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Pathophysiology
Clinical meaning
Guillain-Barré syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy triggered by molecular mimicry: antibodies generated against microbial antigens cross-react with gangliosides and glycolipids on peripheral nerve myelin or axons. In acute inflammatory demyelinating polyneuropathy (AIDP — most common subtype, 90% in Western countries), T cells and macrophages attack Schwann cell myelin, causing segmental demyelination and conduction block. In acute motor axonal neuropathy (AMAN), anti-GM1 and anti-GD1a antibodies directly attack axonal membranes at nodes of Ranvier, causing primary axonal degeneration (more common in Asia, associated with Campylobacter jejuni). The ascending weakness pattern reflects immune attack starting at nerve roots (proximal) and motor nerve terminals (distal), progressing centrally. Respiratory failure occurs in 20-30% when the immune attack involves phrenic nerves (C3-5) and intercostal motor nerves. Autonomic involvement (dysautonomia) affects 60-70% and is a major cause of mortality through cardiac arrhythmias, labile blood pressure, and urinary retention.
Diagnostics & workup:
- Clinical diagnosis: acute onset symmetric ascending weakness + areflexia/hyporeflexia; progressive over days to 4 weeks (nadir by 4 weeks by definition)
- CSF: albumino-cytological dissociation — elevated protein (> 0.45 g/L) with normal cell count (< 10 cells/μL); may be normal in first week; if cells elevated > 50, consider HIV, CMV, lymphomatous meningitis
- Nerve conduction studies / EMG: demyelinating pattern in AIDP (prolonged distal motor latency, conduction block, F-wave prolongation, reduced conduction velocity); axonal pattern in AMAN (reduced CMAP amplitude with preserved conduction velocity); may be normal in first 1-2 weeks
- Serial FVC and NIF monitoring: q4-6h (q2h if declining) — SINGLE MOST IMPORTANT monitoring parameter; intubate at FVC < 20 mL/kg or NIF < -30 cmH2O or rapid decline (Erasmus GBS Respiratory Insufficiency Score [EGRIS] predicts ventilation need)
- Anti-ganglioside antibodies: anti-GM1 (AMAN), anti-GQ1b (Miller Fisher variant — ophthalmoplegia, ataxia, areflexia), anti-GD1a
- MRI spine with contrast: enhancement of cauda equina nerve roots on T1+Gd (present in ~95% of GBS; helps distinguish from transverse myelitis or compressive myelopathy)
- Stool culture for Campylobacter jejuni; serologies for CMV, EBV, Mycoplasma
- ECG and continuous cardiac monitoring: detect autonomic instability (bradycardia, heart block, tachyarrhythmias)
Risk factors:
- Preceding infection 1-4 weeks before symptom onset (70% of cases): Campylobacter jejuni (most common — 30%; associated with axonal variants and anti-GM1 antibodies), CMV, EBV, Mycoplasma pneumoniae, influenza, Zika virus
- Recent vaccination (rare association — 1-2 per million doses; influenza vaccine most studied; COVID-19 vaccine association extremely rare)
- Surgery within 1-4 weeks before onset
- Pregnancy (especially postpartum period)
- Hodgkin lymphoma and other malignancies (paraneoplastic association)
- HIV infection (particularly during seroconversion)
- Age (bimodal distribution — young adults and elderly; all ages affected)
- Male sex (1.5:1 predominance)
Management
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Prescribing & monitoring
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Takeaways
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