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Casula, Elias Paolo (2015) THE COMBINED USE OF TRANSCRANIAL MAGNETIC STIMULATION AND ELECTROENCEPHALOGRAPHY IN THE INVESTIGATION OF REACTIVITY, CONNECTIVITY AND PLASTICITY OF THE PRIMARY MOTOR CORTEX. [Tesi di dottorato]

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Abstract (inglese)

The present thesis comprises two main parts: one theoretical and one experimental. The first part, composed of two chapters, is an in-depth introduction to transcranial magnetic stimulation (TMS) and its simultaneous use with neuroimaging techniques (coregistration). The second part is composed of some of the studies I conducted during my PhD. I chose to include three studies representing the different aspects of my research in the last three years, mainly regarding the study and the application of TMS-EEG coregistration in research (study 1), clinics (study 2) and technical methodology (study 3). The first study (study 1), conducted at the Department of General Psychology of Padova, was aimed to investigate the neuromodulatory effects of an rTMS protocol on healthy volunteers. The second study (study 2) was conducted at the Institute of Neurology of University College London in the context of the international “TrackOnHD” longitudinal project aimed to investigate Huntington disease (HD) in a multimodal approach. The target of this study was to investigate possible TMS-EEG markers of inhibition deficits in Huntington patients. The third study (study 3), conducted in collaboration with the Department of Information Engineering of Padova, was aimed to develop an algorithm of correction to remove an artefact induced by TMS during EEG recordings.


CHAPTER I – TRANSCRANIAL MAGNETIC STIMULATION
In the last twenty years the development of new techniques able to investigate the brain function in vivo during cognitive and motor tasks lead to impressive advances in understanding the human brain. Transcranial magnetic stimulation (TMS) is a tool whose popularity has grown progressively thanks to its ability to stimulate the brain in a focal and non-invasive way (Barker et al., 1985), permitting to establish a causal link in the brain-cognition/motor-behaviour relationship (Pascual-Leone et al., 2000).
In the first chapter of this thesis the possible applications of TMS in the field of cognition, physiology and rehabilitation are discussed. Specifically, the first part focuses on the operating mechanisms of TMS and on the different stimulation parameters that define the effects of the stimulation. In the second part of the first chapter, the three main TMS protocols are discussed: single-pulse TMS, which is used in the temporal and spatial characterization of cognitive processes, in the study of motor cortex reactivity, and in the investigation of the cortico-spinal tract functioning; paired-pulse TMS, that investigates the connectivity and the interaction of cerebral networks at rest or during a task performance; and repetitive TMS (rTMS), that explores the cerebral plasticity processes both in relation to cognitive processing and for rehabilitation treatments.


CHAPTER II – THE SIMULTANEOUS USE OF TRANSCRANIAL MAGNETIC STIMULATION WITH EEG AND OTHER NEUROIMAGING TECHNIQUES
Despite the widespread use of TMS in current research, its mechanism of action is still poorly understood (Miniussi et al., 2010). This lack in comprehension results from missing a firsthand “visible” marker of cortical response and a need for secondary measures of primary motor and visual cortex stimulation. In the last twenty years, thanks to the progressive improvements in neuroimaging technology, the first attempts to simultaneously use TMS with other neuroimaging techniques have been made possible (e.g. TMS-EEG, Ilmoniemi et al., 1997; TMS-PET, Paus et al., 1997). On one hand, the possibility to actively stimulate the brain with TMS allows to establish “causal” inferences in neuroimaging studies, in which, traditionally, only “correlational” inferences were possible. On the other hand, neuroimaging techniques potentially provide an important contribution through the spatial and temporal information of the neural activation evoked by TMS.
In the second chapter of this thesis, the strong and the weak points of different TMS-neuroimaging coregistration approaches are depicted. Specifically, the middle part of the chapter focuses on the main topic of this thesis, i.e. the TMS-EEG coregistration. TMS-EEG, among the different approaches, is the most successful and widespread, thanks to its promising value in the investigation of brain dynamics. Indeed, EEG is able to record the post-synaptic potentials following the neuronal depolarization evoked by TMS at a high temporal resolution (Ilmoniemi et al., 1997). The analysis of the TMS-evoked EEG activity in terms of time, space, frequency and power, potentially provides important and accurate information in the local activation induced by the stimulation (cerebral reactivity), in the spread of such activation (cerebral connectivity), and in the long-lasting neuromodulatory effects following rTMS protocols (cerebral plasticity).
On the other hand, the TMS-EEG coregistration, presents several technical difficulties mainly due to the different artefacts that electromagnetic stimulation induces in the EEG signal. These aspects are discussed thoroughly in the second chapter. Finally, the last part of the second chapter is dedicated to the other TMS coregistration approaches with magnetic resonance imaging (MRI), functional magnetic resonance imaging (fMRI), positron emission tomography (PET), single-photon emission computed tomography (SPECT) and near-infrared spectroscopy (NIRS).


