The researchers built the system around a modified one-dimensional ResNeXt-29 network that processed four recording channels: three electroencephalography signals from frontal, somatosensory and visual cortex, plus dorsal-neck electromyography. Each four-second window contained 2,000 samples and was converted into a 512-dimensional embedding. Sleep stages were Wake, non-rapid eye movement sleep, REM sleep and Artifact. The dataset was imbalanced, comprising 43.8% Wake, 43.5% NREM, 12.3% REM and 0.3% Artifact windows. Two experienced annotators scored recordings, with Cohen’s kappa reaching 0.84 on a four-stage verification set. The annotators were not blinded to treatment, a limitation acknowledged by the authors because awareness of experimental condition could, in principle, influence labels.

A central architectural element was a 128-dimensional Global Context Vector, or GCV, operating as a learnable memory bank across a sequence of 512 windows, equivalent to about 34 minutes of recording. After each of the three ResNeXt stages, bidirectional cross-attention allowed information to flow both from the convolutional features into the GCV and from the GCV back into the signal representation. Temporal self-attention, position-wise feed-forward networks, residual connections and layer normalization were incorporated at each stage. A four-layer Transformer encoder then classified each window using its full one-minute context, while a lightweight parallel branch classified windows independently and served only as a training regularizer. Only the contextual branch was used for reported test predictions.

The model was trained with label-smoothed cross-entropy and an auxiliary supervised contrastive loss. For contrastive learning, each batch was passed through the network twice with independently sampled physiological augmentations, including mild Gaussian noise, conservative amplitude scaling, circular shifts of up to 40 milliseconds, occasional channel dropout and occasional polarity inversion. Windows with the same sleep-stage label, as well as two augmented versions of the same window, were treated as positive examples. The contrastive objective was intended to group embeddings by stage while reducing sensitivity to nuisance variation. In a separate ablation, gradient-reversal heads attempted to make the embedding uninformative about subject identity and treatment condition, but this adversarial component produced negligible additional benefit and was excluded from the default model.

Across five-fold cross-validation, each fold withheld complete animals from training, allowing the researchers to test whether performance generalized beyond idiosyncratic signal patterns. The full model achieved a macro-averaged F1 score of 0.943, accuracy of 0.944 and ROC-AUC of 0.993, with standard deviations across folds of 0.008, 0.008 and 0.001, respectively. It outperformed SlumberNet, whose F1 was 0.870, and Random Forest, whose F1 was 0.879; the differences were statistically significant under a Nadeau and Bengio corrected resampled t-test, with p values of 0.0001 and 0.0401. AttnSleep achieved 0.801 F1, although its adaptation for four-channel input did not preserve the architecture’s original per-channel attention design. Random Forest also showed a pronounced training-validation gap, reaching 99.9% training F1 but 88.1% validation F1.

Ablation results identified global context as the largest single contributor. Removing the GCV reduced F1 by 2.3 percentage points, equivalent to a 25.3% reduction in classification error relative to the ablated version. Initializing the vector with all zeros performed best, suggesting that a task-specific memory could be learned more effectively than manually supplied spectral summaries or randomly initialized values. Supervised contrastive learning added a more modest 0.6 percentage points in F1 and an 8.2% error reduction. Linear probes offered another view of the representation: sleep stage was decoded from frozen embeddings with balanced accuracy of 0.912, whereas subject identity was decoded at 0.130 against chance of 0.077 and treatment at 0.312 against chance of 0.250. An encoder lacking both the GCV and contrastive loss encoded subject and treatment information more strongly, at 0.214 and 0.421, respectively.

The most demanding evaluation asked whether a model trained without any drug data could classify recordings from unseen animals under pharmacological perturbation. In this saline-only protocol, the same subject-held-out folds were retained, so successful prediction required transfer across both subjects and treatments. Mean F1 was 0.937, less than one percentage point below the 0.943 obtained with the full dataset. Performance was lowest for psilocybin at 0.932, followed by the drug combination at 0.939 and MDL100907 at 0.946. The psilocybin result coincided with pronounced REM suppression and altered theta-band dynamics, while MDL100907 produced the smallest departure from the control distribution. A size-matched random subsample performed comparably to the saline-only model, suggesting that the small residual gap was associated mainly with fewer training examples rather than failure under drug shift.

The system was also relatively economical with expert labels. Training on only one hour of annotated data produced accuracy above 88% and F1 of 0.832. Performance rose substantially by eight hours, reaching F1 of 0.921, and then largely plateaued: F1 was 0.919 with 12 hours and 0.918 with 24 hours, compared with 0.943 for the approximately 1,000-hour dataset. The eight-to-12-hour range represented about 1% of the complete corpus while trailing full-data performance by only 2.4 percentage points in F1. Context-aware Grad-CAM analysis also showed that model saliency tended to concentrate around state transitions and waveform segments that departed from their surrounding baseline. This is consistent with the model using sequence-level information when local four-second evidence is ambiguous, although the maps do not directly reveal the direction of information flow between individual epochs.

Several boundaries limit how broadly the findings can be applied. The experiments involved only 13 adult male rats from a single supplier and laboratory, so performance across other electrode configurations, ages, sexes, species or recording protocols remains unverified. Both psilocybin and MDL100907 act through the serotonergic system; transfer to compounds with fundamentally different GABAergic, dopaminergic or glutamatergic mechanisms is untested. The Transformer also receives at most 34 minutes of context rather than a complete sleep cycle, and the model requires all four input channels at inference despite using channel dropout during training. Per-subject z-scoring may additionally bias predictions when drug treatments substantially change the proportion of time spent in each stage. The method complements established tools such as AccuSleep, SPINDLE, Sleep-deep-learner and Somnivore rather than replacing them, and direct comparison with those pipelines, including any calibration or retraining they require, remains future work. With external validation and broader drug testing, the results nevertheless offer a promising route to reducing manual scoring in drug-discovery sleep studies without treating each new animal or treatment condition as an entirely separate classification problem.

Subject of Research: Deep-learning classification of rodent sleep stages from EEG and EMG under pharmacological conditions

Article Title: Global context integration for pharmacologically robust preclinical sleep stage classification

Article References: Brejtr, V., Aleksić, K., Šíchová, K., Vejmola, Č., Páleníček, T., & Lhotská, L. (2026). Global context integration for pharmacologically robust preclinical sleep stage classification. Scientific Reports, 16(1), Article 33004. https://doi.org/10.1038/s41598-026-57917-0

Image Credits: AI Generated

DOI: 10.1038/s41598-026-57917-0

Keywords: rodent sleep staging, deep learning, electroencephalography, electromyography, pharmacology, domain generalization, psilocybin, MDL100907, Transformer models, preclinical neuroscience, Global, context

According to the editorial notice, the decision stems from a broader review rather than from a specific dispute about the study’s data. The PLOS One Editors state that the article was identified as one of a series of submissions about which the journal has concerns regarding the integrity and reliability of the peer review process. In other words, the question is not, at least so far, whether the measurements themselves are accurate, but whether the manuscript was properly vetted by independent experts before publication. That distinction matters, because peer review is the mechanism that journals rely on to filter out flawed methods, unsupported conclusions, and undisclosed conflicts before a paper becomes part of the citable literature.

The notice is notable for what it does and does not assert. PLOS explicitly states that it did not evaluate the article’s integrity or scientific validity while following up on the matter, and readers are advised to interpret the paper with consideration of the peer review concerns. This is a deliberately cautious formulation. An Expression of Concern sits below a full retraction in the hierarchy of post-publication corrections: it signals unresolved doubt, keeps the paper in the database so that other researchers can still find and cite it, and reserves judgment until an investigation concludes or the situation is otherwise resolved. Journals typically resort to this notice when concerns are credible but the underlying facts have not yet been fully established.

Equally significant is what the editors say about the authors. The notice records that PLOS has no evidence of any author involvement in the peer review concerns. That statement matters because schemes in which reviewers fake their own identities or coordinate approving reviews, sometimes called peer review rings, have historically implicated authors who submitted fabricated reviewer email addresses. By stating that no author involvement is suspected here, PLOS is locating the problem elsewhere in the pipeline, while leaving open exactly where the failure occurred. The editors also note that the academic editor listed on the article is a PLOS staff editor who was not involved in the concerns and was unaware of the peer review issues before the article was published, an apparent attempt to shield that individual from unfair inference.

The underlying study itself addressed a clinically active area of research. The pelvic floor muscles form a hammock-like group of fibers spanning the base of the pelvis, and weakness or dysfunction in these muscles is associated with urinary incontinence, pelvic organ prolapse, and other conditions that affect a large share of the population, particularly after childbirth and with advancing age. Electromyography, or EMG, is the standard tool for assessing such muscles noninvasively: surface or intravaginal electrodes detect the tiny electrical signals generated when muscle fibers contract, allowing researchers and clinicians to quantify activation strength and timing. Because the pelvic floor is invisible from outside the body and difficult to activate consciously, biofeedback devices that help patients learn correct muscle engagement have become a focus of physiotherapy research.

