Management of Mechanical Lumbar Spine Disease

Mechanical disorders of the lumbar spine are the most common causes of low back pain. These disorders are related to overuse of a normal anatomic structure or secondary to deformity or injury of an anatomic structure. The common mechanical lumbosacral disorders include lumbar strain, herniated intervertebral nucleus pulposus with radiculopathy, osteoarthritis, and spinal stenosis. Recent epidemiologic surveys suggest that the US prevalence of low back pain is 59 million in the last 3 months.

An essential clinical difficulty that exists with mechanical disorders of the lumbar spine is the absence of close correlation between anatomic alterations and the presence of symptoms. The absence of correlation does not negate the legitimate complaints of a proportion of individuals with anatomic abnormalities that do cause pain. In older populations, the presence of anatomic variations from normal is common. Therefore, a large number of individuals report mechanical low back pain, although they represent a minority of all individuals with these common anatomic alterations. These “degenerative” processes start during the adolescence of all individuals. Diminished blood flow to the intervertebral disc in the first half of the second life decade appears to initiate tissue breakdown. Through a variety of factors, both genetic and environmental, the progression is more rapid in some populations than in others. Environmental risk factors, such as smoking, obesity, and heavy physical activity, heighten the potential to develop symptomatic forms of mechanical disorders.

The symptoms of mechanical disorders are characteristically relieved by certain positions and activities and exacerbated by others. The pattern of alleviating and aggravating factors helps localize the disorder to particular portions of the spine. For example, lumbar spine flexion exacerbates intervertebral disc disease and alleviates apophyseal (facet) joint disease. Physical examination is unable to identify the exact location of the source of pain in many circumstances. However, physical examination does identify limitations of function and neurologic deficits. Radiographic evaluation is able to identify anatomic alterations in the spine but does not necessarily correlate those changes with the patient’s symptoms.

The diagnosis of causes of mechanical low back pain is more specific when corresponding abnormalities in the neurologic system are present. For example, the diagnosis of a lumbar radiculopathy can be suspected by characteristic physical findings and may be confirmed with neurophysiologic testing with nerve conduction tests and electromyography. Making a more specific diagnosis of mechanical low back pain is worth the effort. The differential diagnosis is different for the various forms of back pain. In addition, different components of medical therapy are more appropriate for specific forms of mechanical low back pain, such as epidural corticosteroid injections for radicular pain related to intervertebral disc herniation ( Table 26-1 ).

Table 26-1

Mechanical Disorders of the Lumbar Spine

Characteristics Muscle Strain HNP Osteoarthritis Spinal Stenosis
Age (y) 20–40 30–50 > 50 > 60
Pain pattern
Location Back (unilateral) Back/leg (unilateral) Back (unilateral) Leg (bilateral)
Onset Acute Acute Insidious Insidious
Standing I D I I
Sitting D I D D
Bending I I D D
Straight leg + + (stress)
Plain radiographs + +
CT Disc herniation Joint arthritis Canal narrowing
MRI Disc herniation Joint arthritis Canal narrowing

-, not present; +, present; CT, computed tomography; D, pain decreases; HNP, herniated nucleus pulposus; I, pain increases; MRI, magnetic resonance imaging.

Many mechanical disorders are self-limited in duration, with the majority of patients improving spontaneously. Other disorders wax and wane over longer periods of time. This progression to “natural healing” makes placebo look efficacious in many clinical trials investigating new therapies for low back pain. This situation results in evidence-based reviews of clinically significant therapies revealing very few categories that have a remarkable impact on the improvement of low back pain. Nonetheless, physicians need to make therapeutic choices for their patients despite this relative paucity of evidence. Therapy for mechanical lumbar spine disorders include controlled physical activity, nonsteroidal anti-inflammatory drugs (NSAIDs), skeletal muscle relaxants, local and epidural corticosteroid injections, and long-term pain therapy. Surgical intervention is reserved for patients who have not had improvement with medical therapy and have a surgically correctable abnormality.


A 28-year-old man is physically active, playing sports regularly. He was well until last weekend, when while playing racquetball, he rotated his spine to reach a ball and experienced acute right-sided back pain. He had to stop playing immediately and found his back to be very stiff and painful. He comes to your office 3 days later with continued localized low back pain. He had tried acetaminophen with minimal benefit. Physical examination of the lumbar spine demonstrates decreased flexion to 40 degrees, right lateral flexion to 15 degrees, left lateral flexion to 0 degrees with increased paraspinous muscle contraction, and extension to 5 degrees. Straight-leg raising test is negative for any radicular pain. Neurologic examination reveals normal sensory, motor, and reflex function. Radiographic tests were not ordered.

Acute-Onset Localized Low Back Pain


Lumbar spine strain can be defined as nonradiating low back pain with onset associated with a prolonged abnormal position or mechanical stress. This group comprises the greatest number of individuals with low back pain. Most people with spinal pain (90%) have it on a mechanical basis. Of patients with mechanical low back pain, back strain may account for 60% to 70% of occurrences.

The cause of lumbar strain is most likely related to muscular, fascial, or ligamentous strain related to a specific traumatic episode or continuous mechanical stress. In proper alignment with good posture, little strain is placed on spinal structures and supporting tissues. These tissues are in a resting state and require little energy to function. Tonic contraction associated with injuries result in relative oxygen deprivation and the development of pain. The lumbar spine and supporting muscles may be damaged when an individual lifts an object beyond the capabilities of those structures to sustain the weight. If the force is too great, the stress is first transferred to the supporting ligaments. Then intradiscal pressure increases, and forces are transferred to the apophyseal joints ( Table 26-2 ). These damaging forces result in injury to these structures and the subsequent reflexive physiologic responses.

Table 26-2

Mechanisms of Muscle Pain

  • Muscle strain pain may be related to muscle disruption from indirect trauma, such as excessive tension or stretch. A source of continued risk for recurrent injury is inelastic scar tissue.

  • Muscle fatigue from overuse is another mechanism. Increased concentrations of lactic acid, a byproduct of anaerobic metabolism, may be associated with increased muscle pain and fatigue. High loads requiring maximal effort of muscles causes ultra structural damage to muscle with a delayed inflammatory response

  • Persistent muscle contraction is a component of muscle spasm. The absence of blood flow with an accumulation of metabolic byproducts may stimulate pain receptors within blood vessels.

  • Muscle injury results in paraspinous muscle deconditioning. Radiographic evaluation of cross-sectional views of patients with back pain demonstrated decreased muscle mass in the paraspinous and psoas muscles. Decreased muscle mass results in decreased muscle power. This situation puts individuals at risk for persistent muscle injury.

The diagnosis of lumbar strain is determined by a history of localized low back pain associated with a traumatic event and a compatible physical examination demonstrating localized pain with palpation or movement, muscle contraction, and a normal neurologic examination.


The course of patients with lumbar spine strain is one of gradual improvement over a 2-week period. At 2 months, 90% of individuals are cured without any residual but an increased risk of a recurrence. The vast majority are at risk for another episode that will be of greater duration and severity. Of occupationally related low back pain, 60% of individuals have recurrent symptoms within a year.

Therapy for lumbar strain includes controlled physical activity, NSAIDs, muscle relaxants, and physical therapy. In regard to controlled physical activity, I ask patients to limit bed rest as much as possible. Studies have demonstrated that regular activity as tolerated has a better outcome than those who have bed rest for as short a period as 2 days. Bed rest is detrimental in causing muscle atrophy and absenteeism from work. As soon as very acute pain is diminished, patients are encouraged to increase physical activity. I describe a “comfort zone” for the patient. I ask them to start by doing one tenth of the activity they did before the event. That would mean one block versus 10 blocks of walking, or 3 minutes of treadmill walking versus 30 minutes. They are encouraged to increase activity incrementally as they improve. Educating the patient about the natural resolution of their pain can have a therapeutic effect.

