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Guillain-Barré Syndrome in Children: A Clinician's Monograph

Concise clinician reference on pediatric GBS — Brighton case definition, albuminocytologic dissociation, IVIG/plasma exchange, and respiratory red flags.

Full criteria: Guillain-Barré Syndrome.

Definition and epidemiology

Guillain-Barré syndrome (GBS) is an acute, immune-mediated polyradiculoneuropathy and the commonest cause of acute flaccid paralysis in children since the near-elimination of poliomyelitis. Annual incidence is roughly 0.4–1.4 per 100,000 children, rising with age. It is typically post-infectious, following Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, Mycoplasma pneumoniae, Zika or other infections by 1–4 weeks. The acute inflammatory demyelinating polyneuropathy (AIDP) subtype predominates in Western series; axonal variants (AMAN/AMSAN) are commoner in Asia, including India, and are associated with Campylobacter and anti-ganglioside antibodies. Miller Fisher syndrome (ophthalmoplegia, ataxia, areflexia) is an important variant.

Clinical features

The hallmark is a progressive, ascending, symmetrical flaccid weakness with areflexia/hyporeflexia. Typical features:

Progression is by definition within 4 weeks (most reach nadir by 2 weeks), distinguishing GBS from chronic inflammatory demyelinating polyneuropathy (CIDP).

Diagnosis

GBS is primarily clinical, supported by two investigations:

The Brighton Collaboration case definition grades diagnostic certainty: Level 1 (highest) requires the clinical picture plus supportive CSF and NCS; Level 2 the clinical picture with either CSF or NCS; Level 3 the clinical picture alone. MRI may show nerve-root enhancement. Exclude mimics: transverse myelitis/cord compression (look for a sensory level and sphincter involvement early), myasthenia, botulism, tick paralysis, hypokalaemia, and toxic neuropathies.

See the full criteria: Guillain-Barré Syndrome Algorithm

Red flags

Management overview

Care is supportive plus immunotherapy. Admit; monitor respiratory function (serial FVC/NIF where feasible), swallowing, and cardiovascular autonomic status, escalating to HDU/PICU for ventilatory or autonomic compromise. Immunotherapy is indicated for non-ambulant or rapidly-progressing children: IVIG 2 g/kg over 2–5 days, or plasma exchange; the two are equally effective and are not combined. Corticosteroids are not effective in GBS and should not be used as monotherapy. Provide neuropathic pain control (gabapentin/carbamazepine; opioids with caution given ileus/autonomic risk), VTE prophylaxis in immobile adolescents, bowel/bladder care, and early physiotherapy/rehabilitation.

Prognosis in children is generally favourable, with most regaining independent walking over weeks to months, though axonal variants and those needing ventilation recover more slowly. Watch for treatment-related fluctuation and the small subset that evolves into CIDP.

References

  1. Sejvar JJ, et al. Brighton Collaboration GBS case definitions. Vaccine. 2011;29:599–612.
  2. Leonhard SE, et al. GBS diagnosis and management in ten steps. Nat Rev Neurol. 2019;15:671–683.
  3. Nelson Textbook of Pediatrics, 21st ed.

Decision support for qualified clinicians only — verify against current primary guidelines and your clinical judgement.

References

Last updated 2026-06-28.

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