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Physiology · Neuromuscular junction: Lambert-Eaton syndrome
Sample itemA 62-year-old heavy smoker has proximal leg weakness, dry mouth and absent knee jerks. Strength and reflexes improve briefly after a 10-second maximal voluntary contraction, and high-frequency nerve stimulation shows a marked increase in the muscle response. Which mechanism explains the improvement?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. Calcium accumulation in the motor nerve terminal during repetitive firing increases acetylcholine release
In Lambert-Eaton syndrome, antibodies against presynaptic P/Q-type calcium channels reduce calcium entry and so the quantal release of acetylcholine. Rapid repetitive stimulation allows residual calcium to accumulate, which facilitates release and increases the response. The association with small cell lung cancer should prompt a search for malignancy.
Option by option
A. Calcium accumulation in the motor nerve terminal during repetitive firing increases acetylcholine release (correct)
Facilitation by accumulated presynaptic calcium explains the increment.
B. Recovery of postsynaptic receptors that were blocked by antibodies
Postsynaptic receptor antibodies are the mechanism of myasthenia gravis, which worsens rather than improves with effort.
C. Reduced acetylcholinesterase activity during muscle activity
Acetylcholinesterase activity is not altered by exercise; the defect is in transmitter release.
D. Increased synthesis of acetylcholine in the axon during exercise
Acetylcholine synthesis is not the limiting step and is not increased within seconds of exercise.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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