CHAPTER 43

Low Back Pain

Stephen A. Ferrara, DNP, RN, FNP-BC, FAANP

Low back pain (LBP) is one of the leading reasons for primary care visits. The prognosis of LBP varies widely in the literature. It has long been believed that 90% of cases improve with nonspecific treatment within 6 weeks. However, recent cohort studies estimate short-term recovery ranging from 39% to 79% (da C Menezes Costa et al., 2012). LBP continues to be a costly condition in terms of actual health care dollars spent, time lost from work, and reduced quality of life (Casazza, 2012; Machado, Maher, Herbert, Clare, & McAuley, 2010; Miller, 2012).

Pain is subjective, and there may be few if any objective findings. In fact, a precise pathognomonic diagnosis can be given in only 10% to 20% of patients with LBP (Casazza, 2012; Stanton et al., 2008). Because back pain may spontaneously resolve on its own, the back pain sufferers who seek health care attention are those for whom the pain is severe or disabling or lasts beyond a reasonable time, or for those seeking secondary gain. In most cases, LBP is labeled as lumbar strain because the physical examination reveals no gross abnormalities and recovery is usually quick.

This chapter discusses the etiologies of LBP and the evaluation and treatment of patients. Primary care providers must have a good understanding of the anatomic, biomechanical, and physiologic factors of back pain, as this will aid in the evaluation and treatment of patients with LBP.

ANATOMY, PHYSIOLOGY, AND PATHOLOGY

Anatomy of the Spine

The spine is divided into 4 sections: there are 7 cervical, 12 thoracic, and 5 lumbar vertebral sections, and the fused sacrum (Hainline, 1995; Figure 43.1). The bony vertebral bodies and intervertebral discs provide weight bearing and shock absorption. The posterior elements—vertebral arches, transverse and spinous processes, and facet joints—protect the spinal cord and nerve roots. The facets, ligaments, and paraspinal muscles provide stability and balance (Brady, 1996; Wipf & Deyo, 1995). Pain may arise from any of these structures. The combined anterior and posterior elements are referred to as a functional unit.

The lumbar vertebra is a static structure made up of the anterior vertebral body and posterior elements (spinous process, articular facets, and transverse process). There is a strong potential for pain at the vertebral body and facet articular cartilage secondary to increased pain sensitivity. The most common etiologies are degenerative joint disease and fracture of any part of the vertebra (body, compression fraction secondary to osteoporosis, pars interarticularis stress fractures).

The intervertebral disc plays a major role in LBP. It is composed of the outer annulus fibrosis, made up of multiple layers of collagen fibers, and the inner nucleus pulposus, made up of a colloidal gel of proteoglycans and collagen. It is 80% fluid (Al-Magdassy, 1996; Cyriax, 1991; Hainline, 1995). Its functions are absorbing shock, providing resistance to compression, and allowing flexibility of the vertebral column (Hainline, 1995). A compromised disc lends itself to abnormal motion and disc herniation, with potential radiculopathy and pain. The neurologic components of spinal anatomy are discussed later in this chapter.

Degenerative disc disease is usually secondary to an annular tear, with subsequent leakage of nuclear material and dehydration of the disc (Hainline, 1995). Large annular tears may lead to prolapse or herniation of the nuclear material and subsequent nerve root compression. With aging, the percentage of water decreases and the disc becomes less able to function normally, increasing the risk of disc herniation in the older population.

The superior and inferior posterior lumbar facets are synovial articulations situated between each vertebral body (Cyriax, 1991; Hainline, 1995; Margo, 1994; Wipf & Deyo, 1995). They play a potential role, along with the intervertebral discs, which play a major role, in lower back dysfunction and pain.

Ligaments play a major role in stability and restriction of motion in the lumbar spine. The key ligamentous structures include the anterior and posterior longitudinal ligaments, which help reinforce the annulus. As the ligament descends toward the sacrum, it narrows, increasing the risk of a herniated nucleus pulposus. The ligamentum flavum and the interspinous and supraspinous ligaments all provide further support to spinal movement (Al-Magdassy, 1996; Hainline, 1995).

Muscles can be divided into anterior and posterior muscle groups. Most posterior is the erector spinae, made up of the lateral iliocostals, the intermediate longissimus, and the medial spinalis. The middle layer is the thick multifidus, and the deep posterior muscles include the rotators, interspinalis, and intertransversarii (Figure 43.2). The anterior muscle group includes the abdominal muscles that play a major role in lumbar stabilization. They include the psoas (which is a primary hip flexor), the outer external obliques, the intermediate internal obliques, and the inner transversus abdominis. The remaining anterior muscles include the midline rectus abdominis and the lateral quadratus lumborum that functions as a lateral trunk flexor (see Figure 43.2). All these muscles play a role in trunk motion and stabilization.

The anatomy of LBP is a combination of fact and theory. Studies have shown that pain can be reproduced by injecting hypertonic saline into the ligamentum flavum in facet joint capsules. Supra- and infraspinous ligaments are innervated by afferent branches of the posterior primary rami, and muscle spasms are thought to be a motor reflex to pain. The role of muscle injury as it relates to back pain has not been fully elucidated. Strains and sprains, however, remain the leading diagnoses.

Sciatic pain requires both mechanical and inflammatory stimuli. The sciatic nerve arises from L4–S3 nerve roots (common peroneal and fibial nerves), passes over the lower edge of the sciatic notch, and lies just beneath the piriformis muscle and just above the obturator internus muscle (see Figure 43.2). The nerve innervates the gluteus medius and minimus as well as the tensor fasciae latae before passing beneath the piriformis muscle. After passing through the main branch of the sciatic nerve, it innervates the hamstring and the muscles of the lower leg, and provides sensory innervation of the leg and foot (Borenstein, Wiesel, & Boden, 1995).

The prevalence of back pain alone and back pain with sciatica (defined as pain radiating along the course of the sciatic nerve to below the knee in one or both legs) is summarized in Table 43.1. The total costs of back pain exceed $100 billion in the United States per year (Katz, 2006).

Back-Extension Exercises

The following exercises are to be performed in accordance with the comfort of the patient. The patient should perform only one exercise on any one particular day, and progress to the next exercise only when the pain from the previous one decreases. For patients with sciatic-type conditions, if symptoms intensify in either or both legs (increased pain, numbness, or tingling), patients should discontinue that exercise and contact with their physical therapist or primary care provider. If symptoms diminish in the legs, continue as instructed, even if accompanied by a temporary increase in lower back pain.

Source: Wheeler (1995).

       4.  Press-ups: While lying on your stomach, place your hand under the shoulders, and slowly straighten your elbows. Keep the lower part of the body relaxed while raising the back upward as far as possible. Then relax and return to the starting position. Only raise the back as far as the pain will allow. Perform 10 repetitions, one to two times per day.

       5.  Back bending: While standing, place your hands on your low back. Slowly bend backward as far as possible, then relax, and return to the starting position. Perform 10 repetitions, one to two times per day.

       6.  Back-strengthening exercises:

            (A)  Lying on your stomach, with your forehead supported by a rolled towel or a pillow, raise one arm off the floor, keeping it straight. Do not lift your head. Hold for 10 seconds. Relax. Repeat 5 to 10 times, then repeat with the other arm.

            (B)  Lying on your stomach, raise one leg off the floor, keeping it straight. Hold for 10 seconds. Relax. Repeat 5 to 10 times, then repeat with the other leg.

            (C)  Lying on your stomach, with your forehead supported by a rolled towel or a pillow, raise both arms off the floor, keeping them straight. Do not lift your head. Hold for 10 seconds. Relax. Repeat 5 to 10 times.

            (D)  Lying on your stomach, with your forehead supported by a rolled towel or a pillow, raise one arm and the opposite leg off the floor at the same time, keeping them straight. Do not lift your head. Hold for 10 seconds. Relax. Repeat 5 to 10 times, then repeat with the other arm and leg.

