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Guillain–Barré syndrome in Asia
  1. Jong Seok Bae1,2,
  2. Nobuhiro Yuki3,
  3. Satoshi Kuwabara4,
  4. Jong Kuk Kim5,
  5. Steve Vucic2,6,
  6. Cindy S Lin2,
  7. Matthew C Kiernan7
  1. 1Department of Neurology, College of Medicine, Hallym University, Seoul, Korea
  2. 2Neuroscience Research Australia, Sydney, Australia
  3. 3Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
  4. 4Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan
  5. 5Department of Neurology, College of Medicine, Dong-A University, Busan, Korea
  6. 6Department of Neurology, Westmead Clinical School, University of Sydney, Sydney, New South Wales, Australia
  7. 7Bushell Chair of Neurology, Brain & Mind Research Institute, University of Sydney, Sydney, New South Wales, Australia
  1. Correspondence to Dr Jong Seok Bae, Department of Neurology, College of Medicine, Hallym University, Seoul, Korea, Kangdong Sacred Heart Hospital, 150 Seongan-ro, Gangdong-gu, Seoul 134-701, Korea; jsb_res{at}


Over the past 20 years, the most notable advance in understanding Guillain–Barré syndrome (GBS) has been the identification of an axonal variant. This advance arose chiefly through studies undertaken in East Asian countries and comprised two major aspects: first, the immunopathogenesis of axonal GBS related to anti-ganglioside antibodies and molecular mimicry of Campylobacter jejuni; and second, the observation that distinct electrophysiological patterns of axonal GBS existed, reflecting reversible conduction failure (RCF). As a consequence, the pathophysiology of acute motor axonal neuropathy (AMAN) has perhaps become better understood than acute inflammatory demyelinating polyneuropathy. Despite these more recent advances, a critical issue remains largely unresolved: whether axonal GBS is more common in Asia than in Europe or North America. If it is more common in Asia, then causative factors must be more critically considered, including geographical differences, issues of genetic susceptibility, the role of antecedent infections and other potential triggering factors. It has become apparent that the optimal diagnosis of AMAN requires serial electrophysiological testing, to better delineate RCF, combined with assessment for the presence of anti-ganglioside antibodies. Recent collaborative approaches between Europe and Asia have suggested that both the electrophysiological pattern of AMAN and the seropositivity for anti-ganglioside antibodies develop similarly. Separately, however, current electrodiagnostic criteria for AMAN limited to a single assessment appear inadequate to identify the majority of cases. As such, diagnostic criteria will need to be revised to improve the diagnostic sensitivity for AMAN.

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