even cause the take-up area to be larger in infants than in adults (Blok and Stegeman, personal communication), increasing the number of visible MUAPs even further. The amplitude of the muscle fiber potentials will be smaller, due to their smaller diameters, but we doubt that this seriously affects the judgment of the recruitment pattern. If this hypothesis is correct, electromyographers have to recalibrate their sense for the relation between strength, recruitment pattern, and degree of nerve fiber loss in infants, requiring the study of normal muscles.
Second, central nervous system (CNS) plasticity is involved in regaining function after nerve repair in adults, 8 which may also be true in infants. Infant movements differ from adult ones. Severe nerve damage might disrupt the normal maturation of CNS motor programs, leading to MUAPs that are not embedded in functional movement programs, rendering their action unnoticeable clinically. Motor unit estimation provided evidence for this view, by revealing a normal number of motor units in the biceps of a 3-year-old with OBPL despite abnormal use of the arm. The abnormal use was thus in part due to a CNS cause and not to nerve damage alone.
Further studies must determine to what degree the clinical/EMG discrepancy in OBPL indeed derives from a methodological overestimation of the number of functional motor units by the electromyographer, and its functional underestimation by the clinician.