Peripheral nerve function during hyperglycemic clamping in insulin-dependent diabetic patients

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Abstract
The influence of hyperglycemia on peripheral nerve function was studied in 9 patients with long-term insulin-dependent diabetes. Blood glucose concentration was raised 13.5 .+-. 0.5 mmol/l (mean .+-. SEM) within 15 min and kept approximately 15 mmo/l over basal level for 120 min by intravenous glucose infusion. Hyperglycemia was accompanied by increased plasma osmolality. Sensory and motor nerve conduction and distal mortor latency in the ulnar nerve were determined bfore, immediately after induction of hyperglycemia, and again after 120 min hyperglycemia. Distal (5th finger - wrist) and proximal (wrist -elbow) sensory nerve conduction showed an insignificant increase as hyperglycemia was induced. During hyperglycemia mean distal sensory conduction decreased from 53.1 ms to 50.4 m/s (P < 0.005) and mean proximal sensory conduction decreased from 56.0 m/s to 54.2 m/s (P < 0.01). A mean of distal and proximal sensory conduction increased (53.5 m/s vs 54.6 m/s) (P < 0.05) as hyperglycemia was induced and decreased (54.6 m/s vs 52.3 m/s) (P < 0.01) during clamping. Motor never conduction decreased insignificantly throughout the study. Mean distal motor latency decreased from 3.1 ms to 2.8 ms (P < 0.005) immediately after induction of hyperglycemia. During hyperglycemia it increased from 2.8 ms to 3.1 ms (P < 0.001). We conclude that acute induction of hyperglycemia in long-term diabetes seems to increase sensory conduction and decrease distal motor latency, while 120 min hyperglycemia seems to decrease sensory conduction and increase distal motor latency. As the changes are small, it may not be necessary to pay attention to the concomitant blood glucose concentration when sequential nerve condition measurements are made in diabetics.