eMedicine Specialties > Physical Medicine and Rehabilitation > Lumbar Spine Disorders

Mechanical Low Back Pain: Treatment & Medication

Author: Everett C Hills, MD, MS, Medical Director, Penn State Hershey Rehabilitation Hospital, Assistant Professor of Orthopaedics and Rehabilitation, Assistant Professor of Neurology, Penn State Milton S. Hershey Medical Center and Penn State University College of Medicine
Contributor Information and Disclosures

Updated: Nov 19, 2009

Treatment

Rehabilitation Program

Physical Therapy

The treatment program for mechanical low back pain (LBP) must have specific functional goals and can be outlined in the following 6 steps:

  • Control of pain and the inflammatory process - Pain treatment should be initiated early and efficiently to gain control. Ice, transcutaneous electrical nerve stimulation (TENS), and relative rest may help with controlling the pain and the inflammatory process. Excessive bedrest, however, may be detrimental by leading to lumbar segment motion, loss of muscle strength, and general deconditioning with blunting of motivation.
  • Restoration of joint ROM and soft tissue extensibility - Extension exercises may reduce neural tension. Flexion exercises reduce articular weight-bearing stress to the facet joints and stretch the dorsolumbar fascia. The use of ultrasound therapy may improve collagen extensibility.
  • Improvement of muscular strength and endurance - Exercise training can begin after the patient has passed successfully through the pain control phase. The key is to attain adequate musculoligamentous control of lumbar spine forces to minimize the risk of repetitive injury to the intervertebral disks, facet joints, and surrounding structures. Start with isometrics, then progress to isotonic exercises with effort directed at concentric strengthening.
  • Coordination retraining - Dynamic exercise in a structured training program maximizes coordinated muscle group activities that lead to postural control and the fusion of muscle control with spine stability.
  • Improvement of general cardiovascular condition - Patients are encouraged to remain active and to initiate brisk walking programs, aquatic activities, or use of stationary bicycles/stair steppers. These activities can increase endorphin levels, promoting a sense of well-being, and allow the patient to perform at a higher level of function before perceiving pain.
  • Maintenance exercise programs - A home program is developed within the tolerance and ability of the patient in order to encourage continued exercise after discharge from physical therapy.

Sertpoyraz et al compared isokinetic and standard exercise programs for chronic low back pain.10 Pain, mobility, disability, psychological status, and muscle strength were measured. Forty patients were randomly assigned to a program that took place in an outpatient rehabilitation clinic. No statistically significant difference was found between the 2 programs with regard to their effect in the treatment of low back pain.

The main goal of physical therapy in persons with acute back pain is not to increase strength but to achieve adequate pain control. No benefit has been demonstrated for strengthening exercises in persons with acute back pain. Exercise should begin with extension exercises in the prone position after lateral trunk shifts and then progress, as tolerated, to prone lying with support. Flexion exercises can be performed only if the patient has no acute dural tension.

The spine should be stabilized using strengthening of segmental muscles followed by the prime movers of the spine (ie, latissimus dorsi, abdominals, erector spinae). Muscle groups should be strengthened in a neutral position to decrease tension on ligaments and joints; this position allows balanced segmental forces between the disks and the zygapophyseal joints and maximizes functional stability with axial loading.

Physical therapy programs should also include positioning the patient to maximize comfort. Loosening of the hamstrings, glutei, gastrocnemius/soleus group, tensor fascia latae, quadriceps group, and hip flexors also contributes to reduction of LBP and effective conditioning.

In a 2004 multicenter randomized trial, patients who were trained in exercises that matched their directional preference (DP) were more likely to achieve immediate, lasting improvement in pain compared with patients who received nondirectional treatment or opposite directional treatment.11 Patients using DP exercises were found to have a 3-fold decrease in medication usage. The idea of patient-specific exercises in managing LBP is recognized as controversial by the authors. Using DP to guide patients may improve outcomes in pain, function, and treatment satisfaction.