Against that background, the flagged paper evaluated electromyographic activity of the pelvic floor muscles in different body positions while participants used what the authors describe as an innovative vaginal educator, a device intended to teach patients how to locate and contract the right muscles. Posture is genuinely consequential in this field, because muscle activation measured standing can differ from activation measured lying down, and rehabilitation protocols often specify positions accordingly. A device that reliably guides patients through contractions in multiple positions could, in principle, improve home-based pelvic floor training, which is why such cross-sectional comparisons attract clinical interest. The Expression of Concern does not dispute the plausibility of that research question; it concerns the process by which the report was reviewed.

The mechanics of peer review, when it functions as designed, are straightforward. A journal editor sends a manuscript to two or more independent experts, who assess the methods, statistics, and interpretations and recommend acceptance, revision, or rejection. The system’s weakness is its dependence on trust: reviewers are usually invited based on email addresses supplied with the manuscript or drawn from a database, and journals historically have had limited tools to verify that a reviewer is who they claim to be. Large open-access journals that process tens of thousands of submissions each year are particularly exposed to abuse at scale, and several publishers have spent recent years tightening identity checks, cross-referencing reviewer accounts, and screening submissions for telltale signs of coordinated manipulation.

PLOS has been among the publishers most visibly affected by such schemes. The publisher has previously issued mass retractions involving large numbers of papers in which peer review was compromised, and expressions of concern have become its preferred instrument when an investigation is incomplete. Grouping this article into a series of submissions with related concerns suggests the journal detected a pattern, perhaps through shared reviewer identities, overlapping manuscript characteristics, or anomalies flagged by screening software, and has chosen to annotate every affected paper rather than quietly removing any single one. That approach preserves transparency: readers, funders, and institutions can see the warning attached directly to the record, and the scientific record is amended rather than erased.

For clinicians and researchers who cite the pelvic floor study, the practical consequences are immediate. Citation managers and databases such as PubMed will continue to list the paper, which appeared in PLOS One in March 2024 and carries PubMed identifier 38536803, but the Expression of Concern is now part of its permanent record, linked through the digital object identifiers of both the notice and the original article. Authors citing the work are expected to disclose the notice; failure to do so can itself be treated as a reporting omission. For patients, the direct implications are more limited, since a single cross-sectional measurement study does not by itself set treatment guidelines, but the episode underscores why rehabilitation devices and protocols should be adopted on the strength of multiple, independently reviewed lines of evidence rather than one publication.

The case also illustrates a broader shift in how science polices itself. Post-publication notices were once rare and carried stigma; they are now a routine tool that allows journals to respond quickly to suspected problems without waiting years for institutional investigations to run their course. Whether this particular study is ultimately validated, corrected, or retracted, the record now tells readers exactly what is known and what remains unresolved: the journal has doubts about the reliability of the peer review that preceded publication, no evidence against the authors, and no finding on the science itself. In an era when a single paper can shape clinical practice within months of appearing online, that calibrated honesty may be the notice’s most valuable contribution.

Subject of Research: Peer review integrity concerns surrounding a 2024 PLOS One study of pelvic floor muscle electromyography during use of a vaginal educator device

Article Title: Expression of Concern: Electromyographic activity of pelvic floor muscles in different positions during the use an innovative vaginal educator: Cross-sectional study

Article References: The PLOS One Editors (2026). Expression of Concern: Electromyographic activity of pelvic floor muscles in different positions during the use an innovative vaginal educator: Cross-sectional study. PLOS One, 21(10), e0360775. https://doi.org/10.1371/journal.pone.0360775

Image Credits: AI Generated

DOI: 10.1371/journal.pone.0360775

Keywords: PLOS One, Expression of Concern, peer review, research integrity, pelvic floor muscles, electromyography, vaginal educator, biofeedback, open access, cross-sectional study, publication ethics, post-publication correction

The study, led by Alessandro Scano of Italy’s National Research Council in Milan, does not present new in vivo data. Instead, it delivers something arguably more disruptive: a conceptual and computational critique of how the field interprets its own most successful framework. Scano’s argument begins with an observation that has long been treated as a nuisance. When researchers extract muscle synergies from multichannel electromyography (EMG), the resulting modules differ systematically between individuals and even within the same person across sessions and contexts. Standard practice has been to average these differences away or dismiss them as measurement error. Scano flips that assumption on its head, proposing that a substantial portion of this variability is structured, meaningful, and traceable to three non-motor layers of control that standard synergy extraction methods simply never measure.

The first layer is cognitive. Before any movement is executed, the brain constructs an internal model of the task—what the goal is, which strategy might work, where attention should be allocated. This internal representation is not fixed. Two people given identical instructions may build qualitatively different models of the same task, leading to different motor solutions. In overlearned actions like walking, the cognitive layer recedes into the background. But in strategically demanding situations—imagine a penalty kick where the shooter must read the goalkeeper’s posture, weigh probabilities, and select not just how to kick but which kick to attempt—the cognitive layer becomes the dominant driver of motor output. Experimental evidence shows that such decision-making can alter movement kinematics and timing even when the final motor goal is unchanged, a finding consistent with the view that motor control is fundamentally decision-making.

The second layer is affective, and its fingerprints on muscle activity are among the best documented in psychophysiology. Anxiety and stress reliably increase muscle co-contraction, stiffen movement, and elevate variability, reflecting a shift toward rigid, conservative control strategies. Confident or positive states, by contrast, are associated with more fluid and energetically economical patterns. The infamous phenomenon of choking under pressure—when well-learned skills disintegrate at the worst possible moment—exemplifies this modulation. Neurophysiologically, these effects align with the classical Yerkes–Dodson law: moderate arousal can sharpen performance, while excessive anxiety degrades it. Scano’s framework interprets affective states as gain modulators that adjust the operating regime of the motor system—muscle tone, variability, responsiveness to feedback—without necessarily specifying new motor commands. The same internal task representation can thus produce markedly different muscle activation patterns depending on the performer’s emotional state.

The third layer is experiential, and it may be the most conceptually radical. Scano argues that what researchers identify as muscle synergies may partially reflect a subject’s motor history rather than a universal organizational principle of the nervous system. Athletes trained in different disciplines—throwing sports, racket sports, or non-athletic backgrounds—often exhibit systematically different coordination patterns when performing superficially identical movements, differences that biomechanics alone cannot explain. These stored patterns are embodied priors: stabilized coordination solutions carved out by repeated practice and reused across tasks. In this reading, the motor primitives that the field has treated as hardwired building blocks may be better understood as the fossilized residue of learning—patterns that emerged through experience and were subsequently consolidated into what looks like intrinsic structure.

To make these ideas testable, Scano proposes a quantitative extension of the standard synergy model. In the classical formulation, EMG activity is decomposed into spatial synergies (the matrix W) and temporal activation coefficients (the vector c). The framework hypothesizes that cognitive, affective, and experiential factors primarily modulate the temporal structure of motor commands—the coefficients c—while the spatial modules W remain comparatively stable during transient contextual shifts. This distinction has a neurophysiological rationale: spatial primitives are widely considered to be encoded in spinal and brainstem premotor networks, whereas acute stress or cognitive load characteristically modulates the descending central drive rather than instantly restructuring low-level anatomical circuitry. The proposal introduces an Augmented Reconstruction Index (ARI), which partitions the variance explained by a synergy-based model into a motor component and an additional context-dependent component, quantified by the incremental contribution of contextual variables such as heart rate variability, electrodermal activity, or brief self-reports of anxiety and effort.

The computational proof-of-concept is where the argument becomes genuinely alarming for anyone who has published synergy analyses. Scano simulated an eight-muscle upper-limb reaching task driven by three ground-truth spatial synergies, then added a simulated internal state—a tonic contextual variable with a fixed value of 0.6 and a sensitivity vector introducing module-specific shifts—to mimic the sustained baseline EMG elevation, heightened sympathetic tone, and generalized low-level co-contraction documented in real subjects under psychological pressure or cognitive load. When standard unconstrained non-negative matrix factorization (NMF) was applied to this contextualized data, it achieved a marginally higher overall reconstruction (R² = 0.9989) than the constrained ARI approach (R² = 0.9983). But it achieved this mathematical edge by distorting the extracted spatial synergies to absorb the contextual offset—a phenomenon Scano terms structural drift. The algorithm misinterpreted context-driven tonic changes as a fundamental reorganization of the underlying motor coordination strategy, even though the true spatial modules had never changed.

