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Polio lores134.jpg|
Poliomyelitis
ICD-10 A80, B91
ICD-9 045, 138
OMIM {{{OMIM}}}
DiseasesDB 10209
MedlinePlus 001402
eMedicine ped/1843 pmr/6
MeSH C02.182.600.700


Poliomyelitis, often called polio or infantile paralysis, is an acute viral infectious disease spread from person to person, primarily via the fecal-oral route.[1] The term derives from the Greek polio (πολίός), meaning "grey", myelon (µυελός), referring to the "spinal cord", and -itis, which denotes inflammation.[2] Although around 90% of polio infections have no symptoms at all, affected individuals can exhibit a range of symptoms if the virus enters the blood stream.[3] In fewer than 1% of cases the virus enters the central nervous system, preferentially infecting and destroying motor neurons, leading to muscle weakness and acute flaccid paralysis. Different types of paralysis may occur, depending on the nerves involved. Spinal polio is the most common form, characterized by asymmetric paralysis that most often involves the legs. Bulbar polio leads to weakness of muscles innervated by cranial nerves. Bulbospinal polio is a combination of bulbar and spinal paralysis.[4]

Poliomyelitis was first recognized as a distinct condition by Jakob Heine in 1840.[5] Its causative agent, poliovirus, was identified in 1908 by Karl Landsteiner.[5] Although major polio epidemics were unknown before the 20th century, polio was one of the most dreaded childhood diseases of the 20th century in the United States. Polio epidemics have crippled thousands of people, mostly young children; the disease has caused paralysis and death for much of human history. Polio had existed for thousands of years quietly as an endemic pathogen until the 1880s, when major epidemics began to occur in Europe; soon after, widespread epidemics appeared in the United States.[6] By 1910, much of the world experienced a dramatic increase in polio cases and frequent epidemics became regular events, primarily in cities during the summer months. These epidemics—which left thousands of children and adults paralyzed—provided the impetus for a "Great Race" towards the development of a vaccine. The polio vaccines developed by Jonas Salk in 1952 and Albert Sabin in 1962 are credited with reducing the annual number of polio cases from many hundreds of thousands to around a thousand.[7] Enhanced vaccination efforts led by the World Health Organization, UNICEF and Rotary International could result in global eradication of the disease.[8]

CauseEdit

File:Polio EM PHIL 1875 lores.PNG
Main article: Poliovirus

Poliomyelitis is caused by infection with a member of the genus enterovirus known as poliovirus (PV). This group of RNA viruses prefers to inhabit the gastrointestinal tract.[1] PV infects and causes disease in humans alone.[3] Its structure is very simple, composed of a single (+) sense RNA genome enclosed in a protein shell called a capsid.[3] In addition to protecting the virus’s genetic material, the capsid proteins enable poliovirus to infect certain types of cells. Three serotypes of poliovirus have been identified—poliovirus type 1 (PV1), type 2 (PV2), and type 3 (PV3)—each with a slightly different capsid protein.[9] All three are extremely virulent and produce the same disease symptoms.[3] PV1 is the most commonly encountered form, and the one most closely associated with paralysis.[10]

Individuals who are exposed to the virus, either through infection or by immunization with polio vaccine, develop immunity. In immune individuals, IgA antibodies against poliovirus are present in the tonsils and gastrointestinal tract and are able to block virus replication; IgG and IgM antibodies against PV can prevent the spread of the virus to motor neurons of the central nervous system.[11] Infection or vaccination with one serotype of poliovirus does not provide immunity against the other serotypes, and full immunity requires exposure to each serotype.[11]

TransmissionEdit

Poliomyelitis is highly contagious and spreads easily from human-to-human contact.[11] In endemic areas, wild polioviruses can infect virtually the entire human population.[12] It is seasonal in temperate climates, with peak transmission occurring in summer and autumn.[11] These seasonal differences are far less pronounced in tropical areas.[12] The time between first exposure and first symptoms, known as the incubation period, is usually 6 to 20 days, with a maximum range of 3 to 35 days.[13] Virus particles are excreted in the feces for several weeks following initial infection.[13] The disease is transmitted primarily via the fecal-oral route, by ingesting contaminated food or water. It is occasionally transmitted via the oral-oral route,[10] a mode especially visible in areas with good sanitation and hygiene.[11] Polio is most infectious between 7–10 days before and 7–10 days after the appearance of symptoms, but transmission is possible as long as the virus remains in the saliva or feces.[10]

Factors that increase the risk of polio infection or affect the severity of the disease include immune deficiency,[14] malnutrition,[15] tonsillectomy,[16] physical activity immediately following the onset of paralysis,[17] skeletal muscle injury due to injection of vaccines or therapeutic agents,[18] and pregnancy.[19] Although the virus can cross the placenta during pregnancy, the fetus does not appear to be affected by either maternal infection or polio vaccination.[20] Maternal antibodies also cross the placenta, providing passive immunity that protects the infant from polio infection during the first few months of life.[21]

Classification Edit

Outcomes of poliovirus infection
Outcome Proportion of cases[4]
Asymptomatic 90–95%
Minor illness 4–8%
Non-paralytic aseptic
meningitis
1–2%
Paralytic poliomyelitis 0.1–0.5%
— Spinal polio 79% of paralytic cases
— Bulbospinal polio 19% of paralytic cases
— Bulbar polio 2% of paralytic cases

The term poliomyelitis is used to identify the disease caused by any of the three serotypes of poliovirus. Two basic patterns of polio infection are described: a minor illness which does not involve the central nervous system (CNS), sometimes called abortive poliomyelitis, and a major illness involving the CNS, which may be paralytic or non-paralytic.[22] In most people with a normal immune system, a poliovirus infection is asymptomatic. Rarely the infection produces minor symptoms; these may include upper respiratory tract infection (sore throat and fever), gastrointestinal disturbances (nausea, vomiting, abdominal pain, constipation or, rarely, diarrhea), and influenza-like illnesses.[4]

The virus enters the central nervous system in about 3% of infections. Most patients with CNS involvement develop non-paralytic aseptic meningitis, with symptoms of headache, neck, back, abdominal and extremity pain, fever, vomiting, lethargy and irritability.[2][23] Approximately 1 in 200 to 1 in 1000 cases progress to paralytic disease, in which the muscles become weak, floppy and poorly-controlled, and finally completely paralyzed; this condition is known as acute flaccid paralysis.[24] Depending on the site of paralysis, paralytic poliomyelitis is classified as spinal, bulbar, or bulbospinal. Encephalitis, an infection of the brain tissue itself, can occur in rare cases and is usually restricted to infants. It is characterized by confusion, changes in mental status, headaches, fever, and less commonly seizures and spastic paralysis.[25]

Mechanism Edit

File:Polio spine.png

Poliovirus enters the body through the mouth, infecting the first cells it comes in contact with—the pharynx (throat) and intestinal mucosa. It gains entry by binding to a immunoglobulin-like receptor, known as the poliovirus receptor or CD155, on the cell surface.[26] The virus then hijacks the host cell's own machinery, and begins to replicate. Poliovirus divides within gastrointestinal cells for about a week, from where it spreads to the tonsils (specifically the follicular dendritic cells residing within the tonsilar germinal centers), the intestinal lymph nodes including the M cells of Peyer's patches, and the deep cervical and mesenteric lymph nodes, where it multiplies abundantly. The virus is subsequently absorbed into the bloodstream.[27]

Known as viremia, the presence of virus in the bloodstream enables it to be widely distributed throughout the body. Poliovirus can survive and multiply within the blood and lymphatics for long periods of time, sometimes as long as 17 weeks.[28] In a small percentage of cases, it can spread and replicate in other sites such as brown fat, the reticuloendothelial tissues, and muscle.[29] This sustained replication causes a major viremia, and leads to the development of minor influenza-like symptoms. Rarely, this may progress and the virus may invade the central nervous system, provoking a local inflammatory response. In most cases this causes a self-limiting inflammation of the meninges, the layers of tissue surrounding the brain, which is known as non-paralytic aseptic meningitis.[2] Penetration of the CNS provides no known benefit to the virus, and is quite possibly an incidental deviation of a normal gastrointestinal infection.[30] The mechanisms by which poliovirus spreads to the CNS are poorly understood, but it appears to be primarily a chance event—largely independent of the age, gender, or socioeconomic position of the individual.[30]

Paralytic polioEdit

File:PHIL 2767 Poliovirus Myotonic dystrophic changes.jpg

In around 1% of infections, poliovirus spreads along certain nerve fiber pathways, preferentially replicating in and destroying motor neurons within the spinal cord, brain stem, or motor cortex. This leads to the development of paralytic poliomyelitis, the various forms of which (spinal, bulbar, and bulbospinal) vary only with the amount of neuronal damage and inflammation that occurs, and the region of the CNS that is affected.

The destruction of neuronal cells produces lesions within the spinal ganglia; these may also occur in the reticular formation, vestibular nuclei, cerebellar vermis, and deep cerebellar nuclei.[30] Inflammation associated with nerve cell destruction often alters the color and appearance of the gray matter in the spinal column, causing it to appear reddish and swollen.[2] Other destructive changes associated with paralytic disease occur in the forebrain region, specifically the hypothalamus and thalamus.[30] The molecular mechanisms by which poliovirus causes paralytic disease are poorly understood.

Early symptoms of paralytic polio include high fever, headache, stiffness in the back and neck, asymmetrical weakness of various muscles, sensitivity to touch, difficulty swallowing, muscle pain, loss of superficial and deep reflexes, paresthesia (pins and needles), irritability, constipation, or difficulty urinating. Paralysis generally develops one to ten days after early symptoms begin, progresses for two to three days, and is usually complete by the time the fever breaks.[31]

The likelihood of developing paralytic polio increases with age, as does the extent of paralysis. In children, non-paralytic meningitis is the most likely consequence of CNS involvement, and paralysis occurs in only 1 in 1000 cases. In adults, paralysis occurs in 1 in 75 cases.[32] In children under five years of age, paralysis of one leg is most common; in adults, extensive paralysis of the chest and abdomen also affecting all four limbs—quadriplegia—is more likely.[33] Paralysis rates also vary depending on the serotype of the infecting poliovirus; the highest rates of paralysis (1 in 200) are associated with poliovirus type 1, the lowest rates (1 in 2,000) are associated with type 2.[34]

Spinal polio Edit

File:Polio spinal diagram.PNG

Spinal polio is the most common form of paralytic poliomyelitis; it results from viral invasion of the motor neurons of the anterior horn cells, or the ventral (front) gray matter section in the spinal column, which are responsible for movement of the muscles, including those of the trunk, limbs and the intercostal muscles.[24] Virus invasion causes inflammation of the nerve cells, leading to damage or destruction of motor neuron ganglia. When spinal neurons die, Wallerian degeneration takes place, leading to weakness of those muscles formerly innervated by the now dead neurons.[35] With the destruction of nerve cells, the muscles no longer receive signals from the brain or spinal cord; without nerve stimulation, the muscles atrophy, becoming weak, floppy and poorly controlled, and finally completely paralyzed.[24] Progression to maximum paralysis is rapid (two to four days), and is usually associated with fever and muscle pain.[35] Deep tendon reflexes are also affected, and are usually absent or diminished; sensation (the ability to feel) in the paralyzed limbs, however, is not affected.[35]

The extent of spinal paralysis depends on the region of the cord affected, which may be cervical, thoracic, or lumbar.[36] The virus may affect muscles on both sides of the body, but more often the paralysis is asymmetrical.[27] Any limb or combination of limbs may be affected—one leg, one arm, or both legs and both arms. Paralysis is often more severe proximally (where the limb joins the body) than distally (the fingertips and toes).[27]

Bulbar polio Edit

File:Brain bulbar region.svg

Comprising about 2% of cases of paralytic polio, bulbar polio occurs when poliovirus invades and destroys nerves within the bulbar region of the brain stem.[4] The bulbar region is a white matter pathway that connects the cerebral cortex to the brain stem. The destruction of these nerves weakens the muscles supplied by the cranial nerves, producing symptoms of encephalitis, and causes difficulty breathing, speaking and swallowing.[23] Critical nerves affected are the glossopharyngeal nerve, which partially controls swallowing and functions in the throat, tongue movement and taste; the vagus nerve, which sends signals to the heart, intestines, and lungs; and the accessory nerve, which controls upper neck movement. Due to the effect on swallowing, secretions of mucus may build up in the airway causing suffocation.[31] Other signs and symptoms include facial weakness, caused by destruction of the trigeminal nerve and facial nerve, which innervate the cheeks, tear ducts, gums, and muscles of the face, among other structures; double vision; difficulty in chewing; and abnormal respiratory rate, depth, and rhythm, which may lead to respiratory arrest. Pulmonary edema and shock are also possible, and may be fatal.[36]

Bulbospinal polio Edit

Approximately 19% of all paralytic polio cases have both bulbar and spinal symptoms; this subtype is called respiratory polio or bulbospinal polio.[4] Here the virus affects the upper part of the cervical spinal cord (C3 through C5), and paralysis of the diaphragm occurs. The critical nerves affected are the phrenic nerve, which drives the diaphragm to inflate the lungs, and those that drive the muscles needed for swallowing. By destroying these nerves this form of polio affects breathing, making it difficult or impossible for the patient to breathe without the support of a ventilator. It can lead to paralysis of the arms and legs and may also affect swallowing and heart functions.[37]

Diagnosis Edit

Paralytic poliomyelitis may be clinically suspected in individuals experiencing acute onset of flaccid paralysis in one or more limbs with decreased or absent tendon reflexes in the affected limbs, that cannot be attributed to another apparent cause, and without sensory or cognitive loss.[38]

A laboratory diagnosis is usually made based on recovery of poliovirus from a stool sample or a swab of the pharynx. Antibodies to poliovirus can be diagnostic, and are generally detected in the blood of infected patients early in the course of infection.[4] Analysis of the patient's cerebrospinal fluid (CSF), which is collected by a lumbar puncture ("spinal tap"), reveals an increased number of white blood cells (primarily lymphocytes) and a mildly elevated protein level. Detection of virus in the CSF is diagnostic of paralytic polio, but rarely occurs.[4]

If poliovirus is isolated from a patient experiencing acute flaccid paralysis, it is further tested through oligonucleotide mapping (genetic fingerprinting), or more recently by PCR amplification, to determine whether it is "wild type" (that is, the virus encountered in nature) or "vaccine type" (derived from a strain of poliovirus used to produce polio vaccine).[39] It is important to determine the source of the virus because for each reported case of paralytic polio caused by wild poliovirus, it is estimated that another 200 to 3,000 contagious asymptomatic carriers exist.[40]

