Aravindakannan Therimadasamy1, Yee Cheun Chan2, Einar P Wilder-Smith2,3. 1. Neurology Diagnostic Laboratory, National University Hospital Systems, Singapore. 2. Department of Medicine, Neurology, National University Hospital Systems, Singapore. 3. Department of Medicine, Neurology, Yong Loo Lin School of Medicine, National University, Singapore 5, Lower Kent Ridge Road, 119074, Singapore.
Abstract
INTRODUCTION: The cause of the double peak observed at submaximal stimulation of sensory nerves is unknown. The first peak is generated under the cathode and the second under the anode. The double peak is thought to arise from intradermal nerves or skin receptors, and in this study we tested this assumption. METHODS: We studied the effect of different stimulus durations on anodal peak latency in volunteers. Biphasic anodal stimulation was used to investigate the latent additive effect of the trailing negative phase on the partial depolarization induced by the initial positive phase. We further tested the maximal amplitude of anode-generated potentials to estimate the number of neural structures involved in their generation. RESULTS: Increased stimulus duration caused anode-generated potential delay. Biphasic stimulation increased anode-generated amplitude 4-fold compared with monophasic stimulation. The anode-generated potential produced up to 85% of the supramaximal cathode-generated amplitude. CONCLUSIONS: The results suggest that the double peak arises from anodal break excitation and not from intradermal nerves or receptors.
INTRODUCTION: The cause of the double peak observed at submaximal stimulation of sensory nerves is unknown. The first peak is generated under the cathode and the second under the anode. The double peak is thought to arise from intradermal nerves or skin receptors, and in this study we tested this assumption. METHODS: We studied the effect of different stimulus durations on anodal peak latency in volunteers. Biphasic anodal stimulation was used to investigate the latent additive effect of the trailing negative phase on the partial depolarization induced by the initial positive phase. We further tested the maximal amplitude of anode-generated potentials to estimate the number of neural structures involved in their generation. RESULTS: Increased stimulus duration caused anode-generated potential delay. Biphasic stimulation increased anode-generated amplitude 4-fold compared with monophasic stimulation. The anode-generated potential produced up to 85% of the supramaximal cathode-generated amplitude. CONCLUSIONS: The results suggest that the double peak arises from anodal break excitation and not from intradermal nerves or receptors.