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Stroke patients with hemiparesis display decreased beta band (13–25 Hz) rolandic activity, correlating to impaired motor function. However, clinically, patients without significant weakness, with small lesions far from sensorimotor cortex, exhibit bilateral decreased motor dexterity and slowed reaction times. We investigate whether these minor stroke patients also display abnormal beta band activity. Magnetoencephalographic (MEG) data were collected from nine minor stroke patients (NIHSS < 4) without significant hemiparesis, at ~1 and ~6 months postinfarct, and eight age-similar controls. Rolandic relative beta power during matching tasks and resting state, and Beta Event Related (De)Synchronization (ERD/ERS) during button press responses were analyzed. Regardless of lesion location, patients had significantly reduced relative beta power and ERS compared to controls. Abnormalities persisted over visits, and were present in both ipsi- and contra-lesional hemispheres, consistent with bilateral impairments in motor dexterity and speed. Minor stroke patients without severe weakness display reduced rolandic beta band activity in both hemispheres, which may be linked to bilaterally impaired dexterity and processing speed, implicating global connectivity dysfunction affecting sensorimotor cortex independent of lesion location. Findings not only illustrate global network disruption after minor stroke, but suggest rolandic beta band activity may be a potential biomarker and treatment target, even for minor stroke patients with small lesions far from sensorimotor areas. [ABSTRACT FROM AUTHOR]

Stroke patients with hemiparesis display decreased beta band (13–25 Hz) rolandic activity, correlating to impaired motor function. However, clinically, patients without significant weakness, with small lesions far from sensorimotor cortex, exhibit bilateral decreased motor dexterity and slowed reaction times. We investigate whether these minor stroke patients also display abnormal beta band activity. Magnetoencephalographic (MEG) data were collected from nine minor stroke patients (NIHSS < 4) without significant hemiparesis, at ~1 and ~6 months postinfarct, and eight age-similar controls. Rolandic relative beta power during matching tasks and resting state, and Beta Event Related (De)Synchronization (ERD/ERS) during button press responses were analyzed. Regardless of lesion location, patients had significantly reduced relative beta power and ERS compared to controls. Abnormalities persisted over visits, and were present in both ipsi- and contra-lesional hemispheres, consistent with bilateral impairments in motor dexterity and speed. Minor stroke patients without severe weakness display reduced rolandic beta band activity in both hemispheres, which may be linked to bilaterally impaired dexterity and processing speed, implicating global connectivity dysfunction affecting sensorimotor cortex independent of lesion location. Findings not only illustrate global network disruption after minor stroke, but suggest rolandic beta band activity may be a potential biomarker and treatment target, even for minor stroke patients with small lesions far from sensorimotor areas.

BackgroundAbnormal synchronization of neuronal activity in dopaminergic circuits is related to motor impairment in Parkinson’s disease (PD). Vibrotactile coordinated reset (vCR) fingertip stimulation aims to counteract excessive synchronization and induce sustained unlearning of pathologic synaptic connectivity and neuronal synchrony. Here, we report two clinical feasibility studies that examine the effect of regular and noisy vCR stimulation on PD motor symptoms. Additionally, in one clinical study (study 1), we examine cortical beta band power changes in the sensorimotor cortex. Lastly, we compare these clinical results in relation to our computational findings.MethodsStudy 1 examines six PD patients receiving noisy vCR stimulation and their cortical beta power changes after 3 months of daily therapy. Motor evaluations and at-rest electroencephalographic (EEG) recordings were assessed off medication pre- and post-noisy vCR. Study 2 follows three patients for 6+ months, two of whom received daily regular vCR and one patient from study 1 who received daily noisy vCR. Motor evaluations were taken at baseline, and follow-up visits were done approximately every 3 months. Computationally, in a network of leaky integrate-and-fire (LIF) neurons with spike timing-dependent plasticity, we study the differences between regular and noisy vCR by using a stimulus model that reproduces experimentally observed central neuronal phase locking.ResultsClinically, in both studies, we observed significantly improved motor ability. EEG recordings observed from study 1 indicated a significant decrease in off-medication cortical sensorimotor high beta power (21—30 Hz) at rest after 3 months of daily noisy vCR therapy. Computationally, vCR and noisy vCR cause comparable parameter-robust long-lasting synaptic decoupling and neuronal desynchronization.ConclusionIn these feasibility studies of eight PD patients, regular vCR and noisy vCR were well tolerated, produced no side effects, and delivered sustained cumulative improvement of motor performance, which is congruent with our computational findings. In study 1, reduction of high beta band power over the sensorimotor cortex may suggest noisy vCR is effectively modulating the beta band at the cortical level, which may play a role in improved motor ability. These encouraging therapeutic results enable us to properly plan a proof-of-concept study.

