Unilateral Cerebellar Lesions Research Articles

Asymmetry in Gaze-Holding Impairment in Acute Unilateral Ischemic Cerebellar Lesions Critically Depends on the Involvement of the Caudal Vermis and the Dentate Nucleus.

Stabilizing the eyes in space when looking at a target is provided by a brainstem/cerebellar gaze-holding network, including the flocculus/paraflocculus complex (non-human primate studies) and the caudal vermis, biventer, and inferior semilunar lobule (human studies). Previous research suggests that acute lateralized cerebellar lesions preferentially lead to gaze-evoked nystagmus (GEN) on ipsilesional gaze. Here, we further characterize the effect of unilateral cerebellar lesions on gaze-holding and hypothesize that the side-specific magnitude of gaze-holding impairment depends on the lesion location. Nine patients (age range = 31-62 years) with acute/subacute (≤ 10 days old) MRI-confirmed unilateral cerebellar stroke were included. Horizontal gaze holding was quantified while looking at a slowly moving (0.5°/s) flashing target (gaze angle = ±40°). Asymmetry in eye-drift velocity was calculated and compared with the different MRI patterns of cerebellar lesions. Individual peak eye-drift velocities (range = 1.7-8.8°/s) occurred at the most eccentric eye positions (gaze angle = 28-38°). We found significantly asymmetric eye-drift velocity (EDV) in eight out of nine patients. The four patients with MRI-confirmed involvement of the caudal vermis and the dentate nucleus all presented with ipsilesionally-predominant EDV, while in the five patients with lesions restricted to the cerebellar hemisphere, EDV was stronger on contralesional gaze in three out of four found with an asymmetric EDV. Involvement of the caudal vermis and the dentate nucleus is critical for determining the directional GEN asymmetry in unilateral cerebellar lesions. Thus, our findings support the occurrence of GEN without floccular/parafloccular lesions and suggest that the EDV asymmetry in relation to the side of the lesion provides information about the involvement of specific structures.

The Caudal Vermis and the Dentate Nucleus are Critical Structures for Determining the Directional Asymmetry in Gaze-Evoked Nystagmus in Unilateral Cerebellar Lesions (S28.004)

The Caudal Vermis and the Dentate Nucleus are Critical Structures for Determining the Directional Asymmetry in Gaze-Evoked Nystagmus in Unilateral Cerebellar Lesions (S28.004)

Persistent geotropic positional nystagmus in unilateral cerebellar lesions.

To determine the prevalence of central lesions in persistent geotropic positional nystagmus, and characteristics and anatomical substrates of the nystagmus in cerebellar lesions. We prospectively recruited 58 patients with persistent geotropic positional nystagmus at the Dizziness Clinic of Pusan National University Hospital. Seven patients with unilateral cerebellar lesions were subjected to analysis of clinical characteristics, oculographic data, and MRI lesions. For comparison, we studied 37 cases of peripheral persistent geotropic positional nystagmus. The prevalence of central lesions in persistent geotropic positional nystagmus was 12% (7/58). Persistent geotropic positional nystagmus in cerebellar lesions was mostly asymmetrical. Horizontal nystagmus changed in direction during the bow-and-lean test with null positions. All patients showed impaired horizontal smooth pursuit bilaterally, and 3 of them also had positional downbeat nystagmus. The peak intensity and asymmetry of persistent geotropic positional nystagmus did not differ between central and peripheral groups (p > 0.05), while there was a difference in the maxima. Lesion overlays revealed that damage to the cerebellar tonsil was responsible for the generation of persistent geotropic positional nystagmus. Although persistent geotropic positional nystagmus in cerebellar lesions shares the characteristics of nystagmus measures with peripheral cases, accompanying central oculomotor signs can aid in differentiation. In tonsillar lesions, compensatory rotational feedback due to erroneous estimation of the direction of gravity may generate constant horizontal geotropic positional nystagmus.

Bilateral effects of unilateral cerebellar lesions as detected by voxel based morphometry and diffusion imaging.

