Chapter 25 Intervertebral Disc Syndrome

Key Words

Intervertebral disc syndrome, discogenic back pain, cauda equina syndrome, sciatica, somatic referred pain, radicular pain

After reading this chapter you should be able to answer the following questions:

Question 1	What is the contribution of disc herniation to spinal subluxation?
Question 2	Why is one type of treatment for all cases of intervertebral disc syndrome not in the best interest of the patient?
Question 3	What signs and symptoms associated with intervertebral disc syndrome suggest the need for referral for a neurologic evaluation?

Clinically, the symptoms associated with intervertebral disc syndrome can respond to the application of spinal manipulation.^1,² Behavior of the spinal motion segment consistent with subluxation (altered alignment, movement integrity, and physiological function) is observed with disc degeneration and herniation. The interrelationship of the spinal three-joint complex³ makes a precise diagnosis of low back pain difficult at best, and in many cases involves more than one component of the spinal motion segment.

When the intervertebral disc is affected, the posterior joints are also involved and vice versa. This means that even when the disc is the site of the main lesion, the posterior joints can be affected and contribute to the patient’s symptoms. Conversely when the function of the posterior joints is abnormal, symptoms may also arise from the disc. This discussion of intervertebral disc syndrome explores the contribution of the intervertebral disc to motion segment subluxation and spinal dysfunction.

Historical Background

The publication in 1934 of a paper describing rupture of the intervertebral disc by Mixter and Barr ³ focused on the disc as the primary source of back pain. For the next 40 years, a period known as the “dynasty of the disc,” spinal surgery was the primary treatment for disc lesions.

In 1964 Chrisman et al.⁴ found that 51% of patients with sciatica improved clinically on side posture manipulation but that no changes in the myelographic appearance occurred, suggesting the possibility that the leg pain may not have been due solely to disc herniation. In 1974 Mathew and Yates⁵ reported on the reduction in size of a disc herniation using epidurography pre- and post-manipulation. In 1979 Valentini reported that 171 of 194 patients with acute disc syndrome were successfully treated with side posture manipulation.⁶

Since that time, many studies have reported successful treatment of mechanical back pain with manipulation, including patients with disc lesions,⁷ but there has not been a clear separation in most cases that identifies the contributing structures. Both side posture manipulation¹ and flexion-distraction² have been demonstrated to be effective in the treatment of intervertebral disc lesions. End-range lumbar extension exercise is another tool being used successfully in the treatment of these patients.

Anatomy of the Intervertebral Disc

Three distinct regions make up the structure of the intervertebral disc. They are the nucleus pulposus, anulus fibrosus, and cartilaginous end plates. The intervertebral discs are interposed between adjacent surfaces of the vertebral bodies, serving to unite as well as separate them.

Anulus Fibrosus

The anular fibers of the lumbar intervertebral disc form an outer ligament made up of fibrocartilaginous rings that restrain the nucleus. The outer anular fibers are more elastic. The enclosing fibers are arranged in successive layers overlapping in alternating oblique directions. The outermost fibers are attached to the periosteum and vertebral body just beyond the epiphyseal ring of cortical bone. The posterior and posterolateral parts of the anulus are much thinner, and there is less reinforcement from the thin posterior longitudinal ligament that narrows caudally from L1. It is less than half of the posterior disc margin by the time it reaches L5.

The differentiation between the inner fibers of the anulus and the nucleus pulposus is often described in ways that draw an image of a clear line of demarcation between the two. Analogies of a jelly donut or tire turned on its side insinuate that the nucleus resides in an open cavity, centered within well-organized walls of the inner anulus and the superior and inferior end plates. In actuality, the demarcation between anulus and nucleus pulposus can be difficult to discern because of a gradual transition from the fibrous network of the nucleus to the well-organized lamella of the anulus.⁸

The cervical disc has recently been shown to rely heavily on the posterior longitudinal ligament (PLL) to support the nucleus pulposus posteriorly, because there is little or no anulus in that region. There is no layering of concentric rings of fibers lying at alternate angles; instead, there is a crescent-shaped collagen mass anteriorly that tapers laterally as it approaches the uncinate processes. There is a thin layer of posterior fibers supporting the disc between the uncinate processes and the lateral edge of the PLL, creating an inherent weakness in this region.⁹

Nucleus Pulposus

The nucleus pulposus is separated from the central parts of the vertebral bodies above and below by thin cartilaginous end plates. The nucleus is an avascular structure, and the end plates provide a permeable barrier between the nucleus pulposus and the vertebral bodies, permitting the transfer of tissue fluid that meets the nutritional demands of the disc.

