8/30/2013

Transcranial Direct Current Stimulation Improves Sleep in Patients with Post-Polio Syndrome

lunes, 26 de agosto de 2013 IOS Press BV

According to Novel Study Published in Restorative Neurology and Neuroscience
Amsterdam, NL, August 26, 2013 – Of the 15 million people around the world who have survived poliomyelitis, up to 80% report progressive deteriorating strength and endurance many years after infection, a condition known as post-polio syndrome (PPS). Researchers in Italy from the National Hospital for Poliomyelitis, the Policlinico G.B. De Rossi in Verona, and the University of Milan have found that transcranial direct current stimulation (tDCS) for 15 days improved sleep and fatigue symptoms in patients with PPS, suggesting this non-invasive tool may be a new therapeutic option for this condition. Their results are published in Restorative Neurology and Neuroscience.
Post-polio syndrome (PPS) is a neurological disorder that may first appear years after an acute polio infection. In addition to worsening weakness and fatigue, pain, depression, cold intolerance, and sleep disturbances also may occur. Although polio vaccines have drastically decreased the incidence of new cases of polio in industrialized countries, new cases still occur in areas of Asia and Africa. As polio survivors age, PPS symptoms emerge, even in people who have been stable for 15 years or more. The cause of PPS still remains elusive, and there are no definitive treatment options.  
The study enrolled 32 patients who had contracted polio at a mean age of 31 months, but then were stable clinically for an average of 55 years. They were referred to a national reference center, the Physical Rehabilitation Medicine Unit at Malcesine Hospital in Verona, Italy, for the treatment of PPS after complaining of progressively worsening weakness and fatigue. Half of the patients were randomly assigned to receive anodal tDCS applied bilaterally to the premotor cortex every day, 5 days a week, for three weeks. The control group received current for 5 seconds (sham tDCS). In preliminary testing, subjects said they could not distinguish between real and sham tDCS.
Patients underwent a battery of tests at baseline and then three weeks later. The tests looked at quality of life, multiple aspects of fatigue, depression, and sleep quality.
The authors found that tDCS treated patients improved more than sham-treated patients on several measures of a patient health survey (the Short Form Health Survey or SF-36), including physical functioning, role limitations due to physical health, vitality, social functioning and role limitations due to emotional health. No significant differences were found between the groups on questions related to bodily pain, general health, or mental health.
One of the most noticeable effects of tDCS treatment was an improvement in sleep quality. Scores on the Pittsburgh Sleep Quality Index (PSQI) decreased 65% compared to 25% in the control group, a significant difference (p<0.05). Significant correlations were found between PSQI scores and physical functioning, social functioning, and emotional health. Interestingly, sleep quality improved more in patients who were younger when poliomyelitis developed.
Whether tDCS relieves fatigue directly is still unclear. While fatigue-related sub-items of the SF-36 improved after tDCS, no significant changes were found using specific fatigue-assessment tests such as the Piper Fatigue Scale or the Fatigue Severity Scale. No changes were noted between groups in depression scores.
“tDCS might work by improving sleep. Because changes in sleep quality affect physical and psychological states, improving sleep quality could improve perceived vitality, social and emotional functioning, and, indirectly, also fatigue,” says lead investigator Laura Bertolasi, MD, Department of Neurological, Neuropsychological, Morphological and Movement Sciences, University of Verona, Italy. “tDCS effects on sleep fit in with results in healthy subjects, fibromyalgia, and schizophrenia.”
Post Polio Litaff, Association A.C _APPLAC Mexico

The Polio Crusade

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Erradicación de La poliomielitis

Polio Tricisilla Adaptada

March Of Dimes Polio History

Dr. Bruno

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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

Questions

1
What is that nature of the acute illness in infancy?
2
What is the nature of the subsequent deterioration?
3
What investigations should be performed?
4
What is the differential diagnosis of the cause of the progressive calf hypertrophy?

Answers

QUESTION 1

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.

QUESTION 2

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

QUESTION 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

QUESTION 4

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

    Myositis

    Infiltration

  • tumours

  • amyloidosis

  • cysticercosis

    Link here