PrognosisEdit

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.[41] 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.[41] Half the patients with spinal polio recover fully, one quarter recover with mild disability and the remaining quarter are left with severe disability.[42] 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.[30] Spinal polio is rarely fatal.[31]

File:Polio sequelle.jpg

Without respiratory support, consequences of poliomyelitis with respiratory involvement include suffocation or pneumonia from aspiration of secretions.[43] 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.[4] Bulbar polio often causes death if respiratory support is not provided;[37] with support, its mortality rate ranges from 25 to 75%, depending on the age of the patient.[4][44] When positive pressure ventilators are available, the mortality can be reduced to 15%.[45]

RecoveryEdit

Many cases of poliomyelitis result in only temporary paralysis.[24] Nerve impulses return to the formerly paralyzed muscle within a month, and recovery is usually complete in six to eight months.[41] 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.[46] Paralysis remaining after one year is likely to be permanent, although modest recoveries of muscle strength are possible 12 to 18 months after infection.[41]

One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons develop new branches, or axonal sprouts.[47] These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection,[48] restoring the fibers' capacity to contract and improving strength.[49] Terminal sprouting may generate a few significantly enlarged motor neurons doing work previously performed by as many as four or five units:[32] 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.[48][50]

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.[50]

ComplicationsEdit

Residual complications of paralytic polio often occur following the initial recovery process.[23] 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.[51] 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).[51] 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.[52][37] 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.[52][37]

Post-polio syndrome Edit

Main article: 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).[53] The symptoms of PPS are thought to involve a failure of the over-sized motor units created during recovery from paralytic disease.[54][55] 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.[53] Post-polio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus.[4]

Treatment Edit

File:Womanonsideinlung.jpg

There is no cure for polio. The focus of modern treatment has been on providing relief of symptoms, speeding recovery and preventing complications. Supportive measures include antibiotics to prevent infections in weakened muscles, analgesics for pain, moderate exercise and a nutritious diet.[56] Treatment of polio often requires long-term rehabilitation, including physical therapy, braces, corrective shoes and, in some cases, orthopedic surgery.[36]

Portable ventilators may be required to support breathing. Historically, a noninvasive negative-pressure ventilator, more commonly called an iron lung, was used to artificially maintain respiration during an acute polio infection until a person could breathe independently (generally about one to two weeks). Today many polio survivors with permanent respiratory paralysis use modern jacket-type negative-pressure ventilators that are worn over the chest and abdomen.[43]

Other historical treatments for polio include hydrotherapy, electrotherapy, massage and passive motion exercises, and surgical treatments such as tendon lengthening and nerve grafting.[24] Devices such as rigid braces and body casts—which tended to cause muscle atrophy due to the limited movement of the user—were also touted as effective treatments.[57]

PreventionEdit

Passive immunization Edit

In 1950, William Hammon at the University of Pittsburgh purified the gamma globulin component of the blood plasma of polio survivors.[58] Hammon proposed that the gamma globulin, which contained antibodies to poliovirus, could be used to halt poliovirus infection, prevent disease, and reduce the severity of disease in other patients who had contracted polio. The results of a large clinical trial were promising; the gamma globulin was shown to be about 80% effective in preventing the development of paralytic poliomyelitis.[59] It was also shown to reduce the severity of the disease in patients that developed polio.[58] The gamma globulin approach was later deemed impractical for widespread use, however, due in large part to the limited supply of blood plasma, and the medical community turned its focus to the development of a polio vaccine.[60]

File:Poliodrops.jpg

Vaccine Edit

Main article: Polio vaccine

Two vaccines are used throughout the world to combat polio. Both vaccines induce immunity to polio, efficiently blocking person-to-person transmission of wild poliovirus, thereby protecting both individual vaccine recipients and the wider community (so-called herd immunity).[61]

The first polio vaccine was developed in 1952 by Jonas Salk, also at the University of Pittsburgh, and announced to the world on April 12, 1955.[62] The Salk vaccine, or inactivated poliovirus vaccine (IPV), is based on poliovirus grown in a type of monkey kidney tissue culture (Vero cell line), which is chemically inactivated with formalin.[11] After two doses of IPV (given by injection), 90% or more of individuals develop protective antibody to all three serotypes of poliovirus, and at least 99% are immune to poliovirus following three doses.[4]

Subsequently, Albert Sabin developed an oral polio vaccine (OPV) using live but weakened (attenuated) virus, produced by the repeated passage of the virus through non-human cells at sub-physiological temperatures.[63] Human trials of Sabin's vaccine began in 1957 and it was licensed in 1962.[64] The attenuated poliovirus in the Sabin vaccine replicates very efficiently in the gut, the primary site of wild poliovirus infection and replication, but the vaccine strain is unable to replicate efficiently within nervous system tissue.[65] A single dose of oral polio vaccine produces immunity to all three poliovirus serotypes in approximately 50% of recipients. Three doses of live-attenuated OPV produce protective antibody to all three poliovirus types in more than 95% of recipients.[4]

Because OPV is inexpensive, easy to administer, and produces excellent immunity in the intestine, (which helps prevent infection with wild virus in areas where it is endemic) it has been the vaccine of choice for controlling poliomyelitis in many countries.[66] On very rare occasions (about 1 case per 750,000 vaccine recipients) the attenuated virus in OPV reverts into a form that can paralyze.[13] Most industrialized countries have switched to IPV, which cannot revert, either as the sole vaccine against poliomyelitis or in combination with oral polio vaccine.[67]

Eradication Edit

Main article: Poliomyelitis eradication

Following the widespread use of poliovirus vaccine in the mid-1950s, the incidence of poliomyelitis declined dramatically in many industrialized countries. A global effort to eradicate polio began in 1988, led by the World Health Organization, UNICEF, and The Rotary Foundation.[68] These efforts have reduced the number of annual diagnosed cases by 99%; from an estimated 350,000 cases in 1988 to fewer than 2,000 cases in 2006.[69] Should eradication be successful it will represent only the second time mankind has ever completely eliminated a disease. The first such disease was smallpox, which was officially eradicated in 1979.[70] A number of eradication milestones have already been reached, and several regions of the world have been certified polio-free. The Americas were declared polio-free in 1994.[71] In 2000 polio was officially eradicated in 36 Western Pacific countries, including China and Australia.[72][73] Europe was declared polio-free in 2002.[74] Today, polio remains endemic in only four countries: Nigeria, India, Pakistan, and Afghanistan.[69]

Much of this work was documented by Brazilian photographer Sebastião Salgado, as a UNICEF Goodwill Ambassador, in the book The End of Polio: Global Effort to End a Disease.[75]

History Edit

Main article: History of poliomyelitis
File:Polio Egyptian Stele.jpg

The effects of polio have been known since prehistory; Egyptian paintings and carvings depict otherwise healthy people with withered limbs, and children walking with canes at a young age.[5] The first clinical description was provided by the British physician Michael Underwood in 1789, where he refers to polio as "a debility of the lower extremities".[76] The work of physicians Jakob Heine in 1840 and Karl Oskar Medin in 1890 led to it being known as Heine-Medin disease.[77] The disease was later called infantile paralysis, based on its propensity to affect children.

