In a groundbreaking exploration of the neurological underpinnings of anxiety, recent research has unveiled how trait anxiety — a stable predisposition towards experiencing anxiety across various situations — influences motor cortical dynamics in the human brain. While anxiety’s cognitive effects have been widely studied, this investigation sheds light on its subtle yet pivotal role in modulating motor cortical oscillations, specifically focusing on the interplay between event-related desynchronization (ERD) and event-related synchronization (ERS). These oscillations, notably within the alpha (α) and beta (β) frequency bands, are critical electrophysiological markers tied respectively to the initiation and termination of voluntary movements.
The study, featured in the latest volume of BMC Psychiatry, commands attention for its innovative approach utilizing electroencephalographic (EEG) recordings during a well-validated motor task known as the Go-Nogo paradigm. This cognitive-executive task not only demands swift motor execution but also response inhibition, thereby providing an excellent window into sensorimotor cortical dynamics. Here, the researchers compared participants with elevated trait anxiety scores with those at the opposite end of the spectrum to determine not just differences in ERD and ERS power but also the functional coupling between these two phenomena.
What makes this investigation particularly compelling is the focus on the synchronized dance between α and β oscillations during movement execution and cessation. Event-related desynchronization (ERD) generally corresponds to the cortical activation necessary for initiating and executing movement, manifesting as a reduction in power in these frequency bands. Conversely, event-related synchronization (ERS) signals the return to baseline or inhibitory state following movement, representing a rebound in oscillatory power. Despite these well-established roles, prior literature had scarcely probed how stable psychological traits like anxiety could influence this neurophysiological coupling.
Twenty participants exhibiting the highest decile of trait anxiety scores—referred to as the high trait anxiety (HTA) cohort—and an equally sized group representing the lowest decile—the low trait anxiety (LTA) cohort—were subjected to EEG while performing the Go-Nogo task. It is worth noting that these individuals were carefully selected from a larger pool of 400 college students, ensuring a robust representation of the extremes in anxiety disposition. This stratification proves crucial in isolating the functional neural correlates specific to trait anxiety rather than transient state factors.
Surprisingly, the researchers observed no statistically significant differences in the absolute power changes of the α or β ERD and ERS bands between these two groups. This finding suggests that trait anxiety may not exert a straightforward influence on the magnitude of these sensorimotor oscillations during movement. However, the study’s true novelty lies in the analysis of the relationship, or coupling, between the movement-related ERD and subsequent ERS oscillatory components.
In the group with lower trait anxiety, there was a robust and significant correlation between β ERD during movement execution and α/β ERS following the action. This coupling indicates a tightly regulated sensorimotor rhythm cadence, reflecting efficient cortical processing of motor commands and movement termination. In stark contrast, the high trait anxiety group exhibited a marked dissociation in this coupling, signifying a disrupted or altered communication between motor initiation and completion neural mechanisms. This uncoupling could potentially underpin motor and executive function inefficiencies observed in anxiety-laden individuals.
From a neurophysiological perspective, these results hint at a scenario where trait anxiety compromises the temporal coordination of oscillatory brain rhythms responsible for seamless motor control. Such disruptions could extend beyond mere motor performance, impacting broader networks involving attention, inhibition, and adaptive behavioral responses, given the known association of α and β oscillations with cognitive control processes. Hence, these oscillatory patterns may represent a neural substrate through which anxiety exerts its wide-ranging influence on behavior.
Importantly, this research advances the field’s understanding of sensorimotor anomalies in psychiatric conditions. While much of the literature on anxiety disorders has focused predominantly on affective and cognitive symptoms, this study highlights sensorimotor oscillations as an underappreciated yet clinically relevant domain. The observed uncoupling in HTA subjects may foreshadow the motor irregularities and psychomotor slowing frequently reported in anxiety and mood disorders, suggesting potential targets for therapeutic interventions focused on neurophysiological rhythm restoration.
Technically, the use of EEG offers an exquisite temporal resolution that captures the rapid succession of cortical changes associated with movement onset and offset. By leveraging sophisticated time-frequency analyses, the study precisely characterizes ERD and ERS dynamics, providing quantifiable biomarkers of motor cortical function. This methodological rigor adds credence to the conclusions drawn and emphasizes the utility of electrophysiological measures in psychiatric neuroscience.
Furthermore, the behavioral task employed—the Go-Nogo paradigm—requires participants to engage inhibitory control, an executive function closely hampered in anxious individuals. Consequently, the observed neurophysiological patterns might reflect an intertwined deficit in motor and inhibitory control mechanisms, mediated through oscillatory coupling disturbances, contingent on trait anxiety levels. This conceptual framework enriches models of anxiety pathophysiology by integrating motor control anomalies within traditionally cognitive-affective frameworks.
Future research directions inspired by this work may involve exploring whether interventions like neurofeedback, transcranial magnetic stimulation, or pharmacological agents can modulate ERD-ERS coupling to ameliorate motor and cognitive symptoms in anxiety disorders. Moreover, longitudinal studies could determine if disrupted oscillatory coupling predicts the onset or severity of anxiety-related impairments, thereby serving as a prognostic biomarker.
In conclusion, this pioneering study makes a significant leap in elucidating how a psychological trait with far-reaching impacts—trait anxiety—can subtly but profoundly alter the neural orchestration of movement. Its findings underscore the importance of considering motor cortical oscillations and their interrelations when deciphering the neural architecture of anxiety and open new avenues for diagnostics and therapeutics that transcend the cognitive domain to embrace sensorimotor function.
Subject of Research: The influence of trait anxiety on motor cortical oscillations, specifically the coupling between event-related desynchronization and synchronization during movement.
Article Title: Trait anxiety negatively modulates the coupling of motor event-related desynchronization and event-related synchronization
Article References:
Cheng, CH., Chan, PY.S., Chen, SY. et al. Trait anxiety negatively modulates the coupling of motor event-related desynchronization and event-related synchronization.
BMC Psychiatry 25, 447 (2025). https://doi.org/10.1186/s12888-025-06901-5
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