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Physiology · Motor system: upper motor neurone lesion
Sample itemA man six weeks after a stroke has a spastic arm, brisk reflexes and an upgoing great toe on the same side. Which mechanism most directly accounts for the spasticity?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Loss of descending inhibitory drive, which disinhibits the stretch reflex
Lesions of the upper motor neurone remove corticoreticular and other descending inhibitory influences, so gamma-motor neurone and stretch reflex gain increase, causing velocity-dependent hypertonia, hyperreflexia, clonus and the extensor plantar response. Lower motor neurone lesions cause flaccidity, atrophy and fasciculations. Spasticity may be delayed after the initial flaccid stage.
Option by option
A. Degeneration of anterior horn cells
Loss of anterior horn cells would produce flaccid weakness with wasting.
B. Loss of descending inhibitory drive, which disinhibits the stretch reflex (correct)
Correct. Disinhibition of spinal reflex circuits produces spasticity.
C. Destruction of muscle spindles
Spindle loss would reduce, not increase, reflex gain.
D. Block of neuromuscular transmission
A junctional block would cause weakness without hyperreflexia.
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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