Before the 20th century, polio infections were rarely seen in infants before six months of age, most cases occurring in children six months to four years of age.[78] Poorer sanitation of the time resulted in a constant exposure to the virus, which enhanced a natural immunity within the population. In developed countries during the late 19th and early 20th centuries, improvements were made in community sanitation, including better sewage disposal and clean water supplies. These changes drastically increased the proportion of children and adults at risk of paralytic polio infection, by reducing childhood exposure and immunity to the disease.

Small localized paralytic polio epidemics began to appear in Europe and the United States around 1900.[6] Outbreaks reached pandemic proportions in Europe, North America, Australia, and New Zealand during the first half of the 20th century. By 1950 the peak age incidence of paralytic poliomyelitis in the United States had shifted from infants to children aged five to nine years, when the risk of paralysis is greater; about one-third of the cases were reported in persons over 15 years of age.[79] Accordingly, the rate of paralysis and death due to polio infection also increased during this time.[6] In the United States, the 1952 polio epidemic became the worst outbreak in the nation's history. Of nearly 58,000 cases reported that year 3,145 died and 21,269 were left with mild to disabling paralysis.[80]

The polio epidemics changed not only the lives of those who survived them, but also affected profound cultural changes; spurring grassroots fund-raising campaigns that would revolutionize medical philanthropy, and giving rise to the modern field of rehabilitation therapy. As one of the largest disabled groups in the world polio survivors also helped to advance the modern disability rights movement through campaigns for the social and civil rights of the disabled. The World Health Organization estimates that there are 10 to 20 million polio survivors worldwide.[81] In 1977 there were 254,000 persons living in the United States who had been paralyzed by polio.[82] According to doctors and local polio support groups, some 40,000 polio survivors with varying degrees of paralysis live in Germany, 30,000 in Japan, 24,000 in France, 16,000 in Australia, 12,000 in Canada and 12,000 in the United Kingdom.[81] Many notable individuals have survived polio and often credit the prolonged immobility and residual paralysis associated with polio as a driving force in their lives and careers.[83]

The disease was very well publicized during the polio epidemics of the 1950s, with extensive media coverage of any scientific advancements that might lead to a cure. Thus, the scientists working on polio became some of the most famous of the century. Fifteen scientists and two laymen who made important contributions to the knowledge and treatment of poliomyelitis are honored by the Polio Hall of Fame at the Roosevelt Warm Springs Institute for Rehabilitation in Warm Springs, Georgia, USA.

