Managing Low-Back Pain
Steps to Optimize Function and Hasten Return to Activity
Jonathan A. Drezner, MD; Stanley A. Herring, MD
Practice Essentials Series Editors:
THE PHYSICIAN AND SPORTSMEDICINE - VOL 29 - NO.8 - AUGUST 2001
In Brief: Low-back pain in active patients is common and often recurs. Comprehensive treatment includes control of pain and inflammation, limited bed rest, early therapeutic exercises within a pain-free range, lumbar stabilization exercises, strengthening of the muscles of the trunk and kinetic chain, aerobic conditioning, and correction of faulty biomechanics. The goal of rehabilitation is to restore normal lumbar spine function and promote independent return to activity. Normal lumbar spine function and the absence of symptoms following sport-specific skills ensure successful return to competition. A patient handout is included.
Low-back pain (LBP) is common in athletes and nonathletes. The lifetime prevalence ranges from 60% to 90%, with a 5% annual incidence (1,2). LBP is second only to the common cold as a cause for primary care office visits, and direct medical costs exceed $25 billion per year (3,4). The lower back is also a frequent site of injury in a variety of sports, including gymnastics, football, weight lifting, rowing, golf, dance, tennis, baseball, basketball, and cycling (5).
The causes of LBP in active people are diverse, and identification of the precise anatomic site of lumbar injury and pain generation is often difficult. Primary care providers frequently diagnose lumbar strain or sprain and mechanical LBP in patients without clear neurologic or complicating features. This article focuses on the subset of patients who have sports-related LBP without clear neurologic, spondylitic, or complicating symptoms. A better understanding of the natural history of LBP and the biomechanics of lumbar spine injury will assist in developing appropriate treatment strategies. A framework for the evaluation and management of LBP emphasizes rehabilitation and return to activity.
Natural History and Clinical Course
Medical training commonly teaches that 90% of LBP will resolve spontaneously within 6 to 12 weeks without medical intervention (6). Given this favorable course, some physicians question whether acute LBP requires any specific treatment. However, closer analysis of long-term outcomes in patients with LBP is less favorable than once perceived.
Recent longitudinal studies suggest that back pain is typically recurrent and that chronic back pain occurs more frequently than previously believed (7). Von Korff and Saunders (8) analyzed short-term and long-term outcomes of LBP treatment in primary care. At 1-month follow-up, only 25% to 33% of patients were completely pain free, 33% reported continuing pain of at least moderate intensity, and 20% to 25% reported substantial activity limitations due to LBP. These problems persisted. At 1-year follow-up, 33% of patients had moderate pain, 15% had severe pain, and 20% to 25% still had substantial activity limitations. Up to 86% of patients reported at least one recurrence of their back pain during the following year, and more than 25% experienced chronic LBP (defined as back pain present on more than half the days during 1 year) (8).
An essential distinction is apparent between the functional outcome and the pain outcome in patients who have low-back problems. Some function may be restored even though pain continues. Similarly, the absence of pain does not indicate the restoration of normal function. The high incidence of recurrent and chronic LBP may represent failure to restore proper functioning and highlights the need for appropriate rehabilitation. More realistic estimates of prognosis may reduce patient anxiety and allow them to adapt to recurrent or chronic LBP and to regain function when pain does not fully resolve.
Anatomy and Biomechanics
Anatomy. The basic motion segment of the spine is a three-joint complex, consisting of one intervertebral disk between adjacent vertebrae and two zygapophyseal (facet) joints (figure 1). The intervertebral disk is composed of the central nucleus pulposus and the peripheral annulus fibrosis. The individual lumbar nerve roots exit bilaterally below the pedicle of each vertebra. Stability of the three-joint complex depends on the integrity of the intervertebral disks. Disk degeneration transfers weight-bearing and rotational loads to the facet joints and may produce facet joint inflammation, arthropathy, and a degenerative cascade in the lumbar spine (6).
