The intervertebral discs in the lumbar spine, owing to trauma, degenerative changes, or a combination of both, may fail to remain in their normal place within the confines of the vertebral bodies, and in turn compress the nerve roots. 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 C1 to S2. 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. The high Type I collagen content to low proteoglycan and water ratio gives the annulus fibrosus its tensile strength and durability. By contrast, the high proteoglycan and water content to low Type II collagen ratio of the nucleus pulposus allows for resistance to compression, allowing the spine to cushion 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
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 (see Figure 4).
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 remainder.
Flexion of the spine causes compression of the anterior disc, 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 branch off within the central canal one level before their exit and descend vertically before exiting through the foramen from which they take their name (see Figure 5). For example, the L5 nerve root exits under the L5 pedicle. The nerve root first branches off the cauda equina [see below] between L4 and L5 and travels distally across the L5 vertebral body before exiting laterally under the pedicle of L5. As such, L5 is subject to compression by a central disc herniation of the L4/L5 disc, and (more commonly) by a lateral disc herniation at L5/S1.
(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).
Compression of the central spinal canal, also known as central prolapse, is rare but can be a surgical emergency when the herniated material impinges on the cauda equina.
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 in large herniations that are centrally located. Oftentimes, patients will describe worsening of pain with sitting or bending since this 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 and usually results in worsening of pain or paresthesias in the case of disc herniation. For this reason, a worsening of symptoms when the patient is asked to bend backwards is more consistent with a diagnosis of degenerative changes or spinal stenosis. Tenderness to palpation over the paraspinal muscles and over the spinous processes is not specific for a herniated disc.
The straight leg raise is the most important special test for diagnosing L5 or S1 radiculopathy. With the patient lying supine, the examiner passively lifts the affected leg (straightened at the knee) to 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 has a higher specificity but lower sensitivity, so may be used for confirmation.
Disc herniation with radiculopathy can be diagnosed on clinical findings but is, in the modern era, invariably confirmed with imaging, MRI in particular. Although an MRI is both highly sensitive and specific for describing the anatomy, it can detect findings that are not truly the cause of the symptoms (if any) and not truly in need of care (Figure 6)
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 recommends classifying the disc herniation as degenerative rather than traumatic.
MRI with gadolinium should be obtained when considering revision surgery since 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, and 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.
The differential diagnosis of disc herniation includes other causes of nerve root compression and inflammation, such as spinal stenosis, other mass lesions such as tumor, fibrosis from previous surgery, and spondylolisthesis. Degenerative joint disease can involve the presence of bone spurs which may also 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.
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, the “cauda equina” 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, also known as the conus medullaris. The cauda equina includes the nerve roots from lumbar and sacral regions. These nerves, 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. The nerves branching off beneath the termination of the spinal cord 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 a 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.
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 which can be done in a traditional open manner or microsurgically. In traditional discectomy, a surgical incision is made that allows for removal of the lamina superficial to the herniated disc and subsequent removal of a part of (or the entire) affected disc. A microdiscectomy is similar but involves use of an operative microscope and special retractors for a smaller incision and hemilaminectomy (removal of part of the lamina as opposed to the entire lamina). The herniated material is then removed.
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 herniation of the disc (in approximately 5% of patients within one year after surgery) and dural tears (which occur in ~1% of patients). Other, far less frequent, complications include vascular injuries and infection/discitis.
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 conservative therapy alone.
Laminotomy and discectomy have been shown to be significantly faster in improving pain over non-operative treatment, though this has not been shown in any sham trial, and thus a plecebo effect might confound the result. Factors associated with positive surgical outcomes include a positive straight leg raise, an MRI that is consistent with the patient’s complaint of weakness, leg pain as the primary symptom, and being married. 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 as 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.
Herniated disc, annulus fibrosis, nucleus pulposus, radiculopathy, neck pain, low back pain, sciatica, straight leg raise, Spurling test, discectomy, 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. https://pubmed.ncbi.nlm.nih.gov/24768732/
Meg's Note: Reorganization of headings was completed. Review: Patient Presentation, was clinical presentation and physical exam combined.