See alsoEdit

References Edit

  1. 1.0 1.1 Cohen JI (2004). "Chapter 175: Enteroviruses and Reoviruses" Kasper DL, Braunwald E, Fauci AS, et al (eds.) Harrison's Principles of Internal Medicine, 16th ed., 1144, McGraw-Hill Professional.
  2. 2.0 2.1 2.2 2.3 Chamberlin SL, Narins B (eds.) (2005). The Gale Encyclopedia of Neurological Disorders, 1859–70, Detroit: Thomson Gale.
  3. 3.0 3.1 3.2 3.3 Ryan KJ, Ray CG (eds.) (2004). "Enteroviruses" Sherris Medical Microbiology, 4th ed., 535–7, McGraw Hill. ISBN 0-8385-8529-9.
  4. 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 Atkinson W, Hamborsky J, McIntyre L, Wolfe S (eds.) (2007). "Poliomyelitis" Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book) (PDF), 10th ed., 101–14, Washington DC: Public Health Foundation.
  5. 5.0 5.1 5.2 Paul JR (1971). A History of Poliomyelitis, 16–18, New Haven, Conn: Yale University Press.
  6. 6.0 6.1 6.2 Trevelyan B, Smallman-Raynor M, Cliff A (2005). The Spatial Dynamics of Poliomyelitis in the United States: From Epidemic Emergence to Vaccine-Induced Retreat, 1910–1971. Ann Assoc Am Geogr 95 (2): 269–293.
  7. Aylward R (2006). Eradicating polio: today's challenges and tomorrow's legacy. Ann Trop Med Parasitol 100 (5–6): 401–13.
  8. Heymann D (2006). Global polio eradication initiative. Bull. World Health Organ. 84 (8): 595.
  9. Katz, Samuel L.; Gershon, Anne A.; Krugman, Saul; Hotez, Peter J. (2004). Krugman's infectious diseases of children, 81–97, St. Louis: Mosby.
  10. 10.0 10.1 10.2 Ohri, Linda K., Jonathan G. Marquess (1999). Polio: Will We Soon Vanquish an Old Enemy?. Drug Benefit Trends 11 (6): 41–54. (Available free on Medscape; registration required.)
  11. 11.0 11.1 11.2 11.3 11.4 11.5 Kew O, Sutter R, de Gourville E, Dowdle W, Pallansch M (2005). Vaccine-derived polioviruses and the endgame strategy for global polio eradication. Annu Rev Microbiol 59: 587–635.
  12. 12.0 12.1 Parker SP (ed.) (1998). McGraw-Hill Concise Encyclopedia of Science & Technology, New York: McGraw-Hill.
  13. 13.0 13.1 13.2 Racaniello V (2006). One hundred years of poliovirus pathogenesis. Virology 344 (1): 9–16.
  14. Davis L, Bodian D, Price D, Butler I, Vickers J (1977). Chronic progressive poliomyelitis secondary to vaccination of an immunodeficient child. N Engl J Med 297 (5): 241–5.
  15. Chandra R (1975). Reduced secretory antibody response to live attenuated measles and poliovirus vaccines in malnourished children. Br Med J 2 (5971): 583–5.
  16. Miller A (1952). Incidence of poliomyelitis; the effect of tonsillectomy and other operations on the nose and throat. Calif Med 77 (1): 19–21.
  17. Horstmann D (1950). Acute poliomyelitis relation of physical activity at the time of onset to the course of the disease. J Am Med Assoc 142 (4): 236–41.
  18. Gromeier M, Wimmer E (1998). Mechanism of injury-provoked poliomyelitis. J. Virol. 72 (6): 5056–60.
  19. Evans C (1960). Factors influencing the occurrence of illness during naturally acquired poliomyelitis virus infections. Bacteriol Rev 24 (4): 341–52.
  20. Joint Committee on Vaccination and Immunisation (Salisbury A, Ramsay M, Noakes K (eds.) (2006). Chapter 26:Poliomyelitis. in: Immunisation Against Infectious Disease, 2006 (PDF), 313–29, Edinburgh: Stationery Office.
  21. Sauerbrei A, Groh A, Bischoff A, Prager J, Wutzler P (2002). Antibodies against vaccine-preventable diseases in pregnant women and their offspring in the eastern part of Germany. Med Microbiol Immunol 190 (4): 167–72.
  22. Falconer M, Bollenbach E (2000). Late functional loss in nonparalytic polio. American journal of physical medicine & rehabilitation / Association of Academic Physiatrists 79 (1): 19–23.
  23. 23.0 23.1 23.2 Leboeuf C (1992). The late effects of Polio: Information For Health Care Providers. (PDF), Commonwealth Department of Community Services and Health. URL accessed 2007-11-10.
  24. 24.0 24.1 24.2 24.3 24.4 Frauenthal HWA, Manning JVV (1914). Manual of infantile paralysis, with modern methods of treatment., 79–101, Philadelphia Davis.
  25. Wood, Lawrence D. H.; Hall, Jesse B.; Schmidt, Gregory D. (2005). Principles of Critical Care, Third Edition, 870, McGraw-Hill Professional.
  26. He Y, Mueller S, Chipman P, et al (2003). Complexes of poliovirus serotypes with their common cellular receptor, CD155. J Virol 77 (8): 4827–35.
  27. 27.0 27.1 27.2 Yin-Murphy M, Almond JW (1996). "Picornaviruses: The Enteroviruses: Polioviruses" Baron's Medical Microbiology (Baron S et al, eds.), 4th ed., Univ of Texas Medical Branch.
  28. Todar K. Polio. Ken Todar's Microbial World. University of Wisconsin - Madison. URL accessed on 2007-04-23.
  29. Sabin A (1956). Pathogenesis of poliomyelitis; reappraisal in the light of new data. Science 123 (3209): 1151–7.
  30. 30.0 30.1 30.2 30.3 30.4 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.
  31. 31.0 31.1 31.2 Silverstein A, Silverstein V, Nunn LS (2001). Polio, Berkeley Heights, NJ: Enslow Publishers.
  32. 32.0 32.1 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.
  33. Young GR (1989). Occupational therapy and the postpolio syndrome. The American journal of occupational therapy 43 (2): 97–103.
  34. Nathanson N, Martin J (1979). The epidemiology of poliomyelitis: enigmas surrounding its appearance, epidemicity, and disappearance. Am J Epidemiol 110 (6): 672–92.
  35. 35.0 35.1 35.2 Cono J, Alexander LN (2002). "Chapter 10, Poliomyelitis." Vaccine Preventable Disease Surveillance Manual (PDF), 3rd ed., p. 10–1, Centers for Disease Control and Prevention.
  36. 36.0 36.1 36.2 (2005) Professional Guide to Diseases (Professional Guide Series), 243–5, Hagerstown, MD: Lippincott Williams & Wilkins.
  37. 37.0 37.1 37.2 37.3 Hoyt, William Graves; Miller, Neil; Walsh, Frank (2005). Walsh and Hoyt's clinical neuro-ophthalmology, 3264–65, Hagerstown, MD: Lippincott Williams & Wilkins.
  38. (1997)Case definitions for infectious conditions under public health surveillance. Centers for Disease Control and Prevention. Morbidity and mortality weekly report 46 (RR-10): 26-7.
  39. Chezzi C (1996). Rapid diagnosis of poliovirus infection by PCR amplification. J Clin Microbiol 34 (7): 1722–5.
