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Guillain-Barré syndrome

Last updated: May 30, 2021

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Guillain-Barré syndrome (GBS) is an acute postinfectious polyneuropathy characterized by symmetric and ascending flaccid paralysis. In affected patients, cross‑reactive autoantibodies attack the host's own axonal antigens, resulting in inflammatory and demyelinating polyneuropathy. Albuminocytologic dissociation, characterized by elevated protein levels and normal cell counts in cerebrospinal fluid (CSF), is a hallmark finding of GBS. Additionally, muscle and nerve electrophysiology are used to diagnose demyelinating processes. Symptomatic and supportive treatment results in disease remission in about 70% of cases. In severe cases or patients who do not respond to treatment, intravenous immunoglobulin (IVIG) administration and/or plasmapheresis may be used. Potentially acute life-threatening complications such as respiratory insufficiency, pulmonary embolism, and/or cardiac arrest increase mortality. Although GBS is associated with a good prognosis overall, up to 20% of patients remain severely disabled and approximately 5% of cases are fatal, despite immunotherapy.

  • Incidence [1]
    • ∼ 1 case per 100,000 individuals
    • Adults are affected more frequently than children.
  • Sex: > (1.5:1) [2]

Epidemiological data refers to the US, unless otherwise specified.

References:[6]

Initial symptoms

Advanced symptoms

GBS paralysis affects the muscles of respiration, possibly leading to death due to respiratory failure.

Overview of subtypes and variants of Guillain-Barré syndrome
Description Etiology Clinical features Treatment
Acute inflammatory demyelinating polyneuropathy (AIDP) [7]
  • Acute variant of Guillain‑Barré syndrome
  • Predominant sub-type affecting 60–80% of GBS patients in North America and Europe
Chronic inflammatory demyelinating polyneuropathy (CIDP) [8][9]
  • Chronic variant of Guillain‑Barré syndrome
  • Similar to those of GBS, but lasting > 2 months
Miller-Fisher syndrome
Multifocal motor neuropathy (MMN) [10]
  • Asymmetric paralysis and areflexia
  • Initially involves the distal upper limbs
Acute motor axonal neuropathy (AMAN)
  • An abrupt-onset variant of GBS
  • Affects motor nerve fibers with variable severity and spares sensory fibers
  • Acute paralysis
  • Areflexia without sensory loss

References:[6]

Although GBS is considered an autoimmune disease, glucocorticoids are not recommended for treatment. They have not shown to hasten recovery or affect the long-term outcome.

  • ∼ 70% of patients with GBS have a good prognosis [13]
    • Disease progression peaks 2–4 weeks after the onset of symptoms.
    • Symptoms then recede in reverse order of their development; (i.e., the last symptoms to appear resolve first, as Schwann cells remyelinate peripheral nerve axons).
  • 3–7% of patients with GBS die due to acute complications such as:
    • Respiratory paralysis (apnea)
    • Pulmonary infection/embolism
    • Cardiac dysfunction
  • 6 months after onset, ∼ 20% of affected individuals are still unable to walk unaided.

Death can occur as many as > 30 days after onset of symptoms, during the recovery phase.

  1. Guillain-Barré Syndrome. https://www.cdc.gov/campylobacter/guillain-barre.html. Updated: December 20, 2019. Accessed: December 23, 2020.
  2. Yuki N, Hartung HP. Guillain–Barré Syndrome. N Engl J Med. 2012; 366 : p.2294-2304. doi: 10.1056/NEJMra1114525 . | Open in Read by QxMD
  3. Uncini A, Vallat J-M, Jacobs BC. Guillain-Barré syndrome in SARS-CoV-2 infection: an instant systematic review of the first six months of pandemic. Journal of Neurology, Neurosurgery & Psychiatry. 2020; 91 (10): p.1105-1110. doi: 10.1136/jnnp-2020-324491 . | Open in Read by QxMD
  4. Hartung HP. Infections and the Guillain-Barré Syndrome. J Neurol Neurosurg Psychiatry. 1999; 66 : p.277. doi: 10.1136/jnnp.66.3.277 . | Open in Read by QxMD
  5. Nelson KE. Invited Commentary: Influenza Vaccine and Guillain-Barre Syndrome--Is There a Risk?. Am J Epidemiol. 2012; 175 (11): p.1129-1132. doi: 10.1093/aje/kws194 . | Open in Read by QxMD
  6. Van Den Berg B, Walgaard C, Drenthen J, Fokke C, Jacobs BC, Van Doorn PA. Guillain–Barré syndrome: pathogenesis, diagnosis, treatment and prognosis. Nature Reviews Neurology. 2014; 10 : p.469–482. doi: 10.1038/nrneurol.2014.121 . | Open in Read by QxMD
  7. AIDP/CIDP Part 2: Treatment. https://now.aapmr.org/aidpcidp-part-2-treatment/. Updated: September 20, 2014. Accessed: April 4, 2018.
  8. Chronic inflammatory demyelinating polyradiculoneuropathy: from pathology to phenotype . http://jnnp.bmj.com/content/early/2015/02/12/jnnp-2014-309697.full. Updated: February 12, 2015. Accessed: April 2, 2017.
  9. Mathey EK, Park SB, Hughes RAC, et al. Chronic inflammatory demyelinating polyradiculoneuropathy: from pathology to phenotype. J Neurol Neurosurg Psychiatry. 2015; 86 (9): p.973-985. doi: 10.1136/jnnp-2014-309697 . | Open in Read by QxMD
  10. Lawson VH, Arnold DW. Multifocal motor neuropathy: a review of pathogenesis, diagnosis, and treatment. Neuropsychiatr Dis Treat. 2014; 10 : p.567–576. doi: 10.2147/NDT.S39592 . | Open in Read by QxMD
  11. Dimachkie MM, Barohn RJ, Katz J. Multifocal Motor Neuropathy, Multifocal Acquired Demyelinating Sensory and Motor Neuropathy, and Other Chronic Acquired Demyelinating Polyneuropathy Variants. Neurol Clin. 2013; 31 (2): p.533-555. doi: 10.1016/j.ncl.2013.01.001 . | Open in Read by QxMD
  12. Hughes RAC, Wijdicks EFM, Barohn R, Benson E, et al. Practice parameter: Immunotherapy for Guillain-Barré Syndrome. Neurology. 2003; 61 (6). doi: 10.1212/WNL.61.6.736 . | Open in Read by QxMD
  13. Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barré syndrome. Lancet. 2016; 388 : p.717-727. doi: 10.1016/ S0140-6736(16)00339-1 . | Open in Read by QxMD