Reversible Conduction Failure in Guillain-Barré Syndrome
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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.
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.
참고문헌 (34)
- van den Berg B, "Guillain-Barré syndrome: pathogenesis, diagnosis, treatment and prognosis", Nat Rev Neurol, 10, pp.469~482 (2014)
- Walgaard C, "Early recognition of poor prognosis in Guillain-Barre syndrome", Neurology, 76, pp.968~975 (2011)
- Feasby TE, "An acute axonal form of Guillain-Barré polyneuropathy", Brain, 109(Pt 6), pp.1115~1126 (1986)
- Ho TW, "Patterns of recovery in the Guillain-Barre syndromes", Neurology, 48, pp.695~700 (1997)
- Kuwabara S, "IgG anti-GM1 antibody is associated with reversible conduction failure and axonal degeneration in Guillain-Barré syndrome", Ann Neurol, 44, pp.202~208 (1998)
- Kokubun N, "Conduction block in acute motor axonal neuropathy", Brain, 133, pp.2897~2908 (2010)
- Guillain G, "Sur un syndrome de radiculo-nevrite avec hyperalbuminose du liquide cephalo-rachidien sans reaction cellulaire : remarques sur les caracters cliniques et graphiques des reflexes tendineux", Bull Mem Soc Med Hop Paris, 40, pp.1462~1470 (1916)
- Wiederholt WC, "The Landry-Guillain-Barre-Strohl syndrome or polyradiculoneuropathy: historical review, report on 97 patients, and present concepts", Mayo Clin Proc, 39, pp.427~451 (1964)
- Austin N, "Chinese paralytic syndrome", Lancet, 339, pp.177~ (1992)
- McKhann GM, "Clinical and electrophysiological aspects of acute paralytic disease of children and young adults in northern China", Lancet, 338, pp.593~597 (1991)
- Yu RK, "Structures, biosynthesis, and functions of gangliosides: an overview", J Oleo Sci, 60, pp.537~544 (2011)
- Waxman SG, "Molecular dissection of the myelinated axon", Ann Neurol, 33, pp.121~136 (1993)
- Uncini A, "Nodopathies of the peripheral nerve: an emerging concept", J Neurol Neurosurg Psychiatry, 86, pp.1186~1195 (2015)
- Susuki K, "Gangliosides contribute to stability of paranodal junctions and ion channel clusters in myelinated nerve fibers", Glia, 55, pp.746~757 (2007)
- Yuki N, "Acute axonal polyneuropathy associated with anti-GM1 antibodies following Campylobacter enteritis", Neurology, 40, pp.1900~1902 (1990)
- Argentino C, "GM1 ganglioside therapy in acute ischemic stroke : Italian Acute Stroke Study : hemodilution + drug", Stroke, 20, pp.1143~1149 (1989)
- Schneider JS, "GM1 ganglioside treatment of Parkinson's disease: an open pilot study of safety and efficacy", Neurology, 45, pp.1149~1154 (1995)
- Harrington H, "Ganglioside therapy for amyotrophic lateral sclerosis : a double-blind controlled trial", Neurology, 34, pp.1083~1085 (1984)
- Figueras A, "Bovine gangliosides and acute motor polyneuropathy", BMJ, 305, pp.1330~1331 (1992)
- Yuki N, "Motoneuron-disease-like disorder after ganglioside therapy", Lancet, 337, pp.1109~1110 (1991)
- Yuki N, "Cross-reactive antigen between nervous tissue and a bacterium elicits Guillain-Barré syndrome: molecular mimicry between ganglioside GM1, and lipopolysaccharide from Penner’s serotype 19 of Campylobacter jejuni", Biomed Res, 13, pp.451~453 (1992)
- Yuki N, "Carbohydrate mimicry between human ganglioside GM1 and Campylobacter jejuni lipooligosaccharide causes Guillain-Barre syndrome", Proc Natl Acad Sci U S A, 101, pp.11404~11409 (2004)
- Capasso M, "Acute motor conduction block neuropathy another Guillain-Barré syndrome variant", Neurology, 61, pp.617~622 (2003)
- Kuwabara S, "Axonal Guillain-Barré syndrome: concepts and controversies", Lancet Neurol, 12, pp.1180~1188 (2013)
- Hadden RD, "Electrophysiological classification of Guillain-Barré syndrome: clinical associations and outcome. Plasma Exchange", Sandoglobulin Guillain-Barré Syndrome Trial Group, 1998, pp.44, 780~788
- Bae JS, "Guillain-Barré syndrome in Asia", J Neurol Neurosurg Psychiatry, 85, pp.907~913 (2014)
- 김종국, "Prevalence of Anti-Ganglioside Antibodies and Their Clinical Correlates with Guillain-Barré Syndrome in Korea: A Nationwide Multicenter Study", Journal of Clinical Neurology, 10(2), pp.94~100 (2014), 대한신경과학회[DOI]
- Uncini A, "Pitfalls in electrodiagnosis of Guillain-Barré syndrome subtypes", J Neurol Neurosurg Psychiatry, 81, pp.1157~1163 (2010)
- Rajabally YA, "Electrophysiological diagnosis of Guillain-Barré syndrome subtype : could a single study suffice?", J Neurol Neurosurg Psychiatry, 86, pp.115~119 (2015)
- Uncini A, "Optimizing the electrodiagnostic accuracy in Guillain-Barré syndrome subtypes: criteria sets and sparse linear discriminant analysis", Clin Neurophysiol, 128, pp.1176~1183 (2017)
- Kaida K, "GalNAc-GD1a in human peripheral nerve: target sites of anti-ganglioside antibody", Neurology, 61, pp.465~470 (2003)
- Kaida K, "Guillain-Barré syndrome with antibody to a ganglioside, N-acetylgalactosaminyl GD1a", Brain, 123(Pt 1), pp.116~124 (2000)
- Kim JK, "Acute pure motor demyelinating neuropathy with hyperreflexia and anti-GalNAc-GD1a antibodies", Clin Neurol Neurosurg, 114, pp.1345~1347 (2012)
- Kusunoki S, "Antibodies against ganglioside complexes in Guillain-Barré syndrome and related disorders", J Neurochem, 116, pp.828~832 (2011)