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Chapter 7 covered a general approach to and a detailed examination of the patient with back or neck pain. In this chapter, a more extensive discussion of specific conditions of the spine is presented. For a review of seronegative spondyloarthropathy (e.g., ankylosing spondylitis), the reader is referred to Chapter 3, “Rheumatology.” Fractures of the spine are addressed in Chapters 9 and 10.

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Cauda equina syndrome refers to nerve compression within the spinal canal that occurs below the L1–2 interspace after the termination of the spinal cord. The clinical picture is that of a lower motor neuron lesion with weakness or paralysis, loss of rectal tone, sensory loss in a dermatomal pattern, decreased deep tendon reflexes, and bladder dysfunction. The classic sensory description is “saddle” anesthesia, with loss of sensation in the buttocks and perineal areas. It should be noted that within the first few days, a complete cord syndrome may present similarly until upper motor neuron symptoms develop.

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The most common cause of cauda equina syndrome is a large midline disk herniation, usually at L4–5 or L5-S1 interspaces. Other causes include spinal metastases, spinal hematoma, epidural abscess, vertebral fracture, or transverse myelitis.1,2 Although anal sphincter tone is decreased in up to 80% of patients, an elevated postvoid residual is the most consistent finding to make the diagnosis.3 A postvoid residual of more than 100 to 200 mL of urine is 90% sensitive and 95% specific for the diagnosis in patients suspected of cauda equina syndrome.4 The diagnosis is confirmed by an emergent magnetic resonance imaging (MRI). Treatment consists of high-dose IV steroids (recommendations range from 4 to 100 mg of dexamethasone) and surgical consultation. Surgical intervention is recommended on an urgent basis to increase the likelihood of neurologic recovery.5

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With aging, degeneration develops in the annulus fibrosis that can lead to herniation of the nucleus pulposus following an acute increase in pressure within the disk. Herniation usually progresses gradually as the posterior longitudinal ligament acts to restrain the nucleus. Eventually, as the ligament weakens, the nucleus migrates into the intravertebral foramen, most commonly in a posterolateral direction (i.e., paramedian herniation). In this location, the disk comes into contact with the nerve root, causing pain and radiculopathy. A large central herniation can compress the spinal cord or cauda equina.

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Approximately 4% to 6% of the population will suffer from a clinically significant disk herniation. The vast majority occurs in the lumbar spine and causes low back and leg pain. In patients with sciatica, 90% of cases are due to a herniated disk, while lumbar stenosis and less often a tumor are other possible causes.6 Approximately 98% of clinically important lumbar disk herniations occur at the L4–5 or L5-S1 intervertebral level.4 In the cervical spine, the C6–7 and C5–6 disks account for 70% and 20% of cases, respectively. Cervical radiculopathy is more likely to be due to degenerative ...

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