Author(s): Michael Derr, DO
Originally published: September 20, 2013 Last updated: July 10, 2025
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Disease/Disorder

Definition

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

Etiology

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 disc) 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 disc to herniation and impacts its ability to retain water, leading to a loss of disc height. Phase 2, the instability phase, involves disc resorption, internal disc disruption, and additional tears, causing loss of mechanical integrity at the 3-joint complex. Phase 3, the stabilization phase, involves further disc space narrowing, fibrosis, and osteophyte formation.1,5

Epidemiology including risk factors and primary prevention

The lifetime prevalence of low back pain is 80%, with disc 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 disc degeneration, with animal models showing increased proinflammatory markers, alterations to annular structure, vasoconstriction, and altered nutrient distribution to the disc.8

Patho-anatomy/physiology

Lumbar discs 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. Nerve innervation to the annulus fibrosis of the disc is provided by the sinuvertebral nerve with the basivertebral nerve branch innervating the endplates.4

Pathophysiology: disc degeneration develops as previously described. Herniations are seen with progressive loss of hydration, which leads to a loss of disc 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 discogenic pain.12 Given the limited ability to isolate the pain generators, establishing the diagnosis of and defining the course of symptomatic lumbar disc 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 disc contributes to improvement of symptoms. The exact mechanism of regression is unclear; hypotheses include dehydration leading to shrinking of discs, retraction of discs, and recognition of discs as a foreign body, resulting in macrophage phagocytosis of the disc.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

History

  • Onset: after an 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, discectomy, or laminectomy make remaining discs 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 disc load), body habitus (excess weight may add load to discs), 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 hyporeflexia may localize associated radiculopathy.
  • Provocative maneuvers: seated and supine straight leg raise and femoral nerve stretch test.1,2

Functional assessment

  • Cognition is 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 disc disorders. Specific laboratory studies may be indicated to evaluate for systemic inflammatory or neoplastic diseases when appropriate but are rarely necessary. If suspicion for discitis, initial lab work including complete blood count, erythrocyte sedimentation rate and C-reactive protein is appropriate.1,16,27

Imaging

  • Lumbar radiograph: initial imaging, obtain anteroposterior and lateral view; signs of pathology include loss of disc 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 disc 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 discography is a controversial diagnostic test for discogenic pain. Contrast material is injected into the suspected disc and adjacent discs. Exact reproduction of the patient’s pain at low pressures with painless adjacent discs indicates a positive test.9,20 Risks include, but not limited to, post-discography discitis and accelerated disc degeration.21 While valuable as a diagnostic tool and mostly safe when performed adhering to established guidelines, the lack of robust evidence supporting any one treatment of disc related pain inevitably decreases the practicality of this tool. If ongoing research can mount evidence supporting treatment, this could shift the risk-benefit ratio of performing discography to favor increasing use of this diagnostic tool to facilitate evidence-based treatment.20 The risk of discitis occurring after intentional disc access is non-zero, with reported rates ranging between 0.4 and 1.9% when performed in the absence of prophylactic antibiotics.36

Early predictions of outcomes

Research involving prognostic factors has focused on outcomes after surgical intervention for disc 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 a back belt may help patients at higher risk particularly those with repetitive tasks involving lifting and carrying heavy objects but should not be used for extended periods of time or replace core exercises.
  • 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 discogenic low back pain, the current options are fusion or disc 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 Prior to considering elective surgical intervention for chronic lumbar disc pain, conservative treatment should be maximized.

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 disc herniation. Of those patients, the use of a transforaminal approach also enabled reduction in the need for surgery following treatment.29
  • Chronic (pain >3 months): 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 patients 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

Over the years, multiple minimally invasive outpatient intradiscal treatments have been tried such as biacuplasty, IDET and chymopapain with questionable benefit. Newer intradiscal therapies continue to focus on biological and regenerative therapies with the goal of restoring disc height and function. For example, fibrin and hyaluronic acid are biologics used to enhance the repair response by helping seal and heal annular tearing, disc degeneration and herniation.34

Platelet Rich Plasma (PRP) and Bone Marrow Aspirate Concentrate (BMAC) injections are another alternative treatment for lumbar disc disorders. Several randomized control clinical trials have shown promise that PRP and BMAC may provide short term to medium improvements in pain and function; however, further refinement of treatment protocol is ongoing.30,31,32 Furthermore, while not specifically targeting the disc, the use of neurostimulation is another avenue being increasingly explored and used due to technologic advances.33

In the past, biacuplasty and IDET were electrothermy treatments specifically treating the disc. A new approach uses electrothermy targeting the basivertebral nerve innervating the endplates. This procedure treats vertebrogenic pain which includes the disc endplate and vertebral body, identified as Modic changes on MRI. Basivertebral nerve ablation is a minimally invasive outpatient procedure targeting the nerve as it enters the vertebral body via transpedicular approach using fluoroscopy.35