Non-narcotic analgesics in the form of NSAIDs are helpful in decreasing pain and inflammation in patients with acute lumbar strain. NSAIDs that are analgesic with a more rapid onset of action are preferred. No one NSAID has been specifically tested against others to determine the best agent for this disorder. I tell patients that the NSAID is being used to facilitate function. By decreasing pain, the individual is able to gradually increase physical activity, which is an important component of healing. The exposure to the toxicities of NSAIDs is short term. These agents have little risk in those who are not aspirin sensitive or who do not have severe renal or hepatic dysfunction. NSAIDs are continued until the patient’s pain has improved significantly and they have returned to normal function. NSAIDs have been shown in meta-analyses to be better than placebo in the relief of acute low back pain.

Muscle relaxants may be of use in patients who have palpable spasm or who have difficulty sleeping at night secondary to muscle tightness. These drugs are used to facilitate movement and decrease pain. For example, in a study of 1445 patients with a majority with back pain, a dose of cyclobenzaprine 5 mg tid was more effective than placebo in improving spasm and pain. The 5-mg tablet was as effective as the 10-mg dose with less toxicity. A number of muscle relaxants are available for treatment of acute muscle spasm ( Table 26-3 ). In general, antispasmodics have greater efficacy than anti-spasticity medicines for this form of muscle contraction. I start with the lowest effective dose and increase doses depending on the patient’s response. I limit the prescription of muscle relaxants that have abuse potential. The muscle relaxant is continued until muscle tightness has resolved. In most circumstances, I use a combination of an NSAID and a skeletal muscle relaxant to treat lumbar strain. Observational studies have demonstrated this combination to be an effective regimen.

Table 26-3

Skeletal Muscle Relaxants (Antispasmodics/Nonbenzodiazepams)

Agent Formulations Recommended Dose Most Common Toxicities

  • 350 mg

  • 250 mg

Four times daily Dizziness, drowsiness, headache, physical or psychological dependence

  • 250 mg

  • 750 mg

Three to four times daily Dizziness, drowsiness GI bleeding – rare

  • 5.0 mg

  • 7.5 mg

  • 10.0 mg

  • 15.0 mg (ER)

  • 30.0 mg (ER)

From 5 mg three times daily to 30 mg once a day Drowsiness, dry mouth, urinary retention, increased intraocular pressure. arrhythmias
Metaxalone 800 mg Three to four times daily Drowsiness, dizziness, headache, paradoxical muscle cramps
Methocarbamol 750 mg Four times daily Mental status impairment
Orphenadrine 100 mg Two times daily Drowsiness, dry mouth, urinary retention, increased intraocular pressure

ER, extended release; GI, gastrointestinal.

Physical therapy in the setting of acute lumbar spasm is directed at decreasing pain. Modalities in the form of ice massage initially or heat packs subsequently may decrease pain and diminish spasm. Patients are instructed in simple stretching exercises for the lumbar spine. These exercises encourage gradual movement of supporting muscles so that they do not become deconditioned. Exercise therapy is superior to no exercise for the treatment of acute low back pain. Some of the advocated exercise programs include Williams flexion exercises, MacKenzie extension exercises, and aerobic conditioning. It is difficult to determine the exact benefit of exercise because studies examine different types of exercise and added modalities. In most circumstances, it is reasonable to advise patients to return to normal activities without a referral to a therapist. I recommend a visit to the therapist for individuals who are willing to do exercises to prevent a recurrence of acute back pain.

Myofascial trigger points can cause localized muscle pain with referred pain to the buttocks and lateral thighs. The muscles that may become affected include the quadratus lumborum, gluteus medius, and gluteus maximus. Injection of these areas with anesthetic and semisoluble corticosteroid has modest benefit. In general, local injections are more helpful for acute low back pain than for longer duration pain. I will use a local injection of lidocaine and corticosteroid if I can identify a specific tender point that has not responded to oral medical therapy.

