PubMed · 13441111
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S BERGENSON, G NILSSON. 1957-04-25. [Bulbospinal polyradiculitis].. https://pubmed.ncbi.nlm.nih.gov/13441111/
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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.
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.
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.