A 24-year-old woman presents with ascending weakness starting in the legs over 8 days after a GI illness. Examination reveals areflexia, symmetric proximal and distal weakness, and diminished proprioception. CSF shows albumino-cytological dissociation (protein 180 mg/dL, WBC 2 cells/µL). Nerve conduction studies show absent F-waves, prolonged distal motor latencies, and reduced CMAP amplitudes with normal sensory action potentials. Which subtype of GBS does this electrophysiology suggest?
- A Acute motor axonal neuropathy (AMAN)
- B Miller Fisher syndrome (MFS)
- C Acute inflammatory demyelinating polyneuropathy (AIDP) ✓
- D Acute motor and sensory axonal neuropathy (AMSAN)
Explanation
AIDP (the classic Western form) shows demyelinating features on NCS: prolonged distal motor latencies, reduced conduction velocity, prolonged/absent F-waves, conduction blocks, and temporal dispersion. CMAP amplitudes may be reduced due to conduction block but are not primarily axonally lost. AMAN (prevalent in Asia, associated with Campylobacter, anti-GM1/GD1a antibodies) shows reduced CMAP amplitudes with preserved conduction velocity and sensory action potentials, indicating motor axonal involvement sparing sensory nerves — this case has reduced CMAPs but also prolonged distal latencies suggesting demyelination. AMSAN affects both motor and sensory axons. Miller Fisher syndrome presents with ophthalmoplegia, ataxia, and areflexia (anti-GQ1b antibodies) without significant limb weakness.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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Written and medically reviewed by the StethoPrep medical team.