A 24-year-old man develops rapidly ascending weakness over 10 days, progressing from legs to arms. Deep tendon reflexes are absent bilaterally. CSF shows protein 180 mg/dL with cell count of 4 cells/µL (albuminocytological dissociation). Nerve conduction study shows reduced CMAP amplitudes with absent F-waves but preserved sensory nerve action potentials. This electrophysiological pattern suggests:
- A Acute inflammatory demyelinating polyneuropathy (AIDP)
- B Miller Fisher syndrome
- C Chronic inflammatory demyelinating polyneuropathy (CIDP)
- D Acute motor axonal neuropathy (AMAN variant of GBS) ✓
Explanation
AMAN is a GBS variant characterised by axonal degeneration predominantly affecting motor fibres, associated with anti-GM1 and anti-GD1a antibodies and often preceded by Campylobacter jejuni infection. NCS shows reduced/absent CMAPs with preserved SNAPs (pure motor axonal pattern) and absent F-waves without demyelinating features (no conduction block, no prolonged distal latency). AIDP, the most common GBS variant in Western countries, shows demyelinating features: prolonged distal latencies, conduction block, and slowed NCV. Miller Fisher syndrome features ophthalmoplegia, ataxia, and areflexia with anti-GQ1b antibodies.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.