Acute Flaccid Myelitis: More Paralyzing Polio-Like Illness This Year Says The CDC

The 'conscious uncoupling' of Gwyneth Paltrow and Chris Martin, the Apple watch, the ice-bucket challenge, John Travolta's inability to say a name correctly - these are all events that occurred two years ago - in 2014. 
If you think back, you may also remember that a mysterious illness made headlines that summer - a previously unknown disease that looked a lot like polio left children paralyzed. And, as the case numbers grew (there were 120 cases between August and December that year) and people became more frightened - scientists grew more baffled. 
Now, we know a bit more about what happened in 2014 - although still not much. The illness that was making headlines is called acute flaccid myelitis (AFM.)  The US Centers for Disease Control and Prevention (CDC) has been actively tracking it since August of 2014 and has reported an increase in the number of cases seen thus far this year. 
The terrifying aspects of AFM are that the cause is unknown, anyone can get it, and it affects the nervous system. Even worse, most of the cases are in children. The only silver lining is that it is rare. In the first eight months of this year, 50 cases have been confirmed in 24 states in the US. 
The CDC reports that multiple different viruses are linked to the cause of AFM including, but not limited to enteroviruses, West Nile virus (WNV) and other viruses in the same family as WNV (Japanese encephalitis virus and Saint Louis encephalitis virus,) and adenoviruses. 
AFM has a list of terrifying signs associated with it. The hallmark of the disease is how quickly the effects take hold with a sudden onset of weakness of limbs, loss of muscle tone and reflexes.  Some people also have facial droop/weakness, difficulty moving the eyes, drooping eyelids, or difficulty with swallowing or slurred speech.
The degree to which someone is affected is extremely variable. A child may be rendered usable to breathe on their own, or, on the other spectrum, left with muscle loss in an arm or leg. 
The outbreak of AFM in 2014 was thought to be linked to an uptick in infections of enterovirus D68 (EV-D68) - a close relative of poliovirus.  However, it could not be proven because every person with AFM did not have evidence of an EV-D68 infection, meaning that no virus or even antibodies (immune proteins made to a virus that is infecting the body) were present in their system. In addition, there were no cases of EV-D68 in 2015 (and 21 cases of AFM) and only a few cases of EV-D68 have been reported this year. Since June of this year, there has been a significant increase in EV-D68 cases in the Netherlands making that an area to watch for AFM cases.


Post Polio Litaff, Association A.C _APPLAC Mexico

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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