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General Medicine · Neurology: amyotrophic lateral sclerosis
Sample itemA 58-year-old man has progressive wasting and fasciculations of the hands with brisk reflexes and spasticity in the legs. Sensation, eye movements and bladder control are normal and EMG shows widespread denervation. He is started on riluzole. What is its mechanism of action?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. Inhibition of presynaptic glutamate release
Amyotrophic lateral sclerosis combines upper and lower motor neuron signs with sparing of sensory, oculomotor and sphincter function. Riluzole reduces glutamate-mediated excitotoxicity by inhibiting presynaptic glutamate release and blocking sodium channels, and prolongs survival by a few months. Respiratory support and nutrition are central to care.
Option by option
A. Inhibition of presynaptic glutamate release (correct)
Correct. Reduced glutamate release lessens excitotoxic motor neuron injury.
B. Inhibition of acetylcholinesterase
Acetylcholinesterase inhibition is the mechanism of pyridostigmine and donepezil.
C. Potentiation of GABA-A receptors
GABA-A potentiation is the mechanism of benzodiazepines, which can worsen respiratory weakness.
D. Blockade of postsynaptic dopamine D2 receptors
D2 receptor blockade is the mechanism of antipsychotics.
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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