The implications extend beyond simulation. In real-world human data, where typical reconstruction quality hovers around 90 percent rather than the near-perfect levels of the toy model, the failure to account for context may force unconstrained decomposition methods to artificially extract an additional, supernumerary synergy to explain variance that actually reflects a stress-induced tonic offset. Scano calls this coefficient pollution: a mathematical artifact that merges genuine biological motor structure with context-dependent modulation, destroying the neurophysiological interpretability of the decomposition. A sudden shift in cognitive load modulates central drive, but it does not instantaneously create a new anatomical primitive. The conventional workaround—simply increasing the number of extracted synergies—lacks physiological justification for transient contextual modulations and risks publishing phantom synergy reorganizations that are actually stress signatures in disguise.

The framework generates five falsifiable predictions that can be tested with standard motor control paradigms augmented with minimal assessments. Experimentally induced stress should systematically alter temporal activation patterns while leaving spatial synergies stable, manifesting as an increase in the context-dependent component of explained variance. Cognitive load under dual-task conditions should similarly inflate context-dependent variance. Experts and novices performing the same task may show comparable motor reconstruction quality but differ systematically in the structure of their latent contextual factors, suggesting that differences traditionally attributed to motor primitives may instead reflect embodied priors. As tasks become familiar through practice, the contextual contribution should progressively shrink. And standard decomposition methods should continue to misattribute contextual offsets to spurious structural changes—a prediction the simulation already demonstrates.

The practical consequences ripple outward from basic research into rehabilitation and human–robot interaction. In clinical settings, altered muscle synergies are typically attributed to neural damage or biomechanical constraint, but the framework highlights that anxiety, motivation, cognitive deficits, and prior experience can also shape patient-specific coordination patterns—meaning that variability currently misread as impairment may partly reflect treatable affective or cognitive states. Rehabilitation protocols could be enhanced by targeting task understanding and emotional regulation alongside motor execution, and Scano notes that in robotic applications, an exoskeleton control system equipped with the ARI framework would avoid confusing user stress with a change in motor intention. The author is careful to acknowledge limitations: the linear coupling between contextual states and temporal activations is a first-order approximation, real psychological factors almost certainly combine non-linearly, and the framework captures instantaneous dynamics rather than longitudinal plasticity. But the core message stands with unusual clarity for a theoretical paper. Muscle synergies are not fixed building blocks of movement; they are context-dependent coordination patterns emerging from an integrated cognitive–motor system. The variability that decades of synergy analysis have treated as noise may be the richest signal in the entire dataset—the measurable trace of a mind shaping every movement it commands.

Subject of Research: From motor primitives to context-dependent coordination: a system neuroscience approach integrating cognitive, affective, and experiential factors into muscle synergy analysis

Article Title: From motor primitives to context-dependent coordination: a system neuroscience approach integrating cognitive, affective, and experiential factors into muscle synergy analysis

Article References: Scano, A. (2026). From motor primitives to context-dependent coordination: a system neuroscience approach integrating cognitive, affective, and experiential factors into muscle synergy analysis. Frontiers in Systems Neuroscience, 20, Article 1838867. https://doi.org/10.3389/fnsys.2026.1838867

Image Credits: AI Generated

DOI: 10.3389/fnsys.2026.1838867

Keywords: motor, primitives, context-dependent, coordination, system, neuroscience, approach, integrating, cognitive, affective, experiential, factors

The choice of a 30-second sustained contraction at 50 percent of maximum bite force is methodologically significant. De Luca’s classic work on fatigue assessment suggested that contractions exceeding roughly 30 percent of maximal voluntary strength generate enough intramuscular pressure to occlude blood flow, restricting oxygen delivery and forcing the muscle toward anaerobic metabolism. This creates a relatively standardized metabolic environment in which fatigue develops predictably, while still allowing the task to be tolerable for participants. Shorter protocols of five to ten seconds at maximal effort, which have dominated much of the prior TMD literature, capture a different physiological regime: the signal is dominated by neural drive and motivation rather than by accumulating metabolic fatigue, and the brief duration limits the time over which spectral compression can develop. By using a longer submaximal task with real-time force feedback from a bilateral bite dynamometer, the present design ensured that participants in both groups worked at genuinely equivalent relative loads, reducing the possibility that differences in effort or force output would confound the comparison between groups.

Several physiological explanations could account for the paradoxical finding of greater fatigue signatures in the asymptomatic group. One possibility involves differences in motor unit recruitment strategies. Individuals with chronic myofascial pain often adopt altered motor strategies, including co-contraction patterns, reduced relaxation between contractions, or a shift toward greater reliance on slower, more fatigue-resistant motor units even during low-intensity tasks. If the TMD group habitually recruits a more homogeneous population of low-threshold motor units, the spectral shift during a sustained contraction may be less pronounced because the already slow-conducting fibers have less room to slow further. The asymptomatic group, by contrast, may recruit a broader spectrum of motor units, including faster, higher-threshold units whose conduction velocities decline more dramatically as fatigue develops, producing the steeper median frequency slopes observed in their masseter muscles.

Another consideration is the role of pain-related protective mechanisms. Persistent masticatory muscle pain is frequently accompanied by a phenomenon in which the central nervous system modulates activation to protect painful tissues, sometimes described as pain-adaptive motor behavior. This can include reduced maximal voluntary force, altered distribution of load across synergistic muscles, and periodic micro-pauses in activation. If participants in the TMD group distributed the bite task differently, for example by intermittently shifting load between the masseter and temporalis or between the two sides, the effective metabolic demand on any single muscle could have been lower, blunting the fatigue signature. The finding that the left anterior temporalis showed a steeper RMS increase in the control group while the masseter slopes differed on both sides is consistent with the idea that the two muscles contribute differently to sustained biting, and that this division of labor may be reorganized in the presence of chronic pain.

The asymmetry between the left and right sides in the results also deserves attention. The significant between-group differences appeared in the right and left masseter for median frequency but only in the left anterior temporalis for root mean square. Bilateral molar biting is not necessarily symmetric; handedness, chewing side preference, occlusal contact patterns, and subtle anatomical asymmetries of the mandible can all produce lateralized differences in muscle activation. In asymptomatic individuals, such asymmetries are usually small and functionally inconsequential, but in individuals with TMD, unilateral symptoms can amplify them. The fact that the TMD group did not show greater fatigue on either side suggests that whatever lateralization exists in their chewing behavior did not translate into a systematically faster fatigue development in this protocol, but the side-specific findings in the control group highlight that masticatory muscle fatigue is not a uniform, bilateral phenomenon even in healthy individuals.

The composition of the TMD group also matters for interpreting the results. Participants were required to have a primary myogenic diagnosis, either myalgia or myofascial pain, but could carry comorbid intra-articular diagnoses such as arthralgia or disc displacement with reduction. This heterogeneity reflects clinical reality, since pure muscle-only TMD is uncommon, but it introduces potential variability. Individuals with concurrent joint involvement may adopt different mandibular positioning or muscle activation patterns than those with isolated muscle pain, and these differences could increase within-group variability, making it harder to detect between-group differences in fatigue slopes. The relatively balanced distribution of myalgia and myofascial pain diagnoses within the group, with and without referral patterns, suggests the investigators aimed to capture the typical clinical presentation, but future studies stratifying by specific diagnosis combinations could clarify whether particular subgroups show distinct fatigue profiles.

The restriction to women aged 18 to 40 with a body mass index below 25 was a deliberate design choice with important implications. Sex differences in masticatory muscle morphology, hormonal influences on pain sensitivity and muscle metabolism, and the higher prevalence of TMD among women all justify studying a single sex, but they also limit generalizability. Estrogen fluctuations across the menstrual cycle have been linked to altered pain perception and potentially to differences in muscle fatigue resistance, and although the study did not report cycle phase control, the homogeneous age range reduces some sources of hormonal variability. Similarly, excluding individuals with elevated body mass index avoids confounding from differences in craniofacial morphology and adipose tissue effects on surface EMG signal quality, since subcutaneous fat acts as a low-pass filter that attenuates high-frequency signal components and can distort median frequency estimates.

The use of the angulation coefficient, the slope of the linear regression of each parameter over the 30-second contraction, rather than simple pre-post differences, represents a methodological refinement worth emphasizing. A slope captures the rate of change continuously across the entire task and is less sensitive to noise at any single time point than a two-point comparison. It also allows detection of differences in the trajectory of fatigue even when the absolute starting and ending values are similar between groups. Two individuals could begin and end a contraction with comparable median frequencies yet differ substantially in how quickly that decline unfolded, and the regression slope distinguishes these patterns. This approach is particularly valuable when comparing clinical populations to controls, because baseline signal characteristics often differ between groups, and slope-based measures partially normalize for those baseline differences.

From a clinical standpoint, the results raise questions about how fatigue testing should be interpreted in TMD assessment. If individuals with chronic masticatory muscle pain do not exhibit exaggerated fatigue responses during standardized sustained tasks, then reduced fatigue capacity may not be a defining feature of myogenic TMD, contrary to models that emphasize muscle overuse and fatigue as primary pain drivers. Alternatively, the altered fatigue signature in the TMD group could reflect a genuinely different, perhaps more economical, motor strategy developed over time, or a protective downregulation of activation that limits metabolic stress. Distinguishing between these interpretations requires studies that combine surface EMG with measures of muscle oxygenation, such as near-infrared spectroscopy, or with intramuscular recordings that can resolve single motor unit behavior, since surface signals aggregate the activity of many units and cannot fully separate peripheral metabolic fatigue from central modulation of drive.

