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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]

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]

The cortex contains multiple motor areas, including the primary motor cortex (M1) and supplementary motor area (SMA). Many muscles are represented in both the M1 and SMA, but the reason for this dual representation remains unclear. Previous work has shown that the M1 and SMA representations of a specific human muscle can be differentiated according to their functional connectivity with different brain areas located outside of the motor cortex. It is our perspective that this differential functional connectivity may be the neural substrate that allows an individual muscle to be accessed by distinct neural processes, such as those implementing volitional vs. postural task control. Here, we review existing human and animal literature suggesting how muscles are represented in the M1 and SMA and how these brain regions have distinct functions. We also discuss potential studies to further elucidate the distinct roles of the SMA and M1 in normal and dysfunctional motor control. [ABSTRACT FROM AUTHOR]

This integrative review rearticulates the notion of human aesthetics by critically appraising the conventional definitions, offerring a new, more comprehensive definition, and identifying the fundamental components associated with it. It intends to advance holistic understanding of the notion by differentiating aesthetic perception from basic perceptual recognition, and by characterizing these concepts from the perspective of information processing in both visual and nonvisual modalities. To this end, we analyze the dissociative nature of information processing in the brain, introducing a novel local-global integrative model that differentiates aesthetic processing from basic perceptual processing. This model builds on the current state of the art in visual aesthetics as well as newer propositions about nonvisual aesthetics. This model comprises two analytic channels: aesthetics-only channel and perception-to-aesthetics channel. The aesthetics-only channel primarily involves restricted local processing for quality or richness (e.g., attractiveness, beauty/prettiness, elegance, sublimeness, catchiness, hedonic value) analysis, whereas the perception-to-aesthetics channel involves global/extended local processing for basic feature analysis, followed by restricted local processing for quality or richness analysis. We contend that aesthetic processing operates independently of basic perceptual processing, but not independently of cognitive processing. We further conjecture that there might be a common faculty, labeled as aesthetic cognition faculty, in the human brain for all sensory aesthetics albeit other parts of the brain can also be activated because of basic sensory processing prior to aesthetic processing, particularly during the operation of the second channel. This generalized model can account not only for simple and pure aesthetic experiences but for partial and complex aesthetic experiences as well. [ABSTRACT FROM AUTHOR]

This paper aims to discuss old and contemporary perspectives in understanding language acquisition taking into account the neural theory of language. Discussing a recent theory by Kuhl (2010), neural substrates of first language learning will be put forward (Berwick et al., 2013). Neural substrates of phonetic learning, word learning, sentence processing, and syntax development are separately discussed. As a novel window to look into language learning in a greater detail, second language learning in relation to the theories of language acquisition is further discussed. Second language learning and dual vs. single coding structure relating to language acquisition are discussed in relation to the theories that have previously been explained. Finally, a discussion of contemporary issues in understanding both first and second language acquisition in relation to bilingualism is presented. In sum, investigating language acquisition requires a multi-disciplinary approach taking psychology, linguistics, and cognitive neuroscience of language into account is necessary. [ABSTRACT FROM AUTHOR]

Mirror-induced visual illusion obtained through mirror therapy is widely used to facilitate motor recovery after stroke. Activation of primary motor cortex (M1) ipsilateral to the moving limb has been reported during mirror-induced visual illusion. However, the mechanism through which the mirror illusion elicits motor execution processes without movements observed in the mirrored limb remains unclear. This study aims to review evidence based on brain imaging studies for testing the hypothesis that neural processes associated with kinaesthetic motor imagery are attributed to ipsilateral M1 activation. Four electronic databases were searched. Studies on functional brain imaging, investigating the instant effects of mirror-induced visual illusion among stroke survivors and healthy participants were included. Thirty-five studies engaging 78 stroke survivors and 396 healthy participants were reviewed. Results of functional brain scans (n = 20) indicated that half of the studies (n = 10, 50%) reported significant changes in the activation of ipsilateral M1, which mediates motor preparation and execution. Other common neural substrates included primary somatosensory cortex (45%, kinaesthesia), precuneus (40%, image generation and self-processing operations) and cerebellum (20%, motor control). Similar patterns of ipsilateral M1 activations were observed in the two groups. These neural substrates mediated the generation, maintenance, and manipulation of motor-related images, which were the key processes in kinaesthetic motor imagery. Relationships in terms of shared neural substrates and mental processes between mirror-induced visual illusion and kinaesthetic motor imagery generate new evidence on the role of the latter in mirror therapy. Future studies should investigate the imagery processes in illusion training for post-stroke patients. [ABSTRACT FROM AUTHOR]