J ü ni et al found that the addition of spinal manipulative therapy to standard care is unlikely to result in relevant early pain reduction in patients with acute LBP.12 In a randomized trial involving 104 patients with acute LBP, pain reduction during days 1-14 and at 6 months were similar (p = 0.13) in patients who received spinal manipulative therapy plus standard care — consisting of general advice and acetaminophen, diclofenac, or dihydrocodeine as needed — and those who received only standard care. Small initial differences in analgesic use diminished over time.

Medical Issues/Complications

Mechanical low back pain (LBP) is not a life-threatening illness. Unfortunately, it does have a far-reaching impact on medical care expenditures for injured workers. An in-depth examination of the impact of mechanical LBP on the US workers' compensation system, which varies from state to state, is beyond the subject of this article. Many interesting perceptions about mechanical LBP have been noted.

  • In studies in which subjects had to answer self-assessment instruments, patients with insurance referrals had poorer self-assessment scores regardless of functional status.
  • Among different health care providers, patients rated care and communication, followed by competence, over efficacy of treatment.
  • Chiropractors often have been favored over internists and orthopedic surgeons on the basis of their "high touch" approach to treatment.
  • Orthopedic surgeons were found to be less restrictive with activities compared with family practitioners.
  • In a Dutch study, factors such as better health, better job satisfaction, status as breadwinner, lower age, and reporting of less pain were favorable prognosticators of return to work in individuals who had not been working for more than 3 months. The authors of the study believed that more focus was necessary on the psychosocial aspects of health behavior and job satisfaction.
  • Exercise was found to be more effective than usual primary care management.

Surgical Intervention

Surgical interventions for mechanical low back pain (LBP) are the last choice for treatment. Diskectomies are performed in the United States at a rate proportional to the number of spine surgeons in the community. The US rate of surgeries is twice that of Europe, Canada, and Australia and is 5 times the rate in the United Kingdom. Better results occur with open excisions compared with percutaneous diskectomies. Results are best when no workers' compensation or litigation is involved.13,14

Other Treatment

Evidence-based clinical practices on selected rehabilitation interventions for low back pain (LBP) have focused on the timing of interventions.

  • Acute LBP is defined as pain that does not radiate below the knees with current symptoms that have been present 4-6 weeks or less.
  • Subacute LBP is defined as pain that does not radiate below the knees with current symptoms that have been present 4-12 weeks from onset.
  • Chronic LBP is defined as pain that does not radiate below the knees with current symptoms that have been present greater than 12 weeks.
  • The Philadelphia Panel evaluated the literature on the treatment of LBP and assigned Grades of Recommendation based on the clinical importance of the studies, statistical significance of the findings, and the study design.3 Randomized control trials with statistically significant findings were assigned an A grade. Any study design without clinically significant findings but thought to have been worth performing was assigned a D grade. Grades of Evidence were assigned to the various studies. The highest grades were I for randomized control trials and III for the opinions of respected authorities.
    • For LBP of less than 4 weeks duration, the Philadelphia Panel found poor evidence (grade C) to include or exclude therapeutic exercises, traction, ultrasonography, or TENS. Return to work was strongly encouraged.
    • For LBP of 4-12 weeks duration, the Philadelphia Panel found good evidence for the inclusion of therapeutic exercise and manual traction.
    • For LBP of greater than 12 weeks' duration, the Philadelphia Panel found good evidence for the inclusion of therapeutic exercises, therapeutic ultrasonography, and electromyographic biofeedback. These treatments were positive interventions for achieving adequate pain control, increasing functional activities of daily living, and promoting return to work.
  • Evidence-based clinical practice guidelines from the American Pain Society (APS) for patients with chronic low back pain describe the use of interventional diagnostic tests and therapies, surgeries, and interdisciplinary rehabilitation.15
    • Practice guidelines for nonradicular pain
      • Interdisciplinary rehabilitation that emphasizes cognitive-behavioral approaches should be considered for patients who fail to respond to usual interventions.
      • Provocative diskography (in which material is injected into a disk nucleus to reproduce the patient's typical pain) is not recommended.
      • Facet joint corticosteroid injection, prolotherapy (stimulation of an inflammatory response through repeated injections of irritant material), and intradiskal corticosteroid injection are not recommended.
      • Degenerative spinal changes and persistent, disabling symptoms should lead to discussion and shared decision-making regarding surgery or interdisciplinary rehabilitation. (The evidence is insufficient to weigh the risks and benefits of vertebral disk replacement in these patients.)
    • Practice guidelines for persistent radiculopathy
      • For patients with herniated disks, the use of epidural steroid injection should be discussed.
      • For patients with herniated disks and disabling leg pain from spinal stenosis, surgical options should be discussed.
      • For patients with persistent pain after surgery, the risks and benefits of spinal cord stimulation should be discussed.

