Sensory and motor nerve conduction has been measured in 56 patients with chronic renal failure. Slowed nerve conduction was present in one or more segments in 38 of 39 patients with a 24‐hour creatinine clearance below 10 ml/min/1.73 m 2 . The impairment involved upper and lower extremities, motor and sensory fibres, distal and proximal segments, and fast and more slowly conducting fibres. The amplitude of sensory action potentials was reduced, mainly due to increased temporal dispersion and to increased incidence of irregularities in the shape of potentials. The electromyographic contraction pattern at maximal effort in the abd. poll. brev. muscle was rarely abnormal, whereas the pattern in the ext. dig. brev. muscle was compatible with a moderate to severe loss of motor units in 21 of 29 patients. All patients with electrophysiological signs of impaired nerve function had slowed motor conduction in the common peroneal nerve and/or slowed sensory conduction in the median nerve. The demonstration in the present material of an almost uniform slowing of nerve conduction in all segments examined contrasts with the reported distribution of structural changes, predominantly located in the distal parts of the legs. The hypothesis is put forward that the slowing of nerve conduction is not solely dependent on structural changes, but also on a universal toxic effect upon the nerve axon membrane by uremic toxin(s) other than urea and creatinine.
No takes yet. Share an insight, caveat, or question.
V. Kamp Nielsen (1973) studied this question.
Synapse has enriched one closely related paper. Consider it for comparative context: