Updated: Apr 24, 2009
Cervical spondylosis is a chronic degenerative condition of the cervical spine that affects the vertebral bodies and intervertebral disks of the neck (in the form of, for example, disk herniation and spur formation), as well as the contents of the spinal canal (nerve roots and/or spinal cord). Some authors also include the degenerative changes in the facet joints, longitudinal ligaments, and ligamentum flavum.
Spondylosis progresses with age and often develops at multiple interspaces. Chronic cervical degeneration is the most common cause of progressive spinal cord and nerve root compression. Spondylotic changes can result in stenosis of the spinal canal, lateral recess, and foramina. Spinal canal stenosis can lead to myelopathy, whereas the latter 2 can cause radiculopathy. (See image below and Image 3)
Intervertebral disks lose hydration and elasticity with age, and these losses lead to cracks and fissures. The surrounding ligaments also lose their elastic properties and develop traction spurs. The disk subsequently collapses as a result of biomechanical incompetence, causing the annulus to bulge outward. As the disk space narrows, the annulus bulges, and the facets override. This change, in turn, increases motion at that spinal segment and further hastens the damage to the disk. Annulus fissures and herniation may occur. Acute disk herniation may complicate chronic spondylotic changes.
As the annulus bulges, the cross-sectional area of the canal is narrowed. This effect may be accentuated by hypertrophy of the facet joints (posteriorly) and of the ligamentum flavum, which becomes thick with age. Neck extension causes the ligaments to fold inward, reducing the anteroposterior (AP) diameter of the spinal canal.
As disk degeneration occurs, the uncinate process overrides and hypertrophies, compromising the ventrolateral portion of the foramen. Likewise, facet hypertrophy decreases the dorsolateral aspect of the foramen. This change contributes to the radiculopathy that is associated with cervical spondylosis. Marginal osteophytes begin to develop. Additional stresses, such as trauma or long-term heavy use, may exacerbate this process. These osteophytes stabilize the vertebral bodies adjacent to the level of the degenerating disk and increase the weight-bearing surface of the vertebral endplates. (See images below and Images 1-2, 4-5.) The result is decreased effective force on each of these structures.
The blood supply of the spinal cord is an important anatomic factor in the pathophysiology. Radicular arteries in the dural sleeves tolerate compression and repetitive minor trauma poorly. The spinal cord and canal size also are factors. A congenitally narrow canal does not necessarily predispose a person to myelopathy, but symptomatic disease rarely develops in individuals with a canal that is larger than 13 mm.
Cervical spondylosis is a common condition that is estimated to account for 2% of all hospital admissions. It is the most frequent cause of spinal cord dysfunction in patients older than 55 years. On the basis of radiologic findings, 90% of men older than 50 years and 90% of women older than 60 years have evidence of degenerative changes in the cervical spine.
Evidence from a 2009 report indicated that cervical spondylosis with myelopathy was the most common primary diagnosis (36%) among elderly US patients admitted to the hospital for surgical treatment of a degenerative cervical spine between 1992 and 2005.4 The study, which looked at 156,820 hospital admissions for elderly Medicare beneficiaries, also determined that fusion was the most common procedure (70%) performed in these patients for cervical spine degeneration, with 58% of the fusions being anterior.
Investigators in a study involving Ghanaians reported, "out of 225 patients who carried loads on their head, 143 (63.6%) had cervical spondylosis, and of the 80 people who did not carry load on their head, 29 (36%) had cervical spondylosis."
No apparent correlation between race and cervical spondylosis exists.
Both sexes are affected equally. Cervical spondylosis usually starts earlier in men than in women.
