GUILLAIN-BARRE-SYNDROME MILLER-FISHER SYN DROME

Citation
Hp. Hartung et al., GUILLAIN-BARRE-SYNDROME MILLER-FISHER SYN DROME, Nervenheilkunde, 15(1), 1996, pp. 15-20
Citations number
42
Categorie Soggetti
Clinical Neurology",Psychiatry
Journal title
ISSN journal
07221541
Volume
15
Issue
1
Year of publication
1996
Pages
15 - 20
Database
ISI
SICI code
0722-1541(1996)15:1<15:GMSD>2.0.ZU;2-Q
Abstract
The Guillain-Barre syndrome (GBS) is the most common cause of acute pa ralysis. It has become evident that the syndrome is heterogeneous and includes classical demyelinating polyneuropathy, axonal variants and a cute motor axonal polyneuropathy. Morbidity and mortality result from autonomic disturbances, involvement of caudal cranial nerves with resp iratory insufficiency and complications secondary to immobilization. P athogenetically, both humoral and cellular immune reactions against co mponents of the myelin sheath play an important role. Glycolipids are considered important target antigens of a humorally mediated immune at tack. In the Miller-Fisher syndrome, circulating antibodies to the gan glioside GQ1b can be detected in serum. Apart from supportive therapy plasma exchange and high dose intravenous immunoglobulin G have been p roved efficacious. Their relative merits are currently being evaluated in a large international multicentre trial.