Sensory-motor Plasticity Research Articles

The Effect of Cognitive Style on Individual Differences in Prismatic Adaptation: A Pilot Study

Prism adaptation (PA) is a well-known and widely used technique for rehabilitating unilateral spatial neglect and studying sensory-motor plasticity. However, there is conflicting evidence in the literature regarding its effectiveness which may arise from differences in the type of prisms used, clinical characteristics of the patients, and the procedure used in training. Individual differences may play a role in PA effectiveness in rehabilitating neglect, affecting both its development and its effects. Field-dependent/independent cognitive style is a pervasive characteristic of individual functioning, affecting how environmental information is processed. Here, we tested the hypothesis that cognitive style plays a role in PA efficacy by submitting to a protocol of prism adaptation to 38 health participants, who were classified as field-dependent (FD, N = 19) or field-independent (FI, N = 19), by using the Embedded Figure Test. Results show that during the exposure phase, FI individuals needed a lesser number of pointing movements to reduce the deviation error than FD individuals. However, there are no differences in the extinction of sensory-motor and cognitive after-effects. These results suggest that prismatic adaptation is affected by individuals' cognitive style since FI individuals will need fewer trials to reach adaptation and this could explain why using this rehabilitation technique with a unique, standard protocol is not always effective.

Сorporeality and bodily practices in educational projects of the pre-war USSR and Nazi Germany

This article examines the practices associated with corporeality and movement, which were an important part of the upbringing of the young generations in the USSR and the Third Reich. A comparative analysis of both educational projects shows that the Soviet one provided more opportunity for schoolchildren to model their corporeality than the Nazi one. The Soviet teachers tried to channel the hyperactivity of students into extracurricular study groups (kruzhki, studii, sektsii), into some kinds of social responsibility, competitions, performances, proms, and other events that allowed them to master different cognitive and motor skills. The pre-war Soviet schools provided greater sensory-motor experience and neural plasticity, which led to the high learning ability of young Soviet conscripts and the variability of their actions in the war compared to the Nazis. If the Soviet project of creating a new person was addressed to individuality, soul and will, the Nazi one was based on the barbaric romanticization of the right of the strongest and was predominantly biotechnological. It was initially aimed at raising a person with an iron will in a magnificent body and was against intellectualism—which could weaken conviction and the desire for power. For this reason the main educational functions were delegated to the Hitler Youth. Built on paramilitary activity (sports and drills, hiking, campfires and songs, and participation in Nazi party celebrations), the HY practice could provide limited and only monotonous military training which was insufficient in the space of total war.

Visual feedback therapy for restoration of upper limb function of stroke patients

ObjectiveTo investigate the effects of mirror neuron theory-based visual feedback therapy (VFT) on restoration of upper limb function of stroke patients and motor-related cortical function using functional magnetic resonance imaging (fMRI). MethodsHemiplegic stroke patients were randomly divided into two groups: a VFT group and a control (CTL) group. Sixteen patients in the VFT group received conventional rehabilitation (CR) and VFT for 8 weeks, while 15 patients in the CTL group received only CR. The Barthel Index (BI) was used to assess the activities of daily living at baseline and the 8th week of the recovery training period. The Fugl–Meyer assessment (FMA) scale, somatosensory evoked potential (SEP), and fMRI were used to evaluate the recovery effect of the training therapies. The latencies and amplitudes of N9 and N20 were measured. Before recovery training, fMRI was performed for all patients in the VFT and CTL groups. In addition, 17 patients (9 in the VFT group and 8 in the CTL group) underwent fMRI for follow-up 2 months after treatment. Qualitative data were analyzed using the χ2 test. The independent sample t-test was used to compare normally distributed data among different groups, the paired sample t-test was used to compare data between groups, and the non-parametric test was used to comparing data without normal distribution among groups. ResultsThere were no significant differences between the VFT and CTL group in all indexes. However, after 8 weeks of recovery training, these indexes were all significantly improved (P < 0.05). As compared with the CTL group, the FMA scores, BI, and N9/N20 latencies and amplitudes of SEP in the VFT group were significantly improved (P < 0.05). Two months after recovery training, fMRI showed that the degree of activation of the bilateral central anterior gyrus, parietal lobe, and auxiliary motor areas was significantly higher in the VFT group than the CTL group (P < 0.05). ConclusionsVFT based on mirror neuron theory is an effective approach to improve upper extremity motor function and daily activity performance of stroke patients. The therapeutic mechanism promotes motor relearning by activating the mirror neuron system and motor cortex. SEP amplitudes increased only for patients who participated in visual feedback. VFT promotes sensory-motor plasticity and behavioral changes in both the motor and sensory domains.

