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Results for “Motor learning”

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At least 73 records · Page 4Linked to original sources

PubMed2002

The relationship between knowledge of results and motor learning in Parkinsonian patients.

A simple timing movement was used to investigate augmented feedback on motor learning in Parkinson's disease (PD) patients and controls. During acquisition, participants received knowledge of results (KR) about their errors after every trial (100%) or every fifth trial (20%). Participants then performed a retention test without KR. Controls performed better on the retention test after having had 20% KR during acquisition. PDs showed superior retention with 100% KR. This suggests that the PD patients are more reliant on KR for learning motor skills; a difference that may be attributable to reduced proprioceptive acuity in PD patients.

Aged↗

PubMed2003

Motor learning and prediction in a variable environment.

Traditional studies of motor learning and prediction have focused on how subjects perform a single task. Recent advances have been made in our understanding of motor learning and prediction by investigating the way we learn variable tasks, which change either predictably or unpredictably over time. Similarly, studies have examined how variability in our own movements affects motor learning.

Biomechanical Phenomena↗

PubMed1995

Unimanual motor learning impaired by frontomedial and insular lesions in man.

We correlated impaired unimanual motor learning with the lesion site in 53 patients with chronic lesions predominantly of the frontal lobe. The lesions were assessed using computed tomography (CT), then transferred to standard templates of nine slices parallel to the canthomeatal plane and digitized with a raster matrix of 3 mm by 3 mm width. The learning task was to track a moving target on a computer screen with a dot guided by the preferred hand, while the horizontal coupling between hand movement and screen was inverted. The mean tracking error was recorded over eight successive trials of 80s duration. If the mean error of the last three trials was not lower than that of the first three trials, impaired motor learning was assumed. We correlated performance and lesion with a contingency table analysis for each raster element. Impaired motor learning was associated with a lesion within the supplementary motor area and adjacent anterior cingulate, and within the anterior insular region. Our results indicate that these regions are critical for motor learning and functional plasticity in man. Our data support activation patterns obtained with positron emission tomography.

Adolescent↗

PubMed2006

On No-KR tests in motor learning, retention and transfer.

In this paper we examine the role of no-knowledge of results (KR) tests in motor learning, retention and transfer. A distinction is drawn between studies of KR and studies of other issues in motor learning that use a No-KR test. Arguments are presented against the currently received position that a No-KR test is an essential protocol to examine motor learning, although a No-KR test is most relevant in the few contexts where the outcome information is not naturally available. Perspectives are provided on the limited though proper role of No-KR tests in motor learning, retention and transfer and these are illustrated through experimental examples. It is proposed that the current restrictive interpretation of KR as only augmented outcome information is narrowing not only the context of KR research but also the study of motor learning in general.

Conditioning, Classical↗

PubMedDate not supplied

Aging and motor learning: a possible role for norepinephrine in cerebellar plasticity.

Norepinephrine is known to act as a neuromodulator in the cerebellar cortex because it can increase the effect of neurotransmitters such as GABA. This neuromodulatory effect of NE is a possible substrate for an effect of NE on cerebellar plasticity. Cerebellar plasticity can be examined by studying the learning of motor skills. A rod walking paradigm is used in our laboratory for such investigations. Learning of this rod walking task is impaired in rats that are depleted of central stores of NE and in rats that have received the beta-adrenergic antagonist propranolol. In addition, in aged rats there is a correlation between the loss of beta-adrenergic receptor mediated neuromodulatory actions of NE in the cerebellum with a decreased ability to learn the rod walking task. Taken together this information supports a role for NE in cerebellar plasticity and suggest that the beta-adrenergic receptor is important for this plasticity.

Aging↗

PubMed1999

Speech and oral motor learning in individuals with cerebellar atrophy.

The purpose of this study was to determine whether cerebellar pathology interferes with motor learning for either speech or novel tasks. Practice effects were contrasted between persons with cerebellar cortical atrophy (CCA) and control participants on previously learned real speech, nonsense speech, and novel nonspeech oral-movement tasks. Studies of limb motor learning suggested that control participants would evidence reduced variability, increased speed of movement, and reduced movement amplitude with practice as compared with the CCA group. No significant differences were found between the real- and nonsense-speech tasks. For both speech tasks, although neither group reduced their movement variability with practice, both groups significantly reduced jaw closing displacement and velocity with practice. For the novel nonspeech oral-movement task, no change with practice was observed in either group in terms of variability, amplitude, or peak velocity. No effects of cerebellar pathology were seen in either the speech- or oral-movement tasks. These results demonstrated that with practice of speech tasks, a previously learned motor skill, movement speed and displacement decreased in both groups. Therefore, the effects of practice differed between previously learned speech tasks and the novel oral-movement task regardless of cerebellar pathology.

