Although measurements of nerve conduction velocity in man were first made nearly a hundred years ago, the procedure was not used clinically until 1948 when Hodes, Larrabee, and German reported reduced conduction velocity in regenerating motor nerves. Later, Hodes (1949) described slow conduction in surviving nerve fibres after poliomyelitis, and more recently it has been shown that conduction may also be slow in certain localized peripheral nerve lesions (Simpson, 1956), in polyneuritis, and in peroneal muscular atrophy (Henriksen, 1956; Lambert, 1956; Gilliatt and Thomas, 1957; Gilliatt and Sears, 1958). The use of conduction velocity measurement as a diagnostic procedure in neurology requires a knowledge of the range of values encountered in healthy individuals. Normal values for maximum conduction velocity in human peripheral nerves have already been described by Norris, Shock, and Wagman (1953) and by Henriksen (1956), but in order to obtain a control series for our own laboratory, we have estimated maximum conduction velocity in 180 normal nerves supplying the small muscles of the hands and feet. Our own results, which are in good agreement with those of previous writers, are contained in the first part of this paper. In estimating conduction velocity, the motor nerve trunk is stimulated at two levels and the time interval between the stimulus and the onset of the muscle action potential recorded in both instances. This interval represents conduction time in the largest and most rapidly conducting motor nerve fibres stimulated, together with a further delay at the neuromuscular junction and in the muscle itself. Provided that both stimuli are supramaximal, the difference in latency of the two muscle responses is a valid estimate of conduction time in the most rapidly conducting fibres in the nerve trunk between the two points stimulated. However, conduction time in the smaller and more slowly conducting fibres of a motor nerve cannot be measured in this way as the time of onset of their muscle action potentials is obscured by the discharge of earlier units. This point is of some clinical importance, as it is not uncommon for patients to show values for maximum conduction velocity that are slightly below the accepted normal range; in such a case the question arises as to whether this represents conduction in abnormal fibres or whether it could be due to conduction in slow normal fibres uncovered by the loss of the larger and more rapidly conducting ones. In order to obtain some evidence on this question, we have attempted to compare the conduction times of different nerve fibres supplying a single muscle; the results of this investigation are presented in the second part of the paper.
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