Medication

Pharmacological interventions for the relief of low back pain (LBP) include acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs), topical analgesics, muscle relaxants, opioids, corticosteroids, antidepressants, and anticonvulsants.

Acetaminophen remains one of the best first-line treatments of acute LBP. It is generally well tolerated, has few adverse effects or drug reactions with other medications, and is inexpensive. Acetaminophen is as effective as aspirin; however, overdoses can result in fatal hepatic injury. The maximum advised dose is 4 g/d.

NSAIDs are the most frequently prescribed analgesic medications for mechanical LBP worldwide. A review of the Cochrane Controlled Trials Registry found 51 randomized control trials (involving 6057 patients) comparing different NSAIDs for the treatment of acute mechanical LBP.16 NSAIDs were found to be effective for short-term symptomatic relief. No specific type was shown to be clearly more effective than the others. Insufficient evidence was found for effective analgesic control in chronic LBP.

NSAIDs augmented with muscle relaxants are a standard medical prescription for LBP in the primary care setting. These agents should be prescribed on a scheduled basis, rather than as needed, for optimal analgesia. Patients on combined NSAIDs and muscle relaxants report reduction of symptoms at 1 week, which is less than when compared with either drug alone. The optimum combination of NSAIDs and muscle relaxants remains to be determined.

Topically applied lidocaine patches (Lidoderm 5% patch) have provided a reduction in pain intensity and pain relief in clinical trials of patients with acute pain.

Opioid medications are mainstays for short-term treatment of severe pain. Their role in the long-term care of patients with mechanical LBP is the subject of intense investigations. Transdermal opioid (fentanyl) has been shown to compare favorably to oral long-acting opioids. Concerns about drug diversion and abuse continue to cloud the benefits of long-term opioid use for LBP.

Corticosteroids may play a role in the treatment of mechanical LBP with acute radiculopathic features of radiating pain down one or both legs.

Antidepressants are thought to be effective when a component of depression is accompanying the mechanical LBP. Antidepressants may contribute to improving the disruption in sleep that patients frequently mention as a part of the constellation of symptoms resulting from LBP.

The basic mechanism of anticonvulsants is to stabilize neural membranes. This concept has been used to support the use of anticonvulsants for adjunct analgesia suspected to come from neuropathic causes.

Botulinum toxin type A has been investigated for pain relief in several small studies. The toxin temporarily paralyzes the lumbar muscles, which may be creating spasms that contribute to the generation of LBP.

Clinicians have found that long-acting oral opioids can be rotated periodically (eg q6-12mo) to maintain effectiveness. The molecular structures of these compounds may be sufficiently different to opioid receptors to counter the affects of diminished and down-regulation of receptors to chronic opioid exposure.

Pharmaceutical companies are exploring various combinations of NSAIDs/opioids, extended-release formulations, and drug delivery (eg topical, mucosal) in an effort to achieve safe and effective pain control.

Analgesic agents

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma or have sustained injuries.


Acetaminophen (Tylenol, Feverall, Tempra)

DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.