The muscular support system of the lumbar spine is divided into anterior and posterior groups. The anterior group consists of the abdominal and psoas muscles. The posterior group contains superficial, middle, and deep layers (figure 2). The superficial layer is the largest paraspinal muscle group and consists of long polysegmental muscles called the erector spinae. The erector spinae muscles are arranged in three vertical columns (iliocostalis, longissimus, and spinalis) and are the chief extensors of the vertebral column. The middle layer consists of short polysegmental muscles (multifidi), and the deep layer consists of small intersegmental muscles. The anterior and posterior muscle groups alternate concentrically and eccentrically to control smooth trunk movement (9).
Biomechanics. The cardinal movements of the lumbar spine include flexion, extension, side flexion, and torsion (rotation). Flexion and extension occur predominantly at the lower two lumbar segments. Rotation at each lumbar segment is limited to only a few degrees because of the vertical orientation of the lumbar facets. Combined movements (ie, flexion and rotation) carry the highest injury potential. Repetitive movements, common in sport, can fatigue the supporting structures of the lumbar spine and overwhelm the viscoelastic protective mechanisms of the intervertebral disks and ligaments (9). Back strains or sprains imply some degree of muscle stretching or microscopic tearing of the muscle fibers and/or ligaments (10). Muscle fatigue can cause reflex muscle spasm and pain (9). Muscle spasms also occur with injury to the three-joint complex and may be influenced by sensory or motor-reflex pathways.
The lumbar spine also links the lower extremities and the torso and coordinates transfer of power through the body in most sports via the kinetic chain. Poor conditioning of the extremities places an athlete at greater risk of low-back injury. For example, proximal leg fatigue or quadriceps weakness may lead to additional strain on the lumbar spine when lifting and reaching down are performed by flexing at the waist rather than bending at the hips and knees. Similarly, athletes who reach overhead or throw despite shoulder injuries that limit upper-trunk rotation may attempt to generate more rotational force through abnormal rotation at the lumbar spine (9).
What Causes Pain?
Pain results from mechanical or chemical irritation of nociceptive nerve fibers. In the lower back, these pain receptors are located in the outer one third of the intervertebral disk, the facet joint capsule, the anterior and posterior longitudinal ligaments, and the musculoligamentous supporting structures of the lumbar spine (10). Back pain, however, cannot be thought of as purely an anatomic or biomedical problem. Psychological factors also play a significant role in the onset of back pain and the transition from acute to chronic pain and disability. Depression, anxiety, distress, and cognitive factors, such as passive coping and catastrophizing (blowing minor events to major proportions), have been closely linked to pain and disability (11).
Steps to Diagnosis
History should focus on the location of the pain, its mechanism of onset, and its relation to body position and movement. Factors that aggravate and relieve the pain, such as lumbar flexion or extension, should be determined. Any radiation of the pain, associated motor or sensory symptoms, history of LBP, or recent change in activity level or trauma should be noted.
Patients with LBP must be screened for more serious medical problems or symptoms that require urgent intervention. Fever, malaise, and the inability to establish a position of comfort suggest serious conditions such as diskitis, osteomyelitis, or malignancy. Bowel or bladder dysfunction, saddle anesthesia, and progressive neurologic deficits may indicate cauda equina or nerve root compromise and the need for emergency lumbar decompression.
Physical exam should begin with evaluation of spinal curvature, lumbar range of motion, and the degree of pain-free movement, all measured with the patient standing. Reproducible painful movements (ie, lumbar flexion or extension) should be noted. Palpation should include the paraspinal muscles, spinous processes, and sacroiliac joints. Assessment of hamstring and hip flexor flexibility and a lower-extremity neurologic exam including the straight-leg raising test should also be performed.