CHAPTER III – STUDY 1: NEUROMODULATORY EFFECTS OF LOW-FREQUENCY RTMS: INSIGHTS FROM TMS-EEG
The neuromodulatory effects of rTMS have been mostly investigated by means of peripheral motor-evoked potentials (MEPs). However, MEPs are an indirect measure of cortical excitability, also being affected by spinal excitability. The development of new TMS-compatible EEG systems allowed the direct investigation of the stimulation effects through the cortical responses evoked by TMS (TEPs). In this study, we investigated the effects of a repetitive TMS (rTMS) protocol delivered at low frequency (1 Hz), which is known to produce an inhibitory effect on cortical excitability (Chen et al., 1997). The protocol was applied over the primary motor cortex of 15 healthy volunteers and, as a control, over the primary visual cortex of 15 different healthy volunteers to examine the spatial specificity of the stimulation. The effects of the stimulation were analyzed in both groups through the single-pulse stimulation of the primary motor cortex, before and immediately after the rTMS protocol. Different measures were tested: MEPs, TEPs, local mean field power and scalp maps of the activity distribution.
Results on MEPs amplitude showed a significant reduction following the rTMS over the primary motor cortex. Results on TEPs, showed a well-known TEPs pattern evoked by single-pulse stimulation of the motor cortex: P30, N45, P60 and N100. Following the motor cortex rTMS, we observed a significant increase of P60 and N100 amplitude, whose origin has been linked to the GABAb-mediated inhibitory post-synaptic potentials (Ferreri et al., 2011; Premoli et al, 2014). Results on LMFP, showed an increase of general activity induced by the single-pulse stimulation of the motor cortex, starting from 90 ms after the TMS pulse. This latency actually corresponds to the peak of GABAb inhibition. No significant effects were detected after rTMS of the primary visual cortex.
The results of this study are relevant in three main aspects: (1) we confirmed the inhibitory effect of 1-hz rTMS, also providing a central correlate of such effect (TEPs); (2) we defined the spatial specificity and the origin of the inhibitory effect of 1-Hz rTMS; (3) we confirmed the possible role of the TMS-evoked N100 as a cortical inhibitory marker. The present findings could be of relevance both for therapeutic purposes, especially for pathologies characterized by inhibitory deficits (e.g. Parkinson’s disease; Huntington’s disease); and for basic research, especially in studies aimed to correlate a behavioral performance to the amount of cerebral excitability.


CHAPTER IV – STUDY 2: TMS-EEG MARKERS OF INHIBITORY DEFICIT IN HUNTINGTON’S DISEASE
Recent studies have shown the potential value of combining TMS and EEG for clinical and diagnostic purposes. Several TMS-EEG measures in terms of evoked potentials (i.e. TEPs), brain sources analysis, oscillatory activity and global power has been used in the assessment of brain dynamics deficits in several pathologies, such as: schizophrenia (Ferrarelli et al., 2008); psychotic disorders (Hoppenbrouwers et al., 2008); depression (Kähkönen et al., 2005); awareness disorders (Massimini et al., 2005); epilepsy (Rotenborg et al., 2008) and autism (Sokhadze et al., 2012). For instance, the potential contribution of TEPs in the investigation of the cerebral facilitatory/inhibitory balance has been demonstrated, given their origin from different GABAergic neuronal populations (Ferreri et al., 2011; Premoli et al., 2014). In particular, the TMS-evoked N100 has been related to the amount of GABAergic inhibition, as shown by pharmacological (e.g. Kähkönen et al., 2003) and behavioral research (e.g. Bender et al., 2005; Bonnard et al., 2009) as well as studies in patients (e.g. Helfrich et al., 2013).
As a part of the multi-site international “TrackOnHD” project, we used TMS-EEG to investigate the electrophysiological markers of motor cortex stimulation in Huntington patients. In Huntington’s disease (HD) the progressive degeneration of GABAergic neurons in the striatum lead to a strong reduction of inhibition, resulting in an excessive increase in glutamatergic excitability (i.e. excitoxicity). Our study compared a group of 12 HD patients with a group of 12 healthy volunteers over several different TMS-EEG, EMG, fMRI and clinical measures (in the chapter only the TMS-EEG results are reported).
We found a specific and significant decrease of the N100 as assessed by the time point-by-time point permutation analysis of TEPs and from the analysis of the global activity from 90 to 104 ms after the TMS pulse. Scalp maps of the activity distribution showed a bilateral decrease of negativity, such effect was stronger over the site of stimulation. Event-related spectral perturbation and inter-trial coherence analysis showed a significant difference in the oscillatory activity of the two groups within the GABAb-ergic time window (i.e. 60-110 ms after the TMS pulse). We speculated that the observed results might be produced by the deficit in GABAergic inhibition as a consequence of the striatum neuronal degeneration in HD patients. Although preliminary, these results provided potentially useful TMS-EEG markers for inhibitory deficits in HD patients. Further analyses are needed to correlate the present findings with the other measures collected.


