Polio natural history, complications and prognosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Many cases of poliomyelitis result in only temporary paralysis. After an interval of 30–40 years, 25%–40% of persons who contracted paralytic poliomyelitis in childhood experience new muscle pain and exacerbation of existing weakness, or develop new weakness or paralysis. This disease entity is referred to as pos-tpolio syndrome. Patients with abortive polio infections recover completely. In those that develop only aseptic meningitis, the symptoms can be expected to persist for two to ten days, followed by complete recovery.

Natural History

Poliovirus enters the body through the mouth, infecting nearby cells, such as those of the oral mucosa, nose and throat. The incubation period is considered the time between the assumed time of infection, and symptom onset. The incubation period often ranges from 7 to 14 days, however, it may vary from 5 to 35 days.[1][2]

Typical manifestations of poliomyelitis may range from asymptomatic disease, to death. 95% of the infections with poliovirus are asymptomatic. 4 to 8% of the cases present as abortive poliomyelitis. In about 1 to 2% of infections with poliovirus, the disease manifests as non-paralytic poliomyelitis. Less than 1% of infected patients develop paralytic disease.

Abortive Poliomyelitis

Abortive poliomyelitis often presents with 2 to 3 days of fever. Neurological exam is normal in this form of the disease, and common symptoms may include: sore throat; headache; anorexia; nausea; vomiting and abdominal pain.[3]

Non-Paralytic Poliomyelitis

This form of the disease presents with the symptoms of abortive poliomyelitis, however, these are often more severe, and signs of meningeal irritation are present.[4] Typically these symptoms last for 2 to 10 days, followed by complete recovery.[5]

Paralytic Poliomyelitis

Paralytic symptoms generally begin 1 to 10 days after prodromal symptoms, and progress for 2 to 3 days. The prodrome may be biphasic, especially in children, with initial minor symptoms separated, by 1 to 7 days, from more major symptoms. Adults commonly present one phase of symptoms, with a prolongation of prodrome until the onset of paralysis.[5][6][7]

Spinal Paralytic Poliomyelitis

Severe paralysis occurs in about 0.1% of the cases. Initial minor symptoms are similar to those of abortive poliomyelitis, lasting 1 to 3 days. After this initial period, the patient recovers during 2 to 5 days, until severe symptoms develop. The severe phase of this form of poliomyelitis is characterized by signs and symptoms of aseptic meningitis. These include: malaise; fever; chills; nausea; vomiting; and neck stiffness.

The more severe phase of this pause begins with hyperesthesia, paresthesia, myalgia, and muscle spasms. Meningeal symptoms start 2 days before the onset of paralysis. Muscular symptoms may vary from mild weakness to quadriplegia.

Bulbar Paralytic Poliomyelitis

Polioencephalitis

Many cases of poliomyelitis result in only temporary paralysis.[8] Nerve impulses return to the formerly paralyzed muscle within a month, and recovery is usually complete in six to eight months. The neurophysiological processes involved in recovery following acute paralytic poliomyelitis are quite effective; muscles are able to retain normal strength even if half the original motor neurons have been lost.[9] Paralysis remaining after one year is likely to be permanent, although modest recoveries of muscle strength are possible 12 to 18 months after infection.

One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons develop new branches, or axonal sprouts.[10] These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection,[11] restoring the fibers' capacity to contract and improving strength.[12] Terminal sprouting may generate a few significantly enlarged motor neurons doing work previously performed by as many as four or five units: [13] a single motor neuron that once controlled 200 muscle cells might control 800 to 1000 cells. Other mechanisms that occur during the rehabilitation phase, and contribute to muscle strength restoration, include myofiber hypertrophy—enlargement of muscle fibers through exercise and activity—and transformation of type II muscle fibers to type I muscle fibers.[11][14]

In addition to these physiological processes, the body possesses a number of compensatory mechanisms to maintain function in the presence of residual paralysis. These include the use of weaker muscles at a higher than usual intensity relative to the muscle's maximal capacity, enhancing athletic development of previously little-used muscles, and using ligaments for stability, which enables greater mobility.

Complications

Potential complications of poliomyelitis may include:[15][16][17][18][19][20][21][22]

Complications Description
Respiratory compromise
Myocarditis
  • Inflammatory infiltration in cardiac muscle
Gastrointestinal
Musculo-Skeletal
Postpoliomyelitis Syndrome
  • Occurs in 20-30% of patients with history of paralytic poliomyelitis (25-35 years before), who have made a partial or full recovery
  • Commonly involves previously affected muscles
  • New onset of:
  • Gradual symptom progression
  • Possible cause:
  • Attrition of motor nerves that innervate previously affected muscles

Prognosis

  • The mortality rate from poliomyelitis is referred to the period during which the disease was epidemic. During that period, acute paralytic poliomyelitis had a mortality rate of 5-10%, however, this number was higher in the case of bulbar poliomyelitis.[23]
  • Patients with abortive poliomyelitis often have a full recovery.[24]
  • Patients who develop aseptic meningitis, can expect symptoms to persist for 2-10 days, followed by complete recovery.[25]
  • Spinal poliomyelitis is rarely fatal.[26]
  • Muscle paralysis usually lasts 1-3 days, and in some cases up to 1 week.[27] Persistent weakness occurs in two thirds of patients with the paralytic form of the disease.
  • Patients with severe form of paralytic poliomyelitis, and those who require mechanical ventilation have less probability to recover.[28]
  • 5 to 10% of patients with paralytic poliomyelitis die due to the paralysis of respiratory muscles. The mortality rate varies with age: 2-5% in children, 15-30% in adult. In the presence of support, bulbar poliomyelitis has a mortality rate of 25-75%, depending on the patient's age.[29] When positive pressure ventilators are available, the mortality can be reduced to 15%.[30]
  • Permanent sequelae is uncommon in patients who have survived bulbar poliomyelitis.[31]

