A benchmark for prediction of psychiatric multimorbidity from resting EEG data in a large pediatric sample.

Psychiatric disorders are among the most common and debilitating illnesses across the lifespan and begin usually during childhood and adolescence, which emphasizes the importance of studying the developing brain. Most of the previous pediatric neuroimaging studies employed traditional univariate statistics on relatively small samples. Multivariate machine learning approaches have a great potential to overcome the limitations of these approaches. On the other hand, the vast majority of existing multivariate machine learning studies have focused on differentiating between children with an isolated psychiatric disorder and typically developing children. However, this line of research does not reflect the real-life situation as the majority of children with a clinical diagnosis have multiple psychiatric disorders (multimorbidity), and consequently, a clinician has the task to choose between different diagnoses and/or the combination of multiple diagnoses. Thus, the goal of the present benchmark is to predict psychiatric multimorbidity in children and adolescents. For this purpose, we implemented two kinds of machine learning benchmark challenges: The first challenge targets the prediction of the seven most prevalent DSM-V psychiatric diagnoses for the available data set, of which each individual can exhibit multiple ones concurrently (i.e. multi-task multi-label classification). Based on behavioral and cognitive measures, a second challenge focuses on predicting psychiatric symptom severity on a dimensional level (i.e. multiple regression task). For the present benchmark challenges, we will leverage existing and future data from the biobank of the Healthy Brain Network (HBN) initiative, which offers a unique large-sample dataset (N = 2042) that provides a wide array of different psychiatric developmental disorders and true hidden data sets. Due to limited real-world practicability and economic viability of MRI measurements, the present challenge will permit only resting state EEG data and demographic information to derive predictive models. We believe that a community driven effort to derive predictive markers from these data using advanced machine learning algorithms can help to improve the diagnosis of psychiatric developmental disorders.

Harmonized-Multinational qEEG norms (HarMNqEEG).

This paper extends frequency domain quantitative electroencephalography (qEEG) methods pursuing higher sensitivity to detect Brain Developmental Disorders. Prior qEEG work lacked integration of cross-spectral information omitting important functional connectivity descriptors. Lack of geographical diversity precluded accounting for site-specific variance, increasing qEEG nuisance variance. We ameliorate these weaknesses. (i) Create lifespan Riemannian multinational qEEG norms for cross-spectral tensors. These norms result from the HarMNqEEG project fostered by the Global Brain Consortium. We calculate the norms with data from 9 countries, 12 devices, and 14 studies, including 1564 subjects. Instead of raw data, only anonymized metadata and EEG cross-spectral tensors were shared. After visual and automatic quality control, developmental equations for the mean and standard deviation of qEEG traditional and Riemannian DPs were calculated using additive mixed-effects models. We demonstrate qEEG "batch effects" and provide methods to calculate harmonized z-scores. (ii) We also show that harmonized Riemannian norms produce z-scores with increased diagnostic accuracy predicting brain dysfunction produced by malnutrition in the first year of life and detecting COVID induced brain dysfunction. (iii) We offer open code and data to calculate different individual z-scores from the HarMNqEEG dataset. These results contribute to developing bias-free, low-cost neuroimaging technologies applicable in various health settings.

Decomposing neurophysiological underpinnings of age-related decline in visual working memory.

Exploring the neural basis of age-related decline in working memory is vital in our aging society. Previous electroencephalographic studies suggested that the contralateral delay activity (CDA) may be insensitive to age-related decline in lateralized visual working memory (VWM) performance. Instead, recent evidence indicated that task-induced alpha power lateralization decreases in older age. However, the relationship between alpha power lateralization and age-related decline of VWM performance remains unknown, and recent studies have questioned the validity of these findings due to confounding factors of the aperiodic signal. Using a sample of 134 participants, we replicated the age-related decrease of alpha power lateralization after adjusting for the aperiodic signal. Critically, the link between task performance and alpha power lateralization was found only when correcting for aperiodic signal biases. Functionally, these findings suggest that age-related declines in VWM performance may be related to the decreased ability to prioritize relevant over irrelevant information. Conversely, CDA amplitudes were stable across age groups, suggesting a distinct neural mechanism possibly related to preserved VWM encoding or early maintenance.

Emotion-Induced Frontal Alpha Asymmetry as a Candidate Predictor of Relapse After Discontinuation of Antidepressant Medication.

BACKGROUND: One in 3 patients relapse after antidepressant discontinuation. Thus, the prevention of relapse after achieving remission is an important component in the long-term management of major depressive disorder. However, no clinical or other predictors are established. Frontal reactivity to sad mood as measured by functional magnetic resonance imaging has been reported to relate to relapse independently of antidepressant discontinuation and is an interesting candidate predictor. METHODS: Patients (n = 56) who had remitted from a depressive episode while taking antidepressants underwent electroencephalography (EEG) recording during a sad mood induction procedure prior to gradually discontinuing their medication. Relapse was assessed over a 6-month follow-up period. Thirty five healthy control participants were also tested. Current source density of the EEG power in the alpha band (8-13 Hz) was extracted and alpha asymmetry was computed by comparing the power across 2 hemispheres at frontal electrodes (F5 and F6). RESULTS: Sad mood induction was robust across all groups. Reactivity of alpha asymmetry to sad mood did not distinguish healthy control participants from patients with remitted major depressive disorder on medication. However, the 14 (25%) patients who relapsed during the follow-up period after discontinuing medication showed significantly reduced reactivity in alpha asymmetry compared with patients who remained well. This EEG signal provided predictive power (69% out-of-sample balanced accuracy and a positive predictive value of 0.75). CONCLUSIONS: A simple EEG-based measure of emotional reactivity may have potential to contribute to clinical prediction models of antidepressant discontinuation. Given the very small sample size, this finding must be interpreted with caution and requires replication in a larger study.