Spatial Integration of Somatosensory Inputs during Sensory-Motor Plasticity Phenomena Is Normal in Focal Hand Dystonia.

Background Surround inhibition is a system that sharpens sensation by creating an inhibitory zone around the central core of activation. In the motor system, this mechanism probably contributes to the selection of voluntary movements, and it seems to be lost in dystonia. Objectives. To explore if sensory information is abnormally processed and integrated in focal hand dystonia (FHD) and if surround inhibition phenomena are operating during sensory-motor plasticity and somatosensory integration in normal humans and in patients with FHD. Methods. We looked at the MEP facilitation obtained after 5 Hz repetitive paired associative stimulation of median (PAS M), ulnar (PAS U), and median + ulnar nerve (PAS MU) stimulation in 8 normal subjects and 8 FHD. We evaluated the ratio MU/(M + U) ∗ 100 and the spatial and temporal somatosensory integration recording the somatosensory evoked potentials (SEPs) evoked by a dual nerve input. Results FHD had two main abnormalities: first, the amount of facilitation was larger than normal subjects; second, the spatial specificity was lost. The MU/(M + U) ∗ 100 ratio was similar in healthy subjects and in FHD patients, and the somatosensory integration was normal in this subset of patients. Conclusions. The inhibitory integration of somatosensory inputs and the somatosensory inhibition are normal in patients with focal dystonia as well as lateral surrounding inhibition phenomena during sensory-motor plasticity in FHD.

Beyond the muscular involvement in non-dystrophic myotonias: The emerging role of neuromodulation.

The central nervous system involvement, in terms of a maladaptive sensory-motor plasticity, is well known in patients with dystrophic myotonias (DMs). To date, there are no data suggesting a central nervous system involvement in non-dystrophic myotonias (NDMs). To investigate sensory-motor plasticity in patients with Myotonia Congenita (MC) and Paramyotonia Congenita (PMC) with or without mexiletine. Twelve patients with a clinical, genetic, and electromyographic evidence of MC, fifteen with PMC, and 25 healthy controls (HC) were included in the study. TMS on both primary motor cortices (M1) and a rapid paired associative stimulation (rPAS) paradigm were carried out to assess M1 excitability and sensory-motor plasticity. patients showed a higher cortical excitability and a deterioration of the topographic specificity of rPAS aftereffects, as compared to HCs. There was no correlation among neurophysiological and clinical-demographic characteristics. Noteworthy, the patients who were under mexiletine showed a minor impairment of the topographic specificity of rPAS aftereffects as compared to those who did not take the drug. our findings could suggest the deterioration of cortical sensory-motor plasticity in patients with NDMs as a trait of the disease.

44. Surround inhibition abnormalities in focal hand dystonia may not depend by alterations in somatosensory integration

Surround inhibition is a system that sharpens sensation by creating an inhibitory zone around the central core of activation. In the motor system, this mechanism probably contributes to the selection of voluntary movements and seems to be lost in dystonia. To explore if sensory information is abnormally processed and integrated in focal dystonia and if surround inhibition phenomena are operating during sensory-motor plasticity and sensory-motor integration in normal humans and in patients with focal hand dystonia. We looked at motor evoked potential (MEP) facilitation, in the APB and ADM muscles, obtained after 5 Hz repetitive paired associative stimulation, stimulating median (PAS M), ulnar (PAS U) and median + ulnar nerve (PAS MU) in 8 normal subjects and 8 dystonic patients. We evaluated the ratio MU/(M + U) × 100. Moreover, we tested the spatial and temporal somatosensory integration recording SEPs evoked by a dual nerve input. Our data confirmed that in dystonic patients the amount of facilitation was larger than normal subjects and the spatial specificity was lost. The MU/(M + U) × 100 ratio was similar in healthy subjects and in dystonic patients and the somatosensory integration was normal in this subset of patients. These data suggest that lateral surround inhibition phenomena during sensory-motor plasticity are normal in focal hand dystonia.

Toward a more personalized motor function rehabilitation in Myotonic dystrophy type 1: The role of neuroplasticity.

Myotonic dystrophy type 1 (DM1) is the most prevalent adult muscular dystrophy, often accompanied by impairments in attention, memory, visuospatial and executive functions. Given that DM1 is a multi-system disorder, it requires a multi-disciplinary approach, including effective rehabilitation programs, focusing on the central nervous system neuroplasticity, in order to develop patient-tailored rehabilitative procedures for motor function recovery. Herein, we performed a transcranial magnetic stimulation (TMS) study aimed at investigating central motor conduction time, sensory-motor plasticity, and cortical excitability in 7 genetically defined DM1 patients. As compared to healthy individuals, DM1 patients showed a delayed central motor conduction time and an abnormal sensory-motor plasticity, with no alteration of cortical excitability. These findings may be useful to define patient-tailored motor rehabilitative programs.

Motor recovery after stroke: the role of overground exoskeletons in shaping brain plasticity

The use of neurorobotic devices into gait rehabilitative programs, including Ekso, is reported to increase the engagement and motivation of the patients while actively performing a task, and to shape the sensory-motor plasticity (SMP) and its balance between the primary motor areas (M1), and the fronto-parietal network (FPN) connectivity, thus contributing to successful gait rehabilitation [1]. Aim of our study was to assess whether Ekso would foster the recovery of deteriorated FPN connectivity and SMP patterns involved in limb coordination during walking [2] in a sample of patients with hemiparesis due to stroke. To this end, we enrolled ten patients who underwent Ekso training (24 sessions) and were evaluated about gait performance, FPN connectivity, and SMP pattern. Esko significantly increased gait performance index as revealed by surface EMG (p=0.01) and the deterioration of prefrontal-SMA and SMA-centroparietal connectivity (both p=0.02), and rebalanced the equilibrium between the SMP patterns of the two M1-leg areas (p=0.03). Moreover, the baseline plasticity and FPN connectivity were the most important factors in using Ekso fruitfully (r=0.9, p=0.03). Even though our findings need to be confirmed by future research further addressing the safety and effectively use of Ekso, our small cohort study provides new cues supporting the role of powered exoskeletons in rehabilitation protocols for persons with stroke.

Functional Plasticity in Somatosensory Cortex Supports Motor Learning by Observing

An influential idea in neuroscience is that the sensory-motor system is activated when observing the actions of others [1, 2]. This idea has recently been extended to motor learning, in which observation results in sensory-motor plasticity and behavioral changes in both motor and somatosensory domains [3-9]. However, it is unclear how the brain maps visual information onto motor circuits for learning. Here we test the idea that the somatosensory system, and specifically primary somatosensory cortex (S1), plays a role in motor learning by observing. In experiment 1, we applied stimulation to the median nerve to occupy the somatosensory system with unrelated inputs while participants observed a tutor learning to reach in a force field. Stimulation disrupted motor learning by observing in a limb-specific manner. Stimulation delivered to the right arm (the same arm used by the tutor) disrupted learning, whereas left arm stimulation did not. This is consistent with the idea that a somatosensory representation of the observed effector must be available during observation for learning to occur. In experiment 2, we assessed S1 cortical processing before and after observation by measuring somatosensory evoked potentials (SEPs) associated with median nerve stimulation. SEP amplitudes increased only for participants who observed learning. Moreover, SEPs increased more for participants who exhibited greater motor learning following observation. Taken together, these findings support the idea that motor learning by observing relies on functional plasticity in S1. We propose that visual signals about the movements of others are mapped onto motor circuits for learning via the somatosensory system.