Adult

500-1000 mg PO q4-6h

Pediatric

<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO q4h; not to exceed 5 doses in 24 h

Rifampin can reduce analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity

Documented hypersensitivity; known G-6-P deficiency

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatotoxicity possible in chronic alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many OTC products and combined use with these products may result in cumulative doses exceeding recommended maximum dose

Nonsteroidal anti-inflammatory drugs

Have analgesic, anti-inflammatory, and antipyretic activities.16 Mechanism of action is not known, but they may inhibit COX activity and prostaglandin synthesis. Other mechanisms may also exist, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.


Aspirin (Anacin, Ascriptin)

Effective in most mechanical LBP cases. Irreversibly inhibits platelet function, leading to prolonged bleeding times.

Adult

500-1000 mg PO q4-6h

Pediatric

Not established

Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses > 2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Documented hypersensitivity; liver damage, hypoprothrombinemia, vitamin K deficiency, bleeding disorders, asthma; due to association of aspirin with Reye syndrome, do not use in children ( <16 y) with flu

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia or history of blood coagulation defects or who are taking anticoagulants


Naprosyn (Naproxen, Naprelan, Naprosyn)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of COX, which results in a decrease of prostaglandin synthesis.

Adult

500 mg PO initially
250 mg PO q6-8h or 500 mg PO q12h

Pediatric

Not established

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug

Cyclooxygenase II inhibitors

Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeding is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost avoidance of GI bleeds will further define the populations that will find COX-2 inhibitors the most beneficial.


Celecoxib (Celebrex)

Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus GI toxicity may be decreased. Seek lowest dose of celecoxib for each patient.

Adult

100-200 mg PO q12h

Pediatric

Not established

Coadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration with rifampin may decrease celecoxib plasma concentrations

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, conditions predisposing to fluid retention, severe heart failure, and hyponatremia because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in presence of existing controlled infections; evaluate symptoms and signs suggesting liver dysfunction, or in abnormal liver laboratory results

Muscle relaxants

Mechanism of action is not fully understood.


Cyclobenzaprine (Flexeril)

Skeletal muscle relaxant that acts centrally and reduces motor activity of tonic somatic origins, influencing alpha and gamma motor neurons.
Structurally related to TCAs and thus carries some of their same liabilities. Given in combination with an NSAID (similar to carisoprodol).

Adult

10 mg PO tid

Pediatric

Not established

Coadministration with MAOIs and TCAs may increase toxicity; may have additive effect when used concurrently with anticholinergics; effects of alcohol, CNS depressants, and barbiturates may be enhanced

Documented hypersensitivity; MAOIs within last 14 d

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in angle-closure glaucoma and urinary hesitance; warn patients not to operate machinery while taking this medication


Orphenadrine (Norflex)

While exact mode of action not well understood, has shown clinical effectiveness in muscular injury. Effectiveness may be related to analgesic properties. May have atropinelike effects and analgesic properties.

Adult

100 mg PO bid
60 mg IV/IM q12h

Pediatric

Not established

Documented hypersensitivity; GI obstruction, glaucoma, myasthenia gravis, or cardiospasm

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiac arrhythmias and congestive heart failure


Carisoprodol (Soma)

Short-acting medication that may have depressant effects at spinal cord level. Often given in combination with an NSAID.

Adult

350 mg PO qid

Pediatric

Not established

Increases toxicity of alcohol, CNS depressants, MAOIs, clindamycin, and phenothiazines

Documented hypersensitivity; acute intermittent porphyria

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal and hepatic impairment

Opioids

Useful only for extremely severe pain. Can be administered by injection.


Oxycodone (OxyContin)

Indicated for relief of moderate to severe pain.

Adult

5-10 mg PO q4-6h

Pediatric

Not established

Phenothiazines may antagonize analgesic effects; MAOIs, general anesthesia, CNS depressants, and TCAs may increase toxicity

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in COPD, emphysema, and renal insufficiency

More on Mechanical Low Back Pain

Overview: Mechanical Low Back Pain
Differential Diagnoses & Workup: Mechanical Low Back Pain
Treatment & Medication: Mechanical Low Back Pain
Follow-up: Mechanical Low Back Pain
Multimedia: Mechanical Low Back Pain
References
Further Reading
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References

  1. Institute for Clinical Systems Improvement. Adult low back pain. Bloomington, Minn: Institute for Clinical Systems Improvement;. Sept 2005.

