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Lumbar disk disorders include degenerative disk disease (disk desiccation, annular fissures and tears, loss of disk height and bulges), disk herniations (displacement of nuclear material outside the annulus fibrosus),1,2 and infectious etiologies (diskitis). When symptomatic, this can lead to axial back pain, radiculopathy, or cauda equina syndrome.3


The Kirkaldy-Willis degenerative spine cascade is the most accepted theory on events that ultimately lead to the development of spondylosis and stenosis. The theory highlights the interaction between the posterior spinal elements (facet joints) and the anterior spinal element (intervertebral disk) in establishing a 3-joint complex that undergoes 3 phases in a parallel fashion with a gradual change in the anterior spine bearing 80% to 90% in a healthy spine to equal weightbearing as degeneration reaches end stage.1 Phase 1, the dysfunctional phase, involves development of annular fissures and tears secondary to repetitive microtrauma which leads to blood vessel damage and subsequent inability to supply cells with nutrients and remove cytotoxic waste.  These factors predispose the disk to herniation and impacts its ability to retain water, leading to a loss of disk height. Phase 2, the instability phase, involves disk resorption, internal disk disruption, and additional tears, causing loss of mechanical integrity at the 3-joint complex. Phase 3, the stabilization phase, involves further diskspace narrowing, fibrosis, and osteophyte formation.1,5

Epidemiology including risk factors and primary prevention

The lifetime prevalence of low back pain is 80%, with disk disorders being the most common cause of adult low back pain.6 The most consistent risk factor for degeneration is increasing age. No difference related to gender has been determined.

Correlations have been found with

  • Body mass index, mechanical loading, and genetic predisposition.5
  • Genes coding for collagen, aggrecan, vitamin D receptors, matrix metalloproteinase, cartilage intermediate layer protein, and interleukins.7
  • Smoking and increased rates of disk degeneration, with animal models showing increased proinflammatory markers, alterations to annular structure, vasoconstriction, and altered nutrient distribution to the disk.8


Lumbar disks are generally 4-cm wide, 7 to 10 mm in height, and are involved with transmitting loads and providing flexibility to facilitate movement. There is an outer ring (annulus fibrosis) and an inner core (nucleus pulposus), both made up of differently organized collagen and elastin fibers with a highly hydrated aggrecan-containing gel found in the nucleus,9 which are surrounded by cartilage endplates superiorly and inferiorly.  The nerves that supply innervation to the disk are located in the outer 1/3 of the annulus fibrosis

Pathophysiology: disk degeneration develops as previously described. Herniations are seen with progressive loss of hydration, which leads to a loss of disk height and inappropriate transfer of load to the annulus and endplates. About 95% of herniations take place at the L4-5 and L5-S1 levels. Next most common are L3-4 and L2-3. Despite knowing the anatomic changes that take place, there is no clear relations between those changes and generation of pain. Inflammatory cascades, mechanical compression, instability, muscular imbalances, and psychosocial factors also contribute to perception of pain.2

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Lumbar disc degeneration is common, often found incidentally in otherwise asymptomatic patients.  It is usually benign, having little correlation with function or pain.10 When symptomatic, the most common complaint is pain.  About 85% of patients seen for low back pain do not receive a specific diagnosis.11 Of those patients with back pain, it is estimated that 39% are related to diskogenic pain. 12Given the limited ability to isolate the pain generators, establishing the diagnosis of and defining the course of symptomatic lumbar disk disorders can be challenging. It is generally reported that 90% of patients with low back pain will have their symptoms subside within 6 weeks,5 without medical intervention. Of those with herniations, it is thought that spontaneous regression of the disk contributes to improvement of symptoms. The exact mechanism of regression is unclear; hypotheses include dehydration leading to shrinking of disks, retraction of disks, and recognition of disks as a foreign body, resulting in macrophage phagocytosis of the disk.13 It has been shown that regression is far more likely in disc extrusion and sequestration compared to bulging and protruding disc.14

Specific secondary or associated conditions and complications

Complications include myelopathy or cauda equina syndrome, which can result in neurogenic bowel, neurogenic bladder, motor weakness, sensory loss or impairment, impaired mobility, and long-term disability.