  40. Gawande A (2004-01-12). The mop-up: eradicating polio from the planet, one child at a time: 34–40.
  41. 41.0 41.1 41.2 41.3 Neumann D (2004). Polio: its impact on the people of the United States and the emerging profession of physical therapy. The Journal of orthopaedic and sports physical therapy 34 (8): 479–92. Reproduced online with permission by Post-Polio Health International; retrieved on 2007-11-10.
  42. Cuccurullo SJ (2004). Physical Medicine and Rehabilitation Board Review, Demos Medical Publishing.
  43. 43.0 43.1 Goldberg A (2002). Noninvasive mechanical ventilation at home: building upon the tradition. Chest 121 (2): 321–4. PMID 11834636.
  44. Miller AH, Buck LS (1950). Tracheotomy in bulbar poliomyelitis. California medicine 72 (1): 34–6.
  45. Wackers, G. (1994). "Constructivist Medicine" (web). PhD-thesis. Maastricht: Universitaire Pers Maastricht. Retrieved on 2008-01-04.
  46. 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.
  47. 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.
  48. 48.0 48.1 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.
  49. Trojan DA, Cashman NR (2005). Post-poliomyelitis syndrome. Muscle Nerve 31 (1): 6–19.
  50. 50.0 50.1 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.
  51. 51.0 51.1 Sanofi Pasteur. Poliomyelitis virus (picornavirus, enterovirus), after-effects of the polio, paralysis, deformations. Polio Eradication. URL accessed on 2007-07-31.
  52. 52.0 52.1 Mayo Clinic Staff. Polio: Complications. Mayo Foundation for Medical Education and Research (MFMER). URL accessed on 2007-02-26.
  53. 53.0 53.1 Trojan D, Cashman N (2005). Post-poliomyelitis syndrome. Muscle Nerve 31 (1): 6–19.
  54. Ramlow J, Alexander M, LaPorte R, Kaufmann C, Kuller L (1992). Epidemiology of the post-polio syndrome. Am. J. Epidemiol. 136 (7): 769–86.
  55. Lin K, Lim Y (2005). Post-poliomyelitis syndrome: case report and review of the literature. Ann Acad Med Singapore 34 (7): 447–9.
  56. Daniel, Thomas M.; Robbins, Frederick C. (1997). Polio, 8–10, Rochester, N.Y., USA: University of Rochester Press.
  57. Oppewal S (1997). Sister Elizabeth Kenny, an Australian nurse, and treatment of poliomyelitis victims. Image J Nurs Sch 29 (1): 83-7.
  58. 58.0 58.1 Hammon W (1955). Passive immunization against poliomyelitis. Monogr Ser World Health Organ 26: 357–70.
  59. Hammon W, Coriell L, Ludwig E, et al (1954). Evaluation of Red Cross gamma globulin as a prophylactic agent for poliomyelitis. 5. Reanalysis of results based on laboratory-confirmed cases. J Am Med Assoc 156 (1): 21–7.
  60. Rinaldo C (2005). Passive immunization against poliomyelitis: the Hammon gamma globulin field trials, 1951–1953. Am J Public Health 95 (5): 790–9.
  61. Fine P, Carneiro I (1999). Transmissibility and persistence of oral polio vaccine viruses: implications for the global poliomyelitis eradication initiative. Am J Epidemiol 150 (10): 1001–21.
  62. includeonly>Spice B. "Tireless polio research effort bears fruit and indignation", The Salk vaccine: 50 years later- second of two parts, Pittsburgh Post-Gazette, April 04, 2005. Retrieved on 2007-04-30.
  63. Sabin AB, Boulger LR (1973). History of Sabin attenuated poliovirus oral live vaccine strains. J Biol Stand 1: 115–8.
  64. (1998). A Science Odyssey: People and Discoveries. PBS. URL accessed on 2007-08-14.
  65. Sabin A, Ramos-Alvarez M, Alvarez-Amezquita J, et al (1960). Live, orally given poliovirus vaccine. Effects of rapid mass immunization on population under conditions of massive enteric infection with other viruses. JAMA 173: 1521–6.
  66. (1997)Poliomyelitis prevention: recommendations for use of inactivated poliovirus vaccine and live oral poliovirus vaccine. American Academy of Pediatrics Committee on Infectious Diseases. Pediatrics 99 (2): 300–5.
  67. WHO: Vaccines for routine use. International travel and health. URL accessed on 2007-11-08.
  68. Mastny, Lisa Eradicating Polio: A Model for International Cooperation. Worldwatch Institute. URL accessed on 2007-02-02.
  69. 69.0 69.1 (2006) Update on vaccine-derived polioviruses. MMWR Morb Mortal Wkly Rep 55 (40): 1093–7.
  70. Smallpox. WHO Factsheet. URL accessed on 2006-09-23.
  71. (1994)International Notes Certification of Poliomyelitis Eradication—the Americas, 1994. MMWR Morb Mortal Wkly Rep 43 (39): 720–2.
  72. (2001)General News. Major Milestone reached in Global Polio Eradication: Western Pacific Region is certified Polio-Free. Health Educ Res 16 (1): p. 109.
  73. D'Souza R, Kennett M, Watson C (2002). Australia declared polio free. Commun Dis Intell 26 (2): 253–60.
  74. European Region of the World Health Organization (2002-06-21). Europe achieves historic milestone as Region is declared polio-free. Press release. Retrieved on 2007-11-07.
  75. Centers for Disease Control and Prevention (August 24 2007). The End of Polio: Photographs of Sebastião Salgado Opens to Public. Press release. Retrieved on 2007-11-27.
  76. Underwood, Michael (1793). Debility of the lower extremities. In: A treatise on the diseases [sic] of children, with general directions for the management of infants from the birth (1789) (fee required), pp. 254–6, Philadelphia: Printed by T. Dobson, no. 41, South Second-Street. URL accessed 2007-02-23.
  77. Pearce J (2005). Poliomyelitis (Heine-Medin disease). J Neurol Neurosurg Psychiatry 76 (1): 128.
  78. Robertson S. Module 6: Poliomyelitis. (PDF) The Immunological Basis for Immunization Series. World Health Organization. Geneva, Switzerland.. URL accessed on 2007-05-08.
  79. Melnick JL (1990). Poliomyelitis. In: Tropical and Geographical Medicine, 2nd ed., p. 558–76, McGraw-Hill.
  80. Zamula E (1991). A New Challenge for Former Polio Patients. FDA Consumer 25 (5): 21–5.
  81. 81.0 81.1 After Effects of Polio Can Harm Survivors 40 Years Later. March of Dimes. URL accessed on 2007-08-07.
  82. Frick NM, Bruno RL (1986). Post-polio sequelae: physiological and psychological overview. Rehabilitation literature 47 (5–6): 106–11.
  83. Richard L. Bruno (2002). The Polio Paradox: Understanding and Treating "Post-Polio Syndrome" and Chronic Fatigue, 105-6, New York: Warner Books.

