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Visuomotor adaptation to gaze-shifting prism glasses requires recalibration of the relationship between sensory input and motor output. Healthy individuals flexibly adapt movement patterns to many external perturbations; however, individuals with cerebellar damage do not adapt movements to the same extent. People with Parkinson disease (PD) adapt normally, but exhibit reduced after-effects, which are negative movement errors following the removal of the prism glasses and are indicative of true spatial realignment. Walking is particularly affected in PD, and many individuals experience freezing of gait (FOG), an episodic interruption in walking, that is thought to have a distinct pathophysiology. Here, we examined how individuals with PD with (PD + FOG) and without (PD - FOG) FOG, along with healthy older adults, adapted both reaching and walking patterns to prism glasses. Participants completed a visually guided reaching and walking task with and without rightward-shifting prism glasses. All groups adapted at similar rates during reaching and during walking. However, overall walking adaptation rates were slower compared to reaching rates. The PD - FOG group showed smaller after-effects, particularly during walking, compared to PD + FOG, independent of adaptation magnitude. While FOG did not appear to affect characteristics of prism adaptation, these results support the idea that the distinct neural processes governing visuomotor adaptation and storage are differentially affected by basal ganglia dysfunction in PD.

Podokinetic after-rotation (PKAR) is a phenomenon in which subjects inadvertently rotate when instructed to step in place after a period of walking on a rotating treadmill. PKAR has been shown to transfer between different forms of locomotion, but has not been tested in a non-locomotor task. We conducted two experiments to assess effects of PKAR on perception of subjective straight ahead and on quiet standing posture. Twenty-one healthy young right-handed subjects pointed to what they perceived as their subjective straight ahead with a laser pointer while they were recorded by a motion capture system both before and after a training period on the rotating treadmill. Subjects performed the pointing task while standing, sitting on a chair without a back, and a chair with a back. After the training period, subjects demonstrated a significant shift in subjective straight ahead, pointing an average of 29.1 ± 10.6 degrees off of center. The effect was direction-specific, depending on whether subjects had trained in the clockwise or counter-clockwise direction. Postures that limited subjects’ ability to rotate the body in space resulted in reduction, but not elimination, of the effect. The effect was present in quiet standing and even in sitting postures where locomotion was not possible. The robust transfer of PKAR to non-locomotor tasks, and across locomotor forms as demonstrated previously, is in contrast to split-belt adaptations that show limited transfer. We propose that, unlike split-belt adaptations, podokinetic adaptations are mediated at supraspinal, spatial orientation areas that influences spinal-level circuits for locomotion.

The purpose of this work was to determine whether walking on a rotating disc would cause changes in perception of active and passive turning. Ten healthy control subjects wore a blindfold and earplugs while completing trials of active and passive turning. For active conditions, subjects were told the direction and amplitude of the desired turn and then attempted to turn in place the specified amount via actively stepping. For passive conditions, subjects were told that the disc they stood on would turn and they were to press a button when they had traveled the specified amplitude. Subjects completed active and passive trials to the left and right with amplitudes of 90, 180, 270, and 360 degrees. Subjects then stepped in place for 15 min on a disc rotating clockwise at 90 degrees /s, after which they repeated the trials of active and passive turning. Following rotating treadmill stimulation, subjects asked to turn in the direction opposite disc rotation (i.e., to the left) consistently and significantly overshot their targets in active trials. There were no changes in accuracy of active turning to the right or passive turning in either direction. This indicates that adaptation to the rotating treadmill is expressed even when subjects have a conscious intent to turn. The positive after-effects of the rotating treadmill add to the intended active turning in the direction of the after-effect but there is no decrement in active turning in the direction opposite the after-effect.

We asked what the role of the vestibular system is in adaptive control of locomotor trajectory in response to walking on a rotating disc. Subjects with bilateral vestibular loss (BVL) were compared to age- and gender-matched controls (CTRL). Subjects walked in place on the surface of a rotating disc for 15 min and then attempted to step in place without vision on a stationary surface for 30 min. CTRL subjects demonstrated podokinetic after-rotation (PKAR), involuntarily and unknowingly turning themselves in circles while attempting to step in place. PKAR in CTRLs was characterized by a rapid rise in turning velocity over the first 1-2 min, followed by a gradual decay over the remaining 28 min. Subjects with BVL also demonstrated PKAR and had no knowledge of their turning. However, PKAR in BVLs was characterized by an extremely rapid, essentially instantaneous rise. Subjects with BVL immediately turned at maximum velocity and exhibited a gradual decay throughout the entire 30 min period. Despite this difference in the initial portion of PKAR in BVLs, their responses were not significantly different from CTRLs during minutes 2 to 30 of the response. These results suggest that vestibular inputs normally suppress PKAR velocity over the first 1-2 min of the response, but do not greatly influence PKAR decay. PKAR is therefore a process mediated primarily by somatosensory information and vestibular inputs are not required for its expression. Additionally, the absence of vestibular inputs does not result in increased somatosensory sensitivity that alters podokinetic intensity or decay time constants.

Previous studies demonstrated a leaning after-effect (LAE) following standing or walking on an inclined surface consistent with a long-lasting, somatosensory memory for body orientation relative to the surface. Here, we asked whether providing a brief visual reference during LAE resets postural orientation to the new visual reference. The results showed that subjects immediately return to upright when eyes were opened briefly during the post-incline period. However, the subjects also immediately resumed leaning after closing their eyes again following 20 s of eyes open. The duration of LAE was not influenced by 1 or 2 brief periods of vision. Also, the amplitude of the lean following the brief vision period was often larger than when subjects had their eyes closed for the entire post-incline period. These results suggest a powerful somatosensory memory contribution to postural orientation in space that is not eliminated or recalibrated with brief exposure to a visual reference.

After sustained stepping in-place on a rotating disc, healthy subjects will inadvertently turn in circles when asked to step in-place on a stationary surface with eyes closed. We asked whether the cerebellum is important for this adaptive phenomenon, called podokinetic after-rotation (PKAR). Subjects with cerebellar degeneration and age-matched control subjects performed 15 min of stepping in-place with eyes open on a rotating disc, then 30 min of attempting to step in-place with eyes closed on a stationary surface. Rotational velocity of PKAR was measured during this 30-min period. All control subjects demonstrated PKAR; average initial rotational velocity for control subjects was 16.4+/-3.5 degrees /s. Five of the eight cerebellar subjects demonstrated impaired PK adaptation, defined as PKAR with an initial velocity more than two standard deviations below the control mean initial velocity. Average initial rotational velocity for cerebellar subjects was 7.8+/-0.2 degrees /s. Impaired PK adaptation was not associated with impaired time constants of decay and was not correlated with variability of PKAR velocity. Our results suggest that the cerebellum is important for regulation of the amplitude of PK adaptation and that reduced PKAR amplitude is not likely the result of dyscoordination or variability of movement in the subjects tested.

Postural responses to head displacements are triggered by the vestibular system; responses to body displacements are triggered by the somatosensory system. We examined the interaction of responses to combinations of head and support surface perturbations. Head displacements were always in the opposite direction of body displacements. The time between head and support surface perturbations was varied. We measured amplitude and latency of gastrocnemius and tibialis anterior EMGs for various head backward/body forward and head forward/body backward displacement combinations. These responses were compared to head-only or body-only displacement trials, which served as controls. Relative to controls, the latency of somatosensory-evoked responses to body displacement was longer and vestibular-evoked responses were absent or of low amplitude for combinations where head and support surface perturbations were presented closely in time (10-50 ms apart). These results illustrate complex integration of vestibular and somatosensory information, suggesting that the vestibulospinal and somatosensory-spinal pathways are not two isolated systems independently driving motor neurons. Rather, these pathways may influence one another at premotoneuronal levels where common circuitry may be shared by both systems.