Bradykinesia and impairment of EEG desynchronization in Parkinson's disease.

It has been suggested that the basal ganglia control the release of cortical elements from low-frequency rhythmic idling activity during voluntary movement. This hypothesis was tested by recording the local idling rhythms of the motor cortex, the alpha and beta rhythms, in 12 untreated and treated patients with Parkinson's disease as they moved a wrist. Recordings were made after overnight withdrawal of medication and again 1 hr after levodopa. The treatment-related attenuation of the alpha and beta rhythms picked up over the cortical motor areas contralateral to the active arm correlated with the improvement in size and speed of movement effected by levodopa. The distribution and degree of attenuation depended on the complexity of the task. These results demonstrate for the first time a specific effect of levodopa on the organization of motor cortical activity in the frequency domain, an effect that correlates with improvements in bradykinesia.     

Abnormal pattern of cortical activation associated with voluntary movement in obsessive-compulsive disorder: an EEG study

OBJECTIVE: Converging evidence in patients with obsessive-compulsive disorder (OCD) shows abnormalities of prefrontal areas and basal ganglia, which are also involved in motor control. Event-related desynchronization of mu and beta EEG rhythms is considered a correlate of motor activation during motor preparation and execution, followed by cortical idling or inhibition indicated by event-related synchronization. The authors investigated the circuits involved in motor behavior in OCD by using event-related desynchronization/synchronization. METHOD: Data on alpha and beta event-related desynchronization/synchronization with self-paced movement of the right thumb were obtained by using 29-channel EEG in 10 untreated OCD patients and 10 normal subjects. RESULTS: OCD patients showed delayed onset of mu event-related desynchronization with movement preparation and less postmovement beta synchronization, compared to normal subjects. CONCLUSIONS: Delayed event-related desynchronization in OCD is consistent with involvement of structures related to motor programming, such as basal ganglia. Lower levels of postmovement beta synchronization suggest impairment of the inhibitory system in OCD.     

Effect of L-Dopa on the pattern of movement-related (de)synchronisation in advanced Parkinson's disease.

In the early stages of Parkinson's disease (PD), impaired motor preparation has been related to a delay of mu rhythm movement-related desynchronisation, suggesting hypoactivation of the contralateral, primary sensorimotor (PSM) cortex. Following movement, a decrease in the amplitude of beta rhythm movement-related synchronisation was observed over the same region. This decrease--not seen in control subjects--was thus thought to be related to an impairment in cortical deactivation. By monitoring movement-related (de)synchronisation, we aimed (i) to extend to advanced PD the observations made in less-advanced situations and (ii) to test the effect of acute L-Dopa on these abnormalities. The United Parkinson's Disease Rating Scale (UPDRS) III score decreased by about 60% following acute L-Dopa administration, and we observed the following concurrent changes: a marked increase in mu desynchronisation pre-movement latency (thus reduced delay) during movement preparation over contralateral, central regions; an increase in mu desynchronisation during movement execution over bilateral central regions; a decrease in mu desynchronisation latency over bilateral frontocentral regions, and a significant increase in beta synchronisation over contralateral, central regions after movement. Changes of mu and beta rhythm parameters seemed to be inversely correlated with bradykinesia. Mu rhythm desynchronisation latency and beta synchronisation amplitude further decreased in advanced PD compared to earlier stages of the disease, suggesting greater impairment of cortical activation/deactivation as the disease progresses. L-Dopa partially restored the abnormal mu and beta rhythm cortical (de)synchronisation patterns over the PSM cortex.     

Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease

In Parkinson's disease, poor motor performance (resulting primarily from abnormal cortical activation during movement preparation and execution) may also be due to impaired sensorimotor integration and defective cortical activity termination of the ongoing movement, thus delaying preparation of the following one. Reduced movement-related synchronization of the beta rhythm in Parkinson's disease compared to controls has been put forward as evidence for impaired postmovement cortical deactivation. We assessed the effects of subthalamic deep brain stimulation and l-dopa on beta rhythm synchronization over the premotor and primary sensorimotor cortex. Ten advanced patients performed self-paced wrist flexion in four conditions according to the presence or not of stimulation and l-dopa. Compared to without treatment, the motor score improved by approximately 60%; the beta synchronization was present over the contralateral frontocentral region and increased significantly over the contralateral central region under stimulation and under l-dopa, with a maximal effect when both treatments were associated. Our advanced patients displayed very focused and attenuated beta rhythm synchronization which, under stimulation, increased over the contralateral premotor and primary sensorimotor cortex. Stimulation and l-dopa both partly restored postmovement cortical deactivation in advanced Parkinson's disease, although the respective mechanisms probably differ. They may improve bradykinesia and cortical deactivation by reestablishing movement-related somatosensory processing at the end of the movement through the basal ganglia into the cortex.     

Pathophysiological mechanisms implicated by high-frequency stimulation in Parkinson's disease: the restoration of high and low frequency oscillatory systems

INTRODUCTION: Increased neuronal activity in the internal pallidum (GPi) and the subthalamic nucleus (STN) has been clearly demonstrated in Parkinsonian models, and the two structures have thus been selected as therapeutic targets for functional neurosurgery. High-frequency electrical stimulation of the GPi or the STN improves the parkinsonian symptoms but also dyskinesias directly by GPi stimulation or indirectly by reduction of L-Dopa associated with STN stimulation. According to Alexander's model of the organisation of the basal ganglia, electrical stimulation of GPi or STN should have led to uncontrolled hyperkinesia. This apparent paradox could be explained on one hand by the involvement of different anatomo-functional areas within these structures and on the other by spatial and temporal changes in neuronal discharge patterns in the basal ganglia which in turn produce variations in synchronisation. RESULTS: Event-related (de)synchronisation (ERD) has enabled us to study variations in subcortico-cortical oscillatory activity: it has been shown that high-frequency electrical stimulation of the GPi/STN increases desynchronisation of low frequency rhythms (mu and beta,<30 Hz) during movement preparation and execution and augments post-movement synchronisation. Stimulation also decreases the abnormal frontocentral spreading of desynchronisation during movement preparation. CONCLUSIONS: In accordance with previous coherence analyses, electrical stimulation of STN is likely to restore the activity of high-frequency and low-frequency systems, as evidenced by a decrease in the hypersynchronisation of low-frequency rhythms at rest and restoral of a high-frequency rhythm during movement. Stimulation may improve spatial selectivity by activating the selected programs in conjunction with the primary sensorimotor cortex, whilst inhibiting competitive programs represented by abnormal spreading outside the primary sensorimotor cortex.     

Impaired movement-related potentials in acute frontal traumatic brain injury.

OBJECTIVE: Focal brain lesions due to traumatic brain injury (TBI) do not only lead to functional deficits in the lesion area, but also disturb the structurally intact neuronal network connected to the lesion site. Therefore we hypothesized dysfunctions of the cortical motor network after frontal TBI. The movement related potential (MRP) is an EEG component related to voluntary movement consisting of the Bereitschaftspotential (BP), the negative slope (NS), and the motor potential (MP). The aim of our study was to demonstrate alterations in the movement related cortical network in the acute stage after TBI by comparing our patients' MRPs to those of a healthy control group. METHODS: EEGs of 22 patients with magnetic resonance imaging defined contusions of the prefrontal cortex were recorded within 8 weeks after TBI. We further recruited a healthy control group. The paradigm consisted of self-paced abductions of the right index finger. RESULTS: Compared to healthy controls, the BP in the patient group was significantly reduced and its onset delayed. Moreover, an enhanced contribution of the postrolandic hemisphere ipsilateral to the movement and a reduced contribution of the left frontal cortex, ipsilateral to the lesion in the majority of the patients, were observed during motor execution (MP). CONCLUSIONS: Anatomical connections between the prefrontal cortex and the supplementary motor area (SMA) are known to exist. We suggest that prefrontal lesions lead to reduced neuronal input into the SMA. This deficit in the preparatory motor network may cause the reduced BPs in our patients. Moreover, an increased need for attentional resources might explain the enhanced motor potentials during movement execution. In conclusion, we demonstrated altered MRPs in the acute stage after frontal TBI, which are a consequence of disturbed neuronal networks involved in the preparation and execution of voluntary movements.     

