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| style="padding: 5px 5px; background: #DCDCDC;" | '''Respiratory compromise'''
| style="padding: 5px 5px; background: #DCDCDC;" | '''Respiratory compromise'''
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
* Resulting from paralysis of respiratory muscles (diaphragm and intercostal muscles)
* Resulting from paralysis of [[respiratory]] muscles (diaphragm and intercostal muscles)
* Airway obstruction
* [[Airway obstruction]]
* Lesions in:
* Lesions in:
:* Cranial nerve nuclei
:* [[Cranial nerve nuclei]]
:* Medullary respiratory center
:* [[Medullary]] [[respiratory center]]
|-
|-
| style="padding: 5px 5px; background: #DCDCDC;" | '''Myocarditis'''
| style="padding: 5px 5px; background: #DCDCDC;" | '''Myocarditis'''
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==Prognosis==
==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.<ref name="pmid13822503">{{cite journal| author=FERRIS BG, AULD PA, CRONKHITE L, KAUFMANN HJ, KEARSLEY RB, PRIZER M et al.| title=Life-threatening poliomyelitis, Boston, 1955. | journal=N Engl J Med | year= 1960 | volume= 262 | issue=  | pages= 371-80 | pmid=13822503 | doi=10.1056/NEJM196002252620801 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13822503  }} </ref>
(Mandel)
 
Muscular paralysis usually progresses or extends for only 1 to 3 days after its onset, but occasionally for as long as 1 week.52 Permanent weakness is observed in approximately two thirds of patients with paralytic poliomyelitis. Complete recovery is less likely when acute paralysis is severe and when patients require mechanical ventilation. An estimate of the eventual outcome can be made after 1 month, when most reversible damage has disappeared. Very little additional return of function can be expected beyond 9 months. Recovery from pharyn- geal paralysis usually is evident by 10 days and is eventually complete. Bulbar poliomyelitis is rarely responsible for permanent sequelae in surviving patients.
 


Available mortality figures date from the era of epidemic poliomy- elitis, a period when critical care medicine was less advanced than it is today. The reported overall mortality for acute paralytic poliomyelitis during this period was 5% to 10%, but was substantially higher with bulbar involvement.53


-->


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. In cases of spinal polio, if the affected nerve cells are completely destroyed, paralysis will be permanent; cells that are not destroyed but lose function temporarily may recover within four to six weeks after onset.<ref name=Neumann>{{cite journal |author=Neumann D |title=Polio: its impact on the people of the United States and the emerging profession of physical therapy |url= http://www.post-polio.org/edu/hpros/Aug04HistPersNeumann.pdf | format = PDF | journal=The Journal of orthopaedic and sports physical therapy |volume=34 |issue=8 |pages=479–92 |year=2004 |pmid=15373011}} Reproduced online with permission by Post-Polio Health International; retrieved on [[2007-11-10]].</ref> Half the patients with spinal polio recover fully, one quarter recover with mild disability and the remaining quarter are left with severe disability.<ref>{{cite book |author=Cuccurullo SJ |title=Physical Medicine and Rehabilitation Board Review |url= http://www.ncbi.nlm.nih.gov/books/bv.fcgi?&rid=physmedrehab.table.8357 | publisher=Demos Medical Publishing | year = 2004  |isbn=1-888799-45-5}}</ref> The degree of both acute paralysis and residual paralysis is likely to be proportional to the degree of [[viremia]], and inversely proportional to the degree of [[immunity (medical)|immunity]].<ref>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. PMID 15885840</ref>. Spinal polio is rarely fatal.<ref>Silverstein A, Silverstein V, Nunn LS (2001). Polio, Diseases and People. Berkeley Heights, NJ: Enslow Publishers, 12. ISBN 0-7660-1592-0.</ref>  
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. In cases of spinal polio, if the affected nerve cells are completely destroyed, paralysis will be permanent; cells that are not destroyed but lose function temporarily may recover within four to six weeks after onset.<ref name=Neumann>{{cite journal |author=Neumann D |title=Polio: its impact on the people of the United States and the emerging profession of physical therapy |url= http://www.post-polio.org/edu/hpros/Aug04HistPersNeumann.pdf | format = PDF | journal=The Journal of orthopaedic and sports physical therapy |volume=34 |issue=8 |pages=479–92 |year=2004 |pmid=15373011}} Reproduced online with permission by Post-Polio Health International; retrieved on [[2007-11-10]].</ref> Half the patients with spinal polio recover fully, one quarter recover with mild disability and the remaining quarter are left with severe disability.<ref>{{cite book |author=Cuccurullo SJ |title=Physical Medicine and Rehabilitation Board Review |url= http://www.ncbi.nlm.nih.gov/books/bv.fcgi?&rid=physmedrehab.table.8357 | publisher=Demos Medical Publishing | year = 2004  |isbn=1-888799-45-5}}</ref> The degree of both acute paralysis and residual paralysis is likely to be proportional to the degree of [[viremia]], and inversely proportional to the degree of [[immunity (medical)|immunity]].<ref>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. PMID 15885840</ref>. Spinal polio is rarely fatal.<ref>Silverstein A, Silverstein V, Nunn LS (2001). Polio, Diseases and People. Berkeley Heights, NJ: Enslow Publishers, 12. ISBN 0-7660-1592-0.</ref>  

