## Pathological Hallmark of GBS **Key Point:** Demyelination of peripheral nerves is the most common pathological finding in Guillain-Barré Syndrome, particularly in the demyelinating variant (AIDP — acute inflammatory demyelinating polyneuropathy), which accounts for ~90% of GBS cases in developed countries. ### Pathological Features | Feature | AIDP (Demyelinating) | AMAN/AMSAN (Axonal) | | --- | --- | --- | | Primary pathology | Segmental demyelination | Axonal degeneration | | Frequency (developed nations) | ~90% | ~10% | | Frequency (Asia/developing) | ~30–50% | ~50–70% | | Nerve conduction pattern | Slowing, prolonged latencies, conduction blocks | Normal or mildly reduced velocity, preserved conduction | | Recovery | Remyelination (slower but complete) | Axonal regeneration (slower, may be incomplete) | ### Mechanism of Demyelination 1. Post-infectious immune trigger (Campylobacter jejuni, CMV, EBV) 2. Molecular mimicry → cross-reactive B and T cells 3. Antibody and complement deposition on myelin 4. Macrophage infiltration → stripping of myelin sheath 5. Relative preservation of axons (initially) **High-Yield:** The demyelinating pattern produces the characteristic **slowing of conduction velocity** and **prolonged distal latencies** on nerve conduction studies — key diagnostic clues. **Clinical Pearl:** Axonal variants (AMAN, AMSAN) are more common in Asia and are associated with *Campylobacter jejuni* infection; they carry a worse prognosis because axonal regeneration is slower than remyelination. 
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