Further reading Edit

  • Abaffy, M. (1971). Psychological problems on a ward for patients with severe respiratory difficulties: Magyar Pszichologiai Szemle Vol 28(4) 1971, 538-546.
  • Ahlstrom, G., & Karlsson, U. (2000). Disability and quality of life in individuals with postpolio syndrome: Disability and Rehabilitation: An International, Multidisciplinary Journal Vol 22(9) Jun 2000, 416-422.
  • Allen, G. M., Gandevia, S. C., Neering, I. R., Hickie, I., & et al. (1994). Muscle performance, voluntary activation and perceived effort in normal subjects and patients with prior poliomyelitis: Brain: A Journal of Neurology Vol 117(4) Aug 1994, 661-670.
  • Amaral, M. (1988). Does the early physical handicap protect against suicide? : Jornal Brasileiro de Psiquiatria Vol 37(2) Mar-Apr 1988, 67-69.
  • Becker, H., & Stuifbergen, A. (2004). What Makes It So Hard? Barriers to Health Promotion Experienced by People With Multiple Sclerosis and Polio: Family & Community Health Vol 27(1) Jan-Mar 2004, 75-85.
  • Bouza, C., Munoz, A., & Amate, J. M. (2005). Postpolio syndrome: A challenge to the health-care system: Health Policy Vol 71(1) Jan 2005, 97-106.
  • Brand, N. (1964). Taste response and poliomyelitis: Annals of Human Genetics 27(3) 1964, 233-240.
  • Bruno, R. L., Frick, N. M., Creange, S., Zimmerman, J. R., & Lewis, T. (1996). Polioencephalitis and the brain fatigue generator model of post-viral fatigue syndromes: Journal of Chronic Fatigue Syndrome Vol 2(2-3) 1996, 5-27.
  • Buchanan, B. R. (1992). Physical, emotional, and social adaptation to the late effects of poliomyelitis: Dissertation Abstracts International.
  • Cahill, M., Chant, D., Welham, J., & McGrath, J. (2002). No significant association between prenatal exposure to poliovirus epidemics and psychosis: Australian and New Zealand Journal of Psychiatry Vol 36(3) Jun 2002, 373-375.
  • Cheng-Ping, C. (1965). A comparison of intellectual and personality characteristics of poliomyelitis and normal children in an orphanage environment: Acta Psychologica Taiwanica No 7 1965, 17-33.
  • Chiang, T. T.-K. (1996). The relationship between grief and depression in a group of polio survivors. Dissertation Abstracts International: Section B: The Sciences and Engineering.
  • Ciotti, F., Papperini, R., & Bascucci, S. (1997). Heterochrony of mental retardation of subjects with Down's syndrome and infantile cerebral paralysis: Eta Evolutiva No 56 Feb 1997, 85-93.
  • Clark, K., Dinsmore, S., Grafman, J., & Dalaka, M. C. (1994). A personality profile of patients diagnosed with post-polio syndrome: Neurology Vol 44(10) Oct 1994, 1809-1811.
  • Colin, D., Frischmann-Rosner, M., Liard, J., & Magne, A. (1973). Study of the level of global mental development and of perceptual, memory and reasoning capacities through the use of the Snijders-Oomen Performance Scale with motor handicapped children: Bulletin de Psychologie Vol 27(5-9) 1973-1974, 346-361.
  • Creange, S. J. (1999). Effect of blood glucose level on mood states and attention. Dissertation Abstracts International: Section B: The Sciences and Engineering.
  • Dietvorst, T. F., & Eulberg, M. K. (1986). Self-regulation treatment of post-polio cold limb: Biofeedback & Self Regulation Vol 11(2) Jun 1986, 157-161.
  • Eagles, J. M. (1992). Are polioviruses a cause of schizophrenia? : British Journal of Psychiatry Vol 160 May 1992, 598-600.
  • Elrod, L. M., Jabben, M., Oswald, G., & Szirony, G. M. (2005). Vocational implications of post-polio syndrome: Work: Journal of Prevention, Assessment & Rehabilitation Vol 25(2) 2005, 155-161.
  • Epee-Bounya, A., Gitterman, B. A., & Moon, R. Y. (2001). Parental opinions regarding poliomyelitis immunizations: Clinical Pediatrics Vol 40(8) Aug 2001, 435-440.
  • Eren, I., Inanli, I. C., & Kutluhan, S. (2006). The relationship of psychiatric sign with quality of life in the patients with the polio sequel: Anadolu Psikiyatri Dergisi Vol 7(4) Dec 2006, 223-231.
  • Farbu, E., & Gilhus, N. E. (2002). Education, occupation, and perception of health amongst previous polio patients compared to their siblings: European Journal of Neurology Vol 9(3) May 2002, 233-241.
  • Foster, L. W., Berkman, B., Wellen, M., & Schuster, N. (1993). Postpolio survivors: Needs for and access to social and health care services: Health & Social Work Vol 18(2) May 1993, 139-148.
  • Freidenberg, D. L., Freeman, D., Huber, S. J., Perry, J., & et al. (1989). Postpoliomyelitis syndrome: Assessment of behavioral features: Neuropsychiatry, Neuropsychology, & Behavioral Neurology Vol 2(4) Win 1989, 272-281.
  • Frick, N. M., & Bruno, R. L. (1986). Post-polio sequelae: Physiological and psychological overview: Rehabilitation Literature Vol 47(5-6) May-Jun 1986, 106-111.
  • Gordon, P. A., Feldman, D., Griffing, G., & Bowman, S. L. (2002). A new loss from an old problem: How counselors can assist persons with postpolio syndrome: Journal of Loss & Trauma Vol 7(4) Oct-Dec 2002, 239-249.
  • Hammond, D. C. (1991). Hypnosis for postpolio syndrome & Type-A behavior: American Journal of Clinical Hypnosis Vol 34(1) Jul 1991, 38-45.
  • Hansson, B., & Ahlstrom, G. (1999). Coping with chronic illness: A qualitative study of coping with postpolio syndrome: International Journal of Nursing Studies Vol 36(3) Jun 1999, 255-262.
  • Harris, D. B. (1950). Behavior ratings of post-polio cases: Journal of Consulting Psychology Vol 14(5) Oct 1950, 381-385.
  • Harrison, T. C., & Stuifbergen, A. (2005). A Hermeneutic Phenomenological Analysis of Aging with a Childhood Onset Disability: Health Care for Women International Vol 26(8) Sep 2005, 731-747.
  • Hazendonk, K. M., & Crowe, S. F. (2000). A neuropsychological study of the postpolio syndrome: Support for depression without neuropsychological impairment: Neuropsychiatry, Neuropsychology, & Behavioral Neurology Vol 13(2) Apr 2000, 112-118.
  • Hixon, T. J., Putnam, A. H., & Sharp, J. T. (1983). Speech production with flaccid paralysis of the rib cage, diaphragm, and abdomen: Journal of Speech & Hearing Disorders Vol 48(3) Aug 1983, 315-327.
  • Hollingsworth, L., Didelot, M. J., & Levington, C. (2002). Post-polio syndrome: Psychological adjustment to disability: Issues in Mental Health Nursing Vol 23(2) Mar 2002, 135-156.
  • Hunter, J. (1993). A child of a lesser god: Psychoanalytic Psychotherapy Vol 7(1) 1993, 39-51.
  • Johnson, F. A. (1972). Figure drawings in subjects recovering from poliomyelitis: Psychosomatic Medicine Vol 34(1) Jan 1972, 19-29.
  • Johnson, F. A., & Greenberg, R. P. (1978). Quality of drawing as a factor in the interpretation of figure drawings: Journal of Personality Assessment Vol 42(5) Oct 1978, 489-495.
  • Jonsson, A.-L. T., Moller, A., & Grimby, G. (1999). Managing occupations in everyday life to achieve adaptation: American Journal of Occupational Therapy Vol 53(4) Jul-Aug 1999, 353-362.
  • Kalpakjian, C. Z., & Lequerica, A. (2006). Quality of life and menopause in women with physical disabilities: Journal of Women's Health Vol 15(9) Nov 2006, 1014-1027.
  • Kalpakjian, C. Z., Quint, E. H., Tate, D. G., Roller, S., & Toussaint, L. L. (2007). Menopause characteristics of women with physical disabilities from poliomyelitis: Maturitas Vol 56(2) Feb 2007, 161-172.
  • Kalpakjian, C. Z., Riley, B. B., Quint, E. H., & Tate, D. G. (2004). Hormone replacement therapy and health behavior in postmenopausal polio survivors: Maturitas Vol 48(4) Aug 2004, 398-410.
  • Kemp, B. J., & Krause, J. S. (1999). Depression and life satisfaction among people ageing with post-polio and spinal cord injury: Disability and Rehabilitation: An International, Multidisciplinary Journal Vol 21(5-6) May-Jun 1999, 241-249.
  • Kirichenko, E. I., & Kalizhnyuk, S. S. (1983). Role of biological and social factors in the mechanisms of pathological formation of personality in infantile cerebral paralysis: Zhurnal Nevropatologii i Psikhiatrii imeni S S Korsakova Vol 83(9) 1983, 1390-1394.
  • Kling, C., Persson, A., & Gardulf, A. (2002). The ADL ability and use of technical aids in persons with late effects of polio: American Journal of Occupational Therapy Vol 56(4) Jul-Aug 2002, 457-461.
  • Koh, E. S. C., Williams, A. J., & Povlsen, B. (2002). Upper-limb pain in long-term poliomyelitis: QJM: An International Journal of Medicine Vol 95(6) Jun 2002, 389-395.
  • Kolasa, M. S., Desai, S. N., Bisgard, K. M., Dibling, K., & Prevots, D. R. (2000). Impact of the sequential poliovirus immunization schedule: A demonstration project: American Journal of Preventive Medicine Vol 18(2) Feb 2000, 140-145.
  • Kuehn, A. F., & Winters, R. K. V. (1994). A study of symptom distress, health locus of control, and coping resources of aging post-polio survivors: IMAGE: Journal of Nursing Scholarship Vol 26(4) Win 1994, 325-331.
  • Lewis, A. H. (1992). Life histories of adult survivors of childhood polio: Dissertation Abstracts International.
  • Liston, D. (1965). Housekeeping on wheels: Today's Health 43(5) 1965, 62-66.
