Non invasive Brain Stimulation Unit

Rome, Italy

Non invasive Brain Stimulation Unit

Rome, Italy
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Casula E.P.,Non Invasive Brain Stimulation Unit | Pellicciari M.C.,Non Invasive Brain Stimulation Unit | Picazio S.,Non Invasive Brain Stimulation Unit | Caltagirone C.,Non Invasive Brain Stimulation Unit | And 3 more authors.
NeuroImage | Year: 2016

Changes in the synaptic strength of neural connections are induced by repeated coupling of activity of interconnected neurons with precise timing, a phenomenon known as spike-timing-dependent plasticity (STDP). It is debated if this mechanism exists in large-scale cortical networks in humans. We combined transcranial magnetic stimulation (TMS) with concurrent electroencephalography (EEG) to directly investigate the effects of two paired associative stimulation (PAS) protocols (fronto-parietal and parieto-frontal) of pre and post-synaptic inputs within the human fronto-parietal network. We found evidence that the dorsolateral prefrontal cortex (DLPFC) has the potential to form robust STDP. Long-term potentiation/depression of TMS-evoked cortical activity is prompted after that DLPFC stimulation is followed/preceded by posterior parietal stimulation. Such bidirectional changes are paralleled by sustained increase/decrease of high-frequency oscillatory activity, likely reflecting STDP responsivity. The current findings could be important to drive plasticity of damaged cortical circuits in patients with cognitive or psychiatric disorders. © 2016 Elsevier Inc.


Casellato C.,Polytechnic of Milan | Koch G.,Non invasive Brain Stimulation Unit | D'Angelo E.,University of Pavia
European Journal of Neuroscience | Year: 2014

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.


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 | Year: 2015

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.


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 | Year: 2014

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.


Martorana A.,University of Rome Tor Vergata | Martorana A.,Non Invasive Brain Stimulation Unit | Koch G.,University of Rome Tor Vergata | Koch G.,Non Invasive Brain Stimulation Unit
Frontiers in Aging Neuroscience | Year: 2014

Alzheimer's Disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline and dementia. Recent advances indicate that AD pathogenesis appears more complex than its mere neuropathology. Changes in synaptic plasticity, neuronal disarray and cell death are pathways commonly recognized as pathogenic mechanisms of AD. It is thought that the altered metabolism of certain membrane proteins may lead to the production of amyloid (Aβ) oligomers that are characterized by an highly toxic effect on neurotransmission pathways, such as those mediated by Acetylcholine. The interaction of Aβ oligomers with these neurotansmitters systems would in turn induce cell dysfunction, neurotransmitters signaling imbalance and finally lead to the appearance of neurological signs. In this perspective, it is still debated how and if these mechanisms may also engage the dopaminergic system in AD. Recent experimental work revealed that the dopaminergic system may well be involved in the occurrence of cognitive decline, often being predictive of rapidly progressive forms of AD. However a clear idea on the role of the dopamine system in AD is still missing. Here we review the more recent evidences supporting the notion that the dopaminergic dysfunction has a pathogenic role in cognitive decline symptoms of AD. © 2014 Martorana and Koch.


Martorana A.,University of Rome Tor Vergata | Di Lorenzo F.,University of Rome Tor Vergata | Di Lorenzo F.,Non Invasive Brain Stimulation Unit | Manenti G.,Interventional Imaging | And 2 more authors.
Frontiers in Aging Neuroscience | Year: 2014

Current treatment options for patients with Alzheimer's disease (AD) are limited at providing symptomatic relief, with no effects on the underlying pathophysiology. Recently, advances in the understanding of the AD pathogenesis highlighted the role of ABeta (Aβ) oligomers particularly interfering with mechanisms of cortical plasticity such as long-term potentiation (LTP) and long-term depression (LTD). These findings led to the development of potential antiamyloid therapies, and among them homotaurine, a glycosaminoglycan (GAG) mimetic designed to interfere with the actions of Aβ early in the cascade of amyloidogenic events, and by its γ-aminobutyric acid type (GABA) A receptor affinity. Recently, we showed that AD patients have impaired LTP-like cortical plasticity, as measured by standard theta burst stimulation (TBS) protocols applied over the primary motor cortex (M1). Furthermore, AD patients have a weakened Short Latency Afferent Inhibition (SLAI), a neurophysiological measure of central cholinergic transmission, which changes reflect the cholinergic dysfunction occurring in the pathology. Here we aimed at investigating whether homotaurine administration could modulate in vivo measured mechanisms of synaptic plasticity, namely LTP and LTD, and also SLAI in a group of mild cognitive impaired patients. We observed that homotaurine administration did not induce relevant changes of both LTP and LTD recordings, while induced changes of SLAI in our group of patients. We suggest that homotaurine effects are dependent on changes of cortical GABA transmission suggesting a potential role for this compound in ameliorating the cholinergic transmission by modulating the inhibitory cortical activity. © 2014 Martorana, Di_lorenzo, Manenti, Semprini and Koch.


