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

Intern Med. 2002 May;41(5):360-5. doi: 10.2169/internalmedicine.41.360.

Abstract

Objective: 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.

Methods: 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.

Results: 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).

Conclusions: 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.

Publication types

  • Comparative Study

MeSH terms

  • Action Potentials / physiology
  • Adult
  • Aged
  • Axons / physiology*
  • Blood Glucose / analysis
  • Diabetes Mellitus, Type 1 / drug therapy
  • Diabetes Mellitus, Type 1 / physiopathology
  • Diabetes Mellitus, Type 2 / drug therapy
  • Diabetes Mellitus, Type 2 / physiopathology
  • Diabetic Neuropathies / blood
  • Diabetic Neuropathies / physiopathology*
  • Electromyography
  • Electrophysiology
  • Female
  • Humans
  • Hyperglycemia / drug therapy*
  • Insulin / therapeutic use
  • Male
  • Middle Aged
  • Muscle Contraction / physiology
  • Neural Conduction / physiology
  • Peripheral Nerves / physiopathology*
  • Sodium-Potassium-Exchanging ATPase / metabolism

Substances

  • Blood Glucose
  • Insulin
  • Sodium-Potassium-Exchanging ATPase