Over the last decades, the importance of cerebellar processing for cortical functions has been acknowledged and consensus was reached on the strict functional and structural cortico-cerebellar interrelations. From an anatomical point of view strictly contralateral interconnections link the cerebellum to the cerebral cortex mainly through the middle and superior cerebellar peduncle. Diffusion MRI (dMRI) based tractography has already been applied to address cortico-cerebellar-cortical loops in healthy subjects and to detect diffusivity alteration patterns in patients with neurodegenerative pathologies of the cerebellum. In the present study we used dMRI-based tractography to determine the degree and pattern of pathological changes of cerebellar white matter microstructure in patients with focal cerebellar lesions. Diffusion imaging and high-resolution volumes were obtained in patients with left cerebellar lesions and in normal controls. Middle cerebellar peduncles and superior cerebellar peduncles were reconstructed by multi fiber diffusion tractography. From each tract, measures of microscopic damage were assessed, and despite the presence of unilateral lesions, bilateral diffusivity differences in white matter tracts were found comparing patients with normal controls. Consistently, bilateral alterations were also evidenced in specific brain regions linked to the cerebellum and involved in higher-level functions. This could be in line with the evidence that in the presence of unilateral cerebellar lesions, different cognitive functions can be affected and they are not strictly linked to the side of the cerebellar lesion.

Jules Dejerine, André-Thomas and the pathology of the cerebellum

Jules Dejerine, André-Thomas and the pathology of the cerebellum

Interhemispheric Connectivity Characterizes Cortical Reorganization in Motor-Related Networks After Cerebellar Lesions.

Although cerebellar-cortical interactions have been studied extensively in animal models and humans using modern neuroimaging techniques, the effects of cerebellar stroke and focal lesions on cerebral cortical processing remain unknown. In the present study, we analyzed the large-scale functional connectivity at the cortical level by combining high-density electroencephalography (EEG) and source imaging techniques to evaluate and quantify the compensatory reorganization of brain networks after cerebellar damage. The experimental protocol comprised a repetitive finger extension task by 10 patients with unilateral focal cerebellar lesions and 10 matched healthy controls. A graph theoretical approach was used to investigate the functional reorganization of cortical networks. Our patients, compared with controls, exhibited significant differences at global and local topological level of their brain networks. An abnormal rise in small-world network efficiency was observed in the gamma band (30-40Hz) during execution of the task, paralleled by increased long-range connectivity between cortical hemispheres. Our findings show that a pervasive reorganization of the brain network is associated with cerebellar focal damage and support the idea that the cerebellum boosts or refines cortical functions. Clinically, these results suggest that cortical changes after cerebellar damage are achieved through an increase in the interactions between remote cortical areas and that rehabilitation should aim to reshape functional activation patterns. Future studies should determine whether these hypotheses are limited to motor tasks or if they also apply to cerebro-cerebellar dysfunction in general.

The effects of the cerebral, cerebellar and vestibular systems on the head stabilization reflex.

The head stabilization reflex (HSR) is a brain stem reflex which appears in the neck muscles in response to sudden head position changes and brings the head to its previous position. The reflex mechanism has not been understood. The afferent fibers come from cervical muscle spindles, vestibular structures, and the accessory nerve, the efferents from the accessory nerve. In this study, we aim to investigate the roles of supraspinal neural structures and the vestibular system on the HSR. The patient group consisted of 86 patients (33 cerebral cortical lesion, 14 cerebellar syndrome and 39 vestibular inexcitability or hypoexcitability); the control group was composed of 32 healthy volunteers. Concentric needle electrodes were inserted into the sternocleidomastoid muscle (SCM) and the accessory nerves were stimulated with the electrical stimulator. A reflex response of about 45-55ms was obtained from the contralateral SCM muscle. 50% of cases had bilateral loss whereas 37% of cases with unilateral cerebellar lesions had an ipsilateral reflex loss. Bilateral HSR loss was detected in 84% of cases with bilateral cerebellar lesions. Bilateral reflex loss was observed in 70% of patients with unilateral cortical lesions and 94% of those with bilateral vestibular dysfunction. Ipsilateral HSR loss was observed in 55% of cases with unilateral vestibular dysfunction. It was discovered that supraspinal structures and the vestibular system may have an excitatory effect on HSR. This effect may be lost in supra-segmental and vestibular dysfunctions. The localization value of HSR was found to be rather poor in our study.

