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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Acute ascending flaccid paralysis with areflexia, progressing over days-weeks, following a preceding infection (commonly Campylobacter jejuni)
- CSF: raised protein with normal cell count (albuminocytological dissociation) — may be normal in first week
- Nerve conduction studies confirm demyelinating polyneuropathy
- Treatment: IV immunoglobulin (IVIg 0.4 g/kg/day for 5 days) or plasma exchange
- CRITICAL: monitor respiratory function serially (FVC) — respiratory failure in ~25% requires ITU and ventilation
Overview
Guillain-Barré syndrome (GBS) is an acute immune-mediated polyneuropathy. The most common subtype in the UK is acute inflammatory demyelinating polyneuropathy (AIDP), caused by autoimmune attack on peripheral nerve myelin. Approximately two-thirds of patients report a preceding respiratory or gastrointestinal infection 1–4 weeks before onset. Campylobacter jejuni gastroenteritis is the most commonly identified trigger. Other triggers include CMV, EBV, Mycoplasma pneumoniae, and rarely vaccinations. Miller Fisher syndrome is a variant characterised by ophthalmoplegia, ataxia, and areflexia.
Epidemiology
GBS has a UK incidence of approximately 1–2 per 100,000 per year. It can affect any age but is slightly more common in men and incidence increases with age. It is the most common cause of acute flaccid paralysis in the developed world. C. jejuni is associated with the axonal variant (AMAN) and anti-ganglioside antibodies (anti-GM1).
Clinical Features
Symptoms
Preceding infection 1–4 weeks before (diarrhoeal illness or upper respiratory tract infection)
Ascending symmetrical limb weakness: starts in legs, progresses to arms over days-weeks
Paraesthesiae and numbness (but sensory symptoms usually mild compared to motor)
Back pain and limb pain — common early feature
Breathlessness: diaphragmatic weakness — life-threatening
Dysphagia and facial weakness (bulbar and facial nerve involvement)
Autonomic dysfunction: tachycardia, blood pressure instability, urinary retention, ileus
Signs
Symmetrical ascending flaccid weakness (LMN pattern)
Areflexia or hyporeflexia — typically global
Bilateral facial nerve palsy (~50%)
Reduced FVC — monitor serially (4-hourly). FVC <20 mL/kg = intubation threshold
Miller Fisher variant: ophthalmoplegia + ataxia + areflexia (anti-GQ1b antibodies)
Investigations
First-line
Nerve conduction studies (NCS)Prolonged distal motor latencies, reduced conduction velocities, conduction block, prolonged F-waves — consistent with demyelination. May be normal in first week
Lumbar punctureCSF: raised protein with normal cell count (albuminocytological dissociation). May be normal in first week — repeat if initially normal and clinical suspicion remains
Respiratory function monitoringSerial FVC (forced vital capacity) 4-hourly — most important bedside test. FVC <20 mL/kg or <1 L = consider ITU admission and ventilation
Second-line
Anti-ganglioside antibodiesAnti-GM1 (AMAN), anti-GQ1b (Miller Fisher), anti-GD1a — supportive but not required for diagnosis
BloodsFBC, U&Es, LFTs, CK, TFTs — exclude mimics. Campylobacter stool culture or serology
MRI spineIf cord compression suspected as differential — also may show nerve root enhancement in GBS
Specialist
ECG and cardiac monitoringAutonomic dysfunction — monitor for arrhythmias
1
Immunomodulatory treatment
- IV immunoglobulin (IVIg): 0.4 g/kg/day for 5 days — first-line in most centres
- Plasma exchange (plasmapheresis): 5 exchanges over 1–2 weeks — equally effective alternative
- Corticosteroids are NOT effective in GBS and should NOT be used
- Start treatment if unable to walk unaided or rapidly deteriorating
2
Respiratory monitoring and support
- Monitor FVC 4-hourly (more frequently if deteriorating)
- FVC <20 mL/kg or declining rapidly: discuss ITU admission and intubation
- ~25% of GBS patients require mechanical ventilation
- Single breath count <20 also correlates with need for ventilation
3
Supportive care
- DVT prophylaxis: LMWH + compression stockings
- Pain management: gabapentin or carbamazepine for neuropathic pain; opioids may be needed
- Autonomic monitoring: cardiac monitoring, BP, bowel/bladder function
- Physiotherapy: start early — prevent contractures, begin rehabilitation
- Nutrition: NG tube if bulbar involvement causes unsafe swallowing
Complications
- Respiratory failure: Life-threatening — requires ~25% to be ventilated. Serial FVC monitoring is critical
- Autonomic dysfunction: Arrhythmias, BP instability — continuous cardiac monitoring
- Pain: Severe neuropathic and musculoskeletal pain in >50% — often undertreated
- Residual disability: ~20% have persistent disability at 1 year. ~5% mortality despite treatment
- DVT/PE: Immobility — thromboprophylaxis essential
- Chronic inflammatory demyelinating polyneuropathy (CIDP): If symptoms persist >8 weeks, consider CIDP (chronic form)
UKMLA Exam Tips
- 1Post-infectious ascending flaccid paralysis with areflexia = GBS
- 2CSF: high protein, normal cells (albuminocytological dissociation) — may be normal in first week
- 3Campylobacter jejuni is the most common preceding infection
- 4Treatment: IVIg or plasma exchange — NOT steroids (steroids do not work in GBS)
- 5FVC monitoring is critical — FVC <20 mL/kg = prepare for intubation
- 6Miller Fisher syndrome: ophthalmoplegia + ataxia + areflexia (anti-GQ1b antibodies)
- 7Distinguish from MND: GBS is acute, ascending, areflexic, with sensory symptoms; MND is chronic, asymmetric, mixed UMN+LMN, NO sensory involvement
practicetest your knowledge on guillain-barré syndromeApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — neurology and beyond.
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