Nerve Conduction Defects Are Retarded by Tight Metabolic Control in Type I Diabetes.

Nerve Conduction Defects Are Retarded by Tight Metabolic Control in Type I Diabetes Hyllienmark L, Golster H, Samuelsson U, Ludvigsson J (Department of Clinical Neurophysiology, Karolinska Hospital, Stockholm; Departments of Clinical Neurophysiology, Paediatrics, and Anesthesiology and Intensive Care, University Hospital, Linkoping, Sweden), Muscle Nerve. 2001;24:240-246.

The purpose of this study was to determine the effect of tight metabolic control on nerve conduction abnormalities in people with type I diabetes (insulin-dependent). The authors inquired whether abnormal nerve conduction was retarded or prevented by tight metabolic control, which they defined as a glycosylated hemoglobin ([HbA.sub.1c]) of [is less than] 6.5%. A normal range was listed as being 3.2%-6%.

Although the pathogenesis is unclear, multiple injection therapy (MIT) and metabolic control can reduce the incidence of clinically detectable neuropathy. The authors assumed that overt neuropathy is preceded by nerve conduction defects, but they stated that this assumption was unproven. An earlier study showed that, despite the use of MIT in young patients with insulin-dependent diabetes, they still had nerve conduction defects.

Subjects for the study included an experimental group of 71 patients (mean age=19 years, range=10-26 years of age; mean disease duration=12 years) who were receiving insulin at least 4 times per day by injection or an external subcutaneous infusion pump. The control group included 115 age-matched volunteers who were healthy (range=10-28 years).

Capillary blood glucose and [HbA.sub.1c] were measured before and after the nerve conduction examination. A clinical examination covered factors such as neurological diseases, use of tobacco and alcohol, medications, neuropathic ulcers, tendon reflexes, hypertension, and concurrent diseases.

Motor nerve conduction velocity (MCV), compound muscle action potential (CMAP) amplitude, sensory nerve conduction action potential (SNAP), and sensory nerve velocity (SCV) were measured bilaterally in the peroneal and sural nerves in all participants. All patients were examined by one experienced technician. The results were calculated and statistically analyzed for nerve conduction defects in patients, correlation between metabolic control and conduction velocity, abnormal nerve conduction in relation to diabetes, and clinical symptoms in relation to nerve conduction and metabolic control. The researchers also compared nerve conduction and body length between the control and experimental groups.

The authors concluded that tight metabolic control ([HbA.sub.1c] [is less than] 6.5%) retards nerve dysfunction in persons with type I diabetes with a mean duration of 12 years. Diabetes was associated with a reduction in peroneal MCV of 5.9 meters per second, a reduction in sural SCV of 3.4 meters per second, and a reduction in sural SNAP amplitude of 22%. Nerve dysfunction, however, was found more frequently in patients with poor metabolic control. Abnormal nerve conduction, for example, was found in 2 or more nerves in only 8% of the patients with tight metabolica control ([HbA.sub.1c] [is less than] 6.5). Of those patients with a mean HbA.sub.1c] between 6.5%-8.0%, about 60% had nerve dysfunction in 2 or more nerves. Multiple conduction abnormalities (dysfunction in 2 or more nerves) was found most frequently (88%) in patients with poor metabolic control ([HbA.sub.1c] [is greater than] 8.0).

The researchers concluded that a tight metabolic control may retard the development of nerve dysfunction. A decrease in MCV, they argued, can be reversed after improved metabolic control and, therefore, the changes observed in this study may also be reversible.

Raymond E Hogue, PT, PhD, ECS Emeritus Joplin, Mo