Lumbosacral Disc Injuries 

  • Author: Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM; Chief Editor: Craig C Young, MD   more...
 
Updated: Nov 28, 2011
 

Background

Injuries to the intervertebral discs of the lumbosacral spine are invoked as a causative factor in one of the most common health problems in the United States — low back pain (LBP). Of the many possible etiologies of LBP, the intervertebral disc has been implicated as a more frequent source than muscular strain or ligamentous sprain. Although no single injury to the intervertebral disc has been unequivocally identified as a pain generator, theories of its involvement are common.[1, 2, 3, 4, 5, 6]

For excellent patient education resources, visit eMedicine's Back, Ribs, Neck, and Head Center. Also, see eMedicine's patient education articles Back Pain, Sprains and Strains, and Slipped Disk.

Related eMedicine topics include the following:

Next

Epidemiology

Frequency

United States

The lifetime incidence of LBP has been reported to be 60-90% with an annual incidence of 5%. LBP affects men and women equally. Most people with LBP do not seek medical care, they do not have significant functional impairment, and they recover rapidly. Despite this fact, LBP accounts for 14.3% of new patient visits to physicians each year.

Back pain is the leading cause of lost work productivity and is second only to upper respiratory infection as a cause of time lost from work. Back pain is estimated to result in 175.8 million days of restricted activity in the United States annually. Nearly 2.5 million Americans are disabled by LBP, half of these chronically.

Interestingly, a review of research by Manek and MacGregor reveals that there is a significant genetic effect on LPB.[1] Data from candidate gene studies have shown an association between lumbosacral disc disease and mutations of genes encoding the alpha-2 and alpha-3 subunits of collagen IX.

In 1990, 400,000 industrial low back injuries resulted in disability in the United States.[3] This value accounts for approximately 22% of all workplace injuries, yet LBP represents 31% of all compensation payments. The total cost estimates of LBP range from $25-85 billion.[2]

Previous
Next

Functional Anatomy

The lumbar spine has an average of 5 vertebrae (normal range 4-6) with an intervertebral disc interposed between adjacent vertebral bodies. A cartilaginous endplate exists between the disc and the adjacent vertebral bodies and is considered part of the disc. The disc itself is composed of a central nucleus pulposus surrounded peripherally by the annulus fibrosis.

In normal young adults, the nucleus is a semifluid mass of mucoid material. The nucleus is composed of approximately 70-90% water in a young healthy disc, but this percentage generally decreases with age. The primary nuclear constituents include glycosaminoglycans, proteoglycans, and collagen. Type II collagen predominates in the nucleus. Proteoglycans are the largest molecules in the body and possess an enormous capacity to attract water through oncotic forces. These forces increase their weight by 250% and result in a gel-like composition. Biomechanically, the nucleus can display properties of either a solid or liquid substance depending on the transmitted loads and its posture.

The annulus fibrosis consists of 10-20 concentric collagen fiber layers that surround the nucleus. The layers are arranged in alternating orientation of parallel fibers lying approximately 65° from the vertical. The vertebral endplate is a thin layer of cartilage located between the vertebral body and the intervertebral disc. Although normally composed of both hyaline and fibrocartilage in youth, older endplates are virtually entirely fibrocartilage. Because the intervertebral disc is the largest avascular structure in the body, it is dependent on diffusion across the endplate for nutrition and waste removal. The endplate is considered part of the disc because the endplate almost always remains with the disc when the disc is displaced traumatically from the vertebral body.

The principal functions of the disc are to allow movement between vertebral bodies and to transmit loads from one vertebral body to the next. When axial loads are transmitted to the spine, the annulus and nucleus display a complex intertwined role, allowing for pressure dispersal. The nucleus has the capacity to sustain and transmit pressure. This ability is invoked principally during weight bearing. In this circumstance, the nucleus transmits loads and braces the annulus as described below.

The annular lamellae are capable of sustaining an axial load on the basis of its bulk. When an axial load is applied to the nucleus, it tends to shorten. The nucleus attempts to radially expand, thereby exerting pressure on the annulus. Annular resistance efficiently opposes this outward pressure, creating a hoop-tension effect. The intervertebral disc is so effective at resisting these axial loads that a 40-kg load to a disc causes only 1 mm of vertical compression and only 0.5 mm of radial expansion.