Gaps in the Evidence-Based Knowledge

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

References

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  2. Barr KP, Srtandaert, CJ, Johnson, SC, et al. Low Back Disorders. In: Braddom RL, ed. Physical Medicine and Rehabilitation. 6th ed. Philadelphia, PA: Elsevier Saunders; 2021: 651.
  3. Fujii, K, Yamazaki, M, Kang, KD, et al. Discogenic Back Pain: Literature Review of Definition, Diagnosis and Treatment. JPMR Plus. 3;5:101804. Laplante B, DePalma MJ. Spine osteoarthritis. PM R. 2011;4(5 Suppl):S28-S36.
  4. The Anatomical Study and Clinical Significance of the Sinuvertebral Nerves at the Lumbar Levels., Zhao, Q and Cheng, L and Yan, H and Deng, S and Zhao, J and Liu, Z and Tan, X and Zhong, E and Zhuo, W and Jin, D and Li, Q, Spine (Phila Pa 1976) E61-E66 (2020)
  5. Middleton K, Fish DE. Lumbar spondylosis: clinical presentation and treatment approaches. Curr Rev Musculoskelet Med. 2009;2:94-104.
  6. Huston CW, McCowen SA. Etiologies of painful spinal disorders. In: DePalma MJ, ed. ISpine Evidence Based Interventional Spine. 1st ed. New York, NY: Demos Medical Publishing, 2011: 10.
  7. Kalichman L, Hunter DJ. The genetics of intervertebral disc degeneration. Associated genes. Joint Bone Spine. 2008;75:388-396.
  8. Behrend C, Prasarn M, Coyne E, Horodyski M, Wright J, Rechtine GR. Smoking cessation related to improved patient-reported pain scores following spinal care. J Bone Joint Surg Am. 2012;94:2161-2166.
  9. Raj PP. Intervertebral disc: anatomy-physiology-pathophysiology-treatment. Pain Pract. 2008;8:18-44.
  10. Brinjikji W, Luetmer PH, Comstock B et al. Systematic literature review of imaging features of spinal degeneration in asymptomatic populations. AJNR Am J Neuroradiol 2015;36:811–16
  11. Deyo RA, Rainville J, Kent DL: What can the history and physicalexamination tell us about back pain? JAMA 268:760–765, 1992.
  12. Comer C, Conaghan PG. Tackling persistent low back pain in primary care. Practitioner. 2009;253:32–4 3.
  13. Chang CW, Lai PH, Yip CM, Hsu SS. Spontaneous regression of lumbar herniated disc. J Chin Med Assoc. 2009;72:640-653.
  14. Chiu CC, Chuang TY, Chang KH, Wu CH, Lin PW, Hsu WY. The probability of spontaneous regression of lumbar herniated disc: a systematic review. Clin Rehabil. 2015;29(2):184–195.
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  19. Mailese, J, Togay, H, Unalan, H, et al.  The Sensitivtity and Specificity of the Slump and the Straight Leg Raise in Patients with Lumbar Disc Herniation. J Clin Rheumatolog. April 2008: 14(2):87-91
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  30. Allogeneic mesenchymal precursor cells treatment for chronic low back pain associated with degenerative disc disease: a prospective randomized, placebo-controlled 36-month study of safety and efficacy., Amirdelfan, K and Bae, H and McJunkin, T and Depalma, M and Kim, K and Beckworth, WJ and Ghiselli, G and Bainbridge, JS and Dryer, R and Deer, TR and Brown, RD, Spine J 212-230 (2021)
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  32. Anitua, E., Milani, I., Martinez, A., Cabello, F., Prado, R., Padilla, S., & Sanado, L. (2023). Plasma Rich in Growth Factors (PRGF) in the treatment of patients with Chronic cervical and lumbar pain: a Prospective Observational Clinical study. Pain Physician, 26(6), E725–E736.
  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
  34. Yu J, Taylor W, Verrills P, et al. (July 11, 2021) Results of a Pilot Study on the Safety and Early Efficacy of Novel Polymethyl Methacrylate Microspheres and a Hyaluronic Acid Device for the Treatment of Low Back Pain Caused by Degenerative and Diseased Intervertebral Discs of the Lumbar Spine. Cureus 13(7): e16308. DOI 10.7759/cureus.16308
  35. Basivertebral Nerve Ablation for the Treatment of Chronic Low Back Pain: A Scoping Review of the Literature., Schnapp, W and Martiatu, K and Delcroix, GJ, Pain Physician E551-E562 (2022)
  36. Schneider BJ, Popescu A, Smith CC, McCormick ZL. FactFinders: Antibiotics for Disc Access. Aug 2021. https://cdn.ymaws.com/www.ipsismed.org/resource/resmgr/factfinder/21/08.ff.abx. disc.access.pdf. Accessed July 2, 2025

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

John Antony Donovan, Jr, MD, MS Eng, Charles Taylor, II MD, MS. Lumbar Disc Disorders. 5/4/2022

Author Disclosure

Michael Derr, DO
Nothing to Disclose