Does post-movement beta synchronization reflect an idling motor cortex?

After the completion of a voluntary movement, a synchronization of cortical beta rhythms is recorded over the contralateral central region, which is assumed to reflect the termination of the motor command. In order to test this hypothesis, we compared in eight healthy subjects the synchronization of EEG beta rhythms following active and passive index extension. The passive movement was also performed after deafferentation by ischaemic nerve block in three subjects. Beta synchronization was present in all subjects after both active and passive movements, and disappeared under ischaemia in all three subjects. Post-movement beta synchronization can not solely be explained by an idling motor cortex. It may also, at least in part, reflect a movement-related somatosensory processing.     

Neural correlates of visuomotor adjustments during scaling of human finger movements

Visually guided finger movements include online feedback of current effector position to guide target approach. This visual feedback may be scaled or otherwise distorted by unpredictable perturbations. Although adjustments to visual feedback scaling have been studied before, the underlying brain activation differences between upscaling (visual feedback larger than real movement) and downscaling (feedback smaller than real movement) are currently unknown. Brain activation differences between upscaling and downscaling might be expected because within‐trial adjustments during upscaling require corrective backwards accelerations, whereas correcting for downscaling requires forward accelerations. In this behavioural and fMRI study we investigated adjustments during up‐ and downscaling in a target‐directed finger flexion–extension task with real‐time visual feedback. We found that subjects made longer and more complete within‐trial corrections for downscaling perturbations than for upscaling perturbations. The finger task activated primary motor (M1) and somatosensory (S1) areas, premotor and parietal regions, basal ganglia, and cerebellum. General scaling effects were seen in the right pre‐supplementary motor area, dorsal anterior cingulate cortex, inferior parietal lobule, and dorsolateral prefrontal cortex. Stronger activations for down‐ than for upscaling were observed in M1, supplementary motor area (SMA), S1 and anterior cingulate cortex. We argue that these activation differences may reflect differing online correction for upscaling vs. downscaling during finger flexion‐extension.     

Effects of subthalamic nucleus stimulation on actual and imagined movement in Parkinson's disease : a PET study

BACKGROUND: PET studies in moderately affected Parkinson's disease (PD) patients reveal abnormal cerebral activation during motor execution and imagery, but the effects of subthalamic nucleus (STN) stimulation are not well established. OBJECTIVES: to assess the effect of STN stimulation on cerebral activation during actual and imagined movement in patients with advanced PD. METHODS: seven severely affected PD patients treated with bilateral STN stimulation were studied with PET and H(2)(15)O. The following conditions were investigated: (1). rest; (2). motor execution of a sequential predefined joystick movement with the right hand and (3). motor imagery of the same task. Patients were studied with and without left STN stimulation while right stimulator remained off. RESULTS: Without STN stimulation, the primary motor cortex was activated only during motor execution whereas the dorsolateral prefrontal cortex (DLPFC) was activated only during motor imagery. An activation of the supplementary motor area (SMA) was seen during both motor execution and motor imagery. Left STN stimulation during motor execution increased the regional cerebral blood flow (rCBF) bilaterally in the prefrontal cortex including DLPFC, in the left thalamus and putamen. In addition, a reduction of rCBF was noted in the right primary motor cortex, inferior parietal lobe and SMA. Under left STN stimulation, during motor imagery, rCBF increased bilaterally in the DLPFC and in the left thalamus and putamen and decreased in the left SMA and primary motor cortex. CONCLUSION: STN stimulation during both motor execution and imagery tends to improve the functioning of the frontal-striatal-thalamic pathway and to reduce the recruitment of compensatory motor circuits notably in motor, premotor and parietal cortical areas.     