During movement, the annulus acts like a ligament to restrain movements and partially stabilize the interbody joint. The oblique orientation of the annular fibers provides resistance to vertical, horizontal, and sliding movement. The alternation in the direction of the annular fibers in consecutive lamellae causes the annulus to resist twisting motions poorly. When the segment twists one way, the fibers oriented in that direction are placed on stretch, whereas those fibers oriented in the opposite direction are placed on slack; therefore, the annulus resists the twisting motion with less than its full complement of fibers.

Previous
Next

Sport-Specific Biomechanics

Intervertebral discs of the lumbosacral spine are susceptible to a variety of injuries, which may account for pain in the lower back. The central component to any injury involving the lumbosacral discs is the natural aging process of degeneration that Kirkaldy-Willis identified. The degenerative cascade describes this degenerative process of lumbosacral discs. Kirkaldy-Willis identified the following 3 phases of the degenerative cascade[5] :

  • The first phase, phase I, is known as the dysfunctional phase. This phase is characterized by circumferential tears or fissures in the outer annulus. In addition, endplate separation or failure can disrupt the blood supply, resulting in the loss of nutrition to the disc. These changes are thought to result from repetitive microtrauma. One hypothesis is that the discs' nuclear proteoglycans lose the capacity to absorb water and maintain their protective function.
  • Phase II, or the unstable phase, is characterized by multiple annular tears (both radial and circumferential), internal disc disruption, and resorption or loss of disc space height. This phase is thought to result from the progressive loss of the mechanical integrity of the 3-joint complex.
  • Phase III is also known as the stabilization phase. Further disc resorption, disc space narrowing, endplate destruction, disc fibrosis, and osteophyte formation are present. Disc injuries are more likely to occur in phase I or II of the degenerative process.

Various theories have been proposed as the sources of pain generation in disc injury, involving an intervertebral disc that is degenerative, bulging, or protruding. Mechanical compression and an immunologic or inflammatory response are possibly related to pain from a disc injury. Mechanical compression of a nerve alone is not necessarily painful; however, if that nerve is inflamed, it can produce severe pain with a small amount of mechanical compression.

The basis for an immunologic source for disc-related pain has been based upon the lack of blood supply to the nucleus pulposus, thus hiding it and its contents from the immune system. Injury to the disc would expose these foreign substances, initiating an autoimmune reaction. The nucleus pulposus has been shown to elicit an immune response. Various authors have reported that disc material can incite a leukocyte cell reaction, cytokine, and immunoglobulin response.

A second hypothesis that has gained support as initiating an inflammatory reaction may be the result of biochemical factors rather than an autoimmune response. Central to this idea is the arachidonic cascade. Phospholipase A2 (PLA2) is the rate-limiting step in this pathway, controlling the release of prostaglandins and leukotrienes. Saal showed that human PLA2 levels in the intervertebral disc are 20-10,000 times more active than the PLA2 found in other human tissues.[7, 8] This research led to the investigation of PLA2 and other biochemicals as putative mediators of the inflammatory response to intervertebral disc injury and, thus, inducing back pain.

Previous
Proceed to Clinical Presentation
 
 
Contributor Information and Disclosures
Author

Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM  President and Director, Georgia Pain Physicians, PC; Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Emory University School of Medicine

Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, American Medical Association, International Association for the Study of Pain, and Texas Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Kevin P Sullivan, MD  Consulting Staff, The Boston Spine Group

Kevin P Sullivan, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, International Spine Intervention Society, and North American Spine Society

Disclosure: BioAssets Development Corp Consulting fee Consulting

Erik D Hiester, DO  Fellow in Interventional Pain Management, Emory Medical School/Georgia Pain Physicians

Erik D Hiester, DO is a member of the following medical societies: American Academy of Family Physicians, American Medical Association, American Osteopathic Association, and American Pain Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Andrew D Perron, MD  Residency Director, Department of Emergency Medicine, Maine Medical Center

Andrew D Perron, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Sports Medicine, and Society for Academic Emergency Medicine

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

Henry T Goitz, MD  Academic Chair and Associate Director, Detroit Medical Center Sports Medicine Institute; Director, Education, Research, and Injury Prevention Center; Co-Director, Orthopaedic Sports Medicine Fellowship

Henry T Goitz, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons and American Orthopaedic Society for Sports Medicine

Disclosure: Nothing to disclose.

Jon B Whitehurst, MD  Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital

Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America

Disclosure: Nothing to disclose.