CHAPTER V – STUDY 3: TMS-EEG ARTIFACTS: A NEW ADAPTIVE ALGORITHM FOR SIGNAL DETRENDING
During EEG recording the discharge of the TMS coil may generate an artefact that can last for tens of milliseconds, known as “decay artefact” (Rogasch et al., 2014). This can represent a problem for the analysis of the TMS-evoked potentials (TEPs). So far, two main strategies of correction have been proposed involving the use of a linear detrend or independent component analysis (ICA). However, none of these solutions may be considered optimal: firstly, because in most of the cases the decay artefact shows a non-linear trend; secondly, because the ICA correction (1) might be influenced by individual researcher’s choices and (2) might cause the removal of physiological responses.
Our aim is to verify the feasibility of a new adaptive detrend able to discriminate the different trends of the decay (linear or non-linear). Forty healthy volunteers were stimulated with 55 TMS pulses over the left M1. The TMS-EEG responses were compared among five conditions: RAW (no correction of the decay artefact was applied); INFOMAX29 (the decay components were extracted and removed by the INFOMAX ICA algorithm, using 31 electrodes); FASTICA (the decay components were extracted and removed by the fastICA ICA algorithm, using 31 electrodes); INFOMAX15 (the decay components were extracted and removed by the INFOMAX ICA algorithm, using 15 electrodes) and ALG (the decay artefact was corrected through the use of an adaptive algorithm). To assess whether the artefact correction significantly affected the physiological responses to TMS as well, we examined the differences in the -100 + 400 ms time window around the TMS pulse by means of a non-parametric, cluster-based, permutation statistical test. Then we compared the peak-to-peak TEPs amplitude within the detected time windows. The grand-averaged EEG response revealed five main peaks: P30, N45, P60, N100 and P180. Significant differences (i.e. Monte Carlo p-values < 0.05) were detected in a cluster nearby the TMS coil, and specifically over FC1, CP1, C3 and FC2. Repeated-measures ANOVA revealed a significant corruption of the peak-to-peak amplitude after INFOMAX29 (3 TEPs out of 8), FASTICA (4 TEPs out of 12), INFOMAX15 (5 TEPs out of 15) and ALG correction (2 TEPs out of 15), compared to the original signal. Furthermore, abnormal LMFP and TEPs scalp distribution were detected following the INFOMAX29 and FASTICA correction. When our algorithm was used, however, the TEPs amplitude, morphology and distribution was in line with the literature and not significantly different from the original signal. Also the decay artefact was correctly removed.
The main contribution of this study is the proposal of a new adaptive algorithm to correct the decay artefact induced by TMS in the EEG signal. Our results demonstrated that the proposed adaptive detrend is a reliable solution for the correction of this artefact, especially considering that, contrary to ICA, (1) it is not dependent from the number of recording channels; (2) it does not affect the physiological responses and (3) it is completely independent from the experimenter’s choices.