The cross-sectional design also constrains causal inference. The observed differences in fatigue slopes could be a consequence of living with chronic pain, a pre-existing trait that predisposed individuals to develop TMD, or an artifact of differences in task performance such as force fluctuation, jaw positioning, or motivation. Longitudinal designs following asymptomatic individuals through the onset of TMD symptoms, or intervention studies that reduce pain and then reassess fatigue parameters, would help determine whether the blunted fatigue response is a cause or consequence of the disorder. Additionally, the 30-second duration, while longer than many prior protocols, remains a relatively brief sustained contraction; longer tasks approaching true endurance limits might reveal group differences that a half-minute contraction does not, particularly if the TMD group’s altered recruitment patterns only become metabolically consequential over longer time scales.

Finally, the findings underscore the value of bilateral, force-controlled protocols in masticatory muscle research. Unilateral maximal bites and short isometric bursts, the dominant paradigms in earlier work, may not represent the sustained, submaximal loading that characterizes real-world masticatory function, where muscles repeatedly contract at moderate intensities over extended chewing periods. A sustained bilateral submaximal task with continuous force feedback more closely approximates this functional demand and, as the present results demonstrate, can produce group patterns that contradict those seen in maximal-effort tests. This discrepancy suggests that fatigue assessed under one set of task conditions may not generalize to others, and that a comprehensive characterization of masticatory muscle function in TMD will ultimately require protocols spanning the range from brief maximal efforts to prolonged submaximal endurance tasks, ideally combined with measures of pain, jaw function, and psychological factors that shape how individuals with chronic orofacial pain use their muscles in daily life.

Subject of Research: EMG fatigue signs during sustained bilateral submaximal biting were more pronounced in asymptomatic women than in women with myogenic TMD.

Article Title: Comparison of MF and RMS EMG parameters in women with TMD and asymptomatic women during sustained bilateral submaximal bite force protocol

Article References: Pires, P. F., Pelai, E. B., Galvani, S. C. F., Pulino, B., de Moraes, M., de Castro-Carletti, E. M., Foltran-Mescollott, F., Guerra, R. C., & Rodrigues-Bigaton, D. (2026). Comparison of MF and RMS EMG parameters in women with TMD and asymptomatic women during sustained bilateral submaximal bite force protocol. Frontiers in Pain Research, 7, Article 1962220. https://doi.org/10.3389/fpain.2026.1962220

Image Credits: AI Generated

DOI: 10.3389/fpain.2026.1962220

Keywords: EMG, TMD, muscle fatigue, masseter, temporalis, bite force, median frequency, RMS, orofacial pain, electromyography, Comparison, parameters

The research team, led by investigators at Huazhong University of Science and Technology in Wuhan, China, recruited twenty female college soccer players aged nineteen to twenty-three from two university teams. Each participant completed the Yo-Yo Intermittent Endurance Level 2 Test, a widely validated soccer-specific fatigue protocol involving repeated twenty-meter shuttle runs at progressively increasing speeds. Fatigue was confirmed when athletes reached a heart rate of at least eighty-five percent of their estimated maximum or reported a rating of fifteen or higher on the Borg six-to-twenty perceived exertion scale. All twenty participants met the fatigue criteria before post-fatigue testing began.

Researchers assessed three movement tasks before and after fatigue induction: single-leg landing from a thirty-centimeter platform, double-leg landing from the same height, and a zigzag running course with four five-meter segments and a one-hundred-degree turning angle. Surface electromyography recorded activity from twelve lower limb muscles, including the rectus femoris, vastus lateralis, vastus medialis, biceps femoris, semitendinosus, and tibialis anterior on both legs. Force plates simultaneously captured peak vertical ground reaction forces, stabilization time, and center of pressure displacement, providing a complementary kinetic picture of how fatigue altered landing mechanics.

The most robust finding emerged during double-leg landing, where normalized muscle activation dropped significantly in three key quadriceps muscles. The right vastus lateralis showed a decrease from a median of 8.58 to 7.78 percent peak amplitude, the left vastus lateralis fell from 9.45 to 8.36, and the right vastus medialis declined from 9.86 to 8.27. Critically, these three results survived false discovery rate correction, a statistical safeguard that filters out findings likely to be false positives. Every other significant change in the study remained exploratory, meaning the authors urge caution in interpreting them as definitive fatigue effects.

During single-leg landing, the picture shifted. Peak vertical ground reaction force, normalized to body weight, decreased significantly on both sides after fatigue. The left foot dropped from 2.52 to 2.34 body weights while the right fell from 2.69 to 2.40, both surviving statistical correction. Stabilization time, the duration from ground contact until force fluctuations settled within five percent of body weight, also lengthened on the left side, though this finding did not survive correction and remains tentative. The authors suggest this combination may reflect a more conservative landing strategy adopted under fatigue, where athletes deliberately soften impact forces to maintain control at the expense of explosive cushioning.

In zigzag running, a pre-fatigue asymmetry in rectus femoris activation between the left and right legs, which was statistically significant before correction, disappeared after fatigue. The researchers note this could indicate either a strategic shift toward more symmetrical muscle recruitment or simply bilateral neuromuscular fatigue dampening output on both sides. Without concurrent kinematic data capturing joint angles and moments, the team cannot determine which interpretation is correct. They also acknowledge that because zigzag running was tested last, six to eight minutes after the fatigue protocol, partial recovery may have influenced the result.

The study’s context matters. Women’s soccer participation has surged globally, reaching approximately 16.6 million organized players as of 2023, and female athletes face a substantially elevated risk of non-contact anterior cruciate ligament injuries compared to males, with soccer players sustaining four to six times the risk. Fatigue, bilateral lower limb asymmetry, and neuromuscular control deficits are recognized as key contributors. Collegiate athletes, who often train with less structured periodization than professionals, may be particularly vulnerable to fatigue-induced changes in movement strategy.

The authors are careful to frame their conclusions within the study’s limitations. The sample was drawn from only two university teams, the within-subject design lacked a non-fatigued control group, and the fixed testing sequence means task-order effects cannot be fully separated from fatigue effects. Sleep, nutrition, and menstrual cycle data were not collected. Nonetheless, the findings offer preliminary support for targeted training interventions, including unilateral stability work, quadriceps fatigue resistance, and multidirectional neuromuscular conditioning tailored to the demands of change-of-direction play.

For coaches and sports scientists, the message is that fatigue does not degrade all muscles equally or uniformly across tasks. The knee extensors appear most vulnerable during bilateral landing, while single-leg stability and cutting mechanics show different patterns of adaptation. As women’s soccer continues its rapid global expansion, understanding these task-specific neuromuscular responses may prove essential for designing injury prevention programs that keep athletes healthy deep into matches and tournaments.

Subject of Research: Effects of fatigue on lower limb neuromuscular control and landing biomechanics in female collegiate soccer players

Article Title: The impact of fatigue on lower limb neuromuscular control in female college soccer players

Article References: Xiang, T., Zhu, T., Ma, H., Mu, Z., Han, Z., Imai, K., Shen, S., Guo, Z., & Zhou, X. (2026). The impact of fatigue on lower limb neuromuscular control in female college soccer players. Frontiers in Sports and Active Living, 8, Article 1918634. https://doi.org/10.3389/fspor.2026.1918634

Image Credits: AI Generated

DOI: 10.3389/fspor.2026.1918634

Keywords: sports science, female athletes, soccer, neuromuscular control, fatigue, ACL injury, biomechanics, electromyography, impact, lower, limb, neuromuscular

The research builds on a long-standing theory in motor neuroscience that the central nervous system generates movement from a small set of building blocks known as motor primitives. Within this framework, discrete movements are modeled as point-attractor dynamics: the limb moves from one stable posture to another, then stops. Rhythmic movements, by contrast, are modeled as limit-cycle dynamics, producing continuous periodic oscillations with stable phase relationships. Decades of evidence, from neuroimaging to motor-learning experiments, indicate that these two movement classes recruit partly distinct neural networks. Discrete actions engage broader bilateral and non-primary motor areas, while rhythmic movements rely on more circumscribed cortical and cerebellar circuitry. Stroke patients, tellingly, often retain rhythmic arm movements better than discrete ones.

