What is the pathophysiology of cervical disc disease?

Updated: Apr 16, 2020
  • Author: Michael B Furman, MD, MS; Chief Editor: Dean H Hommer, MD  more...
  • Print
Answer

Manifestations of HNP are divided into subcategories by type (ie, protrusion, extrusion, sequestration). Disc bulge, is not a true herniation, per se. It is described as generalized symmetrical or asymmetrical circumferential extension of the disc margin beyond the margins of the adjacent vertebral endplates.

Disc protrusion describes herniation of nuclear material through a defect in the annulus, producing a focal extension of the disc margin; it can further be defined if the greatest distance, in any plane, between the edges of the disc material beyond the disc space is less than the distance between the edges of the base, in the same plane.

Extrusion applies to herniation of nuclear material when, in at least one plane, any one distance between the edges of the disc material beyond the disc space is greater than the distance between the edges of the base, or when no continuity exists between the disc material beyond the disc space and that within the disc space. Extrusion may be further specified as sequestration, if the displaced disc material has lost completely any continuity with the parent disc.

The term migration may be used to signify displacement of disc material away from the site of extrusion, regardless of whether sequestrated or not. Examples of disc herniation are seen in the images below.

Disc herniation classification. A: Normal disc ana Disc herniation classification. A: Normal disc anatomy demonstrating nucleus pulposus (NP) and annular margin (AM). B: Disc protrusion, with NP penetrating asymmetrically through annular fibers but confined within the AM. C: Disc extrusion with NP extending beyond the AM. D: Disc sequestration, with nuclear fragment separated from extruded disc.
Axial magnetic resonance imaging (MRI) scan (C3-C4 Axial magnetic resonance imaging (MRI) scan (C3-C4) demonstrating left-sided posterolateral protrusion of the nucleus pulposus with compression of the cerebrospinal fluid.
Sagittal magnetic resonance imaging (MRI) scan dem Sagittal magnetic resonance imaging (MRI) scan demonstrating cervical intervertebral disc protrusions at C3-C4 and C7-T1.
Postdiscography axial computed tomography (CT) sca Postdiscography axial computed tomography (CT) scan demonstrating right posterolateral subligamentous protrusion.

Herniation typically occurs secondary to posterolateral annular stress. There are 2 main types of herniation that are described in the literature: focal and broad-based. Focal herniation involves less than 25% of the disc circumference, whereas broad-based herniations involves between 25-50% of the disc circumference. [1] Herniation rarely results from a single traumatic incident. Acute traumatic cervical HNP serves as a major etiology of central cord syndrome. The C6-C7 disc herniates more frequently than discs at other levels.

Acute disc herniation causes radicular pain through chemical radiculitis in which proteoglycans and phospholipases released from the nucleus pulposus mediate chemical inflammation and/or direct nerve root compression. Interleukin 6 and nitric oxide are also released from the disc and play a role in the inflammatory cascade. Denda et al has also recently showed that chronic compression of the spinal canal can lead to higher than normal levels of nitric oxide (NO) in the cerebrospinal fluid (CSF). Excessive NO levels have been shown to be cytotoxic and can induce neuronal apoptosis. [14] Although high levels of NO have not been correlated to severity of pain or disease, this data may play a role in targets for future interventions.

The chemical radiculitis is a key element in the pain caused by HNP because nerve root compression alone is not always painful unless the dorsal root ganglion is also involved. Herniation may induce nerve demyelination with resulting neurologic symptoms. Cervical HNP maybe resorbed during the acute phase. Indeed, studies documenting frequent herniation resorption and correlating herniation regression with symptom resolution support conservative treatment of cervical radicular pain.

A rare trauma-induced high cervical (C2-C3) HNP syndrome manifests as nonspecific neck and shoulder pain, perioral hypesthesia, more radiculopathy than myelopathy, and more upper limb motor and sensory dysfunction than lower limb symptomatology. Decreased middle and/or lower cervical spine mobility from spondylosis, with consequent overload and hypermobility at higher segments, may precipitate high cervical disc lesions in older patients. A retro-odontoid disc may result from an upwardly migrating C2-C3 HNP. Some case reports describe cervical HNPs causing Brown-Séquard syndrome, as well as atypical nonradicular symptoms in patients with congenital insensitivity to pain. Although spondylosis may affect motion at adjacent levels, isolated disc herniation in the cervical spine does not seem to alter motion of adjacent levels, regardless of the degree of disc degeneration or the size of the disc herniation. [15]

A study by Nam et al indicated that in patients with cervical disc herniation, risk factors for motor weakness include decreased disc height, a percentage of the HNP in the spinal canal, and a signal intensity change in the spinal cord. A disc height cutoff value of 5.8 mm produced a sensitivity and specificity of 39.5% and 94.1%, respectively, while a cutoff value of 28.1% for HNP in the spinal canal produced a sensitivity and specificity of 57.9% and 82.4%, respectively. In addition to motor weakness, signal intensity change in the spinal cord also may predict delayed recovery. [16]

Cervical radiculopathy results from mechanical nerve root compression or intense inflammation (ie, chemical radiculitis). Specifically, nerve root compression may occur at the intervertebral foraminal entrance zone at the narrowest segment of the root sleeve anteriorly by disc protrusion and uncovertebral osteophytes and posteriorly by superior articulating process, ligamentum flavum, and periradicular fibrous tissue. [17] Decreased disc height, as well as age-related foraminal width decrease from inferior Z-joint hypertrophy, may impinge subsequently on nerve roots. The cervical region accounts for 5-36% of all radiculopathies encountered. Incidence of cervical radiculopathies by nerve root level is as follows: C7 (70%), C6 (19-25%), C8 (4-10%), and C5 (2%).

The most common cause of cervical radiculopathy is foraminal encroachment (70-75%). The cause is multifactorial, including degeneration of the discs and the uncovertebral joints of Luschka and the zygapophyseal joints. In contrast to lumbar spine disorders, HNP in the cervical spine is responsible for only 20-25% of radiculopathies.

Cervical DDD most commonly is due to age-related changes, but the condition also is affected by lifestyle, genetics, smoking, nutrition, and physical activity. Degenerative disc changes observed on radiographs may reflect simple aging and do not necessarily indicate a symptomatic process.

The disc begins to degenerate in the second decade of life. Degenerative disc disease is essentially a process disrupting homeostasis. This degenerative process of the less hydrated and more fibrous nucleus pulposus fails to withstand the compressive loading, resulting in uneven distribution of forces to the surrounding annulus, which leads to the formation of radial tears. Circumferential tears form in the posterolateral annulus after repetitive use. Several circumferential tears coalesce into radial tears, which progress into radial fissures. The disc then disrupts with tears passing throughout the disc.

Loss of disc height occurs with subsequent peripheral annular bulging. Proteoglycans and water escape through fissures formed from nuclear degradation, resulting in further thinning of the disc space. Changes in the cartilaginous endplates alter nutritional supply to the nucleus that contributes to preexisting dehydration of the disc, compounding the effects of the degenerative cascade. Vertebral sclerosis and osteophytic formation ultimately follow. [5]

IDD describes pathologic annular fissuring within the disc without external disc deformation. This disorder results from trauma-related nuclear degradation, cervical flexion/rotation-induced annular injury, or whiplash.

The intervertebral disc has few pain receptors and little innervation, except in the periphery of the disc. The intervertebral disc may not be irritated until the inflammation process becomes moderate or severe. The nucleus pulposus appears to be the first site of degeneration with the annulus fibrosis being the primary pain generator once injury or degeneration occurs. DDD ultimately may progress to IDD.


Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!