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To the Editor:
Brown et al.1 offer two pieces of evidence that residual weakness after neonatal brachial plexus palsy (NBPP) may represent “developmental apraxia” rather than the effects of poor nerve fiber regeneration. First, the twitch elicited by stimulating the nerve to the muscle of the affected arm is equal to that in the unaffected arm, whereas the maximal voluntary torque generated by the affected muscle is less than that of the unaffected side. This discrepancy is interpreted as a normal contractile muscle mass that cannot be fully activated voluntarily. Second, during maximal voluntary contraction (MVC) of the affected muscle, stimulation of the motor nerve evokes a twitch in 30% of the palsied limbs, but in none of the controls. This is interpreted as evidence of unactivated motor units during MVC.
An alternative interpretation of the results is possible. Aberrant regeneration of agonist axons to innervate antagonists may cause cocontraction of agonist and antagonist muscles,2,3 …
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