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Neuromuscular transmission is not impaired in axonal Guillain–Barré syndrome
  1. S Kuwabara1,
  2. N Kokubun2,
  3. S Misawa1,
  4. K Kanai1,
  5. S Isose1,
  6. K Shibuya1,
  7. Y Noto1,
  8. M Mori1,
  9. Y Sekiguchi1,
  10. S Nasu1,
  11. Y Fujimaki1,
  12. K Hirata2,
  13. N Yuki3
  1. 1Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan
  2. 2Department of Neurology, Dokkyo Medical University, Tochigi, Japan
  3. 3Departments of Microbiology and Medicine, National University of Singapore, Singapore
  1. Correspondence to Professor Satoshi Kuwabara, Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan; kuwabara-s{at}


Background Previous studies have shown that anti-GQ1b antibodies induce massive neuromuscular blocking. If anti-GM1 and -GD1a antibodies have similar effects on the neuromuscular junction (NMJ) in human limb muscles, this may explain selective motor involvement in axonal Guillain–Barré syndrome (GBS).

Methods Axonal-stimulating single-fibre electromyography was performed in the extensor digitorum communis muscle of 23 patients with GBS, including 13 with the axonal form whose sera had a high titre of serum IgG anti-GM1 or -GD1a antibodies.

Results All patients with axonal or demyelinating GBS showed normal or near-normal jitter, and no blocking.

Conclusion In both axonal and demyelinating GBS, neuromuscular transmission is not impaired. Our results failed to support the hypothesis that anti-GM1 or -GD1a antibody affects the NMJ. In GBS, impulse transmission is presumably impaired in the motor nerve terminal axons proximal to the NMJ.

  • Anti-GM1 antibody
  • anti-GD1a antibody
  • Guillain–Barré syndrome
  • acute motor axonal neuropathy
  • neuromuscular transmission
  • single-fibre electromyography
  • EMG
  • neuromuscular
  • neuropathy
  • neurophysiol
  • clinical

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  • Funding This work was supported in part by the Health and Labour Sciences Research Grant on Intractable Diseases (Neuroimmunological Diseases) (SK), and the Research Grant 16B-1 for Nervous and Mental Disorders (SK) from the Ministry of Health, Labour and Welfare of Japan.

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval Ethics approval was provided by the Ethics Committee, Chiba University School of medicine and Dokkyo University.

  • Provenance and peer review Not commissioned; externally peer reviewed.