Childhood Diabetic Neuropathy: A Clinical and Neurophysiological Study

Abstract

SummaryElectrophysiologic studies and a comparative analysis of clinical data have been done on 85 children aged 2‐15 years, with diabetes mellitus but with no clinical signs of neuropathy or known (“complications” in any other respect. Electro‐encephalographic registrations were taken in all 85 cases, electromyography in 74 cases, and determination of the conduction velocity in peripheral motor nerve in 66 cases. The results were compared with a specially selected control material.1. A statistically significant reduction of the conduction velocity was noted in the ulnar and peroneal nerves in the diabetic material as compared to the control material for the age group 8‐15 years. Pathologic conduction velocity was found in the ulnar nerve in 2% and in the peroneal nerve in 9%. The reduced nerve conduction velocity was related to age, duration of diabetes and obviously to “poor” diabetic control.2. The electromyographic analyses showed a pathologic pattern in 5% of the cases‐all from the lower extremities.3. Pathologic EEG's were noted in 35% of the diabetic material and in 13% of the control material, a difference which is statistically significant. No relation to age, age a t onset of diabetes, duration of disease or diabetic control could be found. On the other hand, there was a statistically significant correlation with the frequency of hypoglycemic coma. The alpha activity was statistically significantly lower in the diabetic material as compared with the control material. This difference was pronounced below 9 years of age. Because of this finding, as well as the fact that an age limit of 9 years divides the material into two onset groups, the existence of two different types of childhood diabetes was discussed. In 19% of the diabetic material there were 14 and 6 clsec positive spike potentials, whereas the control material showed an incidence of only 8%. This difference is statistically significant. The findings appear to indicate an increased prevalence of this activity in cases of diabetes of short duration, and possibly in cases of late onset of diabetes in childhood. Alpha activity was compared with the nerve conduction velocity. In both control and diabetic material the nerve conduction velocity remained constant with increasing alpha frequency.4. The pathogenesis of diabetic neuropathy has been discussed. Metabolic factors are considered to constitute the primary cause.