Lumbar Disc Disease

The intervertebral discs in the lumbar spine may fail to remain within the borders defined by the vertebral bodies and in turn compress nerve roots. This process can be caused by trauma, degeneration or a combination of both. In laymen’s terms, this condition is known as a ‘slipped disc.’ Disc pathology is a common cause of low back pain and radicular leg pain, typically affecting the L4-L5 and L5-S1 levels. Diagnosis is made by history and physical examination, with MRI confirmation. Non-operative management with NSAIDs and physical therapy is usually successful, though surgical decompression is indicated for disabling pain or progressive neurological deficits.

Structure and Function

There are 23 spinal discs in the human body, found between adjacent vertebral bodies from C2 to S1. The discs absorb axial forces such as body weight and landing after jumping; they also aid in spinal movements such as flexing and twisting.

Intervertebral discs have a strong, fibrous outer layer, known as the annulus fibrosus, and a gel-like inner layer, known as the nucleus pulposus. Both the annulus fibrosus and the nucleus pulposus contain type-I collagen, proteoglycans and water.In the annulus fibrosus, there is more collagen relative to proteoglycan and water. The high collagen content gives the annulus fibrosus tensile strength. By contrast, the nucleus pulposus has more proteoglycan and water than collagen, and is accordingly particularly good at resisting compression and axial loads.

The normal disc lies wholly within the boundaries of the so-called disc space: this is defined above and below by the vertebral body end plates and peripherally by the outer edges of the vertebral body (see Figure 1).

Figure 1: An axial (A), sagittal (S) and coronal (C) schematic view of the disc. The annulus fibrosus is shown in orange and the nucleus puposus in pink. As seen on the sagittal view (and implicit on the axial view as well), the posterior aspect of the disc is in line with the posterior aspect of the vertebral body. (Modified from Fardon; see acknowledgment below.)

According to the nomenclature recommended by the North American Spine Society, the American Society of Spine Radiology and the American Society of Neuroradiology, a disc that has left its disc space can be termed a “herniation” if there is focal displacement (representing < 25% of the disc circumference), or a “bulge” if the disc material is displaced throughout the circumference of the disc.

A disc herniation in turn can be classified as a protrusion or an extrusion, depending on the geometry of the disc material outside of the disc space. If the base is wider than the distance displaced, a protrusion is present, whereas with extrusion, the displaced disc is narrower than the base (see Figures 2 and 3).

Beyond that, extruded discs may lose their continuity with the disc from which they came. This is known as a sequestered disc herniation. Discs may also herniate into the vertebral body itself, via defects in the end plate. These are called intravertaebral herniations (see Figure 4).

Figure 2: A bulging disc to the right, with a normal disc on the left. As shown in red, there is symmetric bulging of the annulus beyond the edges of the vertebral body, symmetrically throughout the circumference of the disc. (Modified from Fardon.)
Figure 3: Axial views of a herniated disc: protrusion type (P) is shown at left, with an extrusion (E) shown in the right image. Contrasted with a bulge, with a herniation the disc displacement is focal. The distinction between protrusion and extrusion is that in the protrusion type the length of the displaced disc (green line) is less the width (red line). (Modified from Fardon.)

Figure 4: Axial (left) sagittal (right) images show a sequestered disc, cut off from the disc of origin (red star). (Modified from Fardon.)

Disc herniations occur when a tear in the annulus fibrosus allows the nucleus pulposus to push through this outer layer. The herniated material may compress the central spinal canal or nearby nerve roots. Herniations are most commonly posterolateral or paracentral (~90%) because the posterior longitudinal ligament (PLL) is weakest laterally. (Far lateral herniations that can enter the neural foramen directly represent the remaining 10%.)

Flexion of the spine causes compression of the anterior disc, potentially distending the material against the tensed posterior. When the PLL tears along with the annulus fibrosus, the herniation is considered “not contained.” When the PLL fibers are weakened but still preserved, the herniation is “contained.”

