Lambert-Eaton myasthenic syndrome (LEMS) differs from myasthenia gravis in which key clinical and electrophysiological feature?
- A LEMS causes ocular and bulbar weakness as the predominant feature; MG causes proximal limb weakness
- B LEMS is associated with anti-AChR antibodies; MG is associated with anti-VGCC antibodies
- C LEMS shows decremental response at low-frequency nerve stimulation and incremental response at high-frequency stimulation; deep tendon reflexes are reduced but transiently augment post-exercise ✓
- D LEMS responds to pyridostigmine as first-line therapy; MG requires plasma exchange
Explanation
LEMS is caused by antibodies against voltage-gated calcium channels (anti-VGCC) at the presynaptic terminal (not AChR as in MG). The classic electrophysiology shows decrement at low-frequency (3 Hz) stimulation and marked increment (>100%) at high-frequency (50 Hz) stimulation or post-exercise facilitation — the opposite pattern from MG which shows only decrement. Clinically, DTRs are absent or reduced at rest but transiently return after exercise (post-tetanic potentiation). Ocular and bulbar muscles are less affected in LEMS; proximal limb and autonomic features predominate. LEMS is paraneoplastic in ~60% (SCLC).
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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Written and medically reviewed by the StethoPrep medical team.