Picazio S.,Non invasive Brain Stimulation Unit | Koch G.,Non invasive Brain Stimulation Unit | Koch G.,University of Rome Tor Vergata
Cerebellum | Year: 2015

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.


Koch G.,Non Invasive Brain Stimulation Unit | Koch G.,University of Rome Tor Vergata | Di Lorenzo F.,Non Invasive Brain Stimulation Unit | Di Lorenzo F.,University of Rome Tor Vergata | And 6 more authors.
Neuropsychopharmacology | Year: 2014

In animal models of Alzheimer's disease (AD), mechanisms of cortical plasticity such as long-term potentiation (LTP) and long-term depression (LTD) are impaired. In AD patients, LTP-like cortical plasticity is abolished, whereas LTD seems to be preserved. Dopaminergic transmission has been hypothesized as a new player in ruling mechanisms of cortical plasticity in AD. We aimed at investigating whether administration of the dopamine agonist rotigotine (RTG) could modulate cortical plasticity in AD patients, as measured by theta burst stimulation (TBS) protocols of repetitive transcranial stimulation applied over the primary motor cortex. Thirty mild AD patients were tested in three different groups before and after 4 weeks of treatment with RTG, rivastigmine (RVT), or placebo (PLC). Each patient was evaluated for plasticity induction of LTP/LTD-like effects using respectively intermittent TBS (iTBS) or continuous TBS protocols. Short-latency afferent inhibition (SAI) protocol was performed to indirectly assess central cholinergic activity. A group of age-matched healthy controls was recruited for baseline comparisons. Results showed that at baseline, AD patients were characterized by impaired LTP-like cortical plasticity, as assessed by iTBS. These reduced levels of LTP-like cortical plasticity were increased and normalized after RTG administration. No effect was induced by RVT or PLC on LTP. LTD-like cortical plasticity was not modulated in any condition. Cholinergic activity was increased by both RTG and RVT. Our findings reveal that dopamine agonists may restore the altered mechanisms of LTP-like cortical plasticity in AD patients, thus providing novel implications for therapies based on dopaminergic stimulation.


Koch G.,Non Invasive Brain Stimulation Unit | Koch G.,University of Rome Tor Vergata
Frontiers in Neurology | Year: 2013

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.


Picazio S.,Non Invasive Brain Stimulation Unit | Ponzo V.,Non Invasive Brain Stimulation Unit | Koch G.,Non Invasive Brain Stimulation Unit | Koch G.,University of Rome Tor Vergata
Cerebellum | Year: 2015

Converging evidence suggests a crucial role of right inferior frontal gyrus (r-IFG) and right pre-supplementary motor area (r-preSMA) in movement inhibition control. The present work was aimed to investigate how the effective connectivity between these prefrontal areas and the primary motor cortex could change depending on the activity of the cerebellar cortex. Paired transcranial magnetic stimulation (TMS) was delivered in healthy subjects over the r-IFG/left primary motor area (l-M1) and over r-preSMA/l-M1 before (100 ms after the fixation cross onset) and 50, 75, 100, 125, and 150 ms after the presentation of a Go/NoGo visual cue establishing the specific time course and the causal interactions of these regions in relation to l-M1 as measured by motor evoked potentials (MEPs). The same paired-pulse protocol was applied following sham or real cerebellar continuous theta burst stimulation (cTBS). Following sham cTBS, for NoGo trials only, MEPs collected showed the expected pattern of activation for both r-IFG-l-M1 and r-preSMA-l-M1 connectivity, characterized by peaks of increased and decreased MEP amplitude regularly repeated every 50 ms. Following cerebellar cTBS, this pattern of activation related to NoGo trials was modified selectively for the r-IFG-M1 but not for r-preSMA-M1 connection. A common monitoring action of r-IFG and r-preSMA in inhibitory control was confirmed. The effects of cerebellar cTBS showed a specific interaction between cerebellum and r-IFG activity during the inhibitory process. © 2015 Springer Science+Business Media New York

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