Test-retest reliability of resting-state EEG in young and older adults.

The quantification of resting-state electroencephalography (EEG) is associated with a variety of measures. These include power estimates at different frequencies, microstate analysis, and frequency-resolved source power and connectivity analyses. Resting-state EEG metrics have been widely used to delineate the manifestation of cognition and to identify psychophysiological indicators of age-related cognitive decline. The reliability of the utilized metrics is a prerequisite for establishing robust brain-behavior relationships and clinically relevant indicators of cognitive decline. To date, however, test-retest reliability examination of measures derived from resting human EEG, comparing different resting-state measures between young and older participants, within the same adequately powered dataset, is lacking. The present registered report examined test-retest reliability in a sample of 95 young (age range: 20-35 years) and 93 older (age range: 60-80 years) participants. A good-to-excellent test-retest reliability was confirmed in both age groups for power estimates on both scalp and source levels as well as for the individual alpha peak power and frequency. Partial confirmation was observed for hypotheses stating good-to-excellent reliability of microstates measures and connectivity. Equal levels of reliability between the age groups were confirmed for scalp-level power estimates and partially so for source-level power and connectivity. In total, five out of the nine postulated hypotheses were empirically supported and confirmed good-to-excellent reliability of the most commonly reported resting-state EEG metrics.

Decomposing age effects in EEG alpha power.

Increasing life expectancy is prompting the need to understand how the brain changes during healthy aging. Research utilizing electroencephalography (EEG) has found that the power of alpha oscillations decrease from adulthood on. However, non-oscillatory (aperiodic) components in the data may confound results and thus require re-investigation of these findings. Thus, the present report analyzed a pilot and two additional independent samples (total N = 533) of resting-state EEG from healthy young and elderly individuals. A newly developed algorithm was utilized that allows the decomposition of the measured signal into periodic and aperiodic signal components. By using multivariate sequential Bayesian updating of the age effect in each signal component, evidence across the datasets was accumulated. It was hypothesized that previously reported age-related alpha power differences will largely diminish when total power is adjusted for the aperiodic signal component. First, the age-related decrease in total alpha power was replicated. Concurrently, decreases of the intercept and slope (i.e. exponent) of the aperiodic signal component were observed. Findings on aperiodic-adjusted alpha power indicated that this general shift of the power spectrum leads to an overestimation of the true age effects in conventional analyses of total alpha power. Thus, the importance of separating neural power spectra into periodic and aperiodic signal components is highlighted. However, also after accounting for these confounding factors, the sequential Bayesian updating analysis provided robust evidence that aging is associated with decreased aperiodic-adjusted alpha power. While the relation of the aperiodic component and aperiodic-adjusted alpha power to cognitive decline demands further investigation, the consistent findings on age effects across independent datasets and high test-retest reliabilities support that these newly emerging measures are reliable markers of the aging brain. Hence, previous interpretations of age-related decreases in alpha power are reevaluated, incorporating changes in the aperiodic signal.

Decomposing the role of alpha oscillations during brain maturation.

Childhood and adolescence are critical stages of the human lifespan, in which fundamental neural reorganizational processes take place. A substantial body of literature investigated accompanying neurophysiological changes, focusing on the most dominant feature of the human EEG signal: the alpha oscillation. Recent developments in EEG signal-processing show that conventional measures of alpha power are confounded by various factors and need to be decomposed into periodic and aperiodic components, which represent distinct underlying brain mechanisms. It is therefore unclear how each part of the signal changes during brain maturation. Using multivariate Bayesian generalized linear models, we examined aperiodic and periodic parameters of alpha activity in the largest openly available pediatric dataset (N=2529, age 5-22 years) and replicated these findings in a preregistered analysis of an independent validation sample (N=369, age 6-22 years). First, the welldocumented age-related decrease in total alpha power was replicated. However, when controlling for the aperiodic signal component, our findings provided strong evidence for an age-related increase in the aperiodic-adjusted alpha power. As reported in previous studies, also relative alpha power revealed a maturational increase, yet indicating an underestimation of the underlying relationship between periodic alpha power and brain maturation. The aperiodic intercept and slope decreased with increasing age and were highly correlated with total alpha power. Consequently, earlier interpretations on age-related changes of total alpha power need to be reconsidered, as elimination of active synapses rather links to decreases in the aperiodic intercept. Instead, analyses of diffusion tensor imaging data indicate that the maturational increase in aperiodic-adjusted alpha power is related to increased thalamocortical connectivity. Functionally, our results suggest that increased thalamic control of cortical alpha power is linked to improved attentional performance during brain maturation.

The ZuCo benchmark on cross-subject reading task classification with EEG and eye-tracking data.

We present a new machine learning benchmark for reading task classification with the goal of advancing EEG and eye-tracking research at the intersection between computational language processing and cognitive neuroscience. The benchmark task consists of a cross-subject classification to distinguish between two reading paradigms: normal reading and task-specific reading. The data for the benchmark is based on the Zurich Cognitive Language Processing Corpus (ZuCo 2.0), which provides simultaneous eye-tracking and EEG signals from natural reading of English sentences. The training dataset is publicly available, and we present a newly recorded hidden testset. We provide multiple solid baseline methods for this task and discuss future improvements. We release our code and provide an easy-to-use interface to evaluate new approaches with an accompanying public leaderboard: www.zuco-benchmark.com.