Chief Editor

Craig C Young, MD  Professor, Departments of Orthopedic Surgery and Community and Family Medicine, Medical Director of Sports Medicine, Director of Primary Care Sports Medicine Fellowship, Medical College of Wisconsin

Craig C Young, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Medical Society for Sports Medicine, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous coauthor Dr Dennis P White to the development and writing of this article.

References

  1. Manek NJ, MacGregor AJ. Epidemiology of back disorders: prevalence, risk factors, and prognosis. Curr Opin Rheumatol. Mar 2005;17(2):134-40. [Medline].

  2. Frymoyer JW. Epidemiology: the magnitude of the problem. In: Wiesel SW, ed. The Lumbar Spine. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1996:8-16.

  3. Bigos SJ, Battie MC. The impact of spinal disorders in industry. In: Frymoyer JW, ed. The Adult Spine: Principles and Practice. New York, NY: Raven Press; 1991.

  4. Frymoyer JW, Cats-Baril WL. An overview of the incidences and costs of low back pain. Orthop Clin North Am. Apr 1991;22(2):263-71. [Medline].

  5. Kirkaldy-Willis WH, ed. The pathology and pathogenesis of low back pain. Managing Low Back Pain. New York, NY: Churchill Livingstone; 1988:49.

  6. Deyo RA, Tsui-Wu YJ. Descriptive epidemiology of low-back pain and its related medical care in the United States. Spine. Apr 1987;12(3):264-8. [Medline].

  7. Saal JS, Franson RC, Dobrow R, et al. High levels of inflammatory phospholipase A2 activity in lumbar disc herniations. Spine. Jul 1990;15(7):674-8. [Medline].

  8. Saal JS, Sibley R, Dobrow R, et al. Cellular response to lumbar disc herniation: an immunohistologic study. Presented at: Annual Meeting of the International Society for the Study of the Lumbar Spine; June 1990; Boston, Mass.

  9. Beattie PF. Current understanding of lumbar intervertebral disc degeneration: a review with emphasis upon etiology, pathophysiology, and lumbar magnetic resonance imaging findings. J Orthop Sports Phys Ther. Jun 2008;38(6):329-40. [Medline].

  10. Kanemoto M, Hukuda S, Komiya Y, Katsuura A, Nishioka J. Immunohistochemical study of matrix metalloproteinase-3 and tissue inhibitor of metalloproteinase-1 human intervertebral discs. Spine. Jan 1 1996;21(1):1-8. [Medline].

  11. Weinstein SM, Herring SA, Derby R. Contemporary concepts in spine care. Epidural steroid injections. Spine. Aug 15 1995;20(16):1842-6. [Medline].

  12. Malinsky J. The ontogenenetic development of nerve terminationsin the intervertebral disc of man. Acta anat. 1959;38:96-113.

  13. Moneta GB, Videman T, Kaivanto K, et al. Reported pain during lumbar discography as a function of anular ruptures and disc degeneration. A re-analysis of 833 discograms. Spine. Sep 1 1994;19(17):1968-74. [Medline].

  14. Kraemer J. Natural course and prognosis of intervertebral disc diseases. International Society for the Study of the Lumbar Spine Seattle, Washington, June 1994. Spine. Mar 15 1995;20(6):635-9. [Medline].

  15. Bobechko WP, Hirsch C. Auto-immune response to nucleus pulposus in the rabbit. J Bone Joint Surg Br. Aug 1965;47:574-80. [Medline]. [Full Text].

  16. Olmarker K, Nordborg C, Larsson K, Rydevik B. Ultrastructural changes in spinal nerve roots induced by autologous nucleus pulposus. Spine. Feb 15 1996;21(4):411-4. [Medline].

  17. Olmarker K, Blomquist J, Strömberg J, et al. Inflammatogenic properties of nucleus pulposus. Spine. Mar 15 1995;20(6):665-9. [Medline].

  18. McCarron RF, Wimpee MW, Hudkins PG, Laros GS. The inflammatory effect of nucleus pulposus. A possible element in the pathogenesis of low-back pain. Spine. Oct 1987;12(8):760-4. [Medline].

  19. Franson RC, Saal JS, Saal JA. Human disc phospholipase A2 is inflammatory. Spine. Jun 1992;17(6 suppl):S129-32. [Medline].

  20. Ozaktay AC, Cavanaugh JM, Blagoev DC, King AI. Phospholipase A2-induced electrophysiologic and histologic changes in rabbit dorsal lumbar spine tissues. Spine. Dec 15 1995;20(24):2659-68. [Medline].

