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Different forearm postures can modulate corticospinal excitability. However, there is no consensus on whether handedness plays a role in such a mechanism. This study investigated the effects of 3 forearm postures (pronation, neutral, and supination) on the corticospinal excitability of muscles from the dominant and nondominant upper limbs. Surface electromyography was recorded from the abductor digiti minimi, flexor pollicis brevis, and flexor carpi radialis from both sides of 12 right-handed volunteers. Transcranial magnetic stimulation pulses were applied to each muscle's hotspot in both cerebral hemispheres. Motor-evoked potential peak-to-peak amplitude and latency and resting motor threshold were measured. The data were evaluated by analysis of variance. The level of significance was set at 5%. The resting motor threshold was similar for the 3 muscles and both sides. Motor-evoked potential peak-to-peak amplitude from flexor pollicis brevis was lower during supination, and the dominant upper limb latency was longer. The flexor carpi radialis presented lower motor-evoked potential peak-to-peak amplitudes for neutral and shorter latencies during supination. Abductor digiti minimi seemed not to be affected by posture or side. Different muscles from dominant and nondominant sides may undergo corticospinal modulation, even distally localized from a particular joint and under rest. [ABSTRACT FROM AUTHOR]

Connections between neurons can be mapped by acquiring and analysing electron microscopic brain images. In recent years, this approach has been applied to chunks of brains to reconstruct local connectivity maps that are highly informative1-6, but nevertheless inadequate for understanding brain function more globally. Here we present a neuronal wiring diagram of a whole brain containing 5 × 107 chemical synapses7 between 139,255 neurons reconstructed from an adult female Drosophila melanogaster8,9. The resource also incorporates annotations of cell classes and types, nerves, hemilineages and predictions of neurotransmitter identities10-12. Data products are available for download, programmatic access and interactive browsing and have been made interoperable with other fly data resources. We derive a projectome-a map of projections between regions-from the connectome and report on tracing of synaptic pathways and the analysis of information flow from inputs (sensory and ascending neurons) to outputs (motor, endocrine and descending neurons) across both hemispheres and between the central brain and the optic lobes. Tracing from a subset of photoreceptors to descending motor pathways illustrates how structure can uncover putative circuit mechanisms underlying sensorimotor behaviours. The technologies and open ecosystem reported here set the stage for future large-scale connectome projects in other species.

To determine how neuronal circuits encode and drive behavior, it is often necessary to measure and manipulate different aspects of neurochemical signaling in awake animals. Optogenetics and calcium sensors have paved the way for these types of studies, allowing for the perturbation and readout of spiking activity within genetically defined cell types. However, these methods lack the ability to further disentangle the roles of individual neuromodulator and neuropeptides on circuits and behavior. We review recent advances in chemical biology tools that enable precise spatiotemporal monitoring and control over individual neuroeffectors and their receptors in vivo. We also highlight discoveries enabled by such tools, revealing how these molecules signal across different timescales to drive learning, orchestrate behavioral changes, and modulate circuit activity.

Patients with degenerative cervical myelopathy (DCM) experience structural and functional brain reorganization. However, few studies have investigated the influence of sex on cerebral alterations. The present study investigates the role of sex on brain functional connectivity (FC) and global network topology in DCM and healthy controls (HCs). The resting-state functional MRI data was acquired for 100 patients (58 males vs. 42 females). ROI-to-ROI FC and network topological features were characterized for each patient and HC. Group differences in FC and network topological features were examined. Compared to healthy counterparts, DCM males exhibited higher FC between vision-related brain regions, and cerebellum, brainstem, and thalamus, but lower FC between the intracalcarine cortex and frontal and somatosensory cortices, while DCM females demonstrated higher FC between the thalamus and cerebellar and sensorimotor regions, but lower FC between sensorimotor and visual regions. DCM males displayed higher FC within the cerebellum and between the posterior cingulate cortex (PCC) and vision-related regions, while DCM females displayed higher FC between frontal regions and the PCC, cerebellum, and visual regions. Additionally, DCM males displayed significantly greater intra-network connectivity and efficiency compared to healthy counterparts. Results from the present study imply sex-specific supraspinal functional alterations occur in patients with DCM.

Chronic neuropathic pain can result from nervous system injury and can persist in the absence of external stimuli. Although ongoing pain characterizes the disorder, in many individuals, the intensity of this ongoing pain fluctuates dramatically. Previously, it was identified that functional magnetic resonance imaging signal covariations between the midbrain periaqueductal gray (PAG) matter, rostral ventromedial medulla (RVM), and spinal trigeminal nucleus are associated with moment-to-moment fluctuations in pain intensity in individuals with painful trigeminal neuropathy (PTN). Since this brainstem circuit is modulated by higher brain input, we sought to determine which cortical sites might be influencing this brainstem network during spontaneous fluctuations in pain intensity. Over 12 min, we recorded the ongoing pain intensity in 24 PTN participants and classified them as fluctuating (n = 13) or stable (n = 11). Using a PAG seed, we identified connections between the PAG and emotional-affective sites such as the hippocampal and posterior cingulate cortices, the sensory-discriminative posterior insula, and cognitive-affective sites such as the dorsolateral prefrontal (dlPFC) and subgenual anterior cingulate cortices that were altered dependent on spontaneous high and low pain intensity. Additionally, sliding-window functional connectivity analysis revealed that the dlPFC-PAG connection anticorrelated with perceived pain intensity over the entire 12 min period. These findings reveal cortical systems underlying moment-to-moment changes in perceived pain in PTN, which likely cause dysregulation in the brainstem circuits previously identified, and consequently alter the appraisal of pain across time.

Schizophrenia is a prototypical network disorder with widespread brain-morphological alterations, yet it remains unclear whether these distributed alterations robustly reflect the underlying network layout. We tested whether large-scale structural alterations in schizophrenia relate to normative structural and functional connectome architecture, and systematically evaluated robustness and generalizability of these network-level alterations. Leveraging anatomical MRI scans from 2439 adults with schizophrenia and 2867 healthy controls from 26 ENIGMA sites and normative data from the Human Connectome Project (n = 207), we evaluated structural alterations of schizophrenia against two network susceptibility models: (i) hub vulnerability, which examines associations between regional network centrality and magnitude of disease-related alterations; (ii) epicenter mapping, which identifies regions whose typical connectivity profile most closely resembles the disease-related morphological alterations. To assess generalizability and specificity, we contextualized the influence of site, disease stages, and individual clinical factors and compared network associations of schizophrenia with that found in affective disorders. Our findings show schizophrenia-related cortical thinning is spatially associated with functional and structural hubs, suggesting that highly interconnected regions are more vulnerable to morphological alterations. Predominantly temporo-paralimbic and frontal regions emerged as epicenters with connectivity profiles linked to schizophrenias alteration patterns. Findings were robust across sites, disease stages, and related to individual symptoms. Moreover, transdiagnostic comparisons revealed overlapping epicenters in schizophrenia and bipolar, but not major depressive disorder, suggestive of a pathophysiological continuity within the schizophrenia-bipolar-spectrum. In sum, cortical alterations over the course of schizophrenia robustly follow brain network architecture, emphasizing marked hub susceptibility and temporo-frontal epicenters at both the level of the group and the individual. Subtle variations of epicenters across disease stages suggest interacting pathological processes, while associations with patient-specific symptoms support additional inter-individual variability of hub vulnerability and epicenters in schizophrenia. Our work outlines potential pathways to better understand macroscale structural alterations, and inter- individual variability in schizophrenia.

Most of mammalian physiology is under the control of biological rhythms, including the endocrine system with time-varying hormone secretion. Precision neuroimaging studies provide unique insights into how the endocrine system dynamically regulates aspects of the human brain. Recently, we established estrogens ability to drive widespread patterns of connectivity and enhance the global efficiency of large-scale brain networks in a woman sampled every 24 h across 30 consecutive days, capturing a complete menstrual cycle. Steroid hormone production also follows a pronounced sinusoidal pattern, with a peak in testosterone between 6 and 7 A.M. and nadir between 7 and 8 P.M. To capture the brains response to diurnal changes in hormone production, we carried out a companion precision imaging study of a healthy adult man who completed MRI and venipuncture every 12-24 h across 30 consecutive days. Results confirmed robust diurnal fluctuations in testosterone, 17β-estradiol-the primary form of estrogen-and cortisol. Standardized regression analyses revealed widespread associations between testosterone, estradiol, and cortisol concentrations and whole-brain patterns of coherence. In particular, functional connectivity in the Dorsal Attention Network was coupled with diurnally fluctuating hormones. Further, comparing dense-sampling datasets between a man and a naturally cycling woman revealed that fluctuations in sex hormones are tied to patterns of whole-brain coherence in both sexes and to a heightened degree in the male. Together, these findings enhance our understanding of steroid hormones as rapid neuromodulators and provide evidence that diurnal changes in steroid hormones are associated with patterns of whole-brain functional connectivity.

The supraspinal descending pain modulatory system (DPMS) shapes pain perception via monoaminergic modulation of sensory information in the spinal cord. However, the role and synaptic mechanisms of descending noradrenergic signaling remain unclear. Here, we establish that noradrenergic neurons of the locus coeruleus (LC) are essential for supraspinal opioid antinociception. While much previous work has emphasized the role of descending serotonergic pathways, we find that opioid antinociception is primarily driven by excitatory output from the ventrolateral periaqueductal gray (vlPAG) to the LC. Furthermore, we identify a previously unknown opioid-sensitive inhibitory input from the rostroventromedial medulla (RVM), the suppression of which disinhibits LC neurons to drive spinal noradrenergic antinociception. We describe pain-related activity throughout this circuit and report the presence of prominent bifurcating outputs from the vlPAG to the LC and the RVM. Our findings substantially revise current models of the DPMS and establish a supraspinal antinociceptive pathway that may contribute to multiple forms of descending pain modulation.

Converging evidence implicates disrupted brain connectivity in autism spectrum disorder (ASD); however, the mechanisms linking altered connectivity early in development to the emergence of ASD symptomatology remain poorly understood. Here we examined whether atypicalities in the Salience Network - an early-emerging neural network involved in orienting attention to the most salient aspects of ones internal and external environment - may predict the development of ASD symptoms such as reduced social attention and atypical sensory processing. Six-week-old infants at high likelihood of developing ASD based on family history exhibited stronger Salience Network connectivity with sensorimotor regions; infants at typical likelihood of developing ASD demonstrated stronger Salience Network connectivity with prefrontal regions involved in social attention. Infants with higher connectivity with sensorimotor regions had lower connectivity with prefrontal regions, suggesting a direct tradeoff between attention to basic sensory versus socially-relevant information. Early alterations in Salience Network connectivity predicted subsequent ASD symptomatology, providing a plausible mechanistic account for the unfolding of atypical developmental trajectories associated with vulnerability to ASD.

Purpose: To test the effects of mental fatigue (MF) on tackling technique on the dominant and nondominant shoulders in rugby union. Methods: Twenty male amateur rugby union players and a total of 953 tackles were analyzed. A randomized crossover counterbalanced design was used across a non-MF (control) and an MF condition. During each condition, each player performed 24 tackles, divided into 4 sets of 6 tackles (3 tackles on each shoulder). In the MF condition, players performed the Stroop Task between each set of tackles. A video recording of each tackle was used to evaluate each player's technical proficiency. A score of 1 point was awarded if a specific technique was performed correctly, and 0 point was given if not. The total score, measured in arbitrary units (AU) out of 11, represents the player's overall tackling proficiency. Results: Overall, players displayed a significantly lower technical proficiency score in the MF condition compared to control (set 2: control 7.30 [7.04–7.57] AU vs MF 6.91 [6.70–7.12] AU, P =.009, effect size (ES) = 0.30 small and set 3: control 7.34 [7.11–7.57] AU vs MF 6.88 [6.66–7.11] AU, P =.002, ES = 0.37 small). For the nondominant shoulder, players had a significantly lower technical proficiency score during the MF condition at set 2 (control 7.05 [6.68–7.41] AU vs MF 6.69 [6.42–6.96] AU, P =.047, ES = 0.29 small) and set 3 (control 7.14 [6.83–7.45] AU vs MF 6.61 [6.35–6.87] AU, P =.007, ES = 0.49 small). Conclusions: MF can diminish a player's overall tackling proficiency, especially when tackling on the nondominant shoulder. The physiological mechanism for this finding may be impaired executive function and suboptimal functioning of neural signals and pathways, which result in less skillful coordination of movement. To further understand and explain MF-induced physiological changes in tackling, the feasibility of monitoring brain activity (such as electroencephalogram) and neuromuscular function (such as electromyogram) needs to be investigated. The findings from this study may also contribute to the development of more effective tackle training programs for injury prevention and performance. [ABSTRACT FROM AUTHOR]

BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental condition that often persists into adulthood. Underlying alterations in brain connectivity have been identified but some relevant connections, such as the middle, superior, and inferior cerebellar peduncles (MCP, SCP, and ICP, respectively), have remained largely unexplored; thus, we sought to investigate whether the cerebellar peduncles contribute to ADHD pathophysiology among adults. METHODS: We applied diffusion-weighted spherical deconvolution tractography to dissect the cerebellar peduncles of male adults with ADHD (including those who did or did not respond to methylphenidate, based on at least 30% symptom improvement at 2 months) and controls. We investigated differences in tract metrics between controls and the whole ADHD sample and between controls and treatment-response groups using sensitivity analyses. Finally, we analyzed the association between the tract metrics and cliniconeuropsychological profiles. RESULTS: We included 60 participants with ADHD (including 42 treatment responders and 18 nonresponders) and 20 control participants. In the whole ADHD sample, MCP fractional anisotropy (FA; t 78 = 3.24, p = 0.002) and hindrance modulated orientational anisotropy (HMOA; t 78 = 3.01, p = 0.004) were reduced, and radial diffusivity (RD) in the right ICP was increased (t 78 = -2.84, p = 0.006), compared with controls. Although case-control differences in MCP FA and HMOA, which reflect white-matter microstructural organization, were driven by both treatment response groups, only responders significantly differed from controls in right ICP RD, which relates to myelination (t 60 = 3.14, p = 0.003). Hindrance modulated orientational anisotropy of the MCP was significantly positively associated with hyperactivity measures. LIMITATIONS: This study included only male adults with ADHD. Further research needs to investigate potential sex- and development-related differences. CONCLUSION: These results support the role of the cerebellar networks, especially of the MCP, in adult ADHD pathophysiology and should encourage further investigation. CLINICAL TRIAL REGISTRATION: NCT03709940.

Experimental work across species has demonstrated that spontaneously generated behaviors are robustly coupled to variations in neural activity within the cerebral cortex. Functional magnetic resonance imaging data suggest that temporal correlations in cortical networks vary across distinct behavioral states, providing for the dynamic reorganization of patterned activity. However, these data generally lack the temporal resolution to establish links between cortical signals and the continuously varying fluctuations in spontaneous behavior observed in awake animals. Here, we used wide-field mesoscopic calcium imaging to monitor cortical dynamics in awake mice and developed an approach to quantify rapidly time-varying functional connectivity. We show that spontaneous behaviors are represented by fast changes in both the magnitude and correlational structure of cortical network activity. Combining mesoscopic imaging with simultaneous cellular-resolution two-photon microscopy demonstrated that correlations among neighboring neurons and between local and large-scale networks also encode behavior. Finally, the dynamic functional connectivity of mesoscale signals revealed subnetworks not predicted by traditional anatomical atlas-based parcellation of the cortex. These results provide new insights into how behavioral information is represented across the neocortex and demonstrate an analytical framework for investigating time-varying functional connectivity in neural networks.