Most of that evidence, however, comes from the upper limb, where reaching is discrete by default and slow rhythmic movements have been shown to fragment into sequences of discrete submovements. Walking presents the mirror-image case: it is prototypically rhythmic, so finding discrete-like organization in gait is especially informative precisely where the framework is least expected. Slow walking is also clinically important, since reduced gait speed is common in aging and neurological disease, exactly the conditions in which rhythmic locomotor organization may be compromised. If walking speed acts as a control parameter that triggers phase-transition-like shifts in coordination, the transitions might even display hysteresis, the history dependence familiar from the classic walk-to-run transition, which occurs at a higher speed when accelerating than when decelerating.

To capture these shifts, the team recorded 18 healthy adults walking on an instrumented treadmill while a ten-camera motion capture system tracked reflective markers and wireless electrodes recorded activity from 15 lower-limb muscles on each side. Participants completed two protocols: in one, treadmill speed increased from 0.5 to 5.0 kilometers per hour in 0.5 km/h steps; in the other, it decreased along the same range. At each speed, participants completed 15 consecutive strides. The researchers then quantified movement smoothness using two complementary metrics, log dimensionless jerk (LDJ) in the time domain and spectral arc length (SPARC) in the frequency domain, applied to the antero-posterior displacement between the right and left ankles, a low-dimensional descriptor of the inter-limb oscillation that defines gait.

The smoothness results were striking. Both metrics became progressively less negative, indicating smoother movement, as speed increased. Mean LDJ values rose from roughly −16.0 at 0.5 km/h to about −10.5 at 5 km/h, while SPARC climbed from around −8.3 to −4.0. Crucially, the consistency of these changes across participants varied systematically with speed. Between 0.5 and 2.5 km/h, pairwise comparisons of smoothness showed high agreement, with 89 to 100 percent of participants showing significant differences between adjacent low-speed segments. Around 3.0 to 3.5 km/h, that agreement dropped to a moderate range, and at the highest speeds it collapsed almost entirely, with few or no participants showing significant differences between neighboring fast segments. The researchers interpret this intermediate band as a transition window in which individuals shift into a stable rhythmic attractor at slightly different speeds before converging at faster gait.

Smoothness alone, however, is an end-effector readout and cannot by itself prove that a kinematic regime shift reflects reorganized neural control rather than the mere biomechanical consequences of moving slowly. To resolve that ambiguity, the team turned to muscle synergy analysis, decomposing electromyographic signals with non-negative matrix factorization into time-invariant muscle weightings and time-varying activation profiles, selecting the minimum number of synergies that accounted for at least 90 percent of the variance. The number of modules required rose systematically with speed: at the slowest speeds, two synergies sufficed; at intermediate speeds, three; and from roughly 3 to 4 km/h onward, four synergies were needed, stabilizing at the fastest gait. In the decremental condition, the richer four-synergy organization persisted down to about 3 km/h before collapsing back to two at the slowest speeds.

That asymmetry between the incremental and decremental protocols is the study’s most intriguing detail. The neuromuscular system held on to its higher-dimensional coordination state longer when speed was falling than it took to build it when speed was rising, a pattern consistent with hysteresis in a dynamical system settling into stable attractors whose stability depends on a control parameter. The behavior echoes the well-documented hysteresis of the walk-run transition and suggests that the nervous system’s current coordination state depends on its recent history. Notably, smoothness itself showed only minimal directional differences, meaning the history dependence was evident primarily in the neuromuscular measure, while both measures converged on the same overall speed-dependent reorganization.

The link between the two levels of description was remarkably tight. Within every single participant, smoothness metrics and synergy number were strongly and positively correlated across speed segments, with a median Spearman correlation of 0.92 in both ramp directions. As gait became smoother with increasing speed, the modular organization of muscle activity grew richer, in every individual regardless of ramp direction. Merging analyses reinforced the picture: when stepping from a faster to an adjacent slower speed, the lower-speed synergies could be reconstructed with cosine similarities near 0.99 as non-negative combinations of the faster-speed modules, indicating that modules merge rather than vanish as speed drops. The authors draw a parallel to development and stroke recovery, where immature or impaired gait similarly shows fewer, merged modules, and they attribute the richer fast-walking organization to greater dynamic demands: stronger propulsion, tighter phase-specific timing, and increased balance and foot-clearance requirements.

The authors are careful about interpretation. Muscle synergies are estimated from data, and a successful reconstruction does not prove the recovered modules are neurally encoded primitives; the team treats them as a description of the structure of recorded muscle activity rather than direct evidence of discrete neural modules. Yet the speed-dependent changes were reproduced across two protocols, two decomposition levels, and an independently quantified kinematic transition, none of which would be expected from the factorization procedure alone. Limitations include treadmill rather than overground walking, some excluded EMG channels, and a predominantly female sample, though the within-subject design controls for stable participant characteristics.

The broader implications reach toward rehabilitation and wearable technology. Because movement smoothness can be estimated from inertial sensors, the discrete-rhythmic balance could eventually be monitored in real time during adaptive locomotion training, helping clinicians distinguish genuine control adaptations from the kinematic consequences of slow movement. And conceptually, the study extends the dynamic-primitives framework to its least expected domain, showing that even the body’s most iconic rhythm is, at its slowest, something else entirely: a sequence of discrete steps stitched together by a nervous system that switches control modes as the world demands.

Subject of Research: Speed-dependent transitions between discrete and rhythmic control regimes in human walking, assessed via kinematic smoothness and muscle synergies

Article Title: Speed-driven transitions between discrete and rhythmic dynamics in walking revealed by kinematic smoothness and muscle synergies

Article References: Panconi, G., Minciacchi, D., Bravi, R., & Dominici, N. (2026). Speed-driven transitions between discrete and rhythmic dynamics in walking revealed by kinematic smoothness and muscle synergies. iScience, 29(11), Article 117779. https://doi.org/10.1016/j.isci.2026.117779

Image Credits: AI Generated

DOI: 10.1016/j.isci.2026.117779

Keywords: human walking, motor control, muscle synergies, movement smoothness, motor primitives, gait analysis, hysteresis, electromyography, locomotion, dynamic primitives, treadmill, neuromuscular control

Gallium-based liquid metals such as eutectic gallium–indium (EGaIn) have long been viewed as the most promising intrinsically deformable conductors. They combine metallic-level conductivity, on the order of a million siemens per meter, with liquid-like flow at room temperature, allowing them to endure extreme strain without fracturing. Yet their practical adoption has been hampered by two stubborn problems. In air, gallium rapidly forms a self-limiting oxide shell roughly three nanometers thick that stabilizes droplet shape but acts as an electrical insulator, blocking electron transport between neighboring particles. At the same time, the metal’s very high surface tension, near 600 millinewtons per meter, makes it difficult to wet and pattern uniformly on soft elastomeric substrates. As a result, most liquid metal inks are electrically dead when deposited and require a separate thermal, mechanical, laser, or chemical activation step to rupture the oxide and establish conductive pathways.

The new work tackles both obstacles at once by wrapping each liquid metal particle in an ultrathin polymer shell and then exploiting the physics of the spray process itself. Bulk EGaIn is fractured into microscale droplets by tip sonication in a 5 weight percent aqueous PVA solution, run at 20 percent amplitude in pulsed mode to prevent overheating. PVA chains hydrogen-bond to the freshly formed gallium oxide surface, lowering particle surface energy and improving wettability. A centrifugation step removes free, unbound polymer, leaving particles with a controlled PVA layer estimated at 7 to 10 nanometers thick atop the 3 to 5 nanometer native oxide. Transmission electron microscopy and energy-dispersive X-ray spectroscopy confirmed this layered structure, with the carbon signal of the polymer conformally wrapping the oxygen-rich oxide shell. The team emphasizes that the PVA is retained after deposition, where it serves as a fusion mediator and adhesive bridge rather than an insulating barrier.

Getting the shell thickness right proved decisive. Particles carrying an excessively thick PVA coating, produced before the centrifuge refinement, showed improved wettability but could not make direct particle-to-particle contact, yielding films roughly eightfold less conductive than the optimized formulation. The refined PmLMP films reached an electrical conductivity of approximately 1.5 × 10^6 siemens per meter immediately after spraying. Zeta potential measurements help explain why: pristine particles carry a strongly negative surface charge of about −70 millivolts, creating an electrostatic barrier that keeps neighbors apart, while PVA modification reduces this to roughly −38 millivolts, allowing hydrodynamic forces during printing to push particles into intimate contact. Density functional theory calculations, using isopropanol as a model for the PVA repeat unit and hydroxylated gallium oxide as a surface model, supported the feasibility of a moderate hydrogen bond at the interface, with a counterpoise-corrected interaction energy of −23.2 kilojoules per mole.

The heart of the innovation is a synergistic mechano-fluidic mechanism that unfolds in a single deposition event. First, high-velocity impact of aerosolized particles delivers enough mechanical stress to rupture the oxide–polymer shell, exposing fresh metallic surfaces that coalesce on contact. Atomic force microscopy nanoindentation measured a yield force of 266.08 nanonewtons per particle, only slightly above the 200 to 250 nanonewtons reported for bare oxide-shelled particles, confirming that the ultrathin PVA layer does not meaningfully suppress rupturability. X-ray photoelectron spectroscopy provided chemical corroboration: screen-printed control films showed only oxidized gallium signals, whereas spray-printed films revealed distinct indium peaks and metallic Ga^0 features, consistent with shell rupture exposing the metallic core. The researchers estimate a critical impact velocity of only about 4 meters per second, well below the particle speeds achieved at the optimized 30 psi spray pressure.

