Abstract
During movement, there often is a need to control the movement generated sensory input and its perception. A movement related increase in detection threshold of cutaneous stimuli has been demonstrated by several authors (Coquery, 1978; Dyhre-Poulson, 1978). Most studies have concentrated on cutaneous sensation of the hand. In contrast, little is known about movement related modulation of transmission from cutaneous afferents from the foot in humans. To investigate how gait influences the perceived intensity of cutaneous input from the skin of the foot, the tibial or sural nerve was stimulated at the ankle during walking or running on a treadmill in a series of volunteers (with approval of the ethical committee). The task of the subjects was either to verbally report the detection of a stimulus or to press a hand-held force transducer with a force which was equivalent to the intensity of the sensation. As compared to standing, the detection threshold for these stimuli was raised by more than 30 % during locomotion. This relative insensitivity during gait was correlated with a reduction in evoked activity. Following sural nerve stimulation, the amplitude of somatosensory evoked potentials (SEP, P40- N80 complex), recorded at scalp level, was on average 62 % of the level during standing. Moreover, during walking there was a phase-dependent modulation in perceived intensity for all stimulus levels used (in the range between 1-5 and 2-5 times the perception threshold measured while standing). Shocks given just prior to footfall, were perceived as more intense than shocks of equal intensity given in other parts of the step cycle. In contrast there was a decrease in sensitivity for stimuli delivered immediately after ipsi- and contralateral footfall. In agreement with this, during gait the amplitude of the SEP was larger than average at the end of the swing phase and smaller just after foot fall of the stimulated leg. The reduced sensation and the decrease in amplitude of the evoked potentials after touchdown are thought to be due to occlusion or masking by concomitant afferent input from the foot. The phasic increase in sensitivity at end swing may result from a centrally generated facilitation of sensory transmission of signals related to anticipated touchdown.
