidence for diagnostic accuracy.[30]

  • See the images below.

    Cervical discography. Anteroposterior fluoroscopic Cervical discography. Anteroposterior fluoroscopic image.
    Cervical discography. Lateral fluoroscopic image. Cervical discography. Lateral fluoroscopic image.

Other Tests

Electrodiagnostic studies continue to be standard for evaluating neurologic function of the cervical spine. Advantages of these tests include limited expense and low morbidity.

Nerve conduction studies (NCSs) and electromyography (EMG) studies provide physiologic assessment of cervical nerve root and peripheral nerve function.

Needle EMG can detect acute, subacute, and chronic radicular features if motor nerve fiber pathology exists.

A diagnosis of radiculopathy is apparent when needle EMG reveals abnormal spontaneous potentials and/or certain changes in motor unit action potentials, in 2 or more muscles innervated by the same nerve root but by different peripheral nerves. Ideally, EMG abnormalities also should be demonstrated in the paraspinal muscles to confirm the diagnosis of radiculopathy.

In a study by Dillingham et al, cervical radiculopathy may be identified as much as 100% of the time using preset muscle screens. If positive findings are found in 1-2 muscle(s) in such screen, this result is positive.[31]

When paraspinal muscles were one of the screening muscles, 5 muscle screens identified 90-98% of radiculopathies, 6 muscle screens identified 94-99%, and 7 muscle screens identified 96-100%. When paraspinal muscles were not part of the screen, 8 distal limb muscles recognized 92-95% of radiculopathies. An 8 muscle screen that excludes the cervical paraspinal muscles is a valuable tool to help diagnose radiculopathy in those patients with prior history of cervical spinal laminectomy.

A compound motor action potential amplitude drop of 50% or more indicates significant axonal loss. This assessment is made via NCS of motor axons.

NCS/EMG is especially helpful in differentiating cervical radiculopathy from confounding neuropathic conditions (eg, ulnar nerve entrapment, carpal tunnel syndrome, peripheral neuropathy, plexopathy).

Unfortunately, cervical radiculopathies involving exclusively sensory axons (ie, without involvement of motor axons) rarely are detected by electrodiagnostic studies, which is a shortcoming of this diagnostic modality. In addition, routine motor NCSs do not evaluate the C6 and C7 nerve roots, which are most commonly involved, or the levels above.

Unlike needle EMG (which involves intramuscular evaluation and is a well-accepted diagnostic test), surface EMG generally is not considered to have an accepted role in the diagnosis of radiculopathy.

Somatosensory evoked potentials (SEPs) evaluate sensory conduction peripherally and centrally.

Lower limb SEPs involving tibial and peroneal nerves, which assess spinal cord conduction, are more sensitive in diagnosing myelopathy than are upper limb median and ulnar SEPs.

Dermatomal evoked potentials have been used to detect cervical radiculopathy but are of questionable value.

 

Treatment

Rehabilitation Program

Physical Therapy

For most cervical disc disorders, studies support conservative treatment, such as the McKenzie approach and cervicothoracic stabilization programs, combined with aerobic conditioning.

The McKenzie system identifies 3 mechanical syndromes, as follows, that cause pain and compromise function:

  • The postural syndrome provokes pain when normal soft tissues are loaded statically at end ROM; pathology need not be present. Treatment aims to correct posture.

  • The dysfunction syndrome produces pain when the patient, upon attempting full movement, mechanically deforms contracted scarred soft tissue. Consequently, therapy involves stretching and remodeling of such contracted tissue.

  • The derangement syndrome produces intermittent pain when certain movements or postures occur. Specifically, pain may become centralized or peripheralized because of theoretical activity-dependent displacement of intradiscal material. Therapy attempts to correct derangement by promoting activity that centralizes pain.

The McKenzie theory recognizes that although patients may demonstrate similar signs and symptoms, one movement (eg, cervical extension) nevertheless may help some patients and aggravate symptoms in others. Indeed, McKenzie therapy does not use only extension-biased exercise. Consequently, treatment individualization and patient education play key roles.