During the past two decades, the number of animal models of psychiatric disorders has grown exponentially. Of these, genetic animal models that are modeled after rare but highly penetrant mutations hold great promise for deciphering critical molecular, synaptic, and neurocircuitry deficits of major psychiatric disorders, such as schizophrenia. Animal models should aim to focus on core aspects rather than capture the entire human disease. In this context, animal models with strong etiological validity, where behavioral and neurophysiological phenotypes and the features of the disease being modeled are in unambiguous homology, are being used to dissect both elementary and complex cognitive and perceptual processing deficits present in psychiatric disorders at the level of neurocircuitry, shedding new light on critical disease mechanisms. Recent progress in neuroscience along with large-scale initiatives that propose a consistent approach in characterizing these deficits across different laboratories will further enhance the efficacy of these studies that will ultimately lead to identifying new biological targets for drug development. [ABSTRACT FROM AUTHOR]

Background: Wilson's disease manifests as neuro-psychological or psychiatric symptoms along with neurological and liver disease. The present study aimed to probe into the declarative and non-declarative memory profile of Wilson's disease patients from a neurocognitive perspective. Methods: The study involved a sample of 12 Wilson's disease patients and 12 matched non-patient individuals who were assessed on Global Assessment Scale for Wilson's disease, the Edinburgh handedness inventory, memory scales from PGI Battery of Brain Dysfunction, Rey Auditory Verbal Learning Test, and mirror tracing task. Results: The overall result indicated that the Wilson's disease patient group differed with their non-patient counterparts with respect to immediate memory, recall, recognition, semantic memory, and procedural learning. Conclusion: The neural substrates related to the neuro-psychological symptoms of Wilson's disease patients are found to be a neural network involving basal ganglia, fronto-striatal circuits, and cerebellar region. [ABSTRACT FROM AUTHOR]

In this commentary, I critically assess Rex Welshon’s position on the neural substrates of ownership unity. First, I comment on Welshon’s definition of ownership unity and underline some of the problems stemming from his phenomenological analysis. Second, I analyze Welshon’s proposal to establish a mechanistic relation between neural substrates and ownership unity. I show that it is insufficient and defend my own position on how neural mechanisms may give rise to whole subjects of experience, which I call the neuro-integrative account of consciousness. Lastly, I comment on Welshon’s (2013) philosophical contribution and claim that it leaves the reader theoretically stranded. [ABSTRACT FROM AUTHOR]

Infants born prematurely are at risk for cardiovascular events causing hypoxia-ischemia (HI; reduced blood and oxygen to the brain). HI in turn can cause neuropathology, though patterns of damage are sometimes diffuse and often highly variable (with clinical heterogeneity further magnified by rapid development). As a result, though HI injury is associated with long-term behavioral and cognitive impairments in general, pathology indices for specific infants can provide only limited insight into individual prognosis. The current paper addresses this important clinical issue using a rat model that simulates unilateral HI in a late preterm infant coupled with long-term behavioral evaluation in two processing domains - auditory discrimination and spatial learning/memory. We examined the following: (1) whether deficits on one task would predict deficits on the other (suggesting that subjects with more severe injury perform worse across all cognitive domains) or (2) whether domain-specific outcomes among HI-injured subjects would be uncorrelated (suggesting differential damage to orthogonal neural systems). All animals (sham and HI) received initial auditory testing and were assigned to additional auditory testing (group A) or spatial maze testing (group B). This allowed within-task (group A) and between-task (group B) correlation. Anatomic measures of cortical, hippocampal and ventricular volume (indexing HI damage) were also obtained and correlated against behavioral measures. Results showed that auditory discrimination in the juvenile period was not correlated with spatial working memory in adulthood (group B) in either sham or HI rats. Conversely, early auditory processing performance for group A HI animals significantly predicted auditory deficits in adulthood (p = 0.05; no correlation in shams). Anatomic data also revealed significant relationships between the volumes of different brain areas within both HI and shams, but anatomic measures did not correlate with any behavioral measure in the HI group (though we saw a hippocampal/spatial correlation in shams, in the expected direction). Overall, current data provide an impetus to enhance tools for characterizing individual HI-related pathology in neonates, which could provide more accurate individual prognoses within specific cognitive/behavioral domains and thus improved patient-specific early interventions. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The duration and quality of human performance depend on both intrinsic motivation and external incentives. However, little is known about the neuroscientific basis of this interplay between internal and external motivators. Here, we used functional magnetic resonance imaging to examine the neural substrates of intrinsic motivation, operationalized as the free-choice time spent on a task when this was not required, and tested the neural and behavioral effects of external reward on intrinsic motivation. We found that increased duration of free-choice time was predicted by generally diminished neural responses in regions associated with cognitive and affective regulation. By comparison, the possibility of additional reward improved task accuracy, and specifically increased neural and behavioral responses following errors. Those individuals with the smallest neural responses associated with intrinsic motivation exhibited the greatest error-related neural enhancement under the external contingency of possible reward. Together, these data suggest that human performance is guided by a 'tonic' and 'phasic' relationship between the neural substrates of intrinsic motivation (tonic) and the impact of external incentives (phasic). [ABSTRACT FROM AUTHOR]

