Guillain-Barré syndrome
Acute immune-mediated demyelinating polyneuropathy (post-infective)
Overview
An acute, immune-mediated, ASCENDING demyelinating polyneuropathy, classically a few weeks after an infection (especially Campylobacter jejuni). Progressive symmetrical weakness with areflexia; the danger is respiratory failure and autonomic instability. Treated with IVIG or plasma exchange (NOT steroids).
Recognise
- Progressive, symmetrical, ASCENDING weakness (legs then arms) with AREFLEXIA
- ~1–3 weeks after a GI/respiratory infection (Campylobacter, CMV, EBV); mild sensory/paraesthesiae
- Respiratory muscle weakness (monitor FVC); autonomic instability; cranial/bulbar involvement
Red flags
- FALLING FVC (respiratory failure → ventilation), autonomic instability (arrhythmia, BP swings), bulbar weakness
Differentials & how to tell them apart
Investigations
Clinical + nerve conduction studies (demyelination); LP shows ALBUMINOCYTOLOGICAL DISSOCIATION (raised protein, normal cell count); SERIAL FVC/spirometry to monitor respiratory function.
Management
IVIG (or plasma exchange) + respiratory monitoring (serial FVC); NOT steroids
- 1Admit; SERIAL FVC monitoring (the key safety measure — ventilate before crisis); IVIG or plasma exchange; VTE prophylaxis.Gate: Steroids do NOT work in GBS (unlike MS/CIDP); and a falling FVC, not oxygen saturation, is what flags impending respiratory failure → ICU/ventilation
- 2Supportive care, autonomic monitoring, rehabilitation; most recover well over months.
Key points
Ascending weakness + areflexia + recent infection + albuminocytological dissociation = GBS. Monitor FVC (not just sats). Treat with IVIG/plasma exchange — steroids do not help. Miller-Fisher variant = ophthalmoplegia + ataxia + areflexia (anti-GQ1b).
Monitor & prognosis
Serial FVC, autonomic status (ECG/BP), swallow, progression then recovery.
~80% recover well; respiratory failure and autonomic instability are the acute risks.
Source: NICE CKS; neurology guidance