Motor unit territory and muscle fiber concentration in paresis due to peripheral nerve injury and anterior horn cell involvement

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Abstract
The changes in motor unit organization which accompany paresis caused by traumatic lesions of the peripheral nerve and paresis secondary to involvement of the anterior horn cells are described. By means of multilead recording, the spread of the action potentials of a motor unit over the cross section of the muscle and the maximum voltage within the motor unit were determined. The spread of the action potentials is a measure of the territory of the motor units and the maximum voltage, a gauge of the density of muscle fibers within it. In paresis secondary to peripheral nerve injury investigated 8 months or longer after nerve injury, the maximum voltage was 2.4 to 3.5 times that of normal muscle and the motor unit territory was increased by an average of 15 to 40%, depending on the muscle investigated. In muscles in which the motor nerve supply was damaged less than 3 months before the investigation, the maximum voltage was 1.8 times that of normal muscle in the deltoid and unchanged in the branchial biceps and the extensor digitorum com-munis. The motor unit territory was within the limits of normal muscle. The changes in motor unit territory and maximum voltage did not correlate with the degree of paresis as determined by muscle grading. In paresis due to involvement of the anterior horn cells (amyotrophic lateral sclerosis and spinal muscular atrophy [Werdnig-Hoffmann] the increase in motor unit territory and maximum voltage exceeded by far that of equally paretic muscles in peripheral nerve injuries. In severely involved muscles, the maximum voltage was 5 to 8 times that of normal muscle and the motor unit territory was increased by 80 to 140%. A considerable fraction of motor units had territories and maximum voltages never found in normal muscle. In less involved muscles, the values of territory and maximum voltage were in between those of severely involved and normal muscles, the maximum voltage being increased by 3 times and the territory by 40 to 130% as compared with normal muscle. Findings in peroneal muscular atrophy (Charcot-Marie-Tooth) were similar to those in amyotrophic lateral sclerosis. In syringomyelia, the motor unit territory was unchanged as compared with normal muscle but maximum voltage was increased 3 times. The increase in territory observed in neurogenic paresis of peripheral and central origin indicates that muscle fibers are included in the surviving motor units which originally were situated outside the area of these motor units. The increase in maximum voltage indicates that the motor units contain a greater number of muscle fibers per unit area. This increase in fiber concentration can be explained by the reinnervation of denervated muscle fibers through peripheral branching of nerve fibers from surviving motor units. The increase in motor unit territory of 5 to 7 mm. in paretic muscles in amyotrophic lateral sclerosis is thought to be due to synchronized activity of different anterior horn cells causing an enlargement of the electrophysiologically defined motor units. There is evidence that the enlargement of the electrophysiologically defined motor unit precedes loss of muscle fibers. A statistical evaluation of the findings is given for purposes of differential diagnosis.

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