Second and third, the drying process itself consolidates the network. Because the ink uses a binary solvent of deionized water and ethanol in a 3:1 volume ratio, a surface-tension gradient arises within each deposited droplet, driving Marangoni convection. High-speed imaging of fluorescent tracer particles and microparticle image velocimetry showed flow velocities up to 50 times faster, averaging a 22.4-fold increase, compared with a single-solvent system. These vortical flows redistribute particles, counteract gravitational sedimentation, and wedge smaller particles into the voids between larger ones, creating nanoscale point contacts where capillary stress concentrates. The team’s capillary-bridge model predicts a lateral force of roughly 79 nanonewtons at each interparticle meniscus, and under an illustrative contact radius of about 11 nanometers this corresponds to local stresses near 200 megapascals, plausibly sufficient to rupture residual shells. Transmission electron microscopy captured metallic neck formation at particle contacts, and the binary-solvent formulation delivered a threefold conductivity enhancement over the water-only control.

Process optimization revealed how sensitively the mechanism depends on spray parameters. Ultrasonic amplitudes above 50 percent, despite producing smaller particles, introduced enough energy to generate gallium oxide and hydroxide byproducts that interfered with coalescence, so 20 percent amplitude proved optimal. Conductivity saturated at carrier-gas pressures above 30 psi, where kinetic energy reliably exceeds the rupture threshold. Working distance mattered too: at 6 centimeters, air resistance dissipated too much particle energy, while at 3 centimeters the balance of partial solvent evaporation and retained impact energy enabled efficient fusion. The resulting process patterned conductive traces with nominal linewidths down to 50 micrometers and coated areas larger than 20 by 20 square centimeters, and a batch-printed 4 by 4 array showed an average conductivity of 1.55 × 10^6 siemens per meter with limited pixel-to-pixel variation.

Electromechanical testing underscored the practical payoff. Under monotonic tension, PmLMP traces retained electrical continuity beyond 200 percent strain and up to 800 percent, with relative resistance rising only gradually to about 2.8, whereas unmodified particle films lost continuity through droplet beading and over-coated films fractured near 100 percent strain. Cyclic testing at 100 percent strain over 50,000 seconds, roughly 1,400 stretch-release cycles, showed reproducible resistance modulation with limited drift. Integrated light-emitting diodes stayed illuminated through twisting, 100 percent stretching, and bending, and star-shaped LED arrays printed on table-tennis balls, tennis balls, and basketballs remained operational, demonstrating conformability across curvatures. On nonpolar substrates such as PDMS and Ecoflex, an oxygen-plasma pretreatment improved trace uniformity by increasing surface polarity for hydrogen bonding.

The team then pushed the platform toward real devices. Because the printed interconnects are conductive on arrival, standard components, including a microcontroller, resistor, and LEDs, could be pick-and-placed directly onto as-printed flexible circuits that remained functional after folding. A flexible wound-healing patch carrying 640-nanometer red LEDs, driven at 10 hertz and encapsulated in Ecoflex, accelerated macroscopic wound closure relative to untreated controls over seven days in a murine full-thickness excisional wound model. Large-area conductive patterns were printed directly onto textile banners, and the same platform, paired with a LiCl-hydrogel skin interface, served as a wearable electromyography and electrocardiography system. Wireless EMG signals transmitted over Bluetooth Low Energy controlled a remote-controlled vehicle in real time, while custom software visualized ECG waveforms and computed heart rate. Together, these demonstrations sketch a manufacturing route in which liquid metal circuits emerge from an ordinary airbrush already alive with current, opening possibilities for wearable healthcare, bio-integrated electronics, and human-interactive devices that no longer wait for a sintering oven to switch them on.

Subject of Research: Post-treatment-free spray deposition of PVA-modified liquid metal particles for soft and wearable electronics

Article Title: Synergistic Mechano‐Fluidic Self‐Fusion of Poly(Vinyl Alcohol)‐Modified Liquid‐Metal Particles for Post‐Treatment‐Free Soft Electronics

Article References: Yook, K.-Y., Kim, S., Kim, C., Kang, M., Lee, Y., Kim, M., Park, K., Han, S. Y., Cho, S.-W., Lee, G.-H., Son, K., Jang, H., Kim, T. Y., & Seo, J. (2026). Synergistic Mechano‐Fluidic Self‐Fusion of Poly(Vinyl Alcohol)‐Modified Liquid‐Metal Particles for Post‐Treatment‐Free Soft Electronics. Advanced Science, Article e78062. https://doi.org/10.1002/advs.78062

Image Credits: AI Generated

DOI: 10.1002/advs.78062

Keywords: liquid metal, soft electronics, spray printing, EGaIn, poly(vinyl alcohol), self-fusion, wearable sensors, Marangoni convection, capillary forces, stretchable conductors, electromyography, wound healing

The diagnostic anchor in this patient was a laboratory finding rather than a physical sign: a strongly positive test for antibodies against U1 ribonucleoprotein, a component of the spliceosome, the cellular machinery that edits messenger RNA before proteins are made. High-titer anti-U1-RNP antibodies are the serological hallmark of mixed connective tissue disease, a systemic autoimmune disorder first described by Gordon Sharp and colleagues in 1972 that combines features of systemic lupus erythematosus, polymyositis, and systemic sclerosis. The condition is rare, with an estimated prevalence of roughly 3 to 37 per 100,000 people, and it disproportionately affects women. Yet the antibodies themselves can appear in patients whose disease never develops the full overlap picture, which is precisely what made this case so difficult to classify.

On admission, the clinical picture was alarming. Proximal muscle strength was graded 4 out of 5 in the deltoids and biceps but only 2 out of 5 in the hip flexors and quadriceps, meaning the patient could not raise her legs off the bed. Cranial nerves were intact, and crucially there was no rash, no Gottron’s papules, no heliotrope discoloration around the eyes, and no Raynaud phenomenon, the finger-whitening response to cold that typically signals connective tissue disease. The absence of these cutaneous and vascular stigmata is one reason the diagnosis eluded clinicians for so long. Inflammatory myopathy usually announces itself in textbooks with visible clues; here the disease confined itself almost entirely to muscle.

The laboratory numbers told a dramatic story. Serum creatine kinase, the enzyme that leaks into blood when muscle fibers rupture, measured 9,883 IU/L, roughly 68 times the upper limit of normal. Aldolase, another muscle enzyme, was similarly elevated at 75.6 U/L against a reference ceiling of 10. Inflammatory markers were high, with C-reactive protein at 116 mg/L, and the erythrocyte sedimentation rate at 67 mm/h. The extractable nuclear antigen panel revealed anti-U1-RNP antibodies at 17.67 U/mL, well above the positivity threshold of 5.0, while antibodies to Sm, Scl-70, and SS-B/La were negative and anti-dsDNA was merely equivocal, arguing against florid lupus. A positive direct Coombs test was noted but, without reticulocytosis, elevated lactate dehydrogenase, or low haptoglobin, could not be taken as proof of autoimmune hemolysis.

Electrodiagnostic testing added an important nuance. Nerve conduction studies were normal, excluding a neuropathy, but needle electromyography across ten muscles showed small, short-duration motor unit potentials with early full recruitment and, tellingly, no fibrillations or positive sharp waves. That non-irritable pattern is more characteristic of a chronic or so-called burnt-out myopathy than of florid active inflammation. The authors interpret it as the electrophysiological fingerprint of the six-year disease course, upon which the massively elevated creatine kinase indicated a fresh, biochemically active wave of muscle injury. Magnetic resonance imaging of the thighs corroborated the picture, showing diffuse T2 and STIR hyperintensity in the quadriceps consistent with muscle edema and inflammation, with no bone marrow abnormality to suggest a dystrophy or malignancy.

Treatment began within days. The patient received intravenous pulse methylprednisolone, 500 mg daily for three consecutive days, a high-dose regimen chosen because of the severity of weakness and the rapidly progressive pharyngeal dysphagia with its attendant aspiration risk. The response was rapid and unequivocal. By day four, swallowing had improved enough to restore safe oral intake, upper limb strength had returned to 5 out of 5, and lower limb strength had climbed to 4 out of 5 on the Medical Research Council scale. She was transitioned to oral prednisolone at 1 mg per kilogram per day, with methotrexate added as a steroid-sparing immunosuppressant alongside folic acid supplementation. At four-week follow-up, creatine kinase had fallen to 560 IU/L, approaching normal, and the dysphagia had not recurred.

