Despite countless recent advances in diagnosis and treatment, low back pain remains one of the most challenging conditions in all of orthopedics. The results of both surgical and nonsurgical treatments often fall short of patient expectations, making low back pain a frustrating diagnosis for patients and providers alike. The goal of this chapter is to provide a practical, logical, and evidence-based approach to patients with this challenging condition.

The basic unit in the anatomy of the spine is the vertebra (Figure 6-1). A single vertebra has a solid mass of bone anteriorly called the vertebral body and a complicated array of bony spines and prominences posteriorly called the posterior elements. In the middle, there is an open passageway called the spinal canal. The spinal canal starts at the foramen magnum, the opening at the base of the skull where the brain stops and the spinal cord begins, and it continues all the way down to the coccyx. Adjacent vertebrae are stacked one on top of the other, and together, they form the skeletal structure of our spines: a long sheath of bony “armor” to protect our fragile spinal cord and nerve roots and a structural frame to support our body mass (Figure 6-2). For most of the lumbar spine, the spinal canal contains a collection of nerve roots, not the spinal cord. Figure 6-3 shows that the spinal cord ends at approximately the level of the second lumbar vertebra, and that, below this level, the spinal canal contains a bundle of nerve roots called the cauda equina. Each vertebra is linked to the vertebrae above and below it by firm but flexible connections that allow motion in this otherwise-rigid bony column. In the front, the tissue that connects adjacent vertebrae is called the intervertebral disk. Each disk consists of a tough, rubbery peripheral ring known as the annulus fibrosus and a soft, jelly-like center known as the nucleus pulposus (Figure 6-4). Behind the spinal canal, the posterior elements of adjacent vertebrae form articulated connections known as the facet joints.

This intricate assembly of bones, connective tissue, and neural elements is what we call the lumbar spine, and it is depicted in Figure 6-5. While problems related to the cervical and thoracic spine do account for a percentage of patients’ complaints, certainly the vast majority of spine-related problems arise from the lumbar spine, specifically from the lower part of the lumbar spine. It is estimated that over 90% of low back pain comes from pathology at the L4-L5 and L5-S1 levels (see sidebar for details).

Low back pain that does not radiate down the lower extremities (below the knees) and is not associated with numbness, tingling, or weakness is relatively common. It may be the result of a muscle strain, facet joint arthritis, or degenerative disk disease.

The intervertebral disks of the spine, especially those between L4 and S1, are continuously exposed to destructive loads and forces as we flex, extend, rotate, compress, and distract our spinal columns with the motions we make on a daily basis. In children, the disks and other supportive structures of the spine are young, strong, and flexible. Low back pain in children is rare, and, when it occurs, it should be investigated thoroughly. Causes of low back pain in children under 10 include infection of an intervertebral disk, leukemia, and scoliosis. Though it is rare in young children, low back pain is quite common in patients over 30. It is said to affect 60%-80% of the adult population at some time in their lives. As we age, the disks and associated supportive structures in our spines wear out and deteriorate. The nucleus pulposus loses much of its water content, and the collagen fibers of the annulus fibrosis begin to fray and fail. These degenerative changes appear to be an inevitable part of the aging process and can be expected to occur at all levels throughout the spine as patients age into their 80s, 90s, and beyond. Magnetic resonance imaging (MRI) studies in patients in these age groups typically show nucleus pulposus dehydration, loss of disk space height, and other signs of disk degeneration. It has been proposed that these degenerative disk changes are the cause of low back pain in some patients, but back pain is certainly present in many patients who lack these degenerative changes, and these degenerative changes are often seen at one or more levels in the spines of patients with little or no back pain.

Alternatively, low back pain may result from a strain of one or more of the many muscles that support the lumbar spine. Figure 6-6 shows the complex assembly of muscles in the low back. Overuse of these muscles or poor lifting ergonomics can cause the muscles or their insertions onto the bones and fascia of the spine to become inflamed, resulting in pain and stiffness. Facet joint arthritis may also cause lumbar back pain. As the intervertebral disks age and collapse, the facet joints are loaded with greater forces, hastening the development of degenerative arthritis in these small, posterior spinal articulations. It has been proposed that pain and stiffness that result from facet joint arthritis are a contributing factor to acute and chronic low back discomfort. In reality, it may be that some element of all three conditions (degenerative disk disease, lumbar muscular strain, and posterior element arthritis) is present in these patients.

Physical Exam

The yield on physical exam for low back pain (without radiculopathy) is very low. Range-of-motion limits can be meticulously measured, but these measurements are rarely helpful. They may or may not be decreased due to pain. Palpation of the paraspinous muscles may reveal areas of tenderness or even muscle firmness due to spasm. Alternatively, the exam may be completely normal. For the sake of completeness, a physical exam for low back pain should include checking for pain to palpation over the spinous processes and flank percussion. While it is not a particularly sensitive or specific sign, tenderness to palpation over an individual spinous process can indicate the presence of a metastatic vertebral lesion in that vertebra. Pain with flank percussion may indicate a renal cause of the patient’s low back pain. The pain may radiate into the buttocks or even the posterior thighs, but true radicular findings such as pain that radiates below the knees, loss of sensation, reflex changes, and motor weakness are absent in these patients who have low back pain without radiculopathy. The examination may be difficult if the patient is very uncomfortable. Weakness due to pain can be confused with weakness secondary to nerve root impingement.

Global weakness that involves multiple muscle groups in the lower extremity is not consistent with a radiculopathy. Figure 6-7 shows the motor deficits, reflex changes, and patterns of sensory loss one would expect for the most common (L4, L5, and S1) nerve root impingement conditions. In actual clinical practice, weakness due to pain and weakness due to nerve root impingement can be hard to distinguish. The straight leg raise test (Figure 6-8) is a physical exam test used to detect lower lumbar nerve root irritation. The test takes advantage of the fact that, if the knee is locked out straight and the leg is raised, tension is applied to the sciatic nerve. The nerve roots that combine to create the sciatic nerve are the nerve roots most commonly affected by nerve root impingement (L4, L5, and S1), so applying tension to the sciatic nerve applies tension to these nerve roots. If one or more of these nerve roots is significantly inflamed or irritated, this test may elicit pain that radiates down the leg or sensory changes such as numbness, tingling, or electrical sensations. In patients with low back pain only (no radiculopathy), the straight leg raise test may elicit pain in the buttock or posterior thigh, but numbness, tingling, and pain that radiates below the knee are not expected.