RESUMEN

Background: Small pilot studies have suggested that transcranial photobiomodulation (tPBM) could help reduce symptoms of neurological conditions, such as depression, traumatic brain injury, and autism spectrum disorder (ASD). Objective: To examine the impact of tPBM on the symptoms of ASD in children aged two to six years. Method: We conducted a randomized, sham-controlled clinical trial involving thirty children aged two to six years with a prior diagnosis of ASD. We delivered pulses of near-infrared light (40 Hz, 850 nm) noninvasively to selected brain areas twice a week for eight weeks, using an investigational medical device designed for this purpose (Cognilum™, JelikaLite Corp., New York, United States). We used the Childhood Autism Rating Scale (CARS, 2nd Edition) to assess and compare the ASD symptoms of participants before and after the treatment course. We collected electroencephalogram (EEG) data during each session from those participants who tolerated wearing the EEG cap. Results: The difference in the change in CARS scores between the two groups was 7.23 (95% CI 2.357 to 12.107, p = 0.011). Seventeen of the thirty participants completed at least two EEGs and time-dependent trends were detected. In addition, an interaction between Active versus Sham and Scaled Time was observed in delta power (Coefficient = 7.521, 95% CI -0.517 to 15.559, p = 0.07) and theta power (Coefficient = -8.287, 95% CI -17.199 to 0.626, p = 0.07), indicating a potential trend towards a greater reduction in delta power and an increase in theta power over time with treatment in the Active group, compared to the Sham group. Furthermore, there was a significant difference in the condition (Treatment vs. Sham) in the power of theta waves (net_theta) (Coefficient = 9.547, 95% CI 0.027 to 19.067, p = 0.049). No moderate or severe side effects or adverse effects were reported or observed during the trial. Conclusion: These results indicate that tPBM may be a safe and effective treatment for ASD and should be studied in more depth in larger studies.Clinical trial registration: https://clinicaltrials.gov/ct2/show/NCT04660552, identifier NCT04660552.

RESUMEN

AIM: Many biophysical and non-biophysical models have been able to reproduce the corticothalamic activities underlying different EEG sleep rhythms but none of them included the known ability of neocortical networks and single thalamic neurons to generate some of these waves intrinsically. METHODS: We built a large-scale corticothalamic model with a high fidelity in anatomical connectivity consisting of a single cortical column and first- and higher-order thalamic nuclei. The model is constrained by different neocortical excitatory and inhibitory neuronal populations eliciting slow (<1 Hz) oscillations and by thalamic neurons generating sleep waves when isolated from the neocortex. RESULTS: Our model faithfully reproduces all EEG sleep waves and the transition from a desynchronized EEG to spindles, slow (<1 Hz) oscillations, and delta waves by progressively increasing neuronal membrane hyperpolarization as it occurs in the intact brain. Moreover, our model shows that slow (<1 Hz) waves most often start in a small assembly of thalamocortical neurons though they can also originate in cortical layer 5. Moreover, the input of thalamocortical neurons increases the frequency of EEG slow (<1 Hz) waves compared to those generated by isolated cortical networks. CONCLUSION: Our simulations challenge current mechanistic understanding of the temporal dynamics of sleep wave generation and suggest testable predictions.

Asunto(s)

