Degenerative Disk Disease 

  • Author: Stephen Kishner, MD, MHA; Chief Editor: Mary Ann E Keenan, MD   more...
 
Updated: Aug 12, 2011
 

Background

The intervertebral disk is a complex structure that has been the focus of much attention in clinical practice. The prevalence of low back and neck pain, which are thought to be associated with degenerative changes in the disk, represent major epidemiological problems. In the United States, back pain is the second leading symptom that prompts visits to physicians. As many as 80% of adults in the United States experience at least 1 episode of low back pain during their lifetime, and 5% experience chronic problems.[1]

Age-related changes and degeneration

Of all connective tissues, the intervertebral disk undergoes the most serious age-related changes. By the third decade of life, the nucleus pulposus becomes replaced with fibrocartilage, and the distinction between the nucleus and the annulus becomes blurred. The proteoglycan, water, and noncollagenous protein concentrations decrease, while the collagen concentration increases. The increase in collagen concentration is more pronounced in the nucleus and in the posterior quadrants of the disk. It is more pronounced with age and moving caudally in the lumbar spine (similar to the Wolff law).

Biochemically, aging increases the ratio of keratin sulfate to chondroitin sulfate, and it also changes the proportion of chondroitin-4-sulfate to chondroitin-6-sulfate, with a parallel decrease in water content. Proteoglycan synthesis decreases, which decreases the osmotic swelling and the traffic of oxygen and nutrients to the disk. Because of this decreased traffic, breakdown products of link and noncollagenous proteins stagnate in the disk. Nonenzymatic glycosylation of these breakdown products accounts for the brown discoloration of the aging connective tissues.

Differentiating aging from degeneration is difficult. According to Pearce et al, "Aging and degeneration may represent successive stages within a single process that occurs in all individuals but at markedly different rates."[2] Aging and degeneration have in common decreased water and proteoglycan content in the disks, combined with increased collagen.

While sagittal alignment, facet joint arthritis, and genetics potentially play a role in intervertebral disk degeneration, the results of one study suggest that the rate of degeneration may be associated with age. Those of African ethnicity also showed a faster rate of degeneration when compared with whites; sex did not show a significant effect on degeneration.[3]

One study demonstrated that the presence of juvenile disk degeneration was strongly associated with overweight and obesity, low back pain, increased low back pain intensity, and diminished physical and social functioning. An elevated body mass index was significantly associated with increased severity of disk degeneration.[4]

Cascade of degenerative changes

This cascade of degenerative changes can be subdivided into 3 stages: dysfunction, instability, and restabilization. The duration of the stages varies greatly, and distinguishing the signs and symptoms from one stage to the next is difficult.

Dysfunction involves outer annular tears and separation of the endplate, cartilage destruction, and facet synovial reaction. The symptoms of dysfunction are low back pain or neck pain, often localized but sometimes referred, and painful movement. The signs are local tenderness, contracted muscles, hypomobility, and painful extension of the back, neck, or both. Results of a neurological examination are usually normal.

The dysfunction stage is followed by the instability stage, in which disk resorption and loss of disk space height occur. Facet capsular laxity may develop, leading to subluxation. The symptoms are those of dysfunction (ie, "giving way" of the back, a "catch" in the back with movement, and pain with standing after flexion). The signs are abnormal movement (ie, during inspection or palpation), including observation of a catch, sway, or shift when standing erect after flexion.

In the stage of restabilization, the progressive degenerative changes lead to osteophyte formation and stenosis. The symptoms are low back pain of decreasing severity. The signs are muscle tenderness, stiffness, reduced movement, and scoliosis.

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Indications

Lumbar surgery is indicated in patients with severe spinal stenosis, in those with intractable pain, and in patients in whom an appropriate 6- to 12-month nonoperative course of treatment fails. Surgery is elective, except in the presence of bowel and bladder symptoms or cauda equina syndrome.

In elective cases, other conservative modalities should have been tried and observed to fail. The patient should be prepared for the operation from a psychological viewpoint. Instability is present at 1 or 2 levels (as mentioned above in the instability phase of degenerative changes).

In the case of cervical disk disease with radiculopathy, the indications for surgical treatment are intractable pain, progressive motor or sensory deficit, or symptoms refractory in a reasonable period of nonoperative therapy. When the symptoms and signs correlate with radiographic evidence of root compression, various groups report a greater than 90% likelihood of a favorable outcome with both anterior and posterior approaches to surgery.

In the case of cervical disk disease with myelopathy, because the natural history is a stepwise worsening course, early surgery to decompress the spinal cord is recommended to arrest progression if the clinical and radiographic changes are well correlated. The best results for myelopathy occur when surgery is performed within 6 months of the onset of symptoms. Some series show improvement of greater than 70% with surgery in patients with myelopathy.

