Herniated Nucleus Pulposus

Updated: Feb 02, 2017
  • Author: Mark R Foster, MD, PhD, FACS; Chief Editor: Jeffrey A Goldstein, MD  more...
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Nuclear material that is displaced into the spinal canal is associated with a significant inflammatory response, as has been demonstrated in animal studies. Disk injury results in an increase in the proinflammatory molecules interleukin (IL)-1, IL-8, and tumor necrosis factor (TNF)-α. Macrophages respond to this displaced foreign material and seek to clear the spinal canal. Subsequently, a significant scar is produced, even without surgery, and substance P, which is associated with pain, is detected.

Acute neural compression is responsible for dysfunction; compression of a motor nerve results in weakness, and compression of a sensory nerve results in numbness. Radicular pain is caused by inflammation of the nerve, which explains the lack of correlation between the actual size of an intervertebral disk herniation or even the consequent degree of neural compression and the associated clinical symptoms. [1]

Furthermore, intervetebral disk degeneration may result in radial tears and leakage of the nuclear material, which leads to neural toxicity. The subsequent inflammatory response often results in neural irritation causing radiating pain without numbness, weakness, or loss of reflex, even when neural compression is absent.

Several factors seem to influence the occurrence of herniated nucleus pulposus (HNP). Smoking is a risk factor in the epidemiology of lumbar disk herniations and has been documented to decrease the oxygen tension in the avascular disk dramatically, presumably by vasoconstrictive and rheologic effects on blood.

Lumbar disk herniation may result from chronic coughing and other stresses on the disk. For example, sitting without lumbar support causes an increase in disk pressures, and driving is also a risk factor because of the resonant coupling of 5-Hz vibrations from the road to the spine. People who drive signifcant amounts have increased spinal problems; truck drivers have the additional risk of spinal problems from lifting during loading and unloading, which, unfortunately, is done after prolonged driving.

Studies have shown that peak stresses within a deteriorated intervertebral disk exceed those from average loads on a normal disk, which is consistent with a pain mechanism. Further repetitive stress at physiologic levels did not produce a herniation after prolonged testing, contradicting the concept of injury accumulation with customary work activities. However, after a simulated injury to the annulus (cutting), a lower mechanical stress did result in disk herniation, consistent with intervertebral disk degeneration and with clinical experience on discography.

The presumed traumatic cause of disk herniations has been questioned scientifically in the literature, particularly with the increased availability of genetic information. [2, 3]

The pathologic state of a weakened annulus is a necessary condition for herniation to occur. Many cases involve trivial trauma even in the presence of repetitive stress. An annular tear or weak spot has not been demonstrated to result from repetitive normal stress from customary activities or from physically stressful activities.

Mixter and Barr first recognized that the cartilaginous masses in the spinal canal of their patients were not tumors or chondromas. [4]  They proposed that herniation of the nucleus pulposus and displacement of nuclear material caused neural irritation, inflammation, and pain. They showed that excising a disk fragment was effective, but their recommendation to perform this procedure with a fusion was necessitated by relatively aggressive laminectomy. This procedure has been replaced by techniques that are less invasive, such as microdiscectomy.



The intervertebral disc is the largest avascular structure in the body. It arises from notochordal cells between the cartilaginous endplates, which regress from about 50% of the disc space at birth to about 5% in the adult, with chondrocytes replacing the notochordal cells.

Intervertebral discs are located in the spinal column between successive vertebral bodies and are oval in cross-section. The height of the discs increases from the peripheral edges to the center, appearing as a biconvex shape that becomes successively larger by about 11% per segment from cephalad to caudal (ie, from the cervical spine to the lumbosacral articulation). A longitudinal ligament attaches to the vertebral bodies and to the intervertebral discs anteriorly and posteriorly; the cartilaginous endplate of each disc attaches to the bony endplate of the vertebral body. (See the images below.)

Nuclear material is normally contained within the Nuclear material is normally contained within the annulus, but it may cause bulging of the annulus or may herniate through the annulus into the spinal canal. This commonly occurs in a posterolateral location of the intervertebral disk, as depicted.
The spinal nerves exit the spinal canal through th The spinal nerves exit the spinal canal through the foramina at each level. Decreased disk height causes decreased foramen height to the same degree, and the superior articular facet of the caudal vertebral body may become hypertrophic and develop a spur, which then projects toward the nerve root situated just under the pedicle. In this picture, L4-5 has loss of disk height and some facet hypertrophy, thereby encroaching on the room available for the exiting nerve root (L4). A herniated nucleus pulposus within the canal would embarrass the traversing root (L5).

The disc's annular structure is composed of an outer annulus fibrosus, which is a constraining ring that is composed primarily of type 1 collagen. This fibrous ring has alternating layers oriented at 60° from the horizontal to allow isovolumic rotation. That is, just as a shark swimming and turning in the water does not buckle its skin, the intervertebral disc has the ability to rotate or bend without a significant change in volume and, thus, does not affect the hydrostatic pressure of the inner portion of the disc, the nucleus pulposus.

The nucleus pulposus consists predominantly of type II collagen, proteoglycan, and hyaluronan long chains, which have regions with highly hydrophilic, branching side chains. These negatively charged regions have a strong avidity for water molecules and hydrate the nucleus or center of the disc by an osmotic swelling pressure effect. The major proteoglycan constituent is aggrecan, which is connected by link protein to the long hyaluronan. A fibril network, including a number of collagen types along with fibronectin, decorin, and lumican, contains the nucleus pulposus.

The hydraulic effect of the contained, hydrated nucleus within the annulus acts as a shock absorber to cushion the spinal column from forces that are applied to the musculoskeletal system. Each vertebra of the spinal column has an anterior centrum or body. The centra are stacked in a weightbearing column and are supported by the intervertebral discs. A corresponding posterior bony arch encloses and protects the neural elements, and each side of the posterior elements has a facet joint or articulation to allow motion.

The functional segmental unit is the combination of an anterior disc and the two posterior facet joints, and it provides protection for the neural elements within the acceptable constraints of clinical stability. The facet joints connect the vertebral bodies on each side of the lamina, forming the posterior arch. These joints are connected at each level by the ligamentum flavum, which is yellow because of the high elastin content and allows significant extensibility and flexibility of the spinal column.

Clinical stability has been defined as the ability of the spine under physiologic load to limit patterns of displacement so as to avoid damage or irritation to the spinal cord or nerve roots and to prevent incapacitating deformity or pain caused by structural changes. [5] Any disruption of the components holding the spine together (ie, ligaments, intervertebral discs, facets) decreases the clinical stability of the spine. When the spine loses enough of these components to prevent it from adequately providing the mechanical function of protection, surgery may be necessary to reestablish stability.



Degeneration: process and models

Low back pain (LBP) is ubiquitous, with 60-80% of people having an activity-limiting episode at least transiently in their lifetime. Genetic factors appear to have a dominant role, with LBP starting at an earlier age than previously suspected on the basis of subsequent structural changes; men begin having LBP about a decade earlier than women. [6]

The water-retaining ability of the nucleus pulposus, or the inner portion of the intervertebral disk, declines progressively with age. The decline in the mechanical properties of the nucleus pulposus is associated with the degree of proteoglycan deterioration and the decrease in hydration, which lead to excessive regional peak pressures within the disk. As the hyaluronan long chains shorten and swelling pressure decreases as a result of this deterioration, the mechanical stiffness of the disk decreases, which causes the annulus to bulge, with a corresponding loss of disk and foramen height. [7]  (See the image below.)

Hyaluronan long chains form a backbone for attract Hyaluronan long chains form a backbone for attracting electronegative or hydrophilic branches, which hydrate the nucleus pulposus and cause a swelling pressure within the annulus to allow it to stabilize the vertebrae and act as a shock absorber. Deterioration within the intervertebral disk results in loss of these water-retaining branches and eventually in the shortening of the chains.

The etiology of back pain for a particular individual cannot be determined, because of the multiplicity of potential sources. Although periosteal disruption causes pain with fractures, bone itself is devoid of pain receptors (eg, asymptomatic compression fractures commonly are seen in the thoracic spine of elderly individuals with osteoporosis). However, the degenerating intervertebral disk is known to have neurovascular elements at the periphery, including pain fibers.

Disk deterioration and loss of disk height may shift the balance of weightbearing to the facet joint; this mechanism has been hypothesized as a cause of LBP through the facet joint capsule, as well as through other tissues attached to and between the posterior bony elements.

When the annulus in animals is incised, a degenerative cascade is initiated that mimics the natural aging process observed in humans, thus providing a model of disk deterioration. [8] As the use of discography has increased for various clinical applications, similar annular tears are seen routinely that are associated with the degeneration of the intervertebral disk, even in patients who are asymptomatic. Annular tears may simply be the result of aging and the degenerative cascade.

Pathology studies of young patients who died as a result of trauma reveal a surprising degree of articular surface damage in the facet joints; magnetic resonance imaging (MRI) routinely reveals disk deterioration in individuals in the second or third decade of life. Injection of chymopapain into the intervertebral disk causes a repeatable and predictable degenerative cascade in the facet joints, illustrating the coupling between the disk and facet joints. Immobilization by facet fusion posteriorly leads to disk deterioration; this avascular structure is solely dependent upon motion to facilitate the diffusion of nutrients into it.

Whether the deterioration of the disk or that of the facet comes first has not been determined; however, deterioration is known to occur in both.

