Polio natural history, complications and prognosis: Difference between revisions
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== Complications== | == Complications== | ||
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 postpolio syndrome. Factors that increase the risk of postpolio syndrome include increasing length of time since acute poliovirus infection, presence of permanent residual impairment after recovery from the acute illness, and female sex. The pathogenesis of postpolio syndrome is thought to involve the failure of oversized motor units created during the recovery process of paralytic poliomyelitis. Postpolio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus. | 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 postpolio syndrome. Factors that increase the risk of postpolio syndrome include increasing length of time since acute poliovirus infection, presence of permanent residual impairment after recovery from the acute illness, and female sex. The pathogenesis of postpolio syndrome is thought to involve the failure of oversized motor units created during the recovery process of paralytic poliomyelitis. Postpolio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus. | ||
Residual complications of paralytic polio often occur following the initial recovery process. <ref>Leboeuf C (1992). The late effects of Polio: Information For Health Care Providers. (PDF), Commonwealth Department of Community Services and Health. ISBN 1-875412-05-0. Retrieved on 2007-11-10.</ref> Muscle [[paresis]] and paralysis can sometimes result in [[skeletal]] deformities, tightening of the joints and movement disability. Once the muscles in the limb become flaccid, they may interfere with the function of other muscles. A typical manifestation of this problem is ''equinus foot'' (similar to [[club foot]]). This deformity develops when the muscles that pull the toes downward are working, but those that pull it upward are not, and the foot naturally tends to drop toward the ground. If the problem is left untreated, the [[Achilles tendon]]s at the back of the foot retract and the foot cannot take on a normal position. Polio victims that develop equinus foot cannot walk properly because they cannot put their heel on the ground. A similar situation can develop if the arms become paralyzed.<ref name= Aftereffects>{{cite web | author = Sanofi Pasteur | title = Poliomyelitis virus (picornavirus, enterovirus), after-effects of the polio, paralysis, deformations | work = Polio Eradication | url = http://www.polio.info/polio-eradication/front/index.jsp?siteCode=POLIO&lang=EN&codeRubrique=14 | accessdate = 2007-07-31}}</ref> In some cases the growth of an affected leg is slowed by polio, while the other leg continues to grow normally. The result is that one leg is shorter than the other and the person limps and leans to one side, in turn leading to deformities of the spine (such as [[scoliosis]]).<ref name= Aftereffects /> [[Osteoporosis]] and increased likelihood of [[bone fracture]]s may occur. Extended use of braces or wheelchairs may cause compression [[neuropathy]], as well as a loss of proper function of the [[vein]]s in the legs, due to pooling of blood in paralyzed lower limbs.<ref name=MayoComps>{{cite web |author = Mayo Clinic Staff | date=[[2005-05-19]] | url = http://www.mayoclinic.com/health/polio/DS00572/DSECTION=7 | title = Polio: Complications| publisher = Mayo Foundation for Medical Education and Research (MFMER)| accessdate=2007-02-26}}</ref><ref name= Hoyt>{{cite book |author=Hoyt, William Graves; Miller, Neil; Walsh, Frank |title=Walsh and Hoyt's clinical neuro-ophthalmology |publisher=Lippincott Williams & Wilkins |location=Hagerstown, MD |year=2005 |pages=3264–65 |isbn=0-7817-4814-3 |oclc= |doi=}}</ref> Complications from prolonged immobility involving the [[lungs]], [[kidney]]s and [[heart]] include [[pulmonary edema]], [[aspiration pneumonia]], [[urinary tract infection]]s, [[kidney stone]]s, [[paralytic ileus]], [[myocarditis]] and [[cor pulmonale]].<ref name=MayoComps /><ref name= Hoyt/> | |||
=== Post-polio syndrome === | |||
{{main|Post-polio syndrome}} | |||
Around a quarter of individuals who survive paralytic polio in childhood develop additional symptoms decades after recovering from the acute infection, notably muscle weakness, extreme fatigue, or paralysis. This condition is known as [[post-polio syndrome]] (PPS).<ref name=Cashman>{{cite journal |author=Trojan D, Cashman N |title=Post-poliomyelitis syndrome |journal=Muscle Nerve |volume=31 |issue=1 |pages=6–19 |year=2005 |pmid = 15599928}}</ref> The symptoms of PPS are thought to involve a failure of the over-sized motor units created during recovery from paralytic disease.<ref name=Ramlow_1992>{{cite journal |author=Ramlow J, Alexander M, LaPorte R, Kaufmann C, Kuller L |title=Epidemiology of the post-polio syndrome |journal=Am. J. Epidemiol. |volume=136 |issue=7 |pages=769–86 |year=1992 |pmid=1442743}}</ref><ref name= Annals>{{cite journal |author=Lin K, Lim Y |title=Post-poliomyelitis syndrome: case report and review of the literature| url= http://www.annals.edu.sg/pdf/34VolNo7200508/V34N7p447.pdf | format = PDF |journal=Ann Acad Med Singapore |volume=34 |issue=7 |pages=447–9 |year=2005 |pmid = 16123820}}</ref> Factors that increase the risk of PPS include the length of time since acute poliovirus infection, the presence of permanent residual impairment after recovery from the acute illness, and both overuse and disuse of neurons.<ref name=Cashman /> Post-polio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus.<ref name=PinkBook /> | |||
==Prognosis== | |||
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.<ref name=Neumann/> 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> | |||
[[Image:Polio sequelle.jpg|thumb|A child with a deformity of her right leg due to polio]] | |||
Without respiratory support, consequences of poliomyelitis with [[Respiration (physiology)|respiratory]] involvement include [[suffocation]] or [[aspiration pneumonia|pneumonia from aspiration of secretions]].<ref name= Goldberg>{{cite journal |author=Goldberg A |title=Noninvasive mechanical ventilation at home: building upon the tradition |url= http://www.chestjournal.org/cgi/content/full/121/2/321 |journal=[[Chest (journal)|Chest]] |volume=121 |issue=2 |pages=321–4 |year=2002 |id=PMID 11834636}}</ref> 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.<ref name= PinkBook /> Bulbar polio often causes death if respiratory support is not provided;<ref name= Hoyt /> with support, its mortality rate ranges from 25 to 75%, depending on the age of the patient.<ref name=PinkBook /><ref>{{cite journal |author=Miller AH, Buck LS |title=Tracheotomy in bulbar poliomyelitis |url= http://www.pubmedcentral.nih.gov/pagerender.fcgi?artid=1520308&pageindex=1#page |journal=California medicine |volume=72 |issue=1 |pages=34–6 |year=1950 |pmid=15398892 |doi=}}</ref> When positive pressure ventilators are available, the mortality can be reduced to 15%.<ref name=Wackers>{{cite paper| author = Wackers, G.| title = Constructivist Medicine| version = PhD-thesis| publisher = Maastricht: Universitaire Pers Maastricht| date = 1994| url = http://www.fdcw.unimaas.nl/personal/WebSitesMWT/Wackers/proefschrift.html#h4| format = [[web]]| accessdate = 2008-01-04 }}</ref> | |||
===Recovery=== | |||
Many cases of poliomyelitis result in only temporary paralysis.<ref>Frauenthal HWA, Manning JVV (1914). Manual of infantile paralysis, with modern methods of treatment.. Philadelphia Davis, 79–101. OCLC 2078290</ref> Nerve impulses return to the formerly paralyzed muscle within a month, and recovery is usually complete in six to eight months.<ref name=Neumann /> The [[neurophysiology|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.<ref>{{cite journal |author=Sandberg A, Hansson B, Stålberg E |title=Comparison between concentric needle EMG and macro EMG in patients with a history of polio |journal=Clinical Neurophysiology |volume=110 |issue=11 |pages=1900–8 |year=1999 |pmid=10576485}}</ref> Paralysis remaining after one year is likely to be permanent, although modest recoveries of muscle strength are possible 12 to 18 months after infection.<ref name=Neumann /> | |||
One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons develop new branches, or ''axonal sprouts''.<ref>{{cite journal |author=Cashman NR, Covault J, Wollman RL, Sanes JR |title=Neural cell adhesion molecule in normal, denervated, and myopathic human muscle |journal=Ann. Neurol. |volume=21 |issue=5 |pages=481–9 |year=1987 |pmid=3296947}}</ref> These sprouts can [[reinnervate]] orphaned muscle fibers that have been denervated by acute polio infection,<ref name=Agre>{{cite journal |author=Agre JC, Rodríquez AA, Tafel JA |title=Late effects of polio: critical review of the literature on neuromuscular function |journal=Archives of physical medicine and rehabilitation |volume=72 |issue=11 |pages=923–31 |year=1991 |pmid=1929813}}</ref> restoring the fibers' capacity to contract and improving strength.<ref>{{cite journal |author=Trojan DA, Cashman NR |title=Post-poliomyelitis syndrome |journal=Muscle Nerve |volume=31 |issue=1 |pages=6–19 |year=2005 |pmid=15599928}}</ref> Terminal sprouting may generate a few significantly enlarged motor neurons doing work previously performed by as many as four or five units: <ref>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.</ref> 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 [[muscle hypertrophy|myofiber hypertrophy]]—enlargement of muscle fibers through exercise and activity—and transformation of [[Muscle fiber#Type II|type II muscle fibers]] to [[Muscle fiber#Type I| type I muscle fibers]].<ref name=Agre /><ref name = Grimby_1989>{{cite journal |author=Grimby G, Einarsson G, Hedberg M, Aniansson A |title=Muscle adaptive changes in post-polio subjects |journal=Scandinavian journal of rehabilitation medicine |volume=21 |issue=1 |pages=19–26 |year=1989 |pmid=2711135}}</ref> | |||
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 contraction#Contractions, by muscle type|muscle's maximal capacity]], enhancing athletic development of previously little-used muscles, and using [[ligament]]s for stability, which enables greater mobility.<ref name = Grimby_1989 /> | |||
==References== | ==References== | ||
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Overview
Complications
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 postpolio syndrome. Factors that increase the risk of postpolio syndrome include increasing length of time since acute poliovirus infection, presence of permanent residual impairment after recovery from the acute illness, and female sex. The pathogenesis of postpolio syndrome is thought to involve the failure of oversized motor units created during the recovery process of paralytic poliomyelitis. Postpolio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus.
Residual complications of paralytic polio often occur following the initial recovery process. [1] Muscle paresis and paralysis can sometimes result in skeletal deformities, tightening of the joints and movement disability. Once the muscles in the limb become flaccid, they may interfere with the function of other muscles. A typical manifestation of this problem is equinus foot (similar to club foot). This deformity develops when the muscles that pull the toes downward are working, but those that pull it upward are not, and the foot naturally tends to drop toward the ground. If the problem is left untreated, the Achilles tendons at the back of the foot retract and the foot cannot take on a normal position. Polio victims that develop equinus foot cannot walk properly because they cannot put their heel on the ground. A similar situation can develop if the arms become paralyzed.[2] In some cases the growth of an affected leg is slowed by polio, while the other leg continues to grow normally. The result is that one leg is shorter than the other and the person limps and leans to one side, in turn leading to deformities of the spine (such as scoliosis).[2] Osteoporosis and increased likelihood of bone fractures may occur. Extended use of braces or wheelchairs may cause compression neuropathy, as well as a loss of proper function of the veins in the legs, due to pooling of blood in paralyzed lower limbs.[3][4] Complications from prolonged immobility involving the lungs, kidneys and heart include pulmonary edema, aspiration pneumonia, urinary tract infections, kidney stones, paralytic ileus, myocarditis and cor pulmonale.[3][4]
Post-polio syndrome
Around a quarter of individuals who survive paralytic polio in childhood develop additional symptoms decades after recovering from the acute infection, notably muscle weakness, extreme fatigue, or paralysis. This condition is known as post-polio syndrome (PPS).[5] The symptoms of PPS are thought to involve a failure of the over-sized motor units created during recovery from paralytic disease.[6][7] Factors that increase the risk of PPS include the length of time since acute poliovirus infection, the presence of permanent residual impairment after recovery from the acute illness, and both overuse and disuse of neurons.[5] Post-polio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus.[8]
