Lumbar radiculopathy refers to any pathologic condition affecting the lumbar nerve roots. In practical terms, radiculopathy is spinal nerve-related symptoms such as pain, with variable presence of paresthesias, weakness, reflex changes, and secondary interference of normal activities.
Lumbar radiculopathy is usually caused by mechanical compression of nerve roots, frequently in combination with inflammatory biochemical and immunological insult. Although disc herniation (DH), synovial cysts and spinal stenosis account for nearly all cases, rarer causes include a multitude of musculoskeletal, vascular, rheumatologic, neurologic, infectious, iatrogenic, and other etiologies.1
Epidemiology including risk factors and primary prevention
Prevalence of lumbar radiculopathy is estimated to be 2-5% in men and 1-3% in women. Peak age at time of disc surgery is 40 in both sexes. Most cases have an atraumatic onset but risk factors include driving occupations, frequent lifting (especially with twisting motions), heavy industry work, back trauma, as well as previous history of back pain, taller height, smoking, overweight (in a dose dependent fashion 2), sedentary lifestyle, multiple pregnancies, high work load, chronic cough and gender. Environmental factors are thought to account for 80% of lumbar radiculopathy onset, although a familial predisposition to lumbar herniated discs (which can be a cause of lumbar radiculopathy has been reported. It should also be noted that lumbar herniated discs are not always associated with lumbar radiculopathy 3.
- Association found between disc herniation and radiculopathy in 1934 4
- Mechanical compression of the spinal nerve was initially presumed to be the cause of radiculopathy due to: 5
- Spinal nerve anatomy poorly resistant to compression (lacking a perineurium, poorly developed epineurium, and more tenuous blood supply versus peripheral nerves).
- High tensile forces on the spinal nerve from tethering.
- Impaired nutrition in compressed roots.
- Intraneural edema (can directly lead to nerve injury/fibrosis or an intraneural ‘compartment syndrome’ as pressures in the spinal nerve exceeds perfusion pressures resulting in ischemia).
- Disc injury is associated with locally increased levels of inflammatory biochemicals.
- Increased levels of cytokines, leukotrienes, nitric oxide, immunoglobulins, interleukins, PGE-2, and metalloproteinases detected at the site of disc injury.
- Phospholipase A2 (PLA2) levels correlate with radicular symptoms in animal models and high levels found in herniated disc material from discectomy patients.
- PLA2 Also causes lumbar dorsal root ectopic discharges and evidence of demyelination 6.
- Tumor necrosis factor (TNF-alpha) induces radiculopathy in animal model; TNF-alpha blockers counter this effect.
- Immunologic factors also contribute to changes responsible for sciatica.
- Markers of glial cell and nerve damage [neurofilament (NFL), glial fibrillary acidic protein, S-100 protein, and neuron-specific enolase] were significantly elevated in the CSF of patients presenting for lumbar disc surgery compared with controls7.
Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)
Lumbar radiculopathy caused by disc herniation has a favorable natural history in the vast majority of patients. Studies reveal that by 4 – 6 weeks, between 70 and 80% of patients had significant improvement in pain and disability with relative rest. However, 30% of patients in one study had persistent pain and work/leisure restrictions at one year 8. Though initial disability can be quite high, consensus is that only 1 – 10% of patients will go on to surgery due to failure of medical management 9. Patients with larger disc herniations show a greater decrease in herniation size with time, which correlates with symptom improvement.
Specific secondary or associated conditions and complications
Cauda Equina Syndrome (CES): Less than 1% develop massive disc herniations that can affect the entire cauda equina with significant limb weakness and/or bowel/bladder sphincter disturbance. This is considered a surgical emergency as neurologic recovery correlates with timely decompression. Seventy percent of these patients develop symptoms within hours to days of onset of pain. Tumor is another important cause of CES.
Progressive neurologic deficit: Single root radicular symptoms with weakness, reflex changes, neuropathic symptoms such as numbness on exam, that is progressively worsening over time is rare (~2% of cases) but also should be treated with urgent surgical treatment.
ESSENTIALS OF ASSESSMENT
Lumbar radicular pain is usually described as any combination of throbbing, aching, sharp, dull, burning, pressure, numbness, tingling, tearing, stretching or shooting. Though back pain is usually present, leg symptoms (including buttock) predominate. 90% of the time the L5 or S1 nerve root is affected which may present as limb pain and paresthesias which may or may not fit a distinct dermatomal distribution7. History must include questions to rule out Cauda Equina Syndrome, progressive weakness, and “red flag” questions for possible occult process: tumor, infection, fracture, inflammatory arthritis, non-mechanical visceral diseases. Ask for exacerbating and alleviating factors and symptom intensity on a numerical rating scale, as well as precipitating factors. In auto collisions this would involve seatbelt usage, airbag deployment, trajectory of vehicles, etc. Details surrounding work injuries and whether there is pending litigation can impact prognosis.
