A patient with Lambert-Eaton myasthenic syndrome (LEMS) has autoantibodies against voltage-gated calcium channels (VGCC) at the presynaptic motor nerve terminal. The clinical consequence that distinguishes LEMS from myasthenia gravis is:

• A Muscles of the eyes and bulbar muscles are preferentially affected compared to proximal limb muscles
• B Tendon reflexes are exaggerated due to lack of presynaptic inhibition
• C Edrophonium (Tensilon) test shows dramatic improvement as in myasthenia gravis
• D Muscle strength paradoxically improves transiently with repeated exercise (incremental response on repetitive nerve stimulation) ✓

Explanation

In LEMS, antibodies reduce presynaptic VGCC number and function, impairing Ca2+-triggered acetylcholine vesicle release. With repeated stimulation, Ca2+ accumulates in the presynaptic terminal (because residual VGCCs can still mediate some Ca2+ entry that summates), increasing ACh release and temporarily improving neuromuscular transmission — the classic 'incremental' or 'facilitated' EMG response and paradoxical post-exercise strength improvement. In contrast, MG has a decremental response on repetitive stimulation because postsynaptic AChR antibodies deplete the end-plate potential reserve. Ocular muscles are more prominently affected in MG, while proximal limb and autonomic features predominate in LEMS.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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