RESUMEN

Sleep is known to promote recovery post-stroke. However, there is a paucity of data profiling sleep oscillations in the post-stroke human brain. Recent rodent work showed that resurgence of physiologic spindles coupled to sleep slow oscillations (SOs) and concomitant decrease in pathological delta (δ) waves is associated with sustained motor performance gains during stroke recovery. The goal of this study was to evaluate bilaterality of non-rapid eye movement (NREM) sleep-oscillations (namely SOs, δ-waves, spindles, and their nesting) in post-stroke patients vs. healthy control subjects. We analyzed NREM-marked electroencephalography (EEG) data in hospitalized stroke-patients (n = 5) and healthy subjects (n = 3). We used a laterality index to evaluate symmetry of NREM oscillations across hemispheres. We found that stroke subjects had pronounced asymmetry in the oscillations, with a predominance of SOs, δ-waves, spindles, and nested spindles in affected hemisphere, when compared to the healthy subjects. Recent preclinical work classified SO-nested spindles as restorative post-stroke and δ-wave-nested spindles as pathological. We found that the ratio of SO-nested spindles laterality index to δ-wave-nested spindles laterality index was lower in stroke subjects. Using linear mixed models (which included random effects of concurrent pharmacologic drugs), we found large and medium effect size for δ-wave nested spindle and SO-nested spindle, respectively. Our results in this pilot study indicate that considering laterality index of NREM oscillations might be a useful metric for assessing recovery post-stroke and that factoring in pharmacologic drugs may be important when targeting sleep modulation for neurorehabilitation post-stroke.

RESUMEN

Memory consolidation related to the hippocampal-cortex connection takes place during sleep. This connection may involve at least two steps- one in the NREM phase of sleep (transmission) and the other in the REM phase (consolidation). In this brief report, we comment on the role of tau protein in these two phases of sleep. The absence of tau decreases δ waves in NREM, whereas the overexpression of modified (phosphorylated and/or mutated) tau alters θ waves in REM.

Asunto(s)

RESUMEN

INTRODUCTION: The purpose of this study is to determine if delta waves, measured by magnetoencephalography (MEG), increase in adolescents due to a sports concussion. METHODS: Twenty-four adolescents (age 14-17) completed pre- and postseason MRI and MEG scanning. MEG whole-brain delta power was calculated for each subject and normalized by the subject's total power. In eight high school football players diagnosed with a concussion during the season (mean age = 15.8), preseason delta power was subtracted from their postseason scan. In eight high school football players without a concussion (mean age = 15.7), preseason delta power was subtracted from postseason delta power and in eight age-matched noncontact controls (mean age = 15.9), baseline delta power was subtracted from a 4-month follow-up scan. ANOVA was used to compare the mean differences between preseason and postseason scans for the three groups of players, with pairwise comparisons based on Student's t-test method. RESULTS: Players with concussions had significantly increased delta wave power at their postseason scans than nonconcussed players (p = .018) and controls (p = .027). CONCLUSION: We demonstrate that a single concussion during the season in adolescent subjects can increase MEG measured delta frequency power at their postseason scan. This adds to the growing body of literature indicating increased delta power following a concussion.

Asunto(s)

RESUMEN

Sleep is vital and the deepest stages of sleep occur within Non-rapid-eye-movement sleep (NREM), defined by high electroencephalographic power in the delta (~0.5-4 Hz) wave frequency range. Delta waves are thought to facilitate a myriad of physical and mental health functions. This review aims to comprehensively cover the historical and recent advances in the understanding of the mechanisms orchestrating NREM delta waves. We discuss a complete neurocircuit - focusing on one leg of the circuit at a time - and delve deeply into the molecular mechanistic components that contribute to NREM delta wave regulation. We also discuss the relatively localized nature in which these mechanisms have been defined, and how likely they might generalize across distinct sensory and higher order modalities in the brain.

Asunto(s)