Abstract (italiano)

La presente tesi si compone di due parti principali: una teorica e una sperimentale. La prima parte, suddivisa in due capitoli, è un approfondimento teorico sullo strumento stimolazione magnetica transcranica (TMS) e sul suo utilizzo simultaneo (ossia, in coregistrazione) con le tecniche di neuroimaging. La seconda parte comprende alcuni degli studi condotti durante il mio dottorato. Nello specifico, si tratta di tre studi che coprono i diversi aspetti applicativi delle ricerche che ho condotto in questi tre anni, ossia lo studio e l’utilizzo della coregistrazione TMS-EEG in ricerca (studio 1), in ambito clinico (studio 2) e per aspetti tecnico-metodologici (studio 3). Il primo studio (studio 1), condotto nel Dipartimento di Psicologia Generale di Padova, era volto all’analisi degli effetti neuromodulatori di un protocollo rTMS su volontari sani. Il secondo studio (study 2) è stato condotto all’Istituto di Neurologia dello University College London (Londra, Regno Unito) all’interno del progetto internazionale “TrackOnHD”, uno studio longitudinale avente come obiettivo l'indagine approfondita della Malattia di Huntington (HD) attraverso un approccio multimodale. L’obiettivo di questo studio era la ricerca di potenziali marker TMS-EEG che riflettessero il deficit di inibizione cerebrale che caratterizza questa patologia. Il terzo studio (study 3), svolto in collaborazione col Dipartimento di Ingegneria dell’Informazione di Padova, aveva l’obiettivo di sviluppare un algoritmo di correzione in grado di rimuovere un artefatto indotto dalla TMS durante la registrazione EEG.


CAPITOLO I - LA STIMOLAZIONE MAGNETICA TRANSCRANICA (TMS)
Negli ultimi anni lo sviluppo di nuove tecniche in grado di analizzare l’attivazione cerebrale durante processi cognitivi e motori, ha portato ad un avanzamento progressivo delle conoscenze sul cervello umano. La stimolazione magnetica transcranica (TMS) è stata uno degli strumenti la cui popolarità è cresciuta in questi ultimi anni, grazie alla possibilità di stimolare, in modo focale e non invasivo, il cervello in vivo (Barker et al., 1985). Tale capacità ha consentito, per la prima volta, la straordinaria possibilità di inferire delle relazioni causali tra cervello, processi cognitivi e motori, e comportamento (Pascual-Leone et al., 2000).
Nel primo capitolo della presente tesi vengono passate in rassegna tutte le possibili applicazioni della TMS in campo cognitivo, fisiologico e riabilitativo. Nello specifico, la prima parte è dedicata ai meccanismi di funzionamento della TMS e ai parametri di stimolazione che ne definiscono i diversi effetti sul cervello. Nella seconda parte vengono invece passati in rassegna i tre principali protocolli di stimolazione: la TMS a singolo impulso, utilizzata per la caratterizzazione spaziale e temporale dei processi cognitivi, per analizzare la reattività della corteccia motoria primaria, e per verificare l’integrità del tratto cortico-spinale; la TMS a doppio impulso, per studiare la connettività e l’interazione di network cerebrali a riposo e durante lo svolgimento di un task; e la TMS ripetitiva (rTMS), utilizzata per analizzare i fenomeni di plasticità cerebrale sia durante processi cognitivi, sia in relazione a trattamenti riabilitativi.


