They also show reduced nerve conduction velocity and increased resistance to ischaemic conduction failure. These phenomena have little clinical importance. They are rapidly corrected by the establishment of diabetic control and are thus presumably related directly to hyperglycaemia or to a metabolic abnormality correlated with it. Possible mechanisms have been discussed by Watkins and Thomas.1 The increased resistance to ischaemic conduction failure may be related to a switch to anaerobic glycolysis in diabetic nerve. The positive sensory symptoms could be related to hypoxia, which is known to be present in human diabetic neuropathy. Experimentally, hyperglycaemic but not normoglycaemic hypoxia gives rise to alterations in fast K+conductance and afterpotentials in axons, related to axoplasmic acidification. This might lead to the generation of ectopic impulses and contribute to the occurrence of positive symptoms.