Social history includes substance use and abuse, including tobacco and opiate use or abuse. Familial history of back problems is pertinent. Asking questions to gauge how the pain impacts lifestyle, sleep and work life is important. As it is also important to note any previous exercise history.
- Neurologic exam in both the upper and lower extremities: strength, reflexes, sensory testing (sacral segments if cauda equina syndrome suspected, with rectal examination). Check for both upper and lower motor neuron signs.
- Functional strength tests: repeated single heel lift or toe walking (S1), heel walking (L5), single leg sit to stand or squat/rise (L3, L4).
- Root tension signs: supine straight leg raise (SLR) and variations, slump test, crossed SLR (low sensitivity high specificity), femoral nerve stretch test (upper lumbar radiculopathy).
- The straight leg raise test is more sensitive but less specific than the contralateral straight leg raise for the diagnosis of radiculopathy due to disc herniation 21
- General musculoskeletal screening and inspection to rule out soft tissue or joint pains mimicking or superimposed with radicular pain:
- Hip range of motion, hip provocative maneuvers such as flexion, adduction and internal rotation.
- Sacroiliac joint maneuvers: (Gaenslen’s, FABER, shear tests, hip hyperextension, etc) Though, these tests are nonspecific and not sensitive.
- Other diseases: screen for ischial or trochanteric bursitis, facet, IT band or knee joint dysfunction, myofascial trigger points, piriformis syndrome, plantar fasciitis, etc.
Assessment of the patient’s disability using validated tools (Oswestry Disability Index, Roland Morris Disability Questionnaire [Radiculopathy version]) or query sleep quality, psychosocial stressors assessment, work/recreation ability, self-care ability.
Imaging is indicated if symptoms have been present for more than one month, unless a progressive neurologic deficit is present, medical “red flags,” exist, or there has been substantial trauma.
X-Ray, once the “first line” modality, has been found less useful in benign settings in patients under the age of 55. X-rays can be helpful in evaluating for alignment abnormalities including scoliosis and spondylolisthesis, transitional segments, and screen for fracture.
Since 20-36% of asymptomatic adults have disc herniations on lumbar Magnetic Resonance Imaging 10, MRI is best used only as a confirmatory test of the clinical impression. MRI should be ordered prior to any spinal procedure or surgical consultation, or if symptoms fail to improve with rehabilitative care. MRI is the preferred imaging modality, though CT (with or without myelography) can be considered if MRI is contraindicated or if better bony detail is required, such as incases of prior instrumentation.
Supplemental assessment tools
- In cases with persistent extremity symptoms for over 3 weeks, electromyography (EMG) can confirm clinical suspicions, identify root level, severity of involvement, acuity of injury, and evaluate other concomitant disorders.
- Injections, such as fluoroscopically guided transforaminal epidurals can confirm the level of radiculopathy and provide therapeutic benefit, especially where multiple disc abnormalities are seen on MRI. Caution should be taken, however, as transforaminals above a certain volume lose their root level selectivity11. Intra-articular hip injection with local anesthetic that alleviates a majority of hip, back, thigh, and inguinal pain symptoms, can confirm alternative hip pathology. Similarly, injections into other nearby structures can add diagnostic information (sacroiliac, facet joint, greater trochanter, knee)
Early predictions of outcomes
Depression, fear avoidance beliefs, and anxiety may negatively influence medical and surgical outcomes in lumbar radiculopathy patients and can be identified at initial evaluation or early follow up period using validated screening tests such as the STarT back tool, PHQ-9, FABQ, and GAD-7.
Occupational hazards and risk factors for non-recovery must be addressed during any encounter with a patient who develops radiculopathy from a work injury. Impairment ratings, disability percentage, vocational rehabilitation, work hardening, and conditioning are all issues that can be addressed. Ergonomic adjustments should be prescribed.
Social role and social support system
Patients who go to rest mode, or take off work for long periods of time, can find themselves quickly moving from the head of the household and “breadwinner” to dependent status, with loss of status and self-esteem. Thus, the affected patient should become an active participant in their recovery program by participating in supervised exercise-based physical therapy as soon as possible. Those who miss work due to back pain for 6 months have a 50% chance of returning to work; if he or she is out for 1 year, then there is a 25% chance of returning to work; if he or she is out for 2 years, then there is a 0% chance of returning to work 22
Whenever possible, evidence-based recommendations should be considered. Prior to any procedure, informed consent must be obtained. Also, one should be aware of the possibility of secondary gain in cases with third-party liability.
REHABILITATION MANAGEMENT AND TREATMENTS
Available or current treatment guidelines
Proposed but not consensus-driven 12,13 rehabilitation management emphasizes resumption and maintenance of activity. Short rest periods and activity modification to accommodate symptoms are recommended over bedrest. Dynamic lumbar stabilization approach includes back school and proper bending/lifting mechanics; exercise training to teach spinal stabilization, i.e., dynamic maintenance of postural control, trunk, and general upper and lower body strengthening exercises; and flexibility exercises.
At different disease stages
New onset/acute management includes 12
- General stretching program, foraminal opening maneuvers “McKenzie” or “MDT (mechanical diagnosis and treatment) assessment and treatment may be of value.
- Modalities including heat, ice, electrical stimulation and education.
- Correct any lateral listing
- Manipulation might be helpful in acute stages
- Activity modification with emphasis on staying as active as possible
- Medications including NSAIDs, acetaminophen, muscle relaxers, anti-neuropathic drugs, and opioids like tramadol if needed for severe breakthrough pain only14.
- Oral steroid tapers are often used but have not been shown to provide superior pain relief compared to placebo, and with many more side effects 15
Subacute management includes
- Continue and advance acute care treatments as needed to assist in staying active.
- Repeat neurologic exam for new or worsening weakness
- Dynamic lumbar stabilization program as able
- Address any radiculopathy-related weakness with strength training
- Epidural corticosteroid injection under fluoroscopic guidance if there is significant pain or symptoms continue to interfere with function, sleep, and employment.
- If no improvement by 4-6 weeks, improvement plateaus over time, patient preference is for surgery, non-improving or progressive weakness, or disability is high, consider surgical consultation16.
- Interspinous Processor Decompression (IPD): An alternative to laminectomy, a lumbar interspinous spacer is intended to treat skeletally mature patients suffering from pain, numbness, and/or cramping in the legs (neurogenic intermittent claudication) secondary to a diagnosis of moderate degenerative lumbar spinal stenosis; this diagnosis is typically accompanied by lumbar radiculopathy. It is inserted using a minimally invasive procedure which leaves a full range of surgical options if revision is needed to to manage return of symptoms. It can reduces the direct and indirect costs associated with lumbar stenosis and may remove or significantly delay the need for a decompressive laminectomy as well as the risk of a revision surgery associated with laminectomy 24,25. This is a viable treatment option for lumbar stenosis patients due to the lower surgical risk, rapid patient recovery, reversibility, and sustained clinical benefits. Contraindications include osteoporosis, Baastrup’s sign, and unstable spondylolisthesis greater than grade one.
Chronic/ stable management
- Complementary treatments: acupuncture or massage therapy
- Other neuropathic agents, Transcutaneous electrical nerve stimulation (TENS) unit14
- Spinal cord stimulation (percutaneous trial prior to implantation) if no surgical solution to neuropathic extremity pain or if patient already had surgery and has persistent pain17
- Consideration for comprehensive multidisciplinary cognitive-behavioral pain rehabilitation program.
Coordination of care
Coordinated practice: Physiatrist functions as “quarterback” working with patient, primary care physician, physical therapist, employer, spine surgeon, and others. The physiatrist usually serves as the interventionalist or works closely with one.
Weighing the pros and cons of surgery versus more conservative management is to be done on an individual basis. Many studies comparing surgery to conservative management favor surgery; however, the conservative management arm is not standardized in trials, and significant crossovers from each treatment arm of these studies to the other treatment arm make drawing conclusions dubious18.
Chiropractic and osteopathic manipulations may be helpful in the short term but have not been shown to provide long term relief19, Acupuncture, massage therapy, psychology referral can be adjunctive treatments.
Patient & family education
- Stay active, short rest periods in a position of comfort are acceptable. Hurt does not equal harm.
- Monitor for progression of weakness (< 2%).
- Acute symptoms typically last less than 1-2 weeks.
- Lumbar radiculopathy has a favorable natural course of disease in most circumstances.
- Recurrence rate is only approximately 8 – 12% .
- Low back pain component commonly persists.
- Epidural injections and surgery most predictably improve leg pain (not back pain).