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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

Many cases of poliomyelitis result in only temporary paralysis.[1] 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.[2] 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.[3] These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection,[4] restoring the fibers' capacity to contract and improving strength.[5] Terminal sprouting may generate a few significantly enlarged motor neurons doing work previously performed by as many as four or five units: [6] 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.[4][7]

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:[8][9][10][11][12][13][14][15]

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.[16]



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. In cases of spinal polio, if the affected nerve cells are completely destroyed, paralysis will be permanent; cells that are not destroyed but lose function temporarily may recover within four to six weeks after onset.[17] Half the patients with spinal polio recover fully, one quarter recover with mild disability and the remaining quarter are left with severe disability.[18] The degree of both acute paralysis and residual paralysis is likely to be proportional to the degree of viremia, and inversely proportional to the degree of immunity.[19]. Spinal polio is rarely fatal.[20]

A child with a deformity of her right leg due to polio

Without respiratory support, consequences of poliomyelitis with respiratory involvement include suffocation or pneumonia from aspiration of secretions.[21] Overall, 5–10% of patients with paralytic polio die due to the paralysis of muscles used for breathing. The mortality rate varies by age: 2–5% of children and up to 15–30% of adults die. Bulbar polio often causes death if respiratory support is not provided;[22] with support, its mortality rate ranges from 25 to 75%, depending on the age of the patient.[23] When positive pressure ventilators are available, the mortality can be reduced to 15%.[24]

References

  1. Frauenthal HWA, Manning JVV (1914). Manual of infantile paralysis, with modern methods of treatment.. Philadelphia Davis, 79–101. OCLC 2078290
  2. 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.
  3. 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.
  4. 4.0 4.1 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.
  5. Trojan DA, Cashman NR (2005). "Post-poliomyelitis syndrome". Muscle Nerve. 31 (1): 6–19. PMID 15599928.
  6. 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.
  7. 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.
  8. Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  9. WEINSTEIN L (1957). "Cardiovascular disturbances in poliomyelitis". Circulation. 15 (5): 735–56. PMID 13427128.
  10. GALPINE JF, WILSON WC (1959). "Occurrence of myocarditis in paralytic poliomyelitis". Br Med J. 2 (5163): 1379–81. PMC 1990933. PMID 13826196.
  11. 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)
  12. 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.
  13. 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.
  14. 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.
  15. Johnson RT (1984). "Late progression of poliomyelitis paralysis: discussion of pathogenesis". Rev Infect Dis. 6 Suppl 2: S568–70. PMID 6330855.
  16. 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.
  17. 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.
  18. Cuccurullo SJ (2004). Physical Medicine and Rehabilitation Board Review. Demos Medical Publishing. ISBN 1-888799-45-5.
  19. 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. PMID 15885840
  20. Silverstein A, Silverstein V, Nunn LS (2001). Polio, Diseases and People. Berkeley Heights, NJ: Enslow Publishers, 12. ISBN 0-7660-1592-0.
  21. Goldberg A (2002). "Noninvasive mechanical ventilation at home: building upon the tradition". Chest. 121 (2): 321–4. PMID 11834636.
  22. Miller AH, Buck LS (1950). "Tracheotomy in bulbar poliomyelitis". California medicine. 72 (1): 34–6. PMID 15398892.
  23. Template:Cite paper

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