PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 15676111

Inflammatory neuropathies.

Hannah R Briemberg·Anthony A Amato
View original source ↗Export metadata ↓

Abstract

We discuss two of the most common of the acquired inflammatory neuropathies: Guillain-Barre syndrome and chronic inflammatory demyelinating polyneuropathy, as well as their variants. We review their clinical presentation, electrophysiologic findings, and management, highlighting knowledge gained from the recent literature. Unfortunately, although treatments exist for both Guillain-Barre syndrome and chronic inflammatory demyelinating polyneuropathy, none are completely curative and all have significant potential side effects and/or expense. Better understanding of the underlying pathophysiology of these diseases is needed in order to develop more targeted therapies.

Explore related subjects

Guillain-Barre SyndromeHumansPolyradiculoneuropathy, Chronic Inflammatory DemyelinatingJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Hannah R Briemberg, Anthony A Amato. 2005. Inflammatory neuropathies.. https://doi.org/10.1007/s11910-005-0026-z

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Guillain-barré syndrome.

Guillain-Barré syndrome (GBS) is currently divided into the two major subtypes: acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). This review highlights relevant recent publications, particularly on the pathophysiology of AMAN. Molecular mimicry of the bacterial lipo-oligosaccharide by the human gangliosides is now considered an important cause of AMAN. Gangliosides GM1, GM1b, GD1a, and GalNAc-GD1a expressed on the motor axolemma are likely to be the epitopes for antibodies in AMAN. At the nodes or paranodes, deposition of antiganglioside antibodies initially cause reversible conduction block followed by axonal degeneration. Electrodiagnostic findings support this process. Disruption of glycolipids, which are important to maintain ion channel clustering at the nodes and paranode, may impair nerve conduction. Genetic polymorphisms of Campylobacter jejuni determine the expression of the gangliosides on the bacterial wall. In contrast, target molecules in AIDP have not yet been identified. Meta-analyses show efficacy of plasmapheresis and immunoglobulin therapy, but not corticosteroids, in hastening recovery.

Guillain-Barre Syndrome↗
PubMed2006

Travel medicine interventions and neurological disease.

As a consequence of increased mobility worldwide, persons with underlying medical conditions set out on a journey more often than in the past. Among pre-existing medical conditions, some neurological diseases, including multiple sclerosis and other demyelinating diseases, Guillain-Barré syndrome and myasthenia gravis often create management problems to travel medicine practitioners. There is some concern that these conditions could be worsened either by naturally acquired infections or by some travel medicine interventions. The aim of this review is to suggest a practical approach to each of these conditions and to examine the feasibility and the impact of travel medicine interventions on the underlying disease.

Guillain-Barre Syndrome↗
PubMed2006

Therapy of immune neuropathies with intravenous immunoglobulins.

Autoimmune-mediated disorders belong to the main causes of neuropathies worldwide. During recent years much progress has been achieved in the understanding of the underlying pathomechanisms, associated with implications for therapeutic approaches. Here we will briefly review the pathogenesis and discuss treatment options of the Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy, and neuropathies associated with paraproteinemias. In most of these disease entities intravenous immunoglobulins play a major role as effective and safe treatment options.

Guillain-Barre Syndrome↗