Adult↗

PubMed1987

Plasticity of cortical function related to voluntary movement motor learning and compensation following brain dysfunction.

Processes of motor learning and of compensation after localized brain dysfunction were studied in the monkey tasked with conditioned (visually-initiated, reaction-time) hand movements. Field potentials in various cortical areas of the cerebral hemisphere were recorded successively for many months with electrodes implanted on the surface and in the depth of the cortex. The potentials associated with the conditioned movement were found to change during processes of learning the movement and during courses of degradation as well as recovery after the brain dysfunction. Motor learning of the reaction-time movement can be categorized into "recognition" and "skill" learnings. The former is the process for associating the visual stimulus with the movement and accompanied mainly by increasing activities of prefrontal, premotor and prestriate cortices. The latter is attaining better performances in executing the movement, particularly with shorter and more fixed reaction time, and is accompanied by recruitment of the cerebro-cerebellar interaction. The conditioned movements which had been well established were experimentally disturbed by transient, local cooling of different cortical areas or by cerebellar hemispherectomy. Three possible mechanisms of compensation are proposed as follow: 1. Substitution: Compensation occurring immediately through substitutional neuronal circuits. On transient cooling of the forelimb motor cortex, the somatosensory cortex became predominant in motor function and replaced the disabled motor cortex in executing the reaction-time movement, although activity was weak and slow (paretic but not paralytic). Resection of the cerebellar hemisphere also induced the compensatory motor function of the somatosensory cortex so that the movement could be performed although it was weak, slow and clumsy. 2. Relearning: Compensation by relearning through normally unused neuronal circuits. Prolonged and variable reaction times after cerebellar hemispherectomy persisted when the operation included both dentate and interpositus nuclei but recovered within about three weeks when the interpositus nucleus was preserved. It is suggested that the information processing for the well accomplished reaction-time movement is mainly mediated by the cerebro-cerebellar neuronal circuit including the dentate nucleus but is gradually relearned through the normally unused circuits involving the interpositus nucleus after the dentate nucleus lesion. 3. Rebuilding: Compensation by rebuilt neuronal circuits, e.g., by sprouting and/or regeneration (see S. Kawaguchi in this book).

Action Potentials↗

PubMed2000

Effects of attentional focus, self-control, and dyad training on motor learning: implications for physical rehabilitation.

In this article, the authors review recent studies on 3 factors that have been shown to affect the learning of motor skills-the performer's attentional focus, self-control, and practice in dyads-and discuss their implications for rehabilitation. Research has shown that directing learners' attention to the effects of their movements can be more beneficial for learning than directing their attention to the details of their own actions. Furthermore, giving learners some control over the training regimen has been found to enhance learning, unlike prescriptive training protocols that dictate when feedback will be delivered, how often, and the order that tasks will be practiced. Finally, not only can practice in dyads (or larger groups) reduce the costs of training, but it can also result in more effective learning than individual practice sessions. The incorporation of these factors into rehabilitation practice can potentially enhance the effectiveness and efficiency of rehabilitation.

Attention↗

PubMed2001

Role of the human motor cortex in rapid motor learning.

Recent studies suggest that the human primary motor cortex (M1) is involved in motor learning, but the nature of that involvement is not clear. Here, learning-related changes in M1 excitability were studied with transcranial magnetic stimulation (TMS) while na subjects practiced either a ballistic or a ramp pinch task to the 0.5-Hz beat of a metronome. Subjects rapidly learned to optimize ballistic contractions as indicated by a significant increase in peak pinch acceleration and peak force after the 60-min practice epoch. The increase in force and acceleration was associated with an increase in motor evoked potential (MEP) amplitude in a muscle involved in the training (flexor policis brevis) but not in a muscle unrelated to the task (abductor digiti minimi). MEPs returned to their baseline amplitude after subjects had acquired the new skill, whereas no practice-induced changes in MEP amplitude were observed after subjects had overlearned the task, or after practicing slow ramp pinches. Since the changes in MEP amplitude were observed only after TMS of M1 but not after direct stimulation of the corticospinal tract, these findings indicate task- and effector-specific involvement of human M1 in rapid motor learning.

Adolescent↗

PubMed1996

The effects of aging on cerebellar beta-adrenergic receptor activation and motor learning in female F344 rats.

Female Fischer 344 (F344) rats were tested for age-related differences in both cerebellar beta-adrenergic receptor activation and motor learning. Three and 20 month old rats were tested on a motor learning paradigm that required the rats to adjust their gait to navigate a runway of unevenly spaced pegs. Rates of acquisition were compared between age groups. After behavioral testing, cerebellar beta-adrenergic receptor function was assessed using extracellular recordings of Purkinje cells during iontophoresis of GABA and isoproterenol (ISO). Aged female rats showed deficits in motor learning and in beta-adrenergic receptor activation. In young rats, ISO modulated GABAergic inhibition of Purkinje cell firing in more cells compared with aged rats. Thus, aging produces deficits in both motor learning and in beta-adrenergic receptor activation in aged female F344 rats.