RESUMEN

OBJECTIVE: To evaluate the parameters of the electroencephalogram (EEG) using the methods of computer processing of EEG data for an approach to the analysis of possible neurophysiological mechanisms underlying the fluctuations detected in the EEG in patients in the somatogenic phase of acute poisoning with opioid receptor agonists. MATERIAL AND METHODS: Thirty-one patients were examined in the somatogenic phase of acute poisoning with opioid receptor agonists with a wakefulness level 3 to 15 points on the Glasgow Coma Scale. The EEG was recorded in accordance with the recommendations of the International Federation of Clinical Neurophysiology. The indicators of electrical activity of the brain were analyzed; computer processing of EEG data, including spectral analysis, localization of equivalent dipole sources of pathological electrical activity of the brain localization of the maximum of the equivalent density of EEG oscillation currents in the neocortex, was performed. RESULTS: Delta-band oscillations dominated in the majority of patients (65%, 20 patients). EEG delta waves were localized mainly at the level of the thalamus; using the method of low-resolution electromagnetic tomography, the localization of the maximum of the equivalent current density of delta oscillations in the projection of the neocortex was noted. Possible neurophysiological mechanisms of «pathological¼ delta waves recorded in the EEG of these patients are discussed. CONCLUSIONS: The changes on the EEG in these patients arise as a result of a disturbance of the function of the generator mechanisms of both cortical and activating structures of the brain, while the recorded slow-wave, mainly delta activity, taking into account the recording time (somatogenic phase), may be due to the action of secondary alternating factors (hypoxia and cerebral edema).

Asunto(s)

RESUMEN

IQSEC2 is an X-linked gene localized to the post synaptic density encoding a GTP exchange factor that regulates NMDA mediated changes in synaptic function. Mutations in the IQSEC2 gene are associated with drug resistant epilepsy, intellectual disability and autism. Precision medicine based therapeutics to treat IQSEC2 associated epilepsy requires the development and characterization of mutation specific animal models. To date no EEG recordings have been presented for any mouse model of any IQSEC2 mutation showing seizures. In this study we characterize the seizures and EEG brain wave abnormalities present in mice with a A350V IQSEC2 missense mutation that is associated with drug resistant epilepsy in man. We show that seizures are associated with a greater than 40% mortality rate in male mice and occur exclusively from post-natal day 16-20. EEG recordings of mouse pups during this window demonstrate seizures and the presence of spikes with a marked increase in delta waves. EEG recordings in adult male mice have persistent excessive slow frequency activity and spikes, but seizures were not recorded. RNAseq analysis of the hippocampi of mice prior to the development of seizures demonstrated marked abnormalities in canonical pathways involved in synaptogenesis and dendritic maturation with the most prominently dysregulated gene being that for TRH suggesting a potential target for therapy given the previous demonstration of TRH to decrease seizures in several forms of drug resistant epilepsy.

Asunto(s)

RESUMEN

Sleep is known to promote recovery after stroke. Yet it remains unclear how stroke affects neural processing during sleep. Using an experimental stroke model in rats along with electrophysiological monitoring of neural firing and sleep microarchitecture, here we show that sleep processing is altered by stroke. We find that the precise coupling of spindles to global slow oscillations (SOs), a phenomenon that is known to be important for memory consolidation, is disrupted by a pathological increase in "isolated" local delta waves. The transition from this pathological to a physiological state-with increased spindle coupling to SO-is associated with sustained performance gains during recovery. Interestingly, post-injury sleep could be pushed toward a physiological state via a pharmacological reduction of tonic γ-aminobutyric acid (GABA). Together, our results suggest that sleep processing after stroke is impaired due to an increase in delta waves and that its restoration can be important for recovery.

Asunto(s)

RESUMEN

Theta oscillations are key brain rhythm involved in memory formation, sensorimotor integration, and control of locomotion and behavioral states. Generation and spatiotemporal synchronization of theta oscillations rely on interactions between brain nuclei forming a large neural network, which includes pontine nucleus incertus (NI). Here we identified distinct populations of NI neurons, based on the relationship of their firing to hippocampal waves, with a special focus on theta oscillations, and the direction and type of interaction with the medial septum (MS) in male, urethane-anesthetized rats. By recording NI neuronal firing and hippocampal LFP, we described NI neurons that fire action potentials in a theta phase-independent or theta phase-locked and delta wave-independent or delta wave-locked manner. Among hippocampal activity-independent NI neurons, irregular, slow-firing, and regular, fast-firing cells were observed, while hippocampal oscillation-/wave-locked NI neurons were of a bursting or nonbursting type. By projection-specific optotagging, we revealed that only fast-firing theta phase-independent NI neurons innervate the MS, rarely receiving feedback information. In contrast, the majority of theta-bursting NI neurons were inhibited by MS stimulation, and this effect was mediated by direct GABAergic input. Described NI neuronal populations differ in reciprocal connections with the septohippocampal system, plausibly forming separate neuronal loops. Our results suggest that theta phase-independent NI neurons participate in theta rhythm generation through direct innervation of the MS, while theta-bursting NI neurons further transmit the rhythmic signal received from the MS to stabilize and/or strengthen rhythmic activity in other structures.SIGNIFICANCE STATEMENT The generation and spatiotemporal synchronization of theta oscillations rely on interactions between nuclei forming a large neural network, part of which is the pontine nucleus incertus (NI). Here we describe that within NI there are populations of neurons that can be distinguished based on the relationship of their firing to hippocampal theta oscillations and delta waves. We show that these neuronal populations largely do not have reciprocal connections with the septohippocampal system, but form separate neuronal loops. Our results suggest that medial septum (MS)-projecting, fast-firing, theta phase-independent NI neurons may participate in theta rhythm generation through direct innervation of the MS, while theta-bursting NI neurons may further transmit the rhythmic signal received from the MS to other structures.

Asunto(s)

RESUMEN

For Alzheimer's disease (AD), aging is the main risk factor, but whether cognitive impairments due to aging resemble early AD deficits is not yet defined. When working with mouse models of AD, the situation is just as complicated, because only a few studies track the progression of the disease at different ages, and most ignore how the aging process affects control mice. In this work, we addressed this problem by comparing the aging process of PS2APP (AD) and wild-type (WT) mice at the level of spontaneous brain electrical activity under anesthesia. Using local field potential recordings, obtained with a linear probe that traverses the posterior parietal cortex and the entire hippocampus, we analyzed how multiple electrical parameters are modified by aging in AD and WT mice. With this approach, we highlighted AD specific features that appear in young AD mice prior to plaque deposition or that are delayed at 12 and 16 months of age. Furthermore, we identified aging characteristics present in WT mice but also occurring prematurely in young AD mice. In short, we found that reduction in the relative power of slow oscillations (SO) and Low/High power imbalance are linked to an AD phenotype at its onset. The loss of SO connectivity and cortico-hippocampal coupling between SO and higher frequencies as well as the increase in UP-state and burst durations are found in young AD and old WT mice. We show evidence that the aging process is accelerated by the mutant PS2 itself and discuss such changes in relation to amyloidosis and gliosis.

Asunto(s)

RESUMEN

The effects of acetylcholine on cortical activation were studied in wild-type (WT) mice, compared to knockout (KO) mice depleted of the vesicular acetylcholine transporter (VAChT) gene in the basal forebrain, and knockdown (KD) mice with heterogeneous depletion of VAChT gene in the brain. Cortical activation was assessed by comparing power spectra of local field potentials (LFPs) during activated states of rapid-eye-movement sleep (REM) or walk (WLK), with those during non-activated states of slow-wave sleep (SWS) or awake-immobility (IMM). Activation-induced suppression of delta (1-4 Hz) and beta (13-30 Hz) power in the hippocampus, and delta power in frontal cortex, were reduced in KO and KD mice compared to WT mice. Mean theta frequency was higher in KD than KO mice during WLK and REM, but not different between WT and KO mice. Peak theta (4-12 Hz) and integrated gamma (30-150 Hz) power were not significantly different among mouse groups. However, theta-peak-frequency selected gamma2 (62-100 Hz) power was lower in KO than WT or KD mice during WLK, and theta-peak-frequency selected theta power during REM decreased faster with high theta frequency in KO than WT/ KD mice. Theta power increase during REM compared to WLK was lower in KO and KD mice compared to WT mice. Theta-gamma cross-frequency coherence, a measure of synchronization of gamma with theta phase, was not different among mouse groups. However, during REM, SWS, and IMM, delta-gamma coherence was significantly higher and proximal-distal delta coherence in CA1 was lower in KO than WT/KD mice. We conclude that a deficiency in basal forebrain acetylcholine release not only enhances slow waves and suppresses theta-associated gamma waves during activation, but also increases delta-gamma cross-frequency coherence during nonactivated states, with a possible effect of disrupting cognitive processing during any brain state.

