Cervical Degenerative Disc Disease
- PMID: 32809607
- Bookshelf ID: NBK560772
Cervical Degenerative Disc Disease
Excerpt
Degenerative disc disease (DDD) of the cervical spine typically develops equally in the aging population regardless of patient sex. Patients most commonly present with pain; when isolated or in combination with other neurological symptoms, pain may necessitate surgical intervention. Treatment options range from nonoperative measures to surgical options, such as decompression, arthroplasty, and instrumented fusion. This section examines the anatomy, natural history, etiology, pathophysiology, evaluation, and treatment options for patients with cervical DDD.
The cervical spine, spanning from C1 to C7, offers remarkable function and mobility. The upper cervical segments—C1 (the atlas, which articulates with the occiput) and C2 (the axis)—are uniquely structured to allow extensive motion, with primary rotation occurring at the C1–C2 joint and flexion-extension at the occiput–C1 joint. Surrounding or contained within these vertebrae are critical structures, including the spinal cord, nerve roots, major blood vessels, the trachea, and esophagus.
The intervertebral disc (IVD) is located from the C2–C3 level down, aiding in cervical spine mobility and stabilization. In contrast to the thoracic and lumbar vertebrae, the cervical vertebrae have a unique bony prominence called the uncinate process, which articulates with the adjacent level to form the joint of Luschka or uncovertebral joint. This joint helps to reinforce the IVD and provides additional stability and motion. The IVD is an intricate structure composed mainly of 2 parts, the peripherally located annulus fibrosus and the centrally located nucleus pulposus, which are responsible for its load distribution function. The anterior and posterior longitudinal ligaments reinforce the IVD.
The annulus fibrosus of the intervertebral discs is mostly of type I collagen in layers (lamellae), proteoglycans, glycoproteins, elastic fibers, and extracellular matrix (ECM) secreting cells. These collagen layers are uniquely positioned to form a strong shell for the inner contents, the nucleus pulposus. The nucleus pulposus has a gel-like consistency composed mainly of water, which decreases with age (90% at birth and 70% by the age of 60). The remaining minority of the nucleus pulposus contents comprises type II collagen and proteoglycans. Aggrecan is a critical proteoglycan in the nucleus pulposus, which, when bound to hyaluronic acid, helps retain water within the nucleus pulposus, allowing for load resistance.
After the first year of life, the IVD becomes the largest avascular structure in the body. Most of the nutrition is delivered via metabolite diffusion from the vertebral endplates. Over time, the IVD loses its water content and proteoglycan supply, resulting in a more fibrotic consistency of the nucleus pulposus and subsequent fissuring as the vertebral endplates calcify with age.
There are different types of nucleus pulposus herniations. If the nucleus pulposus herniates but remains contained by the annulus, it is called disc protrusion. However, the nucleus pulposus can also penetrate through injured annular fibers, and nucleus pulposus contents can extrude through a defect in the annulus, referred to as a disc extrusion. Furthermore, nucleus pulposus fragments can be separated from the extruded disc material, yielding disc sequestration.
The degenerative process of the cervical spine is classified into 3 distinct stages: dysfunction, instability, and stabilization. Dysfunction occurs between the ages of 15 and 45. During this stage, radial and circumferential tears can occur in the annulus, accompanied by facet joint localized synovitis. Instability can occur in individuals between the ages of 35 and 70. This stage is characterized by inner disc disruption, progressive resorption, and degeneration of the facet joints. This condition leads to the final stage of the process, stabilization, which typically occurs after age 60. Here, hypertrophic bone develops around the facet joints as well as the disc, promoting a stiff and possibly ankylosed spine.
Interestingly, each spine segment may be at a different stage of degeneration. One level could complete the dysfunction stage, while another could begin the stabilization phase. Disc herniations appear to occur due to the dysfunction and instability phase; spinal stenosis occurs due to the late instability stage and early stabilization stage due to the bony overgrowth and disc space narrowing. Consequently, patients may present with a combination of disc herniations and spinal stenosis affecting different levels of the cervical spine. The C5–6 segment is most commonly affected because of the cervical spine’s biomechanical stress and mobility patterns.
When discussing the natural history of cervical DDD and treatment options, symptomatic individuals can experience an array of symptoms, from intermittent or constant pain, along with possible neurological symptoms, without pain. Patients generally receive nonoperative treatment when experiencing nonprogressive pain and/or minimal neurological issues. If surgery is indicated, it is typically elective and can be delayed to achieve symptomatic improvement. However, an exception is patients diagnosed with cervical myelopathy, who should have more urgent surgical treatment to avoid neurological deterioration.
The proper diagnosis and treatment for spondylolytic cervical myelopathy can be extremely challenging, especially in patients with or even without ongoing axial neck pain with possible radiculopathy. One must also be aware that 20% of patients with cervical stenosis may also have lumbar stenosis. While many patients may have a straightforward diagnosis with a thorough history and physical examination accompanied by confirmatory imaging modalities, there is a significant subset of patients who have pain without experiencing neurological findings, aside from possible sensory changes, and whose imaging may not easily correlate with physical exam findings. In such cases, additional diagnostic modalities should complement a thorough history and physical examination to ensure an accurate diagnosis. Therefore, a systematic assessment is essential for effectively diagnosing and treating these patients.
Copyright © 2025, StatPearls Publishing LLC.
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