Cerebellar Subjects Research Articles

An intensive task-oriented circuit training positively impacts gait biomechanics in MS patients.

An intensive task-oriented circuit training (TOCT) provides a valid approach in improving motor function in Multiple Sclerosis (MS). We aimed at testing the efficacy of TOCT on gait kinematics in MS patients with mild-moderate disability. Nineteen MS patients able of independent walking performed 3-D Gait Analysis before (T0) and after (T1) a two-week TOCT program. Patients were clustered in two different subgroups, according to clinical neurological impairments assessed with specific functional system of Expanded Disability Status Scale (EDSS): pyramidal (Group 1) and cerebellar (Group 2) subjects. Spatio-temporal and kinematic data were compared before and after the TOCT intervention in the total sample of patients and in the two selected subgroups at two time intervals. Data obtained revealed increased dynamic ROM at knee joint after training in the whole study sample. Of note, knee dynamic excursion improved significantly in Group 1 but not in Group 2 patients after TOCT. Moreover, sagittal plane kinematics revealed significant modifications on knee and ankle biomechanics in Group 1 after rehabilitation. These data point out the benefits of the task specific training on gait dynamics in mild impaired MS subjects, linking to treatment opportunity in patients with a prevalent pyramidal impairment.

The handkerchief guide: A practical method to improve ataxic gait and active involvement in proprioception of the upper limb in cerebellar subjects

The handkerchief guide: A practical method to improve ataxic gait and active involvement in proprioception of the upper limb in cerebellar subjects

Cerebellar patients do not benefit from cerebellar or M1 transcranial direct current stimulation during force-field reaching adaptation.

Several studies have identified transcranial direct current stimulation (tDCS) as a potential tool in the rehabilitation of cerebellar disease. Here, we tested whether tDCS could alleviate motor impairments of subjects with cerebellar degeneration. Three groups took part in this study: 20 individuals with cerebellar degeneration, 20 age-matched controls, and 30 young controls. A standard reaching task with force-field perturbations was used to compare motor adaptation among groups and to measure the effect of stimulation of the cerebellum or primary motor cortex (M1). Cerebellar subjects and age-matched controls were tested during each stimulation type (cerebellum, M1, and sham) with a break of 1 wk among each of the three sessions. Young controls were tested during one session under one of three stimulation types (anodal cerebellum, cathodal cerebellum, or sham). As expected, individuals with cerebellar degeneration had a reduced ability to adapt to motor perturbations. Importantly, cerebellar patients did not benefit from anodal stimulation of the cerebellum or M1. Furthermore, no stimulation effects could be detected in aging and young controls. The present null results cannot exclude more subtle tDCS effects in larger subject populations and between-subject designs. Moreover, it is still possible that tDCS affects motor adaptation in cerebellar subjects and control subjects under a different task or with alternative stimulation parameters. However, for tDCS to become a valuable tool in the neurorehabilitation of cerebellar disease, stimulation effects should be present in group sizes commonly used in this rare patient population and be more consistent and predictable across subjects and tasks.NEW & NOTEWORTHY Transcranial direct current stimulation (tDCS) has been identified as a potential tool in the rehabilitation of cerebellar disease. We investigated whether tDCS of the cerebellum and primary motor cortex could alleviate motor impairments of subjects with cerebellar degeneration. The present study did not find stimulation effects of tDCS in young controls, aging controls, and individuals with cerebellar degeneration during reach adaptation. Our results require a re-evaluation of the clinical potential of tDCS in cerebellar patients.

Pronounced reduction of acquisition of conditioned eyeblink responses in young adults with focal cerebellar lesions impedes conclusions on the role of the cerebellum in extinction and savings

Human cerebellar lesion studies provide good evidence that the cerebellum contributes to the acquisition of classically conditioned eyeblink responses (CRs). As yet, only one study used more advanced methods of lesion-symptom (or lesion-behavior) mapping to investigate which cerebellar areas are involved in CR acquisition in humans. Likewise, comparatively few studies investigated the contribution of the human cerebellum to CR extinction and savings. In this present study, young adults with focal cerebellar disease were tested. A subset of participants was expected to acquire enough conditioned responses to allow the investigation of extinction and saving effects.19 participants with chronic surgical lesions of the cerebellum and 19 matched control subjects were tested. In all cerebellar subjects benign tumors of the cerebellum had been surgically removed. Eyeblink conditioning was performed using a standard short delay protocol. An initial unpaired control phase was followed by an acquisition phase, an extinction phase and a subsequent reacquisition phase. Structural 3T magnetic resonance images of the brain were acquired on the day of testing. Cerebellar lesions were normalized using methods optimized for the cerebellum. Subtraction analysis and Liebermeister tests were used to perform lesion-symptom mapping.As expected, CR acquisition was significantly reduced in cerebellar subjects compared to controls. Reduced CR acquisition was significantly more likely in participants with lesions of lobule VI and Crus I extending into Crus II (p<0.05, Liebermeister test). Cerebellar subjects could be subdivided into two groups: a smaller group (n=5) which showed acquisition, extinction and savings within the normal range; and a larger group (n=14) which did not show acquisition. In the latter, no conclusions on extinction or savings could be drawn.Previous findings were confirmed that circumscribed areas in lobule VI and Crus I are of major importance in CR acquisition. In addition, the present data suggest that if the critical regions of the cerebellar cortex are lesioned, the ability to acquire CRs is not only reduced but abolished. Subjects with lesions outside these critical areas, on the other hand show preserved acquisition, extinction and saving effects. As a consequence, studies in human subjects with cerebellar lesions do not allow drawing conclusions on CR extinction and savings. In light of the present findings, previous reports of reduced extinction in humans with circumscribed cerebellar disease need to be critically reevaluated.

Temporal disruption of upper-limb anticipatory postural adjustments in cerebellar ataxic patients

Voluntary movements induce postural perturbations, which are counteracted by anticipatory postural adjustments (APAs) that preserve body equilibrium. Little is known about the neural structures generating APAs, but several studies suggested a role of sensory-motor areas, basal ganglia, supplementary motor area and thalamus. However, the role of the cerebellum still remains an open question. The aim of this present paper is to shed further light on the role of cerebellum in APAs organization. Thus, APAs that stabilize the arm when the index finger is briskly flexed were recorded in 13 ataxic subjects (seven sporadic cases, four dominant ataxia type III and two autosomal recessive), presenting a slowly progressive cerebellar syndrome with four-limb dysmetria, and compared with those obtained in 13 healthy subjects. The pattern of postural activity was similar in the two groups [excitation in triceps and inhibition in biceps and anterior deltoid (AD)], but apparent modifications in timing were observed in all ataxic subjects in which, on average, triceps brachii excitation lagged the onset of the prime mover flexor digitorum superficialis by about 27 ms and biceps and AD inhibition were almost synchronous to it. Instead, in normal subjects, triceps onset was synchronous to the prime mover and biceps and AD anticipated it by about 40 ms. The observed disruption of the intra-limb APA organization confirms that the cerebellum is involved in APA control and, considering cerebellar subjects as a model of dysmetria, also supports the view that a proper APA chain may play a crucial role in refining movement metria.

Linear and angular control of circular walking in healthy older adults and subjects with cerebellar ataxia

Linear and angular control of trunk and leg motion during curvilinear navigation was investigated in subjects with cerebellar ataxia and age-matched control subjects. Subjects walked with eyes open around a 1.2-m circle. The relationship of linear to angular motion was quantified by determining the ratios of trunk linear velocity to trunk angular velocity and foot linear position to foot angular position. Errors in walking radius (the ratio of linear to angular motion) also were quantified continuously during the circular walk. Relative variability of linear and angular measures was compared using coefficients of variation (CoV). Patterns of variability were compared using power spectral analysis for the trunk and auto-covariance analysis for the feet. Errors in radius were significantly increased in patients with cerebellar damage as compared to controls. Cerebellar subjects had significantly larger CoV of feet and trunk in angular, but not linear, motion. Control subjects also showed larger CoV in angular compared to linear motion of the feet and trunk. Angular and linear components of stepping differed in that angular, but not linear, foot placement had a negative correlation from one stride to the next. Thus, walking in a circle was associated with more, and a different type of, variability in angular compared to linear motion. Results are consistent with increased difficulty of, and role of the cerebellum in, control of angular trunk and foot motion for curvilinear locomotion.

Structural and Functional Magnetic Resonance Imaging of the Human Cerebellar Nuclei

The present review focuses on recent developments in structural and functional magnetic resonance imaging (MRI) of the deep cerebellar nuclei (DCN), the main output structure of the cerebellum. The high iron content in the DCN allows for their visibility in T2*-weighted images. Spatial resolution has improved allowing the identification of DCN in individual cerebellar patients and healthy subjects. Based on findings in larger groups of healthy subjects, probabilistic MRI-based atlases of the deep cerebellar nuclei have been developed, which are important tools in human lesion and functional imaging studies. High iron content in the DCN, on the other hand, decreases the blood oxygenation level dependent-signal making functional imaging a difficult challenge. Compared to the vast amount of studies reporting activation of the cerebellar cortex, the number of studies demonstrating activation of the DCN is much less. Most studies report activation of the dentate nucleus. Dentate activations appear to be more reliable in more complex tasks for reasons currently unknown. As yet, few studies tried to show activations of functional subunits of the dentate nucleus. Increased signal-to-noise ratio and better spatial resolution using higher MR field strength together with recent progress in dentate normalization methods will allow identification of functional subunits and their interactions with the cerebellar cortex in future studies.

Reactive grip force control in persons with cerebellar stroke: effects on ipsilateral and contralateral hand

This study investigates the cerebellar contribution to reactive grip control by examining differences between (22-48 years) subjects with focal cerebellar lesion due to ischaemic stroke (CL) and healthy subjects (HS). The subjects used a pinch grip to grasp and restrain an instrumented handle from moving when it was subject to unpredictable load forces of different rates (2, 4, 8, 32 N/s) or amplitudes (1, 2, 4 N). The hand ipsilateral to the lesion of the cerebellar subjects showed delayed and more variable response latencies, e.g., 278 +/- 162 ms for loads delivered at 2 N/s, compared to HS 180 +/- 53 ms (P = 0.005). The CL also used a higher pre-load grip force with the ipsilateral hand, 1.6 +/- 0.8 N, than the HS, 1.3 +/- 0.6 N (P = 0.017). In addition, the contralateral hand in subjects with unilateral cerebellar stroke showed a delayed onset of the grip response compared to HS. Cerebellar lesions thus impair the reactive grip control both in the ipsilateral and contralateral hand.

Timing of conditioned eyeblink responses is impaired in children with attention-deficit/hyperactivity disorder

Structural changes of the cerebellum have been reported in several psychiatric diseases like schizophrenia, autism and attention-deficit/hyperactivity disorder (ADHD). Beside behavioral deficits children with ADHD often show slight motor abnormalities. Cerebellar malfunction may contribute. The cerebellum is a structure essential for motor coordination, various forms of motor learning and timing of motor responses. In the present study, eyeblink conditioning was applied to investigate learning and timing of motor responses both in children with ADHD and children with cerebellar lesions. Acquisition, timing and extinction of conditioned eyeblink responses were investigated in children with ADHD, children with chronic surgical cerebellar lesions and controls using a standard delay paradigm with two different interstimulus intervals. Timing of conditioned eyeblink responses was significantly impaired in children with ADHD in the long interstimulus interval condition. Also in children with cerebellar lesions conditioned responses (CR) tended to occur earlier than in controls. Incidences of CRs were significantly reduced in children with cerebellar lesions and tended to be less in children with ADHD than in controls. Extinction of the CRs was impaired in children with cerebellar lesions in both interstimulus interval conditions and in children with ADHD in the long interstimulus interval condition. Cerebellar malfunction may contribute to disordered eyeblink conditioning in ADHD. However, because CR abnormalities differed between ADHD and cerebellar subjects, dysfunction of non-cerebellar structures cannot be excluded.

Construction of gait adaptation model in human splitbelt treadmill walking

There are a huge number of studies that measure kinematics, dynamics, the oxygen uptake and so on in human walking on the treadmill. Especially in walking on the splitbelt treadmill where the speed of the right and left belt is different, remarkable differences in kinematics are seen between normal and cerebellar disease subjects. In order to construct the gait adaptation model of such human splitbelt treadmill walking, we proposed a simple control model and made a newly developed 2D biped robot walk on the splitbelt treadmill. We combined the conventional limit-cycle based control consisting of joint PD-control, cyclic motion trajectory planning and a stepping reflex with a newly proposed adjustment of P-gain at the hip joint of the stance leg. We showed that the data of robot normal subject model and cerebellum disease subject model experiments had high similarities with the data of normal subjects and cerebellum disease subjects experiments carried out by Reisman et al. 2005 and Morton and Bastian 2006 in ratios and patterns. We also showed that P-gain at the hip joint of the stance leg was the control parameter of adaptation for symmetric gaits in splitbelt walking and P-gain adjustment corresponded to muscle stiffness adjustment by the cerebellum. Consequently, we successfully proposed the gait adaptation model in human splitbelt treadmill walking and confirmed the validity of our hypotheses and the proposed model using the biped robot.

Construction of Gait Adaptation Model in Human Splitbelt Treadmill Walking

There are a huge number of studies that measure kinematics, dynamics, the oxygen uptake and so on in human walking on the treadmill. Especially in walking on the splitbelt treadmill where the speed of the right and left belt is different, remarkable differences in kinematics are seen between normal and cerebellar disease subjects. In order to construct the gait adaptation model of such human splitbelt treadmill walking, we proposed a simple control model and made a newly developed 2D biped robot walk on the splitbelt treadmill. We combined the conventional limit-cycle based control consisting of joint PD-control, cyclic motion trajectory planning and a stepping reflex with a newly proposed adjustment of P-gain at the hip joint of the stance leg. We showed that the data of robot (normal subject model and cerebellum disease subject model) experiments had high similarities with the data of normal subjects and cerebellum disease subjects experiments carried out by Reisman et al. (2005) and Morton and Bastian (2006) in ratios and patterns. We also showed that P-gain at the hip joint of the stance leg was the control parameter of adaptation for symmetric gaits in splitbelt walking and P-gain adjustment corresponded to muscle stiffness adjustment by the cerebellum. Consequently, we successfully proposed the gait adaptation model in human splitbelt treadmill walking and confirmed the validity of our hypotheses and the proposed model using the biped robot.

Kinematics of Arm Joint Rotations in Cerebellar and Unskilled Subjects Associated with the Inability to Throw Fast

Cerebellar subjects and unskilled throwers cannot produce fast arm movements when throwing. We investigated the arm movement kinematics associated with this lack of skill. Cerebellar subjects and matched controls, and skilled throwers throwing with their skilled (dominant) and unskilled (nondominant) arms, were instructed to make slow, medium, and fast 3-D overarm throws from a sitting position. Only the fast throws were analyzed in detail. Joint motions were computed from angular positions of arm segments recorded with search coils. When throwing, both the cerebellar group and the unskilled-arm group had slower arm movements, and slower elbow extension and wrist flexion velocities than their reference groups. They also had similar magnitudes of many kinematic parameters, e.g., both cerebellar and unskilled groups had similar elbow extension and wrist flexion velocities. Compared to their reference groups, both the cerebellar and unskilled-arm groups also had a smaller elbow extension acceleration, a smaller shoulder adduction deceleration, and the absence of a large elbow extension deceleration before ball release. Similar decreases in joint velocities and in joint accelerations and decelerations in the cerebellar and unskilled groups are consistent with the idea that the absence of the skill of throwing fast in both groups is associated with an inability to exploit interaction torques.

Sensory Prediction Errors Drive Cerebellum-Dependent Adaptation of Reaching

The cerebellum is an essential part of the neural network involved in adapting goal-directed arm movements. This adaptation might rely on two distinct signals: a sensory prediction error or a motor correction. Sensory prediction errors occur when an initial motor command is generated but the predicted sensory consequences do not match the observed values. In some tasks, these sensory errors are monitored and result in on-line corrective motor output as the movement progresses. Here we asked whether cerebellum-dependent adaptation of reaching relies on sensory or on-line motor corrections. Healthy controls and people with hereditary cerebellar ataxia reached during a visuomotor perturbation in two conditions: "shooting" movements without on-line corrections and "pointing" movements that allowed for on-line corrections. Sensory (i.e., visual) errors were available in both conditions. Results showed that the addition of motor corrections did not influence adaptation in control subjects, suggesting that only sensory errors were needed for learning. Cerebellar subjects were comparably impaired in both adaptation conditions relative to controls, despite abnormal and inconsistent on-line motor correction. Specifically, poor on-line motor corrections were unrelated to cerebellar subjects' adaptation deficit (i.e., adaptation did not worsen), further suggesting that only sensory prediction errors influence this process. Therefore adaptation to visuomotor perturbations depends on the cerebellum and is driven by the mismatch between predicted and actual sensory outcome of motor commands.

Contralateral cerebellar damage impairs imperative planning but not updating of aimed arm movements in humans

The specific motor control processes supported by the cerebellum and impaired with cerebellar damage remain unclear. The cerebellum has been implicated in both planning and updating of accurate movements. Previously, we used a statistical model to parcel aiming performance that was constrained by a timed-response paradigm into contributions attributed to a specified plan and feedforward updating. Here, we apply this procedure to determine the putative role of the cerebellum in planning and updating goal-directed aiming by comparing the performance of subjects with unilateral cerebellar stroke to controls. Subjects rapidly moved to targets in predictable or unpredictable conditions and cerebellar subjects used the contralesional limb to control for ipsilesional motor execution deficits. Displacement-derived movement velocity was used in the statistical model to determine the effect of planning and updating on accuracy. Compared to controls, the cerebellar group demonstrated errors in final position that were primarily determined by planning deficits. This finding is manifest in four ways: Cerebellar subjects (1) were less accurate than controls in both predictable and unpredictable conditions; (2) they showed minimal benefit from increased preparation time for target amplitude specification; (3) with ample time to plan direction, wrong direction response frequency was greater; and (4) final position was minimally determined by the plan. Because these deficits were found contralesional to the moving limb, the cerebellum's role in planning is not lateralized to one hemisphere but rather our findings suggest that cerebellar output affects motor planning for both upper limbs. Indeed, a lesion analysis showed that the dentate nucleus, an area implicated in planning motor strategies and the primary cerebellar output nucleus, was the only common region affected by our patient group with contralateral cerebellar strokes.

Children and Adolescents With Chronic Cerebellar Lesions Show No Clinically Relevant Signs of Aphasia or Neglect

We studied language and visuospatial functions of 12 children and adolescents who had undergone surgery for cerebellar astrocytoma without subsequent radiation or chemotherapy and compared them with 27 age-, gender-, and education-matched healthy control subjects. To study possible lateralization of the functions of the left and right cerebellar hemispheres, subjects performed several language tasks including a verb-generation task as well as standard neglect and extinction tests. Three-dimensional-MR images confirmed that lesions affected cerebellar hemispheres in all children but one who had a pure vermal lesion. The right cerebellar hemisphere was affected in six, the left hemisphere in four children, and both hemispheres in one child. There were no signs of aphasia in the children or adolescents with cerebellar lesions. Language abilities did not differ between cerebellar patients and control subjects except for small increases in reaction times in verb generation in patients with left-sided lesions. Visuospatial functions were also intact in cerebellar subjects except for minor group differences in neglect tasks. In sum, chronic focal cerebellar lesions acquired in childhood or youth do not result in persistent language disorders or clinically significant signs of spatial neglect or extinction.

Intact Ability to Learn Internal Models of Arm Dynamics in Huntington's Disease But Not Cerebellar Degeneration

Two different compensatory mechanisms are engaged when the nervous system senses errors during a reaching movement. First, on-line feedback control mechanisms produce in-flight corrections to reduce errors in the on-going movement. Second, these errors modify the internal model with which the motor plan is transformed into motor commands for the subsequent movements. What are the neural mechanisms of these compensatory systems? In a previous study, we reported that while on-line error correction was disturbed in patients with Huntington's disease (HD), it was largely intact in patients with cerebellar degeneration. Here we altered dynamics of reaching and studied the effect of error in one trial on the motor commands that initiated the subsequent trial. We observed that in patients with cerebellar degeneration, motor commands changed from trial-to-trial by an amount that was comparable to control subjects. However, these changes were random and were uninformed by the error in the preceding trial. In contrast, the change in motor commands of HD patients was strongly related to the error in the preceding trial. This error-dependent change had a sensitivity that was comparable to healthy controls. As a result, HD patients exhibited no significant deficits in adapting to novel arm dynamics, whereas cerebellar subjects were profoundly impaired. These results demonstrate a double dissociation between on-line and trial-to-trial error correction suggesting that these compensatory mechanisms have distinct neural bases that can be differentially affected by disease.

Relative contributions of balance and voluntary leg-coordination deficits to cerebellar gait ataxia.

Different cerebellar regions participate in balance control and voluntary limb coordination, both of which might be important for normal bipedal walking. We wanted to determine the relative contributions of balance versus leg-coordination deficits to cerebellar gait ataxia in humans. We studied 20 subjects with cerebellar damage and 20 control subjects performing three tasks: a lateral weight-shifting task to measure balance, a visually guided stepping task to measure leg- coordination, and walking. We recorded three-dimensional joint position data during all tasks and center of pressure coordinates during weight-shifting. Each cerebellar subject was categorized as having no detectable deficits, a balance deficit only, a leg-placement deficit only, or both deficits. We then determined the walking abnormalities associated with each of these categories. Five of 10 measures of gait ataxia were abnormal in cerebellar subjects with a balance deficit, but only 1 was abnormal in cerebellar subjects with a leg-placement deficit. Furthermore, subjects with a balance deficit performed worse than subjects with a leg-placement deficit on 9 of the 10 gait measures. Finally, performance on the balance task, but not the leg-placement task, explained a significant proportion of the variance in walking speed for the entire cerebellar group. We conclude that balance deficits are more closely related to cerebellar gait ataxia than leg-placement deficits. Our findings are consistent with animal literature, which has suggested that cerebellar control of balance and gait are interrelated, and dissociable from cerebellar control of voluntary, visually guided limb movements.

Cerebellar damage impairs automaticity of a recently practiced movement.

It has been suggested that the cerebellum plays a critical role in learning to make movements more "automatic" (i.e., requiring less attention to the details of a movement). We hypothesized that cerebellar damage compromises learning of movement automaticity, resulting in increased attentional demands for movement control. The purpose of our study was to determine whether cerebellar damage disrupts the ability to make a practiced movement more automatic. We developed a dual task paradigm using two tasks that did not have overlapping sensory or motor requirements for execution. Our motor task required subjects to maintain an upright posture while performing a figure-8 movement using their arm. This motor task was chosen to simulate requirements of everyday movements (e.g., standing while reaching for objects), but it was novel enough to require practice for improvement. Our secondary task was an auditory vigilance task where subjects listened to letter sequences and were asked to identify the number of times a target letter was heard. We tested controls and people with cerebellar damage as they practiced the movement task alone and then performed it with the auditory task. We recorded 3D position data from the arm, trunk, and leg during the movement task. Errors were recorded for both the movement and the letter tasks. Our results show that cerebellar subjects can improve the movement to a very limited extent with practice. Unlike controls, the motor performance of cerebellar subjects deteriorates to prepractice levels when attention is focused away from the movement during dual task trials. Control subjects' insensitivity to dual task interference after practice was due to learned movement automaticity and was not a reflection of better dual task performance generally. Overall, our findings suggest that the cerebellum may be important for shifting movement performance from an attentionally demanding (unpracticed) state to a more automatic (practiced) state.

Motor deficits cannot explain impaired cognitive associative learning in cerebellar patients

There is a strong evidence that the cerebellum is involved in associative motor learning. The exact role of the cerebellum in motor learning and whether it is involved in cognitive learning processes too, are still controversially discussed topics. A common problem of assessing cognitive capabilities of cerebellar patients is the existence of additional motor demands in all cognitive tests. Even if the patients are able to cope well with the motor requirements of the task, their performance could still involve compensating strategies which cost them more attentional resources than the normal controls. To investigate such interaction effects of cognitive and motor demands in cerebellar patients, we conducted a cognitive associative learning paradigm and varied systematically the motor demands and the cognitive requirements of the task. Nine patients with isolated cerebellar disease and nine matched healthy controls had to learn the association between pairs of color squares, presented centrally on a computer monitor together with a left or right answer button. In the simple motor condition, the answer button had to be pressed once and in the difficult condition three times. We measured the decision times and evaluated the correctly named associations after the test was completed. The cerebellar subjects showed a learning deficit, compared to the normal controls. However, this deficit was independent of the motor difficulty of the task. The cerebellum seems to contribute to motor-independent processes, which are generally involved in associative learning.

Perturbed step initiation in cerebellar subjects: 2. Modification of anticipatory postural adjustments.

Although ataxias of stance and gait are frequent manifestations of cerebellar disease, the number of human studies examining stance or gait in cerebellar subjects is limited. In the present study, we examined whether anticipatory postural adjustments were impaired in cerebellar subjects during perturbed and unperturbed step initiation. The first aim was to show possible abnormalities in timing, force and kinematic parameters of anticipatory postural adjustments in unperturbed stepping in cerebellar subjects. Second, we examined the ability of cerebellar subjects to modify anticipatory postural adjustments associated with step initiation in response to a backward translation. Finally, we asked whether cerebellar subjects (and controls) make use of predictive knowledge of perturbation amplitude in perturbed stepping. Only few abnormalities of anticipatory postural adjustments were found in cerebellar subjects compared to controls. Both in the unperturbed and perturbed step conditions, force production as well as step length and step velocity were reduced in cerebellar subjects compared to controls, suggesting compensatory slowing. Cerebellar subjects also appeared to be less able to use predictive information of perturbation amplitude to scale anticipatory postural adjustments than control subjects. Nevertheless, in unperturbed steps, temporal parameters of anticipatory postural adjustments were preserved in cerebellar subjects. When subjects voluntarily initiated a step in response to the surface translation, both control and cerebellar subjects adapted by executing the anticipatory postural adjustments for step more rapidly. Furthermore, both control and cerebellar subjects were able to use online information regarding perturbation amplitude to scale parameters of step initiation in perturbed stepping. Overall, our findings suggest that the cerebellum is neither critical for the basic motor program underlying unperturbed step initiation nor for many adaptive changes occurring during perturbed step initiation. Like its role in predictive scaling of automatic postural responses to external perturbations, the cerebellum appears to be important for predictive adaptation of anticipatory postural adjustments during step initiation.