Precise identification of the anatomic pain generator in active people who have LBP is difficult. Athletes who have lumbar strains report unilateral or bilateral LBP, often with painful paraspinal muscle spasms. Injury can occur from repetitive microtrauma or a single major traumatic event. Muscles that produce or control movements of the lumbar spine, such as the erector spinae and musculi multifidi, are most commonly involved. Local tenderness and muscle spasm, limited range of motion, and a normal neurologic exam are the usual findings. Radiating pain is unusual, and walking and sitting are generally uncomfortable but not unbearable.
Muscle pain and spasm can also represent pathology in other structures of the lumbar spine. Injury to the intervertebral disks is a common source of LBP in active people. A tear in the annulus fibrosis causes isolated LBP with a normal neurologic exam and is probably underdiagnosed. Lumbar disk herniations can involve back pain only, leg pain only, or a combination of the two. Athletes who participate in sports involving repeated and forceful hyperextension of the spine (ie, gymnastics and football) may suffer from spondylolysis (stress fracture of the pars interarticularis) or facet joint inflammation and impingement. Older athletes who have spinal canal stenosis may report back pain associated with walking and relieved by rest. The differential diagnosis of LBP with key diagnostic features is presented in table 1.
Diagnostic imaging is seldom needed in the acute setting. Imaging studies should be considered in children and adolescents to rule out serious medical conditions, in adults over age 50 to rule out malignancy, when traumatic fracture is suspected, and when back pain fails to improve with conservative treatment. Abnormal imaging findings, however, may not represent the reason for a patient's pain. For instance, disk degeneration and protrusion have been demonstrated on magnetic resonance imaging in 20% to 25% of asymptomatic individuals (12). Imaging tests must, therefore, be interpreted carefully and correlated closely with the clinical picture.
The high recurrence rate and functional changes known to occur in chronic back pain warrant attempts to maximize rehabilitation of the lumbar spine. Substantial controversy exists, however, on the best way to rehabilitate low-back injuries. Ideally, treatment decisions are based on prospective, randomized, single-intervention studies that assess long-term efficacy. Unfortunately, methodologic discrepancies make interpretation of the available literature on treating low-back injuries very difficult. Major ethical and practical factors make use of control groups nearly impossible, and current outcome measurements may not distinguish small, but clinically relevant, differences between treatment groups (13). Furthermore, when interpreting the back pain treatment studies, the absence of proof does not indicate the proof of absence.
The treatment strategies discussed below are derived from a synthesis of available literature, integration of functional anatomy, and the principle of functional progression (table 2) (6). The overall goal is to restore normal lumbar spine function and promote safe and independent return to activity.
Pain and inflammation control. Treatment of acute or recurrent LBP begins with control of pain and inflammation. Although no study specifically demonstrates the efficacy of nonsteroidal anti-inflammatory drugs in the treatment of LBP, decreased pain and inflammation may permit early and more rapid rehabilitation. Judicious use of narcotic analgesics may be needed for additional pain control. Muscle relaxants have limited efficacy in LBP, and their central sedating effects may inhibit participation in rehabilitation.
Therapeutic modalities such as cryotherapy and electrogalvanic stimulation also assist in reducing pain and muscle spasm. Superficial heat decreases pain and spasm but increases arterial and capillary blood flow and may increase inflammation in the acute setting. Deep heat via ultrasound is contraindicated acutely but may help with soft-tissue and articular inflexibilities later in treatment.
Bed rest. Bed rest should be limited to no more than 2 days for nonspecific LBP. Prolonged inactivity produces a number of deleterious effects, including decreases in muscle strength, flexibility, cardiovascular fitness, bone density, and disk nutrition (14). Relative rest with early activity is preferred because longer periods of bed rest have not produced better recovery rates (15).
Exercises. Therapeutic exercises should begin early to control pain, avoid deconditioning, and restore function. There is no single treatment or exercise regimen that will be effective for all patients with LBP. Customized rehabilitation programs and working closely with a physical therapist skilled in different treatment approaches will optimize the chances for a successful outcome.
Initial exercises should be directed away from the movement that aggravates the patient's symptoms. For patients whose symptoms are aggravated by flexion and reduced by extension of the lumbar spine, extension exercises should be performed (extension bias). Similarly, if pain is worse with extension but reduced by flexion, flexion exercises should be performed (flexion bias). For some patients with acute or recurrent LBP, a combination of flexion and extension exercises will be tolerated. (See "Exercises in the Treatment of Low-Back Pain.")
As pain subsides, more intensive therapy is aimed at improving strength and function.
Spine stabilization exercises are directed at improving function by conditioning the muscles around the lumbar spine. A key component to spine stabilization is establishing a neutral spine position (the midpoint between available anterior and posterior pelvic tilt) that provides the greatest comfort and functional stability.
Lower-extremity muscle tightness is common with LBP and must be addressed to allow normal lumbar motion. Recognizing common inflexibility and muscle weakness patterns will assist in planning appropriate exercises. Two patterns are common. First, tight hip flexor muscles (iliopsoas and rectus femoris) result in excessive anterior pelvic tilt and increased lumbar lordosis. These factors lengthen the hip extensors (gluteus maximus and hamstrings), placing them at a mechanical disadvantage and causing early recruitment of the lumbar extensor muscles (erector spinae). Treatment consists of stretching the hip flexors and strengthening the hip extensors.
The second pattern involves tight hamstring muscles that cause excessive posterior pelvic tilt and decrease lumbar lordosis. These factors place the back extensors at a mechanical disadvantage and also make the spine less resilient to axial loads. Treatment is aimed at stretching the hamstring muscles and strengthening the back extensors (10).
Conditioning the entire kinetic chain and maintaining aerobic fitness are part of comprehensive rehabilitation. Cross-training activities such as cycling, pool jogging, or stair-stepping machines may be helpful early in rehabilitation. Supervised activities that mimic a patient's sport or activity should begin as soon as symptoms allow.
Correction of predisposing factors such as poor posture when sitting or standing, faulty lifting techniques, abnormal biomechanics, muscle inflexibilities, and poor conditioning is essential to treatment, especially for athletes. Education and individualized coaching on proper technique may help prevent recurrence.
Manipulation for LBP is controversial. A selective subset of patients (mostly those with recent-onset LBP without radiculopathy) may obtain temporary benefit from manipulation (6). Manipulation is contraindicated in disk herniations and, when used, should always be used with other appropriate rehabilitative components. Protracted passive treatment places the patient in a dependent role and becomes counterproductive to establishing functional independence.
Other manual therapy techniques such as joint mobilization, myofascial release, and muscle energy techniques may be used to improve soft-tissue flexibility and segmental joint function (6).
Return to Activity
As pain resolves and rehabilitation advances, patients should begin training in sport-specific functional activities. Repetition or intensity of some training elements may need to be eliminated or reduced to prevent recurrence and aggravation of pain. Intensity and progression of activities should be guided by symptoms. Persistence of pain and muscle spasm indicate that progression was advanced too vigorously. Normal lumbar spine function and the absence of major symptoms following sport-specific skills usually indicate that patients can successfully return to their sport or actvitiy.
Implementating a long-term maintenance program is important in preventing recurrence. The single best predictor of low-back injury during athletic activity is a previous low-back injury. Thus, rehabilitation should continue beyond the resolution of symptoms and return to sport. Depending on the patient's participation level (ie, high school, college, or professional) and time of season, activity clearance should be flexible and based on sound clinical judgment.
Dr Drezner is an assistant professor in the department of Family Practice and Community Medicine at the University of Pennsylvania in Philadelphia, and Dr Herring is a clinical associate professor in the departments of Rehabilitative Medicine and Orthopedics at the University of Washington in Seattle. Address correspondence to Jonathan A. Drezner, MD, Dept of Family Practice and Community Medicine, University of Pennsylvania Health System, 51 N 39th St, 6th Floor Mutch Bldg, Philadelphia, PA 19104; e-mail to [email protected].