Spinal Cord Stimulation (SCS)
SCS has been a treatment for patients with chronic, intractable pain for over 40 years. The technology of these devices continues to improve at an almost yearly pace. Some of the indications for SCS include lumbar radiculopathy, failed back surgery syndrome, intractable back and leg pain, and complex regional pain syndrome. One mechanism of conventional SCS is believed to operate on the gate theory of pain modulation. The mechanism for pain relief with conventional SCS is now known to be more complex involving both spinal and supraspinal mechanisms. Conventional SCS (tonic, low-frequency) has been shown to increase expression of inhibitory neurotransmitter GABA in the spinal cord and induce a subsequent decrease in glutamate levels in experimental animals. However, conventional SCS has limited success in treating axial back pain due to anatomic and neurophysiologic reasons. High-frequency SCS (HF-SCS) with stimulation frequencies at 10KHz and burst SCS (five-pulse train with internal frequency of 500Hz delivered at 40Hz) are thought to have its main effect on the dorsal horn of the spinal cord instead of the dorsal column23.
Lumbar Interspinous Spacer
Lumbar interspinous process decompression (IPD) to treat lumbar spinal stenosis (LSS) with radiculopathy was first made available in the 1980s. All three of the first generation devices were implanted by neurosurgeons under general anesthesia. While open surgical options exist for spinal decompression, some patients do not qualify as good candidates for general anesthesia and open surgery. In 2015, the FDA approved a second generation IPD spacer. The main difference is that this surgery may be performed by an interventional pain medicine physician under moderate sedation. 5-year data from an industry sponsored study on IPD have been published showing improvements in quality of life (QOL) and pain scores.24-25
Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills
- Thorough history and examination to rule out Cauda Equina Syndrome and other neurologic or musculoskeletal mimickers.
- Education on favorable natural history in the face of hyperacute symptoms, importance of staying active sets the stage for effective rehabilitative management.
- Close initial follow-up to monitor neurologic status and ensure adequate pain control with initial treatments.
- Coordinate care early on with employer, therapist, psychologist, and interventionalist to minimize disability.
CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE
Cutting edge concepts and practice Novel but unproven treatments include spinal injections using ultrasound guidance, and alternative epidural injectable drugs such as clonidine, Tumor necrosis factor (TNF) blockers, anti-nerve growth factors, ozone and platelet lysate. Alternative percutaneous intradiscal treatments, such as electrothermal disc decompression, percutaneous mechanical and chemical disc decompression, and nucleoplasty have been developed. Gaining better understanding of genetic factors for discogenic radiculopathy through several national twin registries. Genetic screening for OPRM1 (genotype for Mu opioid receptor polymorphism) may predict outcomes from surgery20. Finally, epidural adhesiolysis for chronic neuropathic pain continues to be studied.
GAPS IN THE EVIDENCE-BASED KNOWLEDGE
Gaps in the evidence-based knowledge
- Genetic contributions to the development of radiculopathy and treatment outcomes
- Development of effective standardized, evidence-based medical management guidelines.
- Shelerud R, Paynter K. Rarer causes of radiculopathy: spinal tumors, infections, and other unusual causes. Phys Med Rehabil Clin N Am. 2002; 13: 645-696
- Shiri R, LallukkaT, Karppinen J, Viikara-Juntura E. Obesity as a risk factor for Sciatica: a meta-analysis. Am J Epidemiol.2014; 179 (8): 929-937
- Andersson G. The epidemiology of spinal disorders. In: The Adult Spine: Principles and Practice. 2nd Ed. J.W. Frymoyer, Ed. Philadelphia, PA: Lippincott-Raven 1997; 93-141.
- Mixter WJ, Barr JS. Rupture of the intervertebral disc with involvement of the spinal canal. N Engl J Med 1934 211:210
- Rhee J, Schaufele M, Abdu W. Radiculopathy and the Herniated Lumbar Disk: Controversies Regarding Pathophysiology and Management. AAOS Instructional Course Lectures 2007; 56: 287-299.
- Chen C, Cavanaugh JM, Ozaktay C, et al. Effects of phospholipase A2 on lumbar nerve root structure and function. Spine. 1997; 22: 1057 – 64.
- Stafford MA, Peng P, Hill DA. Sciatica: a review of history, epidemiology, pathogenesis, and the role of epidural steroid injection in management. British Journal of Anesthesia. 2007; 99 (4):461 – 473.