Cervicothoracic stabilization limits pain, maximizes function, and prevents further injury. Such stabilization includes cervical spine flexibility, postural training, and strengthening. This program emphasizes patient responsibility through active participation.

Restoring flexibility prevents further repetitive microtrauma from poor movement patterning. Pain-free ROM is determined by placing the cervical spine in positions that produce and relieve symptoms. Initially, stabilization commences within established pain-free ROM and then progresses outside this ROM as pain diminishes. Soft tissue or joint restriction inhibiting ROM is treated quickly. Anterior and posterior neck muscles are stretched. Indeed, such spine and soft-tissue mobilization, passive ROM, self-stretching, and correct posturing collectively restore ROM.

Postural training commences with the patient, supervised by a therapist, in front of a mirror. The patient performs various transfer maneuvers while maintaining a neutral spine (i.e., correct posturing), with feedback from the mirror and the therapist. Patient goals include maintenance of neutral spine and demonstrating correct posture during daily activities.

These proprioceptive skills, implemented during strengthening exercises, facilitate stable, safe, and pain-free cervical posture during strenuous activity. Indeed, cervicothoracic stabilization requires strengthening and coordination of neck, shoulder, and scapular muscles. Cervical muscles include extensors, flexors, rectus capitis anterior, rectus capitis lateralis, longissimus cervicis, and longissimus capitis. Primary thoracic stabilizers include abdominals, lumbar paraspinal extensors, and latissimus dorsi. Scapular muscles include the middle and lower trapezius, serratus anterior, and rhomboids. Chest muscles include the pectoralis major and minor. Successful stabilization also requires the training of the lumbar spine and lower extremities, which provide a foundation for the cervicothoracic spine.

Stabilization exercises proceed systematically from simple to complex. Isometric and isotonic resistive exercises employ elastic bands, weight machines, and free weights. Such conditioning distributes forces away from the cervical spine. Exercise repetition ultimately encodes an engram that commands immediate, automatic cervicothoracic stabilization during everyday activity.

Butler's therapy techniques treat radicular symptoms by mobilizing the involved nerve. First, the therapist identifies "adverse neural tension," defined as pathologic mechanical and physiologic responses elicited from a nerve when its stretch properties and ROM are evaluated. Specifically, the therapist performs neurodynamic testing to evaluate a nerve's mechanical properties (e.g., its mobilization around neighboring intervertebral discs) and physiological characteristics (e.g., its response to ischemia, inflammation). Having tested the nerve in question, the therapist may institute treatment consisting initially of passive mobilization to provide CNS input without inciting a stress response and neurogenic massage to reduce perineural swelling. Later, the therapist progresses to active neuromobilization, because, according to Butler, recovering nervous tissue (like other connective tissue) requires movement to promote healing and restoration of optimum mechanical properties.

Butler admits that limited evidence suggests that neurodynamic mobilization improves clinical outcomes. However, he believes that optimizing tissue health and cardiovascular fitness, as well as minimizing negative beliefs and environmental factors, can be beneficial.

Functional restoration programs assist patients disabled by chronic cervical pain overcome obstacles to recovery. Such obstacles include deconditioning, secondary gain, poor motivation, and psychopathology. An occupational or physical therapist, athletic trainer, or nurse instructs the patient in cervical anatomy, biomechanics, pathology, and ergonomics. Patients employ preventive measures in order to prohibit further injury during all daily activities. These medically directed interdisciplinary programs have been successful at enabling workers' compensation patients to return to work. Furthermore, Wright and colleagues reported lower rates of recurrent injury, new surgery, and need for health care services for patients with chronic cervical pain who successfully completed functional restoration.

Medical Issues/Complications

An intervertebral disc compressing the spinal cord can provoke myelopathy with associated weakness, hyperreflexia, and neurogenic bowel and bladder dysfunction. Radiculopathy can manifest significant upper limb weakness or numbness. Intractable axial or radicular pain may result from cervical disc disorders.

