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Back Pain Handbook  Vertebral Fractures Most traumatic fractures of the lumbar vertebral bodies result from compression or flexion injuries producing anterior wedging or compression. With more severe trauma, the patient may sustain a fracture-dislocation or a "burst" fracture involving not only the vertebral body but posterior elements as well. Traumatic vertebral fractures are caused by falls from a height (a pars interarticularis fracture of the L5 vertebra is common), sudden deceleration in an automobile accident, or direct injury. Neurologic impairment is commonly associated with these injuries, and early surgical treatment is indicated (Chap. 369). When fractures are atraumatic, the bone is presumed to be weakened by a pathologic process. The cause is usually postmenopausal (type 1) or senile (type 2) osteoporosis (Chap. 342). Underlying systemic disorders such as osteomalacia, hyperparathyroidism, hyperthyroidism, multiple myeloma, metastatic carcinoma, or glucocorticoid use may also weaken the vertebral body. The clinical context, neurologic signs, and x-ray appearance of the spine establish the diagnosis. Antiresorptive drugs including biphosphatonates, alendronate, transdermal estrogen, and tamoxifen have been shown to reduce the risk of osteoporotic fractures. Lumbar Disk Disease This disorder is a common cause of chronic or recurrent low back and leg pain. Disk disease is most likely to occur at the L4-L5 and L5-S1 levels, but upper lumbar levels are involved occasionally. The cause of the disk injury is often unknown; the risk is increased in overweight individuals. Degeneration of the nucleus pulposus and the annulus fibrosus increases with age and may be asymptomatic or painful. A sneeze, cough, or trivial movement may cause the nucleus pulposus to prolapse, pushing the frayed and weakened annulus posteriorly. In severe disk disease, the nucleus may protrude through the annulus (herniation) or become extruded to lie as a free fragment in the spinal canal. The mechanism by which intervertebral disk injury causes back pain is controversial. The inner annulus fibrosus and nucleus pulposis are normally devoid of innervation. Inflammation and production of proinflammatory cytokines within the protruding or ruptured disk may trigger or perpetuate back pain. Ingrowth of nociceptive (pain) nerve fibers into inner portions of diseased intervertebral disk may be responsible for chronic "diskogenic" pain. Nerve root injury (radiculopathy) from disk herniation may be due to compression, inflammation, or both; pathologically, varying degrees of demyelination and axonal loss are usually present. The symptoms of a ruptured intervertebral disk include back pain, abnormal posture, limitation of spine motion (particularly flexion), or radicular pain. A dermatomal pattern of sensory loss or a reduction in or loss of a deep tendon reflex is more suggestive of a specific root lesion than the pattern of pain. Motor findings (focal weakness, muscle atrophy, or fasciculations) occur less frequently than sensory or reflex changes, but a myotomal pattern of involvement can suggest specific nerve root injury. Lumbar disk disease is usually unilateral (Fig. 16-4), but bilateral involvement does occur with large central disk herniations that compress several nerve roots at the same level. Clinical manifestations of specific lumbosacral nerve root lesions are summarized in Table 16-1. There is evidence to suggest that lumbar disk herniation with a nonprogressive nerve root deficit can be managed conservatively (i.e., nonsurgically) with a successful outcome. The size of the disk protrusion may naturally decrease over time. continue to page 3 of Back Pain     The above statements have not been evaluated by the Food and Drug Administration and none of these products are intended to diagnose, treat, cure, or prevent any disease.