- Weber H. Spine update: the natural history of disc herniation and the influence of intervention. Spine. 1994; 19: 2234-2238
- Mooney V. Presidential Address: ISSLS 1986: Where is the pain coming from? Spine. 1987; 12: 754-759.
- Boden SC, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects: A prospective investigation. J Bone Joint Surg Am. 1990; 72: 403-408
- Furman MB, O’Brien EM. Is it really possible to do a selective nerve root block? Pain. 2000; Apr. 85(3): 526
- Chiodo A, Haig A. Lumbosacral radiculopathies: conservative approaches to management. Phys Med Rehabil Clin N Am. 2002; 13: 609-621
- Tarulli A, Raynor E. Lumbosacral radiculopathy. Neurol Clin. 2007; 25: 387-405
- Dworkin RH, O’Connor AB, Kent J,, et al. Interventional Management of Neuropathic Pain: NeuPSIG Recommendations. Pain. 2013 Nov.154(11):2249-61,
- Goldberg H, Firtch W, Tyburski M, et al. Oral steroids for acute radiculopathy Due to a herniated lumbar disk: A randomized Clinical Trial. JAMA. 2015; 313(19): 1915 – 1923. doi:10.1001/jama.2015.4468
- Carragee E. Surgical treatment of lumbar disk disorders. JAMA. 2006; 296(20):2485-2487.
- National Institute for Health and Clinical Excellence (NICE). Spinal Cord Stimulation for Chronic Pain of Neuropathic or Ischaemic Origin. London (UK): National Institute for Health and Clinical Excellence; 2008
- Weinstein JN, Tosteson TD, Lurie JD, et al. Surgical vs nonoperative treatment for lumbar disk herniation. The Spine Patient Outcomes Research Trial (SPORT): A randomized trial. JAMA 2006;296: 2441–50.
- Hasvick V, Iordinova Schistad E, Grovle L, et al. Subjective health complaints in patents with lumbar radicular pain and disc herniation are associated with a sex- OPRM1 A118G polymorphism interaction: a prospective 1-year observational study. BMC Musculoskeletal Disorders. 15:161, 2014..
- Leininger B1, Bronfort G, Evans R, Reiter T. Spinal manipulation or mobilization for radiculopathy: a systematic review.Phys Med Rehabil Clin N Am. 2011 Feb;22(1):105-25. doi: 10.1016/j.pmr.2010.11.002. Epub 2010 Dec 30.
- van der Windt DAWM, Simons E, Riphagen II, Ammendolia C, Verhagen AP, Laslett M, Devillé W, Deyo RA, Bouter LM, de Vet HCW, Aertgeerts B. Physical examination for lumbar radiculopathy due to disc herniation in patients with low‐back pain. Cochrane Database of Systematic Reviews 2010, Issue 2. Art. No.: CD007431. DOI: 10.1002/14651858.CD007431.pub2.
- Cuccurullo, S., Lee, J., Freeman, T., Freeman, E., et al. Physical Medicine and Rehabilitation Board Review. 3rd Ed. p286. Demos Medical Publishing, 2015.
- Chakravarthy K, Fishman MA, Zuidema X, Hunter CW, Levy R. Mechanism of Action in Burst Spinal Cord Stimulation: Review and Recent Advances. Pain Med. 2019;20(Suppl 1):S13–S22. doi:10.1093/pm/pnz073
- Nunley PD, Patel VV, Orndorff DG, Lavelle WF, Block JE, Geisler FH. Five-year durability of stand-alone interspinous process decompression for lumbar spinal stenosis. Clin Interv Aging. 2017;12:1409-1417 https://doi.org/10.2147/CIA.S143503
- Kevin Cairns, MD, Tim Deer, MD, Dawood Sayed, MD, Kim van Noort, MSc, Kevin Liang, PhD, Cost-effectiveness and Safety of Interspinous Process Decompression (Superion), Pain Medicine, Volume 20, Issue Supplement_2, December 2019, Pages S2–S8, https://doi.org/10.1093/pm/pnz245
Original Version of the Topic:
Randy Shelerud, MD. Lumbar Radiculopathy. Publication Date: 2011/11/05.
Previous Revision(s) of the Topic
Randy Shelerud, MD Lumbar Radiculopathy. Publication Date: 4/8/2016
Casey A. Murphy, M.D., F.A.A.P.M.R., D.A.A.P.M.
Nothing to Disclose
Randolph L. Roig
Nothing to Disclose
Jack Pines, M.D.
Nothing to Disclose
Ibrahim Samarra’e, MS-3
Nothing to Disclose