1,721,142 research outputs found

    Combining reward and M1 transcranial direct current stimulation enhances the retention of newly learnt sensorimotor mappings

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    Background: Reward-based feedback given during motor learning has been shown to improve the retention of the behaviour being acquired. Interestingly, applying transcranial direct current stimulation (tDCS) during learning over the primary motor cortex (M1), an area associated with motor retention, also results in enhanced retention of the newly formed motor memories. However, it remains unknown whether combining these distinct interventions result in an additive benefit of motor retention. Methods: We investigated whether combining both interventions while participants learned to account for a visuomotor transformation results in enhanced motor retention (total n = 56; each group n = 14). To determine whether these interventions share common physiological mechanisms underpinning learning, we assessed motor cortical excitability and inhibition (i.e. SICI) on a hand muscle before and after all participants learned the visuomotor rotation using their entire arm and hand. Results: We found that both the Reward-Stim (i.e. reward + tDCS) and Reward-Sham (i.e. reward-only) groups had increased retention at the beginning of the retention phase, indicating an immediate effect of reward on behaviour. However, each intervention on their own did not enhance retention when compared to sham, but rather, only the combination of both reward and tDCS demonstrated prolonged retention. We also found that only the Reward-Stim group had a significant reduction in SICI after exposure to the perturbation. Conclusions: We show that combining both interventions are additive in providing stronger retention of motor adaptation. These results indicate that the reliability and validity of using tDCS within a clinical context may depend on the type of feedback individuals receive when learning a new motor pattern

    Reply: Pentameric repeat expansions: Cortical myoclonus or cortical tremor? And Cortical tremor: A tantalizing conundrum between cortex and cerebellum

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    We are thankful for van Rootselaar et al’s and Striano et al’s interest in our work, and for sharing their considerations on the subject (Striano et al., 2020; van Rootselaar et al., 2020). The rare and poorly understood disorder that is familial cortical myoclonic tremor and epilepsy (FCMTE) captivates the curiosity of movement disorder and epilepsy specialists, because of its complex phenomenology and its intriguing genetic and pathophysiological underpinnings. We agree that the mechanisms whereby expansions in non-coding regions contribute to disease, regardless of the gene involved, could potentially be ‘textbook material’ as van Rootselaar et al. propose. Indeed, recent genetic discoveries (i.e. intronic pentanucleotide repeat expansions in different genes) have paved the way for the und

    Intracortical circuits, sensorimotor integration and plasticity in human motor cortical projections to muscles of the lower face

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    Previous studies of the cortical control of human facial muscles documented the distribution of corticobulbar projections and the presence of intracortical inhibitory and facilitatory mechanisms. Yet surprisingly, given the importance and precision in control of facial expression, there have been no studies of the afferent modulation of corticobulbar excitability or of the plasticity of synaptic connections in the facial primary motor cortex (face M1). In 25 healthy volunteers, we used standard single- and paired-pulse transcranial magnetic stimulation (TMS) methods to probe motor-evoked potentials (MEPs), short-intracortical inhibition, intracortical facilitation, short-afferent and long-afferent inhibition and paired associative stimulation in relaxed and active depressor anguli oris muscles. Single-pulse TMS evoked bilateral MEPs at rest and during activity that were larger in contralateral muscles, confirming that corticobulbar projection to lower facial muscles is bilateral and asymmetric, with contralateral predominance. Both short-intracortical inhibition and intracortical facilitation were present bilaterally in resting and active conditions. Electrical stimulation of the facial nerve paired with a TMS pulse 5-200 ms later showed no short-afferent inhibition, but long-afferent inhibition was present. Paired associative stimulation tested with an electrical stimulation-TMS interval of 20 ms significantly facilitated MEPs for up to 30 min. The long-term potentiation, evoked for the first time in face M1, demonstrates that excitability of the facial motor cortex is prone to plastic changes after paired associative stimulation. Evaluation of intracortical circuits in both relaxed and active lower facial muscles as well as of plasticity in the facial motor cortex may provide further physiological insight into pathologies affecting the facial motor system. © 2013 The Authors. The Journal of Physiology © 2013 The Physiological Society

    The Signature of Primary Writing Tremor Is Dystonic

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    Background: It has been debated for decades whether primary writing tremor is a form of dystonic tremor, a variant of essential tremor, or a separate entity. We wished to test the hypothesis that primary writing tremor and dystonia share a common pathophysiology. Objectives: The objective of the present study was to investigate the pathophysiological hallmarks of dystonia in patients affected by primary writing tremor. Methods: Ten patients with idiopathic dystonic tremor syndrome, 7 with primary writing tremor, 10 with essential tremor, and 10 healthy subjects were recruited. They underwent eyeblink classic conditioning, blink recovery cycle, and transcranial magnetic stimulation assessment, including motor-evoked potentials and short- and long-interval intracortical inhibition at baseline. Transcranial magnetic stimulation measures were also recorded after paired-associative plasticity protocol. Results: Primary writing tremor and dystonic tremor syndrome had a similar pattern of electrophysiological abnormalities, consisting of reduced eyeblink classic conditioning learning, reduced blink recovery cycle inhibition, and a lack of effect of paired-associative plasticity on long-interval intracortical inhibition. The latter 2 differ from those obtained in essential tremor and healthy subjects. Although not significant, slightly reduced short-interval intracortical inhibition and a larger effect of paired-associative plasticity in primary writing tremor and dystonic tremor syndrome, compared with essential tremor and healthy subjects, was observed. Conclusions: Our initial hypothesis of a common pathophysiology between dystonia and primary writing tremor has been confirmed. Primary writing tremor might be considered a form of dystonic tremor. © 2021 International Parkinson and Movement Disorder Society