Surgical Intervention

Studies indicate that cervical HNP with radiculopathy can be managed conservatively. Surgery is warranted when neurogenic bowel or bladder dysfunction, deteriorating neurologic function, or intractable radicular or discogenic neck pain exists. Specifically, cervical spine surgical outcomes are most favorable for radicular pain, spinal instability, progressive myelopathy, or upper extremity weakness.[32]

Surgical outcomes for patients with myelopathy have been shown to be significantly greater with regard to motor recovery if surgical intervention is performed less than 1 year after the onset of symptoms.[8] A study by Fay et al suggested that cervical arthroplasty is about as effective in treating DDD-related cervical spondylotic myelopathy (CSM) as it is in treating DDD-related cervical radiculopathy. The study involved 151 patients with cervical DDD who underwent arthroplasty, including 72 patients with CSM and 53 with radiculopathy. The investigators found at 3-year postoperative follow-up that the clinical and radiographic outcomes in the myelopathy group were similar to those in the radiculopathy patients.[33]

The literature has demonstrated favorable cervical spine fusion outcomes for chronic discogenic axial neck pain when the presurgical evaluation has incorporated provocative cervical discography. Provocative discography identified the painful segment(s) and confirmed adjacent pain-free levels.

Fusion can increase intradiscal pressure and other stress at adjacent unfused levels, thereby accelerating postsurgical spinal degeneration.[9, 10, 11, 12, 13]

The possibility of obtaining the goals of anterior cervical decompression and fusion (ACDF) while maintaining adjacent segment motion led to the advent of total disc replacement (TDR). Currently, 3 devices for disc replacement have been approved with other trials underway. Studies have shown several advantages of TDR over ACDF, including reduction of bone graft site morbidity, adjacent segment disease, pseudarthrosis, reoperation rate, and anterior cervical plating.[34, 35]

For example, a literature review by Luo et al comparing TDR (889 patients) to ACDF (837 patients) found that in patients with one-level cervical DDD, TDR led to a significantly reduced rate of adjacent segment disease compared with ACDF, at 24-month postoperative follow-up.[36]

In another report, a nonblinded, prospective, randomized, industry-sponsored outcome study with 5-year follow-up (n=209), the rate of reoperation was less following cervical TDR (2.9%) than after conventional anterior cervical discectomy and fusion (14.5%).[37]

A prospective, randomized, multicenter, controlled clinical trial by Jackson and Johnson comparing anterior cervical discectomy and fusion with TDR, both performed at two contiguous levels, indicated that TDR produces better long-term results (7 years postsurgery) with regard to neurologic deterioration and adverse events, with range of motion preserved, less neck and arm pain experienced, and fewer subsequent surgeries required.[38]

However, disc replacement is not without complications and can lead to implant failure and bone-implant interface failure. Another documented complication is heterotrophic ossification and osteolysis, which can reduce the ROM at the replacement level. To date, no one surgical technique has been found to be statistically more favorable or superior to another.[39, 8, 40, 41]

A 2009 study sought to determine which factors are predictive of patient outcome following anterior discectomy and fusion.[42] Surgical outcomes that developed over a 2-year period were examined in patients who were treated for recalcitrant single-level subaxial radiculopathy or myelopathy. The study's results indicated that important prognostic factors include whether or not a patient is gainfully employed, has normal sensory function prior to surgery, has higher preoperative disability scores, and is involved in spine-related litigation.

A literature review by Joaquim and Riew suggested that multilevel cervical arthroplasty offers at least the same safety and efficacy as anterior cervical discectomy and fusion, with cervical motion preserved and potentially fewer reoperations required.[43]

Similarly, in a review of published and ongoing studies, Laratta et al indicated that the clinical outcomes of single-level cervical disc arthroplasty are equivalent to those of anterior cervical discectomy and fusion, while total cost and the need for secondary procedures are reduced. The investigators also reported that the efficacy of two-level cervical disc arthropathy and hybrid surgery may be the same as that of the single-level operation but that the evidence is not yet as strong.[44]

