Increase In Beta Power Research Articles

Medication effects on EEG biomarkers in attention-deficit/hyperactivity disorder

EEG biomarkers have become increasingly used to aid in diagnosis of ADHD. Despite several studies suggesting that EEG theta/beta ratio may help discriminating ADHD from other disorders, the effect of medications on theta/beta ratio is not known. Forty-three children with ADHD that were evaluated with quantitative EEG before and after methylphenidate were included in the study. Theta/beta ratio, theta and beta powers for whole brain, central and frontal areas were calculated. Theta/beta power decreased significantly after treatment; however this change was largely due to an increase in beta power, rather than a fall in theta power. The results suggest that beta power is sensitive to medication effects, while theta power remains as a trait biomarker unaffected by medication status. The value of EEG biomarkers for monitoring neuropsychological performance and clinical status should be explored by future studies.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Unravelling the effect of experimental pain on the corticomotor system using transcranial magnetic stimulation and electroencephalography

The interaction between pain and the motor system is well-known, with past studies showing that pain can alter corticomotor excitability and have deleterious effects on motor learning. The aim of this study was to better understand the cortical mechanisms underlying the interaction between pain and the motor system. Experimental pain was induced on 19 young and healthy participants using capsaicin cream, applied on the middle volar part of the left forearm. The effect of pain on brain activity and on the corticomotor system was assessed with electroencephalography (EEG) and transcranial magnetic stimulation (TMS), respectively. Compared to baseline, resting state brain activity significantly increased after capsaicin application in the central cuneus (theta frequency), left dorsolateral prefrontal cortex (alpha frequency), and left cuneus and right insula (beta frequency). A pain-evoked increase in the right primary motor cortex (M1) activity was also observed (beta frequency), but only among participants who showed a reduction in corticospinal output (as depicted by TMS recruitment curves). These participants further showed greater beta M1-cuneus connectivity than the other participants. These findings indicate that pain-evoked increases in M1 beta power are intimately tied to changes in the corticospinal system, and provide evidence that beta M1-cuneus connectivity is related to the corticomotor alterations induced by pain. The differential pattern of response observed in our participants suggest that the effect of pain on the motor system is variable from on individual to another; an observation that could have important clinical implications for rehabilitation professionals working with pain patients.

Motor Cortex Theta and Gamma Architecture in Young Adult APPswePS1dE9 Alzheimer Mice.

Alzheimer’s disease (AD) is a multifactorial disorder leading to progressive memory loss and eventually death. In this study, an APPswePS1dE9 AD mouse model has been analyzed for motor cortex theta, beta and gamma frequency alterations using computerized 3D stereotaxic electrode positioning and implantable video-EEG radiotelemetry to perform long-term M1 recordings from both genders considering age, circadian rhythm and activity status of experimental animals. We previously demonstrated that APPswePS1dE9 mice exibit complex alterations in hippocampal frequency power and another recent investigation reported a global increase of alpha, beta and gamma power in APPswePS1dE9 in females of 16–17 weeks of age. In this cortical study in APPswePS1dE9 mice we did not observe any changes in theta, beta and particularly gamma power in both genders at the age of 14, 15, 18 and 19 weeks. Importantly, no activity dependence of theta, beta and gamma activity could be detected. These findings clearly point to the fact that EEG activity, particularly gamma power exhibits developmental changes and spatial distinctiveness in the APPswePS1dE9 mouse model of Alzheimer’s disease.

Eliminating stroop effects with post-hypnotic instructions: Brain mechanisms inferred from EEG