60. The effect of cerebellar degeneration on human sensori-motor plasticity

We investigated how cerebellar degeneration influences the plasticity of the tprimary motor cortex (M1) by using PAS (paired associative plasticity) technique. PAS involves repeated pairs of electrical stimuli to the median nerve and transcranial magnetic stimuli of the motor cortex. If the interval between peripheral and cortical stimulation is around 21–25 ms, corticospinal excitability is increased via a long-term potentiation (LTP)-like effect within M1. Our aims were: (i) to explore the presence of a time-specific influence of cerebellar degeneration on human associative plasticity; (ii) to evaluate the role of the somatosensory pathway on the cerebellar modulation of sensory-motor plasticity. We studied 10 patients with pure cerebellar atrophy and 10 age-matched healthy subjects. Motor evoked potentials amplitudes, short-afferent inhibition, motor thresholds, I/O curves, somatosensory-evoked-potentials (SEPs) were measured before, just after and 30 min after PAS at interstimulus intervals of 21.5 and 25 ms. In cerebellar patients, LTP-like effect induced by PAS was abolished at 25 ms, but not at 21.5 ms. SEPs showed that the P25 wave amplitude was markedly reduced in patients with a more severe clinical and radiological impairment of the cerebellum. Patients with cerebellar atrophy have an altered capability to process time-specific sensory volleys, influencing the M1 plasticity.

Neuropsychiatric consequences in sleep breathing disorders

Sleep Breathing Disorders (SBD), especially Obstructive Sleep Apnea Syndromes (OSAS) lead to a lot of physical problems like hypertension and arrhythmias and even to neuropsychiatric consequences like Brain atrophy, Depression, Anxiety and Insomnia. Apart from a multitude of physical complaints, OSAS patients suffer from Excessive Daytime Sleepiness (EDS), reduced sustained attention, limited memory processes and cognitive functions and reduced Quality of Life (QoL). The apnea related neuropsychiatric diseases could be associated with conditions interfering with the mechanisms of mental and sensory-motor plasticity. In our study we used neuropsychological and neuropsychiatric methods in different patient groups in a sleep laboratory. Over the past five years we have tested more than 2000 patients. During admission to the clinic, all patients were selected according to their clinical diagnosis (ICD-10) and all patients were examined neurologically, neuro-psychologically and psychiatrically. All test persons must not suffer from any severe psychiatric disorders. The study was carried out involving all groups of randomly selected patients with OSAS on a number of neuropsychiatric parameters. In this context we analyzed e.g. (1) excessive daytime sleepiness by Epworth Sleepiness Scale (ESS) and Reading Test (2) attention deficits by vigilance test Carda and Clock Test and by sustained attention test Carsim, (3) memory dysfunction by Number Connection Test (ZVT) and Benton Test, (4) psychiatric consequences (e.g. depression by BDI, anxiety by HADS) and (5) quality of life by different questionnaires (SWLS, MLDL, FOSQ, SAQLI). Testing of neuropsychiatric diseases, memory processes and quality of life revealed a highly significant difference between healthy persons and OSAS patients ( p < 0.05). Examination of specific domains of neuropsychiatric diseases, memory processes and quality of life showed significant differences in patients with OSAS. In all dimensions of neuropsychiatric diseases, memory processes and quality of life, untreated OSAS patients had inferior scores to those who had undergone therapy. After more than 6 weeks of nCPAP therapy, the neuropsychiatric diseases of the OSAS patients, memory processes and quality of life improved to a significant degree ( p < 0.05). Analysis of the degree of severity showed for OSAS that on the whole, there is a significant difference concerning neuropsychiatric diseases, memory processes and quality of life. The study revealed that patients with OSAS show neuropsychiatric problems and deficits concerning their vigilance achievements, their memory processes and their quality of life. The improvement of vigilance achievements and memory processes show a lower driving fitness (traffic safety) in untreated patients and increasing traffic safety in treated patients. In summary, based on our results, it is to be said that although a continuous nCPAP therapy improves the OSAS symptoms; neuropsychiatric consequences, memory processes and the quality of life require longer-term recovery.