An argument is developed for the conclusion that certain neurological conditions and disorders are directly relevant for understanding the self 's embodiment and the ownership of conscious experience enjoyed by such an embodied self. Since these neurological conditions and disorders provide evidence that there can be shifts of, and compromises to, ownership, they help identify neural substrates and realizers of such ownership. However, even if recent neuroimaging and neuropsychological nominees for neural substrates of ownership unity are core realizers of ownership, they are not its total realizers. Implications of the distinction between core and total realizers are discussed. [ABSTRACT FROM PUBLISHER]

Adolescence reflects a period of increased rates of anxiety, depression, and suicide. Yet most teens emerge from this period with a healthy, positive outcome. In this article, we identify biological factors that may increase risk for some individuals during this developmental period by: (1) examining changes in neural circuitry underlying core phenotypic features of anxiety as healthy individuals transition into and out of adolescence; (2) examining genetic factors that may enhance the risk for psychopathology in one individual over another using translation from mouse models to human neuroimaging and behavior; and (3) examining the effects of early experiences on core phenotypic features of anxiety using human neuroimaging and behavioral approaches. Each of these approaches alone provides only limited information on genetic and environmental influences on complex human behavior across development. Together, they reflect an emerging field of translational developmental neuroscience in forming important bridges between animal models of neurodevelopmental and neuropsychiatric disorders. Depression and Anxiety, 2011. © 2011 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

A central part of the brain's limbic system, the amygdala is crucial for emotional learning, aversive conditioning, and response to fear and other emotions. Although the amygdala is a vibrant area of study in the neurosciences, it is virtually ignored in criminology. Here, we review the anatomical location, connectivity, and functions of the amygdala, explore its role in James Blair and colleagues' recently advanced theory of psychopathy, explicate amygdala abnormalities in diverse populations, and explore genetics research relating to amygdala functioning. Because of its role in the regulation of fear and other emotional memory and response, the amygdala is importantly related to psychopathy; callous-unemotional traits; and the vibrant, neuroscience-based investigations of the etiology of antisocial behavior. [ABSTRACT FROM AUTHOR]

Abstract: Although the brainstem plays an important role in breathing–swallowing coordination (BSC), the role of suprabulbar structures is ill defined. Given the known decrease in global cerebral activity during sleep, the sleep–wake paradigm was used to elucidate suprabulbar influences. Non-nutritive BSC of 10 healthy human infants was monitored longitudinally during wakefulness and sleep from birth to 1 year of age. Time-locked recordings of submental muscle activity, nasal airflow, and thyroid acoustics enabled the categorization of swallows depending on the preceding and following respiratory phase. In contrast to the change in the overall pattern of BSC with age, and despite well-known marked postnatal cortical development over this time, no arousal-related differences were seen during the first year of life. This most likely reflects complete brainstem control of non-nutritive BSC in infants. [Copyright &y& Elsevier]

This study was designed to examine the correlations between resting-state brain glucose metabolism (CMRglc), as measured with Positron Emission Tomography and performance on executive function tasks in Alzheimer's disease (AD), while taking into account the severity of cognitive deterioration. We addressed this issue in 50 AD patients, classified as very mild (n = 22) and mild (n = 28) AD on the basis of an extensive neuropsychological battery. Thirteen healthy subjects were selected as controls for the neuropsychological measures. Statistical Parametric Mapping (SPM) was used to examine voxel-wise correlations between CMRglc and scores on selected cognitive tests of executive functions: the Stroop Test, the Trail Making Test, the Dual Task and the Phonemic Fluency, while correcting for age and global CMRglc. All analyses were done separately for the two AD subgroups. The very mild AD patients showed significant associations between Stroop and Trail Making Test scores and prefrontal regions metabolism, whereas the mild AD patients exhibited more widely distributed cognitive–metabolic correlations extending to the posterior brain regions. These data suggest that a large cortical network is implicated in executive dysfunction in AD, and that the pattern of cognitive–metabolic correlations varies according to disease severity. [ABSTRACT FROM AUTHOR]

Research has shown that individuals with autism and Asperger syndrome are impaired in humor appreciation, although anecdotal and parental reports provide some evidence to the contrary. This paper reviews the cognitive and affective processes involved in humor and recent neurological findings. It examines humor expression and understanding in autism and Asperger syndrome in the context of the main psychological theories (Theory of Mind, Executive Functions, Weak Central Coherence and Laterization models) and associated neural substrates. In the concluding sections, examples of humor displayed by individuals with autism/Asperger syndrome which appear to challenge the above theories are analyzed and areas for further research are suggested. [ABSTRACT FROM AUTHOR]

