Abstract
The literature concerning the measurement of conduction velocity in human motor nerves and its clinical applications is reviewed. The chief value of the test to the clinician lies in the demonstration of a peripheral neuropathy and in its differentiation from myelopathy and myopathy. It is pointed out that this investigation is often particularly useful in infants and children as it is an objective and relatively painless test requiring little co-operation from the patient. Starting from approximately half the normal adult value at birth in full-term infants the motor nerve conduction velocity normally increases to the full adult level during the first 3 to 5 years of life. In premature infants it begins at a still lower level. This increase is of clinical interest and can be studied serially. There is also a particular developmental aspect in infants in relation to possible delays or disturbances of innervation or myelination. The results of measurements of conduction velocity, chiefly in the median nerves, are reported in 45 "normal" infants and children and in 100 others who had a variety of neurological disorders. The rate was normal in all but one of 33 children with miscellaneous cerebral disorders, including nonspecific mental retardation, Down's syndrome (mongolism), D1 trisomy, hydrocephalus, and organic convulsive disorders. There was a distinct reduction in metachromatic leucodystrophy (2 cases), infantile amaurotic idiocy (1 case), and recurrent and chronic polyneuropathy (3 cases). In 4 children with acute neuronitis there were no demonstrable gross changes in conduction velocity during the first 2 months, while the diminished voltage and increased temporal dispersion of the action potential were more helpful early diagnostic features. Normal results were obtained in benign congenital hypotonia (10 cases), phenylketonuria (3 cases), and ataxia-telangiectasia (1 case). Five children with Friedreich's ataxia were examined and 2 of these had marked clinical fluctuations in the extent of their weakness suggestive of peripheral neuropathy. One of the latter was seen during an acute exacerbation of his weakness when he had a distinctly reduced nerve conduction velocity, and prolonged terminal latency from wrist to thenar eminence. The other was tested during a phase of relative well-being and had a normal conduction velocity but even more prolonged terminal latency than the first. The remaining children had a slowly progressive illness; all of them had normal conduction velocity, but one had just significantly prolonged terminal conduction time. Somewhat slow conduction rates for the age appeared to be present in 1 of 6 infants with arthrogryposis multiplex congenita and in 4 of 14 with clubfoot below the age of 2 years, but the statistical significance of these deviations cannot yet be indicated. The results are discussed, with particular emphasis on developmental aspects and the involvement of the peripheral nervous system in "dysmyelination" and demyelination.
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