Diagnosis and management of low back pain and sciatica

Diagnosis and management of low back pain and sciatica

Anthony H. Wheeler

Approximately 80 percent of the population will experience low back pain at some point during their lives.[1] Although low back pain is usually benign and self-limiting, disability from low back pain has reached epidemic proportions in our Western culture[1] Disability from low back problems is second only to the common cold as a cause of lost work time[2] and is the most common cause of disability in persons under the age of 45.[3]

Pathology affecting the disc has been popularized as a cause of low back pain and sciatica, but cases of asymptomatic disc herniation are commonly identified on computerized tomography (CT) and magnetic resonance imaging (MRI) of the lumbar spine. A recent study of MRI of the lumbar spine in patients without back pain revealed abnormal lumbar discs at some level in 64 percent of these asymptomatic adults.[4] Additionally, the extent of disc protrusion and the degree of clinical symptoms often do not correlate.[1,5]

Degenerative change and injury to spinal structures produce low back and leg pain in various combinations, but with similar activity-related or mechanical characteristics.[6] The term “sciatica” is used to describe leg pain that predominates in the distribution of a lumbosacral nerve root, with or without neurologic deficit. Mechanical low back pain is usually aggravated by static loading of the spine (e.g., prolonged sitting or standing), long-levered activities (e.g., vacuuming) or levered postures (bending forward). It is eased when the spine is balanced by multidirectional forces (e.g., walking) or when the spine is unloaded (e.g., reclining). Mechanical conditions of the spine, including disc disease, spondylosis, spinal stenosis and fractures, account for up to 98 percent of cases of back pain, with the remaining cases due to systemic and visceral disease[7] (Table 1).

TABLE 1

Classification of Low Back Pain Syndromes

Comparison studies of treatments for acute low back pain have demonstrated benefit from an exercise approach developed by the physical therapist Robin McKenzie.[18,20] These exercises are performed in the direction that causes referred pain to centralize, or retract, from the periphery (leg) to the lumbar midline. Studies have shown this approach to be more effective than the popularly prescribed Williams, exercises, which advocate lumbar flexion only.[20] McKenzie exercises act to centralize low back pain in the coronal plane by reducing a lateral lumbar list, or in the sagittal plane by using repeated extension or flexion maneuvers.[20] After the pain is centralized and a lumbar list is corrected, the physiotherapist teaches the patient to find the “neutral” position of the spine, which is the lumbar posture that produces the least pain and the least potential risk for injury.[20]

OTHER ADJUNCTS

In cases of intractable low back pain, therapeutic injections into painful lumbosacral soft tissues and myofascial trigger points have been widely advocated as an adjunctive treatment, although long-term benefit is unproved. Studies have demonstrated that use of a dry needle is as effective as lidocaine (Xylocaine) or corticosteroid injection.[21] While reports on the use of lumbar epidural injections are conflicting, they may reduce pain in some patients with sciatica or predominantly radicular symptoms, at least on a short-term basis (Table 3).[7,22]

Manual therapy for dysfunction of the soft tissues and joints is frequently prescribed during the acute period. Skill level and technique vary among practitioners, including chiropractors, osteopaths, physical therapists and physicians. More controlled trials have evaluated joint manipulation than other conservative measures, but problems with methodologv make interpretation of these studies difficult.[20,23] Spinal manipulation is probably most beneficial for the treatment of acute low back pain without sciatica or neurologic impairment.[24]

Corsets and braces may provide benefit as a treatment adjunct, although their mechanism of action or efficacy has yet to be proved.[6,10,13,23] Rigid bracing is often indicated in patients with spinal fracture or severe pathologic instability. Elastic compression may provide support for patients with weakened trunk muscles. Corsets with a firm molded insert or molded braces may help patients maintain a neutral or protective lumbar posture while performing certain risky biomechanical activities, such as yard work or vacuuming.

Subacute Low Back Pain and Sciatia

When lock back pain and sciatica, especially with neurologic deficit, persist into the subacute phase (defined as back pain for six to 12 weeks) despite adequate treatment, appropriate consultation and diagnostic imaging are indicated (Figure 1). Referral to a physician with expertise in spinal disorders should be considered before expensive diagnostic tests are ordered.

DIAGNOSTIC STUDIES

CT scanning is usually an effective diagnostic study when the spinal or neurologic level is clear and when bony pathology is suspected. Magnetic resonance imaging (MRI) is more useful when the exact spinal or neurologic level is unclear, when a pathologic condition of the spinal cord or soft tissues is suspected or when an underlying infectious or neoplastic process is possible. Contrast-enhanced CT or MRI can be useful in delineating recurrent disc herniation from epidural scarring. Myelography is useful to clarify nerve root pathology, particularly in patients with previous lumbar spine surgery or with a metal fixation device in place. CT myelography can provide further information in patients who have had multiple spinal operations or who have spinal stenosis.[18]

When leg pain predominates and imaging studies provide ambiguous information, clarification may be gained by electromyography (EMG), somatosensory evoked potentials (SSEPs) or selective nerve root blocks.[18] When the cause of subacute sciatica is clear, surgical intervention may be indicated. However, if data are inconclusive, a multidisciplinary evaluation may help in the assessment of physical and psychosocial factors that may be contributing to the prolonged pain and disability.