Introduction: Depression is prevalent after traumatic brain injury (TBI). However, there is a lack of understanding of the brain-based correlates of depression post-TBI. This systematic review aimed to synthesize findings of structural and functional magnetic resonance imaging (MRI) studies to identify consistently reported neural correlates of depression post-TBI. Methods: A search for relevant published studies was conducted through OVID (MEDLINE, APA PsycINFO, and Embase), with an end date of August 3rd, 2023. Fourteen published studies were included in this review. Results: TBI patients with depression exhibited distinct changes in diffusion- based white matter fractional anisotropy, with the direction of change depending on the acuteness or chronicity of TBI. Decreased functional connectivity (FC) of the salience and default mode networks was prominent alongside the decreased volume of gray matter within the insular, dorsomedial prefrontal, and ventromedial prefrontal cortices. Seven studies reported the correlation between observed neuroimaging and depression outcomes. Of these studies, 42% indicated that FC of the bilateral medial temporal lobe subregions was correlated with depression outcomes in TBI. Discussion: This systematic review summarizes existing neuroimaging evidence and reports brain regions that can be leveraged as potential treatment targets in future studies examining depression post-TBI. [ABSTRACT FROM AUTHOR]

The activation of autonomic and hypothalamo-pituitary-adrenal (HPA) systems occurs interdependently with behavioral adjustments under varying environmental demands. Nevertheless, laboratory rodent studies examining the neural bases of stress responses have generally attributed increments in these systems to be monolithic, regardless of whether an active or passive coping strategy is employed. Using the shock probe defensive burying test (SPDB) to measure stress-coping features naturalistically in male and female rats, we identify a neural pathway whereby activity changes may promote distinctive response patterns of hemodynamic and HPA indices typifying active and passive coping phenotypes. Optogenetic excitation of the rostral medial prefrontal cortex (mPFC) input to the ventrolateral periaqueductal gray (vlPAG) decreased passive behavior (immobility), attenuated the glucocorticoid hormone response, but did not prevent arterial pressure and heart rate increases associated with rats' active behavioral (defensive burying) engagement during the SPDB. In contrast, inhibition of the same pathway increased behavioral immobility and attenuated hemodynamic output but did not affect glucocorticoid increases. Further analyses confirmed that hemodynamic increments occurred preferentially during active behaviors and decrements during immobility epochs, whereas pathway manipulations, regardless of the directionality of effect, weakened these correlational relationships. Finally, neuroanatomical evidence indicated that the influence of the rostral mPFC→vlPAG pathway on coping response patterns is mediated predominantly through GABAergic neurons within vlPAG. These data highlight the importance of this prefrontal→midbrain connection in organizing stress-coping responses and in coordinating bodily systems with behavioral output for adaptation to aversive experiences. [ABSTRACT FROM AUTHOR]

Chronic prostatitis/chronic pelvic pain syndrome is a prevalent condition affecting the male urinary system. The urinary dysfunction resulting from this disorder has a direct or indirect impact on the patient's quality of life. Recent studies have suggested that organ cross-sensitization between the prostate and bladder may elucidate this phenomenon; however, the specific molecular mechanisms remain unclear. In this study, we simulated the urinary symptoms of prostatitis patients using an animal model and examined the expression of relevant proteins within the prostate-bladder sensitized neural pathway. We found that transient receptor potential vanilloid 1 (TRPV1) protein is highly expressed in the dorsal root ganglia (DRG) that co-innervate both the prostate and bladder, potentially increasing the sensitivity of TRPV1 channels via the substance P-neurokinin 1 (SP-NK-1) pathway, which may exacerbate micturition symptoms. Furthermore, in the absence of bladder inflammation, elevated levels of neurogenic substances in bladder tissue were found to sensitize bladder sensory afferents. Collectively, these results underscore the significant role of TRPV1 in bladder sensitization associated with prostatitis, suggesting that the inhibition of TRPV1 along this sensitization pathway could be a promising approach to treating urinary dysfunction linked to prostatitis in the future. [ABSTRACT FROM AUTHOR]

Dynamic gain control of aversive signals enables adaptive behavioral responses. Although the role of amygdalar circuits in aversive processing is well established, the neural pathway for amplifying aversion remains elusive. Here, we show that the brainstem circuit linking the interpeduncular nucleus (IPN) with the nucleus incertus (NI) amplifies aversion and promotes avoidant behaviors. IPN GABA neurons are activated by aversive stimuli and their predicting cues, with their response intensity closely tracking aversive values. Activating these neurons does not trigger aversive behavior on its own but rather amplifies responses to aversive stimuli, whereas their ablation or inhibition suppresses such responses. Detailed circuit dissection revealed anatomically distinct subgroups within the IPN GABA neuron population, highlighting the NI-projecting subgroup as the modulator of aversiveness related to fear and opioid withdrawal. These findings unveil the IPN-NI circuit as an aversion amplifier and suggest potential targets for interventions against affective disorders and opioid relapse. • IPN GABA neurons encode aversive value • The activity of these neurons amplifies aversive responses • The IPN-NI pathway controls aversive evaluation and fear learning • This pathway strengthens the aversive response to opioid withdrawal Liang et al. demonstrate that the brainstem circuit from the interpeduncular nucleus (IPN) to the nucleus incertus (NI) is an aversion amplifier, offering potential therapeutic targets for affective disorders and opioid relapse prevention. [ABSTRACT FROM AUTHOR]

Recent advances in neural engineering have opened new ways to investigate the impact of topology on neural network function. Leveraging microfluidic technologies, it is possible to establish modular circuit motifs that promote both segregation and integration of information processing in the engineered neural networks, similar to those observed in vivo. However, the impact of the underlying topologies on network dynamics and response to pathological perturbation remains largely unresolved. In this work, we demonstrate the utilization of microfluidic platforms with 12 interconnected nodes to structure modular, cortical engineered neural networks. By implementing geometrical constraints inspired by a Tesla valve within the connecting microtunnels, we additionally exert control over the direction of axonal outgrowth between the nodes. Interfacing these platforms with nanoporous microelectrode arrays reveals that the resulting laminar cortical networks exhibit pronounced segregated and integrated functional dynamics across layers, mirroring key elements of the feedforward, hierarchical information processing observed in the neocortex. The multi-nodal configuration also facilitates selective perturbation of individual nodes within the networks. To illustrate this, we induced hypoxia, a key factor in the pathogenesis of various neurological disorders, in well-connected nodes within the networks. Our findings demonstrate that such perturbations induce ablation of information flow across the hypoxic node, while enabling the study of plasticity and information processing adaptations in neighboring nodes and neural communication pathways. In summary, our presented model system recapitulates fundamental attributes of the microcircuit organization of neocortical neural networks, rendering it highly pertinent for preclinical neuroscience research. This model system holds promise for yielding new insights into the development, topological organization, and neuroplasticity mechanisms of the neocortex across the micro- and mesoscale level, in both healthy and pathological conditions. [ABSTRACT FROM AUTHOR]

Background: New daily persistent headache (NDPH) is a rare primary headache disorder characterized by daily and persistent sudden onset headaches. Specific abnormalities in gray matter and white matter structure are associated with pain, but have not been well studied in NDPH. The objective of this work is to explore the fiber tracts and structural connectivity, which can help reveal unique gray and white matter structural abnormalities in NDPH. Methods: The regional radiomics similarity networks were calculated from T1 weighted (T1w) MRI to depict the gray matter structure. The fiber connectivity matrices weighted by diffusion metrics like fractional anisotropy (FA), mean diffusivity (MD) and radial diffusivity (RD) were built, meanwhile the fiber tracts were segmented by anatomically-guided superficial fiber segmentation (Anat-SFSeg) method to explore the white matter structure from diffusion MRI. The considerable different neuroimaging features between NDPH and healthy controls (HC) were extracted from the connectivity and tract-based analyses. Finally, decision tree regression was used to predict the clinical scores (i.e. pain intensity) from the above neuroimaging features. Results: T1w and diffusion MRI data were available in 51 participants after quality control: 22 patients with NDPH and 29 HCs. Significantly decreased morphological similarity was found between the right superior frontal gyrus and right hippocampus. The superficial white matter (SWM) showed significantly decreased FA in fiber tracts including the right superficial-frontal, left superficial-occipital, bilateral superficial-occipital-temporal (Sup-OT) and right superficial-temporal, meanwhile significant increased RD was found in the left Sup-OT. For the fiber connectivity, NDPH showed significantly decreased FA in the bilateral basal ganglion and temporal lobe, increased MD in the right frontal lobe, and increased RD in the right frontal lobe and left temporal-occipital lobe. Clinical scores could be predicted dominantly by the above significantly different neuroimaging features through decision tree regression. Conclusions: Our research indicates the structural abnormalities of SWM and the neural pathways projected between regions like right hippocampus and left caudate nucleus, along with morphological similarity changes between the right superior frontal gyrus and right hippocampus, constitute the pathological features of NDPH. The decision tree regression demonstrates correlations between these structural changes and clinical scores. [ABSTRACT FROM AUTHOR]