  2. National Guideline Clearinghouse. Listing of Guidelines for Low Back Pain. Accessed December 29, 2005. Available at: http://www.guidelines.gov. [Full Text].

  3. Philadelphia Panel evidence-based clinical practice guidelines on selected rehabilitation interventions for low back pain. Phys Ther. Oct 2001;81(10):1641-74. [Medline]. [Full Text].

  4. Bigos SJ, Boyer OR, Braen GR. Acute Low Back Problems in Adults. Clinical Practice Guideline, Quick Reference Guide Number 14. Public Health Agency, Agency for Health Care Policy and Research. Rockville, Md:. Department of Health and Human Services;1994.

  5. Bone and Joint Decade. US Bone and Joint Decade Web site. Accessed December 28, 2005. Available at: http://www.usbjd.org/index.cfm. [Full Text].

  6. Datta S, Lee M, Falco FJ, et al. Systematic assessment of diagnostic accuracy and therapeutic utility of lumbar facet joint interventions. Pain Physician. Mar-Apr 2009;12(2):437-60. [Medline]. [Full Text].

  7. Rupert MP, Lee M, Manchikanti L, et al. Evaluation of sacroiliac joint interventions: a systematic appraisal of the literature. Pain Physician. Mar-Apr 2009;12(2):399-418. [Medline].

  8. Chen SM, Liu MF, Cook J, et al. Sedentary lifestyle as a risk factor for low back pain: a systematic review. Int Arch Occup Environ Health. Mar 20 2009;[Medline].

  9. Cocchiarella L, Andersson GBJ. AMA Guides to the Evaluation of Permanent Impairment. 5th ed. 2000.

  10. [Best Evidence] Sertpoyraz F, Eyigor S, Karapolat H, et al. Comparison of isokinetic exercise versus standard exercise training in patients with chronic low back pain: a randomized controlled study. Clin Rehabil. Mar 2009;23(3):238-47. [Medline].

  11. Long A, Donelson R, Fung T. Does it matter which exercise? A randomized control trial of exercise for low back pain. Spine. Dec 1 2004;29(23):2593-602. [Medline].

  12. [Best Evidence] Juni P, Battaglia M, Nuesch E, et al. A randomised controlled trial of spinal manipulative therapy in acute low back pain. Ann Rheum Dis. Sep 2009;68(9):1420-7. [Medline].

  13. Epter RS, Helm S, Hayek SM, et al. Systematic review of percutaneous adhesiolysis and management of chronic low back pain in post lumbar surgery syndrome. Pain Physician. Mar-Apr 2009;12(2):361-378. [Medline].

  14. Veresciagina K, Ambrozaitis KV, Spakauskas B. The measurements of health-related quality-of-life and pain assessment in the preoperative patients with low back pain. Medicina (Kaunas). 2009;45(2):111-22. [Medline].

  15. [Guideline] Chou R, Loeser JD, Owens DK, et al. Interventional therapies, surgery, and interdisciplinary rehabilitation for low back pain: an evidence-based clinical practice guideline from the American Pain Society. Spine. May 1 2009;34(10):1066-77. [Medline].

  16. van Tulder MW, Scholten RJ, Koes BW, et al. Non-steroidal anti-inflammatory drugs for low back pain. Cochrane Database Syst Rev. 2000;CD000396.

  17. Adams MA, May S, Freeman BJ, et al. Effects of backward bending on lumbar intervertebral discs. Relevance to physical therapy treatments for low back pain. Spine. Feb 15 2000;25(4):431-7; discussion 438. [Medline].

  18. Atkinson JH, Slater MA, Wahlgren DR, et al. Effects of noradrenergic and serotonergic antidepressants on chronic low back pain intensity. Pain. Nov 1999;83(2):137-45. [Medline].