HELPING THE PATENT RESUME ACTIVITIES

During the subacute and chronic phases, patients should become more active and independent by performing strengthening, flexibility and stabilization exercises. Reliance on narcotic analgesics and muscle spasmolytics for pain relief should be stopped.[13] Alternatively, tricyclic antidepressants may reduce pain, depression, insomnia and other associated disorders, such as headache.[10,25]

The benefit of traction beyond forced bed rest is unclear.[6,7,10,13] Traction may be useful in the subacute or chronic phase if it can be self-administered, which may be accomplished by instructing the patient to hang by his or her arms from a doorway or stand between two sturdy chairs and use his or her arms to push up from the backs of the chairs. Other simple aids, such as a walker, can be used to temporarily “unload” the trunk and thus alleviate low back pain during an active exercise program or functional activities.

When the patient is able, he or she should begin aerobic conditioning. If the pain of weight-bearing is severe, the microgravity environment of a swimming pool is a useful place to start walking exercises. Walking is coupled with water resistance against the trunk, which entails isometric bracing to maintain a neutral spine position. Since dynamic loading of the spine usually produces less discomfort, activities such as stair climbing or walking may produce less pain. Activities that apply flexion or torsional stress to the spine should be avoided.

Chronic Low Back Pain

During the chronic phase (defined as back pain for 12 weeks or longer), bed rest should be avoided. NSAIDs often have long-term side effects and should he used selectively.[6,18] Use of oral glucocorticoids, opioids and muscle spasmolytics should be avoided, although tricyclic antidepressants may be beneficial on a long-term basis.[18,25] Local injections into soft tissues and epidural corticosteroid injections may be used in selected patients, with careful monitoring for flare-ups. Traction, heat or ice applications may reduce symptoms and should be self-administered.

Functional restoration is a treatment method that addresses the complex interwoven physical and psychosocial factors that play a role in chronic low back pain and disability.[3] The scientific basis for functional restoration comes from research pertaining to the behavioral aspects of chronic pain and the physiologic deterioration that results from prolonged musculoskeletal disuse.

FUNCTIONAL RESTORATION

Emphasizing the multifactorial nature of chronic low back pain, functional restoration typically uses a team approach that includes a physician, psychologist, physical therapist, occupational therapist, nurse and vocational consultant. The program consists of daily intensive physical training to restore normal flexibility, strength and endurance, coupled with cognitive-behavioral intervention. With measured physical and functional improvement, the patient participates in increasing levels of task-oriented rehabilitation and work simulation. The regimen ends with an evaluation of functional capabilities, which can be used as a guideline for returning to work and resuming other physical activities.[3]

The treatment model for chronic low back pain was originally developed by Mayer, who demonstrated return to work in 87 percent of program graduates who could be contacted at two-year follow-up, compared with 41 percent of an untreated group and 29 percent of program dropouts.[26] Another study also showed similar results with a multicenter and multistate functional restoration program that emphasized work hardening but excluded psychosocial programs.[27]

Functional restoration programs are costly by most standards, and the ideal formula for combining psychologic and physical treatment components is not yet determined. Furthermore, it has been difficult for some programs to produce similar success because of flawed program design or faulty methodology.[28]

Rehabilitation programs that purport to manage low back pain should offer patients basic instruction on back care, body mechanics and neutral positioning of the lumbar spine; stabilization exercises to maintain this protected posture during functional activities; an appropriate home exercise program, and self-care instructions to be used in the event of a flare-up. However, the patient must provide the self-motivation, discipline and determination to follow through once given these tools.

Prevention

Morbid obesity and smoking epidemiologically correlate with low back pain and may affect the pathogenesis of the disorder.[29,30] Overall physical fitness may correlate with recovery from low back pain and return to work, but isometric lifting strength and cardiovascular fitness have not been found to be predictive of back injury.[31,32] Training, education and ergonomic intervention may reduce the incidence of back disorders, but this effect has not yet been proved. Psychosocial factors have been shown to have the most significant influence on the development of chronic disability from low back pain. Early treatment of preexisting psychologic disorders or interventions that address job dissatisfaction may provide an opportunity for prophylaxis.[33][Figure 1: ILLUSTRATION OMITTED]