A literature review by Hu et al indicated that in the treatment of symptomatic cervical disc disease, the outcome of cervical disc arthroplasty is better than that of anterior discectomy and fusion with regard to overall and neurologic success, Neck Disability Index results, secondary procedures, functional outcomes, patient satisfaction, degeneration of the superior adjacent segment, and serious adverse events related to implants and surgery.[45]

A systematic literature review by Wullems et al indicated that percutaneous cervical nucleoplasty is a safe and effective treatment for contained herniated discs, even at long-term follow-up. The investigators cautioned, however, that the level of evidence found in their review was only moderate.[46]

Consultations

See the list below:

  • Consultation with an internal medicine specialist is indicated when neck pain suggests an underlying systemic illness (eg, malignancy, infection, metabolic bone disease).

  • Consider consultation with a rheumatologist when neck pain suggests a rheumatologic condition (eg, polymyalgia rheumatica).

  • Consultation with a surgeon for cervical disc disorders is warranted for resulting neurogenic bowel/bladder dysfunction, deteriorating neurologic status (eg, myelopathy), segmental instability, and/or intractable radicular or discogenic pain.

Other Treatment

See the list below:

  • Physical modalities should be used to reduce pain only in the acute phase. Once past the acute phase, modalities are used sparingly on an as-needed basis.

    • Superficial heat modalities relax muscle and relieve soft-tissue pain.

    • Conversely, deep-heating modalities (eg, ultrasonography) should be avoided in acute cervical radiculopathy, because they augment inflammation and, consequently, exacerbate radicular pain and nerve root injury.

  • Cervical traction may relieve radicular pain from nerve root compression. Traction does not improve soft-tissue injury pain. Hot packs, massage, and/or electrical stimulation should be applied prior to traction to relieve pain and relax muscles.

    • Traction regimens include heavy weight-intermittent or light weight-continuous. The neck is flexed 15-20º (ie, not extended) during traction. In the cervical spine, approximately 10 lb of force is necessary to counter gravity and 25 lb of force is necessary to achieve separation of the posterior vertebral segments.

    • Light weight-continuous home traction is cost effective and provides the patient with more autonomy.

    • Pneumatic traction devices afford greater patient comfort and, consequently, increased compliance.

  • A soft cervical collar is recommended only for acute soft-tissue neck injuries and for short periods of time (ie, not to exceed 3-4 days' continuous use). Risks include limiting cervical ROM and losing neck strength if the collar is worn continuously for longer periods.

    • When worn for radiculopathy caused by foraminal stenosis, the wide part of the collar is placed posteriorly and the thin part is placed anteriorly to promote neck flexion, discourage extension, and open the intervertebral foramina.

    • Collars can be worn during certain activities, such as sleeping or driving, for longer periods.

    • Although not commonly used, a Philadelphia collar can be worn at night to position the neck rigidly in flexion, thereby maintaining open foramina.

  • Spinal manipulation and mobilization may restore normal ROM and decrease pain; however, no clear therapeutic mechanism of action is known. Some believe that zygapophysial joint adjustment improves afferent signals from mechanoreceptors to peripheral and central nervous systems.

    • Normalization of afferent impulses improves muscle tone, decreases muscle guarding, and promotes more effective local tissue metabolism. These physiologic modifications subsequently improve ROM and pain reduction.

    • Studies document short-term improvement in the acutely injured patient and in those with cervicogenic headache and radiculopathy secondary to disc herniation.

    • No evidence exists that manipulation confers long-term benefit, improves chronic conditions, or alters the natural course of the disorder.

  • Cervical epidural, spinal nerve (or root), Z-joint, and sympathetic injections serve diagnostic and therapeutic roles. These procedures can be instrumental in determining the anatomic pain generator (eg, nerve root, facet) and providing aggressive, conservative treatment.

  • Therapeutic cervical epidural injections treat radicular pain, although some literature has demonstrated reduced axial pain as well. (See the images below.)