Asunto(s)

RESUMEN

Normal brain function requires an integrated, simultaneous communication between brain regions in a coordinated manner. In our studies on cortical spreading depolarization (CSD) induced electrically in the rat brain while recording electrocorticography (ECoG) and delta wave activity, we found for the first time that CSD suppressed delta wave activity, which began even before the CSD was fully developed. We pursued this observation to determine whether repeated CSD suppressed delta wave activity in rats. CSD was produced by electrical stimulation of the neocortex while recording the development of CSD and changes in the coupling of low-frequency band cross coupling to four typical physiological neuronal activity frequency bands, i.e., 5-7 Hz, 8-12 Hz, 13-30 Hz, and 30-80 Hz. Band-pass filters were applied to achieve the corresponding physiological band signals. Besides the cross-frequency coupling (CFC) analysis, the distribution of delta wave density in time domain was analyzed. We calculated the delta wave density per 30 seconds but represent the density as frequency per minute. A Generalized Linear Models (GLM) was used to carry out the CFC analysis in Matlab. Because delta waves dominated the ECoG recorded, we modeled the higher-frequency amplitude envelope as a function of low-frequency phase using a spline basis. Besides the CFC analysis, we also characterized the distribution of the delta wave density in time domain. Four CFC, Theta, Alpha, Beta, and Gamma were at very small values after CSD, and after about 8 minutes, the CFC recovered to the pre-CSD level. CFC were seen to decrease before a CSD occurred at the higher-frequency bands and tended to decrease quickly. Whether the attenuated CFC by CSD has long-term consequences remains to be determined. Future studies will explore the impact of cortical CSD on CFC with deeper brain structures, including the thalamus and the caudate putamen.

Asunto(s)

RESUMEN

Sleep spindles have been implicated in motor learning in human subjects, but their occurrence, timing in relation to cortical slow oscillations, and relationship to offline gains in motor learning have not been examined in animal models. In this study, we recorded EEG over bilateral primary motor cortex in conjunction with EMG for 24 h following a period of either baseline handling or following rotarod motor learning to monitor sleep. We measured several biophysical properties of sleep spindles and their temporal coupling with cortical slow oscillations (SO, <1 Hz) and cortical delta waves (1-4 Hz). Following motor learning, we found an increase in spindles during an early period of NREM sleep (1-4 h) without changes to biophysical properties such as spindle power, peak frequency and coherence. In this same period of early NREM sleep, both SO and delta power increased after motor learning. Notably, a vast majority of spindles were associated with minimal SO power, but in the subset that were associated with significant SO power (>1 z-score above the population mean), spindle-associated SO power was greater in spindles following motor learning compared to baseline sleep. Also, we did not observe a group-level preferred phase in spindle-SO or spindle-delta coupling. While SO power alone was not predictive of motor performance in early NREM sleep, both spindle density and the difference in the magnitude of the mean resultant vector length of the phase angle for SO-associated spindles, a measure of its coupling precision, were positively correlated with offline change in motor performance. These findings support a role for sleep spindles and their coupling to slow oscillations in motor learning and establish a model in which spindle timing and the brain circuits that support offline plasticity can be mechanistically explored.

