4/07/2010

EFECTO DE LA INMUNOGLOBULINA EN SPP


EFECTO DE LA INMUNOGLOBULINA INTRAVENOSA EN PACIENTES CON EL SÍNDROME DE POST-POLIO UN ESTUDIO EXPERIMENTAL INCONTROLADO

Autores: Jorge Kaponides a; Henrik González a; Tomas Olsson b; Kristian Borg a

unidad de b Neuroimmunology, centro para el hospital molecular de MedicineKarolinska, Estocolmo, Suecia
Afiliaciones:De los departamentos de ciencias de la salud pública, división de medicina de la rehabilitación, Estocolmo, Suecia

DOI: 10.1080/16501970500441625

Frecuencia de la publicación: 6 ediciones por año
Publicado en: El diario de la medicina de la rehabilitación, volumen 38, edición el 2 de marzo de 2006, pagina 138 - 140
Da formato a disponible: HTML (inglés): Pdf (inglés)
Publicado previamente como: Diario escandinavo de la medicina de la rehabilitación (0036-5505) hasta 2001

Extracto

Objetivo

Para analizar cambios en fuerza muscular, funcionamiento físico y calidad de vida durante el tratamiento intravenoso de la inmunoglobulina (IVIg) en pacientes con síndrome de la post-poliomielitis.
Diseño:
Abra el ensayo clínico.
Pacientes: Un total de 14 pacientes (6 mujeres, 8 hombres; la edad media 57 años, se extiende 43-67 años) fue incluida en el estudio.
Intervención: Tratamiento con 90 g IVIg(30 g diarios por 3 días).
Resultado principal: La fuerza muscular, medida con dynamometry dinámico, función del músculo, por medio de realizar una prueba minuciosa de la caminata 6, y la calidad de vida, analizada por medio del cuestionario SF-36, fue realizada antes y después del tratamiento.
Resultados: Para la calidad de vida había una mejora estadística significativa para todos una de las 8 escalas del multi-artículo de SF-36 al comparar datos antes y después del tratamiento con IVIg. El la mayoría de la escala del multi-artículo mejorado era vitalidad
No había aumento significativo en fuerza muscular y funcionamiento físico.

Conclusión: Los datos indican que IVIg puede tener un efecto clínico relevante, con una mejora en calidad de vida. El efecto puede ser debido a una disminución de un proceso inflamatorio en el sistema nervioso central, que se ha divulgado anterior en pacientes con síndrome de la más allá-poliomielitis después del tratamiento de IVIg. Puesto que un efecto posible del placebo no puede ser eliminado, un estudio controlado seleccionado al azar es necesario.































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Erradicación de La poliomielitis

Polio Tricisilla Adaptada

March Of Dimes Polio History

Dr. Bruno

video

movie

movie2

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