Isolated absence of F waves and proximal axonal dysfunction in Guillain-Barre syndrome with antiganglioside antibodies

Objectives-To investigate the pathophysiology of selective absence of F wav es and its relation with antiganglioside antibodies in Guillain-Barre syndr ome (GBS). Some patients with GBS show the absence of F waves as an isolate d conduction abnormality, which has been interpreted as demyelination in th e proximal nerve segments. Methods-In 62 consecutive patients with GBS, sequential nerve conduction an d F wave studies were reviewed, and antibodies against ganglioside GM1, GM1 b, GD1a, GalNAc-GD1a, GD1b, and GQ1b were measured by an enzyme linked immu nosorbent assay. Results-In the first electrophysiological studies, isolated absence of F wa ves was found in 12 (19%) patients. Sequential studies in 10 of these patie nts showed two electrophysiological sequel patterns; rapid restoration of F waves (six patients), and persistent absence of F waves with distal motor nerve degeneration (acute motor axonal neuropathy, four patients). None of the 10 patients showed evidence of demyelination in the proximal, intermedi ate, or distal nerve segments throughout the course. Of the 62 patients, Ig G antibodies against GM1, GM1b, GalNAc-GD1a, or GD1b were significantly ass ociated with the electrodiagnosis of acute motor axonal neuropathy, and pat ients with these antibodies more often had isolated absence of F waves than patients without them (11 of 36 (31%) v one of 26 (4%); p<0.01). Eleven of the 12 patients with isolated absence of F waves had positive serology for one or more antiganglioside antibodies. Conclusions-In GBS with antiganglioside antibodies, isolated absence of F w aves is a frequent conduction abnormality especially in the early phase of the disease, and may be caused by axonal dysfunction, such as physiological conduction block or axonal degeneration at the nerve roots.