    Right C7 cervical transforaminal epidural steroid Right C7 cervical transforaminal epidural steroid injection demonstrating epidural and radicular spread of radiologic contrast dye.
    Cervical epidural steroid injection at the C7-T1 i Cervical epidural steroid injection at the C7-T1 interlaminar space.

    See the list below:

    • An anesthetic and corticosteroid mixture may be injected into the epidural space (interlaminar) or along the nerve root (transforaminal) after precise radiologic, contrast-enhanced fluoroscopic localization.[7]

    • The anesthetic can relieve sympathetically mediated pain.

    • The corticosteroid provides long-term relief if pain results from an intense inflammatory component.

    • Such injections provide a pain-free window of opportunity for more aggressive physical therapy.

  • Diagnostic selective spinal nerve or ventral ramus blocks inject a small anesthetic volume extraforaminally at a single spinal segment level (eg, C5 versus C6); consequently, they are more precise than the "gunshot" interlaminar approach in identifying the symptomatic nerve.

    • Precise symptomatic nerve identification permits the physician to design a more focused treatment protocol.

    • Patients record pain changes in a pain diary following the injection, to confirm diagnostic accuracy.

    • A double injection paradigm previously reported in the literature for facet injections can provide information to the physician for use in determining a diagnosis of radicular pain and to help confirm the symptomatic nerve level. This paradigm identifies patients who have tested false-positive or may have a tendency to respond to a placebo, by determining whether, on separate injection days, they received short-term relief with a short-acting anesthetic (eg, lidocaine) and long-term relief with a long-acting anesthetic (eg, bupivacaine).

  • Adverse effects include those from anesthesia, corticosteroids, and radiologic contrast dye.

    • Blood clotting parameters should be drawn prior to injection in patients with suspected bleeding diathesis. Indeed, spinal cord compression could result if bleeding occurs in the presence of relative spinal stenosis (ie, midsagittal diameter less than 12 mm) in which little room exists to accommodate an epidural hematoma.

    • Nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, should be discontinued prior to the procedure in accordance with their half-life and hematologic profile.

    • Other potential risks include seizure, vertebral artery spasm, infection, temporary quadriparesis from anesthetic, and respiratory arrest.

    • One study, however, suggested that selective cervical nerve blocks carry low morbidity when performed under contrast-enhanced fluoroscopic guidance.

    • In any event, proper patient monitoring and emergency equipment always should be present.

  • Reports of serious CNS complications, including spinal cord injuries and strokes, following cervical transforaminal steroid injections have gained the attention of many practitioners. The mechanism of the injury is believed to be related to the introduction of particulate matter within the corticosteroid preparations, causing occlusion of a vessel.

    • Hodges and colleagues described 2 case reports in which intrinsic spinal cord damage resulted from cervical epidural steroid injection despite fluoroscopic guidance; the patients, because of intravenous sedation, were unable to perceive and report pain and paresthesias from needle-induced spinal cord trauma during the procedure.[47]

    • Furman et al demonstrated a relatively high incidence of entering the intravascular space with transforaminal epidural steroid injections.[48] They also showed that attempting to use a flash of blood in the needle hub to predict intravascular compromise was 97% specific but only 45.9% sensitive. This article underscored the importance of using fluoroscopy and contrast dye to ensure proper placement of the therapeutic agents. Using a flash of blood in the hub without fluoroscopy cannot reliably predict intravascular compromise.

    • Brouwers et al reported a fatal case of spinal cord infarction following a cervical transforaminal steroid injection.[49]

    • Baker et al demonstrated that a radicular artery supplying the cervical spinal cord can be infiltrated by a transforaminal epidural steroid injection.[50] In this report, prior to steroid injection for a left C6-C7, contrast was administered. Using digital subtraction technique, it was clear that a radicular artery filled with contrast; the procedure was aborted without adverse effects. This report revealed a potential access point for an injection-related spinal cord infarction.