Although there are no true diagnostic criteria for LBP, Table 43.1 shows the multitude of LBP syndromes. This section focuses on the more common etiologies, or specific diagnoses of secondary back pain. The provider must be able to differentiate between benign causes, such as lumbar strain and disc disease, and the more ominous and life-threatening disorders that require quick referral, such as cauda equina syndrome, malignancy, and vertebral fracture with neurologic compromise. A thorough history and a detailed physical examination, including a neurologic examination, are warranted.

LBP can be divided into three clinical courses: acute, subacute, and chronic. It is useful to differentiate these three categories when approaching treatment protocols. The definitions are as follows:

It is also important to categorize back pain along with its etiology for correct treatment and accurate referral.

Mechanical or Activity-Related Causes

DEGENERATIVE DISC DISEASE

There appears to be a correlation between annular tears of the disc and degenerative disc disease. As previously stated, there is also a correlation with herniated nucleus pulposus. A slow leak over time of the nuclear material will lead to desiccation of the disc. How does this lead to back pain? One explanation is an inflammatory pathway involving chemical factors. This pathway may explain why pain is relieved when a corticosteroid or nonsteroidal anti-inflammatory agent is administered (Miller, 2008; Rudy, Weiner, Lieber, Slaboda, & Boston, 2007). The other theory is an immunologic phenomenon, described by in vitro studies. It is theorized that the nuclear material, previously sheltered from the immune system, generates an autoimmune response once it is exposed.

Herniated discs occur at the L4–5 or L5–S1 level in 95% of cases (Miller, 2008; Stanton et al., 2008). The neurologic examination should focus on the L5 and S1 nerve roots. A herniated disc at the L5 nerve root may cause pain and numbness radiating from the back to the anterior thigh, anterolateral leg, medial foot, and great toe. There are no reflex changes, and the motor examination reveals weakness in the great toe extensor as well as the dorsiflexors of the foot (Table 43.2).

Patients with an L5–S1 disc herniation (sacroiliac [SI] root) have pain and numbness of the posterior thigh and leg, posterior–lateral foot, and lateral toes; a diminished ankle reflex; and weakness of the plantar flexors of the foot that can be seen with difficulty on toe walking (see Table 43.2). It is rare to see clinical herniations above the level of L4.

A positive straight-leg raise (SLR) test helps confirm nerve root irritation. This test has a sensitivity of 95% with proven disc herniation, and its absence can actually rule out disc herniation. A crossover test or crossed SLR is less sensitive but more specific for disc herniation (Figure 43.3). Electromyography may aid in the diagnosis of a particular radiculopathy, but it is better used to discriminate radicular pain from peripheral neuropathy.

Plain x-rays are not helpful in diagnosing a herniated disc, but they should be used to rule out tumor, infection, fracture, and spondylolisthesis as clinically warranted. A herniated disc is usually confirmed when an imaging study such as CT or MRI shows an abnormality corresponding to the clinical examination. However, these sophisticated and expensive studies should not be ordered too early in the course of a workup for LBP, especially if the patient is not considered a surgical candidate. These tests should be ordered in patients who have a long protracted course, or early in the case of cauda equina syndrome, a progressive neurologic deficit, or the suspicion of tumor or infection (Beattie, 1996).

SPINAL STENOSIS

Spinal stenosis (narrowing of the spinal canal) may be secondary to hypertrophy of the facet joints (osteoarthritis), hypertrophy of the ligamentum flavum, or spondylosis of the intervertebral disc that is often superimposed on a congenitally narrow canal (Stanton et al., 2008).

Spinal stenosis is most likely in the older population. Patients present with an insidious onset of pain and numbness that worsens with walking. The pain of spinal stenosis is referred to as pseudoclaudication because of its similarity to vascular claudication (Casazza, 2012). Patients may have adermatomal distribution of pain and sensory deficit as well as an abnormal SLR test. To differentiate this from a herniated disc, the factors that exacerbate and relieve the pain should be noted. Spinal stenosis is relieved by sitting and aggravated by standing; a herniated disc is exacerbated by sitting and relieved by standing (Casazza, 2012).