Impaired Modulation of the Otolithic Function in Acute Unilateral Cerebellar Infarction

To define the cerebellar contribution in modulating the otolithic signals, we investigated the otolithic function in 27 patients with acute unilateral cerebellar infarctions in the territory of the posterior inferior cerebellar artery (PICA, n = 17, 63%), combined PICA and superior cerebellar artery (SCA) (n = 7, 30%), SCA (n = 2, 7%), and anterior inferior cerebellar artery (n = 1, 4%) from 2010 to 2012. The patients had evaluation of the ocular tilt reaction [head tilt, ocular torsion (OT), and skew deviation], tilt of the subjective visual vertical (SVV), cervical vestibular evoked myogenic potentials (VEMPs) in response to air conducted tone bursts, and ocular VEMPs induced by tapping the head at AFz. The evaluation was completed within 2 weeks after symptom onset. Patients often showed OT or SVV tilt (15/27, 55.6%) that was either ipsi- (n = 6) or contraversive (n = 9). Overall, there were no differences in the amplitudes and latencies of cervical and ocular VEMPs between the ipsi- and contralesional sides. However, individual analyses revealed frequent abnormalities of cervical (11/27, 41%) and/or ocular (9/27, 33%) VEMPs. While 11 (73%) of the 15 patients with the OTR/SVV tilt showed abnormalities of cervical (n = 9) and/or ocular (n = 7) VEMP responses, only three (25%) of the 12 patients without the OTR/SVV tilt had abnormal cervical (n = 2) and/or ocular (n = 2) VEMPs (73% vs. 25%, Fisher's exact test, p = 0.021). The concordance rate in the results of cervical and ocular VEMPs was marginally significant (19/27, 70%, p = 0.052, binominal). Unilateral cerebellar lesions may generate otolithic imbalances, as evidenced by the OTR/SVV tilt and asymmetric ocular or cervical VEMP responses, but without directionality according to the lesion side. Patients with the OTR/SVV tilt had abnormal VEMPs more often than those without.

Is there a link between spatial neglect and vestibular function at the cerebellar level?

The role of the cerebellum in vestibular function is well known and generally accepted [1, 3]. In the past, claims of the occurrence of spatial neglect have been raised in patients with cerebellar lesions [9, 12, 15], although, data regarding spatial neglect due to cerebellar lesions are inconsistent [6, 13]. The aims of this study were two-fold: to answer the questions, first, if neglect is a common sign in patients with acute cerebellar lesions, and second, if so, if there is an anatomical link between neglect and vestibular otolith function at the cerebellar level. We investigated a series of 16 acute stroke patients with unilateral leftand right-sided cerebellar lesions (Table 1). Figure 1a illustrates a lesion overlay map of all patients in which the subjects with left-sided lesions were flipped to the right side. Neglect and visual extinction were assessed as described previously [7, 8, 10]. All patients underwent vestibular otolith testing by means of tilts of the subjective visual vertical (SVV) [1, 4]. A mean tilt of more than 2.5 of the static SVV determined binocularly was considered pathological [1, 4]. Lesion analysis was done by brain imaging lesion techniques using MRIcron software [14]. The lesions of all patients were documented by MRI; the MRI protocol was described previously [2]. Only one of the sixteen patients (patient MS) showed neglect (6%), i.e., had six omissions in the Bell’s test on the contralesional side. None of the patients, including the one with a right-sided lesion, patient MS (formally diagnosed as neglect), showed typical behaviour of patients with neglect. Patient MS showed a performance of 23 out of 30 achievable points in the mini-mental state exam (MMSE) [5] compatible with a cognitive impairment. Ipsilesional neglect and extinction was not diagnosed in any of the patients. In contrast, eight out of 16 patients (50%) showed a vestibular otolith dysfunction with a contralesional tilt of SVV, whereas three patients (19%)—including the one patient (MS) with six contralesional omissions in the Bell’s test—had an ipsilesional SVV tilt. Thus, signs of neglect and vestibular otolith function were not associated (Fisher’s exact test p = 0.687). The cerebellar lesions distribution of the patients with SVV tilts affected parts of the biventer lobule, the deep nuclei, the hemispheres and midline structures. However, the location of maximum overlap of the patients with SVV tilts at the lateral border of the dentate nucleus reaching into the cerebellar hemisphere (x = -23; y = 62; z = -37; x = -13; y = 56; z = -37) was not affected in the MRI of patient MS (Fig. 1b, c, d). Contrary to data from patients with lesions of the cerebral cortex [11], our data show no relationship between SVV deviation, i.e. vestibular otolith dysfunction, and spatial neglect at cerebellar level. In accordance with B. Baier (&) F. Thomke F. Birklein M. Dieterich Department of Neurology, University of Mainz, Langenbeckstr. 1, 55131 Mainz, Germany e-mail: baierb@uni-mainz.de

Lateralized cerebellar contributions to word generation: a phonemic and semantic fluency study.

