Autor(es): Lin Hsin Hsin,Spies Judith M,Lu Jun Lan,Pollard John D

Resumo: High-dose intravenous immunoglobulin (IVIg) is an effective treatment for inflammatory demyelinating neuropathies, although the mechanism(s) of action remain incompletely understood. Experimental autoimmune neuritis (EAN) is an animal model of inflammatory demyelinating neuropathies; however, there have been conflicting reports regarding the efficacy of human IVIg in EAN. To obtain a model suitable for the study of the mechanism(s) of action of IVIg in Guillain-Barré syndrome, we investigated the effect of IVIg in EAN in the rat using clinical, electrophysiological and morphological measures. Human IVIg administered at the onset of signs of disease proved effective in preventing further progression of disease and shortening disease duration. This effectiveness was associated with significant differences in electrophysiological parameters including less prolongation of somatosensory evoked potential (S wave) latencies, better maintained S wave amplitudes, less reduction of distal motor nerve conduction velocity, and better maintained amplitudes of compound muscle action potentials of the dorsal foot muscles after stimulation at ankle and hip. Moreover, treatment with IVIg resulted in significantly lower histological grades in rat EAN. The current study provides evidence that human IVIg is effective in the treatment of EAN in the rat, indicating that this model may facilitate further investigation of the mechanism(s) of action of IVIg in inflammatory demyelinating neuropathies.

Palavras-Chave: Intravenous immunoglobulin; Experimental autoimmune neuritis; Inflammatory demyelinating neuropathy; Electrophysiology; Histology

Imprenta: Journal of the Neurological Sciences, v. 256, n. 1-2, p. 61-67, 2007

Identificador do objeto digital: 10.1016/j.jns.2007.02.017

Descritores: Guillain-Barre Syndrome - Cytopathology ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Antibodies

Data de publicação: 2007

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