  • Lo, S.-l. (1991). The effects of succeeding and failing experiences on problem solving: A comparison of people with disabilities and without disabilities: Japanese Journal of Educational Psychology Vol 39(4) Dec 1991, 392-399.
  • Loetscher, T., Regard, M., & Brugger, P. (2006). Misoplegia: A review of the literature and a case without hemiplegia: Journal of Neurology, Neurosurgery & Psychiatry Vol 77(9) Sep 2006, 1099-1100.
  • Long, E. R., Gemski, L., & DeLeon, P. H. (1999). Rotary International--A private partner in a public health battle: A model for psychology? : Professional Psychology: Research and Practice Vol 30(1) Feb 1999, 3-4.
  • Lowman, C. L., & Seidenfeld, M. A. (1947). A preliminary report of the psychosocial effects of poliomyelitis: Journal of Consulting Psychology Vol 11(1) Jan 1947, 30-37.
  • Mastiukova, E. M. (1983). Speech comprehension peculiarities in children with cerebral palsy: Defektologiya No 3 1983, 3-9.
  • McNeal, D. R., Somerville, N. J., & Wilson, D. J. (1999). Work problems and accommodations reported by persons who are postpolio or have a spinal cord injury: Assistive Technology Vol 11(2) 1999, 137-157.
  • Miller, N. E. (1974). Applications of psychophysiological research: Rehabilitation Psychology Vol 21(4) 1974, 137-141.
  • Morgoulis, J., & Tournay, A. (1963). Poliomyelitis and the body schema: Enfance No 4-5 1963, 277-291.
  • Myers, N. A. (2004). The analysis of a biopsychosocial model to assess polio survivors' likelihood of diagnosis with post-polio syndrome. Dissertation Abstracts International Section A: Humanities and Social Sciences.
  • No authorship, i. (1949). Review of Poliomyelitis: Journal of Consulting Psychology Vol 13(5) Oct 1949, 384.
  • Nollet, F., Ivanyi, B., Beelen, A., de Haan, R. J., Lankhorst, G. J., & de Visser, M. (2002). Perceived health in a population based sample of victims of the 1956 polio epidemic in the Netherlands: Journal of Neurology, Neurosurgery & Psychiatry Vol 73(6) Dec 2002, 695-700.
  • Obadare, E. (2005). A crisis of trust: History, politics, religion and the polio controversy in Northern Nigeria: Patterns of Prejudice Vol 39(3) Sep 2005, 265-284.
  • On, A. Y., Oncu, J., Uludag, B., & Ertekin, C. (2005). Effects of lamotrigine on the symptoms and life qualities of patients with post polio syndrome: A randomized, controlled study: NeuroRehabilitation Vol 20(4) 2005, 245-251.
  • Outland, P., & Coonerty, S. (1995). Polio survivors: Self concept and body image: Journal of Applied Rehabilitation Counseling Vol 26(3) Fal 1995, 23-25.
  • Outland, P. M. (1991). Polio survivors: Self-concept and body image: Dissertation Abstracts International.
  • Paul, Y., & Dawson, A. (2006). Some ethical issues arising from polio eradication programmes in India. Malden, MA: Blackwell Publishing.
  • Rekand, T., & Farbu, E. (2005). Lifestyle and Late Symptoms after Poliomyelitis: A Review. Hauppauge, NY: Nova Science Publishers.
  • Rekand, T., Korv, J., Farbu, E., Roose, M., Gilhus, N. E., Langeland, N., et al. (2004). Lifestyle and late effects after poliomyelitis. A risk factor study of two populations: Acta Neurologica Scandinavica Vol 109(2) Feb 2004, 120-125.
  • Renne, E. (2006). Perspectives on polio and immunization in Northern Nigeria: Social Science & Medicine Vol 63(7) Oct 2006, 1857-1869.
  • Rodriguez, R. M. (2001). Explanatory style and health among polio survivors. Dissertation Abstracts International: Section B: The Sciences and Engineering.
  • Samsonova, L. N. (1982). Condition of manual motor function in cerebral-palsied students as judged from orthopaedic data: Defektologiya No 2 1982, 59-64.
  • Sanchez, D. I. (1997). Stress, coping, and psychological adaptation of individuals with post-polio sequelae. Dissertation Abstracts International: Section B: The Sciences and Engineering.
  • Sangorrin, J. (1977). The "Corporal Scheme" and motor deficiency: Anuario de Psicologia No 16 1977, 95-111.
  • Schanke, A.-K. (1997). Psychological distress, social support and coping behaviour among polio survivors: A 5-year perspective on 63 polio patients: Disability and Rehabilitation: An International, Multidisciplinary Journal Vol 19(3) Mar 1997, 108-116.
  • Seidenfeld, M. A. (1947). Psychological elements in work interference from physical disability: Journal of Consulting Psychology Vol 11(6) Nov 1947, 326-333.
  • Seidenfeld, M. A. (1955). Psychological implications of breathing difficulties in poliomyelitis: American Journal of Orthopsychiatry 25 1955, 788-801.
  • Silver, J., & Wilson, D. (2007). Polio voices: An oral history from the American polio epidemics and worldwide eradication efforts. Westport, CT: Praeger Publishers/Greenwood Publishing Group.
  • Silverstein, A. B., & Robinson, H. A. (1956). The representation of orthopedic disability in children's figure drawings: Journal of Consulting Psychology Vol 20(5) Oct 1956, 333-341.
  • Smith, D. W. (1992). A study of power and spirituality in polio survivors using the nursing model of Martha E. Rogers: Dissertation Abstracts International.
  • Sternburg, L. L. (1982). Some adaptive compensations in speech control achieved after respiratory paralysis: Four cases: Dissertation Abstracts International.
  • Stuifbergen, A. K., Seraphine, A., Harrison, T., & Adachi, E. (2005). An explanatory model of health promotion and quality of life for persons with post-polio syndrome: Social Science & Medicine Vol 60(2) Jan 2005, 383-393.
  • Suvisaari, J., Haukka, J., Tanskanen, A., Hovi, T., & Lonnqvist, J. (1999). Association between prenatal exposure to poliovirus infection and adult schizophrenia: American Journal of Psychiatry Vol 156(7) Jul 1999, 1100-1102.
  • Tan, U. (2007). A Wrist-Walker Exhibiting no "Uner tan Sydnrome": A theory for possible mechanisms of human devolution toward the atavistic walking patterns: International Journal of Neuroscience Vol 117(1) Jan 2007, 147-156.
  • Thoren-Jonsson, A.-L. (2001). Coming to terms with the shift in one's capabilities: A study of the adaptive process in persons with poliomyelitis sequelae: Disability and Rehabilitation: An International, Multidisciplinary Journal Vol 23(8) 2001, 341-351.
  • Tollen, A. (1998). Assessment instrument for problem-focused coping: Reliability test of APC. Part 1: Scandinavian Journal of Caring Sciences Vol 12(1) 1998, 18-24.
  • Trojan, D. A., Collet, J. P., Shapiro, S., Jubelt, B., Miller, R. G., Agre, J. C., et al. (1999). A multicenter, randomized, double-blinded trial of pyridostigmine in postpolio syndrome: Neurology Vol 53(6) Oct 1999, 1225-1233.
  • Tyroler, H. A., Johnson, A. L., & Fulton, J. T. (1965). Patterns of preventive health behavior in populations: I. Acceptance of oral poliomyelitis vaccine within families: Journal of Health & Human Behavior 6(3) 1965, 128-140.
  • Umble, K. E., Cervero, R. M., Yang, B., & Atkinson, W. L. (2000). Effects of traditional classroom and distance continuing education: A theory-driven evaluation of a vaccine-preventable diseases course: American Journal of Public Health Vol 90(8) Aug 2000, 1218-1224.
  • van Kraayenoord, C. (2005). The "Extra Benefits" of Polio Eradication: International Journal of Disability, Development and Education Vol 52(3) Sep 2005, 169-174.
  • Vasconcelos, O. M., Prokhorenko, O. A., Salajegheh, M. K., Kelley, K. F., Livornese, K., Olsen, C. H., et al. (2007). Modafinil for treatment of fatigue in post-polio syndrome: A randomized controlled trial: Neurology Vol 68(20) May 2007, 1680-1686.
  • Ville, I., & Paicheler, H. (2000). Descriptions of self in a context of limited activity: Cahiers Internationaux de Psychologie Sociale No 445 Mar 2000, 14-28.
  • Ware, K. E., Fisher, S., & Cleveland, S. (1957). Body-image boundaries and adjustment to poliomyelitis: The Journal of Abnormal and Social Psychology Vol 55(1) Jul 1957, 88-93.
  • Watts, M. J. (1991). Post-polio syndrome: The role of Type A behavior in psychosocial adaptation: Dissertation Abstracts International.
  • Weissenborn, I. (2004). Post-Polio Syndrome: A Disease of the Body as Indication for an Analytical Psychotherapy: Analytische Psychologie Vol 35(136) Jun 2004, 182-204.
  • Wendland, L. V. (1952). Employment prognosis of the post-poliomyelitic: Journal of Applied Psychology Vol 36(5) Oct 1952, 328-332.
  • White, C., Brock, K., Kennedy, G., & Joubert, L. (2005). Data-mining polio service needs in Victoria, Australia: Implications for the multi-disciplinary team: Journal of Social Work Research and Evaluation Vol 6(2) Fal-Win 2005, 177-184.
  • Williams, C. G. (1991). Health conceptions and practices of individuals who have had poliomyelitis: Dissertation Abstracts International.
  • Yekutiel, M., Jariwala, M., & Stretch, P. (1994). Sensory deficit in the hands of children with cerebral palsy: A new look at assessment and prevalence: Developmental Medicine & Child Neurology Vol 36(7) Jul 1994, 619-624.
  • Young, G. R. (1989). Occupational therapy and the postpolio syndrome: American Journal of Occupational Therapy Vol 43(2) Feb 1989, 97-103.


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