Spinal manipulation is also mentioned frequently by patients as a component of therapy for acute low back pain. Manipulation involves abrupt movement of spinal structures beyond their physiologic but not their anatomic range of movement. A number of studies have shown no specific benefit compared with regular medical care. For example, the addition of chiropractic care to an exercise program offers no additional benefit. In fact, the “benefit” of chiropractic care may have nothing to do with movement of the spine. In a study of 467 patients, overall satisfaction was three times greater with chiropractors than with the physicians. Physicians were perceived as being less concerned about the patient’s condition and pain. Physicians were also perceived as being less confident about the cause of the patient’s pain. I recommend physical therapy as a substitute for chiropractic manipulation for those who want to participate in a movement program.

Case Study 1 Treatment

The patient was placed on naproxen 500 mg twice a day with meals and cyclobenzaprine 5 mg three times a day. The patient was given a list of flexion stretching exercises to complete as his pain improved. He was told to maintain his daily, nonexercise activities as tolerated. The patient took these medicines for two weeks. He gradually decreased cyclobenzaprine first. He then discontinued naproxen therapy. He had resolution of pain by the third week and returned to his sports activities after 4 weeks from the onset of his pain.

Had this patient not improved, he would have been given another NSAID with analgesic properties from a different chemical group. An alternate muscle relaxant would be prescribed if he received no benefit or experienced drug toxicities. A local injection would be considered if he identified a singular location that remained painful and was the source of limited function. Physical therapy would be prescribed at week four if he demonstrated continued muscle contraction and limited motion.


A 38-year-old woman has had intermittent low back pain that has resolved spontaneously. She was moving into an apartment carrying a number of boxes. She developed low back pain that quickly expanded into left-sided low back pain that radiated to the big toe. She had great difficulty sitting. She was more comfortable standing or supine in bed. Physical examination demonstrates decreased flexion to 30 degrees, right lateral bending to 15 degrees, left lateral bending to 5 degrees with increased radicular symptoms, and extension to 10 degrees of the lumbar spine. Straight-leg raising test is positive on the left in the seated and supine position. Cross-leg straight leg raising test is negative. Neurologic examination reveals decreased sensory function in L5 distribution, no motor abnormalities, and no reflex abnormalities. Radiographic tests include a magnetic resonance imaging (MRI) scan demonstrating a herniated disc with compression of the left L5 nerve root.

Acute-Onset Low Back And Leg Pain


A herniated disc is defined as the extrusion of the nucleus pulposus through the fibers of the annulus fibrosus. Most disc ruptures occur during the third and fourth decades of life when the nucleus pulposus remains gelatinous. The most likely time of day associated with increased force on the disc is in the morning. The morning is the time the disc is distended to its greatest volume from absorbing water throughout the evening. Alterations in the properties of the nucleus pulposus start in the second decade. A number of factors, including excessive force on disc structures, can result in a breach of the annulus fibrosus by material in the nucleus pulposus.

The most common levels for disc herniation are L4-L5 and L5-S1 which account for 98% of lesions. In general, disc herniations at L5-S1 usually compromise the first sacral root, and a lesion at the L4-L5 affect the fifth lumbar root. It is important to remember that disc resorption is part of the natural healing process associated with disc herniation. The enhanced ability to resorb disc contents has the potential for resolving clinical symptoms more rapidly. Tumor necrosis factor is a product that may help to attract phagocytic cells that resorb herniated tissues.

The pathophysiology of disc herniation causing radicular pain is not fully elucidated. Compression of a nerve root by a herniated disc explains only part of the pathophysiology of radicular pain. A variety of inflammatory mediators are released. These mediators are important in the resorption of extruded tissues. At the same time, leakage of these factors may produce excitation of the nerve root and enhancement of pain-producing substances. Tumor necrosis factor recreates the neurophysiologic abnormalities associated with radicular pain in animal models of radiculopathy. Therefore, the generation of the clinical symptoms of disc herniation is related to a varying ratio of mechanical compression and inflammatory mediators.

