CHAPTER 4 Rajiv K. Dixit1 and John Dickson2 1 University of California, San Francisco; Northern California Arthritis Center, Walnut Creek, USA 2 University of Bradford, Bradford, UK Low back pain (LBP) is the most common musculoskeletal symptom and represents a major socioeconomic burden. An estimated 80% of the population will experience back pain during their lifetime; 90% of these patients will be largely pain free within 6 weeks. Recurrence, also generally self‐limited, is common. Sciatica is the result of nerve root impingement and occurs in <1% of patients. The pain is radicular (and almost invariably radiates below the level of the knee) in the distribution of a lumbosacral nerve root, sometimes accompanied by sensory and motor deficits. Sciatica should be differentiated from non‐neurogenic sclerotomal pain, which arises from pathology within the disc, facet joint or paraspinal muscles and ligaments. Sclerotomal pain is non‐dermatomal in distribution and often radiates into the lower extremities but rarely below the knee or with associated paraesthesiae as with sciatica. Low back pain usually originates from the lumbar spine (Figure 4.1); pain is occasionally referred to the spine from other structures (Box 4.1). Over 95% of LBP is mechanical. Mechanical pain is due to an anatomical abnormality, generally the result of degenerative change, in the lumbar spine that increases with physical activity and is relieved by rest and recumbency. Systemic disease (infection, neoplasm and spondyloarthritis) accounts for only 1–2% of LBP. Figure 4.1 Basic anatomy of the lumbar spine; (a) cross‐sectional view through a normal lumbar vertebra; (b) lateral view of the lumbar spine The most common cause of mechanical LBP is degenerative change. In lumbar spondylosis (lumbar osteoarthritis), degenerative changes occur in the intervertebral disc and facet joint. Imaging evidence of lumbar spondylosis (disc space and facet joint narrowing, osteophytes and subchondral sclerosis) is common, increases with age and is often asymptomatic. The clinical spectrum of mechanical LBP secondary to lumbar spondylosis is wide. Patients may present with self‐limited acute LBP (with recurrent episodes in some), whereas chronic LBP (often with periods of acute exacerbation) may develop in others. Some patients may develop sclerotomal pain that radiates into the buttocks and lower extremities. Lumbar spondylosis predisposes patients to intervertebral disc herniation, spondylolisthesis and spinal stenosis. The nucleus pulposus in a degenerated disc may prolapse and push out from the weakened annulus, usually posterolaterally. Imaging evidence of disc herniation is common even in asymptomatic adults. Occasionally, disc herniation may result in nerve root impingement (Figure 4.2), causing sciatica. Of all clinically significant herniations, 95% involve the L4–5 or L5–S1 disc. Generally, the more caudal nerve root is impinged; that is, the L5 nerve root with L4–5 herniation and S1 nerve root with L5–S1 herniation. In most patients the sciatic pain resolves over a period of weeks. Figure 4.2 Posterolateral disc herniation resulting in nerve root impingement Rarely, a large midline disc herniation, usually L4–5, compresses the cauda equina. This is a surgical emergency because neurological results are affected by the time to decompression. The full cauda equina syndrome has a symptom complex that includes LBP, bilateral sciatica, bilateral motor weakness of the lower extremities, loss of sensation in a saddle distribution (over the genitals, anus and inner thighs), with bladder and bowel incontinence. Whenever possible, the cauda equina syndrome should be recognized before incontinence becomes established. The spectrum of symptoms is presented in Box 4.2. Spondylolisthesis is the anterior displacement of a vertebra on the one beneath it. It is usually secondary to degenerative changes in the disc and facet joints (degenerative spondylolisthesis) but may result from a developmental defect in the pars interarticularis of the vertebral arch (spondylolysis), which produces isthmic spondylolisthesis (Figure 4.3). Patients with minor degrees of spondylolisthesis are usually asymptomatic, although some may have mechanical LBP. Greater degrees of spondylolisthesis occasionally cause sciatica, spinal stenosis or cauda equina syndrome. Figure 4.3 (a) Spondylolysis with bilateral defects in the pars interarticularis (arrows); (b) spondylolysis at L5 resulting in spondylolisthesis at L5–S1 Spinal stenosis (ST) is defined as a narrowing of the spinal canal and its lateral recesses and neural foramina, which may result in a compression of lumbosacral nerve roots (20% of adults over age 60 have imaging evidence of ST but are asymptomatic). Degenerative changes (leading to disc herniation, facet joint osteophytes and ligamentum flavum hypertrophy) are the causes of ST in most patients (Figure 4.4, Box 4.3). The prevalence of ST increases with age. Figure 4.4 Spinal stenosis secondary to a combination of disc herniation (A), facet joint hypertrophy (B) and hypertrophy of the ligamentum flavum (C)
Low Back Pain
Causes of low back pain
Lumbar spondylosis
Disc herniation
Spondylolisthesis
Spinal stenosis
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