REFERENCES

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In: Physical medicine and rehabilitation. State of the Art Reviews 1990;4:191-9. [9.] Weinstein JN. The role of neurogenic and non-neurogenic mediators as they relate to pain and the development of osteoarthritis. A clinical review. Spine 1992:17(Supl 10):356-61. [10.] Frymoyer JW. Back pain and sciatica. N Engl J Med 1988;318:291-300. [11.] Weber H. Lumbar disc herniation. A controlled, prospective study with ten years of observation. Spine 1983;8:131-40. [12.] Saal JA, Saal JS. Nonoperative treatment of herniated lumbar intervertebral disc with radiculopathy. An outcome study. Spine 1989;14:431-7. [13.] Saal JA, Saal JS, Herzog RJ. The natural history of lumbar intervertebral disc extrusions treated nonoperatively. Spine 1990;15:683-6. [14.] Delauche-Cavallier MC, Budet C, Laredo JD, Debie B, Wybier M, Dorfmann H, et al. Lumbar disc herniation. Computed tomography scan changes after conservative treatment of nerve root compression. Spine 1992;17:927-33. [15.] Maigne JY, Rime B, Deligne B. Computed tomographic follow-up study of forty-eight cases of nonoperatively treated lumbar intervertebral disc herniation. Spine 1992;17:1071-4. [16.] Bozzao A, Gallucci M, Masciocchi C, Aprile I, Barile A, Passariello R. Lumbar disc herniation. MR imaging assessment of natural history in patients treated without surgery. Radiology 1992;185:135-41. [17.] Deyo RA, Diehl AK, Rosenthal M. How many days of bed rest for acute low back pain? A randomized clinical trial. N Engl J Med 1986;315:1064-70. [18.] Common diagnostic and therapeutic procedures of the lumbosacral spine. The North American Spine Society’s Ad Hoc Committee on Diagnostic and Therapeutic Procedures. Spine 1991;16:1161-7. [19.] Faas A, Chavannes AW, van Eijk JT, Gubbels JW A randomized, placebo-controlled trial of exercise therapy in pabents with acute low back pain. Spine 1993;18:1388-95. [20.] White AH, Anderson RT, eds. Conservative care of low back pain. Baltimore: Williams & Wilkins, 1991;97-119,159-68. [21.] Garvey TA, Marks MR, Wiesel SW A prospechve, randomized, double-blind evaluation of triggerpoint injection therapy for low-back pain. Spine 1989;14:962-4. [22.] Bowman SJ, Wedderburn L, Whaley A, Grahame R, Newman S. Outcome assessment after epidural corticosteroid injechon for low-back pain and sciatica. Spine 1993;18:1345-50. [23.] Deyo RA. Conservative therapy for low back pain. Distinguishing useful from useless therapy. JAMA 1983;250:1057-62. [24.] Shekelle PG. Spinal manipulation. Spine 1994;19: 858-61 . [25.] Ward NG. Tricyclic antidepressants for chronic lowback pain. Spine 1986;11:661-5. [26.] Mayer TG, Gatchel RJ, Mayer H, Kishino ND, Keeley J, Mooney V. A prospective two-year study of functional restoration in industrial ow back injury. An objective assessment procedure. JAMA 1987;258:1763-7 [Published erratum appears in JAMA 1988;259:220]. [27.] Burke SA, Harms-Constas CK, Aden PS. Return to work/work retention outcomes of a functional restoration program. A multi-center, prospective study with a comparison group. Spine 1994;19:1880-5. [28.] Gatchel RJ, Mayer TG, Hazard RG, Rainville J, Mooney V. Functional restoration. Pitfalls in evaluating efficacy [Editorial]. Spine 1992;17:988-95. [29.] Battie MC, Videman T, Gill K, Moneta GB, Nyman R, Kaprio J, et al. Smoking and lumbar intervertebral disc degeneration: an MRI study of identical twins. Spine 1991;16:1015-21. [30.] Deyo RA, Bass JE. Lifestyle and low-back pain. The influence of smoking and obesity. Spine 1989;14:501-6. [31.] Battie MC, Bigos SJ, Fisher LD, Hansson TH, Jones ME, Wortley MD. Isometric lifting strength as a predictor of industrial back pain reports. Spine 1989;14: 851-6. [32.] Battie MC, Bigos SJ, Fisher LD, Hansson TH, Nachemson AL, Spengler DM, et al. A pl ospechve study of the role of cardiovascular risk factors and fitness in industrial back pain complaints. Spine 1989;14:141-7. [33.] Bigos SJ, Battie MC, Spengler DM, Fisher LD Fordyce WE, Hansson TH, et al. A prospective study of work perceptions and psychosocial factors affecting the report of back injury Spine 1991;16:1-6 [Published erratum appears in Spine 1991;16:688].

ANTHONY H. WHEELER, M.D. is a neurologist in pnvate practice with Charlotte (N.C.) Orthopedic Specialists at the Charlotte Spine Center. Dr. Wheeler received a medical degree from the University of North Carolina at Chapel Hill School of Medicine and served an internship and a residency at the affiliated hospitals of Baylor College of Medicine in Houston, Tex. Address correspondence to Anthony H. Wheeler, M.D., Charlotte Spine Center, 2001 Randolph Road, Charlotte, NC 28207.

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