RESUMO
This work was done to study the clinical sensory findings and to investigate the influence of hyperglycaemia on nerve sensory conduction. A group of 120 maturity-onset diabetic patients [86 females and 34 males] and 30 normal control subjects were studied. The patients were classified into two groups according to whether they had diabetic neuropathy [32 patients] or not had [88 patients]. The modalities of light touch and vibration sense were the most frequently diminished, two-point discrimination was less frequently affected and proprioception was rarely affected. Sensory nerve conduction velocity of median, ulnar and sural nerves, using the antidromic technique, was significantly [P < 0.001] slowed in the diabetic patients compared to controls. Levels of fasting plasma glucose as well as levels of glycosylated haemoglobin, and index of long-term glycaemia, were correlated with slowing of sensory conduction velocity of the tested nerves. These associations could not be explained by patient age or duration of diabetes. These findings suggest that the degree of hyperglycemia of maturity-onest diabetes contributes to the sensory nerve abnormalities in this disease. We can conclude that sensory nerve conduction parameters are the objective criteria for peripheral nerve involvement. It tends to be impaired in diabetics even those without clinical evidence of neuropathy. Moreover, the sensory nerve conduction parameters are probably the most sensitive index of peripheral neuropathy in diabetic patients. The present study also concluded that altered nerve metabolism associated with hyperglycaemia may contribute to the distal sensory polyneuropathy of diabetes. This support the hypothesis for the existence of endoneurial oedema and hydration of peripheral nerves secondary to overactivity of aldolase reductase pathway. These structural changes are recently quantitatively defined by magnetic resonance proton image. This increased level of peripheral nerve water represents a new finding in the development of diabetic neuropathy. Treatment with an aldolase reductase inhibior is a prospect which might halt, if not reverse, the development of diabetic neuropathy