How does LEMS differ clinically from myasthenia gravis?

LEMS: proximal lower limb weakness predominant (difficulty rising from chair), reduced/absent DTRs, autonomic features (dry mouth, constipation, impotence), transient improvement with exercise (post-tetanic potentiation); MG: ocular and bulbar predominant, normal DTRs, worsens with exercise.

What cancer causes paraneoplastic LEMS?

Small cell lung cancer (SCLC) causes ~60% of LEMS; VGCC antibodies cross-react between SCLC voltage-gated calcium channels and presynaptic motor nerve terminals; SCLC detection is urgent as LEMS may precede SCLC diagnosis by months-years.

What is the 3,4-DAP dosing for LEMS?

3,4-Diaminopyridine (amifampridine) 15-60 mg/day in 3-4 divided doses; blocks potassium channels, prolonging nerve terminal depolarization and increasing calcium influx for ACh release; FDA-approved for LEMS; paresthesias are common side effect.

What EMG pattern is diagnostic for LEMS?

CMAP amplitude low at rest; >100% CMAP increment with repetitive nerve stimulation at 50 Hz (high frequency facilitation) or post-exercise is diagnostic; SFEMG shows jitter (similar to MG but with different pattern); anti-VGCC antibodies in 85%.

What immunosuppression treats non-paraneoplastic LEMS?

Prednisolone + azathioprine as for MG; IVIG for rapid improvement; plasma exchange; pyridostigmine has modest benefit (less effective than in MG as ACh release rather than AChR degradation is primary defect); 3,4-DAP is the primary symptomatic treatment.

Lambert-Eaton Myasthenic Syndrome Clinical Score

Assesses Lambert-Eaton myasthenic syndrome (LEMS) severity using the QMG-LEMS score, VGCC antibody titer, paraneoplastic SCLC screening priority score, and 3,4-diaminopyridine dosing.

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Frequently Asked Questions

How does LEMS differ clinically from myasthenia gravis?

What cancer causes paraneoplastic LEMS?

What is the 3,4-DAP dosing for LEMS?

What EMG pattern is diagnostic for LEMS?

What immunosuppression treats non-paraneoplastic LEMS?