    • The potentially catastrophic complications that can follow a cervical transforaminal epidural steroid injection cannot be underestimated. While these procedures are perceived as posing less of a risk than surgery, they still carry substantial hazards. They should be performed by skilled practitioners and under fluoroscopic guidance. Baker et al further suggest the use of digital subtraction, because intravascular compromise may be missed on routine spot films.[50]

Emerging concepts

Biologic therapies for symptomatic intervertebral discs offer a novel approach to treatment. By effectively targeting the primary pain generator (ie, the intervertebral cervical disc) clinicians may treat the source of the pain and not just the sequelae of the degenerative cascade (ie, radiculopathy or discogenic pain). These treatments may also offer alternatives to conservative or surgical measures. Because these agents can be injected with contrast-enhanced fluoroscopic guidance, they may result in reduced morbidity to the patient.

To date several biologic compounds are under clinical and laboratory investigations. These include:

  • Growth factors, including tumor growth factor (TGF)-beta, bone morphogenetic proteins (BMP)-2, BMP -7, BMP-14: Infusion of growth factors has been shown in animal models to cause an anabolic response with increases in disc height and proteoglycan synthesis. BMP-7 and BMP-14 are currently in phase I clinical trials.

  • Gene transfer: The gene encoding the growth factor or therapeutic protein would be implanted into the disc to produce the protein in situ. Preliminary results have been promising, showing increased proteoglycan synthesis when injected into human disc cells in vitro.[51]

  • Cell therapy, including autologous disc cells, articular chondrocytes, and mesenchymal stem cells: These substances can be transplanted into vertebral discs, slowing disc degeneration. Several in vivo animal studies have shown that mesenchymal stem cells slow the progression of disc degeneration as well as regenerate the matrix.[52] Numerous other studies have demonstrated the ability of injected cells to survive, differentiate toward disc cells, and produce matrix components, including collagen II and proteoglycans.[51, 52]

  • Tissue engineering: Therapeutic agents, when injected into the intervertebral disc function to alter both biochemical and biomechanical stressors. At this time, a US Food and Drug Administration (FDA)-approved trial is underway evaluating the efficacy and safety of a fibrin sealant derived from human plasma derivatives (fibrinogen and thrombin). This substance (fibrinogen and thrombin) has been shown in animal studies to inhibit nucleus pulposus fibrosis, promote recovery of proteoglycan content, and facilitate repair of the annulus. A pilot study showed reduction in pain and disability at 1 and 2 years after a single injection.[53, 54]

In the early stage of disc degeneration, protein factors such as growth factors and proteinase inhibitors may be effective. In the intermediate stage of degeneration, cell or gene therapy may be required. In the advanced stages of disc degeneration, tissue engineering approaches will be needed.

Biologic substances offer a great potential for therapy of the degenerative disc. There have been numerous studies indicating in vitro and in vivo success in rebuilding or repairing the structure of the intervertebral disc. With these rapid advancements, these interventions may soon be available in clinical practice. What remains to be answered is if these biomechanical and biochemical alterations will offer clinically relevant findings. Whether structural changes to the disc will lead to decreased pain and increased function of the patient is unclear.

 

Medication

Medication Summary

NSAIDs are first-line pharmacologic intervention for most cervical conditions. NSAIDs reduce pain at low doses and decrease inflammation at high doses. Patients require a therapeutic NSAID plasma level to achieve an anti-inflammatory effect. NSAIDs with once-a-day dosing improve compliance and increase the probability of achieving therapeutic levels. Controlling inflammation is paramount when treating cervical radiculopathy.

Aspirin rarely is recommended, because it binds irreversibly to cyclooxygenase (COX) and incites gastritis, requiring large doses to reach anti-inflammatory effect. Traditional NSAIDs provoke multiorgan toxicity, including peptic ulcer disease, renal insufficiency, and hepatic dysfunction. COX isomer type 2 (COX-2) NSAID inhibitors confer the same analgesic/anti-inflammatory benefits without multiorgan toxicity. All NSAIDs have a dose-related ceiling point for analgesia above which higher doses fail to provide additional pain relief. The same precautions should be observed with COX-2 NSAIDs, despite their reduced risk of organ toxicity.