Common clinical syndromes associated with cervical spondylosis include the following:
Findings at physical examination may include the following:
| Adhesive Capsulitis | Diabetic Neuropathy |
| Brown-Sequard Syndrome | Multiple Sclerosis |
| Carpal Tunnel Syndrome | Myofascial Pain |
| Central Cord Syndrome | Neoplastic Brachial Plexopathy |
| Cervical Disc Disease | Osteoporosis and Spinal Cord Injury |
| Cervical Myofascial Pain | Radiation-Induced Brachial Plexopathy |
| Cervical Sprain and Strain | Rheumatoid Arthritis |
| Chronic Pain Syndrome | Traumatic Brachial Plexopathy |
OPLL
Occipital neuralgia as a result of spondylotic changes at C1-C2
Shoulder problems
Primary spinal cord tumors
Syringomyelia
Extramedullary lesions (tumors, thoracic disk herniation)
Hereditary spastic paraplegia
Normal pressure hydrocephalus
Spinal cord infarction
Spinal sepsis
Whiplash syndrome (hyperextension-hyperflexion injury)
Pancoast tumors
Double crush syndrome (coexistence of a radiculopathy and peripheral nerve compression in the carpal or cubital tunnel)
Thinning and fragmentation of the articular cartilage may be observed. The normal smooth, white articular surface becomes irregular and yellow. Continued loss of articular cartilage leads to exposure of areas of subchondral bone, which appear as shiny foci on the articular surface (eburnation). Fibrosis, increased bone formation, and cystic changes frequently occur in the underlying bone. Loss of articular cartilage stimulates new bone formation, usually in the form of nodules (osteophytes) at the bone edges.
The recreational therapist can use recreational and community activity to accomplish the following:
Cervical spondylosis may result in complications (see Mortality/Morbidity), including the following:
Consultations with the following specialists may be helpful:
The goal of pharmacotherapy is to reduce morbidity and prevent complications.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are used in the treatment of cervical spondylosis. If one class seems to be ineffective after a 2-week trial, a formulation from another class may be tried. The most commonly used NSAIDs are ibuprofen, acetylsalicylic acid, naproxen, indomethacin, mefenamic acid, and piroxicam.
Relieves mild to moderately severe pain and inhibits inflammatory reactions, probably by decreasing the activity of the enzyme cyclooxygenase, thus inhibiting prostaglandin synthesis.
250-500 mg PO bid; may increase to 1.5 g/d for limited periods; generally, not to exceed 1.25 g/d
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Co-administration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with pre-existing renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug
NSAID from propionic acid derivatives group. Effective inhibitor of cyclo-oxygenase, which is responsible for biosynthesis of prostaglandins. Rapidly absorbed after oral administration. Half-life in plasma is about 2 h. Ibuprofen passes slowly into the synovial spaces and may remain there in higher concentration as the concentration in plasma declines. Excretion is rapid and complete (mainly excreted in urine as metabolites or conjugates).
1200-1800 mg PO divided q4-6h; not to exceed 3200 mg in divided doses
<6 years: Not established
6-12 years: 4-10 mg/kg/dose PO tid/qid
>12 years: Administer as in adults
May reduce diuretic and natriuretic effects of furosemide; may decrease antihypertensive effects of such agents as thiazide diuretics, beta-adrenergic antagonists, and inhibitors of angiotensin-converting enzyme; co-administration with anticoagulants may increase PT (monitor and watch for signs of bleeding); may increase serum lithium levels; may increase risk of methotrexate toxicity; probenecid may increase toxicity of NSAIDs
Documented hypersensitivity to ibuprofen, other NSAIDs, or aspirin; avoid in peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, and high risk of bleeding
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; discontinue if clinical symptoms and signs of liver disease develop or if abnormal liver test results persist; caution in anticoagulation abnormalities or during anticoagulant therapy; GI adverse effects may occur; common adverse side effects include thrombocytopenia, skin rashes, headache, dizziness, and blurred vision, as well as (in a few cases) toxic amblyopia
Rapidly absorbed; metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation. Indomethacin inhibits prostaglandin synthesis.
25-50 mg PO bid/tid
75 mg SR PO bid; not to exceed 200 mg/d
1-2 mg/kg/d divided PO bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d
Co-administration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; GI bleeding or renal insufficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with pre-existing renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if there is persistent leukopenia, granulocytopenia, or thrombocytopenia)
Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
500 mg PO initially, followed by 250 mg q4h prn
<12 years: Not established
>12 years: Administer as in adults
Co-administration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, and high risk of bleeding
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
May have adverse effects in fetus; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
Decreases the activity of cyclooxygenase, which in turn inhibits prostaglandin synthesis; piroxicam's effects decrease the formation of inflammatory mediators.
10-20 mg/d PO qd
0.2-0.3 mg/kg/d PO qd; not to exceed 15 mg/d
Co-administration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; active GI bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with pre-existing renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if there is persistent leukopenia, granulocytopenia, or thrombocytopenia)
Treats mild to moderately severe pain and headache. The drug inhibits prostaglandin synthesis, which prevents the formation of platelet-aggregating thromboxane A2; aspirin acts on the heat-regulating center of the hypothalamus and vasodilates peripheral vessels to reduce fever. By inhibiting prostaglandin synthesis, aspirin may also inhibit key steps in the inflammation process.
Treatment is administered for at least 8 wk.
90-100 mg/kg/d PO divided q6-8h for 2 wk initially, then 60-70 mg/kg/d for 6 wk; not to exceed 3.6-5.4 g/d
60-90 mg/kg/d PO divided q6-8h for 8 wk; adjust according to serum levels
Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with co-administration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs; simultaneous administration of other NSAIDs may decrease the cardioprotective and stroke-preventive effects
Documented hypersensitivity; liver damage, hypoprothrombinemia, vitamin K deficiency, bleeding disorders, asthma; due to association of aspirin with Reye syndrome, do not use in children (<16 y) with viral infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants
Corticosteroids have potent anti-inflammatory properties. These medications can be given orally or as a single intramuscular (IM) injection.
Glucocorticoid steroid used to treat a variety of inflammatory conditions. Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Dosages may be adjusted for individual sensitivities and associated medical conditions.
<60 years: 5-200 mg/d PO qd or in divided doses; not to exceed 200 mg/d; adjust to lowest effective dose once desired response achieved
>60 years: Reduced dose may be necessary
4-5 mg/m2/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2 wk as symptoms resolve
Co-administration with estrogens may decrease clearance; when used with digoxin, digitalis toxicity secondary to hypokalemia may increase; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with co-administration of diuretics
Documented hypersensitivity; viral infection, peptic ulcer disease, hepatic dysfunction, connective tissue infections, and fungal or tubercular infections; diabetes; recent abdominal surgery; congestive heart failure; hypertension; myasthenia gravis; current or recent illness with chicken pox or measles
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Take qd or qod doses in the morning; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, pancreatitis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use; take with food;
adverse effects include dizziness (intensified by alcohol consumption), increased appetite, insomnia, indigestion, restlessness, confusion, convulsions, reddish-purple lines on skin, muscle cramps, blood in stool, skin rash, swollen legs or feet, mood swings, weight gain, weakness or fatigue, hives, thirst, and frequent urination; overdose symptoms include convulsions, headache, hallucinations, and heart failure
Muscle relaxants are used to treat muscle spasm, which may play a role in patient discomfort.
Skeletal muscle relaxant used in conjunction with other therapies to treat pain and discomfort associated with musculoskeletal conditions. Reduces nerve impulse transmission from spinal cord to skeletal muscle.
<60 years: 1.5 g PO qid for first 48-72 h; not to exceed 6 or 8 g/d in severe conditions; usual maintenance dose is 750 mg to 1 g PO qid or 1.5 g tid
>60 years: Reduced dose may be necessary
Maintenance dose: 800 mg (2 tabs) PO qid
<12 years: Not established
>12 years: Administer as in adults
Increases toxicity of CNS depressants
Documented hypersensitivity; renal impairment
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in history of seizures; take with food; adverse effects include lightheadedness, blurred vision, dizziness, drowsiness (patient should avoid performing dangerous tasks while on medication), itching, conjunctivitis, fever, headache, hives, nasal congestion, nausea or vomiting, rash, urticaria (ie, itching attack, possibly as a result of drug sensitivity), extreme weakness, temporary vision loss, and transient paralysis; overdose symptoms include, convulsions, vomiting, diarrhea, headache, nausea, difficult breathing, sensation of paralysis, and coma; may cause color interference in certain screening tests for 5-hydroxyindoleacetic acid (5-HIAA) and vanillylmandelic acid (VMA); patient should avoid drinking alcoholic beverages or taking other CNS depressants, because of the potential for additive CNS depression (excessive sleepiness, slurred speech, decreased awareness); caution in impaired liver or kidney function; adverse effects likely in patients >60 y; avoid use while breastfeeding (potential risk to newborn); prolonged use requires monitoring
These agents are useful in select cases of chronic pain.
Antidepressant with sedative effects. The mechanism of action is unknown. Amitriptyline is not an MAOI and does not act primarily by stimulating CNS.