Dehydration results from shortening of the hyaluronic chains, deterioration of the state of aggregation, and decreases in the ratio of chondroitin sulfate to keratan sulfate, leading to the disk bulging and disk height loss. The consistency of the nuclear material undergoes a change from a homogeneous material to clumps, which leads to the altered distribution of pressures within the disk and resistance to the flow of nuclear material; the nuclear material thereby becomes mechanically unstable. [9] The clumping of the degenerating nuclear material can be likened to a marble held between two books—that is, it is difficult to contain.

These clumps may be lateral to the posterior longitudinal ligament and, therefore, may have the least resistance to herniating through the corner of the intervertebral disk and into the spinal canal or foramen. Surgical removal of the herniated fragments is achieved by grasping them with a pituitary rongeur.

This method of surgical removal is not possible with normal, homogeneous material, which is encountered when healthy interverterbral disks are excised anteriorly in patients having surgery because of deformity or trauma. Using the pituitary rongeur technique to perform a microdiscectomy on a herniated fragment necessitates a preexisting state of deterioration; the weakened areas in the annulus provide a path of least resistance for the nuclear material to egress.

Natural history

Much has been written concerning the process of spinal deterioration or spondylosis, which occurs over a lifetime. Intervertebral disk deterioration leads to decreased stiffness of the disk, as well as diminished stability, resulting in episodic pain that is common and may be temporarily severe. However, continued deterioration ultimately leads to restabilization of the spine by collagenization, which stiffens the disk. Patients in their 50s and 60s customarily have stiffer spines but less pain than patients in their 30s and 40s who are undergoing initiation of the degenerative cascade.

Patients who ask if they have to live with this pain "for the rest of their lives" can be reassured to some extent by this natural history. Furthermore, spontaneous recovery from an acute pain episode routinely occurs, so any treatment must be demonstrated as effective by positively altering the expected course without treatment.

In general practice, the overall incidence of HNP in patients who have new LBP onset is lower than 2%. Therefore, most of these patients have deterioration of the intervertebral disk and dysfunction of the functional segmental unit. They will have LBP, and some will have associated leg pain but without sciatica (an intractable, radiating pain, below the knee) or radiculopathy. A disk fragment that is no longer contained within the annulus but is displaced into the spinal canal has decreased hydration and deteriorated proteoglycan that can be expected to undergo further deterioration and consequent annular desiccation, essentially like a grape being transformed into a raisin.

Spontaneous resolution of sciatica may result from shrinkage of a herniated fragment, aided by macrophages and the evoked inflammatory reaction, but practitioners too often attribute this clinical improvement to their favorite treatments. Intractable symptoms of sciatica from intervertebral disk displacements may benefit dramatically from surgical intervention.

Within 20 years of Mixter and Barr's 1934 report, Friedenberg compared operative treatment with nonoperative treatment. [4, 10] Nonoperative treatment yielded three groups of results: pain free, occasional residual pain, and disabling pain. Proportions of these groups remained similar after 5 years. Friedenberg concluded that even recurrent severe episodes may resolve without surgery; the problem was and remains patient selection.

Weber presented a randomized, controlled study (marred by dropouts in the surgery control group because of severe pain) and concluded that patient results were the same with operative as with conservative treatment, except that those who were treated operatively had better results at 1 year. [11]

The Spine Patient Outcomes Research Trial (SPORT) observational cohort is similarly limited in its conclusions by crossovers: 50% of the surgery arm had surgery within 3 months and 30% of the nonsurgical group had surgery, but at long-term follow-up, the two groups again were not statistically different. [12]



Patients with "broad-based" intervertebral disk herniations generally have a deterioration of the disk or a failure of clinical stability with associated back pain, rather than isolated sciatica. These patients are not appropriate candidates for microdiscectomy alone.

Lumbar fusion is being used increasingly in these cases, and arthroplasty is also being considered; however, this treatment remains controversial because it is, again, based inevitably on subjective patient pain and clinical judgment without objective determination. Many reports in the literature have described specific cytokines elevated, but not comprehensively; endplate changes are observed but no clear correlation identified to this point. Various nuclear replacements that reduce postoperative loss of disc height restoring compressive loading are being studied. [13]

With a discectomy, patients with dominant leg pain have excellent results, with 85-90% returning to full function. However, as many as 15% of patients have continued back pain that may limit their return to full function, despite the absence of radiculopathy. Patients who undergo surgery do not necessarily show better results than patients who defer surgery. [14]

The remaining concern of recurrent herniation is small, though it is correlated with obesity. [15]  Efforts to minimize this complication have included annulus repair [16]  and injecting hemostatic materials or bioactive molecules. Etanercept was shown in a small study to be of no benefit for sciatica, although the addition of butorphanol with corticosteroid was helpful with an epidural injection. [17]

Intervertebral disk degeneration that causes clumping of the nuclear material and relative mechanical instability is the necessary preceding condition for HNP. However, it is impossible to tell which patients will do well after microdiscectomy for a herniation and which will have continued problems, of varying severity, from the disk degeneration. Studies have shown that degenerated discs have different growth factors and other molecules; thus, even introducing mesenchymal stem cells requires significant further research and development. [18]

Significant deterioration and accompanying LBP increasingly are being treated with stabilization, via either an anterior lumbar interbody fusion (ALIF) or a posterior lumbar interbody fusion (PLIF) in association with posterior decompression (when necessary) and instrumentation. Results are not yet available, as techniques are still evolving, but experience is accumulating.