  21. Grönblad M, Virri J, Tolonen J, et al. A controlled immunohistochemical study of inflammatory cells in disc herniation tissue. Spine. Dec 15 1994;19(24):2744-51. [Medline].

  22. Haro H, Kato T, Komori H, Osada M, Shinomiya K. Vascular endothelial growth factor (VEGF)-induced angiogenesis in herniated disc resorption. J Orthop Res. May 2002;20(3):409-15. [Medline].

  23. Doita M, Kanatani T, Harada T, Mizuno K. Immunohistologic study of the ruptured intervertebral disc of the lumbar spine. Spine. Jan 15 1996;21(2):235-41. [Medline].

  24. Takahashi H, Suguro T, Okazima Y, et al. Inflammatory cytokines in the herniated disc of the lumbar spine. Spine. Jan 15 1996;21(2):218-24. [Medline].

  25. Crock HV. Internal disc disruption. A challenge to disc prolapse fifty years on. Spine. Jul-Aug 1986;11(6):650-3. [Medline].

  26. Lindblom K. Diagnostic puncture of intervertebral disks in sciatica. Acta Orthop Scand. 1948;17:213-39.

  27. Hirsch C. An attempt to diagnose the level of a disc lesion clinically by disc puncture. Acta Orthop Scand. 1948;18:132-40.

  28. Holt EP Jr. The question of lumbar discography. J Bone Joint Surg Am. Jun 1968;50(4):720-6. [Medline]. [Full Text].

  29. Simmons JW, Aprill CN, Dwyer AP, Brodsky AE. A reassessment of Holt's data on: "The question of lumbar discography". Clin Orthop Relat Res. Dec 1988;237:120-4. [Medline].

  30. Wiley JJ, Macnab I, Wortzman G. Lumbar discography and its clinical applications. Can J Surg. Jul 1968;11(3):280-9. [Medline].

  31. Walsh TR, Weinstein JN, Spratt KF, et al. Lumbar discography in normal subjects. A controlled, prospective study. J Bone Joint Surg Am. Aug 1990;72(7):1081-8. [Medline]. [Full Text].

  32. Guyer RD, Ohnmeiss DD. Lumbar discography. Position statement from the North American Spine Society Diagnostic and Therapeutic Committee. Spine. Sep 15 1995;20(18):2048-59. [Medline].

  33. Sachs BL, Vanharanta H, Spivey MA, et al. Dallas discogram description. A new classification of CT/discography in low-back disorders. Spine. Apr 1987;12(3):287-94. [Medline].

  34. Aprill C, Bogduk N. High-intensity zone: a diagnostic sign of painful lumbar disc on magnetic resonance imaging. Br J Radiol. May 1992;65(773):361-9. [Medline].

  35. Schellhas KP, Pollei SR, Gundry CR, Heithoff KB. Lumbar disc high-intensity zone. Correlation of magnetic resonance imaging and discography. Spine. Jan 1 1996;21(1):79-86. [Medline].

  36. Gundry CR, Fritts HM. Magnetic resonance imaging of the musculoskeletal system. Part 8. The spine, section 2. Clin Orthop Relat Res. Oct 1997;343:260-71. [Medline].

  37. Ricketson R, Simmons JW, Hauser BO. The prolapsed intervertebral disc. The high-intensity zone with discography correlation. Spine. Dec 1 1996;21(23):2758-62. [Medline].

  38. Smith BM, Hurwitz EL, Solsberg D, et al. Interobserver reliability of detecting lumbar intervertebral disc high-intensity zone on magnetic resonance imaging and association of high-intensity zone with pain and anular disruption. Spine. Oct 1 1998;23(19):2074-80. [Medline].

  39. German JW, Foley KT. Disc arthroplasty in the management of the painful lumbar motion segment. Spine. Aug 15 2005;30(16 suppl):S60-7. [Medline].

  40. Gamradt SC, Wang JC. Lumbar disc arthroplasty. Spine J. Jan-Feb 2005;5(1):95-103. [Medline].

  41. [Best Evidence] Peul WC, van den Hout WB, Brand R, Thomeer RT, Koes BW. Prolonged conservative care versus early surgery in patients with sciatica caused by lumbar disc herniation: two year results of a randomised controlled trial. BMJ. Jun 14 2008;336(7657):1355-8. [Medline]. [Full Text].

