Reversible Conduction Failure in Guillain-Barré Syndrome

Abstract

Gangliosides are the primary antigenic target in acute motor axonal neuropathy. When anti-ganglioside antibodies bind to gangliosides near the motor axon node of Ranvier, complement system activation and Wallerian degeneration occur. Nevertheless, debate persists regarding the impact of anti-ganglioside antibodies on Guillain-Barré syndrome (GBS). Certain patients with these antibodies experience a swift recovery or exhibit conduction abnormalities indicative of demyelination in nerve conduction studies. The concept of reversible conduction failure was introduced by Kuwabara et al. in 1998. They proposed that this could result from compromised physiological conduction at the node of Ranvier. Auto-antibodies that bind to GM1 or GD1a gangliosides at this node can activate the complement system and disrupt sodium channel and axo-glial junctions, causing conduction failure. In 2003, Cappaso et al. described two cases of rapidly improving flaccid paralysis following Campylobacter jejuni infection. Initial nerve conduction studies indicated motor conduction block, which resolved quickly within 2 to 5 weeks. The authors termed this phenomenon acute motor conduction block neuropathy and considered it a form of arrested or partial acute motor axonal neuropathy. Since acute motor conduction block neuropathy could be misclassified as acute inflammatory demyelinating polyneuropathy based on existing electrophysiological criteria, several suggestions were made to refine the classification of GBS subtypes.