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Patterns and serial changes in electrodiagnostic abnormalities of axonal Guillain–Barré syndrome

From the Department of Neurology (Drs. Hiraga, Kuwabara, Ogawara, Misawa, Kanesaka, Hattori, and Mori), Chiba University Graduate School of Medicine, and Department of Neurology (Drs. Koga and Yuki), Dokkyo University School of Medicine, Tochigi, Japan.

Address correspondence and reprint requests to Dr. A. Hiraga, Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba, 260-8670 Japan; e-mail: hiragaa{at}mail3.alpha-net.ne.jp

Background: In Guillain–Barré syndrome (GBS), anti-ganglioside antibodies are strongly associated with the acute motor axonal neuropathy (AMAN) form, but there are also cases of the demyelinating form of GBS (acute inflammatory demyelinating polyneuropathy [AIDP]) with anti-ganglioside antibodies.

Objective: To elucidate the patterns and sequential changes in electrodiagnostic abnormalities of anti-ganglioside-positive GBS.

Methods: Detailed serial electrodiagnostic findings were reviewed for 51 patients with GBS. Anti-ganglioside antibodies were measured by ELISA.

Results: Antibodies to GM1, GM1b, GD1a, or GalNAc-GD1a were present in 25 patients. Of these, 12 (48%) showed the AMAN pattern, 5 (20%) the AIDP pattern, and 3 (12%) isolated F-wave absence in the first examination. All five patients with the AIDP pattern showed prolonged distal latencies, but three eventually showed the AMAN pattern or rapid normalization. The remaining two still had similarly prolonged distal latencies in weeks 4 to 6, but the serial changes were distinct from those in the anti-ganglioside-negative AIDP patients who showed progressive increases in distal latencies over 2 months after onset.

Conclusions: Besides the simple axonal degeneration pattern, patients with anti-ganglioside-positive Guillain–Barré syndrome can show transient conduction slowing/block in the distal or proximal nerve segments, mimicking demyelination, but anti-ganglioside antibodies do not appear to be associated with acute inflammatory demyelinating polyneuropathy.

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