The diagnosis of a herniated disc is made on the basis of the history and physical examination ( Table 26-4 ). Plain radiographs of the lumbar spine are obtained if there are other causes of spinal pathology such as an infection or tumor. Other radiographic tests, MRI scan, computed tomography (CT) scan, or myelograms are used to confirm the clinical correlation with clinical complaints and anatomic alterations ( Fig. 26-1 ). Patients with osteoarthritis of the spine may develop facet syndrome that is associated with leg pain. Spinal stenosis patients with radicular pain tend to be older than those in whom herniated discs develop.

Table 26-4

Sensory, Motor, Reflex Distribution of Lumbar Roots

Root Cutaneous Area Muscle Weakness/Movement Affected Tendon Reflex

  • Anterior thigh

  • Upper buttock

Hip flexion, adduction

  • Lower anterior thigh

  • Buttock

  • Lateral posterior thigh

  • Hip adduction

  • Knee extension

Knee jerk

  • Anterior lower leg Lateral knee

  • Medial ankle

  • Knee extension

  • Foot inversion, dorsiflexion

Knee jerk

  • Lateral calf

  • Dorsum of foot

  • Knee flexion

  • Large toe—plantar surface

  • Hip extension, abduction

  • Foot/toe dorsiflexion


  • Small toe

  • Medial calf

  • Sole of foot

  • Knee flexion

  • Foot/toe plantar flexion

  • Foot eversion

Ankle jerk

Figure 26-1

Disc hernation. A, Herniated intervertebral lumbar disc. Sagittal magnetic resonance imaging (MRI) scan demonstrates a herniated disc with caudal migration of the disc at the L4/5 interspace. B, Herniated intervertebral lumbar disc. Axial MRI scan demonstrates a herniated disc ( arrowhead ) blocking the left neural foramen.

(From Hochberg M, Silman A, Smolen J, Weinblatt M, Weisman M. Rheumatology. 4th ed. Philadelphia: Elsevier; 2008. p. 609-10. Figures 58.34 and 58.35.)


Treatment for most patients with a herniated disc can be nonoperative or surgical depending on the severity of symptoms inasmuch herniated intervertebral discs can resorb spontaneously. Investigators have documented improvement in symptoms at a time before the complete resorption of intervertebral discs. In these patients, the control of inflammatory mediators has a greater effect on the lessening of clinical symptoms. Individuals who have contrast-enhanced extruded discs have a greater opportunity to resorb the herniated portion.

Controlled physical activity is a component of nonoperative therapy for patients with herniated discs. Bed rest is kept to a minimum. When in bed, patients use a semi-Fowler position, with hips and knees comfortably flexed. This position is ideal because it keeps intradiscal pressure down and reduces nerve root tension.

NSAIDs, analgesics, and muscle relaxants are important components of drug therapy for low back and radicular pain. Inasmuch as some of the symptoms of low back and leg pain are inflammatory in nature, as well as mechanical compression, anti-inflammatory medications are indicated. Doses at the upper ranges of therapeutic index are indicated. No specific NSAID is better than another. I choose between chemical classes if the initial drug is ineffective or causes toxicity. I am concerned about gastrointestinal toxicities, although the NSAID is prescribed for a relatively short period of time. I will prescribe a proton pump inhibitor if the patient has gastrointestinal symptoms or is older than the usual younger patient with a herniated disc.

The use of oral corticosteroids as a component of therapy for radiculopathy secondary to a herniated disc is a controversial issue. Although many practitioners admit to prescribing corticosteroids for radiculopathy, clinical trial results demonstrating benefits are nonexistent. In this circumstance, absence of proof is not proof of absence. I do not prescribe large doses of dexamethasone. I prefer prescribing prednisone in doses up to 20 mg per day. I will continue prednisone for a period of about 4 to 6 weeks before deciding if the medicine has been helpful. I will discontinue the medicine if patients have not responded or have developed intolerable toxicities. I will gradually taper the prednisone in 5-mg decrements over a number of weeks monitoring the continued improvement measured in decreased pain and a normalization of neurologic function.