  42. Saal JS, Saal JA. Management of chronic discogenic low back pain with a thermal intradiscal catheter. A preliminary report. Spine. Feb 1 2000;25(3):382-8. [Medline].

  43. Iwamoto J, Sato Y, Takeda T, Matsumoto H. The return to sports activity after conservative or surgical treatment in athletes with lumbar disc herniation. Am J Phys Med Rehabil. Dec 2010;89(12):1030-5. [Medline].

  44. Hsu WK, McCarthy KJ, Savage JW, Roberts DW, Roc GC, Micev AJ, et al. The Professional Athlete Spine Initiative: outcomes after lumbar disc herniation in 342 elite professional athletes. Spine J. Mar 2011;11(3):180-6. [Medline].

  45. Andersson GB. Epidemiologic aspects on low-back pain in industry. Spine. Jan-Feb 1981;6(1):53-60. [Medline].

  46. Andersson GB, Brown MD, Dvorak J, et al. Consensus summary of the diagnosis and treatment of lumbar disc herniation. Spine. Dec 15 1996;21(24 suppl):75S-78S. [Medline].

  47. Brown KR, Pollintine P, Adams MA. Biomechanical implications of degenerative joint disease in the apophyseal joints of human thoracic and lumbar vertebrae. Am J Phys Anthropol. Jul 2008;136(3):318-26. [Medline].

  48. Fardon D, Pinkerton S, Balderston R, et al. Terms used for diagnosis by English speaking spine surgeons. Spine. Feb 1993;18(2):274-7. [Medline].

  49. Garfin SR, Rydevik B, Lind B, Massie J. Spinal nerve root compression. Spine. Aug 15 1995;20(16):1810-20. [Medline].

  50. Garfin SR, Rydevik BL, Brown RA. Compressive neuropathy of spinal nerve roots. A mechanical or biological problem?. Spine. Feb 1991;16(2):162-6. [Medline].

  51. Habtemariam A, Grönblad M, Virri J, et al. Immunocytochemical localization of immunoglobulins in disc herniations. Spine. Aug 15 1996;21(16):1864-9. [Medline].

  52. Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med. Jul 14 1994;331(2):69-73. [Medline]. [Full Text].

  53. Kuslich SD, Ulstrom CL, Michael CJ. The tissue origin of low back pain and sciatica: a report of pain response to tissue stimulation during operations on the lumbar spine using local anesthesia. Orthop Clin North Am. Apr 1991;22(2):181-7. [Medline].

  54. Lotan R, Oron A, Anekstein Y, Shalmon E, Mirovsky Y. Lumbar stenosis and systemic diseases: is there any relevance?. J Spinal Disord Tech. Jun 2008;21(4):247-51. [Medline].

  55. Nguyen CM, Ho KC, Yu SW, Haughton VM, Strandt JA. An experimental model to study contrast enhancement in MR imaging of the intervertebral disk. AJNR Am J Neuroradiol. Jul-Aug 1989;10(4):811-4. [Medline].

  56. Palmgren T, Grönblad M, Virri J, et al. Immunohistochemical demonstration of sensory and autonomic nerve terminals in herniated lumbar disc tissue. Spine. Jun 1 1996;21(11):1301-6. [Medline].

  57. Ross JS, Modic MT, Masaryk TJ. Tears of the anulus fibrosus: assessment with Gd-DTPA-enhanced MR imaging. AJNR Am J Neuroradiol. Nov-Dec 1989;10(6):1251-4. [Medline].

  58. Slipman C, Sawchuck TC. Discogenic pain: state of art reviews. Phys Med Rehab. 1999;13:601-24.

  59. Takahashi H, Suguro T, Okazima Y, et al. Inflammatory cytokines in the herniated disc of the lumbar spine. Spine. Jan 15 1996;21(2):218-24. [Medline].

  60. Troup JD, Martin JW, Lloyd DC. Back pain in industry. A prospective survey. Spine. Jan-Feb 1981;6(1):61-9. [Medline].

  61. Von Korff M, Saunders K. The course of back pain in primary care. Spine. Dec 15 1996;21(24):2833-7; discussion 2838-9. [Medline].

  62. Wu CG, Li YD, Li MH, Gu YF, Li M. Prospective evaluation of transabdominal percutaneous lumbar discectomy for L5-S1 disc herniation: initial clinical experience. J Neurosurg Spine. Apr 2008;8(4):321-6. [Medline]. [Full Text].

 
Previous
Next
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.