My grandmother had polio when she was little

Q: My grandmother had polio when she was little, but except for some mild weakness in her right leg she had gotten better. The doctors think she is coming down with it again. How can she have gotten polio again here in the U.S.?
A: This sounds like post-polio syndrome (PPS), and that is what I will discuss in today's column.
Poliomyelitis is caused by a virus that is shed in the stool of infected people. Poor sanitary conditions and poor hygiene contribute to its spread. After ingestion, the virus replicates in the nose/throat mucosa and/or the gastrointestinal tract of the patient. It then invades the lymph nodes and possibly spreads to the blood; in some cases it can also invade the neurons in the patient's brain and/or spinal cord.
About 90 percent to 95 percent of those infected with the polio virus have minor non-specific symptoms such as low-grade fevers, malaise, sore throat and/or headache, and these people recover with no problems. Some people also have GI symptoms such as nausea, vomiting and/or abdominal pain, and again typically have a full recovery.
About 1 percent of those infected develop paralytic polio (damage to muscle innervating neurons), causing muscle weakness (most often in one limb or on one side of the body) which can progress to flaccidity and paralysis. About half of these patients recover fully, a quarter have mild residual weakness and about a quarter have severe permanent disability. Overall, the prognosis is better for younger children.
Polio infection is definitively diagnosed by cultures of certain body fluids or blood antibody tests. The only treatment for polio is supportive care, but a 95 percent effective preventative vaccine exists and is routinely given to all children in the U.S. This not only helps prevent infection from the polio virus, but also helps eradicate the disease from the population since polio is only transmitted from person to person by the fecal-oral route discussed above.
From this discussion it should not be surprising that new cases of polio in the U.S. are essentially all contracted outside the country. In fact, worldwide vaccination programs are attempting to eradicate polio completely, as was done for smallpox.
Post-polio syndrome occurs in people years after they have had paralytic polio. One theory as to why PPS occurs is that the partially damaged neurons from the initial infection "wear out." This explains why there is no active viral infection in people with PPS, and why their symptoms are typically fatigue and slowly progressive muscle weakness affecting the same muscles as in the initial infection.
There is no specific test for PPS. In fact, it may be difficult to diagnose since the slow onset and subtlety of initial symptoms may be caused by many other conditions. The criteria to diagnose PPS are:
  • A history of paralytic polio (even if there was an essentially complete recovery)
  • A stable period after the initial infection, which can be decades long
  • Gradual onset of persistent muscle weakness and sometimes muscle atrophy
  • Symptoms that persist for over a year
  • Other possible causes of the symptoms must be ruled out
PPS is actually pretty common in survivors of paralytic polio, affecting a quarter to half of these patients.
The slow progression of the symptoms, and the fact that they occur in a distribution that the patient survived in the past, make the prognosis for PPS good in the sense that it is rarely life threatening. However it can significantly impact the patient's quality of life.
Appropriate exercise to strengthen certain muscles to help offset the weakness from PPS can be beneficial in many patients; to date, no other treatments have been shown to be very effective.
Although new cases of polio are rare in the U.S., there are still about half a million Americans who are survivors of this disease (typically contracted before mass vaccination efforts helped minimize its occurrence) and, hence, are at risk for PPS; worldwide there are many millions of people at risk.
Although there is no known way to prevent PPS, regular exercise to keep muscles fit and strong as well as to stay healthy overall can help minimize the negative impact this condition may have.
Jeff Hersh, Ph.D., M.D., F.A.A.P., F.A.C.P., F.A.A.E.P., can be reached at DrHersh@juno.com.
Clasificación Internacional de Enfermedades Codifico al Síndrome de Post Polio con el Código G14 Síndrome Postpolio   Incluye :  Síndrome postpoliomielítico  Excluyéndolo del código B91Secuelas de poliomielitis

The Polio Crusade

THE POLIO CRUSADE IN AMERICAN EXPERIENCE A GOOD VIDEO THE STORY OF THE POLIO CRUSADE pays tribute to a time when Americans banded together to conquer a terrible disease. The medical breakthrough saved countless lives and had a pervasive impact on American philanthropy that ... Continue reading..http://www.pbs.org/wgbh/americanexperience/polio/

Erradicación de La poliomielitis

Polio Tricisilla Adaptada

March Of Dimes Polio History

Dr. Bruno




A 41-year-old man developed an acute illness at the age of 9 months during which, following a viral illness with headache, he developed severe weakness and wasting of the limbs of the left side. After several months he began to recover, such that he was able to walk at the age of 2 years and later was able to run, although he was never very good at sports. He had stable function until the age of 18 when he began to notice greater than usual difficulty lifting heavy objects. By the age of 25 he was noticing progressive difficulty walking due to weakness of both legs, and he noticed that the right calf had become larger. The symptoms became more noticeable over the course of the next 10 years and ultimately both upper as well as both lower limbs had become noticeably weaker.

On examination there was wasting of the muscles of upper and lower limbs on the left, and massively hypertrophied gastrocnemius, soleus and tensor fascia late on the right. The calf circumference on the right exceeded that on the left by 10 cm (figure1). The right shoulder girdle, triceps, thenar eminence and small muscles of the hand were wasted and there was winging of both scapulae. The right quadriceps was also wasted. The wasted muscles were also weak but the hypertrophied right ankle plantar flexors had normal power. The tendon reflexes were absent in the lower limbs and present in the upper limbs, although the right triceps was reduced. The remainder of the examination was normal.

Figure 1

The patient's legs, showing massive enlargement of the right calf and wasting on the left


What is that nature of the acute illness in infancy?
What is the nature of the subsequent deterioration?
What investigations should be performed?
What is the differential diagnosis of the cause of the progressive calf hypertrophy?



An acute paralytic illness which follows symptoms of a viral infection with or without signs of meningitis is typical of poliomyelitis. Usually caused by one of the three polio viruses, it may also occur following vaccination and following infections with other enteroviruses.1 Other disorders which would cause a similar syndrome but with upper motor neurone signs would include acute vascular lesions, meningoencephalitis and acute disseminated encephalomyelitis.


A progressive functional deterioration many years after paralytic poliomyelitis is well known, although its pathogenesis is not fully understood.2 It is a diagnosis of exclusion; a careful search for alternative causes, for example, orthopaedic deformities such as osteoarthritis or worsening scoliosis, superimposed neurological disorders such as entrapment neuropathies or coincidental muscle disease or neuropathy, and general medical causes such as respiratory complications and endocrinopathies.3


Investigations revealed normal blood count and erythrocyte sedimentation rate and normal biochemistry apart from a raised creatine kinase at 330 IU/l (normal range 60–120 IU/l), which is commonly seen in cases of ongoing denervation. Electromyography showed evidence of denervation in the right APB and FDI with polyphasic motor units and complex repetitive discharges, no spontaneous activity in the left calf and large polyphasic units in the right calf consistent with chronic partial denervation. Motor and sensory conduction velocities were normal. A lumbar myelogram was normal. Magnetic resonance imaging (MRI) scan of the calves is shown in figure2.

Figure 2

Axial T1 weighted MRI scan (TR 588 ms, TE 15 ms) of the calves, showing gross muscle atrophy and replacement by adipose tissue on the left, and hypertrophy of the muscles on the right, with only minor adipose tissue deposition


The differential diagnosis of the progressive calf hypertrophy is given in the box.

Causes of calf muscle hypertrophy

Chronic partial denervation

  • radiculopathy

  • peripheral neuropathy

  • hereditary motor and sensory neuropathy

  • spinal muscular atrophy

  • following paralytic poliomyelitis

    Neuromyotonia and myokymia

  • Isaac's syndrome

  • generalised myokymia

  • neurotonia

  • continuous muscle fibre activity due to: chronic inflammatory demyelinating polyradiculopathy, Guillain Barre syndrome, myasthenia gravis, thymoma, thyrotoxicosis, thyroiditis

    Muscular dystrophies



  • tumours

  • amyloidosis

  • cysticercosis

    Link here