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Managing postpolio syndrome pain

GEVIRTZ, CLIFFORD MD, MPH

COMBATING INFECTION

POLIO IS A DISTANT MEMORY for most health care providers, but post-polio syndrome (PPS) is becoming increasingly common in patients who survived the last polio epidemics in the 1950s and 1960s. As the survivors of polio age, their struggles with the disease's residual effects become more problematic.

These are the diagnostic criteria for PPS:

  • prior poliomyelitis confirmed by history, neurologic exam, and electrodiagnostic test if needed to rule out other causes
  • a period of neurologic recovery from the acute illness followed by an extended interval of neurologic and functional stability
  • gradual or abrupt onset of new weakness accompanied by abnormal muscle fatigue, with or without generalized fatigue, muscle atrophy, or muscle or joint pain
  • exclusion of other medical, orthopedic, or neurologic causes of the problems listed above.1

The cause of PPS isn't known, but researchers have several theories. One is that the ongoing process of denervation and reinnervation of motor neurons gets out of balance, with denervation exceeding reinnervation. A second theory is that persistent latent poliovirus becomes reactivated. A third theory is that a different virus infects the motor neurons, causing weakness. Or, PPS may reflect a normal loss of strength due to aging and weight gain that's simply more noticeable in patients who've had polio.

About 640,000 Americans have PPS, which occurs in 22% to 68% of patients who've had polio. Time of onset ranges from 15 to 40 years after the acute polio episode. Some researchers believe that all polio survivors eventually will develop some symptoms of PPS.

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Signs and symptoms

A patient with PPS may describe the muscle pain as a deep ache. Pain often is accompanied by a gait disturbance, and patients who had residual respiratory muscle weakness are likely to have respiratory problems. New-onset respiratory problems can be caused by new respiratory muscle weakness or by progressive scoliosis.

Muscle atrophy can lead to decreased production of body heat and autonomic dysfunction. Some patients develop central or obstructive sleep apnea. Another complication is “flat-back syndrome,” the inability to stand erect because of forward flexion in the trunk and pain in the lower back and legs.2

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Therapeutic interventions

Physical therapy for PPS focuses on energy conservation, pacing activities, and strengthening exercises directed at the deconditioned muscle groups. Transcutaneous electrical nerve stimulation (TENS) can help strengthen weakened muscles and decrease pain. Magnet therapy (applied over trigger points) also may help.

Drug therapy consists of centrally acting anti-Parkinson's drugs such as bromocriptine and selegiline. Although these drugs aren't approved by the Food and Drug Administration (FDA) to treat PPS, small studies have suggested that they may offer some benefit to patients with PPS; further research is needed.3,4

Medications that address fatigue have been used with only partial success in patients with PPS. Anticholinesterases such as pyridostigmine (also not FDA-approved for PPS) have been tried to treat deficiencies in neuromuscular junction transmission. These drugs have worked in only about half the cases, possibly because PPS involves various neuromuscular junction defects.5

Pain medications are indicated when rest and rehabilitation don't provide adequate relief. Nonsteroidal anti-inflammatory drugs and acetaminophen are most frequently prescribed with excellent results.

Although PPS can't be cured, patients can have periods of stability that last 3 to 10 years. Physical therapy and analgesics can offer some respite during the slow downward course of PPS.

Clifford Gevirtz is clinical associate professor in the department of anesthesiology at Louisiana State University-New Orleans, and medical director of Somnia Pain Management in Harrison, N.Y. Dr. Gevirtz is editor of Topics in Pain Management; this article was adapted from that publication's January 2006 issue.

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REFERENCES

1. March of Dimes. Post-polio Syndrome: Identifying Best Practices in Diagnosis and Care. White Plains, N.Y., 2001.
2. Ring D, et al. An association between the flat back and postpolio syndrome: A report of three cases. Archives of Physical Medicine and Rehabilitation. 78(3):324–326, March 1997.
3. Bruno RL, et al. Bromocriptine in the treatment of post-polio fatigue: A pilot study with implications for the pathophysiology of fatigue. American Journal of Physical Medicine and Rehabilitation. 75(5):340–347, September-October 1996.
4. Bamford CR, et al. Post-polio syndrome-response to deprenyl (selegiline). International Journal of Neuroscience. 71(1–4):183–188, July-August 1993.
5. Maselli RA, et al. Function and ultrastructure of the neuromuscular junction in post polio syndrome. Annuals of the New York Academy of Science. 753:129–137, May 25, 1995.
© 2006 Lippincott Williams & Wilkins, Inc.