A 42-year-old woman from Delhi presents with acute-onset bilateral foot drop and inability to climb stairs over 3 days. She denies recent infections but reports a Campylobacter jejuni gastroenteritis 3 weeks ago. On examination, she has symmetrical weakness of hip flexors and foot dorsiflexors (MRC grade 3/5), with preserved reflexes in lower limbs and normal sensation. Electromyography shows active denervation potentials in lower limb muscles with normal conduction velocities. CSF protein is mildly elevated at 55 mg/dL with 2 lymphocytes/μL. What is the most likely variant of GBS in this patient?

Explanation

## Diagnosis: Acute Motor Axonal Neuropathy (AMAN) **Key Point:** This patient presents with **axonal GBS**, characterized by: 1. **Normal or near-normal conduction velocities** (preserved NCS velocities) 2. **Active denervation** on EMG (fibrillations, positive sharp waves) 3. **Preserved reflexes** (distinguishes from demyelinating GBS) 4. **Motor-predominant weakness** (lower limbs, foot drop) 5. **Mild CSF protein elevation** (less pronounced than AIDP) ## Comparison of GBS Variants | Feature | AIDP | AMAN | Miller Fisher | Pharyngeal-Cervical-Brachial | |---------|------|------|---------------|------------------------------| | **Frequency** | 60–70% (worldwide) | 30% (Asia) | 3–5% | Rare | | **NCS Pattern** | Demyelination (slow CV, blocks) | Axonal (normal/near-normal CV) | Normal or mild slowing | Axonal | | **Reflexes** | Absent/↓ | **Preserved** | Preserved | Preserved | | **Weakness** | Ascending, proximal + distal | **Motor predominant, distal** | Ophthalmoplegia + ataxia | Bulbar + neck + shoulder | | **Antecedent** | URI, diarrhea | **C. jejuni gastroenteritis** | C. jejuni, Zika | C. jejuni | | **CSF Protein** | Markedly ↑ (>100) | Mildly ↑ (50–80) | Normal or mild ↑ | Mildly ↑ | | **Prognosis** | Good (80% recover) | Slower recovery, more disability | Good | Variable | **High-Yield:** AMAN is the **most common variant in Asia** (30% of GBS cases), particularly after *Campylobacter jejuni* infection. The preserved reflexes are the **key discriminator** from AIDP. **Clinical Pearl:** AMAN has a **slower and less complete recovery** than AIDP. Patients often require longer ICU stays and have higher rates of residual disability. Early recognition is important for prognostication. **Mnemonic:** **AMAN = Axonal, Motor, Asia, Absent reflexes are NOT a feature** (preserved reflexes help identify it). ## Pathophysiology ```mermaid flowchart TD A[Campylobacter jejuni infection]:::outcome --> B[Molecular mimicry]:::action B --> C[Anti-GM1 antibodies]:::action C --> D[Axonal membrane attack]:::action D --> E[Motor nerve degeneration]:::action E --> F[AMAN phenotype]:::outcome ``` **Warning:** Do not confuse preserved reflexes in AMAN with normal neurological status — this is still a severe neuropathy requiring ICU monitoring and immunotherapy.