Impairment on verbal fluency tasks has been one of the more consistently reported neuropsychological findings after cerebellar lesions, but it has not been uniformly observed and the possible underlying cognitive basis has not been investigated. We tested twenty-two patients with chronic, unilateral cerebellar lesions (12 Left, 10 Right) and thirty controls on phonemic and semantic fluency tasks. We measured total words produced, words produced in the initial 15 seconds, errors and strategy switches. In the phonemic fluency task, the right cerebellar lesion (RC) group produced significantly fewer words compared to the left cerebellar lesion (LC) group and healthy controls, particularly over the first 15 seconds of the task with no increase in errors and significantly fewer switches over the entire task. In the semantic fluency task there was only a modest decrease in total words in the RC group compared to controls. RC lesions impair fluency with many of the same performance characteristics as left prefrontal lesions. This supports the hypotheses of a prefrontal-lateral cerebellar system for modulation of attention/executive or strategy demanding tasks.

Lateralized Cerebellar Contributions to Word Generation: A Phonemic and Semantic Fluency Study

Impairment on verbal fluency tasks has been one of the more consistently reported neuropsychological findings after cerebellar lesions, but it has not been uniformly observed and the possible underlying cognitive basis has not been investigated. We tested twenty-two patients with chronic, unilateral cerebellar lesions (12 Left, 10 Right) and thirty controls on phonemic and semantic fluency tasks. We measured total words produced, words produced in the initial 15 seconds, errors and strategy switches. In the phonemic fluency task, the right cerebellar lesion (RC) group produced significantly fewer words compared to the left cerebellar lesion (LC) group and healthy controls, particularly over the first 15 seconds of the task with no increase in errors and significantly fewer switches over the entire task. In the semantic fluency task there was only a modest decrease in total words in the RC group compared to controls. RC lesions impair fluency with many of the same performance characteristics as left prefrontal lesions. This supports the hypotheses of a prefrontal-lateral cerebellar system for modulation of attention/executive or strategy demanding tasks.

Reinstating the ability of the motor cortex to modulate cutaneomuscular reflexes in hemicerebellectomized rats

The pathways passing through the cerebellum calibrate cutaneomuscular responses. Indeed, the enhancement of cutaneomuscular responses associated with subthreshold high-frequency trains of stimulation applied on motor cortex following a period of peripheral repetitive stimulation (PRS) is prevented by hemicerebellectomy. We analysed the effects of low-frequency repetitive stimulation of motor cortex (LFRSM1) on interhemispheric inhibition (IHI) and on the modulation of cutaneomuscular reflexes in rats with left hemicerebellar ablation. IHI was assessed by paired-pulse method with a conditioning stimulus (CS) to M1 followed by a test stimulus (TS) to the opposite M1. LFRSM1 reduced IHI. Combination of LFRSM1 with PRS increased significantly the magnitudes of cutaneomuscular responses evoked ipsilaterally to the hemicerebellar ablation. The increase of the intensity of cutaneomuscular responses was correlated with the reduction of IHI. Excitability of anterior horn motoneurons pool, assessed by F-wave, remained unchanged. Conjunction of LFRSM1 with PRS can be used to restore the ability of the motor cortex to modulate the intensity of cutaneomuscular responses in case of extensive unilateral cerebellar lesion. This study underlines for the first time the potential role of callosal pathways in the deficits of corticomotor tuning of cutaneomuscular responses contralaterally to acute extensive cerebellar lesion.

Cerebellar damage impairs detection of somatosensory input changes. A somatosensory mismatch-negativity study