Background: Abnormal synchronization of neuronal activity in dopaminergic circuits is related to motor impairment in Parkinson's disease (PD). Vibrotactile coordinated reset (vCR) fingertip stimulation aims to counteract excessive synchronization and induce sustained unlearning of pathologic synaptic connectivity and neuronal synchrony. Here, we report two clinical feasibility studies that examine the effect of regular and noisy vCR stimulation on PD motor symptoms. Additionally, in one clinical study (study 1), we examine cortical beta band power changes in the sensorimotor cortex. Lastly, we compare these clinical results in relation to our computational findings. Methods: Study 1 examines six PD patients receiving noisy vCR stimulation and their cortical beta power changes after 3 months of daily therapy. Motor evaluations and at-rest electroencephalographic (EEG) recordings were assessed off medication pre- and post-noisy vCR. Study 2 follows three patients for 6+ months, two of whom received daily regular vCR and one patient from study 1 who received daily noisy vCR. Motor evaluations were taken at baseline, and follow-up visits were done approximately every 3 months. Computationally , in a network of leaky integrate-and-fire (LIF) neurons with spike timing-dependent plasticity, we study the differences between regular and noisy vCR by using a stimulus model that reproduces experimentally observed central neuronal phase locking. Results: Clinically , in both studies, we observed significantly improved motor ability. EEG recordings observed from study 1 indicated a significant decrease in off-medication cortical sensorimotor high beta power (21—30 Hz) at rest after 3 months of daily noisy vCR therapy. Computationally , vCR and noisy vCR cause comparable parameter-robust long-lasting synaptic decoupling and neuronal desynchronization. Conclusion: In these feasibility studies of eight PD patients, regular vCR and noisy vCR were well tolerated, produced no side effects, and delivered sustained cumulative improvement of motor performance, which is congruent with our computational findings. In study 1, reduction of high beta band power over the sensorimotor cortex may suggest noisy vCR is effectively modulating the beta band at the cortical level, which may play a role in improved motor ability. These encouraging therapeutic results enable us to properly plan a proof-of-concept study. [ABSTRACT FROM AUTHOR]

Background: Quality of life is severely impaired in patients with depressive disorders. Previous studies have focused on biomarkers predicting depressive symptomatology; however, studies investigating biomarkers predicting quality of life outcomes are limited. Improving quality of life is important because it is related not only to mental health but also to physical health. We need to develop a biomarker related to quality of life as a therapeutic target for patients with depressive disorders. Resting-state electroencephalography (EEG) is easy to record in clinical settings. The index of bandwidth spectral power predicts treatment response in depressive disorders and thus may be a candidate biomarker. However, no longitudinal studies have investigated whether EEG-recorded power could predict quality of life outcomes in patients with depressive disorders.Methods: The resting-state EEG-recorded bandwidth spectral power at baseline and the World Health Organization Quality of Life (QOL)-26 scores at 3-year follow-up were measured in 44 patients with depressive disorders.Results: The high beta band power (20-30 Hz) at baseline significantly predicted QOL at the 3-year follow-up after considering depressive symptoms and medication effects in a longitudinal investigation in patients with depressive disorders (β = 0.38, p = 0.01).Limitations: We did not have healthy subjects as a comparison group in this study.Conclusions: Our findings suggest that resting-state beta activity has the potential to be a useful biomarker for predicting future quality of life outcomes in patients with depressive disorders. [ABSTRACT FROM AUTHOR]

Across languages and linguistic phenomena, rises in spoken pitch seem to occupy a privileged position compared to steady F 0 or pitch lowering. Speakers are more likely to use sudden rises in pitch to arouse listener attention, rather than using falls; e.g., contrastive stress, questions seeking a response, beginnings of units of discourse, expressions of intense emotion, etc. The study evaluated whether there are brain responses that are more sensitive to stepwise raised vs. lowered spoken F 0, and whether any such responses were also caused by pure tone stimuli. Three types of brain response were evaluated. Mismatch negativity (MMN), which reflects pre-attentive mechanisms, was only sensitive to degrees of F 0 change, and not to direction. P300, which is an indicator of attention orientation, did not show sensitivity to F 0 direction to non­speech stimuli, but showed greater sensitivity to raised F 0 than to lowered F 0 in speech. Time–frequency analysis of EEG data showed beta-band response in the right parietal area, when presented with spoken F 0 elevation. Taken together, the P300 and beta band results suggest that attention modulation mechanisms are triggered when listeners are exposed to sudden rises in spoken F 0. However, there was a lack of attention orientation response when non-speech F 0 changes were presented, or when subjects were exposed to lowering of F 0 in speech. [ABSTRACT FROM AUTHOR]

Code-switching, i.e. the alternation between languages in a conversation, is a typical, yet socially-constrained practice in bilingual communities. For instance, code-switching is permissible only when other conversation partners are fluent in both languages. Studying code-switching provides insight in the cognitive and neural mechanisms underlying language control, and their modulation by linguistic and non-linguistic factors. Using time-frequency representations, we analyzed brain oscillation changes in EEG data recorded in a prior study (Kaan et al., 2020). In this study, Spanish-English bilinguals read sentences with and without switches in the presence of a bilingual or monolingual partner. Consistent with prior studies, code-switches were associated with a power decrease in the lower beta band (15-18 Hz). In addition, code-switches were associated with a power decrease in the upper gamma band (40-50 Hz), but only when a bilingual partner was present, suggesting the semantic/pragmatic processing of code-switches differs depending on who is present. [ABSTRACT FROM AUTHOR]