CAPITOLO II - L’UTILIZZO SIMULTANEO DELLA TMS CON L’EEG ED ALTRE TECNICHE DI NEUROIMAGING
Nonostante la grande popolarità che la TMS ha conosciuto negli ultimi anni, molti aspetti del suo meccanismo d’azione sono ancora poco chiari (Miniussi et al., 2010). Tale ambiguità è dovuta al fatto che, fatta eccezione per la corteccia motoria e visiva primaria, la stimolazione TMS non fornisce dei marker “visibili” di eccitabilità corticale. Negli ultimi anni, grazie al miglioramento tecnologico degli strumenti di indagine neuroscientifica, si è iniziato a utilizzare simultaneamente (in coregistrazione) la TMS con diverse tecniche di neuroimaging. Ciò ha consentito di trarre delle inferenze di tipo “causale” e non più solo “correlazionale” (come nei tradizionali studi di neuroimaging) grazie alle informazioni spaziali e temporali sull’effetto della TMS che le tecniche di neuroimaging offrono.
Nel secondo capitolo della presente tesi, vengono trattati dettagliatamente le potenzialità e i limiti delle diverse coregistrazioni TMS-neuroimaging. In particolare, nella parte centrale del capitolo è dato ampio spazio all’argomento centrale di questa tesi, ossia la coregistrazione TMS-EEG. L’approccio TMS-EEG, tra i vari metodi di coregistrazione, è stato quelli che negli ultimi anni ha riscontrato maggiore successo e diffusione, dovuto all’enorme potenzialità che questo metodo garantisce nello studio delle dinamiche cerebrali. L’EEG, infatti, è in grado di registrare, ad altissima risoluzione temporale, i potenziali post-sinaptici indotti dalla depolarizzazione neuronale evocata dalla TMS (Ilmoniemi et al., 1997). L’analisi dell’attività EEG indotta dalla TMS - in termini di tempo, spazio, frequenza e potenza - è in grado di fornire delle preziose informazioni sia sull’attivazione locale indotta dalla stimolazione (reattività cerebrale), sia su quella distale (connettività cerebrale), sia sulle modificazioni a seguito di protocolli di stimolazione ripetitiva (plasticità cerebrale).
D’altra parte, la coregistrazione TMS-EEG presenta numerose difficoltà di tipo tecnico, dovuto ai numerosi artefatti che la stimolazione elettromagnetica induce sul segnale EEG (così come sui segnali delle altre tecniche di neuroimaging), questi aspetti sono trattati in maniera dettagliata all’interno del capitolo. Infine, l’ultima parte del capitolo è dedicata agli altri metodi di coregistrazione TMS con risonanza magnetica (MRI), risonanza magnetica funzionale (fMRI), tomografia a emissione di positroni (PET), tomografia a emissione di fotone singolo (SPECT) e spettroscopia del vicino infrarosso (NIRS).


CAPITOLO III – STUDIO 1: EFFETTI NEUROMODULATORI DELLA RTMS A BASSA FREQUENZA: EVIDENZE DALL’APPROCCIO TMS-EEG
Tradizionalmente gli effetti neuromodulatori della rTMS sono stati studiati attraverso l’analisi dei potenziali motori evocati (MEP). Tuttavia, come noto, i MEP sono una misura indiretta dell’eccitabilità corticale avendo una forte componente anche spinale. Con lo sviluppo di nuovi sistemi EEG compatibili con la TMS, è stato possibile analizzare gli effetti della stimolazione in modo più diretto, tramite l’analisi dei potenziali corticali evocati dalla TMS (TEPs). In questo studio abbiamo analizzato l’effetto di un protocollo di TMS ripetitiva (rTMS) a bassa frequenza (1 Hz) molto noto, soprattutto in ambito riabilitativo, per sortire un effetto di inibizione dell’eccitabilità corticale. Il protocollo è stato applicato sulla corteccia motoria primaria di quindici volontari sani e sulla corteccia visiva primaria di altri quindici volontari sani, assunti come gruppo di controllo per analizzare la specificità spaziale della stimolazione. Gli effetti della stimolazione ripetitiva sono stati testati su diverse misure elettrofisiologiche evocate da una stimolazione a singolo impulso della corteccia motoria, prima e subito dopo il protocollo rTMS, ossia: MEP, TEPs, local mean field power (LMFP) e distribuzione dell’attività sullo scalpo.
I risultati sui MEP hanno mostrato una diminuzione significativa dell’ampiezza a seguito del protocollo rTMS sulla corteccia motoria. I risultati sui TEP hanno mostrato un pattern noto composto di quattro principali picchi: P30, N45, P60 e N100. A seguito del protocollo rTMS sulla corteccia motoria si è osservato un incremento significato dell’ampiezza dei TEP P60 e N100, la cui origine è legata all’attività dei potenziali post-sinaptici inibitori GABAb (Ferreri et al., 2011; Premoli et al., 2014). I risultati sul LMFP hanno mostrato un incremento di attività generale indotta dalla TMS sulla corteccia motoria a partire da circa 90 ms dalla stimolazione, ossia la latenza del picco massimo di inibizione GABAb. A seguito del protocollo di stimolazione di controllo, applicato sulla corteccia visiva, non si è riscontrato nessun cambiamento significativo.
I risultati di questo studio hanno una rilevanza su tre aspetti: (1) si è confermato l’effetto inibitorio del protocollo rTMS a 1-Hz, offrendo anche un correlato centrale di inibizione (TEPs) oltre che periferico (MEPs); (2) sono state definite la spazialità e l’origine dell’inibizione indotta dalla rTMS a bassa frequenza; (3) la N100 evocata dalla TMS si conferma essere un marker affidabile del grado di inibizione corticale. I risultati di questo studio potrebbero avere una rilevanza sia in campo terapeutico e riabilitativo, specie per i disturbi alla cui base si suppone vi sia un deficit di inibizione corticale (ad es. malattia di Parkinson, malattia di Huntington); sia in campo di ricerca, specie in studi in cui si vogliano correlare performance a task cognitivi o motori con il grado di eccitazione/inibizione corticale.


