By stimulating a motor nerve at multiple sites along its course, it is possible to demonstrate segments in which conduction is partially “blocked” or is differentially slowed. From such data one infers the presence of a multifocal demyelinative process in motor nerves. This contrasts with the findings in certain of the inherited and metabolic demyelinating neuropathies, in which all parts of the nerve fiber are altered to more or less the same degree, that is, there is uniform slowing and reduction in amplitude and no conduction block.
As a technical matter, conduction block is demonstrated by a reduction in the amplitude of the CMAP elicited from the proximal site along the motor nerve, compared to stimulation at a distal site. Generally, a 40 percent reduction in amplitude over a short distance of nerve, or 50 percent over a longer distance, qualifies as a block, one possible exception being along the tibial nerve, in which there is some degree of physiologic dispersion; therefore, a slight drop in amplitude over the length of the nerve is normally expected. It is important to be sure that any reduction in amplitude along the course of the nerve is not solely a result of dispersion of the waveform as mentioned previously. The presence of a conduction block can also be inferred from the finding of poor recruitment of muscle action potentials and the concurrent absence of active denervation (see further on). The finding of conduction block is a main feature of a number of acquired immune demyelinating neuropathies, including Guillain-Barré syndrome, chronic inflammatory demyelinating neuropathy, and multifocal conduction block associated with the GM1 antibody, which are discussed in
Chap. 46.
Focal conduction block may be caused simply by nerve compression at certain common sites (fibular head, across the elbow, flexor retinaculum at the wrist, etc.) rather than to an intrinsic disease of the peripheral nerves. Focal compression of nerve, as occurs in these entrapment syndromes, produces localized slowing or blocks in conduction, perhaps because of segmental demyelination at the site of compression. The demonstration of such localized changes of conduction affords ready confirmation of nerve entrapment; for example, if the distal latency of the median nerve (Fig. 2-11A) exceeds 4.5 ms while that of the ulnar nerve remains normal, compression of the median nerve in the carpal tunnel is likely. Similar focal slowing or partial block of conduction may be recorded from the ulnar nerve at the elbow and from the peroneal nerve at the fibular head.
The examiner should also be aware of a normal variant, the Martin-Gruber anastomosis that exists in close to 20 percent of individuals; in this configuration, axons from the median nerve cross into the ulnar nerve in the mid-forearm to innervate normally ulnar associated muscles in the hand. Distal stimulation of the ulnar nerve then gives higher amplitude ulnar CMAP than proximal stimulation, simulating conduction block, but without weakness or atrophy. The anastomosis can be demonstrated by obtaining a normal CMAP when stimulating the proximal median nerve and recording over ulnar innervated muscles.
Information about the conduction of impulses through the proximal segments of a nerve, including the spinal roots, is provided by the study of the H reflex and the F wave (Fig. 2-14).