title: The acute effects of glycemic control on nerve conduction in human diabetics.
abstract: OBJECTIVE
  To investigate acute changes in nerve conduction associated with glycemic control. In diabetes, nerve dysfunction can result from reversible metabolic factors associated with hyperglycemia, as well as structural changes.
  
  
  METHODS
  Multiple nerve conduction parameters including F-wave latencies were measured in 47 diabetic patients with prominent hyperglycemia before and after intensive insulin treatment.
  
  
  RESULTS
  Four weeks after the start of treatment, there was a significant improvement in minimal F-wave latencies of the median (P<0.001) and tibial (P<0.001) nerves, and in distal latencies (P=0.01) and sensory nerve conduction velocities (P<0.001) of the median nerves. Amplitudes of motor and sensory responses did not change significantly. These findings were similar for patients with type 1 (n=8) and those with type 2 (n=39) diabetes. Patients with poorer glycemic control or milder neuropathy tended to show greater changes after treatment.
  
  
  CONCLUSIONS
  Glycemic control quickly alters the speed of nerve conduction. F-wave latencies and conduction times across the carpal tunnel are very sensitive parameters.
  
  
  CONCLUSIONS
  Serial nerve conduction studies can detect reversible slowing of nerve conduction presumably caused by metabolic factors, such as decreased Na+/K+-ATPase activity, the altered polyol pathway, and tissue acidosis.
authors.affiliation: Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
authors.forename: Yuriko
authors.initials: Y
authors.lastname: Kikkawa
authors.forename: Satoshi
authors.initials: S
authors.lastname: Kuwabara
authors.forename: Sonoko
authors.initials: S
authors.lastname: Misawa
authors.forename: Noriko
authors.initials: N
authors.lastname: Tamura
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Kitano
authors.forename: Kazue
authors.initials: K
authors.lastname: Ogawara
authors.forename: Takamichi
authors.initials: T
authors.lastname: Hattori
mesh_terms: D000200:Action Potentials; D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism*; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000503:physiopathology*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000503:physiopathology*; D004576:Electromyography; D005071:Evoked Potentials; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia / Q000188:drug therapy; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009431:Neural Conduction; D011930:Reaction Time; D013497:Sural Nerve / Q000503:physiopathology; D013979:Tibial Nerve / Q000503:physiopathology
chemical_list: D001786:Blood Glucose; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin