Acute motor axonal neuropathy: A frequent cause of acute flaccid paralysis in China

McKhann, Guy M.; Cornblath, David R.; Griffin, John W.; Ho, Tony W.; Li, C. Y.; Jiang, Zhenxing; Wu, Heng; Zhaori, Getu; Liu, Y.; Jou, L. P.; Liu, T. C.; Gao, Chongyang; Mao, Jianren; Blaser, Martin J.; Mishu, Ban; Asbury, Arthur K.

doi:10.1002/ana.410330402

Cited by 562 publications

(409 citation statements)

References 22 publications

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“…This observation is rather different from the observed in northern China with a clear correlation with the summer months for the Acute Motor Axonal Neuropathy (AMAN) type of GuillainBarré, 16 and in other regions such as in Argentina with two peaks for both forms of the disease Acute Demyelinating Peripheral Neuropathy (AIDP) and AMAN at the summer and at the winter months 7 .…”

Section: Discussioncontrasting

confidence: 84%

Guillain Barré syndrome in a population less than 15 years old in Brazil

Dias‐Tosta

Kückelhaus²

2002

Arq. Neuro-Psiquiatr.

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-To know the impact of the Guillain Barré syndrome (GBS) in the population less than 15 years old, after the eradication of poliomyelitis. Data bank from the program of epidemiological surveillance of acute flaccid palsies (AFP) from the Fundação Nacional de Saúde were analyzed between 1990 -1996. From 3619 notifications of AFP there were 1678 GBS. GBS yearly incidence rates is 0.39-0.63 cases/100,000. No consistent seasonal variation existed or relationship to vaccines. Weakness at inclusion were, moderate 52.1%, severe in 47.9%, sixty days after 57.1% normal, 7.4% mild, 15.7% moderate, 10.4% with severe deficits, death in 5.4%. 67 (4.0%) cases unknown. Death rates varies from 2.8% in southeast to 7.9% in the northeast. GBS was the most frequent cause of AFP. In spite of the severity of this disease being similar in the different regions, the outcome varies according to origin of the cases, possibly reflecting the economical conditions in those places.KEY WORDS: Guillain Barré syndrome, epidemiology, vaccines, follow up.Síndrome de Guillain-Barré na população menor de quinze anos no Brasil Síndrome de Guillain-Barré na população menor de quinze anos no Brasil Síndrome de Guillain-Barré na população menor de quinze anos no Brasil Síndrome de Guillain-Barré na população menor de quinze anos no Brasil Síndrome de Guillain-Barré na população menor de quinze anos no Brasil RESUMO -Com o objetivo de conhecer a importância da síndrome de Guillain Barré (SGB) na população menor de quinze anos, após a erradicação da poliomielite, foi analizado o banco de dados do programa da vigilância epidemiológica das paralisias agudas e flácidas (PAF) da Fundação Nacional de Saúde, entre 1990 e 1996. De 3619 notificações de PAF encontraram-se 1678 com SGB, com incidência anual de 0,39-0,63 casos/ 100.000. Não se comprovou variação sazonal nem relação com a vacina. Os casos eram de acometimento: moderado em 52,1%, grave em 47,9%, 60 dias após 57,1% eram normais, 7,4% leves, 15,7% moderados, 10,4% graves, morte em 5,4%, 67 (4,0%) casos perdidos para o acompanhamento. Mortes ocorreram em 2,8% no sudeste, e 7,9% no nordeste. SGB é a causa mais frequente de PAF. Embora a gravidade da doença seja semelhante nas diferentes regiões, a evolução varia conforme o local de origem, possivelmente refletindo diferentes condições econômicas. PALAVRAS-CHAVE: síndrome de Guillain Barré, epidemiologia, vacina, evolução.The acute flaccid palsies (AFP) are a group of diseases, with many etiologies, variable incidences and variable prognoses, that affect population around the year in the world. Until mid 80's the acute poliomyelitis was the main cause of acute flaccid palsies but with the program of eradication of poliomyelitis had emerged the Guillain-Barré syndrome (GBS) as the major etiology, such statement is already proved in the developed countries, but still unknown in many communities. The epidemiological data has been shown valuable in evaluating the frequency of GBS in various populations, studying changes in incidence over time, detec...

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Section: Discussioncontrasting

confidence: 84%

Guillain Barré syndrome in a population less than 15 years old in Brazil

Dias‐Tosta

Kückelhaus²

2002

Arq. Neuro-Psiquiatr.

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“…IgG was deposited on some axons in the cauda equina of rabbit Cj-12. These findings, compatible with the features of human axonal GBS (3,4), provide evidence that the rabbits inoculated with C. jejuni LOS constitute a valid GBS model. This definitive replica of a human autoimmune disease produced by immunizing with the mimic of the infectious agent associated with epidemiological evidence of microbial infection has not been reported previously.…”

Section: Discussionsupporting

confidence: 82%

Carbohydrate mimicry between human ganglioside GM1 and Campylobacter jejuni lipooligosaccharide causes Guillain–Barré syndrome

Yuki

Susuki

Koga

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

461

357

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Molecular mimicry between microbial and self-components is postulated as the mechanism that accounts for the antigen and tissue specificity of immune responses in postinfectious autoimmune diseases. Little direct evidence exists, and research in this area has focused principally on T cell-mediated, antipeptide responses, rather than on humoral responses to carbohydrate structures. Guillain-Barré syndrome, the most frequent cause of acute neuromuscular paralysis, occurs 1-2 wk after various infections, in particular, Campylobacter jejuni enteritis. Carbohydrate mimicry [Gal␤1-3GalNAc␤1-4(NeuAc␣2-3)Gal␤1-] between the bacterial lipooligosaccharide and human GM1 ganglioside is seen as having relevance to the pathogenesis of Guillain-Barré syndrome, and conclusive evidence is reported here. On sensitization with C. jejuni lipooligosaccharide, rabbits developed anti-GM1 IgG antibody and flaccid limb weakness. Paralyzed rabbits had pathological changes in their peripheral nerves identical with those present in GuillainBarré syndrome. Immunization of mice with the lipooligosaccharide generated a mAb that reacted with GM1 and bound to human peripheral nerves. The mAb and anti-GM1 IgG from patients with Guillain-Barré syndrome did not induce paralysis but blocked muscle action potentials in a muscle-spinal cord coculture, indicating that anti-GM1 antibody can cause muscle weakness. These findings show that carbohydrate mimicry is an important cause of autoimmune neuropathy.

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“…2,3 In China, a form, acute motor axonal neuropathy (AMAN), in which the primary pathophysiological process involves disruption of motor axonal function, not demyelination was identified. 4 Severe axonal cases also have sensory nerve fiber involvement and are called acute motor sensory axonal neuropathy (AMSAN). Minor forms of GBS include Fisher, sensory-ataxic and other variants.…”

Section: Gangliosidesmentioning

confidence: 99%

Autoantobodies activate small GTPase RhoA to modulate neurite outgrowth

Sheikh

2011

Small GTPases

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Acute motor axonal neuropathy: A frequent cause of acute flaccid paralysis in China

Cited by 562 publications

References 22 publications

Guillain Barré syndrome in a population less than 15 years old in Brazil

Guillain Barré syndrome in a population less than 15 years old in Brazil

Carbohydrate mimicry between human ganglioside GM1 and Campylobacter jejuni lipooligosaccharide causes Guillain–Barré syndrome

Autoantobodies activate small GTPase RhoA to modulate neurite outgrowth

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