Previous studies on the control of human balance suggested that increased pressure under the feet, leading to reduced plantar sole mechanoreceptors sensitivity, increases body sway. Although this suggestion is attracting, it is unclear whether increased plantar sole pressure simply reduces the transmission of plantar sole afferent to the cortex or also alters the sensorimotor integrative mechanisms. Here we used electrical stimulation applied under the sole of the foot to probe the sensorimotor mechanisms processing foot mechanoreceptors. Balance control of healthy individuals was assessed either when wearing a loaded vest or in normal-weight condition. In the Loaded condition, we observed decreased cortical activity over the primary somatosensory cortex (SI) for both an early P50-N90 somatosensory evoked potential (SEP) and for oscillatory brain activity within the gamma band (30–80 Hz). These reductions were interpreted as a disrupted early sensory transmission (i.e., decreased early SEP) leading to a decreased perception of plantar sole sensory information (i.e., decreased gamma band power). These early sensory mechanisms for the Loaded condition were associated with an increase in the late P170-N210 SEP and oscillatory brain activity within the beta band (19–24 Hz). These neural signatures involved areas which are engaged in sensorimotor integrative processes (secondary somatosensory cortex (SII) and right temporoparietal junction). Altered early and late sensory processes may result from the increase pressure on the mechanoreceptors of the foot sole and not from postural instability per se. Indeed, postural instability with normal weight condition did not lead to SEP changes.
The weighting of the sensory inputs is not uniform during movement preparation and execution. For instance, a transient increase in the transmission to the cortical level of cutaneous input ~700 ms was observed before participants initiated a step forward. The sensory facilitation occurred at a time when feet cutaneous information is critical for setting the forces to be exerted onto the ground to shift the center of mass toward the supporting side prior to foot-off. Despite clear evidence of task-dependent modulation of the early somatosensory signal transmission, the neural mechanisms are mainly unknown. One hypothesis suggests that during movement preparation the premotor cortex and specifically the supplementary motor area (SMA) can be the source of an efferent signal that facilitates the somatosensory processes irrespectively of the amount of sensory inputs arriving at the somatosensory areas. Here, we depressed mechanically the plantar sole cutaneous transmission by increasing pressure under the feet by adding an extra body weight to test whether the task-dependent modulation is present during step preparation. Results showed upregulation of the neural response to tactile stimulation in the extra-weight condition during the stepping preparation whereas depressed neural response was still observed in standing condition. Source localization indicated the SMA and to a lesser extent the superior parietal lobule (SPL) areas as the likely origin of the response modulation. Upregulating cutaneous inputs (when mechanically depressed) at an early stage by efferent signals from the motor system could be an attempt to restore the level of sensory afferents to make it suitable for setting the anticipatory adjustments prior to step initiation.
Human adaptive behavior in sensorimotor control is aimed to increase the confidence in feedforward mechanisms when sensory afferents are uncertain. It is thought that these feedforward mechanisms rely on predictions from internal models. We investigate whether the brain uses an internal model of physical laws (gravitational and inertial forces) to help estimate body equilibrium when tactile inputs from the foot sole are depressed by carrying extra weight. As direct experimental evidence for such a model is limited, we used Judoka athletes thought to have built up internal models of external loads (i.e., opponent weight management) as compared with Non-Athlete participants and Dancers (highly skilled in balance control). Using electroencephalography, we first (experiment 1) tested the hypothesis that the influence of tactile inputs was amplified by descending cortical efferent signals. We compared the amplitude of P1N1 somatosensory cortical potential evoked by electrical stimulation of the foot sole in participants standing still with their eyes closed. We showed smaller P1N1 amplitudes in the Load compared to No Load conditions in both Non-Athletes and Dancers. This decrease neural response to tactile stimulation was associated with greater postural oscillations. By contrast in the Judoka’s group, the neural early response to tactile stimulation was unregulated in the Load condition. This suggests that the brain can selectively increase the functional gain of sensory inputs, during challenging equilibrium tasks when tactile inputs were mechanically depressed by wearing a weighted vest. In Judokas, the activation of regions such as the right posterior inferior parietal cortex (PPC) as early as the P1N1 is likely the source of the neural responses being maintained similar in both Load and No Load conditions. An overweight internal model stored in the right PPC known to be involved in maintaining a coherent representation of one’s body in space can optimize predictive mechanisms in situations with high balance constraints (Experiment 2). This hypothesis has been confirmed by showing that postural reaction evoked by a translation of the support surface on which participants were standing wearing extra-weight was improved in Judokas.
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