Cervical Spondylosis 

  • Author: Hassan Ahmad Hassan Al-Shatoury, MD, PhD, MHPE; Chief Editor: Consuelo T Lorenzo, MD   more...
 
Updated: Apr 18, 2012
 

Background

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)

A T2-weighted cervical magnetic resonance imaging A T2-weighted cervical magnetic resonance imaging scan shows obliteration of the subarachnoid space as a result of spondylotic changes.
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Pathophysiology

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) The result is decreased effective force on each of these structures.

A cervical myelogram shows advanced spondylotic chA cervical myelogram shows advanced spondylotic changes and multiple compression of the spinal cord by osteophytes. A 59-year-old woman presented with a spastic gait A 59-year-old woman presented with a spastic gait and weakness in her upper extremities. A T2-weighted sagittal magnetic resonance imaging scan shows cord compression from cervical spondylosis, which caused central spondylotic myelopathy. Note the signal changes in the cord at C4-C5, the ventral osteophytosis, buckling of the ligamentum flavum at C3-C4, and the prominent loss of disk height between C2 and C5. A 48-year-old man presented with neck pain and preA 48-year-old man presented with neck pain and predominantly left-sided radicular symptoms in the arm. The patient's symptoms resolved with conservative therapy. An axial, gradient-echo magnetic resonance imaging scan shows moderate anteroposterior narrowing of the cord space due to a ventral osteophyte at the C4 level, with bilateral narrowing of the neural foramina (more prominently on the left side). A 48-year-old man presented with neck pain and preA 48-year-old man presented with neck pain and predominantly left-sided radicular symptoms in the arm. The patient's symptoms resolved with conservative therapy. A T2-weighted sagittal magnetic resonance imaging scan shows ventral osteophytosis, most prominent between C4 and C7, with reduction of the ventral cerebrospinal fluid sleeve.

Degeneration of the joint surfaces and ligaments decreases motion and can act as a limiting mechanism against further deterioration. Thickening and ossification of the posterior longitudinal ligament (OPLL) also decreases the diameter of the canal.[1, 2, 3]

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.

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Epidemiology

Frequency

United States

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.

International

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."

Mortality/Morbidity

  • The course of cervical spondylosis may be slow and prolonged, and patients may either remain asymptomatic or have mild cervical pain.
  • Long periods of nonprogressive disability are typical, and in a few cases, the patient's condition progressively deteriorates.
  • Morbidity ranges from chronic neck pain, radicular pain, diminished cervical range of motion (ROM), headache, myelopathy leading to weakness, and impaired fine motor coordination to quadriparesis and/or sphincteric dysfunction (eg, difficulty with bowel or bladder control) in advanced cases. The patient may eventually become chair-bound or bedridden.

Race

No apparent correlation between race and cervical spondylosis exists.

Sex

Both sexes are affected equally. Cervical spondylosis usually starts earlier in men than in women.

Age

  • Symptoms of cervical spondylosis may appear in persons as young as 30 years but are found most commonly in individuals aged 40-60 years. Radiologic spondylotic changes increase with patient age; 70% of asymptomatic persons older than 70 years have some form of degenerative change in the cervical spine. See also Frequency.
  • Cervical spondylosis usually starts earlier in men than in women.
  • When cervical spondylosis develops in a young individual, it is almost always secondary to a predisposing abnormality in 1 of the joints between the cervical vertebrae, probably as a result of previous mild trauma.
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Contributor Information and Disclosures
Author

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.

Coauthor(s)

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.

Specialty Editor Board

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  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Patrick M Foye, MD  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 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  Medical Director, Medevals

Disclosure: Nothing to disclose.

Chief Editor

Consuelo T Lorenzo, MD  Physiatrist, Department of Physical Medicine and Rehabilitation, Alegent Health 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.

Additional Contributors

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.

References

  1. Epstein N. Posterior approaches in the management of cervical spondylosis and ossification of the posterior longitudinal ligament. Surg Neurol. Sep-Oct 2002;58(3-4):194-207; discussion 207-8. [Medline].

  2. Epstein N. Ossification of the cervical posterior longitudinal ligament: a review. Neurosurg Focus. Aug 15 2002;13(2):ECP1. [Medline].

  3. Ozer AF, Oktenoglu T, Cosar M, et al. Long-term follow-up after open-window corpectomy in patients with advanced cervical spondylosis and/or ossification of the posterior longitudinal ligament. J Spinal Disord Tech. Feb 2009;22(1):14-20. [Medline].

  4. Wang MC, Kreuter W, Wolfla CE, et al. Trends and variations in cervical spine surgery in the United States: Medicare beneficiaries, 1992 to 2005. Spine. Apr 2 2009;[Medline].

  5. Miranda P, Gomez P, Alday R. Acute traumatic central cord syndrome: analysis of clinical and radiological correlations. J Neurosurg Sci. Dec 2008;52(4):107-12; discussion 112. [Medline].

  6. Patel AA, Spiker WR, Daubs M, Brodke DS, Cannon-Albright LA. Evidence of an inherited predisposition for cervical spondylotic myelopathy. Spine (Phila Pa 1976). Jan 1 2012;37(1):26-9. [Medline]. [Full Text].

  7. Young WF. Cervical spondylotic myelopathy: a common cause of spinal cord dysfunction in older persons. Am Fam Physician. Sep 1 2000;62(5):1064-70, 1073. [Medline]. [Full Text].

  8. Kuijper B, Tans JT, van der Kallen BF, Nollet F, Lycklama A Nijeholt GJ, de Visser M. Root compression on MRI compared with clinical findings in patients with recent onset cervical radiculopathy. J Neurol Neurosurg Psychiatry. May 2011;82(5):561-3. [Medline].

  9. Tsiptsios I, Fotiou F, Sitzoglou K, et al. Neurophysiological investigation of cervical spondylosis. Electromyogr Clin Neurophysiol. Jul-Aug 2001;41(5):305-13. [Medline].

  10. Weber M, Eisen A. Are motor evoked potentials (MEPs) helpful in the differential diagnosis of spondylotic cervical myelopathy (SCM)?. Suppl Clin Neurophysiol. 2000;53:419-23. [Medline].

  11. Stetkarova I, Kofler M. Cutaneous silent periods in the assessment of mild cervical spondylotic myelopathy. Spine. Jan 1 2009;34(1):34-42. [Medline].

  12. Uribe JS, Sangala JR, Duckworth EA, et al. Comparison between anterior cervical discectomy fusion and cervical corpectomy fusion using titanium cages for reconstruction: analysis of outcome and long-term follow-up. Eur Spine J. Feb 12 2009;[Medline].

  13. Ramzi N, Ribeiro-Vaz G, Fomekong E, et al. Long term outcome of anterior cervical discectomy and fusion using coral grafts. Acta Neurochir (Wien). Dec 2008;150(12):1249-56; discussion 1256. [Medline].

  14. Epstein NE. Laminectomy for cervical myelopathy. Spinal Cord. Jun 2003;41(6):317-27. [Medline].

  15. Wang MY, Shah S, Green BA. Clinical outcomes following cervical laminoplasty for 204 patients with cervical spondylotic myelopathy. Surg Neurol. Dec 2004;62(6):487-92; discussion 492-3. [Medline].

  16. Fehlings MG, Smith JS, Kopjar B, Arnold PM, Yoon ST, Vaccaro AR, et al. Perioperative and delayed complications associated with the surgical treatment of cervical spondylotic myelopathy based on 302 patients from the AOSpine North America Cervical Spondylotic Myelopathy Study. J Neurosurg Spine. Feb 10 2012;[Medline].

  17. Seebach CL, Kirkhart M, Lating JM, Wegener ST, Song Y, Riley LH 3rd, et al. Examining the role of positive and negative affect in recovery from spine surgery. Pain. Mar 2012;153(3):518-25. [Medline].

  18. Wang MC, Chan L, Maiman DJ, et al. Complications and mortality associated with cervical spine surgery for degenerative disease in the United States. Spine. Feb 1 2007;32(3):342-7. [Medline].

  19. Alexander JT. Natural history and nonoperative management of cervical spondylosis. In: Menezes AH, Sonnatage VH, eds. Principles of Spinal Surgery. New York, NY: McGraw-Hill; 1996:547-57.

  20. Binder AI. Cervical spondylosis and neck pain. BMJ. Mar 10 2007;334(7592):527-31. [Medline].

  21. Braddom RL. Management of common cervical pain syndromes. In: DeLisa JA, ed. Rehabilitation Medicine: Principles and Practice. Philadelphia, Pa: Lippincott Williams & Wilkins; 1993:1036-46.

  22. Carr RG. The physiatrist and cervical spondylosis. In: Saunders RL, Bernini PM, eds. Cervical Spondylotic Myelopathy. Boston, Mass: Blackwell Scientific; 1992:96-109.

  23. Chan CW. Spinal cord injury. In: Sinaki M, ed. Basic Clinical Rehabilitation Medicine. Minneapolis, Minn: Mosby-Year Book; 1993:183-94.

  24. Clark CR. Degenerative conditions of the spine: differential diagnosis and non-surgical treatment. In: Frymoyer JW, ed. The Adult Spine: Principles and Practice. New York, NY: Raven Press; 1991:1154-64.