In spinal stenosis, deep tendon reflexes may be decreased, with weakness in one or both lower extremities. The diagnosis is confirmed by MRI imaging revealing a narrow spinal canal. Plain films would point out only the degenerative changes that lead to spinal stenosis.

SPONDYLOLYSIS/SPONDYLOLISTHESIS

These disorders are most common in young adolescents and young adults who are involved in sports such as gymnastics, tennis, weight lifting, and football (linemen). These sports put the lumbar spine into hyperextension. Spondylolisthesis is the slipping of one vertebral body forward on the one below. The extent of slippage is graded from grade I to grade IV (total forward displacement). Often spondylolisthesis is secondary to bilateral spondylolysis. Spondylolisthesis is best seen on plain lateral radiographs.

Vertebral compression fractures are most consistent with osteoporosis in women over age 65 and men over age 75 with decreased bone mass. Osteoporosis in itself has no signs and symptoms and may progress silently for years until an ominous compression fracture leads to pain and disability. The patient may have pain and a tender point at the level of fracture and may splint the back to avoid mobility at the fracture site. Plain films may reveal the fracture or a decrease in vertebral height. Bone mineral densitometry can be used to diagnose osteoporosis by calculating the patient’s bone mineral density and comparing it to the normal bone density for age (see Chapter 45).

FACET SYNDROME (ARTHROPATHY)

Arthropathy of the facet joints may be difficult to diagnose. Patients may have LBP with or without radiation to the buttocks. Hyperextension may precipitate facet impingement and exacerbate symptoms (Casazza, 2012). The physical examination may be unremarkable except for pain on extension of the trunk. SLR and the neurologic examination are usually unremarkable. A plain radiograph may or may not demonstrate changes at the facet joints. MRI demonstrates degenerative changes at the intervertebral discs and at the facet joints.

PIRIFORMIS SYNDROME

Piriformis syndrome has become a common diagnosis, especially when it relates to buttock pain without LBP symptoms. The piriformis muscle is an external rotator of the hip. It traverses over the sciatic notch and inserts on the greater trochanter of the femur. Piriformis syndrome is common in athletes, persons who excessively abduct the hip or overuse the muscles of the buttock, and persons who have excessive compression over the sciatic notch (e.g., sitting on an overstuffed wallet). The physical examination may reveal tenderness over the sciatic notch, pain with forced internal rotation of the hip, and pain and weakness with simultaneous abduction and external rotation of the hip. The neurologic examination is normal, as are plain radiographs (Scheele, Luijsterburg, Bierma-Zeinstra, & Koes, 2012).

SI SPRAIN

The SI joints are often overlooked as an etiology for LBP. There is controversy as to whether the SI joints can be sprained, because they are among the strongest joints in the body. True subtle motion at this joint may predispose a person to injury of this joint. Clinically, the patient may present with pain at the SI joint. This SI pain should be differentiated from that of piriformis syndrome or other pathology that may be referred to the groin and posterior thigh. Pain may increase when the patient lies on the affected side. There are several provocative tests, including Gaenslen’s extension test (Figure 43.4), the Patrick/FABER test (Figure 43.5), and the SI compression test. Unlike patients with sciatica and piriformis syndrome, there is no tenderness at the sciatic notch. Plain radiographs may or may not show changes at the SI joint; nevertheless, they are valuable in ruling out other potential diagnoses (e.g., fracture, malignancy, infection, ankylosing spondylitis).

Degenerative Disorders: Osteoarthritis

Osteoarthritis is the most common degenerative disorder. Degeneration of the articular cartilage involving both the facet joints (as previously described) and vertebral columns occurs. It is easily diagnosed by correlation of symptoms and plain x-ray findings. Other possibilities that cause back pain must still be considered before making a diagnosis.

Systemic Disorders

INFLAMMATORY DISEASES

The seronegative arthropathies, rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, Reiter’s syndrome, and arthritis associated with inflammatory bowel disease are a few of the inflammatory arthropathies that may lead to LBP. The diagnosis is made usually after the failure of other diagnoses. The workup includes laboratory tests specific for each disorder (see the “Diagnostic Studies” section later in this chapter).

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