Essentials of Assessment


  • Onset: after inciting event, which required flexion and rotation, some may not have an identifiable event.
  • Character: aching, sore, and stabbing.
  • Location: most likely midline lower back pain,15 but can refer to groin, genitals, abdomen, buttocks, and extremities.
  • Worse with flexion, sitting, twisting, lifting, vibration, coughing, and sneezing. Better with frequent position change or extension.1,6
  • Medical history: prior spine surgeries (lumbar arthrodesis, diskectomy, or laminectomy make remaining disks susceptible),1 history of cancer, steroid/drug use, and recent systemic or local infections. Because psychosocial factors also play a role in pain, review psychiatric and social history.
  • Red flags: bowel or bladder issues (retention/incontinence), saddle anesthesia, and motor weakness are concerning for myelopathy or cauda equina syndrome. Fevers/chills should raise suspicion for infectious etiology. Night sweats, constant pain that is worse at night, unintentional weight loss, and pain not improved with conservative therapy should raise suspicion for malignancy. Low back pain in older adults or the immunosuppressed merit workup for fracture.

Physical examination

  • Vitals: fever, tachycardia, or blood pressure abnormalities may indicate systemic pathology.
  • Inspection: need for repositioning, preferred position (standing or sitting in extension decreases disk load), body habitus (excess weight may add load to disks), surgical scars, mood, and reaction to exam maneuvers.
  • Range of motion: Lumbar range of motion may be limited, particularly in flexion.
  • Palpation: paraspinals may be tender or tight and spinous tenderness or step deformity may indicate spondylolisthesis.
  • Neurologic exam: sensation, strength, reflexes, and gait may be full and symmetric. Impaired sensation, focal weakness, or hyperreflexia may localize associated radiculopathy.
  • Provocative maneuvers: seated and supine straight leg raise and femoral nerve stretch test.1,2

Functional assessment

  • Cognition usually within normative limits, unless a preexisting condition exists.
  • Behavior: pain out of proportion to exam may indicate nonorganic pathology.
  • Mobility/gait: evaluate tandem, heel, and toe walking, which may assist in identifying associated radiculopathy or myelopathy.

Laboratory studies

There is no indicated laboratory study or marker for lumbar disk disorders. Specific laboratory studies may be indicated to evaluate for systemic inflammatory or neoplastic diseases when appropriate, but are rarely necessary.1,16


  • Lumbar radiograph: initial imaging, obtain anteroposterior and lateral view; signs of pathology include loss of disk height and end plate sclerosing.1
  • Magnetic resonance imaging (MRI): current standard, may see desiccation, herniations, Modic endplate changes, and high intensity zones, indicating annular tears.1,17 While considered the gold standard, MRI is overused, despite evidence-based guidelines and recommendations to avoid obtaining an MRI within the first six weeks of pain without red flags, or before conservative treatments have been attempted given the sensitivity rate as low as 0.52 and a sensitivity of 0.82. Based on these results, MRI findings need to be correlated to symptoms and physical examination findings.18,19
  • Computed tomography: an alternative when MRI is contraindicated (pacemakers, non-clinical tattoos, aneurysm clips).2 Can see calcified disk herniations, which might predict that surgery could be indicated.
  • Bone scan: sensitive in identifying occult fractures, bone metastasis, and infections.2
  • Of note, diagnostic studies are not recommended in otherwise healthy patients with no red-flag symptoms as above where pain has been present for less than 6 weeks without the completion of physical therapy with the exception of pain causing complete immobilization or hospital admission.16

Supplemental assessment tools

Provocative diskography is a controversial diagnostic test for diskogenic pain. Contrast material is injected into the suspected disk and adjacent disks. Exact reproduction of the patient’s pain at low pressures with painless adjacent disks indicates a positive test.9,20 Despite its questionable safety and diagnostic utility given the poor correlation with outcomes after spinal surgery, diskogram is still being widely performed although rates are trending downward.20 Postdiskography diskitis is considered one of the more severe possible complications. Other complications include triggering degeneration of a previously healthy disk, vasovagal reactions, paravertebral muscle pain and penetration of the disk’s ventral ramus. Retrospective studies have shown a significant increase in lumbar surgeries, prolonged back pain episodes, and work loss in diskography patients compared to controls over the long term (10 years), showing that some of the negative outcomes from this procedure may take up to a decade or more to become apparent.21

Early predictions of outcomes

Research involving prognostic factors has focused on outcomes after surgical intervention for disk herniation. In that setting, lack of back pain, absence of a work-related injury, radicular symptoms, or leg pain on straight leg raise were predictive of satisfactory outcomes.22 Poor prognostic factors for development of chronic low back pain and disability include smoking, lower level of education, being out of work while receiving worker’s compensation, and depression.1,2,23

Rehabilitation Management and Treatments

Available or current treatment guidelines

  • Guidelines published in 1994 by the Agency for Health Care Policy and Research.24 and more recent guidelines from American College of Physicians (ACP) published in 2017 emphasize conservative, non-pharmacological, medical treatment and reduction of diagnostic testing, except in cases where red flags were apparent.25
  • Prevention: use of back belt in populations at higher risk particularly those with repetitive tasks involving lifting and carrying heavy objects
  • Conservative: having excluded red flags, initial treatment includes superficial heat, myofascial release, massage and nonsteroidal anti-inflammatory drugs if needed and for more chronic issues, exercise, multi-modal rehabilitation, stress reduction and even behavioral therapy are recommended before stronger pharmacologic options. Epidural steroid injections may be considered for radicular leg symptoms, if greater than axial pain.
  • Surgical: for diskogenic low back pain, the current options are fusion or disk arthroplasty. However, in the setting of predominantly axial pain (without cauda equina syndrome or progressive neurological deficit, which are surgical indications), role of surgery has been questioned given the unclear benefit of surgery long term despite statistical improvement with surgery at the 4- and 8-year marks given the numerous cofounders.26 Despite this, surgical rates for lumbar degenerative disk disease have increased 2.4-fold over the last decade.27

At different disease stages

  • Emergency: if progressive neurologic deficits or cauda equina syndrome is present, surgical intervention is indicated.28
  • Acute: evaluate for red flags, conservative management, and relative rest with avoidance of painful movements. Epidural injections are also an option, which provide pain relief and functional improvement for at least 6 weeks, particularly in patients with radicular pain because of disk herniation. Of those patients, the use of a transforaminal approach also enabled reduction in the need for surgery following treatment.29
  • Chronic (pain >3 mo): assess psychosocial factors/comorbidities (depression) and encourage regular exercise focusing on muscle strengthening and endurance to return to prior activities, while reducing medication use. If this fails, consider steroid injections or surgical intervention.

Coordination of care

  • Initial plan involves referring to a primary care provider, physiatrist, and physical therapist.
  • If conservative management fails, consider referral to an interventional spine or pain physician, orthopedic or neurosurgeon, psychologist, or psychiatrist.

Patient & family education

Educate patient on

  • Injury prevention
  • Proper posture (sitting and standing)
  • Proper lifting/bending techniques (spine straight, knees bent, no twisting)
  • Role of strengthening, stretching, and aerobic exercise program
  • Weight loss

Cutting Edge/Emerging and Unique Concepts and Practice

Cutting edge concepts and practice

New therapies are focused on biological therapies with goals of restoring disk height and function.9 These include fibrin glue, intradiskal glucosamine, and chondroitin sulfate to enhance repair response by promoting an environment rich in necessary protein build block, gene therapy to enhance presence of growth factors, autologous disk cell transfer, and synthetic protein polymer to replace natural nucleus pulposus and prosthetic disks. Annular repair may also be necessary with these treatments.

Platelet Rich Plasma (PRP) and Bone Marrow Aspirate Concentrate (BMAC) injections are another alternative treatment for lumbar disk disorders. Several randomized control clinical trials have shown promise that PRP and BMAC may provide short term to medium improvements in pain and function but promise exists given the superior outcomes seen in vitro models with further refinement of techniques ongoing.30,31,32 The mechanism by which these improvements have occurred is still debated.  Furthermore, the use of spinal cord stimulation given the advances in technology over the last several years is another avenue being increasingly explored.33

Large scale trials currently in process are focused on elucidating possible biomarkers of chronic back pain through genome-wide association studies (GWAS).4 These studies and others like them may provide not only a direction for treatment but a better understanding of the source of many lumbar disc disorders.

Gaps in the Evidence-Based Knowledge

Gaps in the evidence-based knowledge

  • No specific treatment has been proven for diskogenic pain; treatments overlap with those for general low back pain.
  • Controversy around reliability and risk of accelerated disk degeneration with diskography.16
  • Outcomes of epidural steroid injections, prosthetic disk replacement, and other biological therapy intervention are still overall unknown.
  • Long-term benefits of surgical interventions are still being evaluated for each individual patient.


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  33. Kallewaard JW, Edelbroek C, Terheggen M, Raza A, Geurts JW. A Prospective Study of Dorsal Root Ganglion Stimulation for Non-Operated Discogenic Low Back Pain. Neuromodulation. 2020 Feb;23(2):196-202

Original Version of the Topic

Clifford R. Everett, MD MPH, Claudia Ramirez, MD, Matthew Perkowski, DO. Lumbar disc disorders. 9/20/2013

Previous Revision(s) of the Topic

Thiru M. Annaswamy, MD, Charles Taylor, II MD, Ph O. Lumbar disc disorders. 8/18/2017

Author Disclosure

John Antony Donovan, Jr, MD, MS Eng
Nothing to Disclose

Charles Taylor, II, MD, MS
Nothing to Disclose