Action Potentials↗

PubMed2004

Skilled motor learning does not enhance long-term depression in the motor cortex in vivo.

Learning of motor skills may occur as a consequence of changes in the efficacy of synaptic connections in the primary motor cortex. We investigated if learning in a reaching task affects the excitability, short-term plasticity, and long-term plasticity of horizontal connections in layers II-III of the motor cortex. Because training in this task requires animals to be food-deprived, we compared the trained animals with similarly food-deprived untrained animals and normal controls. The results show that the excitability, short-term plasticity, and long-term plasticity of the studied horizontal connections were unaffected by motor learning. However, stress-related effects produced by food deprivation and handling significantly enhanced the expression of long-term depression in these pathways. These results are compatible with the hypothesis that the acquisition of a complex motor skill produces bi-directional changes in synaptic strength that are distributed throughout the complex neural networks of motor cortex, which remains synaptically balanced during learning. The results are incompatible with the idea that learning causes large unidirectional changes in the population response of these neural networks, which may occur instead during certain behavioral states, such as stress.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed2005

Cerebellar complex spike firing is suitable to induce as well as to stabilize motor learning.

BACKGROUND: Cerebellar Purkinje cells (PC) generate two responses: the simple spike (SS), with high firing rates (>100 Hz), and the complex spike (CS), characterized by conspicuously low discharge rates (1-2 Hz). Contemporary theories of cerebellar learning suggest that the CS discharge pattern encodes an error signal that drives changes in SS activity, ultimately related to motor behavior. This then predicts that CS will discharge in relation to the error and at random once the error has been nulled by the new behavior. RESULTS: We tested this hypothesis with saccadic adaptation in macaque monkeys as a model of cerebellar-dependent motor learning. During saccadic adaptation, error information unconsciously changes the endpoint of a saccade prompted by a visual target that shifts its final position during the saccade. We recorded CS from PC of the posterior vermis before, during, and after saccadic adaptation. In clear contradiction to the "error signal" concept, we found that CS occurred at random before adaptation onset, i.e., when the error was maximal, and built up to a specific saccade-related discharge profile during the course of adaptation. This profile became most pronounced at the end of adaptation, i.e., when the error had been nulled. CONCLUSIONS: We suggest that CS firing may underlie the stabilization of a learned motor behavior, rather than serving as an electrophysiological correlate of an error.

Action Potentials↗

PubMed1989

Motor learning in monkeys (Macaca fascicularis) with lesions in motor thalamus.

The study examines the nature of the influence that the basal ganglia exert on frontal cortex via the motor nuclei of the thalamus. Twelve monkeys were trained to pull a handle given one colour cue and to turn it given another. Bilateral lesions were then placed in the ventral thalamus. Four monkeys with large anterior lesions including the VA nucleus and the anterior part of VLo were severely impaired at relearning the task. Monkeys with small lesions in VAmc or with lesions centred on VLo were not impaired. The analysis of the histology suggests that the impairment in the four monkeys did not result from involvement of the cerebellar relay through nucleus X. It is argued that the animals are not impaired because of faulty execution. This suggests that the basal ganglia have an influence on motor learning.

Animals↗

PubMed2004

Consolidation of dynamic motor learning is not disrupted by rTMS of primary motor cortex.

Motor skills, once learned, are often retained over a long period of time. However, such learning first undergoes a period of consolidation after practice. During this time, the motor memory is susceptible to being disrupted by the performance of another motor-learning task. Recently, it was shown that repetitive transcranial magnetic stimulation (rTMS) over the primary motor cortex could disrupt the retention of a newly learned ballistic task in which subjects had to oppose their index finger and thumb as rapidly as possible. Here we investigate whether the motor cortex is similarly involved during the consolidation that follows learning novel dynamics. We applied rTMS to primary motor cortex shortly after subjects had either learned to compensate for a dynamic force field applied to their index finger or learned a ballistic finger abduction task. rTMS severely degraded the retention of the learning for the ballistic task but had no effect on retention of the dynamic force-field learning. This suggests that, unlike learning of simple ballistic skills, learning of dynamics may be stored in a more distributed manner, possibly outside the primary motor cortex.

Adult↗

PubMed1995

Tissue plasminogen activator induction in Purkinje neurons after cerebellar motor learning.

The cerebellar cortex is implicated in the learning of complex motor skills. This learning may require synaptic remodeling of Purkinje cell inputs. An extracellular serine protease, tissue plasminogen activator (tPA), is involved in remodeling various nonneural tissues and is associated with developing and regenerating neurons. In situ hybridization showed that expression of tPA messenger RNA was increased in the Purkinje neurons of rats within an hour of their being trained for a complex motor task. Antibody to tPA also showed the induction of tPA protein associated with cerebellar Purkinje cells. Thus, the induction of tPA during motor learning may play a role in activity-dependent synaptic plasticity.