CAPITOLO IV – STUDIO 2: DEFICIT DI INIBIZIONE NELLA MALATTIA DI HUNTIGTON: EVIDENZE DALLA COREGISTRAZIONE TMS-EEG
Evidenze recenti hanno mostrato le potenzialità dell’utilizzo della coregistrazione TMS-EEG in ambito clinico e diagnostico. Diverse misure TMS-EEG in termini di potenziali evocati (TEPs), analisi di sorgenti, attività oscillatoria e potenza dell’attività globale, sono state utilizzate per lo studio di dinamiche cerebrali deficitarie in diverse patologie, come: schizofrenia (Ferrarelli et al., 2008); disordini psicotici (Hoppenbrouwers et al., 2008); depressione (Kähkönen et al., 2005); disturbi di coscienza (Massimini et al., 2005); epilessia (Rotenborg et al., 2008) e autismo (Sokhadze et al., 2012). Ad esempio, diverse evidenze hanno mostrato il potenziale contributo dei TEPs nello studio degli equilibri eccitatori/inibitori corticali, data la loro origine GABAergica (Ferreri et al., 2011; Premoli et al., 2014). In particolare, la N100 TMS-evocata sembra essere strettamente correlata al grado di inibizione GABAergica, come mostrato da evidenze a carattere farmacologico (ad es. Kähkönen et al., 2003; Premoli et al., 2014); studi comportamentali (ad es. Bender et al., 2005; Bonnard et al., 2009) e studi in pazienti (ad es. Helfrich et al., 2013).
Nel presente studio, facente parte di un ampio progetto internazionale multicentrico (“TrackOnHD”), abbiamo utilizzato la coregistrazione TMS-EEG per analizzare dei possibili marker elettrofisiologici della malattia di Huntington, tramite stimolazione della corteccia motoria primaria. La malattia di Huntington (HD) è caratterizzata da una progressiva degenerazione dei neuroni striatali di natura GABAergica. Tale degenerazione porta a un eccessivo incremento del tono eccitatorio mediato dal glutammato, un fenomeno noto come eccitossicità. Nel presente studio sono stati analizzati dodici pazienti HD e dodici volontari sani su varie misure TMS-EEG, EMG, fMRI e cliniche (nel capitolo sono riportati solo i risultati relativi alle misure TMS-EEG).
I risultati hanno mostrato una riduzione significativa e specifica della N100, come rilevato dall’analisi dei TEP per permutazioni punto-per-punto e dall’analisi dell’attività media globale da 94 a 104 ms dopo l’impulso TMS. Le mappe dello scalpo della distribuzione dell’attività hanno mostrato una riduzione della negatività su entrambi gli emisferi, con un effetto maggiore sul sito di stimolazione. Le analisi di perturbazione dello spettro evento-relata e della coerenza inter-trial hanno mostrato una differenza significativa nell’attività oscillatoria dei due gruppi all’interno della finestra di interesse GABAb-ergico (60-110 ms dopo l’impulso TMS). I risultati osservati potrebbero essere prodotti dal deficit di inibizione GABAergica nei pazienti HD conseguente alla degenerazione neuronale nello striato. Anche se preliminari, i risultati dello studio hanno rilevato dei marker TMS-EEG potenzialmente d’interesse per la valutazione dei deficit inibitori in pazienti HD. Ulteriori analisi sono necessarie per correlare i risultati ottenuti con le altre misure raccolte all’interno del progetto.


