Tips and Techniques for Polio Survivors

Tips and Techniques for Polio Survivorsby Dr. Richard L. Bruno

Recently I had a fever with muscle and chest pain. The only abnormal blood tests showed high C-reactive protein and high creatine kinase. My blood pressure and cholesterol are normal, I have never smoked, and I'm thin. Because of the chest pain I had an angiogram, which was normal. Could high CRP and high CK be related to PPS?
C-reactive protein is a blood marker for inflammation somewhere in the body. High CRP can be seen with type 2 diabetes, autoimmune diseases and cancers.Could inflammation somewhere in your body, as indicated by your elevated CRP, be related to PPS? Fifty consecutive patients evaluated at The Post-Polio Institute had CRP measured. The patients were on average 59 years old and 55% were women. Thirteen percent had an elevated CRP, 66% of
whom were men. CRP was on average nearly three times the normal value. However, there was no significant difference between those with high and normal CRP on self-ratings of daily fatigue, difficulty with self-care or ability to perform activities inside or outside of the home. So, there is no evidence that elevated CRP or inflammation is related to PPS, either to post-polio fatigue or difficulty in functioning.
Recent studies have found that elevated CRP is related to having a heart attack or stroke. The theory is that a bacterial or viral infection (although definitely not a poliovirus infection) somehow inflames arteries and causes them to clog. Our 1985 National Survey found no more heart disease or high blood pressure in polio survivors than in the general
population. But two studies found that 5% more male post-polio patients had abnormally elevated cholesterol as compared to the general population. In one of the studies, only 33% of those with high cholesterol had been given a
cholesterol screening test by their doctor and not even 25% were on cholesterol-lowering medications, like the statin drugs such as Lipitor, Pravachol and Zocor. This is not good, since reducing cholesterol reduces heart attack risk. What's more, research has shown that taking statins to reduce cholesterol can also lower CRP and may thereby increase survival even after having a first heart attack.
Statin drugs provide a connection between CRP and CK--in polio survivors. CK is an enzyme released when muscle is damaged. One half of one percent of anyone taking a statin develops muscle breakdown, which causes muscle
pain (especially in the calves), muscle weakness and an increase in CK. Even without muscle breakdown or an elevated CK, some polio survivors report muscle pain or weakness when taking a statin, usually one of the older statins like Lipitor. And polio survivors can have an elevated CK without taking a statin. Two studies found that 40% of polio survivors had abnormally elevated CK, with men having significantly higher CK than did women. In one study, CK increased with the number of steps polio survivors walked in a day. In our fifty Post-Polio Institute patients, 21% had
abnormally elevated CK levels (on average about 33% higher than normal) with men also having higher CK than did women. But, as with CRP, there was no significant difference between those with high and normal CK on self-ratings
of daily fatigue, difficulty with self-care or the ability to perform activities inside or outside of the home. However, an elevated CK may mean that polio survivors are making their muscles work too hard and are causing them to break down.
So, neither CRP nor CK is related to fatigue or loss of functional abilities in polio survivors. However, all polio survivors need to have their cholesterol and CRP measured to assess heart disease risk. And since an elevated CK indicates muscle breakdown, either from taking a statin or from muscle overuse, polio survivors should have CK measured before taking a statin. If you are worried about possible muscle weakness or breakdown with the statins, or the newer cholesterol-lowering drugs like Zetia and Vytorin, ask your doctor about using older medications like slow-acting niacin or bile acid sequestrants. Besides medication, polio survivors need to eat high fiber foods, reduce saturated fat, treat high blood pressure and stop smoking to keep their tickers ticking.

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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