Prognosis
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.[9] 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.[9] Half the patients with spinal polio recover fully, one quarter recover with mild disability and the remaining quarter are left with severe disability.[10] 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.[11]. Spinal polio is rarely fatal.[12]
Without respiratory support, consequences of poliomyelitis with respiratory involvement include suffocation or pneumonia from aspiration of secretions.[13] 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.[8] Bulbar polio often causes death if respiratory support is not provided;[4] with support, its mortality rate ranges from 25 to 75%, depending on the age of the patient.[8][14] When positive pressure ventilators are available, the mortality can be reduced to 15%.[15]
Recovery
Many cases of poliomyelitis result in only temporary paralysis.[16] Nerve impulses return to the formerly paralyzed muscle within a month, and recovery is usually complete in six to eight months.[9] 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.[17] Paralysis remaining after one year is likely to be permanent, although modest recoveries of muscle strength are possible 12 to 18 months after infection.[9]
One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons develop new branches, or axonal sprouts.[18] These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection,[19] restoring the fibers' capacity to contract and improving strength.[20] Terminal sprouting may generate a few significantly enlarged motor neurons doing work previously performed by as many as four or five units: [21] 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.[19][22]
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.[22]
References
- ↑ Leboeuf C (1992). The late effects of Polio: Information For Health Care Providers. (PDF), Commonwealth Department of Community Services and Health. ISBN 1-875412-05-0. Retrieved on 2007-11-10.
- ↑ 2.0 2.1 Sanofi Pasteur. "Poliomyelitis virus (picornavirus, enterovirus), after-effects of the polio, paralysis, deformations". Polio Eradication. Retrieved 2007-07-31.
- ↑ 3.0 3.1 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) - ↑ 4.0 4.1 4.2 Hoyt, William Graves; Miller, Neil; Walsh, Frank (2005). Walsh and Hoyt's clinical neuro-ophthalmology. Hagerstown, MD: Lippincott Williams & Wilkins. pp. 3264–65. ISBN 0-7817-4814-3.
- ↑ 5.0 5.1 Trojan D, Cashman N (2005). "Post-poliomyelitis syndrome". Muscle Nerve. 31 (1): 6–19. PMID 15599928.
- ↑ 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.
- ↑ Lin K, Lim Y (2005). "Post-poliomyelitis syndrome: case report and review of the literature" (PDF). Ann Acad Med Singapore. 34 (7): 447–9. PMID 16123820.
- ↑ 8.0 8.1 8.2
- ↑ 9.0 9.1 9.2 9.3 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.
- ↑ Cuccurullo SJ (2004). Physical Medicine and Rehabilitation Board Review. Demos Medical Publishing. ISBN 1-888799-45-5.
- ↑ 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
- ↑ Silverstein A, Silverstein V, Nunn LS (2001). Polio, Diseases and People. Berkeley Heights, NJ: Enslow Publishers, 12. ISBN 0-7660-1592-0.
- ↑ Goldberg A (2002). "Noninvasive mechanical ventilation at home: building upon the tradition". Chest. 121 (2): 321–4. PMID 11834636.
- ↑ Miller AH, Buck LS (1950). "Tracheotomy in bulbar poliomyelitis". California medicine. 72 (1): 34–6. PMID 15398892.
- ↑ Template:Cite paper
- ↑ Frauenthal HWA, Manning JVV (1914). Manual of infantile paralysis, with modern methods of treatment.. Philadelphia Davis, 79–101. OCLC 2078290
- ↑ 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.
- ↑ 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.
- ↑ 19.0 19.1 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.
- ↑ Trojan DA, Cashman NR (2005). "Post-poliomyelitis syndrome". Muscle Nerve. 31 (1): 6–19. PMID 15599928.
- ↑ 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.
- ↑ 22.0 22.1 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.