Jun 13, 2002

The acute effects of glycemic control on axonal excitability in human diabetic nerves

Internal Medicine
Satoshi KuwabaraNaotake Hashimoto

Abstract

To investigate whether glycemic control is associated with reversible changes in axonal excitability in human diabetic nerves. It is known that voluntary contraction or compression ischemia alters nerve Na+/K+ pump activity, and axonal excitability changes due to the pump activity can be estimated by threshold tracking. Threshold, the current required to produce a compound muscle action potential 50% of maximum, was determined from the stimulus-response curve, and threshold changes produced by maximal voluntary contraction or ischemia were measured before and after insulin treatment in 10 diabetic patients. Within 3 weeks of the start of treatment, the threshold changes became greater following voluntary contractions (+13+/-4% versus +23+/-5%; mean+/-SEM; p=0.04) and during ischemia (-5+/-2% versus -11+/-2%; p=0.04). The extent of threshold fluctuation depends on multiple metabolic factors associated with diabetes such as decreased Na+/K+ ATPase activity, increased anaerobic glycolysis, and tissue acidosis, and nerve excitability can respond quickly to glycemic control in diabetic patients.

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Mentioned in this Paper

Surface Electromyography
Metabolic Process, Cellular
Ischemia
Diabetes Mellitus, Non-Insulin-Dependent
Nervousness
Fluctuation
Contraction (Finding)
Nerve Conduction Function
Insulin B Chain
Axon

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