The classic Stroop task demonstrates the persistent and automatic effects of the meaning of color words that are very hard to inhibit when the task is to name the word color. Post-hypnotic instructions may enable highly-hypnotizable participants to inhibit the automatic access to word meaning. Here we compared the consequences of hypnosis alone and hypnosis with post-hypnotic instructions on the Stroop effect and its facilitation and inhibition components. Importantly, we studied the mechanisms of the hypnosis effects at the neural level by analyzing EEG frequencies. Highly hypnotizable participants performed the Stroop task in a counterbalanced design following (1) post-hypnotic suggestions that words had lost their meaning, (2) after hypnosis alone, and (3) in a control condition without hypnosis. The overall Stroop effect and both its facilitation and interference components, were not significant after the post-hypnotic suggestion but in both other conditions. Hypnosis alone neither affected the Stroop effect nor – in contrast to some previous reports and claims – overall performance. EEG recorded during the Stroop task showed a significant increase in both frontal theta and frontal beta power when participants were under the impact of post-hypnotic suggestions, in comparison to the two other sessions. Together, these findings indicate that post-hypnotic suggestions – but not hypnosis alone - are powerful tools for eliciting top down processes. Our EEG findings could be interpreted as clue that this is due to the investment of additional cognitive control.

Medication Effects on EEG Biomarkers in Attention-Deficit/Hyperactivity Disorder.

EEG biomarkers have become increasingly used to aid in diagnosis of attention-deficit/hyperactivity disorder (ADHD). Despite several studies suggesting that EEG theta/beta ratio may help discriminating ADHD from other disorders, the effect of medications on theta/beta ratio is not known. Forty-three children with ADHD that were evaluated with quantitative EEG before and after methylphenidate were included in the study. Theta/beta ratio, theta and beta powers for whole brain, central, and frontal areas were calculated. Theta/beta power decreased significantly after treatment; however, this change was largely due to an increase in beta power, rather than a fall in theta power. The results suggest that beta power is sensitive to medication effects, while theta power remains as a trait biomarker unaffected by medication status. The value of EEG biomarkers for monitoring neuropsychological performance and clinical status should be explored by future studies.

Timing of beta oscillatory synchronization and temporal prediction of upcoming stimuli

Modulations of beta oscillatory power serve a predictive role, in preparation of future actions. It is well known that beta amplitude decreases prior to voluntary movements and expected tactile stimuli. Paradoxically, recent studies have reported a beta amplitude increase prior to expected visual and auditory stimuli. Moreover, it has been suggested that, in isochronic stimulus series, the rising beta slope is adjusted to the duration of the interstimulus interval. We investigated the characteristics of such timing related pre-stimulus beta power increases using visual stimulus sequences that were presented at three regular rates (0.61, 0.74 and 0.95Hz). EEG was recorded from twenty participants while they attended the sequences by performing a clock reading task. Time-frequency analyses showed a consistent pattern of beta modulation: the post-stimulus beta power decrease was followed by a steep increase. Contrary to recent views, we found that the peaks of beta power, for the three presentation rates, were reached at a similar latency post-stimulus, instead of a fixed interval preceding the next stimulus. This demonstrates that, at interstimulus intervals between 1–2s, beta synchronization slopes are not modulated by timing mechanisms related to prediction of upcoming stimuli. We reconcile the discrepant results by proposing that when shorter interval durations are used, as in previous studies, beta resynchronization is interrupted by the presentation of a new stimulus, making it seem as if beta power peaks prior to upcoming stimuli. We emphasize caution with respect to the notion that the timing of beta synchronization is an expression of predictive timing.

Is an absolute level of cortical beta suppression required for proper movement? Magnetoencephalographic evidence from healthy aging

Previous research has connected a specific pattern of beta oscillatory activity to proper motor execution, but no study to date has directly examined how resting beta levels affect motor-related beta oscillatory activity in the motor cortex. Understanding this relationship is imperative to determining the basic mechanisms of motor control, as well as the impact of pathological beta oscillations on movement execution. In the current study, we used magnetoencephalography (MEG) and a complex movement paradigm to quantify resting beta activity and movement-related beta oscillations in the context of healthy aging. We chose healthy aging as a model because preliminary evidence suggests that beta activity is elevated in older adults, and thus by examining older and younger adults we were able to naturally vary resting beta levels. To this end, healthy younger and older participants were recorded during motor performance and at rest. Using beamforming, we imaged the peri-movement beta event-related desynchronization (ERD) and extracted virtual sensors from the peak voxels, which enabled absolute and relative beta power to be assessed. Interestingly, absolute beta power during the pre-movement baseline was much stronger in older relative to younger adults, and older adults also exhibited proportionally large beta desynchronization (ERD) responses during motor planning and execution compared to younger adults. Crucially, we found a significant relationship between spontaneous (resting) beta power and beta ERD magnitude in both primary motor cortices, above and beyond the effects of age. A similar link was found between beta ERD magnitude and movement duration. These findings suggest a direct linkage between beta reduction during movement and spontaneous activity in the motor cortex, such that as spontaneous beta power increases, a greater reduction in beta activity is required to execute movement. We propose that, on an individual level, the primary motor cortices have an absolute threshold of beta power that must be reached in order to move, and that an inability to suppress beta power to this threshold results in an increase in movement duration.