P 182. Normal lateral inhibition mechanism during sensory-motor plasticity in dystonia

Objective To explore if sensory information is processed and integrated during sensory-motor plasticity phenomena by using lateral inhibition mechanisms in normal humans and in patients with dystonia. Background Several evidence suggest that lateral inhibition is a system within sensory-motor cortex operating during the acquisition of new motor tasks in order to select the appropriate muscle sequence to be stored within the final motor engram. This mechanism is thought to be lost in dystonia and this should explain the development of redundant motor memories which could culminate in overflow phenomena and overt dystonia. Methods We have used transcranial magnetic stimulation to explore lateral inhibition during sensory-motor plasticity in 12 dystonic patients (7 focal hand dystonia, 5 cranial dystonia) and in 8 healthy subjects. In particular we looked at motor evoked potential (MEP) facilitation, in the abductor pollicis brevis (APB) and abductor digiti minimi (ADM), obtained after 5 Hz repetitive paired associative stimulation after median (PAS M), ulnar nerve stimulation (PAS U) and median + ulnar nerve (PAS MU) stimulation. In this way we evaluated the ratio MU/M + Ux100 (lateral inhibition index). Moreover, we evaluated the lateral inhibition index (Li index). This parameter is easily obtained by using the following formula: ratio MU/(M + U) x 100. MU is the MEP facilitation measured after PAS with simultaneous stimulation of median and ulnar and M + U is the amount of MEP facilitation, after PAS, induced from stimulation of the individual nerves. Results Our data confirmed that patients with dystonia had two main abnormalities: first the amount of facilitation was larger than normal subjects; second and more important the spatial specificity was lost. A three-factorial ANOVA demonstrated a significant time × group × conditioning interaction ( F = 7.9; p = 0.005). Lateral inhibition index was similar (about 50%) in healthy subjects and dystonic patients. Conclusions These data suggest that lateral inhibition is normal in dystonia during sensory-motor plasticity. Another mechanism could contribute to the formation of motor memories with redundant information, which could culminate in overt dystonia.

History of exposure to dopaminergic medication does not affect motor cortex plasticity and excitability in Parkinson’s disease

ObjectiveLittle is known whether and how chronic exposure to dopaminergic treatment alters physiological mechanisms in Parkinson’s disease (PD). MethodsTwo clinically similar groups of PD patients, one consisting of drug-naïve patients and another of patients already on chronic dopaminergic medication (when off medication), were compared to each other and to a control group. Plasticity and excitability of the hand primary motor cortex of the more affected side were evaluated using transcranial magnetic stimulation (TMS) techniques. ResultsThere was little difference between two patient groups, and both groups showed similar differences in comparison to controls: decreased facilitatory sensory-motor plasticity (as measured by paired associative stimulation [PAS] protocol), impaired short-interval intracortical inhibition (SICI), and diminished slope of input–output curves at higher TMS intensities. The exception was that 30min after PAS, intracortical facilitation (ICF) was significantly reduced in drug-naïve patients, whereas it changed much less in other two groups. ConclusionsChronic exposure to dopaminergic drugs does not affect substantially the features of motor cortex excitability and plasticity in PD. There is little interaction between plasticity and excitability features of motor cortex in PD. SignificanceReduced response to facilitatory PAS protocol, reduced SICI, and reduced slope of the input–output curve at higher TMS pulse intensities, seem to be physiological markers for the presence of the pathological disease process in PD. Long term treatment does not seem to change the underlying physiology of the disease.

Impairment of sensory-motor plasticity in mild Alzheimer’s disease

BackgroundPrimary motor cortex (M1) is relatively spared in the early stages of Alzheimer’s disease (AD). ObjectiveAim of the present study was to investigate whether abnormal M1 synaptic plasticity is present at an early stage of AD. We employed an electrophysiological protocol, named rapid paired associative stimulation (rPAS), involving repetitive transcranial magnetic stimulation (rTMS) paired with electrical stimulation of the contralateral median nerve, that modifies corticospinal excitability and short latency afferent inhibition (SAI). MethodsWe studied 10 patients with a diagnosis of probable mild AD according to the Mini Mental State Examination score (minimum 21) and 14 age-matched control subjects. Motor evoked potentials (MEP) amplitudes and short-afferent inhibition (SAI) were measured at baseline before and for up to 60 min after 5Hz-rPAS in abductor pollicis brevis (APB). rPAS consisted of 600 pairs of transcranial magnetic stimuli, at a rate of 5 Hz for 2 min, coupled with electrical median nerve stimulation preceding TMS over the contralateral M1 at an inter-stimulus interval of 25 ms. ResultsBaseline SAI was significantly reduced in AD patients. In the control subjects rPAS induced a significant increase in MEP amplitudes and a decrease of SAI in the APB muscle persistently for up to 1 h. Conversely 5Hz-rPAS did not induce any significant changes in MEP amplitudes and SAI in mild AD patients. ConclusionsSensory-motor plasticity is impaired in the motor cortex of AD at an early stage of the disease.