Attention is a complex process whose disturbance is considered a core deficit in a number of disorders [e.g., Attention Deficit Hyperactivity Disorder (ADHD), schizophrenia]. In 1956, Rosvold and colleagues [J. Consult. Psychol. 20 (1956) 343.] demonstrated that the continuous performance test (CPT) as a measure of sustained attention was highly sensitive to brain damage or dysfunction. These findings have been replicated with various populations and with various versions of the CPT. The CPT is now cited as the most frequently used measure of attention in both practice and research. Across studies, results are consistent with models of sustained attention that involve the interaction of cortical (frontal, temporal, parietal), subcortical (limbic, basal ganglia), and functional systems including the pathways between the basal ganglia, thalamus, and frontal lobes. Right hemisphere involvement (asymmetric response) is also evident across multiple studies. As such, the CPT demonstrates sensitivity to dysfunction of the attentional system whether this is due to diffuse or more focal damage/dysfunction or in conjunction with any specific disorder. CPT performance can be viewed as symptom specific (attentional disturbance), but it is not disorder specific (e.g., ADHD). Implications for neuropsychological interpretation of CPT results are presented. [Copyright &y& Elsevier]

We studied the electrodermal skin conductance responses (SCRs) of 36 subjects with well-characterized lesions in various regions of the cerebral hemispheres. Several lesion loci were consistently associated with defective electrodermal responding: the ventromedial frontal region (right and left), the right inferior parietal region, and the anterior cingulate gyrus (right and left). Our findings provide direct information regarding neural correlates of skin conductance responses in bumans. [ABSTRACT FROM AUTHOR]

Recent water maze experiments suggest that rats performing place navigation primarily use the geometric information provided by a set of landmarks, and neglect the featural information provided by the identities of the landmarks. Here, I develop a model that explains how an animal may perform place navigation by relying only on geometric information. The core of the model is the representation of places as panoramas defined by circular bar-codes embodying the relative bearings and apparent sizes of the landmarks, irrespective of their identities. There are two stages in the model. During the first stage, the animal freely explores its environment in order to acquire spatial information at the local level. During the second stage, the animal uses the information previously memorized to perform place navigation towards the goal it intends to reach. The possible role of two brain areas in place navigation is discussed within this framework. Beyond their primary role in landmark-based representations of places, hippocampal place cells may be involved in computing the current distances to the landmarks. Beyond their primary role in landmark-based representations of headings, post-subicular head-direction cells may be involved in computing the “compass bearings” of the landmarks. [ABSTRACT FROM AUTHOR]

Purpose of Review: Aphasia is often characterized in terms of subtype and severity, yet these constructs have limited explanatory power, because aphasia is inherently multifactorial both in its neural substrates and in its symptomatology. The purpose of this review is to survey current and emerging multivariate approaches to understanding aphasia. Recent Findings: Techniques such as factor analysis and principal component analysis have been used to define latent underlying factors that can account for performance on batteries of speech and language tests, and for characteristics of spontaneous speech production. Multivariate lesion-symptom mapping has been shown to outperform univariate approaches to lesion-symptom mapping for identifying brain regions where damage is associated with specific speech and language deficits. It is increasingly clear that structural damage results in functional changes in wider neural networks, which mediate speech and language outcomes. Summary: Multivariate statistical approaches are essential for understanding the complex relationships between the neural substrates of aphasia, and resultant profiles of speech and language function. [ABSTRACT FROM AUTHOR]

Summary Sparse manipulation of neuron excitability during free behavior is critical for identifying neural substrates of behavior. Genetic tools for precise neuronal manipulation exist in the fruit fly, Drosophila melanogaster , but behavioral tools are still lacking to identify potentially subtle phenotypes only detectible using high-throughput and high spatiotemporal resolution. We developed three assay components that can be used modularly to study natural and optogenetically induced behaviors. FlyGate automatically releases flies one at a time into an assay. FlyDetect tracks flies in real time, is robust to severe occlusions, and can be used to track appendages, such as the head. GlobeDisplay is a spherical projection system covering the fly's visual receptive field with a single projector. We demonstrate the utility of these components in an integrated system, FlyPEZ, by comprehensively modeling the input-output function for directional looming-evoked escape takeoffs and describing a millisecond-timescale phenotype from genetic silencing of a single visual projection neuron type. Graphical Abstract Highlights • FlyGate automatically releases flies one at a time into an assay • FlyDetect tracks flies in real time and is robust to severe occlusions • GlobeDisplay is a panoramic spherical projection system that uses a single projector • FlyPEZ uses these tools to quantify natural and optogenetically induced behavior Williamson et al. developed a high-throughput device to automatically isolate individual flies and record their behavior with high-speed video. They demonstrate the system's utility for studying the Drosophila brain using modern genetic tools by discovering behavioral phenotypes that result from manipulation of small groups of neurons. [ABSTRACT FROM AUTHOR]