Guillain-Barré Syndrome
Neurology
Illness script · Neurology
Guillain-Barré Syndrome
Acute post-infectious autoimmune demyelinating polyradiculoneuropathy causing ascending flaccid paralysis, areflexia, and potential respiratory failure.
This illness script for Guillain-Barré Syndrome covers predisposing factors, classic presentation, mechanism, workup, management, and the clinical pivots that separate it from look-alikes—written for USMLE Step 1 and clerkship reasoning.
01
Predisposing factors
- Preceded by infection 2–4 weeks prior in ~70% of cases
- Campylobacter jejuni most common trigger (esp. axonal variant AMAN)
- Also: CMV, EBV, Zika, influenza, COVID-19, flu vaccine (rare)
- Any age; slight male predominance
- Prior surgery or immunization can occasionally precede onset
02
Presentation
- Ascending symmetric limb weakness beginning distally, progressing over days–4 weeks
- Areflexia (universal) — loss of DTRs is the key early exam finding
- Back/leg pain and paresthesias common early; sensory deficits mild
- Cranial nerve involvement in ~50%: bilateral facial palsy most classic
- Autonomic dysfunction: labile BP, bradycardia, urinary retention
- Respiratory failure in ~30% — monitor FVC; intubate if FVC <20 mL/kg or <1 L
03
Pathophysiology
- Molecular mimicry: antibodies against microbial antigens cross-react with peripheral nerve gangliosides (GM1, GQ1b)
- Complement-mediated attack on Schwann cells → segmental demyelination (AIDP) or axonal damage (AMAN/AMSAN)
- Disruption of saltatory conduction → progressive weakness and areflexia
- Autonomic involvement: unstable BP, arrhythmias, ileus
04
Diagnostics
- LP: albuminocytologic dissociation — elevated protein (>45 mg/dL) with normal WBC; hallmark finding
- EMG/NCS: gold standard — demyelination (slowed conduction, prolonged F-waves) in AIDP
- LP may be normal in first 1–2 weeks — do not rule out GBS on early normal LP
- Anti-GQ1b antibodies in Miller Fisher variant (ophthalmoplegia, ataxia, areflexia)
- MRI spine to exclude cord compression if diagnosis uncertain
05
Management
- Admit all patients; serial FVC q4–6h to anticipate respiratory failure
- IVIg (2 g/kg over 5 days) OR plasmapheresis — equivalent efficacy, choose one
- Steroids are NOT beneficial and not recommended in GBS
- DVT prophylaxis, pain management (neuropathic agents), bowel/bladder care
- Most patients recover; ~10% have permanent disability; nadir at 4 weeks then plateau
06
Clinical pivots
How to separate this script from the look-alikes that show up on exams and on the wards.
Spinal Cord Compression/Transverse Myelitis
GBS has NO sensory level and NO upper motor neuron signs; reflexes are absent not hyperreflexic
Myasthenia Gravis
MG has fatigable weakness, preserved reflexes, and normal CSF; no ascending pattern
Botulism
Botulism is descending paralysis with dilated fixed pupils and no sensory symptoms
Miller Fisher Syndrome
MFS is GBS variant: ophthalmoplegia + ataxia + areflexia triad with anti-GQ1b antibodies
Keep reading
Full library- Greater Trochanteric Pain SyndromeLateral hip pain arising from gluteal tendinopathy and/or trochanteric bursitis at the greater trochanter, formerly called trochanteric bursitis.
- HyperkalemiaSerum potassium >5.5 mEq/L causing life-threatening cardiac and neuromuscular dysfunction via altered membrane potential.
Educational use only. This illness script is a study framework, not medical advice. Confirm decisions with current guidelines and your clinical supervisors.