Why did swallowing fail so suddenly? The report explains that oropharyngeal dysphagia in inflammatory myopathy arises when inflammation strikes the striated pharyngeal musculature, specifically the cricopharyngeus and the inferior pharyngeal constrictors, the muscles that coordinate the pharyngeal phase of swallowing. This feature is well recognized in polymyositis and dermatomyositis but underreported in mixed connective tissue disease, and it carries a grim prognosis when missed, being associated with aspiration, malnutrition, and death. Its abrupt emergence here, progressing from solids to liquids in roughly ten days, underscores why clinicians are urged to treat new dysphagia in any patient with myopathy as an emergency demanding immediate immunosuppression.

The classification question is where the case becomes genuinely instructive. Four sets of criteria, those of Sharp, Alarcón-Segovia and Villareal, Kasukawa and Miyawaki, and Kahn and Appeboom, are used to define mixed connective tissue disease, and all four require high-titer anti-U1-RNP antibodies. But each also demands at least one classic overlap manifestation beyond myositis: Raynaud phenomenon, swollen fingers or hands, synovitis, acrosclerosis, or sclerodactyly. This patient had none of them. Formally, therefore, she did not fulfill any of the four classification systems, and the authors designate her condition an anti-U1-RNP-positive inflammatory myopathy rather than definite mixed connective tissue disease. Such patients are increasingly viewed as occupying an early, incomplete, or myositis-dominant point on the disease spectrum, and a proportion evolve to meet full criteria over time, which is why the authors emphasize longitudinal surveillance rather than a fixed label.

The case also carries a lesson about anemia. Hematological abnormalities affect an estimated 30 to 40 percent of mixed connective tissue disease patients, and Coombs-positive hemolytic anemia has been described, yet this patient’s refractory microcytic anemia was attributed to iron deficiency for years despite supplementation failing. In retrospect, the authors write, that persistent anemia was a missed opportunity for earlier systemic evaluation. They recommend that any patient with proximal muscle weakness and unexplained, supplementation-resistant anemia undergo an autoimmune workup, including an extractable nuclear antigen panel and myositis-specific antibodies, early rather than late.

The authors acknowledge limitations: no muscle biopsy was performed to confirm the histological subtype, the burnt-out EMG pattern may simply reflect the prolonged delay, swallowing improvement was assessed clinically rather than by videofluoroscopy, and a broader myositis-specific antibody panel was not run. As a single case, the findings cannot be generalized to all populations. Still, the patient’s own account captures the stakes. She described years of declining function, sudden distress when swallowing failed, and relief at finally having a clear diagnosis after treatment restored her strength and her ability to eat normally. For clinicians, the message is blunt: autoimmune myopathy belongs on the differential for any longstanding unexplained proximal weakness, and the antibody that defines it is a simple blood test away.

Subject of Research: Anti-U1-RNP-positive inflammatory myopathy presenting with oropharyngeal dysphagia

Article Title: Anti‐U1‐RNP‐Positive Inflammatory Myopathy Presenting With Dysphagia: A Case Report

Article References: Anjlee, Rasheed, S., Ashfaq, M., Bai, S., Yaqubi, A. J., & Raza, A. A. (2026). Anti‐ U1 ‐ RNP ‐Positive Inflammatory Myopathy Presenting With Dysphagia: A Case Report. Clinical Case Reports, 14(10), Article e73676. https://doi.org/10.1002/ccr3.73676

Image Credits: AI Generated

DOI: 10.1002/ccr3.73676

Keywords: anti-U1-RNP antibodies, mixed connective tissue disease, inflammatory myopathy, dysphagia, myositis, creatine kinase, electromyography, methylprednisolone, autoimmune disease, anemia, rheumatology, case report

The research team recruited fifty adults between the ages of 55 and 90, dividing them into two groups of twenty-five: older adults with mild cognitive impairment, identified through the Montreal Cognitive Assessment and confirmed with a multi-domain neuropsychological battery, and cognitively intact older adults. Anyone with neurological or musculoskeletal diagnoses, recent hospitalization, or an inability to walk ten meters without an assistive device was excluded. Each participant then walked on a motorized ActiveStep treadmill at a self-selected speed of either 0.8 or 1.0 meters per second while wearing a safety harness connected to a load cell. After several unperturbed steps, the treadmill delivered its ambush: the belt abruptly decelerated to a standstill and then accelerated violently forward, yanking the support surface out from under the swinging foot and pitching the body toward a forward fall.

What happened next was remarkably consistent across nearly everyone. Rather than immediately throwing the swinging leg far forward in the classic elevating strategy seen with obstacle trips, almost all participants first slammed the swing limb down almost in line with the stance foot, a rapid lowering step that restored a base of support as quickly as possible. Only then did they take the long forward recovery step that actually arrested the fall, and here the group split into two camps. Some stepped forward with the contralateral limb, others with the ipsilateral limb, and a handful of ipsilateral steppers showed an aborted contralateral step or a weight shift without liftoff before the recovery step began, hinting at a momentary failure of step initiation. Just three participants, one with impairment and two without, immediately executed a long forward step with the swing limb, resembling an elevating strategy, and they were excluded from the primary analysis because their response was biomechanically distinct and too rare to support statistical conclusions.

The headline result was not who fell, but how close everyone came. Falls were defined by a harness load exceeding thirty percent of body weight, verified on video, and the fall rates were strikingly high in both groups: ninety-two percent among those with mild cognitive impairment and seventy-eight percent among the cognitively intact, a difference that did not reach statistical significance. But the margin of stability, a normalized measure of how far the extrapolated center of mass sits beyond the front boundary of the base of support at the moment the recovery foot lands, told a sharper story. Participants with mild cognitive impairment showed significantly higher margins of stability at recovery touchdown, meaning their center of mass had traveled even further past the safe zone than their cognitively intact counterparts. This group difference persisted even after the researchers statistically controlled for baseline mobility, walking speed, and treadmill velocity, and it held regardless of which limb each person used for the recovery step.

The likely culprit was the recovery step itself. Regression modeling showed that the margin of stability at touchdown was predicted primarily by reactive step length, and participants with mild cognitive impairment took recovery steps roughly fifteen percent shorter than the cognitively intact group. A shorter step establishes a smaller base of support and a shorter lever arm against the forward momentum of the trunk, leaving the body’s center of mass stranded further beyond the toes. Notably, the pre-trip picture looked identical between groups: unperturbed walking showed no differences in margin of stability, step length, or trunk angle, suggesting that the deficit was not a feedforward consequence of a cautious or shuffling gait but a genuine failure of the feedback-driven emergency response. The one proactive exception was toe clearance, which was significantly lower in the impaired group, about 5.5 centimeters versus 7.1 centimeters, a detail that matters because low toe clearance is a well-known risk factor for actually catching a foot on an obstacle in the first place.

Beneath these kinematic differences lay something even more intriguing: a rewiring of the muscle coordination itself. Using wireless electromyography from eight lower limb muscles, including the biceps femoris, vastus lateralis, medial gastrocnemius, and tibialis anterior on both legs, the team extracted muscle synergies, the stereotyped co-activation patterns that the nervous system deploys as building blocks for movement. Seven distinct synergies emerged across the cohort. In an exploratory analysis, at least three of these showed low structural similarity between the two groups within each stepping strategy, falling below the similarity threshold the researchers had defined. Cognitively intact older adults recruited highly similar synergy structures regardless of which limb they stepped with, while those with mild cognitive impairment showed more variability between strategies and even recruited a unique synergy not seen in the control group.

The texture of those synergy differences was telling. Cognitively intact participants showed greater contribution from the stepping limb quadriceps in one key synergy, consistent with generating the knee extension needed for a longer, more effective recovery step. Meanwhile, participants with mild cognitive impairment tended to recruit synergies dominated by a single muscle, such as the stance limb tibialis anterior or medial gastrocnemius, whereas the intact group showed richer co-activation of multiple stance limb muscles working together to generate support. The authors interpret this as a shift toward more fractionated, simplistic motor modules rather than the integrated, multi-muscle coordination that efficient balance recovery demands. Such fragmentation could stem from impaired sensorimotor integration, altered executive function, or the structural and functional brain changes, including reduced grey matter volume and disrupted functional connectivity, that are well documented in mild cognitive impairment.

The mechanistic picture the authors sketch runs from the brainstem to the cortex. Reactive balance responses are believed to be initiated by rapid subcortical brainstem loops driven primarily by fast somatosensory signals, and people with mild cognitive impairment often show reduced brainstem grey matter volume and delayed onset latencies of stepping limb muscles, which could slow perturbation detection and response initiation. Later phases of the response, such as scaling step length to the demands of the moment, likely recruit cortical networks, and altered cerebellar functional connectivity has been linked to reactive stability in this population. Muscle synergies themselves may be stored as pre-existing templates in the brainstem or spinal cord, with the cortex priming the appropriate templates through central set, a process that depends on cerebellar-cortical and basal ganglia-cortical loops vulnerable to the neural changes of early cognitive decline. In this framing, the trip response fails not because the legs are weak but because the neural machinery that selects and executes the right motor program at the right moment is degraded.