    Inhibitory action of forearm flexor muscle afferents on corticospinal outputs to antagonist muscles in humans

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    1. To find out whether muscle afferents influence the excitability of corticospinal projections to antagonist muscles, we studied sixteen healthy subjects and one patient with a focal brain lesion. 2. Using transcranial magnetic and electrical brain stimulation we tested the excitability of corticomotoneuronal connections to right forearm muscles at rest after conditioning stimulation of the median nerve at the elbow. Somatosensory potentials evoked by median nerve stimulation were also recorded in each subject. 3. Test stimuli delivered at 13-19 ms after median nerve stimulation significantly inhibited EMG responses elicited in forearm extensor muscles by transcranial magnetic stimulation, but did not inhibit responses to electrical stimulation. In contrast, magnetically and electrically elicited responses in forearm flexor muscles were suppressed to the same extent. 4. The higher the intensity of the test shocks, the smaller was the amount of median nerve-elicited inhibition. Inhibition in extensor muscles was also smaller during tonic wrist extension, or if the induced electrical stimulating current in the brain flowed from posterior to anterior over the motor strip rather than vice versa. Test responses evoked by magnetic transcranial stimulation in the first dorsal interosseous and in brachioradialis muscles were not inhibited after median nerve stimulation at the elbow. Stimulation of digital nerves failed to inhibit motor potentials in extensor muscles. 5. Test stimuli delivered at 15 and 17 ms after radial nerve stimulation significantly inhibited EMG responses elicited in forearm flexor muscles by magnetic transcranial stimulation. 6. In the patient with a focal thalamic lesion, who had dystonic postures and an absent N20 component of the somatosensory-evoked potentials but normal strength, median nerve stimulation failed to inhibit magnetically evoked responses in forearm extensor muscles. 7. We propose that activation of median nerve muscle afferents can suppress the excitability of cortical areas controlling the antagonist forearm extensor muscles acting on the hand. The inhibitory effect occurs at short latency and might assist spinal pathways mediating reciprocal inhibition by contrasting the co-activation of antagonistic pools of corticospinal cells

    Exploring the connectivity between the cerebellum and facial motor cortex

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    ranscranial magnetic stimulation (TMS) delivered over the cer-ebellum 5e7 ms prior to a stimulus applied over the contralateralM1 reduced the excitability of M1 corticospinal outputs. This phenomenon is termed cerebellar brain inhibition (CBI). It remains unknown whether CBI is pre-sent in face M1 (fM). Fourteen right-handed healthy volunteers (9 females;28.77±1.11 years old) participated in this study. Electromyographic activity (EMG) was recorded from the right depressor anguli oris muscle (DAO). We reported the first evidence of cerebellar-M1 connectivity for the representation of the DAO in healthy subjects. Similar to CBIfor the hand and leg representations, the timing and location of cerebellar stimulation prior to probing cortical excitability was critical suggesting that the same pathways targeted with paired-pulseTMS for limb M1 extends to the cerebellar connection with fM1

    Sensory functions in dystonia: Insights from behavioral studies

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    The pathophysiology of primary dystonia is thought to involve dysfunction of the basal ganglia cortico-striatal-thalamo-cortical motor circuits. In the past, emphasis was placed on the role of the basal ganglia in controlling movements; in more recent times, however, it has also become clear that they play an important part in sensory as well as cognitive functions. Here, we review evidence for dysfunction of sensory processing in patients with dystonia, and speculate that this may lead to abnormalities in a crucial role of the basal ganglia that links sensory information to appropriate motor output. Sensory function, particularly in the somatosensory domain, has been shown to be compromised in patients with primary dystonia, both in adult onset focal dystonia and in genetically characterized DYT1 dystonia. Given that nonaffected DYT1 gene carriers may show similar abnormalities to clinically affected individuals, sensory deficits could constitute a subclinical endophenotypic trait of disease that precedes overt clinical manifestations. Whether they can trigger primary dystonia or are an epiphenomenon is an issue warranting further study, but the fact that a number of different neurorehabilitative approaches explicitly manipulate somatosensory inputs to improve motor function suggests there may be a causal link between them. We believe that in future, randomized, blind and controlled studies in large patient populations should address this issue, providing efficient strategies to aid functional recovery, particularly in focal hand dystonia, where the available medical treatments offer little benefit. (c) 2009 Movement Disorder Society
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