In the lumbar spine, the nerve roots are named by the level of the pedicle under which they exit the spine. For example, the L5 nerve root exits under the L5 pedicle (see Figure 5). Note that the nerve roots branch off the cauda equina [see below] within the central canal one level above their exit point, and descend vertically within the canal before exiting through the foramen. The L5 nerve, again by example, branches off the cauda equina between the L4 and L5 vertebrae, and travels distally across the L5 vertebral body before exiting laterally under the pedicle of L5. As such, L5 is subject to compression at two distinct places: by a central disc herniation of the L4/L5 disc, and (more commonly) by a lateral disc herniation at L5/S1.

Figure 5: The lumbar nerve roots are shown. The branching off of the L5 root is shown by the green star, with the areas of central and lateral compression shown by the red and purple boxes, respectively.Figure 5: The lumbar nerve roots are shown. The branching off of the L5 root is shown by the green star, with the areas of central and lateral compression shown by the red and purple boxes, respectively.

(The lumbar arrangement lies in contrast to that of the cervical spine, where nerve roots transverse horizontally across one disc and exit under the pedicle of the body numbered above (so-called “mismatch”). That is, the C5 root exits under the C4 pedicle. Because of the root’s horizontal path in the cervical spine, a herniation at C4-5 herniation will affect the C5 nerve root, if any, independent of whether the disc herniation is central or lateral).

Severe compression of the central spinal canal that causes severe stenosis is rare but can be a surgical emergency when the herniated material impinges on the cauda equina. Cases where the compression causes significant bilateral lower extremity motor/sensory deficits or bowel/bladder dysfunction requires urgent surgical intervention.

Patient Presentation

Lumbar disc bulges and herniations can present as axial pain when associated with degenerative disc disease. If there is nerve root compression or irritation, patients might complain of pain or paresthesias traveling from the back to the buttock and down the posterior leg, so-called radicular symptoms. When the L4-L5 level is involved, pain may wrap around the leg to the dorsum of the foot. With L5-S1 herniations, symptoms are more commonly present on the plantar side of the foot. Muscle weakness may also be a complaint. Symptoms are usually unilateral but can be bilateral when large herniations are centrally located. Oftentimes, patients will describe worsening of pain with sitting or bending, a motion that exacerbates disc bulging.

The physical examination begins with an assessment of gait. Strength testing of the lower extremity muscles should be performed and graded on a 0 to 5 scale. Knee extension and ankle dorsiflexion tests L4 motor function, and physical exam for L4 nerve root injury may also reveal a weakened patellar reflex. L5 is the major nerve root controlling hip abduction and great toe extension (which may be easier to test). The S1 nerve root can be tested by having the patient toe walk: plantar flexion via gastrocnemius and soleus function relies on this nerve root.

Active and passive range of motion as well as strength testing of the hip can reveal abnormalities and is important to perform since hip pain is commonly mislabeled as back pain. Range of motion of the spine should be evaluated by flexion, extension, rotation, and bending to either side. Flexion of the spine increases the load on the posterior disc. This motion therefore usually results in worsening of pain or paresthesias when a disc herniation is present. In contrast, a worsening of symptoms on extension is more consistent with a diagnosis of degenerative arthritis. Tenderness to palpation over the paraspinal muscles and over the spinous processes is not specific for a herniated disc.

The straight leg raise is an important, albeit subjective, test for diagnosing L5 or S1 radiculopathy. With the patient lying supine, the examiner passively lifts the affected leg (straightened at the knee) from 30 to 70 degrees. If this maneuver reproduces the patient’s radiating pain or paresthesias, it is considered positive. Pain reproduction when testing the contralateral leg (lifting the asymptomatic leg and causing pain of the symptomatic leg) has a higher specificity but lower sensitivity, so may be used for confirmation.

Objective Evidence

Disc herniation with radiculopathy can be diagnosed on clinical grounds, but is invariably diagnosed by MRI(Figure 6). MRI is both highly sensitive and specific for describing the anatomy, although it may detect findings that are clinically incidental. As such, MRI is best used to answer a specific clinical question, and not as a screening or surveillance modality.