Brain activity correlates differentially with increasing temporal complexity of rhythms during initialisation, synchronisation, and continuation phases of paced finger tapping

Activity in parts of the human motor system has been shown to correlate with the complexity of performed motor sequences in terms of the number of limbs moved, number of movements, and number of trajectories. Here, we searched for activity correlating with temporal complexity, in terms of the number of different intervals produced in the sequence, using an overlearned tapping task. Our task was divided into three phases: movement selection and initiation (initiate), synchronisation of finger tapping with an external auditory cue (synchronise), and continued tapping in absence of the auditory pacer (continue). Comparisons between synchronisation and continuation showed a pattern in keeping with prior neuroimaging studies of paced finger tapping. Thus, activation of bilateral SMA and basal ganglia was greater in continuation tapping than in synchronisation tapping. Parametric analysis revealed activity correlating with temporal complexity during initiate in bilateral supplementary and pre-supplementary motor cortex (SMA and preSMA), rostral dorsal premotor cortex (PMC), basal ganglia, and dorsolateral prefrontal cortex (DLPFC), among other areas. During synchronise, correlated activity was observed in bilateral SMA, more caudal dorsal and ventral PMC, right DLPFC and right primary motor cortex. No correlated activity was observed during continue at P<0.01 (corrected, cluster level), though left angular gyrus was active at P<0.05. We suggest that the preSMA and rostral dorsal PMC activities during initiate may be associated with selection of timing parameters, while activation in centromedial prefrontal cortex during both initiate and synchronise may be associated with temporal error monitoring or correction. The absence of activity significantly correlated with temporal complexity during continue suggests that, once an overlearned timed movement sequence has been selected and initiated, there is no further adjustment of the timing control processes related to its continued production in absence of external cues.     

Effects of rTMS on Parkinson’s disease: a longitudinal fMRI study

Parkinson’s disease is a movement disorder whose principal symptoms are tremor, rigidity, bradykinesia and postural instability. Initially, drugs like l-dopa or dopaminergic agonists are able to control these symptoms, but with the progress of the disease these drugs become less effective. Previous studies have reported that repetitive transcranial magnetic stimulation (rTMS) can improve these motor symptoms. The objective of this study was to investigate the neural mechanisms through which 25 Hz rTMS may improve motor symptoms in Parkinson’s disease. In a double-blind placebo-controlled study, we evaluated the effects of 25 Hz. rTMS in 10 Parkinson’s disease patients. Fifteen rTMS sessions were performed over the primary cortex on both hemispheres (one after the other) during a 12-week period. The patients were studied using functional magnetic resonance imaging during performance of a simple tapping and a complex tapping task, 1 week before the administration of the first rTMS session and just after the last session. rTMS improved bradykinesia, while functional magnetic resonance imaging showed different cortical patterns in prefrontal cortex when patients performed the complex tapping test. Furthermore, the improvement in bradykinesia is associated with caudate nucleus activity increases in simple tapping. Finally, we observed a relative change in functional connectivity between the prefrontal areas and the supplementary motor area after rTMS. These results show a potential beneficial effect of repetitive transcranial magnetic stimulation on bradykinesia in Parkinson’s disease which is substantiated by neural changes observed in functional magnetic resonance imaging.     

