Neural control of standing posture

Sammanfattning: When humans are asked to stand normally, they are not completely motionless. Rather, small amounts of body movement, termed postural sway, can be observed. Although the postural sway of standing has been well described, the manner in which this sway is neurally controlled and its influence in tasks involving postural re-stabilization are not known. Therefore, the aim of this thesis was to investigate the neural control of human standing posture, with a special emphasis on 1) whether the neuromuscular responses to an unexpected perturbation are influenced by the postural sway, 2) whether spinallymediated changes occur as a function of postural sway position and/or direction, and 3) whether the excitability of the cortical and corticospinal pathways are altered with respect to postural sway. In each study, subjects stood quietly on a force platform. For Studies I-III, the anteroposterior center of pressure (COP) signal from the force platform was monitored online such that when the position and/or velocity of the COP was of the desired magnitude and direction, a perturbation was administered to the subject. The perturbation consisted of either a sudden support surface translation (Study I) or a percutaneous electrical stimulation to the posterior tibial nerve (Studies II-IV). In Study IV, a perturbation, in the form of either a transcranial magnetic (TMS) or electric (TES) stimulation to the left motor cortex, was triggered at a random time, regardless of the COP signal. The neuromuscular responses to the mechanical, electrical or magnetic perturbations were assessed by measuring the body kinematics from a motion capture system or electromyographic (EMG) recordings from surface electrodes placed over various lower limb muscles. Specific dependent measures included the number of stepping responses, the latencies and amplitudes of the EMG recordings, the peak-to-peak amplitudes of the Hoffmann reflex (Hreflex) and M-wave from tibial nerve stimulation, as well as the peak-to-peak amplitudes of the motor evoked potentials (MEPs) elicited by TMS and TES. Study I indicated that when subjects were standing normally, the position of postural sway influenced the postural responses to an unexpected surface translation. EMG activity of various lower limb and trunk muscles were generally delayed in time and larger in amplitude when subjects were swaying in the direction opposite to the upcoming perturbation. The altered postural responses may be related to the ongoing modulation of the synaptic efficacy, as reflected by the size of the H-reflex, to the triceps surae Ia pathways. In Studies II-IV, it was found that when subjects were swaying in the forward as compared to the backward direction or position, depolarization of the soleus and medial gastrocnemius motoneurone pools, via synaptic transmission of the Ia afferents, was easier to achieve. However, this sway direction- and sway position-dependent modulation of neural excitability was limited to the spinal and corticospinal levels. Study IV revealed that TMS- and TES-evoked MEPs were similarly modulated during the naturally occurring sway of normal standing, suggesting that the excitability of the motor cortex was not dependent on postural sway. A facilitation in cortical excitability, as shown by the differential MEP response between TMS and TES, was however found during normal as compared supported (i.e. no postural sway) standing. This thesis demonstrates that human standing posture is controlled via an overall enhancement of cortical excitability, concurrently with an ongoing sway-dependent modulation of spinal and corticospinal processes. The constantly changing neural inputs to the motoneurone pool may give insight into the influence of postural sway to the neuromuscular responses to an unexpected perturbation.