The clinical implications cut in two directions. On one hand, the results align with earlier work showing that people with mild cognitive impairment also respond poorly to slip-like backward perturbations, suggesting a direction-general deficit in reactive stepping that could undermine recovery from many kinds of everyday destabilization, especially when attention is divided. On the other hand, the study raises a caution about the treadmill paradigms increasingly marketed for balance assessment and training. Surface translations produce continual posterior displacement of the support surface, which appears to favor lowering strategies more often than obstacle-induced trips do, and prior research has found that repeated treadmill slip training did not transfer to improved recovery from a novel overground obstacle trip. Commercialized perturbation systems remain attractive for their scalability, but the authors argue that truly effective fall prevention for this population may need to incorporate more ecologically valid elements such as obstacle avoidance and navigation.

The study has limits the authors acknowledge candidly: a single high-intensity perturbation that pushed fall rates above seventy percent in both groups may have created ceiling effects that masked group differences in the binary fall outcome, the regression and synergy analyses were exploratory with modest subgroup samples, and electromyography captured only eight lower limb muscles when hip and trunk musculature also matter for trip recovery. Still, the core finding stands with unusual clarity. Older adults with mild cognitive impairment do not simply trip more often; when the ground moves beneath them, their recovery steps land shorter, their center of mass drifts further past the point of no return, and their muscles fire in fragmented, less reproducible patterns. It is a vivid demonstration that cognitive decline reaches deep into the body’s most ancient reflexes, and that protecting the aging brain may be inseparable from protecting the aging step.

Subject of Research: Reactive balance and trip recovery strategies in older adults with mild cognitive impairment

Article Title: Recovery strategies during trip-like support surface perturbations while walking in older adults with mild cognitive impairment

Article References: Pitts, J., & Bhatt, T. (2026). Recovery strategies during trip-like support surface perturbations while walking in older adults with mild cognitive impairment. GeroScience. https://doi.org/10.1007/s11357-026-02490-7

Image Credits: AI Generated

DOI: 10.1007/s11357-026-02490-7

Keywords: mild cognitive impairment, reactive balance, trip perturbation, fall risk, muscle synergies, treadmill perturbation, margin of stability, gait, electromyography, aging, sensorimotor integration, GeroScience

A team of sleep neurologists at the Cleveland Clinic Sleep Disorders Center analyzed 1,474 video polysomnograms performed between September 2018 and October 2023, drawing on the center’s STARLIT registry. Of these patients, 624—about 42 percent—were taking antidepressants, while 850 were not. The researchers manually scored RSWA using chin (submentalis) and bilateral flexor digitorum superficialis (FDS) electromyography, following the American Academy of Sleep Medicine’s current scoring criteria. Unlike many earlier studies that relied on leg muscles prone to artifact, this approach captured the upper limb signals now considered the most accurate diagnostic markers for REM sleep behavior disorder.

The technical rigor of the scoring matters. RSWA was flagged when any of three criteria were met: tonic activity, in which chin EMG amplitude runs at least twice the atonia level for at least half of a 30-second epoch; phasic activity, in which at least five of ten consecutive three-second mini-epochs contain brief bursts of doubled-amplitude muscle activity in the chin or forearm muscles; or any sustained EMG activity meeting amplitude thresholds regardless of duration. To avoid confounding by sleep apnea, REM epochs during or within 30 seconds of a respiratory event were excluded from analysis.

The headline result is a clear class effect. After adjusting for age, body mass index, gender, and race, patients on selective serotonin reuptake inhibitor (SSRI) monotherapy showed a 3.39 percent increase in the proportion of REM epochs containing RSWA compared with medication-free patients, while those on serotonin norepinephrine reuptake inhibitors (SNRIs) showed a substantially larger 6.66 percent increase. Both findings were statistically significant. In striking contrast, tricyclic antidepressant (TCA) monotherapy was not associated with any increase in RSWA—in fact, the point estimate trended downward, though it did not reach significance.

Combination therapies produced the highest estimates of all. Patients taking both an SSRI and an SNRI showed a 10.44 percent increase in RSWA, and those combining an SNRI with a TCA showed a 12.81 percent increase, although the authors caution that these combination subgroups were small—14 and 9 patients respectively—and the results did not reach conventional statistical significance. Overall, mean RSWA was significantly higher among antidepressant users than non-users, at 15.0 percent versus 9.7 percent of REM epochs, and 18.9 percent of medicated patients crossed the 27 percent RSWA threshold used to diagnose REM sleep behavior disorder on polysomnography, compared with 11.4 percent of non-users.

Why would serotonergic and noradrenergic drugs loosen the grip of sleep paralysis? The answer lies in the brainstem circuitry that governs REM atonia. Glutamate-releasing neurons in the pontine sublaterodorsal nucleus activate inhibitory premotor neurons in the ventral medulla, which in turn silence spinal motor neurons during REM sleep. SSRIs and SNRIs boost serotonin and norepinephrine signaling, and the study’s authors suggest that activation of the dorsal raphe serotonergic and locus coeruleus noradrenergic nuclei during REM may interfere with this normal inhibitory cascade, allowing muscle tone to leak back into dreaming sleep.

The clinical stakes are high because RSWA is the polysomnographic biomarker of REM sleep behavior disorder (RBD), a parasomnia in which patients physically enact their dreams—punching, kicking, and shouting—sometimes injuring themselves or their bed partners. Isolated RBD in older adults is one of the strongest known harbingers of neurodegenerative disease, frequently preceding Parkinson’s disease, dementia with Lewy bodies, or multiple system atrophy by years or even decades. Yet increased REM muscle tone is not specific to neurodegeneration. It also appears with antidepressant exposure, psychiatric illness, and narcolepsy, which creates a genuine diagnostic dilemma for sleep physicians evaluating a depressed patient on an SSRI who also shows excessive REM EMG activity.

One emerging hypothesis, supported by the new data, is that antidepressants do not create RBD from scratch but rather unmask a pre-existing, subclinical neurodegenerative process. Patients with antidepressant-associated RBD have been found to harbor markers of neurodegeneration—olfactory impairment, color vision deficits, and autonomic dysfunction—that cannot be explained by the medications alone. If serotonergic drugs simply reveal an underlying tendency toward RSWA, then a patient whose sleep study shows drug-associated muscle activity may still warrant closer neurological follow-up rather than reassurance that the finding is merely a side effect.

The Cleveland Clinic study is not without caveats, and the authors are candid about them. The cohort was clinically selected: RSWA scoring was performed only for studies with suspected parasomnia or observed dream enactment, enriching the sample for muscle activity and inflating absolute percentages relative to an unselected sleep laboratory population. The cross-sectional design precludes causal inference, potential confounders such as melatonin use could not be assessed, and the software could not distinguish tonic from phasic RSWA. The cohort was also predominantly White, and the medicated group skewed female and slightly younger, limiting generalizability. Formal inter-reader reliability testing was not performed, though average RSWA percentages did not differ significantly across the four scorers.

Even with those limitations, the study stands as the largest to date to quantify RSWA with modern AASM criteria and the SINBAR-style montage incorporating upper extremity EMG, and its message is unambiguous: SSRIs and SNRIs, but not TCAs, are associated with measurably more REM sleep without atonia in patients evaluated for parasomnia. For clinicians, the practical takeaway is that medication history must be weighed carefully when interpreting a sleep study suggestive of RBD, particularly since the proportion of patients meeting electrodiagnostic criteria for RBD was higher among antidepressant users in this cohort. For the millions of people taking these widely prescribed drugs, the findings are not a reason to stop treatment—but they are a reason for sleep medicine to look more closely at what antidepressants do to the sleeping brain, and at what those changes might reveal about the decades to come.

Subject of Research: Differential effects of antidepressant classes on REM sleep without atonia measured by chin and upper extremity EMG

Article Title: Antidepressant medications have differential effects on REM sleep without atonia quantified by chin and upper extremity EMG

Article References: Ahdab, J. E., Rodriguez, C. L., Grigg-Damberger, M., Araujo, M. L. D., Andrews, N. D., Thanaviratananich, S., & Foldvary-Schaefer, N. (2026). Antidepressant medications have differential effects on REM sleep without atonia quantified by chin and upper extremity EMG. Journal of Clinical Sleep Medicine, 22(1), Article 109. https://doi.org/10.1007/s44470-026-00127-2

Image Credits: AI Generated

DOI: 10.1007/s44470-026-00127-2

Keywords: REM sleep without atonia, REM sleep behavior disorder, antidepressants, SSRIs, SNRIs, tricyclic antidepressants, polysomnography, electromyography, sleep medicine, neurodegeneration, Parkinson's disease, parasomnia