Relations between the basal ganglia and the thalamus of the primate. New morphologic data. New physiopathologic interpretations

Considerable progress has been made over the last few years in our knowledge of the thalamus and basal ganglia and their relationships to the cerebral cortex. More detailed topographic studies in the macaque have demonstrated the separation, in the lateral region of the thalamus, between afferent cerebellar and basal ganglia territories. These territories fail to correlate with the subdivision between ventral and dorsal elements or the limits of a single cytoarchitectonic nucleus. The cerebellar territory corresponds to VIL (or VPLo) which projects towards the primary cortex, and to VIM (or area X) and DI (or VLc) which project towards premotor cortex. The nigral (and tectal) territory corresponds to VOM (or VAmc) and to some parts of the medial nucleus and projects mainly towards the oculomotor area, supplementary motor area and prefrontal cortex. In return, the oculomotor area and substantia nigra project towards the colliculus superior. Several thalamic nuclei constitute the pallidal territory: VOL (or VLo) projects mainly towards supplementary motor area, LPo (or VApc) and Do towards the prefrontal cortex. The median center, which receives afferents from pallidum and motor cortex, projects towards the striatum but also the motor cortex. The parafascicular nucleus projects towards the striatum and premotor cortex. It is still not possible to transpose data acquired in the macaque to man, but functional reinterpretations are possible. A system which involves the median pallidum, VOL and supplementary motor area could control motor initiative and flow of movement. A second system, involving the substantia nigra, colliculus superior, thalamic relay and oculomotor area could control posture. The pallidum and substantia nigra, anterior part of lateral mass, medial nucleus and prefrontal cortex could elaborate motor programmes.     

Comparison of cerebral activation between motor execution and motor imagery of self-feeding activity

Motor imagery is defined as an act wherein an individual contemplates a mental action of motor execution without apparent action. Mental practice executed by repetitive motor imagery can improve motor performance without simultaneous sensory input or overt output. We aimed to investigate cerebral hemodynamics during motor imagery and motor execution of a self-feeding activity using chopsticks. This study included 21 healthy right-handed volunteers. The self-feeding activity task comprised either motor imagery or motor execution of eating sliced cucumber pickles with chopsticks to examine eight regions of interest: pre-supplementary motor area, supplementary motor area, bilateral prefrontal cortex, premotor area, and sensorimotor cortex. The mean oxyhemoglobin levels were detected using near-infrared spectroscopy to reflect cerebral activation. The mean oxyhemoglobin levels during motor execution were significantly higher in the left sensorimotor cortex than in the supplementary motor area and the left premotor area. Moreover, significantly higher oxyhemoglobin levels were detected in the supplementary motor area and the left premotor area during motor imagery, compared to motor execution. Supplementary motor area and premotor area had important roles in the motor imagery of self-feeding activity. Moreover, the activation levels of the supplementary motor area and the premotor area during motor execution and motor imagery are likely affected by intentional cognitive processes. Levels of cerebral activation differed in some areas during motor execution and motor imagery of a self-feeding activity. This study was approved by the Ethical Review Committee of Nagasaki University(approval No. 18110801) on December 10, 2018.     

Influence of internal globus pallidus stimulation on motor cortex activation pattern in Parkinson's disease.

OBJECTIVES: Indications of the functional neurosurgical treatments become more and more numerous, however, few methods were used to study the mechanism of action and some discrepancies came to light. We assessed the influence of internal globus pallidus (GPI) stimulation and L-Dopa on cortical activation during the preparation and execution phases of the movement compared to clinical improvement of Parkinson's disease.METHODS: We recorded the movement-related cortical potential and movement-related desynchronization.RESULTS: The Unified Parkinson's Disease Rating Scale was improved by 46% under stimulation and 64% under stimulation with L-Dopa. Premovement desynchronization was significantly increased on central contralateral derivation under stimulation with L-Dopa and decreased on frontocentral ipsilateral derivation under stimulation with and without L-Dopa. Movement desynchronization was improved on the contralateral motor cortex under stimulation with and without L-Dopa (benefit correlated with bradykinesia improvement). The movement-related postmotor potential was significantly increased under stimulation with L-Dopa.CONCLUSIONS: GPI stimulation alone influenced the premotor cortex activation during the planning and induced a selective and focal effect on the organisation of motor cortical activity during the movement execution which may explain bradykinesia improvement. The motor cortex activation improvement under stimulation with L-Dopa concerned both the movement preparation and execution but remained very localised to the contralateral motor cortex.     