CAPITOLO V – STUDIO 3: ARTEFATTI TMS-EEG: UN NUOVO ALGORITMO ADATTATIVO PER IL DETREND DEL SEGNALE
Durante un EEG, la stimolazione TMS può generare un artefatto a lunga latenza, noto come artefatto “decay”. Tale artefatto rappresenta un problema per l’analisi dei potenziali evocati dalla TMS (TEP). In letteratura, per risolvere il problema, sono comunemente utilizzate due principali strategie: l’utilizzo di un detrend lineare e l’utilizzo dell’independent component analysis (ICA). Tuttavia, nessuna di queste soluzioni può essere considerata ottimale. Per quanto riguarda l’utilizzo di un detrend lineare, dal momento che nella maggior parte dei casi l’artefatto decay non segue un andamento lineare, questo tipo di correzione risulta inefficiente. Per quanto invece riguarda l’ICA, anche questa procedura presenta dei limiti intrinseci: (1) può essere eccessivamente influenzato dalle scelte dello sperimentatore e (2) può causare la rimozione di componenti fisiologiche, oltre che artefattuali.
Il nostro obiettivo è di verificare l’efficienza di un nuovo detrend adattivo, sviluppato su MATLAB, in collaborazione col dipartimento di Ingegneria Informatica di Padova, capace di discriminare i diversi trend dell’artefatto decay (ossia lineare e non-lineare). Quaranta volontari sani sono stati stimolati con 55 impulsi TMS singoli sulla corteccia motoria primaria di sinistra. Le risposte EEG indotte dalla TMS sono state analizzate in cinque condizioni: RAW (in cui non veniva applicata nessuna correzione dell’artefatto decay); INFOMAX29 (in cui l’artefatto decay veniva corretto con un algoritmo ICA-INFOMAX, considerando tutti i 29 canali); FASTICA (in cui l’artefatto decay veniva corretto con un algoritmo fastICA, considerando tutti i 29 canali); INFOMAX15 (in cui l’artefatto decay veniva corretto con un algoritmo ICA-INFOMAX, considerando solo 15 canali) e ALG (in cui l’artefatto decay veniva corretto tramite il nostro algoritmo adattivo). Per verificare se la correzione dell’artefatto avesse influenzato anche i TEP, sono state analizzare le differenze in una finestra temporale da -100 a +400 ms dall’impulso TMS attraverso l’utilizzo di un test per permutazioni, non-parametrico e corretto per cluster. Successivamente, sono state comparate le ampiezze e le latenze picco-picco dei TEP all’interno delle finestre temporali negli elettrodi risultati significativi. La risposta grand-average ha rilevato cinque picchi principali: P30, N45, P60, N100 e P180. Sono state rilevate delle differenze significative (i.e. Monte Carlo p < 0.05) in un cluster di elettrodi vicino alla stimolazione, comprendente i canali FC1, CP1, C3 e FC2. Le analisi sull’ampiezza picco-picco hanno rilevato una significativa modulazione dell’ampiezza dopo la correzione INFOMAX29 (in 3 TEP su 8), FASTICA (in 4 TEP su 12), INFOMAX15 (in 5 TEP su 15) e ALG (in 2 TEP su 15), rispetto al segnale RAW originale. I risultati LMFP e delle mappe di distribuzione sullo scalpo hanno rilevato diverse anomalie a seguito della correzione INFOMAX29 e FASTICA.
I risultati hanno mostrato che la correzione ICA modifica in modo significativo l’ampiezza, la morfologia e la distribuzione di una parte dei TEP analizzati e nello stesso tempo non garantisce una completa rimozione dell’artefatto decay. Al contrario, a seguito della correzione col nostro algoritmo (condizione ALG), l’ampiezza, la morfologia e la distribuzione dei TEP rimanevano fedeli a quella originale, con una rimozione pressoché completa dell’artefatto decay. Il principale contributo di questo studio è stato la proposta di un nuovo algoritmo di correzione per un artefatto a lunga latenza che la TMS induce sul segnale EEG (artefatto decay) rendendo difficoltosa l’analisi. I risultati hanno dimostrato che questo metodo è più efficiente delle strategie attualmente in utilizzo in letteratura, non avendo i limiti intrinseci presentati dall’algoritmo ICA.

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Tipo di EPrint:Tesi di dottorato
Relatore:Bisiacchi, Patrizia Silvia
Dottorato (corsi e scuole):Ciclo 27 > scuole 27 > SCIENZE PSICOLOGICHE
Data di deposito della tesi:30 Gennaio 2015
Anno di Pubblicazione:30 Gennaio 2015
Parole chiave (italiano / inglese):TMS EEG coregistration plasticity connectivity reactivity
Settori scientifico-disciplinari MIUR:Area 11 - Scienze storiche, filosofiche, pedagogiche e psicologiche > M-PSI/02 Psicobiologia e psicologia fisiologica
Struttura di riferimento:Dipartimenti > Dipartimento di Psicologia Generale
Codice ID:7848
Depositato il:13 Nov 2015 09:05
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