The nucleus pulposus is a thick semifluid gel that makes up 40% of the intervertebral disc. It is composed of stellate cells sparsely scattered throughout a three-dimensional lattice gel of fine interlaced collagen fibrils that enmesh fibroblastic cells, and proteoglycans.⁸ The nucleus is much more accurately thought of as a porous sponge filled with a thick, viscous material than as a well-demarcated fluid-filled space. Changes in the disc on maturation occur in the nucleus pulposus, with an increase in collagen fibers and breakdown of proteoglycans. This decreases the disc’s ability to absorb fluid with resulting loss of disc height.

Cartilaginous End Plates

The outer end plate is a hard, bony ring with a larger central cartilaginous part that anchors the disc to the vertebral body. They are also important pathways for the diffusion of nutrients from the vascular spongiosa of the vertebrae into the central part of the disc. Ten percent of each bony vertebral end plate is perforated by small vascular buds that make contact with the cartilage plate.

The Disc and Spinal Motion

The spinal motion segment with its three joint complex is a marvel of function that combines both stability and flexibility. The intervertebral disc is central to the typical spinal motion segment. Each segment is composed of the anterior amphiarthrodial joint formed by the disc between the two vertebral bodies and two posterior (zygapophyseal) diarthrodial joints. In the cervical spine, the joints of Luschka on the lateral aspect of the vertebral bodies add additional stability. Whereas the intervertebral disc allows for six degrees of freedom (rotation around the three axes and translation along the three axes; see Chapter 11), the posterior joints guide and restrict motion. Segmental movement is determined by the direction of the facet planes that produces different patterns of movement in the various spinal regions. The contribution of the intervertebral disc to spinal motion is dependent on the discal turgor.

Intrinsic Equilibrium

Motion in the healthy spine is dependent on the elastic properties of the noncontractile structures that contribute to a comparatively stable mechanical unit. The forces acting on the typical spinal segment include the axial pressure of the nucleus pulposus against the vertebral end plates (that resist compression and separate adjacent vertebrae) and the tension exerted by ligaments holding each segment together. These forces form an intrinsic equilibrium that depends on the turgor of the nucleus pulposus and the integrity of the spinal ligaments that form a delicate balance mechanism.¹⁰ This mechanism allows for erect posture with relatively little muscular force. Disruption of this balance mechanism occurs with disc degeneration. With reduced turgidity of the nucleus, segmental instability and subluxation result.

Pathology

Disc Degeneration

Unequivocal findings of disc degeneration in the form of cleft and radial tears in the central anulus fibrosus are abundant beginning at age 11 to 16 years. This is thought to be caused by a diminution of the blood supply to the disc through the end plate, which begins before age 2 but becomes most pronounced between the ages of 3 and 10 years.¹¹

Three stages of disc degeneration in the cervical spine were described by Hall ¹² in 1965. A transverse fissure was observed in the early stage with a slight increase in the apposition of the vertebrae. A second stage of degeneration was described, with a further decrease in disc height and a flaring of the joints of Luschka. In the later stage, a transverse fissure from one side of the intervertebral region to the other was noted with the uncus forming an oblique shelf with a flattened superior surface.

In 1971 Schmorl and Junghanns described loosening of the spinal motion segment.¹³ Kirkaldy-Willis¹⁴ in turn described the pathology and pathogenesis of the lumbar spine in 1978. He labeled the three phases of the spectrum of degenerative disc disease as dysfunction, the unstable phase, and late stage stabilization.¹⁵ He noted that the changes in the stage of dysfunction are minor and perhaps reversible. Movement of the posterior joints may be restricted, and palpation at the level of the lesion may demonstrate that one spinous process is out of line with the next.¹⁵

Changes in the intervertebral disc as degeneration progresses are characterized by small circumferential tears and increasing laxity, which allows subluxation of the joint surfaces to occur. Manipulation of subluxated facet joints most likely brings relief at this stage.¹⁶ Later these tears become larger and coalesce to become radial tears that pass from the anulus into the nucleus. Motion caused by an axial rotatory torque is increased by radial and transverse tears in the anulus more than motion caused by flexion, extension, or lateral bending.¹⁷ Therefore one would expect to see increased rotational stresses in the three joint complex with significant radial or transverse anular tears.

These tears increase until there is complete internal disruption of the disc. The normal disc height is greatly reduced because of the loss of proteoglycans and water from the nucleus. The anulus becomes lax and bulges around the circumference. This bulge must be distinguished from disc herniation, which is a protrusion of nuclear material through the anulus and into the epidural space.

In the stabilization phase described by Kirkaldy-Willis,¹⁴ the spinal motion segment becomes increasingly stiff due to facet joint fibrosis and the formation of osteophytes at the disc and vertebral body following disc resorption to create a stable spinal motion segment.¹⁵ The stabilization of a spinal motion segment creates added stress and advances degeneration at least at the two levels immediately above the stabilized joint complex, creating findings similar to the findings immediately cephalad to a lumbosacral fusion.¹⁸

Disc Herniation

The mechanism of disc herniation may be a series of recurrent rotational injuries that produce circumferential and radial tears leading to disc bulge. In some cases the anulus is completely ruptured and the nucleus protrudes through the anulus. In severe cases, part of the nucleus breaks free and becomes sequestrated. The sequestrated fragment may move about, causing variations in symptoms from level to level and side-to-side.

A severe compression injury with the spine flexed may cause a sudden rupture of the anulus.¹⁵ However, once the anulus is torn, the degree of flexion and the level of nucleus pulposus hydration are the two most influential factors with respect to whether or not the nucleus breaks loose and extrudes through the torn anulus. The rate of loading is not thought to be very important once the anular tear is present.¹⁹ Disc herniation can compromise the nerve roots, and posterior herniation in the cervical spine can affect the spinal cord. Because the conus medullaris is superior to the lumbar spine, the cord is not affected by a central bulge or herniation in the lumbar spine.

Extremity pain can be the significant symptom of a patient presenting with a disc injury. Involvement of the nerve root is certainly one source of extremity symptoms in these patients. The nerve root is compressed by the extruded nucleus, or even by a focal bulge in the anulus, with the result being ischemic changes to the nerve root and possible long-term or even permanent neurologic damage. This type of mechanical compression of the nerve root causes true radicular signs and symptoms of pain in the dermatomal distribution of the affected nerve root, sensory changes (hyperesthesia, paresthesia, hypoesthesia, anesthesia) along the same dermatome, motor loss or weakness of muscles innervated in whole or part by the affected root, and a decrease in the deep tendon reflex of corresponding muscles.

Mechanical compression of nerve roots may not be the only cause of nerve root involvement in the clinical picture. The presence of nucleus pulposus material in the epidural space without compression of the root has been shown to produce nerve root inflammation and even irritation of the dorsal root ganglion, both of which can cause radicular signs and symptoms.²⁰ Epidural presence of nucleus pulposus has also been shown to reduce nerve root and DRG blood flow with a measurable reduction in nerve conduction velocity.²¹

There is a significant association between recent episodes of low back pain and disc degeneration demonstrable on MRI.²² Even without the demonstrable presence of nucleus pulposus in the epidural space, patients may report buttock, hip, groin, or lower limb pain. Tears in the posterior anulus common to the degenerative disc have been shown capable of producing these symptoms with²² or without²³ a posterior disc bulge.

Additionally, herniation can affect nonadjacent structures. For example, patients with documented lumbar disc herniations with back and leg pain have been found to have a high incidence of sacroiliac joint dysfunction, perhaps due to direct effects from the mechanical changes at the injured level or perhaps from changes in hamstring and iliopsoas muscle function as a result of nerve root irritation. These symptoms respond well to manual therapy of the SI joints.²⁴ (See Chapter 26.) This effect on a joint as complex and important to the totality of spinal motion as the sacroiliac joint demonstrates the importance of ensuring proper segmental motion on either side of a disc lesion as an important step to prevent secondary pain syndromes and biomechanical deficits throughout the kinetic chain.

Biomechanical changes associated with disc degeneration or herniation change the mechanics of adjacent vertebral three joint complexes, causing added or unusual stress and changes in function. These stresses may be expressed as a facet syndrome with referred pain patterns that mimic radicular pain in the extremity. This type of pain syndrome generally responds well to chiropractic adjustments.

Finally, a significant number of asymptomatic people have been shown to have disc bulges and, to a lesser extent, even herniations.²⁵ This supports the notion that the disc’s effect on surrounding structures and the mechanics of the region may be as important as the direct effect on the nerve root.

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