Asunto(s)

RESUMEN

Sleep has been implicated in both memory consolidation and forgetting of experiences. However, it is unclear what governs the balance between consolidation and forgetting. Here, we tested how activity-dependent processing during sleep might differentially regulate these two processes. We specifically examined how neural reactivations during non-rapid eye movement (NREM) sleep were causally linked to consolidation versus weakening of the neural correlates of neuroprosthetic skill. Strikingly, we found that slow oscillations (SOs) and delta (δ) waves have dissociable and competing roles in consolidation versus forgetting. By modulating cortical spiking linked to SOs or δ waves using closed-loop optogenetic methods, we could, respectively, weaken or strengthen consolidation and thereby bidirectionally modulate sleep-dependent performance gains. We further found that changes in the temporal coupling of spindles to SOs relative to δ waves could account for such effects. Thus, our results indicate that neural activity driven by SOs and δ waves have competing roles in sleep-dependent memory consolidation.

Asunto(s)

RESUMEN

In spite of the uniform appearance of sleep as a behavior, the sleeping brain does not produce electrical activities in unison. Different types of brain rhythms arise during sleep and vary between layers, areas, or from one functional system to another. Local heterogeneity of such activities, here referred to as local sleep, overturns fundamental tenets of sleep as a globally regulated state. However, little is still known about the neuronal circuits involved and how they can generate their own specifically-tuned sleep patterns. NREM sleep patterns emerge in the brain from interplay of activity between thalamic and cortical networks. Within this fundamental circuitry, it now turns out that the thalamic reticular nucleus (TRN) acts as a key player in local sleep control. This is based on a marked heterogeneity of the TRN in terms of its cellular and synaptic architecture, which leads to a regional diversity of NREM sleep hallmarks, such as sleep spindles, delta waves and slow oscillations. This provides first evidence for a subcortical circuit as a determinant of cortical local sleep features. Here, we review novel cellular and functional insights supporting TRN heterogeneity and how these elements come together to account for local NREM sleep. We also discuss open questions arising from these studies, focusing on mechanisms of sleep regulation and the role of local sleep in brain plasticity and cognitive functions.

RESUMEN

BACKGROUND: The inverse problem solution in the field of ElectroEncephaloGraphy (EEG) analysis has been addressed in the scientific literature for many decades, utilizing either mathematical techniques for measurement fitting or pure ElectroMagnetic (EM) methods involving complex head models for the prediction of the near field. NEW METHOD: A novel radiated EM field estimation analysis scheme is proposed for EEG analysis, based on the determination of a grid of equivalent distributed EM sources with equal magnetic moments, in order to compute the extrapolated far field. A Pattern Search approach is adopted to minimize the Mean Absolute Relative Error between the EM near field created by the source grid and the EM field extracted by the measurements. RESULTS: The application of the method on a subject's brain activity recordings in the context of "Protagoras" mental-auditory experiment demonstrates the capability of the proposed scheme to compare the subject's concentration differences between the limit of present and past versus the limit of present and future. COMPARISON WITH EXISTING METHODS: The proposed method combines features from different existing methods, both in terms of mathematical and EM theory techniques, in order to extend their capabilities and transform the conventional analysis of EEG recordings to a far field radiation basis. CONCLUSIONS: The treatment of the brain as an equivalent far field radiator can be a useful and promising new perspective to the established analysis of EEG recordings arising from brain activity during mental processing.

Asunto(s)

RESUMEN

OBJECTIVE: The P300 component of a sensory event-related potential is one of the major electrophysiological markers used to explore remnants of cognitive function in patients with disorders of consciousness (DoC). However, measuring the P300 in patients is complicated by significant inter-trial variability commonly observed in levels of arousal and awareness. To overcome this limitation, we analyzed single-trial modulation of power in the delta and theta frequency bands, which underlie the P300. METHODS: In a preliminary cross-sectional study using a 24-channel EEG and a passive own-name oddball paradigm, we analyzed event-related synchronization (ERS) across trials in the delta and theta bands in a sample of 10 control and 12 DoC subjects. RESULTS: In comparison to controls, DoC subjects presented a low percentage of trials where delta ERS was observed. In particular, coordinated modulation between delta and theta in response to the stimulus was absent, with a high percentage of trials where only theta ERS was observed. Further, we found a positive correlation between the percentage of epochs with delta ERS and the strength of the P300. CONCLUSIONS: Reduced modulation of spectral activity in the delta band in response to stimuli indicates a dissociation in the activity of the neural networks that oscillate in delta and theta ranges and contribute to the generation of the P300. SIGNIFICANCE: The reduction in spectral modulation observed in DoC provides a deeper understanding of neurophysiological dysfunction and the means to develop a more fine-grained marker of residual cognitive function in individual patients.