Bruxism is a complex orofacial behavior that can occur during sleep or wakefulness, characterized by the involuntary grinding or clenching of teeth, involving repetitive activity of the jaw muscles. Its etiology is multifactorial, influenced by genetic, psychological, physiological, and lifestyle factors. While the mild bruxism may not necessitate treatment, severe bruxism can lead to significant consequences, including tooth damage, jaw pain, fatigue, and headaches. The bruxism has been associated with medical conditions, such as stress, anxiety, sleep disorders, and various neurological disorders; however, the exact pathophysiology remains elusive. Although the central nervous system is strongly implicated in the development of bruxism, specific neural substrates have not yet been conclusively established. Furthermore, there is evidence to suggest that individuals with bruxism may exhibit neural plasticity, resulting in the establishment of distinct neural circuitry that control the jaw movements. The application of various neurophysiological techniques in both clinical and pre-clinical studies provides valuable insights into the neural mechanisms underlying bruxism. This review aims to comprehensively examine the current literature on the neural pathways involved in bruxism, with the goal of improving the clinical approach and therapeutics for this condition. A deeper understanding of the neural circuitry controlling bruxism holds the potential to advance future treatment approaches and improve the management of patients with bruxism. [ABSTRACT FROM AUTHOR]

Implanted cortical neuroprosthetics (ICNs) are medical devices developed to replace dysfunctional neural pathways by creating information exchange between the brain and a digital system which can facilitate interaction with the external world. Over the last decade, researchers have explored the application of ICNs for diverse conditions including blindness, aphasia, and paralysis. Both transcranial and endovascular approaches have been used to record neural activity in humans, and in a laboratory setting, high-performance decoding of the signals associated with speech intention has been demonstrated. Particular progress towards a device which can move into clinical practice has been made with ICNs focussed on the restoration of speech and movement. This article provides an overview of contemporary ICNs for speech and movement restoration, their mechanisms of action and the unique ethical challenges raised by the field. [ABSTRACT FROM AUTHOR]

A central pursuit of cognitive neuroscience is to find neural mechanisms of cognition, with research programs favoring different strategies to look for them. But what is a neural mechanism, and how do we know we have captured them? Here I answer these questions through a framework that integrates Marr's levels with philosophical work on mechanism. From this, the following goal emerges: What needs to be explained are the computations of cognition, with explanation itself given by mechanism—composed of algorithms and parts of the brain that realize them. This reveals a delineation within cognitive neuroscience research. In the premechanism stage, the computations of cognition are linked to phenomena in the brain, narrowing down where and when mechanisms are situated in space and time. In the mechanism stage, it is established how computation emerges from organized interactions between parts—filling the premechanistic mold. I explain why a shift toward mechanistic modeling helps us meet our aims while outlining a road map for doing so. Finally, I argue that the explanatory scope of neural mechanisms can be approximated by effect sizes collected across studies, not just conceptual analysis. Together, these points synthesize a mechanistic agenda that allows subfields to connect at the level of theory. [ABSTRACT FROM AUTHOR]

Purpose: This review highlights the importance of functional connectivity in pediatric neuroscience, focusing on its role in understanding neurodevelopment and potential applications in clinical practice. It discusses various techniques for analyzing brain connectivity and their implications for clinical interventions in neurodevelopmental disorders. Methods: The principles and applications of independent component analysis and seed-based connectivity analysis in pediatric brain studies are outlined. Additionally, the use of graph analysis to enhance understanding of network organization and topology is reviewed, providing a comprehensive overview of connectivity methods across developmental stages, from fetuses to adolescents. Results: Findings from the reviewed studies reveal that functional connectivity research has uncovered significant insights into the early formation of brain circuits in fetuses and neonates, particularly the prenatal origins of cognitive and sensory systems. Longitudinal research across childhood and adolescence demonstrates dynamic changes in brain connectivity, identifying critical periods of development and maturation that are essential for understanding neurodevelopmental trajectories and disorders. Conclusion: Functional connectivity methods are crucial for advancing pediatric neuroscience. Techniques such as independent component analysis, seed-based connectivity analysis, and graph analysis offer valuable perspectives on brain development, creating new opportunities for early diagnosis and targeted interventions in neurodevelopmental disorders, thereby paving the way for personalized therapeutic strategies. [ABSTRACT FROM AUTHOR]

The effects of acute dehydration on neuromuscular function have been studied. However, whether the mechanisms underpinning such function are central or peripheral is still being determined, and the results are inconsistent. This systematic review aims to elucidate the influence of acute dehydration on neuromuscular function, including a novel aspect of investigating the central and peripheral neuromuscular mechanisms. Three databases were used for the article search: PubMed, Web of Science, and Scopus. Studies were included if they had objective measurements of dehydration, muscle performance, and electromyography data or transcranial magnetic stimulation or peripheral nerve stimulation measurements with healthy individuals aged 18–65 years. Twenty-three articles met the eligibility criteria. The studies exhibited considerable heterogeneity in the methods used to induce and quantify dehydration. Despite being inconsistent, the literature shows some evidence that acute dehydration does not affect maximal strength during isometric or moderate-speed isokinetic contractions. Conversely, acute dehydration significantly reduces maximal strength during slow-speed isokinetic contractions and fatigue resistance in response to endurance tasks. The studies report that dehydration does not affect the motor cortical output or spinal circuity. The effects occur at the peripheral level within the muscle. [ABSTRACT FROM AUTHOR]

The cognitive neuroscience of language aims at revealing how linguistic information is represented and manipulated in the brain to enable communication and meaningful behaviour. An important aspect of the underlying brain processes is the integration and transformation of information across multiple brain systems. In order to understand these processes, a detailed characterisation of brain connectivity is key. For the most accurate characterisation of brain connectivity, connectivity methods should make use of the full multivariate and multidimensional information available from neuroimaging data. This should include a characterisation of transformations between patterns of activation across brain regions, and in particular their dependence on stimulus features, task and context. Methods for this type of analysis in event-related experimental designs have only recently begun to emerge. This paper describes these novel developments and their potential to transform the neuroscience of language, with a focus on fMRI and EEG/MEG research. [ABSTRACT FROM AUTHOR]

Electroencephalography may be a valuable tool for assessing lexico-semantic processing in conditions where behavioural measures are unreliable. Detecting and quantifying effects in individuals is crucial for clinical applications, but individual-subject analyses are frequently not reported, and are hampered by low signal-to-noise. Multivariate analyses (MVPA) may be more sensitive than traditional approaches, so we asked how robustly they could detect differential neural responses to semantically matched and mismatched word/picture pairs in individuals. With clinical application in mind, we compared data from a research-grade EEG system to concurrently recorded data from the wireless Emotiv EPOC +. In both EEG systems, despite robust group-level effects, we only detected statistically significant processing of lexico-semantic condition in 50% of individuals. Surprisingly, detection rates were similar for MVPA and univariate analyses. MVPA may be advantageous when individual responses are heterogeneous, but in this simple paradigm, lexico-semantic processing could not be reliably detected at the individual level. [ABSTRACT FROM AUTHOR]

Background: This study explores the compensatory neural mechanisms associated with congenital deafness through an examination of tactile discrimination abilities using high-resolution functional magnetic resonance imaging (fMRI). Objective: To analyze the neural substrates underlying tactile processing in congenitally deaf individuals and compare them with hearing controls. Methods: Our participant pool included thirty-five congenitally deaf individuals and thirty-five hearing controls. All participants engaged in tactile discrimination tasks involving the identification of common objects by touch. We utilized an analytical suite comprising voxel-based statistics, functional connectivity multivariate/voxel pattern analysis (fc-MVPA), and seed-based connectivity analysis to examine neural activity. Results: Our findings revealed pronounced neural activity in congenitally deaf participants within regions typically associated with auditory processing, including the bilateral superior temporal gyrus, right middle temporal gyrus, and right rolandic operculum. Additionally, unique activation and connectivity patterns were observed in the right insula and bilateral supramarginal gyrus, indicating a strategic reorganization of neural pathways for tactile information processing. Behaviorally, both groups demonstrated high accuracy in the tactile tasks, exceeding 90%. However, the deaf participants outperformed their hearing counterparts in reaction times, showcasing significantly enhanced efficiency in tactile information processing. Conclusion: These insights into the brain's adaptability to sensory loss through compensatory neural reorganization highlight the intricate mechanisms by which tactile discrimination is enhanced in the absence of auditory input. Understanding these adaptations can help develop strategies to harness the brain's plasticity to improve sensory processing in individuals with sensory impairments, ultimately enhancing their quality of life through improved tactile perception and sensory integration. [ABSTRACT FROM AUTHOR]

The document titled "Appendix F: Means and SDs of frequency of prompts per group" provides data on the frequency of prompts in different tasks for two groups, Inq and Inq+ SE. It includes trivia questions related to neuroscience topics, such as brain lobes, neurons, and reflexes, which were used in an online competition. The document also features questions on somatosensation and memory formation, aimed at assessing students' understanding of these concepts. [Extracted from the article]

Background: Olfactory dysfunction stands as one of the most prevalent nonmotor symptoms in the initial stage of Parkinson’s disease (PD). Nevertheless, the intricate mechanisms underlying olfactory deficits in Parkinson’s disease still remain elusive. Methods: This study collected rs-fMRI data from 30 PD patients [15 with severe hyposmia (PD-SH) and 15 with no/mild hyposmia (PD-N/MH)] and 15 healthy controls (HC). To investigate functional segregation, the amplitude of lowfrequency fluctuation (ALFF) and regional homogeneity (ReHo) were utilized. Functional connectivity (FC) analysis was performed to explore the functional integration across diverse brain regions. Additionally, the graph theory-based network analysis was employed to assess functional networks in PD patients. Furthermore, Pearson correlation analysis was conducted to delve deeper into the relationship between the severity of olfactory dysfunction and various functional metrics. Results: We discovered pronounced variations in ALFF, ReHo, FC, and topological brain network attributes across the three groups, with several of these disparities exhibiting a correlation with olfactory scores. Conclusion: Using fMRI, our study analyzed brain function in PD-SH, PDN/MH, and HC groups, revealing impaired segregation and integration in PD-SH and PD-N/MH. We hypothesize that changes in temporal, frontal, occipital, and cerebellar activities, along with aberrant cerebellum-insula connectivity and node degree and betweenness disparities, may be linked to olfactory dysfunction in PD patients. [ABSTRACT FROM AUTHOR]

Brain-computer interfaces (BCIs) represent a groundbreaking approach to enabling direct communication for individuals with severe motor impairments, circumventing traditional neural and muscular pathways. Among the diverse array of BCI technologies, electroencephalogram (EEG)-based systems are particularly favored due to their non-invasive nature, user-friendly operation, and cost-effectiveness. Recent advancements have facilitated the development of adaptive bidirectional closed-loop BCIs, which dynamically adjust to users’ brain activity, thereby enhancing responsiveness and efficacy in neurorehabilitation. These systems support real-time modulation and continuous feedback, fostering personalized therapeutic interventions that align with users’ neural and behavioral responses. By incorporating machine learning algorithms, these BCIs optimize user interaction and promote recovery outcomes through mechanisms of activity-dependent neuroplasticity. This paper reviews the current landscape of EEG-based adaptive bidirectional closed-loop BCIs, examining their applications in the recovery of motor and sensory functions, as well as the challenges encountered in practical implementation. The findings underscore the potential of these technologies to significantly enhance patients’ quality of life and social interaction, while also identifying critical areas for future research aimed at improving system adaptability and performance. As advancements in artificial intelligence continue, the evolution of sophisticated BCI systems holds promise for transforming neurorehabilitation and expanding applications across various domains. [ABSTRACT FROM AUTHOR]

Background Purpose Postoperative ileus (POI) is a condition marked by a temporary suppression of gastrointestinal motility following abdominal surgery. The mechanism of POI encompasses various factors and is characterized by two phases: the early neurogenic phase involving both adrenergic and non‐adrenergic neural pathways; the later immune‐mediated phase is characterized by a sterile inflammatory response that lasts several days. Activation of muscularis macrophages triggers a sterile inflammatory process that results in dysfunction of the enteric nervous system (ENS) and a reversible inhibition of gastrointestinal motility.In this minireview, recent insights in the pathophysiological mechanisms underlying POI and potential new therapeutic strategies are described. [ABSTRACT FROM AUTHOR]

Cognitive impairment is a leading component of several neurodegenerative and neurodevelopmental diseases, profoundly impacting on the individual, the family, and society at large. Cognitive pathologies are driven by a multiplicity of factors, from genetic mutations and genetic risk factors, neurotransmitter-associated dysfunction, abnormal connectomics at the level of local neuronal circuits and broader brain networks, to environmental influences able to modulate some of the endogenous factors. Otherwise healthy older adults can be expected to experience some degree of mild cognitive impairment, some of which fall into the category of subjective cognitive deficits in clinical practice, while many neurodevelopmental and neurodegenerative diseases course with more profound alterations of cognition, particularly within the spectrum of the dementias. Our knowledge of the underlying neuropathological mechanisms at the root of this ample palette of clinical entities is far from complete. This review looks at current knowledge on synaptic modifications in the context of cognitive function along healthy ageing and cognitive dysfunction in disease, providing insight into differential diagnostic elements in the wide range of synapse alterations, from those associated with the mild cognitive changes of physiological senescence to the more profound abnormalities occurring at advanced clinical stages of dementia. I propose the term "cognitive synaptopathy" to encompass the wide spectrum of synaptic pathologies associated with higher brain function disorders. [ABSTRACT FROM AUTHOR]

Background: The creative arts have long been known for their therapeutic potential. These modalities, which include dance, painting, and music, among others, appear to be effective in enhancing emotional expression and alleviating adverse physiological and psychological effects. Engagement in creative arts can be pursued as a personal hobby, in a classroom setting, or through a formal therapeutic intervention with a qualified therapist. Engagement can be active (i.e., creating) or passive (i.e., viewing, listening). Regardless of the modality and manner of engagement, the mechanisms explaining the therapeutic efficacy of creative arts remain poorly understood. Objective: This study aims to systematically review research investigating the neurological mechanisms activated during active or passive engagement in creative arts, with a specific emphasis on the roles of the medial prefrontal cortex (mPFC) and the amygdala in emotional regulation (ER) and creative behaviors. The review seeks to provide preliminary evidence for the possible existence of common neural mechanisms underlying both phenomena, which could inform the development of targeted therapeutic interventions leveraging creative arts for ER. Methods: A systematic review was conducted following the Cochrane Collaboration guideline and PRISMA standards to identify studies examining the neurological mechanisms underlying creative activities. Results: A total of six out of 85 records meet the inclusion criteria, with all being basic research studies. Preliminary findings suggest that active and passive engagement with creative arts consistently activate neural circuits implicated in adaptive emotional regulation, including the mPFC and amygdala. These activations mirror the neural pathways engaged in effective ER strategies, suggesting the possible existence of shared mechanisms between creative expression and emotional processing. Conclusion: The evidence underscores the potential of creative arts as a complementary therapeutic strategy alongside conventional care and other evidence-based mind-body modalities. By elucidating the shared neural mechanisms between creative arts engagement and ER, this review contributes to the theoretical and practical understanding of the role of creative arts in mental health. Future research is recommended to further explore these neural correlations and their implications for therapeutic practice. [ABSTRACT FROM AUTHOR]

The claustrum is a brain structure that remains shrouded in mystery due to the limited understanding of its cellular structure, neural pathways, functionality and physiological aspects. Significant research has unveiled connections spanning from the claustrum to the entire cortex as well as subcortical areas. This widespread connectivity has led to speculations of its role in integrating information from different brain regions, possibly contributing to processes such as attention, consciousness, learning and memory. Our working hypothesis posits that claustrum neural activity contributes to the acquisition, consolidation and reconsolidation of long-term memories in mice. We found evidence in CF-1 mice of a decline in behavioral performance in an inhibitory avoidance task due to intra-claustral administration of 2% lidocaine immediately after a training session or memory recall. Nevertheless, this does not seem to be the case for the acquisition or retrieval of this type of memory, although its neural activity is significantly increased after training, evaluated through c-Fos expression. Moreover, inhibition of the claustrum's synaptic activity appears to impair the consolidation but not acquisition or retrieval of an unconditioned memory formed in a nose-poke habituation task. [ABSTRACT FROM AUTHOR]

Cough is one of the most common reasons leading to pediatric consultations, negatively impacting the quality of life of patients and caregivers. It is defined as a sudden and forceful expulsion of air from the lungs through the mouth, typically triggered by irritation or the stimulation of sensory nerves in the respiratory tract. This reflex is controlled by a neural pathway that includes sensory receptors, afferent nerves, the brainstem's cough center, efferent nerves, and the muscles involved in coughing. Based on its duration, cough in children may be classified as acute, lasting less than four weeks, and chronic, persisting for more than four weeks. Neuromodulators have shown promise in reducing the frequency and severity of cough by modulating the neural pathways involved in the cough reflex, although they require careful monitoring and patient selection to optimize the outcomes. This review aims to examine the rationale for using neuromodulators in the management of cough in children. [ABSTRACT FROM AUTHOR]

Background: Although neuroimaging investigations have consistently demonstrated that "hyperresponsive" and "hyperconnected" visual cortices may represent the functional substrate of cortical spreading depolarization in patients with migraine with aura, the mechanisms which underpin the brain "tendency" to ignite the cortical spreading depolarization and, consequently, aura phenomenon are still matter of debate. Considering that triggers able to induce aura phenomenon constrain brain to increase global (such as physical activity, stressors and sleep abnormalities) or local (such as bright light visual stimulations) energy demand, a vascular supply unable to satisfy the increased energy requirement could be hypothesized in these patients. Methods: Twenty-three patients with migraine with aura, 25 patients with migraine without aura and 20 healthy controls underwent a 3-Tesla MRI study. Cerebral blood flow and local functional connectivity (regional homogeneity) maps were obtained and registered to the MNI space where 100 cortical regions were derived using a functional local-global normative parcellation. A surrogate estimate of the regional neurovascular coupling for each subject was obtained at each parcel from the correlation coefficient between the z-scored ReHo map and the z-scored cerebral blood flow maps. Results: A significantly higher regional cerebral blood flow across the visual cortex of both hemispheres (i.e. fusiform and lingual gyri) was detected in migraine with aura patients when compared to patients with migraine without aura (p < 0.05, corrected for multiple comparisons). Concomitantly, a significantly reduced neurovascular coupling (p < 0.05, false discovery rate corrected) in the primary visual cortex parcel (VIS-4) of the large-scale visual network was observed in the left hemisphere of patients with migraine with aura (0.23±0.03), compared to both patients with migraine without aura (0.32±0.05) and healthy controls (0.29±0.05). Conclusions: Visual cortex neurovascular "decoupling" might represent the "link" between the exposure to trigger factors and aura phenomenon ignition. While physiological vascular oversupply may compensate neurovascular demand-supply at rest, it becomes inadequate in case of increased energy demand (e.g. when patients face with trigger factors) paving the way to the aura phenomenon ignition in patients with migraine with aura. Whether preventive treatments may exert their therapeutic activity on migraine with aura restoring the energy demands and cerebral blood flow trade-off within the visual network should be further investigated. [ABSTRACT FROM AUTHOR]

Delirium is an acute, global cognitive disorder syndrome, also known as acute brain syndrome, characterized by disturbance of attention and awareness and fluctuation of symptoms. Its incidence is high among critically ill patients. Once patients develop delirium, it increases the risk of unplanned extubation, prolongs hospital stay, increases the risk of nosocomial infection, postintensive care syndrome-cognitive impairment, and even death. Therefore, it is of great importance to understand how delirium occurs and to reduce the incidence of delirium in critically ill patients. This paper reviews the potential pathophysiological mechanisms of delirium in critically ill patients, with the aim of better understanding its pathophysiological processes, guiding the formulation of effective prevention and treatment strategies, providing a basis for clinical medication. [ABSTRACT FROM AUTHOR]

Bruxism is a complex orofacial behavior that can occur during sleep or wakefulness, characterized by the involuntary grinding or clenching of teeth, involving repetitive activity of the jaw muscles. Its etiology is multifactorial, influenced by genetic, psychological, physiological, and lifestyle factors. While the mild bruxism may not necessitate treatment, severe bruxism can lead to significant consequences, including tooth damage, jaw pain, fatigue, and headaches. The bruxism has been associated with medical conditions, such as stress, anxiety, sleep disorders, and various neurological disorders; however, the exact pathophysiology remains elusive. Although the central nervous system is strongly implicated in the development of bruxism, specific neural substrates have not yet been conclusively established. Furthermore, there is evidence to suggest that individuals with bruxism may exhibit neural plasticity, resulting in the establishment of distinct neural circuitry that control the jaw movements. The application of various neurophysiological techniques in both clinical and pre-clinical studies provides valuable insights into the neural mechanisms underlying bruxism. This review aims to comprehensively examine the current literature on the neural pathways involved in bruxism, with the goal of improving the clinical approach and therapeutics for this condition. A deeper understanding of the neural circuitry controlling bruxism holds the potential to advance future treatment approaches and improve the management of patients with bruxism. [ABSTRACT FROM AUTHOR]

In mammals, action potentials fired by rapidly adapting mechanosensitive afferents are known to reliably time lock to the cycles of a vibration. How and where along the ascending neuraxis is the peripheral afferent temporal code transformed into a rate code are currently not clear. Here, we probed the encoding of vibrotactile stimuli with electrophysiological recordings along major stages of the ascending somatosensory pathway in mice. We discovered the main transformation step was identified at the level of the thalamus, and parvalbumin-positive interneurons in thalamic reticular nucleus participate in sharpening frequency selectivity and in disrupting the precise spike timing. When frequency-specific microstimulation was applied within the brainstem, it generated frequency selectivity reminiscent of real vibration responses in the somatosensory cortex and could provide informative and robust signals for learning in behaving mice. Taken together, these findings could guide biomimetic stimulus strategies to activate specific nuclei along the ascending somatosensory pathway for neural prostheses. [Display omitted] • Electrophysiological recording reveals a shift of neural coding for tactile vibration • Transformation from a temporal to a rate code involves thalamic inhibitory networks • Microstimulation in brainstem DCN can reproduce cortical selectivity for vibration • Microstimulation in DCN, but not in S1, can be used for vibrotactile discrimination Lee et al. show that the transformation of the vibrotactile temporal code found in the periphery into a rate code along the ascending somatosensory pathway involves thalamic processing, particularly through parvalbumin-positive interneurons in the reticular nucleus. Brainstem microstimulation mimics vibration responses in the somatosensory cortex, offering insights for neural prostheses. [ABSTRACT FROM AUTHOR]

