Nerve conduction defects are retarded by tight metabolic control in type I diabetes.
This follow-up study examines whether the development of nerve dysfunction is retarded by tight metabolic control in patients with type I diabetes mellitus. Seventy-one patients and 115 age-matched healthy control subjects underwent studies of nerve conduction in peroneal and sural nerves. The presence of diabetes was associated with a reduction in peroneal motor nerve conduction velocity (MCV) by 5.9 m/s, sural sensory nerve conduction velocity (SCV) by 3.4 m/s, and sural sensory nerve action potential (SNAP) amplitude by 22%. Dysfunction in peroneal MCV, sural SCV, and sural SNAP were related to long-term poor metabolic control. Eleven of 12 patients with HbA1c <6.5% had normal nerve conduction or abnormality in only one nerve as compared to 2 of 15 patients with HbA1c >8.0%. It is concluded that tight long-term metabolic control (HbA1c <6.5%) can retard nerve dysfunction in patients with type I diabetes mellitus and a mean disease duration of 12 years.
Hyllienmark
L
L
Department of Clinical Neurophysiology, Karolinska Hospital, Stockholm S-17176, Sweden. lars.hyllienmark@neuro.ks.se
Golster
H
H
Samuelsson
U
U
Ludvigsson
J
J
D000200:Action Potentials / Q000502:physiology; D000293:Adolescent; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D002648:Child; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy* / Q000503:physiopathology*; D004594:Electrophysiology; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000627:therapeutic use*; D008297:Male; D009431:Neural Conduction / Q000502:physiology*; D009469:Neuromuscular Junction / Q000502:physiology; D010543:Peroneal Nerve / Q000503:physiopathology; D012026:Reflex, Stretch / Q000502:physiology; D013497:Sural Nerve / Q000503:physiopathology
D001786:Blood Glucose; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin