Postural ataxia related to somatosensory loss.
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Biomedical subjects
Publications and source records attributed to F B Horak.
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We tested the hypothesis that basal ganglia dysfunction in Parkinson's disease impairs the ability to quickly change set. The ability to change set was inferred by measuring the change in the amplitude of automatic gastrocnemius or tibialis anterior muscle responses in standing subjects: (1) when the direction of a surface perturbation changed from a backward translation to a toes up rotation; and (2) when subjects were instructed to 'give' or 'resist' while responding to the translations and rotations. In experiment 1, a change in sensorimotor set was assessed by the suppression of gastrocnemius responses to toes up rotations following a series of backward translations. Unlike healthy young and older subjects, Parkinson subjects did not change sensorimotor set immediately to the first rotation, but needed several rotations to change their responses. When required to alternate their responses between backward translations and toes up rotations, Parkinson subjects showed a smaller amplitude change in gastrocnemius responses. In experiment 2, Parkinson subjects had more difficulty in using cognitive set to modify their responses, especially when instructed to 'resist' the perturbations. A small number of healthy older subjects also had difficulties changing set quickly, but to a lesser extent than the Parkinson subjects. Levodopa medication did not improve the Parkinson subjects' ability to change set quickly. These results suggest that the basal ganglia, which are affected in Parkinson's disease, are critical neural substrates in the ability to change set quickly.
The effects of predictability of load magnitude on anticipatory and triggered grip-force adjustments were studied as nine normal subjects used a precision grip to lift, hold, and replace an instrumented test object. Experience with a predictable stimulus has been shown to enhance magnitude scaling of triggered postural responses to different amplitudes of perturbations. However, this phenomenon, known as a central-set effect, has not been tested systematically for grip-force responses in the hand. In our study, predictability was manipulated by applying load perturbations of different magnitudes to the test object under conditions in which the upcoming load magnitude was presented repeatedly or under conditions in which the load magnitudes were presented randomly, each with two different pre-load grip conditions (unconstrained and constrained). In constrained conditions, initial grip forces were maintained near the minimum level necessary to prevent pre-loaded object slippage, while in unconstrained conditions, no initial grip force restrictions were imposed. The effect of predictable (blocked) and unpredictable (random) load presentations on scaling of anticipatory and triggered grip responses was tested by comparing the slopes of linear regressions between the imposed load and grip response magnitude. Anticipatory and triggered grip force responses were scaled to load magnitude in all conditions. However, regardless of pre-load grip force constraint, the gains (slopes) of grip responses relative to load magnitudes were greater when the magnitude of the upcoming load was predictable than when the load increase was unpredictable. In addition, a central-set effect was evidenced by the fewer number of drop trials in the predictable relative to unpredictable load conditions. Pre-load grip forces showed the greatest set effects. However, grip responses showed larger set effects, based on prediction, when pre-load grip force was constrained to lower levels. These results suggest that anticipatory processes pertaining to load magnitude permit the response gain of both voluntary and triggered rapid grip force adjustments to be set, at least partially, prior to perturbation onset. Comparison of anticipatory set effects for reactive torque and lower extremity EMG postural responses triggered by surface translation perturbations suggests a more general rule governing anticipatory processes.
This study investigates the effects of parkinsonism and dopamine replacement therapy (levodopa) on centrally initiated postural activity preceding rising onto the toes. The electromyographic (EMG) and force magnitude, scaling, sequencing, and postural stabilization were compared when rising-to-toes under two conditions, slow/low versus fast/high, for parkinsonian patients and elderly control subjects. Parkinsonian subjects were tested after withholding their levodopa medication for 12-16 h and again 1 h after taking their medication when parkinsonian signs were diminished. Parkinsonian subjects showed reduced magnitudes and delayed timing of the postural and voluntary components of the rise-to-toes task, as if they had difficulty turning off the postural, tibialis anterior (TIB) component and initiating the voluntary, gastrocnemius (GAS) component. Dopamine improved the relative timing, as well as the magnitude of both postural and voluntary components of rise-to-toes. Although the magnitude of dorsiflexion torque was smaller for parkinsonian subjects ON and OFF than for healthy elderly controls, the parkinsonian subjects showed intact scaling of the magnitude of postural activity. Parkinsonian subjects do not perform the rise-to-toes task like normal subjects who are instructed to rise slowly; the relative timing of TIB and GAS activation was different even at comparable speeds of performance. Parkinsonian subjects, both ON and OFF, exhibited greater risk of falling than elderly control subjects when rising to toes. This increased risk of falling was reflected in a smaller safety margin between the peak center of mass (CoM) and peak center of pressure (CoP) during the task. The magnitude of mean postural dorsiflexion torque in the rise-to-toes task was highly correlated with a clinical rating scale of gait and balance, suggesting that force control is a critical factor influencing postural control in patients with Parkinson's disease.
We compared the effects of galvanic vestibular stimulation applied at 0, 0.5, 1.5 and 2.5 s prior to a backward platform translation on postural responses. The effect of the galvanic stimulation was largest on the final equilibrium position of the center of pressure (CoP). The largest effects occurred for the 0.5 and 0-s pre-period, when the dynamic CoP pressure changes in response to both the galvanic stimulus and the platform translation coincided. The shift in the final equilibrium position was also larger than the sum of the shifts for the galvanic stimulus and the platform translation alone for the 0.5 and 0-s pre-periods. The initial rate of change of the CoP response to the platform translation was not significantly affected in any condition. Changes in the peak CoP position could be accounted for by local interaction of CoP velocity changes induced by the galvanic and translation responses alone, but the changes in final equilibrium position could only be accounted for by a change in global body orientation. These findings suggest that the contribution of vestibulospinal information is greatest during the dynamic phase of the postural response, and that the vestibular system contributes most to the later components of the postural response, particularly to the final equilibrium position. These findings suggest that a nonlinear interaction between the vestibular signal induced by the galvanic current and the sensory stimuli produced by the platform translation occurs when the two stimuli are presented within 1 s, during the dynamic phase of the postural response to the galvanic stimulus. When presented at greater separations in time, the stimuli appear to be treated as independent events, such that no interaction occurs.
These experiments tested the hypothesis that the ability to change sensorimotor set quickly for automatic responses depends on the time interval between successive surface perturbations. Sensorimotor set refers to the influence of prior experience or context on the state of the sensorimotor system. Sensorimotor set for postural responses was influenced by first giving subjects a block of identical backward translations of the support surface, causing forward sway and automatic gastrocnemius responses. The ability to change set quickly was inferred by measuring the suppression of the stretched antagonist gastrocnemius responses to toes-up rotations causing backward sway, following the translations. Responses were examined under short (10-14 s) and long (19-24 s) inter-trial intervals in young healthy subjects. The results showed that subjects in the long-interval group changed set immediately by suppressing gastrocnemius to 51% of translation responses within the first rotation and continued to suppress them over succeeding rotations. In contrast, subjects in the short-interval group did not change set immediately, but required two or more rotations to suppress gastrocnemius responses. By the last rotation, the short-interval group suppressed gastrocnemius responses to 33%, similar to the long-interval group of 29%. Associated surface plantarflexor torque resulting from these responses showed similar results. When rotation and translation perturbations alternated, however, the short-interval group was not able to suppress gastrocnemius responses to rotations as much as the long-interval group, although they did suppress more than in the first rotation trial after a series of translations. Set for automatic responses appears to linger, from one trial to the next. Specifically, sensorimotor set is more difficult to change when surface perturbations are given in close succession, making it appear as if set has become progressively stronger. A strong set does not mean that responses become larger over consecutive trials. Rather, it is inferred by the extent of difficulty in changing a response when it is appropriate to do so. These results suggest that the ability to change sensorimotor set quickly is sensitive to whether the change is required after a long or a short series of a prior different response, which in turn depends on the time interval between successive trials. Different rate of gastrocnemius suppression to toes-up rotation of the support surface have been reported in previous studies. This may be partially explained by different inter-trial time intervals demonstrated in this study.
Previous studies have identified two discrete strategies for the control of posture in the sagittal plane based on EMG activations, body kinematics, and ground reaction forces. The ankle strategy was characterized by body sway resembling a single-segment-inverted pendulum and was elicited on flat support surfaces. In contrast, the hip strategy was characterized by body sway resembling a double-segment inverted pendulum divided at the hip and was elicited on short or compliant support surfaces. However, biomechanical optimization models have suggested that hip strategy should be observed in response to fast translations on a flat surface also, provided the feet are constrained to remain in contact with the floor and the knee is constrained to remain straight. The purpose of this study was to examine the experimental evidence for hip strategy in postural responses to backward translations of a flat support surface and to determine whether analyses of joint torques would provide evidence for two separate postural strategies. Normal subjects standing on a flat support surface were translated backward with a range of velocities from fast (55 cm/s) to slow (5 cm/s). EMG activations and joint kinematics showed pattern changes consistent with previous experimental descriptions of mixed hip and ankle strategy with increasing platform velocity. Joint torque analyses revealed the addition of a hip flexor torque to the ankle plantarflexor torque during fast translations. This finding indicates the addition of hip strategy to ankle strategy to produce a continuum of postural responses. Hip torque without accompanying ankle torque (pure hip strategy) was not observed. Although postural control strategies have previously been defined by how the body moves, we conclude that joint torques, which indicate how body movements are produced, are useful in defining postural control strategies. These results also illustrate how the biomechanics of the body can transform discrete control patterns into a continuum of postural corrections.
BACKGROUND: The cause of frequent falling in patients with dementia of the Alzheimer type (AD) is not well understood. Distraction from incongruent visual stimuli may be an important factor as suggested by their poor performance in tests of shifting visual attention in other studies. The purpose of this study was to determine whether AD patients have difficulty maintaining upright balance under absent and/or incongruent visual and other sensory conditions compared to nondemented healthy elderly persons and individuals with Parkinson's disease (PD). METHODS: Seventeen healthy older adults, 15 medicated PD subjects, and 11 AD subjects underwent the Sensory Organization Test protocol. The incidence of loss of balance ("falls"), and the peak-to-peak amplitude of body center of mass sway during stance in the six sensory conditions were used to infer the ability to use visual, somatosensory, and vestibular signals when they provided useful information for balance, and to suppress them when they were incongruent as an orientation reference. Vestibular reflex tests were conducted to ensure normal vestibular function in the subjects. RESULTS: AD subjects had normal vestibular function but had trouble using it in condition 6, where they had to concurrently suppress both incongruent visual and somatosensory inputs. All 11 AD subjects fell in the first trial of this condition. With repeated trials, only three AD subjects were able to stay balanced. AD subjects were able to keep their balance when only somatosensory input was incongruent. In this condition, all AD subjects were able to maintain balance whereas some falls occurred in the other groups. In all conditions, when AD subjects did not fall, they were able to control as large a sway as the healthy controls, except when standing with eyes closed in condition 2: AD subjects did not increase their sway whereas the other groups did. In the PD group, the total fall incidence was similar to the AD group, but the distribution was generalized across more sensory conditions. PD subjects were also able to improve with repeated trials in condition 6. CONCLUSION: Patients with dementia of the Alzheimer type have decreased ability to suppress incongruent visual stimuli when trying to maintain balance. However, they did not seem to be dependent on vision for balance because they did not increase their sway when vision was absent. Parkinsonian patients have a more general balance control problem in the sensory organization test, possibly related to difficulty changing set.
BACKGROUND: It has been suggested that patients with dementia of the Alzheimer type have abnormalities in the basal ganglia, and thus, may have similar sensorimotor problems as patients with basal ganglia degeneration from Parkinson's disease. Whether the similarity extends to balance control is unknown. One distinguishing feature of balance disorder in Parkinson's disease is difficulty with changing postural set in terms of adapting the amplitude of leg muscle activity as a function of support condition. We, therefore, tested whether patients with Alzheimer's disease without extrapyramidal signs would show a similar problem in changing postural set as patients with Parkinson's disease. METHODS: The ability to quickly change postural set was measured by comparing leg muscle activity under two conditions of support (free stance, versus grasping a frame, or sitting) during backward surface translations, during toes up surface rotations, and during voluntary rise to toes. Results were compared among 12 healthy adults, 8 nondemented Parkinson's patients on their usual dose of medication, and 11 Alzheimer patients without extrapyramidal signs. RESULTS: Subjects with Alzheimer's, but not Parkinson's, disease performed similarly to the healthy control subjects. They changed postural set immediately, by suppressing leg muscle activity to low levels when supported. Parkinson subjects did not change postural set immediately. They did not suppress the tibialis anterior in voluntary rise to toes when holding, nor the soleus in perturbed sitting as much as the healthy control and Alzheimer subjects in the first trial. Instead, the Parkinson subjects changed set more slowly, over repeated and consecutive trials in both protocols. The onset latencies of soleus responses to backward surface translations and perturbed sitting, as well as tibialis anterior responses to toes up rotations, were the same for all three groups. CONCLUSION: Alzheimer patients without extrapyramidal signs, unlike nondemented Parkinson's disease patients, have no difficulty in quickly changing postural set in response to altered support conditions. Our results, therefore, do not support the hypothesis that Parkinson's and uncomplicated Alzheimer's diseases share common postural set problems that may contribute to disordered balance control.
Emergence of postural patterns as a function of vision and translation frequency. We examined the frequency characteristics of human postural coordination and the role of visual information in this coordination. Eight healthy adults maintained balance in stance during sinusoidal support surface translations (12 cm peak to peak) in the anterior-posterior direction at six different frequencies. Changes in kinematic and dynamic measures revealed that both sensory and biomechanical constraints limit postural coordination patterns as a function of translation frequency. At slow frequencies (0.1 and 0.25 Hz), subjects ride the platform (with the eyes open or closed). For fast frequencies (1.0 and 1.25 Hz) with the eyes open, subjects fix their head and upper trunk in space. With the eyes closed, large-amplitude, slow-sway motion of the head and trunk occurred for fast frequencies above 0.5 Hz. Visual information stabilized posture by reducing the variability of the head's position in space and the position of the center of mass (CoM) within the support surface defined by the feet for all but the slowest translation frequencies. When subjects rode the platform, there was little oscillatory joint motion, with muscle activity limited mostly to the ankles. To support the head fixed in space and slow-sway postural patterns, subjects produced stable interjoint hip and ankle joint coordination patterns. This increase in joint motion of the lower body dissipated the energy input by fast translation frequencies and facilitated the control of upper body motion. CoM amplitude decreased with increasing translation frequency, whereas the center of pressure amplitude increased with increasing translation frequency. Our results suggest that visual information was important to maintaining a fixed position of the head and trunk in space, whereas proprioceptive information was sufficient to produce stable coordinative patterns between the support surface and legs. The CNS organizes postural patterns in this balance task as a function of available sensory information, biomechanical constraints, and translation frequency.
Recent experiments in healthy subjects have demonstrated that automatic postural responses can be suppressed when subjects are instructed to step instead of maintain stance in response to the surface translation. The aim of the present study was to investigate the role of the cerebellum in coordinating this interaction between the central command to step and peripherally triggered automatic postural responses. Eight subjects with cerebellar degeneration and eight control subjects were instructed to either maintain stance or step forward in response to a backward translation. In order to determine whether prediction of perturbation amplitude assisted suppression of postural responses, three platform translations were presented in both a serial (predictable) and a random (unpredictable) order. Cerebellar subjects were able to suppress their initial postural responses to the same amount as control subjects when instructed to step forward in response to backward translations, despite their hypermetria and inability to scale responses to predictable perturbation amplitudes. Control, but not cerebellar, subjects scaled the size of their postural responses to predictable perturbation amplitudes. The perturbation amplitude, however, had no effect on the size of early automatic responses when they were suppressed by instruction to step. The size of the suppressed postural response was independent of predictability of perturbation amplitudes in both control and cerebellar subjects. The dynamic interaction between automatic postural responses to an external perturbation and anticipatory postural adjustments for step initiation seems independent of prediction of perturbation amplitude and the integrity of the cerebellum. Although cerebellar subjects show larger-than-normal magnitude and variability of postural responses and an inability to scale the size of responses to predictable perturbation amplitudes, the cerebellum does not seem to be critical for suppression of the early postural response with a centrally intended movement.
Multivariate descriptors of sway were used to test whether altered sensory conditions result not only in changes in amount of sway but also in postural coordination. Eigenvalues and directions of eigenvectors of the covariance of shnk and hip angles were used as a set of multivariate descriptors. These quantities were measured in 14 healthy adult subjects performing the Sensory Organization test, which disrupts visual and somatosensory information used for spatial orientation. Multivariate analysis of variance and discriminant analysis showed that resulting sway changes were at least bivariate in character, with visual and somatosensory conditions producing distinct changes in postural coordination. The most significant changes were found when somatosensory information was disrupted by sway-referencing of the support surface (P = 3.2 x 10(-10)). The resulting covariance measurements showed that subjects not only swayed more but also used increased hip motion analogous to the hip strategy. Disruption of vision, by either closing the eyes or sway-referencing the visual surround, also resulted in altered sway (P = 1.7 x 10(-10)), with proportionately more motion of the center of mass than with platform sway-referencing. As shown by discriminant analysis, an optimal univariate measure could explain at most 90% of the behavior due to altered sensory conditions. The remaining 10%, while smaller, are highly significant changes in posture control that depend on sensory conditions. The results imply that normal postural coordination of the trunk and legs requires both somatosensory and visual information and that each sensory modality makes a unique contribution to posture control. Descending postural commands are multivariate in nature, and the motion at each joint is affected uniquely by input from multiple sensors.
Patients with bilateral vestibular loss have difficulty maintaining balance without stepping when standing in tandem, on compliant surfaces, across narrow beams, or on one foot, especially with eyes closed. Normal individuals (with no sensory impairment) maintain balance in these tasks by employing quick, active hip rotation (a "hip strategy"). The absence of a hip strategy in vestibular patients responding to translations of a short support surface has previously been taken as evidence that the use of hip strategy requires an intact vestibular system. However, many tasks requiring hip strategy alter one or a combination of important system characteristics, such as initial state of the body (tandem stance), dynamics (compliant surfaces), or biomechanical limits of stability (narrow beams). Therefore, the balance deficit in these tasks may result from a failure to account for these support surface alterations when planning and executing sensorimotor responses. In this study, we tested the hypothesis that vestibular information is critical to trigger a hip strategy even on an unaltered support surface, which imposes no changes on the system characteristics. We recorded the postural responses of vestibular patients and control subjects with eyes closed to rearward support surface translations of varying velocity, in erect stance on a firm, flat surface. Subjects were instructed to maintain balance without stepping, if possible. Faster translation velocities (25 cm/s or more) produced a consistent pattern of early hip torque (first 400 ms) in control subjects (i.e., a hip strategy). Most of the patients with bilateral vestibular loss responded to the same translation velocities with similar torques. Contrary to our hypothesis, we conclude that vestibular function is not necessary to trigger a hip strategy. We postulate, therefore, that the balance deficit previously observed in vestibular patients during postural tasks that elicit a hip strategy may have been due to the sensorimotor consequences of the system alterations imposed by the postural tasks used in those studies. Preliminary results from two younger patients who lost vestibular function as infants indicate that age, duration of vestibular loss, and/or the timing of the loss may also be factors that can influence the use of hip strategy as a rapid postural response.
The purpose of this study was to compare and contrast postural responses to lateral and A/P surface translations by quantifying joint positions, bilateral three-dimensional (3-D) ground reaction forces, and lower limb and trunk muscle electromyographic (EMG) activity. Subjects stood on a movable platform which was randomly translated in four different directions. The kinematic patterns in response to lateral and anterior/posterior (A/P) surface translations were similar in that there was a sequential displacement and reversal of the shank/thigh and then trunk segments. While the body center of mass (CoM) was displaced equally in response to lateral and A/P translations, equilibrium was maintained by redistributing the vertical forces and changing the shear forces exerted against the support surface. These force responses were bilaterally symmetrical for A/P translations but not for lateral translations. With respect to EMG activity, the first muscle activated was the proximal tensor fascia latae for lateral translations whereas the distal muscles were recruited first for A/P translations. Results from this study suggest that control of postural equilibrium may be similar for A/P and lateral translations, although specific differences in patterns may reflect various biomechanical constraints of the trunk and the lower extremities associated with the two planes of movement.
OBJECTIVE: To investigate the role of the cerebellum in postural adaptation for changes to the stimulus type of support surface displacements (backward translations v "toes up" rotations). METHODS: A group of 13 patients with chronic, isolated lesions of the cerebellum and 15 control subjects were tested. Automatic postural responses of the medial gastrocnemius and anterior tibial muscles were recorded. The first paradigm consisted of 10 rotational perturbations followed by 10 backward translations of the platform, and 10 backward translations followed by 10 rotations. The second paradigm consisted of 18 rotations and two randomly interposed translational perturbations, and 18 translations with two rotations randomly interposed. RESULTS: When the type of perturbation changed from an expected translation to an unexpected rotation and vice versa both control subjects and cerebellar patients showed an immediate and significant change in the response amplitude of the medial gastrocnemius and at the same time an immediate and significant change in the response amplitude of the anterior tibial muscles. Neither controls nor cerebellar patients showed effects of prediction in surface displacements of unexpected types of perturbation. Both controls and cerebellar patients showed no gradual increase in the gastrocnemius response in subsequent trials of surface translations following a block of 10 surface rotations and no gradual increase in the response amplitude of the anterior tibial muscle in subsequent trials of surface rotations following a block of 10 surface translations. CONCLUSIONS: Despite postural hypermetria, the integrity of the cerebellum does not seem critical for adaptation of postural synergies to changing stimulus types of surface displacements. The present results support previous findings suggesting that the main role of the cerebellum in automatic postural responses may be gain control.
To characterize muscle synergy organization underlying multidirectional control of stance posture, electromyographic activity was recorded from 11 lower limb and trunk muscles of 7 healthy subjects while they were subjected to horizontal surface translations in 12 different, randomly presented directions. The latency and amplitude of muscle responses were quantified for each perturbation direction. Tuning curves for each muscle were examined to relate the amplitude of the muscle response to the direction of surface translation. The latencies of responses for the shank and thigh muscles were constant, regardless of perturbation direction. In contrast, the latencies for another thigh [tensor fascia latae (TFL)] and two trunk muscles [rectus abdominis (RAB) and erector spinae (ESP)] were either early or late, depending on the perturbation direction. These three muscles with direction-specific latencies may play different roles in postural control as prime movers or as stabilizers for different translation directions, depending on the timing of recruitment. Most muscle tuning curves were within one quadrant, having one direction of maximal activity, generally in response to diagonal surface translations. Two trunk muscles (RAB and ESP) and two lower limb muscles (semimembranosus and peroneus longus) had bipolar tuning curves, with two different directions of maximal activity, suggesting that these muscle can play different roles as part of different synergies, depending on translation direction. Muscle tuning curves tended to group into one of three regions in response to 12 different directions of perturbations. Two muscles [rectus femoris (RFM) and TFL] were maximally active in response to lateral surface translations. The remaining muscles clustered into one of two diagonal regions. The diagonal regions corresponded to the two primary directions of active horizontal force vector responses. Two muscles (RFM and adductor longus) were maximally active orthogonal to their predicted direction of maximal activity based on anatomic orientation. Some of the muscles in each of the synergic regions were not anatomic synergists, suggesting a complex central organization for recruitment of muscles. The results suggest that neither a simple reflex mechanism nor a fixed muscle synergy organization is adequate to explain the muscle activation patterns observed in this postural control task. Our results are consistent with a centrally mediated pattern of muscle latencies combined with peripheral influence on muscle magnitude. We suggest that a flexible continuum of muscle synergies that are modifiable in a task-dependent manner be used for equilibrium control in stance.
We studied anticipatory postural adjustments contributing to gait initiation deficits in patients with Parkinson's disease (PD) to determine if these deficits could be improved by administration of levodopa or by external stimuli. Ground reaction forces and body kinematics were recorded for self-generated and cutaneous cue-triggered step initiation in normal subjects and in PD subjects when OFF and when ON. The effects of assisting anticipatory postural sway with a surface translation coupled with a cutaneous cue were also examined. Decreased force production, decreased velocity of movement, and slowed execution of the anticipatory postural adjustments for self-generated step characterized step initiation in PD subjects when OFF. These impairments were significantly less evident when the PD subjects were ON. Both PD and normal subjects increased force and velocity of movement when a cutaneous cue was used as a go signal. When subjects voluntarily initiated a step in response to the surface translation, both PD and normal subjects executed the anticipatory postural adjustments for step more rapidly, but the PD subjects, both ON and OFF, failed to increase force to execute push-off more rapidly. In conclusion, dopaminergic therapy and an external stimulus similarly improve the deficient force production for the anticipatory postural adjustments associated with step initiation in PD. The findings also suggest that force production during the postural adjustment phase of self-generated, but not externally triggered, step initiation is influenced by dopaminergic pathways.
We reported previously that patients with cerebellar deficits were unable to scale the magnitude of their early automatic postural responses to the predicted amplitudes of surface translations based on central set from prior experience. The present study investigated whether this deficit in set-dependent amplitude scaling was based predominantly on the cerebellar patient's disability (i) to predict perturbation amplitudes on the basis of prior experience, (ii) to scale the gain or magnitude of upcoming postural responses or (iii) to habituate postural responses. The increase in size of the early postural response when a larger than actual platform amplitude was expected and decrease when a smaller one was expected was defined as a measure of set-dependent amplitude prediction. The suppression of the postural response when the same platform velocity was repeated was used as a measure of habituation. The correlation between the size of early postural responses and platform amplitudes when presented serially, but not randomly, tested the ability to scale the gain of postural responses based on prior experience. Results show that although cerebellar patients could predict perturbation amplitudes based on prior experience, they could not use this prediction to modify precisely the gain of responses. The ability to habituate the magnitude of postural responses was not affected by cerebellar lesions. Thus, the cerebellum might not be critical for predicting upcoming events or for habituating to repeated postural stimuli, although it is important for accurate tuning of response gain based on prediction.