Figure 6: Sagittal (left) and axial (right) images of an extrude disc herniation [red circles]. (Case courtesy of, rID: 2670)

MRI can help discern the cause of disc herniation. If there is imaging evidence of violent trauma and no evidence of degeneration, causality can be established. On the other hand, in the presence of degenerative changes and without significant imaging evidence of an associated violent injury such as fracture or dislocation, the Fardon task force (see Acknoledgwments, below) recommends classifying the disc herniation as degenerative rather than traumatic.

MRI with gadolinium should be obtained when considering revision surgery, because post-surgical scarring will enhance with contrast while recurrent disc herniation will not. Gadolinium is also necessary if there is suspicion of neoplastic or infectious etiology. If plain radiography is performed, findings may include narrowing of the space between adjacent vertebral bodies, loss of lumbar or cervical lordosis, or spondylosis.

Additionally, electrodiagnostic studies can help rule out peripheral neuropathy as the cause of extremity symptoms.


More than 90% of disc herniations occur in the lumbar spine, due to its prominent role in flexion and extension. Most lumbar herniations are at the L4-L5 or L5-S1 levels. Lumbar disc herniations occur most frequently between the ages of 40 and 60, but can occur at almost any age after 18 years. Males have nearly a three times higher incidence of lumbar disc herniation.

Notably, many disc herniations may not cause symptoms. In the classic study of Boden et al [J Bone Joint Surg Am 1990 Mar;72(3):403-8.], about one-third of the population of asymptomatic volunteers were seen to have a “substantial abnormality” on MRI: of those who were less than sixty years old, 20% had a herniated disc and in the group that was sixty years old or older, 36% of the subjects had a disc herniation.

Differential Diagnosis

The differential diagnosis of disc herniation includes other causes of nerve root compression and inflammation, including spinal stenosis, mass lesions such as a tumor, fibrosis from previous surgery, and spondylolisthesis. Degenerative joint disease can produce bone spurs which may impinge on a nerve root. A hematoma should be considered in patients taking anticoagulants, who have recently had a spinal puncture procedure, or who have suffered trauma to the back.

Axial pain from facet joint degenerative joint disease usually presents as ill-defined pain, worse with activity and relieved with rest. Degenerative joint disease usually does not cause pain to radiate down the extremities, but some patients may describe low back pain traveling below the buttocks. Infectious etiologies such as osteomyelitis and discitis usually present as localized pain and do not radiate.

Red Flags

Cauda equina syndrome is a very rare and serious presentation of massive disc herniation in which the bundle of nerve roots at the end of the spinal cord are compressed within the spinal canal. The cauda equina consists of the nerve roots and rootlets that branch off of the lower end of the spinal cord (the conus medullaris). The cauda equina includes the nerve roots from lumbar and sacral regions. These nerve roots, although branched off the spinal cord itself at roughly the L1 vertebral level, remain within the central canal until they exit at their appropriate neural foramen. These nerves are said to resemble a horse's tail, hence the name cauda equina (Figure 7).

Cauda equina syndrome occurs when the nerves of the cauda equina are compressed by any space-occupying lesion, including a large herniated disc, tumor, epidural abscess, or bony protrusion. The compression of multiple nerves in the cauda equina often leads to unilateral or bilateral lower extremity pain and sensorimotor changes, bowel/bladder dysfunction, which can manifest as incontinence or urinary retention (with overflow incontinence and increased post-void residuals). Patients may also present with sexual dysfunction, saddle anesthesia, and absence of lower extremity reflexes.

Figure 7: The cauda equina. The neural elements are shown in yellow. The region of the spinal cord (SC), ending usually at L1-L2, is identified by the green brackets, and that of the cauda equina (CE) distal to that.

Weight loss or a diagnosis of cancer elsewhere in the body are red flags for spinal metastases. A history of IV drug use, fevers, or an elevated WBC count should raise suspicion for an abscess, osteomyelitis, or discitis.