  25. Fiscgrund JS, Herkowitz HN. Cervical spondylotic radiculopathy, natural history and pathophysiology. In: Herkowitz HN, Rothman RH, Simeone FA, eds. Rothman-Simeone, the Spine. 4th ed. Philadelphia, Pa: WB Saunders; 1999:461-5.

  26. Fouyas IP, Statham PF. Operative treatment of cervical spondylosis. Br J Neurosurg. Dec 1998;12(6):594-5. [Medline].

  27. Hoff JT, Panadopoulos SM. Cervical disc disease and cervical spondylosis. In: Wilkins RH, Rengachary SS, eds. Neurosurgery. New York, NY: McGraw-Hill; 1996:3756-74.

  28. Iwabuchi M, Kikuchi S, Sato K. Pathoanatomic investigation of cervical spondylotic myelopathy. Fukushima J Med Sci. Dec 2004;50(2):47-54. [Medline].

  29. Jumah KB, Nyame PK. Relationship between load carrying on the head and cervical spondylosis in Ghanaians. West Afr J Med. Jul-Sep 1994;13(3):181-2. [Medline].

  30. Kadanka Z, Mares M, Bednarík J, et al. Predictive factors for mild forms of spondylotic cervical myelopathy treated conservatively or surgically. Eur J Neurol. Jan 2005;12(1):16-24.

  31. Kadanka Z, Mares M, Bednarík J, et al. Predictive factors for spondylotic cervical myelopathy treated conservatively or surgically. Eur J Neurol. Jan 2005;12(1):55-63.

  32. Kawaguchi Y, Kanamori M, Ishihara H, et al. Pathomechanism of myelopathy and surgical results of laminoplasty in elderly patients with cervical spondylosis. Spine. Oct 1 2003;28(19):2209-14. [Medline].

  33. Kimura R, Park YS, Nakase H, et al. Syringomyelia caused by cervical spondylosis. Acta Neurochir (Wien). Feb 2004;146(2):175-8. [Medline].

  34. Nurick S. The pathogenesis of the spinal cord disorder associated with cervical spondylosis. Brain. 1972;95(1):87-100. [Medline].

  35. Papadopoulos CA, Katonis P, Papagelopoulos PJ, et al. Surgical decompression for cervical spondylotic myelopathy: correlation between operative outcomes and MRI of the spinal cord. Orthopedics. Oct 2004;27(10):1087-91. [Medline].

  36. Rao RD, Currier BL, Albert TJ, et al. Degenerative cervical spondylosis: clinical syndromes, pathogenesis, and management. J Bone Joint Surg Am. Jun 2007;89(6):1360-78. [Medline].

  37. Sakaura H, Hosono N, Mukai Y, et al. Long-term outcome of laminoplasty for cervical myelopathy due to disc herniation: a comparative study of laminoplasty and anterior spinal fusion. Spine. Apr 1 2005;30(7):756-9. [Medline].

  38. Sari-Kouzel H, Cooper R. Managing pain from cervical spondylosis. Practitioner. Apr 1999;243(1597):334-8. [Medline].

  39. Singh A, Crockard HA, Platts A, et al. Clinical and radiological correlates of severity and surgery-related outcome in cervical spondylosis. J Neurosurg. Apr 2001;94(2 Suppl):189-98. [Medline].

 
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A cervical myelogram shows advanced spondylotic changes and multiple compression of the spinal cord by osteophytes.
A 59-year-old woman presented with a spastic gait and weakness in her upper extremities. A T2-weighted sagittal magnetic resonance imaging scan shows cord compression from cervical spondylosis, which caused central spondylotic myelopathy. Note the signal changes in the cord at C4-C5, the ventral osteophytosis, buckling of the ligamentum flavum at C3-C4, and the prominent loss of disk height between C2 and C5.
A T2-weighted cervical magnetic resonance imaging scan shows obliteration of the subarachnoid space as a result of spondylotic changes.
A 48-year-old man presented with neck pain and predominantly left-sided radicular symptoms in the arm. The patient's symptoms resolved with conservative therapy. An axial, gradient-echo magnetic resonance imaging scan shows moderate anteroposterior narrowing of the cord space due to a ventral osteophyte at the C4 level, with bilateral narrowing of the neural foramina (more prominently on the left side).
A 48-year-old man presented with neck pain and predominantly left-sided radicular symptoms in the arm. The patient's symptoms resolved with conservative therapy. A T2-weighted sagittal magnetic resonance imaging scan shows ventral osteophytosis, most prominent between C4 and C7, with reduction of the ventral cerebrospinal fluid sleeve.
 
 
 
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