  19. Batt ME, Todd C. Five facts and five concepts for rehabilitation of mechanical low back pain. Br J Sports Med. Aug 2000;34(4):261. [Medline].

  20. Borenstein D. Epidemiology, etiology, diagnostic evaluation, and treatment of low back pain. Curr Opin Rheumatol. Mar 1996;8(2):124-9. [Medline].

  21. Brigham CR, Babitsky S, Mangraviti JJ. The Independent Medical Evaluation Report: A Step-by-Step Guide with Models. SEAK Inc;1996.

  22. Cherkin DC, Wheeler KJ, Barlow W, et al. Medication use for low back pain in primary care. Spine. Mar 1 1998;23(5):607-14. [Medline].

  23. Chrubasik S, Eisenberg E, Balan E, et al. Treatment of low back pain exacerbations with willow bark extract: a randomized double-blind study. Am J Med. Jul 2000;109(1):9-14. [Medline].

  24. Consumer Reports. Back pain: the best treatment is surprisingly simple. Consumer Reports;1995:620-621.

  25. Cox ME, Asselin S, Gracovetsky SA, et al. Relationship between functional evaluation measures and self-assessment in nonacute low back pain. Spine. Jul 15 2000;25(14):1817-26. [Medline].

  26. Derby R, Bogduk N, Anat D, et al. Precision percutaneous blocking procedures for localizing spine pain. Part 1: the posterior lumbar compartment. Pain Digest. 1993;3:89-100.

  27. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain?. JAMA. Aug 12 1992;268(6):760-5. [Medline].

  28. Di Fabio RP, Mackey G, Holte JB. Physical therapy outcomes for patients receiving worker''s compensation following treatment for herniated lumbar disc and mechanical low back pain syndrome. J Orthop Sports Phys Ther. Mar 1996;23(3):180-7. [Medline].

  29. Dishman JD, Bulbulian R. Spinal reflex attenuation associated with spinal manipulation [In Process Citation]. Spine. Oct 1 2000;25(19):2519-25. [Medline].

  30. Drugs for pain. Med Lett Drugs Ther. Aug 21 2000;42(1085):73-8. [Medline].

  31. Duance VC, Crean JK, Sims TJ, et al. Changes in collagen cross-linking in degenerative disc disease and scoliosis. Spine. Dec 1 1998;23(23):2545-51. [Medline].

  32. Ferguson SA, Marras WS, Gupta P. Longitudinal quantitative measures of the natural course of low back pain recovery. Spine. Aug 1 2000;25(15):1950-6. [Medline].

  33. Frymoyer JW. Back pain and sciatica. N Engl J Med. Feb 4 1988;318(5):291-300. [Medline].

  34. Furlan AD, Brosseau L, Welch V, Wong J. Massage for low back pain. Cochrane Database Syst Rev. 2000;CD001929.

  35. Guidelines for the assessment and management of chronic pain. WMJ. 2004;103(3):13-42. [Medline].

  36. Handa N, Yamamoto H, Tani T, et al. The effect of trunk muscle exercises in patients over 40 years of age with chronic low back pain. J Orthop Sci. 2000;5(3):210-6. [Medline].

  37. Hanson P, Qvortrup K, Magnusson SP. The superficial annulus fibrosus ligament. an incipient description of a separate ligament between the lumbar anterior longitudinal ligament and the intervertebral disc [In Process Citation]. Cells Tissues Organs. 2000;167(4):259-65. [Medline].

  38. Harrington JF, Messier AA, Bereiter D, et al. Herniated lumbar disc material as a source of free glutamate available to affect pain signals through the dorsal root ganglion. Spine. Apr 15 2000;25(8):929-36. [Medline].

  39. Hart LG, Deyo RA, Cherkin DC. Physician office visits for low back pain. Frequency, clinical evaluation, and treatment patterns from a U.S. national survey. Spine. Jan 1 1995;20(1):11-9. [Medline].

