Biology subjects

Quiquempoix, M.

Publications and source records attributed to Quiquempoix, M..

3 recordsLinked to original sources

bioRxiv2026

Revisiting post-stimulus theta activity: evidence for an aperiodic rather than oscillatory origin

The aperiodic, 1/f-like component of electrophysiological activity is increasingly recognized as a meaningful feature of neural function, rather than background noise. In parallel, many EEG studies report transient changes in oscillatory power following stimulus onset and interpret these effects as signatures of attention, salience, or cognitive control. However, such conclusions usually rely on baseline normalization procedures that assume aperiodic activity remains stable from pre-to post-stimulus periods. Using high-density EEG recordings from typically developing children, we tested this assumption in two paradigms: an audiovisual simple reaction-time task (n = 36) and a visual oddball task (n = 38). For each task, conventional spectral analyses were compared with analyses that explicitly modeled and removed the aperiodic component in both pre- and post-stimulus windows. Across tasks, stimulus onset was associated with robust increases in aperiodic exponent and offset, indicating systematic changes in the 1/f component of the spectrum. In the audiovisual task, these changes were modality-specific, with central, parieto-occipital, or combined topographies depending on stimulus type. These effects were reduced but remained significant after ERP removal, indicating that they were not fully explained by phase-locked activity. Critically, once aperiodic activity was accounted for, the apparent post-stimulus increase in theta power was largely abolished in both tasks, including the canonical fronto-central theta enhancement to infrequent targets in the oddball paradigm. The conventional method also overestimated the magnitude of beta desynchronization, particularly in the induced (ERP-removed) signal. The apparent gamma desynchronization detected by conventional analyses was reversed after aperiodic correction, revealing either synchronization or no change, indicating that it reflects a spurious consequence of spectral slope steepening rather than a true suppression of gamma oscillatory activity. In contrast, alpha desynchronization remained robust after aperiodic correction and was in fact enhanced, suggesting it reflects genuine oscillatory suppression. Together, these findings indicate that a substantial portion of conventional time-frequency effects, particularly apparent theta synchronization, may reflect changes in aperiodic activity in response to stimulation rather than genuine periodic oscillations, challenging core assumptions of conventional time-frequency analyses. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=123 SRC="FIGDIR/small/732609v1_ufig1.gif" ALT="Figure 1"> View larger version (38K): org.highwire.dtl.DTLVardef@1d25f43org.highwire.dtl.DTLVardef@6c476aorg.highwire.dtl.DTLVardef@c4a02aorg.highwire.dtl.DTLVardef@ef417d_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphical abstractC_FLOATNO C_FIG

neuroscience↗

bioRxiv2026

Instability of Alpha Oscillatory States in Autism and Familial Liability: Evidence from Burst-Resolved High-Density Electroencephalography (EEG)

Atypical sensory experiences are highly prevalent in autistic children and include both hyper- and hypo-responsivity, often accompanied by sensory overload. Alpha oscillations (7-13 Hz), which dynamically regulate cortical excitability, represent a plausible neural mechanism underlying these phenomena: reduced alpha activity is associated with enhanced sensory responsiveness, whereas increased alpha supports suppression of external input. Although decreased alpha power has been repeatedly reported in autism, it remains unclear whether this reduction reflects lower oscillatory amplitude or reduced temporal stability of alpha rhythms, two mechanisms with distinct neurophysiological implications. To better characterize alpha activity in autism, we examined resting-state alpha dynamics in non-autistic children (NA; n = 39), autistic children (AU; n = 52), and siblings of autistic children (SIB; n = 26), aged 8-14 years. We combined traditional broadband measures of relative alpha power, parametric separation of periodic and aperiodic activity, and single-event analyses that quantify the temporal structure of alpha oscillations. Both broadband relative alpha power and periodic alpha power were reduced in autism over parietal regions, replicating prior findings. Importantly, ordinal analyses revealed an intermediate profile in siblings, supporting a liability-related gradient of alpha alterations. However, single-event analyses demonstrated that the average amplitude of individual alpha bursts did not differ between groups. Instead, autistic children showed significantly shorter alpha burst duration and reduced alpha abundance (i.e., proportion of time occupied by rhythmic alpha episodes), with siblings again exhibiting intermediate values. Linear regression analyses confirmed that reductions in relative and periodic alpha power were primarily driven by decreased alpha abundance rather than diminished burst amplitude. These findings indicate that altered alpha activity in autism reflects reduced temporal stability and density of alpha events rather than weaker oscillatory amplitude per se. Reduced persistence of alpha rhythms may therefore represent a neural marker of altered cortical excitability and sensory regulation in autism. Lay summaryAutistic children often experience the world differently at the sensory level, including being more easily overwhelmed by sounds, lights, or other stimuli. In this study, we looked at a type of brain activity called alpha rhythms, which help regulate how strongly the brain responds to incoming information. We found that, in autistic children, these alpha rhythms were not weaker when they occurred, but they lasted for a shorter time and happened less often. Siblings of autistic children showed an intermediate pattern. These results suggest that sensory differences in autism may be linked to less stable brain rhythms that normally help control sensory input. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=158 SRC="FIGDIR/small/716324v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@1be733dorg.highwire.dtl.DTLVardef@7fea49org.highwire.dtl.DTLVardef@1ee9124org.highwire.dtl.DTLVardef@17af139_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2024

Neural Mechanisms of Intersensory Switching: Evidence for Delayed Sensory Processing and Increased Cognitive Effort

Intersensory switching (IS), the ability to shift attention between different sensory systems, is essential for cognitive flexibility, yet leads to slower responses compared to repeating the same sensory modality. The underlying neural mechanisms of IS remain largely unknown. In this study, high-density EEG was used to investigate these mechanisms in healthy adults (n=53) performing a speeded reaction time (RT) task involving visual and auditory stimuli. Trials were categorized as Repeat (same preceding modality) or Switch (different preceding modality). Switch trials showed slower RTs and delayed sensory responses (N1 and P2 components). Furthermore, across both Repeat and Switch trials, RT correlated with the latency of these neural responses. Additionally, lower alpha-band inter-trial phase coherence (ITPC) in primary sensory regions was noted for Switch compared to Repeat trials, suggesting reduced efficiency of sensory processing. Greater induced theta activity over fronto-central scalp regions in Switch trials suggested increased cognitive control demands, potentially involving the anterior cingulate cortex (ACC). These findings reveal that IS is characterized by delayed sensory processing and heightened cognitive load, supporting a model where prior stimulus primes the sensory cortex for faster processing in Repeat trials, while Switch trials demand more cognitive resources for adjustment. The similarity of effects across both auditory and visual sensory modalities suggests that IS effects represent core features of sensory processing, potentially reflecting a fundamental, modality-independent mechanism of attentional switching across sensory domains.

neuroscience↗