Treatment Options and Outcomes

Nearly all patients will have sufficient improvement of symptoms within 3 months with non-operative care. Non-operative treatment includes the use NSAIDs or acetaminophen, exercise and dieting for weight loss, and physical therapy.

Patients should gradually increase activity as tolerated. Bedrest is unwise.

Second-line medications include muscle relaxants such as cyclobenzaprine or a corticosteroid taper.

Surgery should be reserved for patients who have failed non-operative therapy or patients with significant or progressive neurologic deficits, such as those with cauda equina syndrome.

Operative treatment includes hemilaminotomy and discectomy of which can be done in a traditional open manner or microsurgically. In traditional discectomy, a surgical incision is made that allows for removal of a portion of the lamina superficial to the herniated disc. The herniated material is then removed. A microdiscectomy is a similar procedure, but involves use of an operative microscope and special retractors for a smaller incision.

Post-operative rehabilitation is relatively simple, with the majority of patients returning to medium or high-intensity activity after 4 to 6 weeks. Complications of surgery include recurrent herniated disc (most common approximately 4% during the first year after surgery), dural tear (in 1-2% of patients), and discitis (less than 0.5% of patients).

The natural progression of a herniation is to decrease in size over time via reabsorption, which is mediated by macrophage phagocytosis. Within 3 months, over 90% of patients will see an improvement in their symptoms through non-operative treatment alone.

Laminotomy and discectomy have been shown to produce a significantly faster reduction in pain compared with non-operative treatment in observational studies. (Note that this result has not been shown in any sham trial, and thus a placebo effect might confound the result.) Factors associated with better surgical outcomes include a positive straight leg raise test pre-operatively, an MRI that is consistent with the patient’s complaint of weakness, and leg pain as the primary symptom. Social factors may play a role too, as being married is also associated with better outcomes. When worker’s compensation is involved in the case, surgical patients are less likely to see improvement in their symptoms and quality of life. Revision surgery outcomes for herniation recurrence are not significantly worse than primary surgery outcomes.

Risk Factors and Prevention

The incidence of disc herniation increases with age. With aging, the vertebral discs lose water content and flexibility and the gel-like nucleus pulposus is replaced with fibrocartilage. Several genes have been implicated in the development accelerated degeneration including those coding for extracellular matrix proteins such as type I collagen, Vitamin D Receptor, and matrix metalloproteinases.

Obesity is associated with disc herniation due to the increased load placed on the spine. Likewise, a sedentary lifestyle, itself associated with obesity, is a risk factor for herniation as the seated position focuses pressure on the internal part of the disc.

Athletes playing contact sports are prone to disc herniation via sudden rotational movements and flexion of the spine.

Disease prevention is aimed at maintaining a healthy weight, strengthening core and back muscles for spine support, practicing good posture, and education on proper technique of lifting heavy objects (using one’s legs and not bending over at the waist). Weightlifters should be encouraged to use support belts and to recognize signs of fatigue before they regress into improper lifting form.


Harrison Ford suffered a herniated disc while riding an elephant in Sri Lanka during the filming of Indiana Jones: Temple of Doom.

Key Terms

Herniated disc, annulus fibrosis, nucleus pulposus, radiculopathy, neck pain, low back pain, sciatica, straight leg raise, Spurling test, discectomy, cauda equina syndrome


Distinguish radicular pain from axial and referred low back pain by taking a focused history. Perform strength testing of ankle dorsiflexion, hallux extension, and ankle plantarflexion to distinguish between the L4, L5, and S1 level, respectively. Be able to perform a straight leg raise and contralateral straight leg raise to provoke lumbar radiculopathy. Know the red flags for low back pain and identify the indications for obtaining an MRI study.


This chapter draws heavily on the paper by Fardon et al, Lumbar disc nomenclature: version 2.0: Recommendations of the combined task forces of the North American Spine Society, the American Society of Spine Radiology and the American Society of Neuroradiology. Spine J. 2014 Nov 1;14(11):2525-45.

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