Transcranial magnetic stimulation and motor plasticity in human lateral cerebellum: dual effect on saccadic adaptation.

The cerebellum is a key area for movement control and sensory-motor plasticity. Its medial part is considered as the exclusive cerebellar center controlling the accuracy and adaptive calibration of saccadic eye movements. However, the contribution of other zones situated in its lateral part is unknown. We addressed this question in healthy adult volunteers by using magnetic resonance imaging (MRI)-guided transcranial magnetic stimulation (TMS). The double-step target paradigm was used to adaptively lengthen or shorten saccades. TMS pulses over the right hemisphere of the cerebellum were delivered at 0, 30, or 60 ms after saccade detection in separate recording sessions. The effects on saccadic adaptation were assessed relative to a fourth session where TMS was applied to Vertex as a control site. First, TMS applied upon saccade detection before the adaptation phase reduced saccade accuracy. Second, TMS applied during the adaptation phase had a dual effect on saccadic plasticity: adaptation after-effects revealed a potentiation of the adaptive lengthening and a depression of the adaptive shortening of saccades. For the first time, we demonstrate that TMS on lateral cerebellum can influence plasticity mechanisms underlying motor performance. These findings also provide the first evidence that the human cerebellar hemispheres are involved in the control of saccade accuracy and in saccadic adaptation, with possibly different neuronal populations concerned in adaptive lengthening and shortening. Overall, these results require a reappraisal of current models of cerebellar contribution to oculomotor plasticity.

Motor cortical plasticity is impaired in Unverricht–Lundborg disease

Patients with Unverricht-Lundborg disease, also referred to as progressive myoclonus epilepsy type 1, exhibit widespread motor symptoms and signs in addition to epileptic seizures, which suggest abnormal excitability of the primary motor pathways. To explore the plasticity of the sensory-motor cortex, we employed a modern neurophysiological method, the paired associative stimulation protocol, which resembles the concept of long-term potentiation of experimental studies. Seven patients with genetically verified Unverricht-Lundborg disease and 13 healthy control subjects were enrolled in the study to characterize cortical sensory-motor plasticity. In the study protocol, peripheral electric median nerve stimulation preceded navigated transcranial magnetic stimulation targeted to the representation area of thenar musculature on the contralateral primary motor cortex. The protocol consisted of 132 transcranial magnetic stimulation trials at 0.2 Hz, preceded by peripheral sensory stimulation at 25 ms. Motor-evoked potential amplitudes were analyzed at baseline and after the paired associative stimulation protocol at an intensity of 130% of the individual motor threshold. The patients with Unverricht-Lundborg disease exhibited an average decrease of 15% in motor-evoked potential amplitudes 30 minutes after paired associative stimulation, whereas in the control subjects, a significant increase (101%) was observed (P < .05), as expected. The results indicate a lack of normal cortical plasticity in Unverricht-Lundborg disease, which stresses the role of abnormal motor cortical functions or sensorimotor integration as possible pathophysiological contributors to the motor symptoms. The impaired cortical plasticity may be associated with the previously reported structural and physiological abnormalities of the primary motor cortex.

Neural mechanisms underlying spatial realignment during adaptation to optical wedge prisms

Visuomotor adaptation to a shift in visual input produced by prismatic lenses is an example of dynamic sensory-motor plasticity within the brain. Prism adaptation is readily induced in healthy individuals, and is thought to reflect the brain's ability to compensate for drifts in spatial calibration between different sensory systems. The neural correlate of this form of functional plasticity is largely unknown, although current models predict the involvement of parieto-cerebellar circuits. Recent studies that have employed event-related functional magnetic resonance imaging (fMRI) to identify brain regions associated with prism adaptation have discovered patterns of parietal and cerebellar modulation as participants corrected their visuomotor errors during the early part of adaptation. However, the role of these regions in the later stage of adaptation, when ‘spatial realignment’ or true adaptation is predicted to occur, remains unclear. Here, we used fMRI to quantify the distinctive patterns of parieto-cerebellar activity as visuomotor adaptation develops. We directly contrasted activation patterns during the initial error correction phase of visuomotor adaptation with that during the later spatial realignment phase, and found significant recruitment of the parieto-cerebellar network – with activations in the right inferior parietal lobe and the right posterior cerebellum. These findings provide the first evidence of both cerebellar and parietal involvement during the spatial realignment phase of prism adaptation.

