eMedicine Specialties > Physical Medicine and Rehabilitation > Cervical Spine Disorders

Cervical Disc Disease: Treatment & Medication

Author: Michael B Furman, MD, MS, Physiatrist, Interventional Spine Care Specialist, Electrodiagnostics, Orthopedic and Spine Specialists
Coauthor(s): Jeremy Simon, MD, Attending Physician, Department of Physical Medicine, The Rothman Institute; Kirk M Puttlitz, MD, Consulting Staff, Pain Management and Physical Medicine, Arizona Neurological Institute; Frank John English Falco, MD, Physiatrist, MidAtlantic Spine
Contributor Information and Disclosures

Updated: Apr 6, 2009

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 follow, 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 (ie, 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 (eg, its mobilization around neighboring intervertebral discs) and physiological characteristics (eg, 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. The literature has demonstrated favorable cervical spine fusion outcomes for chronic discogenic axial neck pain when the presurgical evaluation 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.12,13,14

A 2009 study sought to determine which factors are predictive of patient outcome following anterior discectomy and fusion.15 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.

Consultations

  • 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

  • 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 15-20 º (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. (See images below and Images 4-5.) These procedures can be instrumental in determining the anatomic pain generator (eg, nerve root, facet) and providing aggressive, conservative treatment.
Right C7 cervical transforaminal epidural steroid...

Right C7 cervical transforaminal epidural steroid injection demonstrating epidural and radicular spread of radiologic contrast dye.

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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 ...

Cervical epidural steroid injection at the C7-T1 interlaminar space.

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Cervical epidural steroid injection at the C7-T1 ...

Cervical epidural steroid injection at the C7-T1 interlaminar space.

  • Therapeutic cervical epidural injections treat radicular pain, although some literature has demonstrated reduced axial pain as well.
    • 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.16
    • 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 "gun shot" 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.17
    • Furman et al demonstrated a relatively high incidence of entering the intravascular space with transforaminal epidural steroid injections.18 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.19
    • Baker et al demonstrated that a radicular artery supplying the cervical spinal cord can be infiltrated by a transforaminal epidural steroid injection.20 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.20

Medication

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. 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 contract 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

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 (Deltasone, Orasone Sterapred)

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

Adult

70 mg/d PO initial; subsequently decrease 10 mg/d for total course of 200-300 mg

Pediatric

Not established

Activity may increase with estrogens, salicylates, oral contraceptives, ketoconazole, indomethacin, and macrolide antibiotics; decreased action with barbiturates, cholestyramine, ephedrine, phenytoin, colestipol, theophylline, rifampin; increased side effects with salicylates, cyclosporin, digitalis, alcohol, indomethacin, diuretics, and amphotericin B; decreased effects of antidiabetics with neostigmine, vaccines, somatrem, anticoagulants, anticonvulsants, ambenonium chloride, isoniazid, toxoids, and anticholinesterases

Documented hypersensitivity, psychosis, idiopathic thrombocytopenia, acute glomerulonephritis, fungal infections, amebiasis, nonasthmatic bronchial disease, TB, and AIDS

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use


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

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

Adult

24 mg PO initially; taper to discontinue over 7 d

Pediatric

Not established

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics

Documented hypersensitivity, psychosis, idiopathic thrombocytopenia, acute glomerulonephritis, fungal infections, amebiasis, nonasthmatic bronchial disease, TB, and AIDS

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use

Anticonvulsants

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.

Adult

900-1800 mg/d PO in 3 divided doses; may start 300 mg the first day, 300 mg bid on second day, and 300 mg tid on third day
May increase up to 1800 mg/d by adding 300 mg on following days
Can titrate to effect over several days (300 mg on day 1, 300 mg bid on day 2, and 300 mg tid on day 3)

Pediatric

Not established

Antacids may reduce bioavailability of gabapentin significantly (administer at least 2 h following antacids); may increase norethindrone levels significantly

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Renal disease, hepatic disease, breastfeeding, and advanced age; caution in severe renal disease


Carbamazepine (Tegretol)

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

Adult

100 mg PO bid with meals
May increase 100 mg PO q12h until pain diminishes; not to exceed 1.2 g/d
Maintenance dose 200-400 mg PO bid

Pediatric

Not established

Serum levels may increase significantly within 30 d of danazol coadministration (avoid whenever possible); do not coadminister with MAOIs; cimetidine may increase toxicity especially if taken in first 4 wk of therapy; carbamazepine may decrease primidone and phenobarbital levels (their coadministration may increase carbamazepine levels)

Documented hypersensitivity, bone marrow depression, and concomitant MAOI use

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Do not use to relief minor aches or pains; caution with increased intraocular pressure; obtain CBC counts and serum-iron baseline prior to treatment, during first 2 mo, and yearly or every other year thereafter; can cause drowsiness, dizziness, and blurred vision; caution while driving or performing other tasks requiring alertness

Analgesics

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.

