[Pathophysiology and therapeutic approach in inflammatory demyelinating polyneuropathy--recent advances].
Recent advances on pathogenetic mechanism and therapeutic approach for Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIPD) were briefly reviewed. As for GBS, an axonal form has been recognized as a clinicopathological variant, in which Campylobacter jejuni infection and elevated anti-GM1 antibody tires are frequently observed. Other anti-glycolipid antibodies to GQ1b, GD1b and GM2 would also be significant as a determinant factor for a clinical phenotype. Beneficial effects of IVIg therapy and plasmapheresis have been established. Although CIDP has also been considered to be demyelinating neuropathy, axonal pathology is frequently noted, and in such cases, a substantial motor neuron loss is present. Clinical recovery in the cases with high anti-MAG and anti-SGPG titers is not necessarily favorable. Corticosteroid therapy, plasmapheresis and IVIg have been all established as therapies beneficial for CIDP.
Sobue
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Department of Neurology, Nagoya University School of Medicine.
D000906:Antibodies / Q000032:analysis; D002169:Campylobacter Infections; D016123:Campylobacter jejuni; D005915:Globosides / Q000276:immunology; D006801:Humans; D018992:Myelin-Associated Glycoprotein / Q000276:immunology; D011129:Polyradiculoneuropathy / Q000382:microbiology / Q000503:physiopathology / Q000628:therapy
D000906:Antibodies; D005915:Globosides; D018992:Myelin-Associated Glycoprotein; C051917:sulfate-3-glucuronyl paragloboside