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Relevant Anatomy

Vertebrae anatomy

The spine is composed of 7 cervical, 12 thoracic, 5 lumbar, and a fused set of sacral and vestigial coccygeal vertebrae. Spine stability is the result of 3 columns in 1 as described by Dennis. Fracture or loss of 2 columns results in instability. The anterior column consists of the anterior longitudinal ligament and the anterior portion of the vertebral body. The middle column consists of the posterior wall of the vertebral body and the posterior longitudinal ligament. The posterior column is formed by the posterior bony arch; this consists of transverse processes, facets, laminae, and spinous processes.

Intervertebral disks form one quarter of the total length of the spinal column. Each vertebra has the potential for 6° of freedom, translation in all 3 axes of movement, and rotation around each axis. Not all vertebrae are created equal; the cervical vertebrae have the greatest freedom of flexion, extension, lateral rotation, and lateral flexion. This is because they are larger, they have concave lower and convex upper vertebral body surfaces, and they have transversely aligned facet joints.

Thoracic vertebrae have restricted flexion, extension, and rotation but freer lateral flexion because they are attached to the rib cage, are smaller, have flatter vertebral surfaces, have frontally aligned facet joints, and have larger overlapped spinous processes. The lumbar spine has good flexion and extension and free lateral flexion because its disks are large, the spinous processes are posteriorly directed, and the facet joints are sagittally directed. Lateral lumbar rotation is limited because of facet alignment.

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Contraindications

Relative contraindications to spinal fusion include smoking, morbid obesity, active infection, and severe medical or psychological problems.

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Contributor Information and Disclosures
Author

Stephen Kishner, MD, MHA  Professor of Clinical Medicine, Physical Medicine and Rehabilitation Residency Program Director, Louisiana State University School of Medicine in New Orleans

Stephen Kishner, MD, MHA is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Edward Babigumira, MD  Interventional Spine and Pain Medicine Specialist, Lewes Medical and Surgical Associates, Delaware

Edward Babigumira, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, and International Spine Intervention Society

Disclosure: Nothing to disclose.

James Monroe Laborde, MD, MS  Clinical Assistant Professor, Department of Orthopedics, Louisiana State University Health Sciences Center and Tulane Medical School; Adjunct Assistant Professor, Department of Biomedical Engineering, Tulane University; Adjunct Assistant Professor, Department of Physical Medicine and Rehabilitation, Louisiana State University Medical School

James Monroe Laborde, MD, MS is a member of the following medical societies: American Academy of Orthopaedic Surgeons

Disclosure: Nothing to disclose.

Specialty Editor Board

K Daniel Riew, MD  Mildred B Simon Distinguished Professor of Orthopedic Surgery, Professor of Neurologic Surgery, Washington University School of Medicine; Chief, Cervical Spine Surgery, Department of Orthopedic Surgery, Barnes-Jewish Hospital

K Daniel Riew, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, AO Foundation, Cervical Spine Research Society, North American Spine Society, and Scoliosis Research Society

Disclosure: Medtronic Royalty Medtronic Vertex; Biomet Royalty Maxan anterior cervical plate; Osprey Royalty Interbody Graft; Osprey Stock Options None; SpineMedica None None; Synthes Consulting fee Other

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

William O Shaffer, MD  Professor, Vice-Chairman and Residency Program Director, Department of Orthopedic Surgery, University of Kentucky at Lexington

William O Shaffer, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, International Society for the Study of the Lumbar Spine, Kentucky Medical Association, Kentucky Orthopaedic Society, North American Spine Society, Southern Medical Association, and Southern Orthopaedic Association

Disclosure: DePuySpine 1997-2007 (not presently) Royalty Consulting; DePuySpine 2002-2007 (closed) Grant/research funds SacroPelvic Instrumentation Biomechanical Study; DePuyBiologics 2005-2008 (closed) Grant/research funds Healos study just closed; DePuySpine 2009 Consulting fee Design of Offset Modification of Expedium

Dinesh Patel, MD, FACS  Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital

Dinesh Patel, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Mary Ann E Keenan, MD  Professor, Vice Chair for Graduate Medical Education, Department of Orthopedic Surgery, University of Pennsylvania School of Medicine; Chief of Neuro-Orthopedics Program, Department of Orthopedic Surgery, Hospital of the University of Pennsylvania

Mary Ann E Keenan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, American Society for Surgery of the Hand, and Orthopaedic Rehabilitation Association

Disclosure: Nothing to disclose.

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