Ask the Experts - Reduced Nerve Conduction Amplitude in the Setting of...
What meaning does decreased nerve conduction amplitude have in light of normal conduction velocity and normal muscle testing on EMG?

The morphology of the peripheral nerve response is formed by the contribution of the different populations of nerve fibers of varying diameters within the peripheral nerve bundle. The amplitude of the nerve response is actually a representation of the various groupings of fiber populations having differing diameters and degrees of myelination.

The earlier portion of the evoked peak represents the larger-diameter fibers and the latter portion of the response, progressively smaller-diameter fibers. Collectively, the height of the nerve conduction amplitude is a representation of all the axon bundles comprising the nerve. Injury to axons within the nerve bundle will result in a dropout in the total number of axons actually stimulated in the nerve bundle and hence a reduction in the amplitude of the evoked compound motor action potential. Therefore, reduction of the nerve conduction amplitude indicates the degree of axonal injury in the nerve bundle.

Latency is a reflection of the activation pattern of individual neurons comprising the peripheral nerve. In the compound action potential produced in a nerve conduction test, the fastest arriving fibers (the most myelinated) determine the onset latency and hence the velocity of that nerve. Prolonged latencies reflect the dropout of faster myelinated fibers and result in slower nerve velocities.

In the case in question, reduced nerve conduction amplitude in the presence of a normal nerve conduction velocity would indicate a dropout of smaller-diameter axons in the nerve, accounting for the decreased amplitude of the compound muscle action potential while maintaining a normal nerve conduction velocity. The lack of change of the nerve conduction velocity would indicate that the axonal injury has not affected the faster (most militated) fibers contained in the nerve bundle.

Selective injury of fiber types can be observed in various hereditary neuropathies. By contrast, nerve compression injuries cause damage at the point of compression and can involve a mixed population of large- and small-diameter axons resulting in a decrease in both the amplitude and the latency of the evoked nerve response (representing an axonal, demyelinating polyneuropathy).

The EMG signal recorded represents a population of discharging motor units within the muscle. Elevated motor unit amplitudes recorded by an EMG represent reorganization of the motor unit innervation pattern secondary to injury. Loss of an axon supplying a group of muscle fibers results in denervation of those fibers. Eventually those denervated fibers are reinnervated by nearby healthy axon terminals. This results in an increased density of innervated muscle fibers within a motor unit (remodeling), which is visualized as an increase in the amplitude of the motor unit when recorded by the EMG electrode. A selective dropout of small-diameter axons (resulting in a lower amplitude of the nerve conduction response) with a normal nerve conduction could result in denervation of a select population of smaller motor units.

Because of time limitations, an EMG exam typically samples only small areas of the active muscle. Given this fact an EMG recording could miss sampling smaller motor unit populations that have undergone remodeling as a result of denervation/reinnervation (resulting from axonal injury of select population of axons).

In the present case a normal EMG in the presence of decreased amplitude and normal nerve conduction velocity can reflect:

1. Loss of a subpopulation of smaller axons and hence remodeling of smaller motor units that were not sampled in the EMG; or possibly diffuse axonal loss that did not result in significant enough remodeling of motor units to bring about a change in the recorded motor unit potential.

2. Performance of the EMG early on after the injury. EMG changes will lag behind noted nerve conduction changes by 3-4 weeks as a result of the ongoing remodeling of the affected muscle. If there is fairly significant axonal loss (decreased nerve conduction amplitude), the EMG should eventually yield increased insertion activity and increased amplitudes of motor units surveyed.