Abstract
Objectives: To investigate peripheral and central somatosensory conduction in diabetic patients. Methods: We recorded sensory nerve action potentials and 5‐channel somatosensory evoked potentials (SEPs) with non‐cephalic reference after median nerve stimulation in 55 diabetic patients and 41 age/height matched normal subjects. We determined onset latencies of the spinal N13‐P13 and the cortical N20‐P20 components, and obtained the central conduction time (CCT). Results: Onset latencies of all SEP components were prolonged in diabetic patients. The mean onset CCT in the diabetic group was 6.3 ± 0.5ms (mean ± SD), being significantly longer than that in the control group (6.1 ± 0.2 ms). The peripheral sensory conduction velocity was also decreased in the diabetic group, but there was no significant correlation between peripheral conduction slowing and the onset CCT prolongation. Conclusions: Diabetes affects conductive function in the central as well as peripheral somatosensory pathways. The CCT abnormality does not coincide with lowering of the peripheral sensory conduction. The present results do not favor the hypothesis that a central‐peripheral distal axonopathy plays an important role in development of diabetic polyneuropathy.
Published Version
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