Several recent studies support the view that the cerebellum's contribution to sensory processing is not limited to movement regulation. In a previous paper (Restuccia D, Valeriani M, Barba C, Le Pera D, Capecci M, Filippini V, Molinari M. Functional changes of the primary somatosensory cortex in patients with unilateral cerebellar lesions. Brain 2001; 124: 757-68) we showed that the cerebellum influences somatosensory input processing at very early stages. The present study was aimed at verifying whether an analogous influence is also exerted at higher levels. For some time it has been known that in the auditory modality a specific event-related potential (ERP), that is, mismatch negativity (MMN), reflects preattentive detection of changes in the incoming stimulus by comparing the new stimulus with sensory memory traces. To test the cerebellar influence on the processing of incoming somatosensory stimuli we first verified whether the electrical stimulation of fingers, according to an 'oddball' paradigm within a stimulus-ignored condition, was able to elicit event-related components specifically linked to the preattentive detection of change. We analysed scalp responses obtained from eight healthy volunteers during frequent and rare electrical stimulation of the first and fifth finger of the left hand, respectively. To ensure that responses to deviant stimuli were due to changes in detection mechanisms, rather than to activation of new afferents, we also analysed responses to rare stimulation alone ('standard-omitted' condition). The 'oddball' stimulation was able to elicit a parieto-occipital extra negativity that was different in scalp distribution and latency from the N140 response to the 'standard-omitted' stimulation. We considered that this response was related to changes in detection mechanisms and labelled it somatosensory mismatch negativity (S-MMN). When the same procedure was applied to six patients with unilateral cerebellar lesions we found that the S-MMN was clearly abnormal after stimulation of the affected hand (ipsilateral to the affected cerebellar hemisphere). Earlier ERPs, as well as ERPs elicited during the 'standard-omitted' condition, were fully normal. Present data indicate that cerebellar processing is involved in preattentive detection of somatosensory input changes. In conclusion, this study demonstrates the reliability of S-MMN recordings and indicates that subjects with cerebellar damage may be impaired in the cortical processing of incoming somatosensory inputs.

Unilateral cerebellar stroke disrupts movement preparation and motor imagery

Objective To assess motor cortex excitability, motor preparation and imagery in patients with unilateral cerebellar stroke with damage of the dentate nucleus by using transcranial magnetic stimulation (TMS). Method Eight patients with unilateral cerebellar lesions due to tromboembolic stroke and 10 age matched healthy subjects were enrolled. Resting (RMT) and active (AMT) motor threshold, cortical and peripheral silent period, evaluation of motor imagery, reaction time and premovement facilitation of motor evoked potential (MEP) were tested bilaterally using TMS. Results The RMT and AMT were found to be increased contra lateral to the affected cerebellar hemisphere while the cortical silent period was prolonged. In addition the amount of MEP facilitation during motor imagery and the pre-movement facilitation were reduced in the motor cortex contra lateral to the affected cerebellar hemisphere. The reaction time, performed with the symptomatic hand, was slower. Conclusions On the whole, our data confirm a role for the cerebellum in maintaining the excitability of primary motor area. Furthermore, patients with unilateral cerebellar stroke exhibit lateralized deficit of motor preparation and motor imagery. Significance Our results add to evidence that cerebellum contributes to specific aspects of motor preparation and motor imagery.

Olfactory Impairments in Patients with Unilateral Cerebellar Lesions Are Selective to Inputs from the Contralesional Nostril

Functional imaging studies of olfaction have consistently reported odorant-induced activation of the cerebellum. However, the cerebellar role in olfaction remains unknown. We examined the olfactory and olfactomotor abilities of patients with unilateral cerebellar lesions, comparing performance within subjects across nostrils, as well as between subjects with age-matched and young controls. Regarding olfactory performance, initial testing revealed that patients had a contralesional impairment in olfactory identification but not olfactory detection threshold. However, when tested under conditions that prevented compensatory sniffing strategies, the patients also exhibited a contralesional olfactory detection impairment. Regarding olfactomotor function, a healthy olfactomotor system generates sniffs that are (1) sufficiently vigorous and (2) inversely proportional to odorant concentration in sniff mean airflow velocity, maximum airflow velocity, volume, and duration. Patients' sniffs were lower in overall airflow velocity and volume in comparison with control participants. Furthermore, reduced sniff velocity predicted poorer detection thresholds in patients. Finally, whereas young controls used concentration-dependent sniffs, there was a trend in that direction only for age-matched controls. Patients used sniffs that were concentration invariant. In conclusion, cerebellar lesions impacted olfactory and olfactomotor performance. These findings strongly implicate an olfactocerebellar pathway prominent in odor identification and detection that functionally connects each nostril primarily to the contralateral cerebellum.

Interlimb coordination deficits during cyclic movements in cerebellar hemiataxia

The authors report a 35-year-old man whose unilateral cerebellar lesion resulted in marked deficits in coordinating simultaneous cyclic movements of the arm and leg on his ipsilesional side. He exhibited no such deficits when making simultaneous movements of the contralesional limbs or when moving paired left and right limbs. Thus, the cerebellum, which is already known to underlie within-limb interjoint coordination, also contributes to coordination between limbs.

