1. The effect of central set on automatic postural responses was studied in humans exposed to horizontal support-surface perturbations causing forward sway. Central set was varied by providing subjects with prior experience of postural stimulus velocities or amplitudes under 1) serial and random conditions, 2) expected and unexpected conditions, and 3) practiced and unpracticed conditions. In particular, the influence of central-set conditions was examined on the pattern and magnitude of six leg and trunk electromyograph (EMG) activations and associated ankle torque responses to postural perturbations with identical stimulus parameters. 2. The scaling of initial agonist integrated EMG (IEMG) and torque responses to postural perturbation amplitude disappeared when perturbation amplitudes were randomized. This finding suggests that the initial magnitude of postural responses were centrally set to anticipated postural perturbation amplitudes based on sequential experience with the stimulus. 3. Expectation of postural stimulus amplitude had a significant effect on initial torque responses; subjects overresponded when a larger perturbation was expected and underresponded when a smaller perturbation was expected. Expectation of postural stimulus velocity had a smaller effect on initial torque responses, and subjects consistently overresponded when the velocity of the perturbation was unexpected. This difference in amplitude and velocity expectation may be because of the capacity to encode stimulus velocity, but not amplitude information, into the earliest postural responses of the current trial. The relative strength of amplitude and velocity central-set effects varied widely with individual subjects. 4. Central-set conditions did not affect initial EMG response latencies (100 +/- 20 ms, mean +/- SD) or the relative onset of proximal and distal agonists and antagonists. Unexpected or unpracticed stimulus amplitudes, however, were associated with significant late activation of ankle antagonist, tibialis. Thus errors in initial response magnitude because of central-set effects appear to be partially corrected by reciprocal antagonist activity. Agonist IEMG, however, did not always reflect significant changes in torque responses with central-set conditions. 5. Expectation of postural stimulus amplitude and velocity had two different types of effects on the magnitudes of postural responses: 1) a directionally specific, central-set effect consisting of either increased or decreased responses, depending on expectation of stimulus amplitude; and 2) a nonspecific enhanced response to novel stimulus velocities with a gradual reduction when a velocity was presented repeatedly. Two different neural mechanisms are proposed for these two adaptive effects. 6. Reduction of postural response magnitude and antagonist activity during practice may be partially explained by adaptive mechanisms based on expectation because of prior experience with stimulus velocity and amp

1. The effects of cerebellar deficits in humans on scaling the magnitude of automatic postural responses based on sensory feedback and on predictive central set was investigated. Electromyographic (EMG) and surface reactive torques were compared in patients with anterior lobe cerebellar disorders and in normal healthy adults exposed to blocks of four velocities and five amplitudes of surface translations during stance. Correlations between the earliest postural responses (integrated EMG and initial rate of change of torque) and translation velocity provided a measure of postural magnitude scaling using sensory information from the current displacement. Correlations of responses with translation amplitude provided a measure of scaling dependent on predictive central set based on sequential experience with previous like displacements because the earliest postural responses occurred before completion of the displacements and because scaling to displacement amplitude disappeared when amplitudes were randomized in normal subjects. 2. Responses of cerebellar patients to forward body sway induced by backward surface displacements were hypermetric, that is, surface-reactive torque responses were two to three times larger than normal with longer muscle bursts resulting in overshooting of initial posture. Despite this postural hypermetria, the absolute and relative latencies of agonist muscle bursts at the ankle, knee, and hip were normal in cerebellar patients. 3. Although they were hypermetric, the earliest postural responses of cerebellar patients were scaled normally to platform displacement velocities using somatosensory feedback. Cerebellar patients, however, were unable to scale initial postural response magnitude to expected displacement amplitudes based on prior experience using central set. Randomization of displacement amplitudes eliminated the set effect of amplitude on initial responses in normal subjects, but responses to randomized and blocked trials were not different in cerebellar patients. 4. Cerebellar patients compensated for hypermetric responses and lack of anticipatory scaling of earliest gastrocnemius activity by scaling large, reciprocally activated tibialis and quadriceps antagonist activity with the displacement velocity and amplitude. Correlations between these antagonist EMG integrals and displacement amplitudes were preserved when amplitudes were randomized, suggesting that feedback-dependent and not set-dependent mechanisms were responsible for scaling of antagonists by cerebellar patients. Antagonist compensation for initial hypermetric responses also could be induced in normals when they overresponded to unexpectedly small amplitudes of surface displacements. 5. The major effects of anterior lobe cerebellar damage on human postural responses involves impairment of response magnitude based on predictive central set and not on use of velocity feedback or on the temporal synergic organization of multijoint postural coordination.(ABSTRACT TRUNCATED AT 400 WORDS)

1. Experiments were performed in standing subjects to determine whether low-threshold cutaneous and muscle afferents from mechanoreceptors in the human foot reflexly influence fusimotor neurons innervating pretibial flexor muscles. Recordings were made from 30 identified muscle-spindle afferents, four tendon-organ afferents, and one alpha-motor axon innervating the pretibial flexor muscles. The subjects stood without support or vision on a force platform while trains of electrical stimuli (5 stimuli, 300 Hz) were delivered at nonpainful intensities to the sural nerve or to the posterior tibial nerve at the ankle. 2. Seventeen of the 30 spindle endings had no background discharge, and none was activated by the sural or posterior tibial stimuli. Five silent afferents were given a background discharge by sustained pressure on the relevant tendon, but with two the discharge was dominated by a tremor rhythm obscuring any reflex response to the stimuli. Based on peristimulus time histograms (PSTHs), the sural stimuli then produced increases in discharge of two of the remaining three endings at latencies of 84 and 90 ms. These effects could not be explained by muscle stretch and are presumed to have been fusimotor mediated. 3. When the subjects stood freely without support or vision, 13 muscle-spindle endings had a background discharge, but with three endings tremor developed at the ankle and dominated the spindle discharge. Sural stimuli affected the discharge of five of nine endings unaffected by tremor. With three of these endings, there were changes in discharge that could be explained by muscle stretch.(ABSTRACT TRUNCATED AT 250 WORDS)

Displacements of the center of foot pressure, the hip and the head were recorded in six subjects standing on a platform, sinusoidally tilting in pitch (anterior-posterior). Stimulus frequencies ranged between 0.01 and 1 Hz. Stimulus amplitudes were 2, 4 and 6 degrees. With eyes open the displacements were minimal at 0.3 Hz. With eyes closed, however, induced sway was maximal at this frequency. The apparent lack of visual stabilization at the lowest frequency (0.01 Hz) might be attributed to a subthreshold velocity of the retinal image motion induced by the swaying body. A similar absence of visual stabilization of 1 Hz is assumed to indicate the limit of the working range of visual stabilization of posture. Independent of stimulus amplitude a phase lead of about 90 degrees was found at 0.01 Hz. This decreased with increasing frequency up to a phase lag of 100 degrees at the highest frequency (1 Hz). Head stabilization was generally more effective than hip stabilization. EMG recordings from the leg muscles suggest that with eyes closed the center of force is mainly stabilized by leg muscle activity, while with eyes open this stabilization is best, when vision allows for stabilization of body posture by intersegmental movements between head, trunk and legs.