Analgesics are an important component of therapy to improve patient comfort as they heal. Analgesics are adjunctive therapy. Analgesics, in addition to NSAIDs, may include acetaminophen, tramadol, and opioids. The patient should understand that the dose of analgesics should not be increased without discussion with their physician. Increasing doses may offer little benefit but an increased risk of toxicity. Requests for increasing doses of analgesics for control of severe leg pain are indications for consideration of surgical intervention.

Muscle relaxants can help with uncontrolled muscle contraction associated with nerve impingement. The mechanism of action of these agents is unknown. The beneficial effects of this group of drugs were thought to be related to their tranquilizing effects. In a large study of low-dose cyclobenzaprine that demonstrated efficacy, the benefits were unassociated with the presence or absence of somnolence. Muscle relaxants without abuse potential are preferred.

Epidural corticosteroid injections are considered for patients with radiculopathy who are not responding to modified activities, NSAIDs, and muscle relaxants. Carette and coworkers studied the efficacy of epidural corticosteroid injections for sciatica secondary to disc herniation. At 3 weeks, patients receiving 80 mg of methylprednisolone acetate had fewer physical limitations than the control group. At 6 weeks, the improvement persisted. At 3 months, no significant differences were found between groups. At 12 months, the number of disc surgeries was similar in active and placebo groups. Other studies have had less success with periradicular injections. I prescribe three epidural injections to be given over a 6-week period. I evaluate the patient after every injection to determine if additional injections in the series are indicated. Epidural injections can be helpful in relieving leg pain as a temporizing intervention. This therapy is less invasive than discectomy.

Surgical Therapy

Surgical intervention is considered for patients with motor weakness or intractable pain. Patients who have failed conservative therapy are also candidates. Clinical trials have attempted to demonstrate the relative benefit of surgical versus medical therapy for intervertebral disc herniation. In general, patients who undergo discectomy resolve symptoms more rapidly than those treated without surgery. Also earlier surgery tends to have a more timely resolution of symptoms, although delayed surgery of 4 to 6 months continues to have benefits for pain resolution. Discectomy for disc herniation at superior levels of the lumbar spine (L2-L3, L3-L4) may have greater treatment effects. Medical therapy for these upper lumbar herniations may be less effective. Despite these early benefits, when evaluated 2 years after surgery, disc herniation patients have similar improved outcomes whether treated with discectomy or medical therapy. Also of concern are the long-term consequences of spine surgery. Patients who have one surgery may be at greater risk for additional surgery because of re-herniation at the same level, or herniation at neighboring disc levels. A study by Mariconda et al suggests that discectomy patients have a satisfactory self-reported health-related quality of life and continued pain relief up to 25 years after surgery.

Case Study 2 Treatment

The patient was treated with diclofenac 100 mg bid for 2 weeks. The patient had a partial response but continued with mild weakness. The patient received prednisone 20 mg qd. At re-evaluation at 4 weeks, the patient’s leg pain was decreased. A physical therapy program with MacKenzie exercises was started. The patient’s symptoms improved over the next 4 months. This prednisone was decreased 5 mg every 2 to 4 weeks as her symptoms improved. At month 4 she discontinued diclofenac therapy. She was encouraged to continue strengthening exercises to maintain lumbar spine strength.

Epidural injections would be offered had the patient not responded to oral corticosteroid therapy. Analgesic therapy would be added if the NSAID therapy was inadequate to allow completion of activities of daily living. Surgical consultation would be recommended if weakness or severe pain increased.

May 19, 2019 | Posted by in RHEUMATOLOGY | Comments Off on Management of Mechanical Lumbar Spine Disease

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