Cumulative blood oxygenation-level-dependent signal changes support the 'time accumulator' hypothesis

We studied time-related changes in the blood oxygenation-level-dependent signal during a time reproduction task. Nine healthy study participants retained and reproduced stimuli of varying durations in the multi-second range. During the encoding phase of the task, activity in the left dorsolateral prefrontal cortex inversely correlated with the interval duration, while an adjacent region in the dorsolateral prefrontal cortex showed positive correlation with duration in the reproduction phase. Cumulative signal increase during the reproduction phase, as found in the primary motor and supplementary motor areas, may also reflect the time-sensitive behavior. Signal accumulation in the right caudate nucleus is in agreement with presumed role of basal ganglia in time perception. These results support the 'time accumulator' hypothesis.     

Cerebral blood flow changes induced by subthalamic stimulation in Parkinson's disease

The authors used PET to show that the abnormal pattern of cerebral blood flow (CBF) activation described in PD is normalized by electrical stimulation of subthalamic nucleus. Improvement in bradykinesia correlated with increase in CBF due to stimulation in the supplementary motor area and anterior cingulate cortex. Compared to unilateral stimulation, bilateral stimulation induced a greater extent of activation in bilateral cortical areas and additional bilateral activation of globus pallidus.     

Motor imagery in normal subjects and in asymmetrical Parkinson's disease: a PET study

OBJECTIVE: To investigate, using PET and H2(15)O, brain activation abnormalities of patients with PD during motor imagery. To determine whether motor imagery activation patterns depend on the hand used to complete the task. BACKGROUND: Previous work in PD has shown that bradykinesia is associated with slowness of motor imagery. METHODS: The PET study was performed in eight patients with PD with predominantly right-sided akinesia, and in eight age-matched control subjects, all right-handed. Regional cerebral blood flow was measured by PET and H2(15)O while subjects imagined a predetermined unimanual externally cued sequential movement with a joystick with either the left or the right hand, and during a rest condition. RESULTS: In normal subjects, the prefrontal cortex, supplementary motor area (SMA), superior parietal lobe, inferior frontal gyrus, and cerebellum were activated during motor imagery with either the left or the right hand. Contralateral primary motor cortex activation was noted only when the task was imagined with the right (dominant) hand, whereas activation of the dorsolateral prefrontal cortex was observed only during imagery with the left hand. In patients with PD, motor imagery with the right ("akinetic") hand was characterized by lack of activation of the contralateral primary sensorimotor cortex and the cerebellum, persistent activation of the SMA, and bilateral activation of the superior parietal cortex. Motor imagery with the left ("non-akinetic") hand was also abnormal, with lack of activation of the SMA compared with controls. CONCLUSIONS: In patients with PD with predominantly right-sided akinesia, brain activation during motor imagery is abnormal and may appear even with the less affected hand. In normal subjects, brain activation during motor imagery depends on the hand used in the imagined movement.     

Motor processing after movement execution as revealed by evoked and induced activity