Although swallowing has been reviewed extensively, the coordination of the phases of swallowing have not. The phases are controlled by the brainstem, but peripheral factors help coordinate the phases. The occurrence, magnitude, and duration of esophageal phase depends upon peripheral feedback activated by the bolus. The esophageal phase does not occur without peripheral feedback from the esophagus. This feedback is mediated by esophageal slowly-adapting mucosal tension receptors through the recurrent and superior laryngeal nerves. A similar reflex mediated by the same peripheral pathway is the activation of swallowing by stimulation of the cervical esophagus. This reflex occurs primarily in human infants and animals, and this reflex may be important for protecting against aspiration after esophago-pharyngeal reflux. Not only are there inter-phase excitatory processes, but also inhibitory processes. A significant inhibitory process is deglutitive inhibition. When one swallows faster than peristalsis ends, peristalsis is inhibited by the new pharyngeal phase. This process prevents the ongoing esophageal peristaltic wave from blocking the bolus being pushed into the esophagus by the new wave. The esophageal phase returns during the last swallow of the sequence. This process is probably mediated by mucosal tension receptors through the superior laryngeal nerves. A similar reflex exists, the pharyngo-esophageal inhibitory reflex, but studies indicate that it is controlled by a different neural pathway. The pharyngo-esophageal inhibitory reflex is mediated by mucosal tension receptors through the glossopharyngeal nerve. In summary, there are significant peripheral processes that contribute to swallowing, whereby one phase of swallowing significantly affects the other. [ABSTRACT FROM AUTHOR]

Purpose: This article reports on jaw articulation, in connection with the segmental articulations of tongue tip and lips. The jaw is considered a syllable articulator as it opens and closes for each syllable, and the amount of jaw opening is related to syllable strength, given the same phonemic vowel. Here, we investigate the syllabic and the segmental articulations relationships to the acoustic segments. Method: We analyze electromagnetic articulography data of 18 Southern Swedish speakers by testing hypotheses based on the Descriptive Approach to Segmental Articulations. In this approach, articulatory movements are divided into fast intervals and steady states, and the crucial ("primary") articulators' deceleration and acceleration peaks align with the acoustic segment boundaries. Results: Previous findings on the lips and the tongue tip are confirmed. New results are the jaw as noncrucial ("nonprimary") does not align with the acoustic segment boundaries: Its steady states are shorter than consonant and vowel segments. Moreover, place of articulation of the coda affects the jaw cycle, while syllable type only affects jaw closing. No such effects are found on the edges of the jaw cycle, instead only gender affects jaw deceleration at syllable onset. Conclusions: The jaw is not crucial for the timing of the acoustic segment boundaries; also, syllable borders seem to not be affected by place of segmental articulation. The results strengthen the view of the jaw as syllable articulator providing a frame and the other articulators (e.g., lips and tongue tip) as the segmental articulators providing the content. [ABSTRACT FROM AUTHOR]

The article discusses tips and tricks for performing endoscopic ultrasound guided celiac plexus interventions. Celiac plexus interventions are used to manage abdominal pain associated with pancreaticobiliary cancers and chronic pancreatitis. The article provides information on when to consider these interventions, patient preparation, technique optimization, alternative procedures, management of adverse events, and the efficacy of the interventions. It also mentions the potential use of endoscopic ultrasound guided radiofrequency ablation as an alternative to celiac plexus interventions. Overall, the article emphasizes the importance of these interventions as an adjunct to medical therapy for managing pain in a safe and effective manner. [Extracted from the article]

Transient receptor potential ankyrin 1 (TRPA1), a member of the TRP superfamily of cation channels, is broadly expressed in sensory neural pathways, including the trigeminal neurons innervating the nasal cavity and vagal neurons innervating the trachea and the lung. TRPA1 acts as a detector of various irritant chemicals as well as hypoxia and hyperoxia. For the past 15 years, we have characterised its role in respiratory and behavioural modulation in vivo using Trpa1 knockout (KO) mice and wild‐type (WT) littermates. Trpa1 KO mice failed to detect, wake up from sleeping, and escape from formalin vapour and a mild hypoxic (15% O2) environment. Respiratory augmentation induced by mild hypoxia was absent in either Trpa1 KO mice or WT mice treated with a TRPA1 antagonist. Irritant gas introduced into the nasal cavity inhibited respiratory responses in WT mice but not in the KO mice. The effect of TRPA1 on the olfactory system seemed minimal because olfactory bulbectomized WT mice reacted similarly to the intact mice. Immunohistological analyses using a cellar activation marker, the phosphorylated form of extracellular signal‐regulated kinase, confirmed activation of trigeminal neurons in WT mice but not in Trpa1 KO mice in response to irritant chemicals and mild hypoxia. These data collectively show that TRPA1 is necessary for multiple chemical‐induced protective responses in respiration and behaviour. We propose that TRPA1 channels in the airway may play a sentinel role for environmental threats and prevent incoming damage. [ABSTRACT FROM AUTHOR]

Objective – To study the correlation between P1 latency and the results of clinical language tests (Reynell III and TROG-2), the latter were used as they are recommended for follow-up assessments of children with cochlear implants (Cis) by the Swedish National Quality Register for children with hearing impairment. Design – A clinical cohort study. Study sample – Cross-sectional and consecutive sampling of 49 children with CIs coming for clinical follow-up assessment from March 2017 – December 2019. Results – For all children tested, there was a significant negative correlation (Spearman's rho= −0.403, p = 0.011) between hearing age and P1 latency. A significant correlation between P1 latency and the Reynell III result (Spearman's rho = −0.810, p = 0.015) was found. In the TROG-2 group, there was no significant correlation between their P1 latency and their language test results (Spearman's rho −0.239, p = 0.196). Conclusion – This method seems to be feasible and easily accepted. The study was conducted in a heterogeneous group of children that we meet daily in our clinic. The results indicated that P1 latency has a negative correlation with language development among our youngest patients fitted with CIs and might be a clinical tool to assess the maturation of central auditory pathways. [ABSTRACT FROM AUTHOR]

Objectives: To determine whether idiopathic intracranial hypertension (IIH) may affect white matter integrity and optic pathways by using diffusion tensor imaging (DTI) and to correlate the DTI metrics with intracranial pressure (ICP). Methods: This study is a retrospective case–control study. A total of 42 patients who underwent lumbar puncture and those with elevated ICP, meeting the diagnostic criteria for IIH, were included in the study. All patients had supportive magnetic resonance imaging findings for the diagnosis of IIH. The headache control group comprised 36 patients who presented to the Neurology Department with infrequent episodic tension‐type headache, had a normal neurologic examination, and had clinical and radiological findings suggestive of normal ICP. For each patient with IIH, clinical findings and ophthalmological measurements were recorded. The apparent diffusion coefficient (ADC), fractional anisotropy (FA), axial diffusivity (AD), and radial diffusivity (RD) values were calculated using a region of interest‐based method in different white matter tracts and optic pathways and compared. Results: A total of 42 patients diagnosed with IIH (three males, 39 females), with a mean (standard deviation [SD] age of 38.1 (8.9) years), and 36 headache controls (10 males, 26 females, mean [SD] age; 38.1 [9.4] years) were included in the study. The mean (SD) body mass index (BMI) of the patients with IIH was 25.2 (1.9) kg/m2, and the mean (SD) BMI of the headache controls was 23.3 (1.5) kg/m2 (p < 0.001). Decreased FA values and increased RD values in the cingulum were detected in patients with IIH compared to the headache controls (p = 0.003, Cohen's d = 0.681; p = 0.002 Cohen's d = −0.710). Decreased AD values in the left and right superior cerebellar peduncle and increased ADC values in the middle cerebellar peduncle were detected in patients with IIH compared to the headache controls (p < 0.001, Cohen's d = 0.961; p = 0.009, Cohen's d = 0.607; p = 0.015, Cohen's d = −0.564). Increased ADC and RD values and decreased FA values in optic nerve were detected in patients with IIH (p = 0.010, Cohen's d = −0.603; p = 0.004, Cohen's d = −0.676; p = 0.015 Cohen's d = 0.568). A positive correlation was found between the cerebrospinal fluid pressure and ADC values of the left and right superior and left inferior longitudinal fasciculus, genu of the corpus callosum, and right optic radiation (r = 0.43, p = 0.005; r = 0.31, p = 0.044; r = 0.39, p = 0.010; r = 0.35, p = 0.024; r = 0,41, p = 0.007). There was a positive correlation between the retinal nerve fiber layer thickness and the ADC values of the optic nerve (r = 0.32, p = 0.039). Conclusions: Intracranial hypertension can be associated with deteriorated DTI values, which might be interpreted as a sign of impaired white matter microstructural integrity in many brain regions beyond the periventricular white matter. Pressure‐induced edema and axonal degeneration may be the potential underlying mechanisms of this microstructural damage. Plain Language Summary: Females of reproductive age with obesity are disproportionately affected by idiopathic intracranial hypertension (IIH), and the incidence of this diagnosis is increasing along with the prevalence of obesity. We do not yet understand how IIH develops, but dysregulation of intracranial pressure is an important area of research interest, so we hypothesized that increased intracranial pressure may affect white matter microstructure and optic pathways in patients with IIH. Using data from a specialized imaging technique, we found that patients with IIH may have impaired white matter microstructural integrity in several areas of the brain and microstructural alterations in the optic nerve. [ABSTRACT FROM AUTHOR]

