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Physiology · Muscle physiology: denervation
Sample itemA 45-year-old man with a lumbar radiculopathy has had weakness of ankle dorsiflexion for six weeks. Needle electromyography at rest shows spontaneous fibrillation potentials in the tibialis anterior. What is the mechanism of these potentials?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
C. Spread of acetylcholine receptors over the whole muscle fibre membrane, with spontaneous depolarisation of single denervated fibres
After denervation, the muscle fibre expresses acetylcholine receptors beyond the end plate and develops spontaneous membrane oscillations, causing random contraction of single fibres. These fibrillations are invisible through the skin but are seen on needle EMG from about two to three weeks after nerve injury. Fasciculations, in contrast, are visible twitches of whole motor units.
Option by option
A. Discharge of muscle spindles from stretch of the denervated muscle
Spindle discharge does not generate muscle fibre potentials at rest.
B. Spontaneous firing of surviving motor units that have increased their territory
Firing of enlarged surviving motor units gives fasciculations and large polyphasic potentials on voluntary activation.
C. Spread of acetylcholine receptors over the whole muscle fibre membrane, with spontaneous depolarisation of single denervated fibres (correct)
Extrajunctional receptor expression and membrane instability produce single-fibre fibrillations.
D. Continuous acetylcholine release from regenerating axon terminals
Regenerating terminals produce a different pattern, and the fibrillations appear before reinnervation.
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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