References

  1. ↑ Mueller S, Wimmer E, Cello J (2005). "Poliovirus and poliomyelitis: a tale of guts, brains, and an accidental event". Virus Res. 111 (2): 175–93. doi:10.1016/j.virusres.2005.04.008. PMID 15885840.
  2. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  3. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  4. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  5. ↑ 5.0 5.1 "Poliomyelitis" (PDF).
  6. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  7. ↑ HORSTMANN DM (1949). "Clinical aspects of acute poliomyelitis". Am J Med. 6 (5): 592–605. PMID 18126001.
  8. ↑ Frauenthal HWA, Manning JVV (1914). Manual of infantile paralysis, with modern methods of treatment.. Philadelphia Davis, 79–101. OCLC 2078290
  9. ↑ Sandberg A, Hansson B, Stålberg E (1999). "Comparison between concentric needle EMG and macro EMG in patients with a history of polio". Clinical Neurophysiology. 110 (11): 1900–8. PMID 10576485.
  10. ↑ Cashman NR, Covault J, Wollman RL, Sanes JR (1987). "Neural cell adhesion molecule in normal, denervated, and myopathic human muscle". Ann. Neurol. 21 (5): 481–9. PMID 3296947.
  11. ↑ 11.0 11.1 Agre JC, Rodríquez AA, Tafel JA (1991). "Late effects of polio: critical review of the literature on neuromuscular function". Archives of physical medicine and rehabilitation. 72 (11): 923–31. PMID 1929813.
  12. ↑ Trojan DA, Cashman NR (2005). "Post-poliomyelitis syndrome". Muscle Nerve. 31 (1): 6–19. PMID 15599928.
  13. ↑ Gawne AC, Halstead LS (1995). "Post-polio syndrome: pathophysiology and clinical management". Critical Review in Physical Medicine and Rehabilitation 7: 147–88. Reproduced online with permission by Lincolnshire Post-Polio Library; retrieved on 2007-11-10.
  14. ↑ Grimby G, Einarsson G, Hedberg M, Aniansson A (1989). "Muscle adaptive changes in post-polio subjects". Scandinavian journal of rehabilitation medicine. 21 (1): 19–26. PMID 2711135.
  15. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  16. ↑ WEINSTEIN L (1957). "Cardiovascular disturbances in poliomyelitis". Circulation. 15 (5): 735–56. PMID 13427128.
  17. ↑ GALPINE JF, WILSON WC (1959). "Occurrence of myocarditis in paralytic poliomyelitis". Br Med J. 2 (5163): 1379–81. PMC 1990933. PMID 13826196.
  18. ↑ Mayo Clinic Staff (2005-05-19). "Polio: Complications". Mayo Foundation for Medical Education and Research (MFMER). Retrieved 2007-02-26. Check date values in: |date= (help)
  19. ↑ Ramlow J, Alexander M, LaPorte R, Kaufmann C, Kuller L (1992). "Epidemiology of the post-polio syndrome". Am J Epidemiol. 136 (7): 769–86. PMID 1442743.
  20. ↑ Dalakas MC, Sever JL, Madden DL, Papadopoulos NM, Shekarchi IC, Albrecht P; et al. (1984). "Late postpoliomyelitis muscular atrophy: clinical, virologic, and immunologic studies". Rev Infect Dis. 6 Suppl 2: S562–7. PMID 6330854.
  21. ↑ Dalakas MC, Elder G, Hallett M, Ravits J, Baker M, Papadopoulos N; et al. (1986). "A long-term follow-up study of patients with post-poliomyelitis neuromuscular symptoms". N Engl J Med. 314 (15): 959–63. doi:10.1056/NEJM198604103141505. PMID 3007983.
  22. ↑ Johnson RT (1984). "Late progression of poliomyelitis paralysis: discussion of pathogenesis". Rev Infect Dis. 6 Suppl 2: S568–70. PMID 6330855.
  23. ↑ FERRIS BG, AULD PA, CRONKHITE L, KAUFMANN HJ, KEARSLEY RB, PRIZER M; et al. (1960). "Life-threatening poliomyelitis, Boston, 1955". N Engl J Med. 262: 371–80. doi:10.1056/NEJM196002252620801. PMID 13822503.
  24. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  25. ↑ Neumann D (2004). "Polio: its impact on the people of the United States and the emerging profession of physical therapy" (PDF). The Journal of orthopaedic and sports physical therapy. 34 (8): 479–92. PMID 15373011. Reproduced online with permission by Post-Polio Health International; retrieved on 2007-11-10.
  26. ↑ Silverstein A, Silverstein V, Nunn LS (2001). Polio, Diseases and People. Berkeley Heights, NJ: Enslow Publishers, 12. ISBN 0-7660-1592-0.
  27. ↑ Ritchie Russell, W.; Fischer-Williams, M. (1954). "RECOVERY OF MUSCULAR STRENGTH AFTER POLIOMYELITIS". The Lancet. 263 (6807): 330–333. doi:10.1016/S0140-6736(54)91084-3. ISSN 0140-6736.
  28. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  29. ↑ Miller AH, Buck LS (1950). "Tracheotomy in bulbar poliomyelitis". California medicine. 72 (1): 34–6. PMID 15398892.
  30. ↑ Template:Cite paper
  31. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.

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