Dopamine agonists restore cortical plasticity in patients with idiopathic restless legs syndrome

In the present work, we aimed at assessing whether patients with idiopathic restless legs syndrome (RLS) showed alterations of sensory-motor plasticity, an indirect probe for motor learning, within the motor cortex (M1). Previous findings suggest that learning in human M1 occurs through LTP-like mechanisms. To test our hypothesis, we employed the paired associative stimulation (PAS) protocol by transcranial magnetic stimulation (TMS), which is able to induce LTP-like effects in the motor cortex of normal subjects. Twelve patients with idiopathic RLS and 10 age- and sex-matched control subjects were recruited. PAS protocol consisted of 0.05 Hz electrical median nerve stimulation (90 stimuli), paired with 0.05 Hz TMS (90 stimuli) over the hot spot for stimulating the abductor pollicis brevis (APB) muscle given 25 milliseconds after the onset of the electrical stimulus. Corticospinal excitability recorded in APB muscle, as indexed by MEP obtained after single stimulus, was tested before and up to 30 minutes after PAS protocol. Eight of 12 patients were studied before and after 4 weeks of dopaminergic treatment. PAS protocol increased significantly corticospinal excitability as long as 30 minutes in healthy subjects. On the contrary, PAS protocol did not change the amplitude of MEPs in patients with idiopathic RLS without treatment. PAS associative plasticity was restored after 4 weeks of dopaminergic treatment. Our data demonstrated that associative sensory-motor plasticity, an indirect probe for motor learning, is impaired in idiopathic RLS patients but may be reverted to normal after dopaminergic treatment.

Separate Neural Substrates in the Human Cerebellum for Sensory-motor Adaptation of Reactive and of Scanning Voluntary Saccades

Sensory-motor adaptation processes are critically involved in maintaining accurate motor behavior throughout life. Yet their underlying neural substrates and task-dependency bases are still poorly understood. We address these issues here by studying adaptation of saccadic eye movements, a well-established model of sensory-motor plasticity. The cerebellum plays a major role in saccadic adaptation but it has not yet been investigated whether this role can account for the known specificity of adaptation to the saccade type (e.g., reactive versus voluntary). Two patients with focal lesions in different parts of the cerebellum were tested using the double-step target paradigm. Each patient was submitted to two separate sessions: one for reactive saccades (RS) triggered by the sudden appearance of a visual target and the second for scanning voluntary saccades (SVS) performed when exploring a more complex scene. We found that a medial cerebellar lesion impaired adaptation of reactive-but not of voluntary-saccades, whereas a lateral lesion affected adaptation of scanning voluntary saccades, but not of reactive saccades. These findings provide the first evidence of an involvement of the lateral cerebellum in saccadic adaptation, and extend the demonstrated role of the cerebellum in RS adaptation to adaptation of SVS. The double dissociation of adaptive abilities is also consistent with our previous hypothesis of the involvement in saccadic adaptation of partially separated cerebellar areas specific to the reactive or voluntary task (Alahyane et al. Brain Res 1135:107-121 (2007)).

Sensory-motor Integration and Synaptic Plasticity in Cerebellar Córtex

The present study aims to investigate the synaptic plasticity in the cerebellum as a result of the learning process of complex (acrobatic) motor skills. It begins with an anatomical and physiological description of the cerebellum, which includes its division into lobes, the relationship with other areas of the Central Nervous System, and a detailed analysis of its internal circuits. Next, an approach regarding disitnct models which attempt to explain how the cerebellum functions as it incorporates new motor patterns to the system is made. Finally, results of different experimental studies which investigated the cerebellar synaptic remodelling in acrobatic trained rats are assembled. The acrobatic training consisted of activities demanding a high level of coordination and balance. The trainned rats were compared to others submitted to simple exercises and to inactive groups. The three groups of rats were sacrifi ced and studied with an electronic microscope.