Event-related synchronization (ERS) in the beta frequency band following movement execution has shown that motor processing is not completed yet when a movement ends. It is known that induced and evoked activities reflect different aspects of cortical processing which may result in different time courses. In the current study, we analyzed topography of postimperative negative variation (PINV) in 39 healthy right-handed adolescents in an acoustic forewarned reaction time (contingent negative variation, CNV) task using a 64-electrode high-density sensor array. We dissociated different PINV components in their time course from postmovement beta ERS in order to provide fundamental knowledge about evoked and induced EEG components after movement execution as a basis for further analysis of postmovement processing. A postmovement negativity occurred from about 500 to 1200 ms after the imperative stimulus (peaking about 600 ms after a right-hand button press) at central electrodes, contralateral to the response movement side. Current source density (CSD) analysis confirmed the current sinks over motor areas [contralateral primary motor/premotor and supplementary/cingulate motor area]. The described DC component (motor PINV, mPINV) differed in time course and localization from later "classical" PINV (cPINV) which is thought to reflect contingency reappraisal. mPINV could also be distinguished topographically from a mere delayed CNV resolution. When mPINV and ERS at the same left central electrode were compared, both parameters showed different time courses. Left central mPINV rather paralleled ERS at midcentral electrodes. Therefore, we suggest that the topography of mPINV provides first hints towards an involvement of contralateral primary motor cortex in postmovement processing beyond a mere idling state as reflected by later beta ERS. mPINV could be a useful tool to investigate the role of primary motor cortex in motor-learning processes. The combined analysis of induced and evoked activities seems to be able to elucidate different aspects of cortical connectivity and motor processes following movement.     

Voluntary tic suppression and the normalization of motor cortical beta power in Gilles de la Tourette syndrome: an EEG study

Gilles de la Tourette syndrome (GTS) is a neurological condition characterized by motor and vocal tics. Previous studies suggested that this syndrome is associated with abnormal sensorimotor cortex activity at rest, as well as during the execution of voluntary movements. It has been hypothesized that this abnormality might be interpreted as a form of increased tonic inhibition, probably to suppress tics; however, this hypothesis has not been tested so far. The present study was designed to formally test how voluntary tic suppression in GTS influences the activity of the sensorimotor cortex during the execution of a motor task. We used EEG to record neural activity over the contralateral sensorimotor cortex during a finger movement task in adult GTS patients, in both free ticcing and tic suppression conditions; these data were then compared with those collected during the same task in age‐matched healthy subjects. We focused on the levels of activity in the beta frequency band, which is typically associated with the activation of the motor system, during three different phases: a pre‐movement, a movement, and a post‐movement phase. GTS patients showed decreased levels of beta modulation with respect to the healthy controls, during the execution of the task; however, this abnormal pattern returned to be normal when they were explicitly asked to suppress their tics while moving. This is the first demonstration that voluntary tic suppression in GTS operates through the normalization of the EEG rhythm in the beta frequency range during the execution of a voluntary finger movement.     

Impaired antagonist inhibition may contribute to akinesia and bradykinesia in Huntington's disease.

OBJECTIVE: To test the hypothesis that besides impaired agonist facilitation, impaired antagonist inhibition also contributes to delayed initiation (akinesia) and slow execution (bradykinesia) of voluntary movements in Huntington's disease. METHODS: Fifteen patients with Huntington's disease and 11 age-matched controls participated in the study. The amount of agonist facilitation was measured as the increase in soleus H-reflex amplitude prior to ballistic voluntary plantar flexion (soleus contraction). Antagonist inhibition was measured as the decrease in soleus H-reflex prior to ballistic dorsiflexion (tibialis anterior (TA) contraction). The amount of agonist facilitation and antagonist inhibition was correlated with the time needed for motor initiation (reaction time) and movement execution (movement time). RESULTS: Starting 50ms prior to soleus contraction, soleus H-reflex increased in control subjects but less so in patients. Soleus H-reflexes decreased in controls 25ms prior to TA contraction, while this antagonist inhibition was completely lacking in patients. Thus, patients with Huntington's disease not only displayed reduced agonist facilitation, but impaired antagonist inhibition as well. Moreover, more impairment of antagonist inhibition correlated significantly with more severe akinesia and bradykinesia. CONCLUSIONS: Antagonist inhibition prior to and during agonist contractions is markedly impaired in Huntington's disease. This impairment might contribute to motor slowness in these patients.