Guillain-Barré syndrome (GBS)
Overview
Guillain-Barré syndrome is an acute, immune‑mediated polyradiculoneuropathy that typically presents with rapidly progressive, symmetrical weakness and reduced or absent tendon reflexes. It is a core emergency medicine condition because of the risk of respiratory failure, bulbar dysfunction and autonomic instability; all suspected cases require urgent inpatient assessment and early neurology and critical‑care discussion (NICE NG127; GOV.UK).
High‑yield facts (rapid orientation)
- Incidence ≈ 1-2 per 100,000 per year; more common in men (≈1.5:1); incidence increases with age.
- Antecedent infection is reported in about two‑thirds of cases; respiratory or gastrointestinal infections are typical and Campylobacter jejuni is commonly implicated (GOV.UK).
- Natural history: progressive weakness over days to weeks (usually maximal by 2 weeks; rarely beyond 4 weeks), followed by a plateau and then recovery over weeks to months.
- Major early risks are evolving respiratory failure and autonomic dysfunction; about 20-30% require mechanical ventilation.
- Disease‑modifying treatments for eligible patients (non‑ambulant or respiratory compromise) are IV immunoglobulin (IVIG) or plasma exchange (PE); start early (ideally within the first 2 weeks) but do not delay airway or ventilatory support while arranging treatment (GOV.UK).
Pathophysiology and major variants
GBS is caused by an aberrant immune response (molecular mimicry) targeting peripheral nerves and roots. Injury patterns include demyelination or axonal damage; clinical phenotype reflects the pathological target.