Role of the cerebellum in movements: control of timing or movement transitions?

Patients with cerebellar damage are impaired on a range of timed tasks. However, recent research has indicated that the impairment on temporal production tasks is limited to discontinuous movements. The present experiments were designed to compare two accounts for the increased temporal variability observed in these patients when producing discontinuous movements. First, the impairment on discontinuous movements may be the result of the requirements associated with transitioning between movement onsets and offsets, requirements unique to discontinuous movement production. Second, the impairment may reflect a requirement to represent the temporal goal in timed, discontinuous movements. Patients with unilateral or bilateral cerebellar lesions and matched control subjects performed a key-pressing task. In one condition, the participants pressed and immediately released the key. The other conditions required the participants to press the key, and after either a 550-ms or 950-ms delay, release the key. Individuals with cerebellar damage were impaired on the two timed conditions. These results do not support the transition hypothesis. Rather, they are consistent with the hypothesis that the cerebellum is essential for tasks requiring precise event-like temporal control.

Amplitude changes of unconditioned eyeblink responses in patients with cerebellar lesions.

Timing and amplitude parameters of unconditioned eyeblink responses were investigated in 24 patients with unilateral cerebellar lesions following infarcts within the territory of the superior cerebellar artery (SCA, n=12) and of the posterior inferior cerebellar artery (PICA, n=12). The extent of cortical cerebellar lesions, i.e., which lobules were affected and possible involvement of cerebellar nuclei, was determined by three-dimensional magnetic resonance imaging (3D MRI). Amplitude parameters of eyeblink responses were normalized and expressed as percentage of the unaffected side in patients and the second tested side in age-matched controls. Normalized peak amplitudes, burst area and burst duration were significantly increased in SCA patients with lesions restricted to cortical areas. Burst onset and time to peak were not significantly different compared with controls. Temporal and amplitude parameters of eyeblink responses were unchanged in SCA patients with additional involvement of cerebellar nuclei and in patients with lesions of the PICA territory. Consistent with animal lesion and recording studies and a recent human functional magnetic resonance imaging (fMRI) study, the present data suggest that cortical areas of the superior cerebellum are of importance in eyeblink control in humans. These areas partly overlap with areas known to be critical in eyeblink conditioning.

Unilateral cerebellar lesions influence arm movements bilaterally.

Limb ataxia is seen as a sign of ipsilateral cerebellar dysfunction. However, imaging studies have shown a bilateral cerebellar activation during unilateral hand movements. We questioned whether unilateral cerebellar lesions affect pointing movements not only of the ipsilateral hand but also of the contralateral hand. Horizontal saccadic pointing movements of 10 patients with unilateral cerebellar infarctions (infarctions of the posterior inferior or superior cerebellar artery) were compared with those of 19 controls. The movements were recorded with an infrared video motion analysis system. The peak velocity, time lag, and dysmetria of the ipsilateral and contralateral hands were calculated. Patients with cerebellar infarctions had significantly slower movements not only for the ipsilateral but also for the contralateral arm. The time lag of these movements in patients was also significantly larger for both arms. In contrast, there was no significant difference in dysmetria at the endpoints. These findings indicate that both ipsilateral and contra-lateral movements of patients with unilateral cerebellar lesions are slightly impaired.

Responses of the red nucleus neurons to limb stimulation after cerebellar lesions.

Two series of experiments concerning the effects induced by unilateral cerebellar lesions on background activity and responses of red nucleus neurons contralateral to lesion sites are reported in this short review. The first series describes the effects of cerebellar cortex ablations, the second reports the results of hemicerebellectomy. The major source of input to the deep cerebellar nuclei, the Purkinje cells of the cerebellar cortex are known to be inhibitory. Removal of this influence by cerebellar cortex lesion results in an increase of the interpositus neurons background activity. This effect strengthens the interpositus excitatory influence upon rubral neurons by evoking exaggerated depolarization and enhancing sensitivity of these cells to somatosensory volleys. This causes a considerable increase in the background firing, eliminates the pauses in discharges occurring in responses generated by somatosensory stimuli, and augments the excitatory rebound. These changes destroy the content and timing of feedback information flowing through the spino-cerebello-rubro-spinal loop, and are, at least in part, responsible for motor deficits of cerebellar dysfunction. Hemicerebellectomy reduces drastically spontaneous firing of rubro-spinal neurons and simplifies response patterns. Due to direct spino-rubral pathways the latency of response is not changed.