Tomasino et al presented radiologic and clinical outcome data on patients who underwent single-level anterior cervical discectomy and fusion (ACDF) for cervical spondylosis and/or disc herniation using bioabsorbable plates for instrumentation. [19] Overall, at 19.5 months postoperatively, 83% of the patients had favorable outcomes based on the Odom criteria.

The authors found that absorbable instrumentation provides better stability than the absence of a plate but that graft subsidence and deformity rates may be higher than those associated with metal implants. In this study, the fusion rate and outcome were found to be comparable to the results achieved with metallic plates, and the authors concluded that the use of bioabsorbable plates is a reasonable alternative to metal, avoiding the need for lifelong metallic implants. [19]

Buchowski et al performed a cross-sectional analysis of two large prospective, randomized multicenter trials to evaluate the efficacy of cervical disc arthroplasty for myelopathy with a single-level abnormality localized to the disc space. [20] The authors found that patients in both the arthroplasty and arthrodesis groups had improvement following surgery, with improvement being similar and with no worsening of myelopathy occurring in the arthroplasty group.

The authors noted that although the findings at 2 years postoperatively suggest that arthroplasty is equivalent to arthrodesis in these cases, they did not evaluate the treatment of retrovertebral compression as occurs with ossification of the posterior longitudinal ligament. [20]

Carragee et al compared progression of common degenerative findings between lumbar discs injected 10 years earlier with those same disc levels in matched subjects who were not exposed to discography. [21] The authors found that in all graded or measured parameters, discs exposed to puncture and injection had greater progression of degenerative findings than the control (noninjected) discs. Progression of disc degeneration was 35% in the discography group, compared to 14% in the control group, with 55 new disc herniations occurring in the discography group and 22 in the control group.

The study also found significantly greater loss of disc height and signal intensity in the discography discs. The authors noted, therefore, that careful consideration of risk and benefit are necessary in regard to disc injection. [21]

McGirt et al performed a prospective cohort study with standardized postoperative lumbar imaging with computed tomography (CT) and magnetic resonance imaging (MRI) every 3 months for a year, then annually, to assess same-level recurrent disc herniation. [22] Improvement in all outcome measures was observed 6 weeks after surgery. At 3 months after surgery, 18% loss of disc height was observed, which progressed to 26% by 2 years. In 11 (10.2%) patients, revision discectomy was required at a mean of 10.5 months after surgery.

According to the authors, patients who had larger anular defects and removal of smaller disc volumes had increased risk of recurrent disc herniation, and those who had greater disc volumes removed had more progressive disc height loss by 6 months after surgery. The authors suggested, based on the findings, that in cases of larger anular defects or less aggressive disc removal, concern for recurrent herniation should be increased and that, in such cases, effective anular repair may behelpful. [22]

Fish et al performed a retrospective single-center study to analyze whether MRI findings could be used to predict therapeutic responses to cervical epidural steroid injections (CESI) in patients with cervical radiculopathy. [23] Patients were categorized by the presence or absence of four types of cervical MRI findings: disc herniation, nerve root compromise, neuroforaminal stenosis, and central canal stenosis.

The authors found that only the presence, versus the absence, of central canal stenosis was associated with significantly superior therapeutic response to CESI. They therefore concluded that the MRI finding of central canal stenosis is a potential indication that CESI may be merited. [23]

Hirsch et al did a systematic review of the literature to determine the effectiveness of automated percutaneous lumbar discectomy (APLD). [24] According to the authors, based on United States Preventive Services Task Force (USPSTF) criteria, the indicated evidence for APLD is level II-2 for short- and long-term relief, indicating that APLD may provide appropriate relief in properly selected patients with contained lumbar disc prolapse. However, the authors noted that there is a paucity of randomized, controlled trials in the literature covering this subject.

Dasenbrock et al performed a meta-analysis of six trials of 837 patients comparing open discectomy with minimally invasive discectomy and found similar visual analogue scale (VAS) scores at short and long-term follow-up. Results showed no significant difference in relief of leg pain between the two approaches. Reoperation was more common with limited (tubular) exposure but not statistically significant, and total complications did not differ. [25]