Increased Low- and High-Frequency Oscillatory Activity in the Prefrontal Cortex of Fibromyalgia Patients.

Recent human neuroimaging studies have suggested that fibromyalgia (FM), a chronic widespread pain disorder, exhibits altered thalamic structure and function. Since the thalamus has extensive reciprocal connection with the cortex, structural and functional thalamic alterations in FM might be linked to aberrant thalamocortical oscillation. This study investigated the presence of abnormal brain rhythmicity in low- and high-frequency bands during resting state in patients with FM and their relationship to clinical pain symptom. Spontaneous magnetoencephalography (MEG) activity was recorded in 18 females with FM and 18 age- and sex-matched healthy control (HC) subjects. The most remarkable finding was that FM patients had general increases in theta, beta and gamma power along with a slowing of the dominant alpha peak. Increased spectral powers in the theta-band were primarily localized to the left dorsolateral prefrontal (DLPFC) and orbitofrontal cortex (OFC). Beta and gamma over-activation were localized to insular, primary motor and primary and secondary somatosensory (S2) cortices, as well as the DLPFC and OFC. Furthermore, enhanced high-frequency oscillatory activities in the DLPFC and OFC were associated with higher affective pain scores in patients with FM. Our results demonstrate that FM patients feature enhanced low- and high-frequency oscillatory activity in the brain areas related to cognitive and emotional modulation of pain. Increased low- and high-frequency activity of the prefrontal cortex may contribute to persistent perception of pain in FM. Therapeutic intervention based on manipulating neural oscillation to restore normal thalamocortical rhythmicity may be beneficial to pain relief in FM.

Bicycling and Walking are Associated with Different Cortical Oscillatory Dynamics.

Although bicycling and walking involve similar complex coordinated movements, surprisingly Parkinson’s patients with freezing of gait typically remain able to bicycle despite severe difficulties in walking. This observation suggests functional differences in the motor networks subserving bicycling and walking. However, a direct comparison of brain activity related to bicycling and walking has never been performed, neither in healthy participants nor in patients. Such a comparison could potentially help elucidating the cortical involvement in motor control and the mechanisms through which bicycling ability may be preserved in patients with freezing of gait. The aim of this study was to contrast the cortical oscillatory dynamics involved in bicycling and walking in healthy participants. To this end, EEG and EMG data of 14 healthy participants were analyzed, who cycled on a stationary bicycle at a slow cadence of 40 revolutions per minute (rpm) and walked at 40 strides per minute (spm), respectively. Relative to walking, bicycling was associated with a stronger power decrease in the high beta band (23–35 Hz) during movement initiation and execution, followed by a stronger beta power increase after movement termination. Walking, on the other hand, was characterized by a stronger and persisting alpha power (8–12 Hz) decrease. Both bicycling and walking exhibited movement cycle-dependent power modulation in the 24–40 Hz range that was correlated with EMG activity. This modulation was significantly stronger in walking. The present findings reveal differential cortical oscillatory dynamics in motor control for two types of complex coordinated motor behavior, i.e., bicycling and walking. Bicycling was associated with a stronger sustained cortical activation as indicated by the stronger high beta power decrease during movement execution and less cortical motor control within the movement cycle. We speculate this to be due to the more continuous nature of bicycling demanding less phase-dependent sensory processing and motor planning, as opposed to walking.

Withholding planned speech is reflected in synchronized beta-band oscillations.

When engaged in a conversation, speakers sometimes have to withhold a planned response, for example, before it is their turn to speak. In the present study, using magnetoencephalography (MEG) outside of a conversational setting, we investigate the oscillatory brain mechanisms involved in the process of withholding a planned verbal response until it is time to speak. Our participants viewed a sequence of four random consonant strings and one pseudoword, which they had to pronounce when the fifth string (the imperative stimulus) was presented. The pseudoword appeared either as the fourth or fifth stimulus in the sequence, creating two conditions. In the withhold condition, the pseudoword was the fourth string and the verbal response was withheld until the imperative stimulus was presented. In the control condition, the fifth string was the pseudoword, so no response was withheld. We compared oscillatory responses to the withhold relative to the control condition in the time period preceding speech. Alpha-beta power (8–30 Hz) decreased over occipital sensors in the withhold condition relative to the control condition. Source-level analysis indicated a posterior source (i.e., occipital cortex) associated with the alpha-beta power decreases. This occipital alpha-beta desynchronization likely reflects attentional allocation to the upcoming imperative stimulus. Moreover, beta (12–20 Hz) power increased over frontal sensors. Source-level analysis indicated a frontal source (i.e., middle and superior frontal gyri) associated with the beta-power increases. We interpret the frontal beta synchronization to reflect a mechanism aiding the maintenance of the current motor or cognitive state. Our results provide a window into a possible oscillatory mechanism implementing the ability of speakers to withhold a planned verbal response until they have to speak.

Reward feedback stimuli elicit high-beta EEG oscillations in human dorsolateral prefrontal cortex.

Reward-related feedback stimuli have been observed to elicit a burst of power in the beta frequency range over frontal areas of the human scalp. Recent discussions have suggested possible neural sources for this activity but there is a paucity of empirical evidence on the question. Here we recorded EEG from participants while they navigated a virtual T-maze to find monetary rewards. Consistent with previous studies, we found that the reward feedback stimuli elicited an increase in beta power (20–30 Hz) over a right-frontal area of the scalp. Source analysis indicated that this signal was produced in the right dorsolateral prefrontal cortex (DLPFC). These findings align with previous observations of reward-related beta oscillations in the DLPFC in non-human primates. We speculate that increased power in the beta frequency range following reward receipt reflects the activation of task-related neural assemblies that encode the stimulus-response mapping in working memory.

Selective Antagonism of mGlu5 Alters Sleep‐wake and Spectral EEG and Ameliorates Behavioral Abnormalities in a Rodent Model of Traumatic Stress

Traumatic stress induces state‐dependent alterations in cortical network activity as measured by sleep‐wake and quantitative electroencephalography (qEEG) that may predict the onset or severity of chronic post‐traumatic stress disorder (PTSD) symptoms. Activation of metabotropic glutamate receptor 5 (mGlu5) promotes fear memory consolidation, and may contribute to sleep disturbances after trauma. The single prolonged stress (SPS) rodent model of traumatic stress recapitulates many physiological and behavioral correlates of the human disorder, but its effect on sleep‐wake and qEEG spectral power has not been examined.Male Sprague‐Dawley rats were implanted with telemetric EEG electrodes continuously recording cortical activity before and after SPS. VU0409106, a selective mGlu5 negative allosteric modulator (NAM) was administered after SPS to assess blockade or reversal of SPS‐induced sleep‐wake and qEEG disturbances.SPS caused persistent PTSD‐like alterations in rapid eye movement (REM) sleep and non‐REM (NREM) sleep as well as changes in state‐dependent spectral power, such as an increase in waking beta (18‐30Hz) power, and a decrease in NREM delta (0.5‐4Hz) power indicative of hyperarousal and poor sleep quality. VU0409106 modulated SPS‐induced sleep‐wake architecture changes and qEEG spectral power alterations and ameliorated accompanying anxiety‐like behaviors.

Cortical oscillatory dynamics and benzodiazepine-site modulation of tonic inhibition in fast spiking interneurons

Tonic conductance mediated by extrasynaptic GABAA receptors has been implicated in the modulation of network oscillatory activity. Using an in vitro brain slice to produce oscillatory activity and a kinetic model of GABAA receptor dynamics, we show that changes in tonic inhibitory input to fast spiking interneurons underlie benzodiazepine-site mediated modulation of neuronal network synchrony in rat primary motor cortex. We found that low concentrations (10 nM) of the benzodiazepine site agonist, zolpidem, reduced the power of pharmacologically-induced beta-frequency (15–30 Hz) oscillatory activity. By contrast, higher doses augmented beta power. Application of the antagonist, flumazenil, also increased beta power suggesting endogenous modulation of the benzodiazepine binding site. Voltage-clamp experiments revealed that pharmacologically-induced rhythmic inhibitory postsynaptic currents were reduced by 10 nM zolpidem, suggesting an action on inhibitory interneurons. Further voltage-clamp studies of fast spiking cells showed that 10 nM zolpidem augmented a tonic inhibitory GABAA receptor mediated current in fast spiking cells whilst higher concentrations of zolpidem reduced the tonic current. A kinetic model of zolpidem-sensitive GABAA receptors suggested that incubation with 10 nM zolpidem resulted in a high proportion of GABAA receptors locked in a kinetically slow desensitized state whilst 30 nM zolpidem favoured rapid transition into and out of desensitized states. This was confirmed experimentally using a challenge with saturating concentrations of GABA. Selective modulation of an interneuron-specific tonic current may underlie the reversal of cognitive and motor deficits afforded by low-dose zolpidem in neuropathological states.

Directional Recording of Subthalamic Spectral Power Densities in Parkinson's Disease and the Effect of Steering Deep Brain Stimulation.

A new 32-contacts deep brain stimulation (DBS) lead, capable of directionally steering stimulation, was tested intraoperatively. The aim of this pilot study was to perform recordings from the multidirectional contacts and to investigate the effect of directional current steering on the local field potentials (LFPs). In eight patients with Parkinson's disease, after standard microelectrode recording and clinical testing, the new lead was temporarily implanted. The 32-channel LFP recordings were measured simultaneously at different depths and directions before and after directional stimulation. The spatial distribution of LFPs power spectral densities across the contact array at baseline marked the borders of the subthalamic nucleus (STN) with a significant increase in beta power and with a mean accuracy of approximately 0.6mm in four patients.The power in the 18.5-30Hz frequency band varied across different directions in all patients. In the three cases that showed improvement of rigidity, this was higher when current was steered toward the direction with the highest LFP power in the beta band. Subthalamic LFPs in six patients showed a differential frequency-dependent suppression/enhancement of the oscillatory activity in the 10-45Hz frequency band after four different 'steering' modes as compared to ring mode, suggesting a higher specificity. Through a new 32-contact DBS lead it is possible to record simultaneous subthalamic LFPs at different depths and directions, providing confirmation of adequate lead placement and multidirectional spatial-temporal information potentially related to pathological subthalamic electrical activity and to the effect of stimulation. Although further research is needed, this may improve the efficiency of steering stimulation.

Are NREM sleep characteristics associated to subjective sleep complaints after mild traumatic brain injury?

IntroductionSleep complaints are common after mild traumatic brain injury (mTBI). While recent findings suggest that sleep macro-architecture is preserved in mTBI, features of non-rapid eye movement (NREM) sleep micro-architecture including electroencephalography (EEG) spectral power, slow waves (SW), and sleep spindles could be affected. This study aimed to compare NREM sleep in mTBI and healthy controls, and explore whether NREM sleep characteristics correlate with sleep complaints in these groups. MethodsThirty-four mTBI participants (mean age: 34.2 ± 11.9 yrs; post-injury delay: 10.5 ± 10.4 weeks) and 29 age-matched controls (mean age: 32.4 ± 8.2 yrs) were recruited for two consecutive nights of polysomnographic (PSG) recording. Spectral power was computed and SW and spindles were automatically detected in three derivations (F3, C3, O1) for the first three sleep cycles. Subjective sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI). ResultsmTBI participants reported significant poorer sleep quality than controls on the PSQI and showed significant increases in beta power during NREM sleep at the occipital derivation only. Conversely, no group differences were found in SW and spindle characteristics. Interestingly, changes in NREM sleep characteristics were not associated with mTBI estimation of sleep quality. ConclusionsCompared to controls, mTBI were found to have enhanced NREM beta power. However, these changes were not found to be associated with the subjective evaluation of sleep. While increases in beta bands during NREM sleep may be attributable to the occurrence of a brain injury, they could also be related to the presence of pain and anxiety as suggested in one prior study.

MEG-based detection and localization of perilesional dysfunction in chronic stroke.

Post-stroke impairment is associated not only with structural lesions, but also with dysfunction in surviving perilesional tissue. Previous studies using equivalent current dipole source localization of MEG/EEG signals have demonstrated a preponderance of slow-wave activity localized to perilesional areas. Recent studies have also demonstrated the utility of nonlinear analyses such as multiscale entropy (MSE) for quantifying neuronal dysfunction in a wide range of pathologies. The current study utilized beamformer-based reconstruction of signals in source space to compare spectral and nonlinear measures of electrical activity in perilesional and healthy cortices. Data were collected from chronic stroke patients and healthy controls, both young and elderly. We assessed relative power in the delta (1–4 Hz), theta (4–7 Hz), alpha (8–12 Hz) and beta (15–30 Hz) frequency bands, and also measured the nonlinear complexity of electrical activity using MSE. Perilesional tissue exhibited a general slowing of the power spectrum (increased delta/theta, decreased beta) as well as a reduction in MSE. All measures tested were similarly sensitive to changes in the posterior perilesional regions, but anterior perilesional dysfunction was detected better by MSE and beta power. The findings also suggest that MSE is specifically sensitive to electrophysiological dysfunction in perilesional tissue, while spectral measures were additionally affected by an increase in rolandic beta power with advanced age. Furthermore, perilesional electrophysiological abnormalities in the left hemisphere were correlated with the degree of language task-induced activation in the right hemisphere. Finally, we demonstrate that single subject spectral and nonlinear analyses can identify dysfunctional perilesional regions within individual patients that may be ideal targets for interventions with noninvasive brain stimulation.

The rotenone-induced rat model of Parkinson's disease: Behavioral and electrophysiological findings

Exposure to rotenone leads to parkinsonian features, such as loss of dopaminergic neurons in the substantia nigra and motor impairment, however, the validity of this model has recently been questioned. In rodent and monkey models of Parkinson's disease (PD) abnormal neuronal activity in the basal ganglia motor loop has been described, with hyperactivity of the subthalamic nucleus (STN) similar to that found in PD. The present study aims at providing new and more specific evidence for the validity of the rotenone rat model of PD by examining whether neuronal activity in the STN is altered.Male Sprague Dawley rats were treated with rotenone injections (2.5mg/kg bodyweight intraperitoneally) for 60 days. Behavioral analysis showed an impairment in the rotarod and hanging wire test in the rotenone group (p<0.05), accompanied by a decline in tyrosine hydroxylase immunoreactive neurons in the nigro-striatal region (p<0.001). Thereafter, single unit (SU) activities and local field potentials were recorded in the STN in urethane anesthetized rats. The SU analysis revealed a higher neuronal discharge rate (p<0.001), more bursts per minute (p=0.006) and a higher oscillatory activity (p=0.008) in the STN of rotenone treated rats. Spectral analysis showed an increase of relative beta power in the STN as well as in the motor cortex.We found electrophysiological key features of PD pathology and pathophysiology in the STN of rotenone treated rats. Therefore, the rotenone-induced rat model of PD deserves further attention since it covers more aspects than dopamine depletion and implies the reproducibility of PD specific features.

A controlled study on the cognitive effect of alpha neurofeedback training in patients with major depressive disorder.