Animals↗

PubMed2003

Motor learning elicited by voluntary drive.

Motor training consisting of voluntary movements leads to performance improvements and results in characteristic reorganizational changes in the motor cortex. It has been proposed that repetition of passively elicited movements could also lead to improvements in motor performance. In this study, we compared behavioural gains, changes in functional MRI (fMRI) activation in the contralateral primary motor cortex (cM1) and in motor cortex excitability measured with transcranial magnetic stimulation (TMS) after a 30 min training period of either voluntarily (active) or passively (passive) induced wrist movements, when alertness and kinematic aspects of training were controlled. During active training, subjects were instructed to perform voluntary wrist flexion-extension movements of a specified duration (target window 174-186 ms) in an articulated splint. Passive training consisted of wrist flexion- extension movements elicited by a torque motor, of the same amplitude and duration range as in the active task. fMRI activation and TMS parameters of motor cortex excitability were measured before and after each training type. Motor performance, measured as the number of movements that hit the target window duration, was significantly better after active than after passive training. Both active and passive movements performed during fMRI measurements activated cM1. Active training led to more prominent increases in (i) fMRI activation of cM1; (ii) recruitment curves (TMS); and (iii) intracortical facilitation (TMS) than passive training. Therefore, a short period of active motor training is more effective than passive motor training in eliciting performance improvements and cortical reorganization. This result is consistent with the concept of a pivotal role for voluntary drive in motor learning and neurorehabilitation.

Adult↗

PubMed1994

Neural basis for motor learning in the vestibuloocular reflex of primates. III. Computational and behavioral analysis of the sites of learning.

1. We have used a combination of eye movement recordings and computer modeling to study long-term adaptive modification (motor learning) in the vestibuloocular reflex (VOR). The eye movement recordings place constraints on possible sites for motor learning. The computer model abides by these constraints, as well as constraints provided by data in previous papers, to formalize a new hypothesis about the sites of motor learning. The model was designed to reproduce as much of the existing neural and behavioral data as possible. 2. Motor learning was induced in monkeys by fitting them with spectacles that caused the gain of the VOR (eye speed divided by head speed) to increase to values > 1.6 or to decrease to values < 0.4. We elicited pursuit by providing ramp motion of a small target at 30 degrees/s along the horizontal axis. Changes in the gain of the VOR caused only small and inconsistent changes in the eye acceleration in the first 100 ms after the onset of pursuit and had no effect on the eye velocity during tracking of steady target motion. Electrical stimulation in the flocculus and ventral paraflocculus with single pulses or trains of pulses caused smooth eye movement toward the side of stimulation after latencies of 9-11 ms. Neither the latency, the peak eye velocity, nor the initial eye acceleration varied as a consistent function of the gain of the VOR. 3. The computer model contained nodes that represented position-vestibular-pause cells (PVP-cells) and flocculus target neurons (FTNs) in the vestibular nucleus, and horizontal gaze-velocity Purkinje cells (HGVP-cells) in the cerebellar flocculus and ventral paraflocculus. Node FTN represented only the "E-c FTNs," which show increased firing for eye motion away from the side of recording. The transfer functions in the model included dynamic elements (filters) as well as static elements (summing junctions, gain elements, and time delays). Except for the transfer functions that converted visual motion inputs into commands for smooth eye movement, the model was linear. 4. The performance of the model was determined both by computer simulation and, for the VOR in the dark, by analytic solution of linear equations. For simulation, we adjusted the parameters by hand to match the output of the model to the eye velocity of monkeys and to match the activity of the relevant nodes in the model to the firing of HGVP-cells, FTNs, and PVP-cells when the gain of the VOR was 0.4, 1.0, and 1.6.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2006

Disrupted motor learning and long-term synaptic plasticity in mice lacking NMDAR1 in the striatum.

Much research has implicated the striatum in motor learning, but the underlying mechanisms have not been identified. Although NMDA receptor (NMDAR)-dependent long-term potentiation has been observed in the striatum, its involvement in motor learning remains unclear. To examine the role of striatal NMDAR in motor learning, we created striatum-specific NMDAR1 subunit knockout mice, analyzed the striatal anatomy and neuronal morphology of these mice, evaluated their performance on well established motor tasks, and performed electrophysiological recordings to assay striatal NMDAR function and long-term synaptic plasticity. Our results show that deleting the NMDAR1 subunit of the NMDAR specifically in the striatum, which virtually abolished NMDAR-mediated currents, resulted in only small changes in striatal neuronal morphology but severely impaired motor learning and disrupted dorsal striatal long-term potentiation and ventral striatal long-term depression.

Animals↗