Outpatients: 75 mg PO qd in divided doses; not to exceed 150 mg/d; therapeutic effect may take as long as 30 d to develop
Hospitalized patients: May require 100 mg/d PO; may gradually increase up to 300 mg/d
Adolescents and elderly patients: Lower doses recommended; 10 mg PO tid with 20 mg hs may be satisfactory if higher dosages not tolerated
<12 years: Not established
>12 years: Administer as in adults
Phenobarbital may decrease effects; co-administration with CYP2D6 enzyme system inhibitors (eg, cimetidine, quinidine) may increase levels; inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram
Documented hypersensitivity; use of MAOIs in past 14 d; history of seizures, cardiac arrhythmias, glaucoma, or urinary retention; should not be used in acute recovery phase after myocardial infarction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in cardiac conduction disturbances and history of hyperthyroidism, renal impairment, or hepatic impairment; avoid in elderly patients; increased and decreased blood glucose levels reported; when possible, discontinue several days before elective surgery
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cervical spondylosis, spine, back pain, cervical spine, neck pain, herniated disc, spinal stenosis, spondylosis, surgery spine, herniated disk, radiculopathy, spine pain, spinal cervical, stenosis, cervical, cervical spine surgery, cervical spondylotic myelopathy, cervical myelopathy, cervical arthritis, degenerative spondylosis, cervical osteoarthritis, spine spondylosis, degenerative arthropathy of the cervical spine, facet joints, longitudinal ligaments, ligamentum flavum, chronic cervical degeneration, cervical disk degeneration, disk herniation, spur formation, nerve root compression, progressive spinal cord compression, foraminal stenosis, spinal canal stenosis, chronic neck pain, quadriparesis, sphincteric dysfunction, chronic suboccipital headache, cervical radiculopathy, acute herniated disk, cervical intervertebral disk degeneration, transverse lesion syndrome, motor syndrome, central cord syndrome, brachialgia, tandem spinal stenosis, neurogenic claudication, gait abnormality, dysphagia, vertebrobasilar insufficiency, elevated hemidiaphragm, Spurling sign, Lhermitte sign, Hoffman sign, degenerative disk disease
Hassan Ahmad Hassan Al-Shatoury, MD, PhD, MHPE,, Associate Professor, Department of Neurosurgery, Suez Canal University; Co-Director, Center of Research and Development in Medical Education and Health Services Suez Canal University Hospital
Disclosure: Nothing to disclose.
Ayman Ali Galhom, MD, PhD, Lecturer (Associated Professor), Department of Neurosurgery, Suez Canal University Faculty of Medicine, Egypt
Ayman Ali Galhom, MD, PhD is a member of the following medical societies: Congress of Neurological Surgeons
Disclosure: Nothing to disclose.
Curtis W Slipman, MD, Director, University of Pennsylvania Spine Center; Associate Professor, Department of Physical Medicine and Rehabilitation, University of Pennsylvania Medical Center
Curtis W Slipman, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, International Association for the Study of Pain, and North American Spine Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
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.
Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.
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.
The editors would like to thank Franklin C Wagner, Jr, MD, Former Chief, Division of Spine and Spinal Cord Surgery, Former Professor, Department of Neurosurgery, University of Illinois at Chicago College of Medicine, for his previous association with this article.
Further ReadingRelated eMedicine topics:
Central Cord Syndrome
Cervical Spondylosis, Diagnosis and Management
Degenerative Disk Disease
Disk Herniation
Herniated Nucleus Pulposus
Spinal Stenosis [Neurosurgery]
Spinal Stenosis [Orthopedic Surgery]
Spinal Stenosis [Radiology]
Spinal Stenosis and Neurogenic Claudication
Clinical guidelines:
ACR Appropriateness Criteria® chronic neck pain. American College of Radiology - Medical Specialty Society. 1998 (revised 2005). 7 pages. [NGC Update Pending] NGC:004629
Clinical trials:
Study and Surgical Treatment of Syringomyelia
The CSM Trial: A Multicenter Study Comparing Ventral to Dorsal Surgery for Cervical Spondylotic Myelopathy
Treatment of Cervical Radiculopathy With Arthroplasty Compared With Discectomy With Fusion and Cage (ACDF)
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