Use muscle relaxants to potentiate the NSAID analgesic effect and not necessarily to control muscle spasm. Muscle relaxants primarily sedate by relaxing muscle with subsequent relaxation of the patient.

Oral corticosteroids treat inflammatory cervical radiculopathy. No documented case of avascular necrosis exists in the literature when the total prednisone dose or corticosteroid equivalent stayed under 550 mg. Some providers use a methylprednisolone dose pack (tapers from 24 to 0 mg over 7 days); however, concern exists regarding adequate dosing to treat radiculopathy. A prednisone dose schedule outlined below stays within the 550-mg limiting amount.

Tricyclic antidepressants (TCAs) decrease pain and reduce nonrestorative sleep. Side effects include dry mouth, constipation, and weight gain. Selective serotonin reuptake inhibitors (SSRIs), despite lacking side effects associated with TCAs, are inferior to TCAs in treating diabetic peripheral neuropathic pain, and their efficacy in relieving neck and back pain compared with that of other antidepressants remains unknown. Additional medications include membrane-stabilizing agents (eg, gabapentin, carbamazepine). Gabapentin has demonstrated efficacy in treating diabetic peripheral neuropathic pain. Pregabalin (Lyrica) has been used as an off-label treatment for radicular pain with some efficacy. Other analgesics (acetaminophen, tramadol) provide pain relief without inflammation control.

Opioids may be prescribed orally, transdermally, rectally, or sublingually on a scheduled basis. Patients on opioids should sign a medication agreement restricting them to a single physician and pharmacy, scheduled medication use, no unscheduled refills, and no sharing or selling medication. Patients with a previous history of alcoholism or other addiction who are prescribed opioids long term are at risk for dependence. Therefore, consider recommending cotreatment of these patients with a psychologist or other addiction specialist.

Lastly, many short-acting opioid preparations contain acetaminophen, which may be toxic in doses above 3 g per day. Consequently, patients should be counseled to avoid toxicity by avoiding other pharmaceuticals containing acetaminophen.

Corticosteroids

Class Summary

Used to treat inflammatory cervical radiculopathy. Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Prednisone (Sterapred)

Decreases inflammation by inhibiting polymorphonuclear leukocyte and fibroblast migration, stabilizing lysosomes, and decreasing capillary permeability.

Methylprednisolone dose pack (Solu-Medrol, Medrol, Depo-Medrol)

Decreases inflammation by inhibiting polymorphonuclear leukocyte and fibroblast migration, stabilizing lysosomes, and decreasing capillary permeability.

Anticonvulsants

Class Summary

Use of certain anti-epileptic drugs, such as the GABA analogue Neurontin (gabapentin), has proven helpful in some cases of neuropathic pain. Have central and peripheral anticholinergic effects, as well as sedative effects, and block the active reuptake of norepinephrine and serotonin. The multifactorial mechanism of analgesia could include improved sleep, altered perception of pain, and increase in pain threshold.

Gabapentin (Neurontin)

Has anticonvulsant properties and antineuralgic effects; however, exact mechanism of action is unknown. Structurally related to GABA but does not interact with GABA receptors.

Carbamazepine (Tegretol)

May reduce polysynaptic responses and block posttetanic potentiation. Inhibits nerve impulses by decreasing influx of sodium ions into cell membrane.

Pregabalin

Structural derivative of GABA. Mechanism of action unknown. Binds with high affinity to alpha2 -delta site (a calcium channel subunit). In vitro, reduces calcium-dependent release of several neurotransmitters, possibly by modulating calcium channel function. FDA approved for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia and as adjunctive therapy in partial-onset seizures.

Analgesics

Class Summary

Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who experience pain.

Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin)

DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.

Tramadol (Ultram)

Inhibits ascending pain pathways, altering perception of and response to pain. Inhibits also reuptake of norepinephrine and serotonin.

 

Follow-up

Further Outpatient Care

See the list below:

  • Most cervical spine disorders are treated successfully with conservative measures on an outpatient basis. Refer to the Physical Therapy and Other Treatment sections for discussion.