Asunto(s)

RESUMEN

During non-REM sleep the EEG shows characteristics waves that are generated by the dynamic interactions between cortical and thalamic oscillators. In thalamic neurons, low-threshold T-type Ca(2+) channels play a pivotal role in almost every type of neuronal oscillations, including slow (< 1 Hz) waves, sleep spindles and delta waves. The transient opening of T channels gives rise to the low threshold spikes (LTSs), and associated high frequency bursts of action potentials, that are characteristically present during sleep spindles and delta waves, whereas the persistent opening of a small fraction of T channels, (i.e., ITwindow) is responsible for the membrane potential bistability underlying sleep slow oscillations. Surprisingly thalamocortical (TC) neurons express a very high density of T channels that largely exceed the amount required to generate LTSs and therefore, to support certain, if not all, sleep oscillations. Here, to clarify the relationship between T current density and sleep oscillations, we systematically investigated the impact of the T conductance level on the intrinsic rhythmic activities generated in TC neurons, combining in vitro experiments and TC neuron simulation. Using bifurcation analysis, we provide insights into the dynamical processes taking place at the transition between slow and delta oscillations. Our results show that although stable delta oscillations can be evoked with minimal T conductance, the full range of slow oscillation patterns, including groups of delta oscillations separated by Up states ("grouped-delta slow waves") requires a high density of T channels. Moreover, high levels of T conductance ensure the robustness of different types of slow oscillations.

Asunto(s)

RESUMEN

OBJECTIVE: Delta waves (DW) are present both during sleep and in wakefulness. In the first case, DW are considered effectors of synaptic plasticity, while in wakefulness, when they appear in the case of brain lesions, their functional meaning is not unanimously recognized. To throw light on the latter, we aimed to investigate the impact on DW exerted by the cortical plasticity-inducing protocol of intermittent theta burst stimulation (iTBS). METHODS: Twenty healthy subjects underwent iTBS (11 real iTBS and nine sham iTBS) on the left primary motor cortex with the aim of inducing long-term potentiation (LTP)-like phenomena. Five-minute resting open-eye 32-channel EEG, right opponens pollicis motor-evoked potentials (MEPs), and alertness behavioral scales were collected before and up to 30 min after the iTBS. Power spectral density (PSD), interhemispheric coherence between homologous sensorimotor regions, and intrahemispheric coherence were calculated for the frequency bands ranging from delta to beta. RESULTS: Real iTBS induced a significant increase of both MEP amplitude and DW PSD lasting up to 30 min after stimulation, while sham iTBS did not. The DW increase was evident over frontal areas ipsilateral and close to the stimulated cortex (electrode F3). Neither real nor sham iTBS induced significant modifications in the PSD of theta, alpha, and beta bands and in the interhemispheric coherence. Behavioral visuo-analogic scales score did not demonstrate changes in alertness after stimulations. No correlations were found between MEP amplitude and PSD changes in the delta band. CONCLUSIONS: Our data showed that LTP induction in the motor cortex during wakefulness, by means of iTBS, is accompanied by a large and enduring increase of DW over the ipsilateral frontal cortex. SIGNIFICANCE: The present results are strongly in favor of a prominent role of DW in the neural plasticity processes taking place during the awake state.

Asunto(s)