Guillain-Barré syndrome pathophysiology

Jump to navigation Jump to search

Guillain-Barré syndrome Microchapters


Patient Information


Historical Perspective




Differentiating Guillain-Barré syndrome from other Diseases

Epidemiology and Demographics

Risk Factors


Natural history, Complications, and Prognosis


Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings



Echocardiography and Ultrasound

CT scan


Other Imaging Findings

Other Diagnostic Studies


Medical Therapy


Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Guillain-Barré syndrome pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides


American Roentgen Ray Society Images of Guillain-Barré syndrome pathophysiology

All Images
Echo & Ultrasound
CT Images

Ongoing Trials at Clinical

US National Guidelines Clearinghouse

NICE Guidance

FDA on Guillain-Barré syndrome pathophysiology

CDC on Guillain-Barré syndrome pathophysiology

Guillain-Barré syndrome pathophysiology in the news

Blogs on Guillain-Barré syndrome pathophysiology

Directions to Hospitals Treating Guillain-Barré syndrome

Risk calculators and risk factors for Guillain-Barré syndrome pathophysiology

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


The exact pathogenesis of Guillain Barre syndrome is not completely understood but in 2/3 of cases there is a history of an infectious disease in the past month.The most common pathogens responsible for these antecedent infections are: Campylobacter jejuni, cytomegalo virus and Hemophilus influenzae. It is believed that the main underlying etiology of GBS is an autoimmune reaction due to molecular mimicry. On microscopic histopathological analysis: Lymphocyte and macrophage infiltration, demyelination in AIDP, Macrophage infiltration and axolemma disruption in motor fibers in AMAN, disruption of both motor and sensory fibers. Little lymphocyte infiltration in AMSAN and Oculomotor nerve demyelination in Miller Fisher type.



  • Dendrites are branched processes which lead the impulse into the neuronal cell body.
  • Axons in a single process which lead the impulse away from the neuronal cell body.
  • This structure leads to fast traveling of electrical impulses.[1]



  • There is no characteristic genetic association with GBS.

Microscopic Pathology


  1. Mattle, Heinrich (2017). Fundamentals of neurology : an illustrated guide. Stuttgart New York: Thieme. ISBN 9783131364524.
  2. Winer JB, Hughes RA, Anderson MJ, Jones DM, Kangro H, Watkins RP (May 1988). "A prospective study of acute idiopathic neuropathy. II. Antecedent events". J. Neurol. Neurosurg. Psychiatry. 51 (5): 613–8. PMC 1033063. PMID 3404161.
  3. Jacobs BC, Rothbarth PH, van der Meché FG, Herbrink P, Schmitz PI, de Klerk MA, van Doorn PA (October 1998). "The spectrum of antecedent infections in Guillain-Barré syndrome: a case-control study". Neurology. 51 (4): 1110–5. PMID 9781538.
  4. 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.
  5. 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 2191246. PMID 8228822.
  6. Chiba A, Kusunoki S, Obata H, Machinami R, Kanazawa I (October 1993). "Serum anti-GQ1b IgG antibody is associated with ophthalmoplegia in Miller Fisher syndrome and Guillain-Barré syndrome: clinical and immunohistochemical studies". Neurology. 43 (10): 1911–7. PMID 8413947.
  7. Irie S, Saito T, Nakamura K, Kanazawa N, Ogino M, Nukazawa T, Ito H, Tamai Y, Kowa H (August 1996). "Association of anti-GM2 antibodies in Guillain-Barré syndrome with acute cytomegalovirus infection". J. Neuroimmunol. 68 (1–2): 19–26. PMID 8784256.
  8. Mori M, Kuwabara S, Miyake M, Dezawa M, Adachi-Usami E, Kuroki H, Noda M, Hattori T (April 1999). "Haemophilus influenzae has a GM1 ganglioside-like structure and elicits Guillain-Barré syndrome". Neurology. 52 (6): 1282–4. PMID 10214761.
  9. 9.0 9.1 Hafer-Macko CE, Sheikh KA, Li CY, Ho TW, Cornblath DR, McKhann GM, Asbury AK, Griffin JW (May 1996). "Immune attack on the Schwann cell surface in acute inflammatory demyelinating polyneuropathy". Ann. Neurol. 39 (5): 625–35. doi:10.1002/ana.410390512. PMID 8619548.
  10. 10.0 10.1 Hafer-Macko C, Hsieh ST, Li CY, Ho TW, Sheikh K, Cornblath DR, McKhann GM, Asbury AK, Griffin JW (October 1996). "Acute motor axonal neuropathy: an antibody-mediated attack on axolemma". Ann. Neurol. 40 (4): 635–44. doi:10.1002/ana.410400414. PMID 8871584.
  11. 11.0 11.1 Ganser AL, Kirschner DA (1984). "Differential expression of gangliosides on the surfaces of myelinated nerve fibers". J. Neurosci. Res. 12 (2–3): 245–55. doi:10.1002/jnr.490120212. PMID 6502752.
  12. 12.0 12.1 Feasby TE, Hahn AF, Brown WF, Bolton CF, Gilbert JJ, Koopman WJ (June 1993). "Severe axonal degeneration in acute Guillain-Barré syndrome: evidence of two different mechanisms?". J. Neurol. Sci. 116 (2): 185–92. PMID 8336165.
  13. 13.0 13.1 Feasby TE, Gilbert JJ, Brown WF, Bolton CF, Hahn AF, Koopman WF, Zochodne DW (December 1986). "An acute axonal form of Guillain-Barré polyneuropathy". Brain. 109 ( Pt 6): 1115–26. PMID 3790970.
  14. Chiba A, Kusunoki S, Obata H, Machinami R, Kanazawa I (October 1993). "Serum anti-GQ1b IgG antibody is associated with ophthalmoplegia in Miller Fisher syndrome and Guillain-Barré syndrome: clinical and immunohistochemical studies". Neurology. 43 (10): 1911–7. PMID 8413947.
  15. Phillips MS, Stewart S, Anderson JR (May 1984). "Neuropathological findings in Miller Fisher syndrome". J. Neurol. Neurosurg. Psychiatry. 47 (5): 492–5. PMC 1027825. PMID 6736980.

Template:WH Template:WS