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Pellicciari M.C.,Irccs Centro San Giovanni Of Dio Fatebenefratelli | Miniussi C.,Irccs Centro San Giovanni Of Dio Fatebenefratelli | Miniussi C.,University of Brescia | Ferrari C.,Irccs Centro San Giovanni Of Dio Fatebenefratelli | And 3 more authors.
Clinical Neurophysiology

Objective: To evaluate the effects of several single TMS pulses, delivered at two different inter-trial intervals (ITIs), on corticospinal excitability. Methods: Twelve healthy volunteers participated in two experimental sessions, during which TMS pulses were delivered at random or at fixed ITIs. The TMS single pulse-induced modulation of corticospinal output (motor evoked potential amplitude - MEP) was evaluated on-line. Each session began with a baseline block, followed by 10 blocks, with 20 TMS pulses each. Intra- and inter-block effects were valuated using an ANOVA model, through nested random effect on subjects considering the subject-specific variability. Results: The delivery of successive TMS pulses significantly changed both intra-block and inter-block cortical excitability, as demonstrated by an increase in the amplitude of MEPs (p < 0.001) and supported through trend analyses, showing a perfect linear trend for inter-block levels (R2 = 1) and nearly linear trend for intra-block levels (R2 = 0.97). The MEPs significantly increased when the TMS pulses were delivered at both random and fixed ITIs. Conclusions: Single TMS pulses induce cumulative changes in neural activity during the same stimulation, resulting in a motor cortical excitability increase. Significance: Particular attention should be taken when several single TMS pulses are delivered in research and clinical settings for diagnostic and therapeutic purposes. © 2015 International Federation of Clinical Neurophysiology. Source

Benussi A.,University of Brescia | Koch G.,Non invasive Brain Stimulation Unit | Koch G.,University of Rome Tor Vergata | Cotelli M.,Irccs Centro San Giovanni Of Dio Fatebenefratelli | And 2 more authors.
Movement Disorders

Background and Objective: Numerous studies have highlighted the possibility of modulating the excitability of cerebellar circuits using transcranial direct current stimulation. The present study investigated whether a single session of cerebellar anodal transcranial direct current stimulation could improve symptoms in patients with ataxia. Methods: Nineteen patients with ataxia underwent a clinical and functional evaluation pre- and post-double-blind, randomized, sham, or anodal transcranial direct current stimulation. Results: There was a significant interaction between treatment and time on the Scale for the Assessment and Rating of Ataxia, on the International Cooperative Ataxia Rating Scale, on the 9-Hole Peg Test, and on the 8-Meter Walking Time (P<0.001). At the end of the sessions, all performance scores were significantly different in the sham trial, compared to the intervention trial. Conclusions: A single session of anodal cerebellar transcranial direct current stimulation can transiently improve symptoms in patients with ataxia and might represent a promising tool for future rehabilitative approaches. © 2015 International Parkinson and Movement Disorder Society. Source

Koch G.,Non invasive Brain Stimulation Unit | Koch G.,University of Rome Tor Vergata
Frontiers in Neurology

Animal models of Parkinson's disease (PD) have shown that key mechanisms of cortical plasticity such as long-term potentiation (LTP) and long-term depression (LTD) can be impaired by the PD pathology. In humans protocols of non-invasive brain stimulation, such as paired associative stimulation (PAS) and theta-burst stimulation (TBS), can be used to investigate cortical plasticity of the primary motor cortex. Through the amplitude of the motor evoked potential these transcranial magnetic stimulation methods allow to measure both LTP-like and LTD-like mechanisms of cortical plasticity. So far these protocols have reported some controversial findings when tested in PD patients. While various studies described evidence for reduced LTP- and LTD-like plasticity, others showed different results, demonstrating increased LTP-like and normal LTD-like plasticity. Recent evidence provided support to the hypothesis that these different patterns of cortical plasticity likely depend on the stage of the disease and on the concomitant administration of l-DOPA. However, it is still unclear how and if these altered mechanisms of cortical plasticity can be taken as a reliable model to build appropriate protocols aimed at treating PD symptoms by applying repetitive sessions of repetitive TMS (rTMS) or transcranial direct current stimulation (tDCS). The current article will provide an up-to-date overview of these issues together with some reflections on future studies in the field. © 2013 Koch. Source

Monaco J.,Connectivity | Casellato C.,Polytechnic of Milan | Koch G.,Non invasive Brain Stimulation Unit | D'Angelo E.,Connectivity | D'Angelo E.,University of Pavia
European Journal of Neuroscience

The cerebellum plays a critical role in forming precisely timed sensory-motor associations. This process is thought to proceed through two learning phases: one leading to memory acquisition; and the other leading more slowly to memory consolidation and saving. It has been proposed that fast acquisition occurs in the cerebellar cortex, while consolidation is dislocated into the deep cerebellar nuclei. However, it was not clear how these two components could be identified in eyeblink classical conditioning (EBCC) in humans, a paradigm commonly used to investigate associative learning. In 22 subjects, we show that EBCC proceeded through a fast acquisition phase, returned toward basal levels during extinction and then was consolidated, as it became evident from the saving effect observed when re-testing the subjects after 1 week of initial training. The results were fitted using a two-state multi-rate learning model extended to account for memory consolidation. Transcranial magnetic stimulation was used to apply continuous theta-burst stimulation (cTBS) to the lateral cerebellum just after the first training session. Half of the subjects received real cTBS and half sham cTBS. After cTBS, but not sham cTBS, consolidation was unaltered but the extinction process was significantly impaired. These data suggest that cTBS can dissociate EBCC extinction (related to the fast learning process) from consolidation (related to the slow learning process), probably by acting through a selective alteration of cerebellar plasticity. © 2014 Federation of European Neuroscience Societies and John Wiley & Sons Ltd. Source

Picazio S.,Non invasive Brain Stimulation Unit | Koch G.,Non invasive Brain Stimulation Unit | Koch G.,University of Rome Tor Vergata

Motor inhibition is an essential skill for fully adapted behavior requiring motor control and higher-order functions of motor cognition. A wide set of cortical and subcortical areas, including the right inferior frontal gyrus, the pre-supplementary motor area, and the subthalamic nucleus in the basal ganglia, contribute to convey the inhibitory command to the motor cortex. In the present review, we discuss how recent evidence supports the idea that the cerebellum may also have a relevant contribution in certain aspects of motor inhibition. This evidence were provided by behavioral data collected in patients with cerebellar lesions, functional magnetic resonance (fMRI) investigations conducted in clinical samples and in healthy participants, and by transcranial magnetic stimulation (TMS) techniques used to non-invasively test cerebello-motor functional connectivity. The application of these methods, combined with the execution of inhibitory tasks, could provide new evidence for a causal role of the effective cerebello-cortical connectivity in motor inhibition. Understanding the neurophysiological mechanisms that mediate motor inhibition through the cerebellum could be essential to design new rehabilitative protocols for treating several neurological and psychiatric disorders characterized by disinhibited behavior such as addiction, schizophrenia, attention deficit hyperactivity disorder (ADHD) and Parkinson’s disease. © 2014, Springer Science+Business Media New York. Source

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