Objective The aim of this study was to assess the reliability of resting-state functional magnetic resonance imaging (rest-fMRI) in mapping language areas for preoperative planning, versus standard task-based techniques, which are at times difficult to perform in clinical settings. Our study also aimed to evaluate the overlap between language areas identified through rest-fMRI and the standard task-fMRI, in neurosurgical cases. Materials and Methods Using a seed-based analysis of rest-fMRI with multiple template seeds, we identified functionally connected language regions in patients undergoing preoperative language mapping. Four language task paradigms (word, verb, picture, and semantics) were evaluated. We quantified the degree of overlap between language areas identified on rest-fMRI and task-fMRI, categorizing the results as more than 50% or less than 50% overlap. Results Seventy-seven percent of patients demonstrated an overlap exceeding 50% between rest- and task-fMRI maps, with the left Broca's area being the most frequently observed region of overlap. This finding was noted even in cases with lesions in Broca's or Wernicke's areas, highlighting the method's robustness. The verb task showed the best blood-oxygen-level dependent activity and overlap with rest-fMRI, highlighting its reliability. To identify a specific language area, the contralateral seed of the same area most commonly displayed connectivity with the area of interest. Conclusion Our findings demonstrate the potential of using rest-fMRI in accurately mapping eloquent language areas, in clinical settings The strong concordance observed, especially in the left Broca's area, underscores the reliability of this method. Further research and larger studies are essential to validate these results, potentially establishing the use of routine rest-fMRI, in clinical preoperative workup. [ABSTRACT FROM AUTHOR]

Recent artificial neural networks that process natural language achieve unprecedented performance in tasks requiring sentence-level understanding. As such, they could be interesting models of the integration of linguistic information in the human brain. We review works that compare these artificial language models with human brain activity and we assess the extent to which this approach has improved our understanding of the neural processes involved in natural language comprehension. Two main results emerge. First, the neural representation of word meaning aligns with the context-dependent, dense word vectors used by the artificial neural networks. Second, the processing hierarchy that emerges within artificial neural networks broadly matches the brain, but is surprisingly inconsistent across studies. We discuss current challenges in establishing artificial neural networks as process models of natural language comprehension. We suggest exploiting the highly structured representational geometry of artificial neural networks when mapping representations to brain data. [ABSTRACT FROM AUTHOR]

Dental pulp stem cells (DPSCs) have demonstrated significant potential for neuroregeneration. However, a full understanding of the specific mechanism underpinning the neural differentiation of DPSCs is still required. The Wnt signaling is crucial for the development of the embryonic neural system and the maintenance of adult neural homeostasis. This study aimed to investigate the role of the Wnt/Ca2+ pathway in the neural differentiation of human DPSCs (hDPSCs) and its modulation of the Wnt/β-catenin pathway. hDPSCs were cultured and divided into the control group and the neurogenic induction group (Neuro group). The mRNA and protein levels of neurogenic markers, Wnt/Ca2+, and Wnt/β-catenin pathway indicators were determined using Quantitative real-time PCR and Western blotting. After inhibition of the Wnt/Ca2+ pathway using a WNT5A short hairpin RNA (shRNA) plasmid and subsequent neurogenic induction, neurogenic markers and Wnt/β-catenin pathway indicators in the NC-sh-Neuro group and WNT5A-sh-Neuro group were determined using Quantitative real-time PCR and Western blotting. Compared with the control group, the expression of the Wnt/Ca2+ pathway indicators (WNT5A, Frizzled 2, calmodulin-dependent protein kinase IIa, and nuclear factor of active T cells 1) decreased in the Neuro group. Conversely, the expression of WNT3A, total β-catenin and active β-catenin in the Wnt/β-catenin pathway increased. Moreover, compared with the NC-sh-Neuro group, the WNT5A-sh-Neuro group exhibited a greater level of mature neural differentiation alongside elevated expression of the Wnt/β-catenin pathway indicators. The Wnt/Ca2+ pathway inhibited neural differentiation of hDPSCs and has a negative effect on the Wnt/β-catenin pathway in vitro. [ABSTRACT FROM AUTHOR]

Background Neuropathic pain is a refractory disease and badly impacts the lives of patients. Urinary kallikrein (UK) acted as a glycoprotein has been discovered to play a pivotal role in neuroprotection. However, the regulatory impacts and correlative pathways of UK in the progression of neuropathic pain remain dimness. Methods The chronic constriction injury (CCI) rat model was firstly established to mimic neuropathic pain. The withdrawal threshold was measured through the Von Frey test. The levels of TNF-α, IL-1β and IL-6 were determined through ELISA. The levels of ROS, GSH, SOD and GSH-Px were examined through the commercial kits. The ectopic discharges were assessed. The protein expressions were inspected through western blot. Results It was demonstrated that withdrawal threshold was reduced in CCI rat model, but this change was reversed after UK treatment, indicating that UK relieved mechanical allodynia. Moreover, UK alleviated the inflammatory response through reducing TNF-α, IL-1β and IL-6 levels. It was uncovered that oxidative stress was strengthened in CCI rat model, but this impact was restrained after UK treatment. Additionally, UK suppressed ectopic discharge. At last, it was proved that UK triggered the Nrf2/ARE signaling pathway in CCI rat model. Conclusion This study manifested that UK reversed neuropathic pain by inhibiting ectopic neural pathways, neural pathways and oxidation via the Nrf2/ARE pathway. This study may offer useful proofs the regulatory functions of UK in the cure of neuropathic pain. [ABSTRACT FROM AUTHOR]

Natural scenes are highly dynamic, challenging the reliability of visual processing. Yet, humans and many animals perform accurate visual behaviors, whereas computer vision devices struggle with rapidly changing background luminance. How does animal vision achieve this? Here, we reveal the algorithms and mechanisms of rapid luminance gain control in Drosophila, resulting in stable visual processing. We identify specific transmedullary neurons as the site of luminance gain control, which pass this property to direction-selective cells. The circuitry further involves wide-field neurons, matching computational predictions that local spatial pooling drive optimal contrast processing in natural scenes when light conditions change rapidly. Experiments and theory argue that a spatially pooled luminance signal achieves luminance gain control via divisive normalization. This process relies on shunting inhibition using the glutamate-gated chloride channel GluClα. Our work describes how the fly robustly processes visual information in dynamically changing natural scenes, a common challenge of all visual systems. Stable vision in quickly changing environments requires a mechanism that ensures that contrast is computed correctly when light conditions change rapidly. Here authors identify the circuits and algorithm of this mechanism in the fruit fly Drosophila. [ABSTRACT FROM AUTHOR]