Guillain-Barré syndrome classification

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.



Guillain barre syndrome may be classified according to the underlying pathophysiology into four groups:[1][2][3][4][5][6][7][8][9]

Subtypes explanation
Acute Motor Axonal Neuropathy (AMAN)
  • The most common type (85-90%).
  • Prior infection can trigger it.
  • Autoimmune disorder.
  • The target is schwann cell surface membrane or the myelin.
  • Causes demyelination.
  • In electrodiagnostic tests we can see slowing of nerve conduction.
  • In pathology we can see lymphocytic infiltration of peripheral nerves and macrophage invasion of myelin sheath and schwann cells.
Acute Motor Axonal Neuropathy (AMAN)
  • It’s common among Chinese and Japanese people.
  • It can be triggered by C. jejuni.
  • It is associated with antiganglioside antibodies.
  • Autoimmune disorder.
  • Target is axonal membrane.
  • Causes axonal degeneration in motor neurons.
  • In electrodiagnostic study we can see reduction of compound muscle action potential.
Acute motor and sensory axonal neuropathy
  • The incidence rate is under 10%.
  • Causes axonal degeneration.
  • It is similar with AMAN but involves both motor and sensory axons.
Miller Fisher syndrome
  • Causes a clinical triad: ophthalmoplegia, ataxia and areflexia.
  • Associated with ganglioside GQ1b antibody.


  1. Hadden RD, Cornblath DR, Hughes RA, Zielasek J, Hartung HP, Toyka KV, Swan AV (November 1998). "Electrophysiological classification of Guillain-Barré syndrome: clinical associations and outcome. Plasma Exchange/Sandoglobulin Guillain-Barré Syndrome Trial Group". Ann. Neurol. 44 (5): 780–8. PMID 9818934. doi:10.1002/ana.410440512. 
  2. Prineas JW (February 1972). "Acute idiopathic polyneuritis. An electron microscope study". Lab. Invest. 26 (2): 133–47. PMID 5059983. 
  3. Ho TW, Mishu B, Li CY, Gao CY, Cornblath DR, Griffin JW, Asbury AK, Blaser MJ, McKhann GM (June 1995). "Guillain-Barré syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies". Brain. 118 ( Pt 3): 597–605. PMID 7600081. 
  4. Prineas JW (1981). "Pathology of the Guillain-Barré syndrome". Ann. Neurol. 9 Suppl: 6–19. PMID 7224616. 
  5. Kuwabara S, Yuki N, Koga M, Hattori T, Matsuura D, Miyake M, Noda M (August 1998). "IgG anti-GM1 antibody is associated with reversible conduction failure and axonal degeneration in Guillain-Barré syndrome". Ann. Neurol. 44 (2): 202–8. PMID 9708542. doi:10.1002/ana.410440210. 
  6. Ogawara K, Kuwabara S, Mori M, Hattori T, Koga M, Yuki N (October 2000). "Axonal Guillain-Barré syndrome: relation to anti-ganglioside antibodies and Campylobacter jejuni infection in Japan". Ann. Neurol. 48 (4): 624–31. PMID 11026446. 
  7. Griffin JW, Li CY, Ho TW, Tian M, Gao CY, Xue P, Mishu B, Cornblath DR, Macko C, McKhann GM, Asbury AK (January 1996). "Pathology of the motor-sensory axonal Guillain-Barré syndrome". Ann. Neurol. 39 (1): 17–28. PMID 8572662. doi:10.1002/ana.410390105. 
  8. FISHER M (July 1956). "An unusual variant of acute idiopathic polyneuritis (syndrome of ophthalmoplegia, ataxia and areflexia)". N. Engl. J. Med. 255 (2): 57–65. PMID 13334797. doi:10.1056/NEJM195607122550201. 
  9. Yuki N, Taki T, Inagaki F, Kasama T, Takahashi M, Saito K, Handa S, Miyatake T (November 1993). "A bacterium lipopolysaccharide that elicits Guillain-Barré syndrome has a GM1 ganglioside-like structure". J. Exp. Med. 178 (5): 1771–5. PMC 2191246Freely accessible. PMID 8228822.