Deterrence

See the list below:

  • Maintaining proper cervical posture and cervicothoracic strength and flexibility, avoiding cervical trauma and repetitive cervical stress, and adhering to a healthy lifestyle that advocates proper nutrition, physical activity, and smoking cessation may help to prevent cervical disc disease.

Complications

See the list below:

  • Complications of cervical spine disorders may include the following:

    • Intractable axial or radicular pain

    • Myelopathy with associated weakness, hyperreflexia, and neurogenic bowel/bladder dysfunction

  • Radiculopathy with associated upper extremity weakness and numbness

Patient Education

See the list below:

  • Educate patients to avoid aggravating factors (eg, vibrational stress from driving, cervical flexion, Valsalva maneuvers) that may exacerbate discogenic pain.

  • Additionally, instruct patients on correct posture and a home exercise program (eg, cervicothoracic stabilization, aerobic conditioning).

  • For excellent patient education resources, see eMedicineHealth's patient education articles Shoulder and Neck Pain, Neck Strain, Whiplash, Chronic Pain, and Pain Medications.

 

Questions & Answers

Overview

What is cervical disc disease?

How is cervical disc disease diagnosed?

How is cervical disc disease treated?

What is the pathophysiology of cervical disc disease?

What is the prevalence of cervical disc disease in the US?

What is the global prevalence of cervical disc disease?

What is the morbidity of cervical disc disease?

What are the sexual predilections of cervical disc disease?

Which age groups have the highest prevalence of cervical disc disease?

Presentation

What is the focus of clinical history for cervical disc disease?

Which clinical history findings are characteristic of cervical disc disease?

What are most common maneuvers to test for cervical radiculopathy in cervical disc disease?

Which physical findings are characteristic of cervical disc disease?

What causes cervical disc disease?

DDX

What are the mechanical etiologies of cervical disc disease?

What are the infectious etiologies of cervical disc disease?

What are the metabolic etiologies of cervical disc disease?

What are the rheumatologic etiologies of cervical disc disease?

What are the differential diagnoses for Cervical Disc Disease?

Workup

What is the role of lab testing in the diagnosis of cervical disc disease?

What is the role of imaging studies in the diagnosis of cervical disc disease?

What is the role of radiography in the diagnosis of cervical disc disease?

What is the role of CT scanning in the diagnosis of cervical disc disease?

What is the role of CT myelography in the diagnosis of cervical disc disease?

What is the role of MRI in the diagnosis of cervical disc disease?

What is the role of discography in the diagnosis of cervical disc disease?

What is the role of electrodiagnostic studies in the evaluation of cervical disc disease?

Treatment

How is cervical disc disease treated?

What are the possible complications of cervical disc disease?

What is the role of surgery in the treatment of cervical disc disease?

Which specialist consultations are beneficial to patients with cervical disc disease?

Which physical modalities are used in the treatment of cervical disc disease?

What is the role of cervical traction in the treatment of cervical disc disease?

What is the role of a soft cervical collar in the treatment of cervical disc disease?

What is the role of spinal manipulation and mobilization in the treatment of cervical disc disease?

What is the role of cervical epidural, spinal nerve (or root), Z-joint, and sympathetic injections in the treatment of cervical disc disease?

What is the role of epidural injections in the treatment of cervical disc disease?

What are the possible adverse effects of cervical disc disease?

What complications are indicated in the central nervous system relative to cervical disc disease?

What is the role of biologic therapies for symptomatic intervertebral discs in the treatment of cervical disc disease?

Medications

Which medications are indicated in the treatment of cervical disc disease?

Which medications in the drug class Analgesics are used in the treatment of Cervical Disc Disease?

Which medications in the drug class Anticonvulsants are used in the treatment of Cervical Disc Disease?

Which medications in the drug class Corticosteroids are used in the treatment of Cervical Disc Disease?

Follow-up

What is included in long-term monitoring of cervical disc disease?

How is cervical disc disease prevented?

What are the potential complications of epidural injections for the treatment of cervical disc disease?

What is included in patient education about cervical disc disease?