Cognitive deficits are core symptoms of depression. This study aims to investigate whether neurofeedback (NF) training can improve working memory (WM) performance in patients with major depressive disorder (MDD). The NF group (n = 40) underwent eight NF sessions and was compared to a non-interventional control group (n = 20). The NF protocol aimed to increase the individual upper alpha power in the parieto-occipital area of the scalp. Main cognitive variable was WM, which was measured pre- and post- training along with other variables such as attention and executive functions. EEG was recorded in both eyes closed resting state and eyes open task-related activity, pre- and post- NF training, and pre- and post- the NF trials within each session. A power EEG analysis and an alpha asymmetry analysis were conducted at the sensor level. Frequency domain standardized low resolution tomography (sLORETA) was used to assess the effect at brain source level. Correlation analysis between the clinical/cognitive and EEG measurements was conducted at both the sensor and brain source level. The NF group showed increased performance as well as improved processing speed in a WM test after the training. The NF group showed pre-post enhancement in the upper alpha power after the training, better visible in task-related activity as compared to resting state. A current density increase appeared in the alpha band (8–12 Hz) for the NF group, localized in the subgenual anterior cingulate cortex (sgACC, BA 25). A positive correlation was found for the NF group between the improvement in processing speed and the increase of beta power at both the sensor and brain source level. These results show the effectiveness of this NF protocol in improving WM performance in patients with MDD.

Circadian modulation of motor-related beta oscillatory responses

Previous electrophysiological investigations have evaluated movement-related beta (14–28Hz) oscillatory activity in healthy participants. These studies have described an abrupt decrease in beta activity that starts before movement onset, and a sharp increase in beta power that peaks after movement termination. These neural responses have been respectively termed the event-related beta desynchronization or pre-movement beta ERD, and the post-movement beta rebound (PMBR). Previous studies have shown that a variety of movement parameters and demographic factors (e.g., age) modulate the amplitude of these oscillatory responses, and in the current study we evaluated whether the amplitudes follow a biological temporal rhythm (e.g., circadian), as it is known that spontaneous beta levels increase from morning to afternoon in some brain areas. To this end, we used magnetoencephalography (MEG) to evaluate oscillatory activity during a right hand finger-tapping task in four participants who were recorded at three different times (09:00, 12:00, 16:00) on three consecutive days (i.e., 36 total MEG sessions). All MEG data were corrected for head motion and examined in the time–frequency domain using beamforming methods. We found a significant linear increase in beta ERD amplitude from 09:00 to 16:00h in the left precentral gyrus, left premotor cortices, left supplementary motor area (SMA), and right precentral and postcentral gyri. In contrast, the amplitude of the PMBR was very steady across the day in all brain regions except the left SMA, which exhibited a linear increase from morning to afternoon. Finally, beta levels during the baseline period also increased from 09:00 to 16:00 in most regions of the cortical sensorimotor network. These data show that both the pre-movement beta ERD and spontaneous beta levels strongly increase from morning to afternoon in the motor cortices, which may indicate that the amplitude of the beta ERD response is determined by the spontaneous beta level during the motor planning period.

Transcranial direct current stimulation and power spectral parameters: a tDCS/EEG co-registration study

Transcranial direct current stimulation (tDCS) delivers low electric currents to the brain through the scalp. Constant electric currents induce shifts in neuronal membrane excitability, resulting in secondary changes in cortical activity. Concomitant electroencephalography (EEG) monitoring during tDCS can provide valuable information on the tDCS mechanisms of action. This study examined the effects of anodal tDCS on spontaneous cortical activity in a resting brain to disclose possible modulation of spontaneous oscillatory brain activity. EEG activity was measured in ten healthy subjects during and after a session of anodal stimulation of the postero-parietal cortex to detect the tDCS-induced alterations. Changes in the theta, alpha, beta, and gamma power bands were investigated. Three main findings emerged: (1) an increase in theta band activity during the first minutes of stimulation; (2) an increase in alpha and beta power during and after stimulation; (3) a widespread activation in several brain regions.