Adult

325-650 mg PO q4h prn; not to exceed 4 g/d

Pediatric

10-15 mg/kg PO q4h

Increases effects of chloramphenicol; effects of acetaminophen increase with caffeine and diflunisal; effects of acetaminophen decrease with colestipol, anticholinergics, oral contraceptives, and cholestyramine; acetaminophen increases potential for hepatotoxicity with alcohol; severe hypothermia may occur with phenothiazines

Documented hypersensitivity; intolerance to saccharin, table sugar, alcohol, or tartrazine (yellow dye #4)

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatotoxicity possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; APAP is contained in many OTC products and combined use with these products may result in cumulative APAP doses exceeding recommended maximum dose


Tramadol (Ultram)

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

Adult

50-100 mg PO q4-6h prn; not to exceed 400 mg/d

Pediatric

Not established

Tramadol levels decrease with carbamazepine; coadministration with opiates, hypnotics, sedatives, and alcohol increases CNS depression

Documented hypersensitivity; acute CNS depressant medication intoxication

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Can cause dizziness, nausea, constipation, sweating, and pruritus; additive sedation with alcohol and TCAs; abrupt discontinuation can precipitate opioid withdrawal symptoms; adjust dose in liver disease, myxedema, hypothyroidism, hypoadrenalism; pregnancy, breastfeeding; seizure; development of tolerance or dependency with extended use; caution with norepinephrine and serotonin reuptake inhibitors, and MAOIs

More on Cervical Disc Disease

Overview: Cervical Disc Disease
Differential Diagnoses & Workup: Cervical Disc Disease
Treatment & Medication: Cervical Disc Disease
Follow-up: Cervical Disc Disease
Multimedia: Cervical Disc Disease
References
Further Reading
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Keywords

cervical disc disease, spine, cervical spine, herniated disc, spinal stenosis, back surgery, degenerative disc disease, disc disease, radiculopathy, cervical spondylosis, disc herniation, back disc, cervical disc, disc surgery, spinal disc, disc pain, disk disease, degenerative spine, cervical disk, herniated discs, spine disc, nucleus pulposus, degenerative disk disease, cervical spinal stenosis, cervical spine surgery, annular tear, DDD, disc degeneration, disc extrusion, disc herniation, disc protrusion, disc sequestration, discogenic pain, herniated nucleus pulposus, HNP, inflammatory radiculopathy, internal disc disruption, IDD, intervertebral disc herniation, radicular pain, radiculitis, degenerative annular tears, cervical radiculopathy, nerve root injury, disc stenosis, myofascial pain, cervical disc disorder, central cord syndrome, CCS, spondylosis, neck pain, shoulder pain, Brown-Séquard syndrome, chemical radiculitis, vertebral sclerosis, osteophytic formation, whiplash, dynatome, Spurling maneuver, abduction sign, repetitive cervical stress, cervical flexion injury, cervical rotation injury

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Contributor Information and Disclosures

Author

Michael B Furman, MD, MS, Physiatrist, Interventional Spine Care Specialist, Electrodiagnostics, Orthopedic and Spine Specialists
Michael B Furman, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, International Spine Intervention Society, North American Spine Society, Pennsylvania Medical Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: pfizer Honoraria Speaking and teaching

Coauthor(s)

Jeremy Simon, MD, Attending Physician, Department of Physical Medicine, The Rothman Institute
Jeremy Simon, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, International Spine Intervention Society, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Kirk M Puttlitz, MD, Consulting Staff, Pain Management and Physical Medicine, Arizona Neurological Institute
Kirk M Puttlitz, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Phi Beta Kappa
Disclosure: Nothing to disclose.

Frank John English Falco, MD, Physiatrist, MidAtlantic Spine
Frank John English Falco, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, American Society of Regional Anesthesia and Pain Medicine, Association of Academic Physiatrists, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: St. Jude's Medical Consulting fee Speaking and teaching

Medical Editor

Everett C Hills, MD, MS, Medical Director, Penn State Hershey Rehabilitation Hospital, Assistant Professor of Orthopaedics and Rehabilitation, Assistant Professor of Neurology, Penn State Milton S. Hershey Medical Center and Penn State University College of Medicine
Everett C Hills, MD, MS is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Congress of Rehabilitation Medicine, American Medical Association, American Society of Neurorehabilitation, Association of Academic Physiatrists, and Pennsylvania Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

 
 
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