  40. Hoogendoorn WE, van Poppel MN, Bongers PM, et al. Systematic review of psychosocial factors at work and private life as risk factors for back pain. Spine. Aug 15 2000;25(16):2114-25. [Medline].

  41. McMorland G, Suter E. Chiropractic management of mechanical neck and low-back pain: a retrospective, outcome-based analysis. J Manipulative Physiol Ther. Jun 2000;23(5):307-11. [Medline].

  42. North American Spine Society. Orthopedic Knowledge Update: Spine. NASS/AAOS;1997:113-119.

  43. Pustaver MR. Mechanical low back pain: etiology and conservative management. J Manipulative Physiol Ther. Jul-Aug 1994;17(6):376-84. [Medline].

  44. Rungee JL. Low back pain during pregnancy. Orthopedics. Dec 1993;16(12):1339-44. [Medline].

  45. Sizer PS Jr, Matthijs O, Phelps V. Influence of age on the development of pathology. Curr Rev Pain. 2000;4(5):362-73. [Medline].

  46. Solomonow M, He Zhou B, Baratta RV, et al. Biexponential recovery model of lumbar viscoelastic laxity and reflexive muscular activity after prolonged cyclic loading. Clin Biomech (Bristol, Avon). Mar 2000;15(3):167-75. [Medline].

  47. Spengler D. Herniated nucleus pulposus surgery: effect of compensation. The Back Letter. 1997;vol 12.

  48. Spitzer WO, Skovron ML, Salmi LR, et al. Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders: redefining "whiplash" and its management. Spine. Apr 15 1995;20(8 Suppl):1S-73S. [Medline].

  49. Von Feldt JM, Ehrlich GE. Pharmacologic therapies. Phys Med Rehabil Clin N Am. May 1998;9(2):473-87, ix. [Medline].

  50. Waddell G, McCulloch JA, Kummel E, Venner RM. Nonorganic physical signs in low-back pain. Spine. Mar-Apr 1980;5(2):117-25. [Medline].

  51. Wilson L, Hall H, McIntosh G, Melles T. Intertester reliability of a low back pain classification system. Spine. Feb 1 1999;24(3):248-54. [Medline].

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Keywords

mechanical low back pain, back pain, pain back, lower back pain, low back pain, sciatica, back problems, back injury, back surgery, back pain relief, lower back pain pregnancy, myofascial low back pain, LBP, mechanical LBP, pulled low back, low back sprain, low back strain, lumbar sprain, lumbar strain, discogenic low back pain, diskogenic low back pain, sacroiliac joint sprain, sacroiliac joint strain, back strain, worker's compensation, workman's comp

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Contributor Information and Disclosures

Author

Everett C Hills, MD, MS, Medical Director, Penn State Hershey Rehabilitation Hospital, Assistant Professor of Orthopaedics and Rehabilitation, Assistant Professor of Neurology, Penn State Milton S. Hershey Medical Center and Penn State University College of Medicine
Everett C Hills, MD, MS is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Congress of Rehabilitation Medicine, American Medical Association, American Society of Neurorehabilitation, Association of Academic Physiatrists, and Pennsylvania Medical Society
Disclosure: Nothing to disclose.

Medical Editor

J Michael Wieting, DO, MEd, Professor of Physical Medicine and Rehabilitation, Professor of Osteopathic Principles and Practices, Director of Sports Medicine, Associate Director of Physician Assistant Training Program, Department of Osteopathic Principles and Practice, Lincoln Memorial University-DeBusk College of Osteopathic Medicine
J Michael Wieting, DO, MEd is a member of the following medical societies: American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners, American College of Sports Medicine, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, and International Society of Physical and Rehabilitation Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Rene Cailliet, MD, Professor-Chairman Emeritus, Department of Rehabilitation Medicine, University of Southern California School of Medicine; Former Director, Department of Rehabilitation Medicine, Santa Monica Hospital Medical Center
Rene Cailliet, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Pain Society, Association of American Medical Colleges, International Association for the Study of Pain, and Pan American Medical Association
Disclosure: Nothing to disclose.

 
 
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