Drain the roots

Guillain–Barré syndrome (GBS) is an acute paralytic disease that produces major mortality and morbidity.1 The clinical–pathologic spectrum of GBS now extends from the classical acute inflammatory demyelinating polyneuropathy to axonal variants with (acute motor sensory axonal neuropathy) and without (acute motor axonal neuropathy) sensory involvement and clinical variants such as Miller Fisher syndrome.1,2⇓ Axonal involvement in GBS, whether primary or secondary, is generally associated with increased long-term disability. Key pathogenetic steps in GBS may include misdirected immune attacks upon nerve antigens in the myelin sheath and axolemma. These responses may be incited in susceptible hosts by aberrant immune responses to infectious agents, such as Campylobacter jejuni, which express epitopes similar to nerve antigens.2,3⇓ Whereas both cellular and humoral immune mechanisms may be involved, most research has centered on the role of gangliosides and related glycoconjugates as targets of specific antibodies, some of which seem to be preferentially associated with specific phenotypes, such as anti-GQ1b and Miller Fisher syndrome.4,5⇓

The key issues in GBS treatment are excellent intensive care unit management, including respiratory care, low-dose heparin to prevent deep vein thrombosis, and good nursing care.1 However, two disease-altering therapies, plasma exchange (PE) and high-dose IV immunoglobulin (IVIg), have shown efficacy in speeding motor recovery. Major North American6 and French trials7 demonstrated improvement with PE and a large Dutch trial8 showed equivalent benefit from IVIg. The international Plasma Exchange Sandoglobulin Trial (PSGBS), the largest …