scholarly journals Dance on the Brain: Enhancing Intra- and Inter-Brain Synchrony

2021 ◽  
Vol 14 ◽  
Author(s):  
Julia C. Basso ◽  
Medha K. Satyal ◽  
Rachel Rugh

Dance has traditionally been viewed from a Eurocentric perspective as a mode of self-expression that involves the human body moving through space, performed for the purposes of art, and viewed by an audience. In this Hypothesis and Theory article, we synthesize findings from anthropology, sociology, psychology, dance pedagogy, and neuroscience to propose The Synchronicity Hypothesis of Dance, which states that humans dance to enhance both intra- and inter-brain synchrony. We outline a neurocentric definition of dance, which suggests that dance involves neurobehavioral processes in seven distinct areas including sensory, motor, cognitive, social, emotional, rhythmic, and creative. We explore The Synchronicity Hypothesis of Dance through several avenues. First, we examine evolutionary theories of dance, which suggest that dance drives interpersonal coordination. Second, we examine fundamental movement patterns, which emerge throughout development and are omnipresent across cultures of the world. Third, we examine how each of the seven neurobehaviors increases intra- and inter-brain synchrony. Fourth, we examine the neuroimaging literature on dance to identify the brain regions most involved in and affected by dance. The findings presented here support our hypothesis that we engage in dance for the purpose of intrinsic reward, which as a result of dance-induced increases in neural synchrony, leads to enhanced interpersonal coordination. This hypothesis suggests that dance may be helpful to repattern oscillatory activity, leading to clinical improvements in autism spectrum disorder and other disorders with oscillatory activity impairments. Finally, we offer suggestions for future directions and discuss the idea that our consciousness can be redefined not just as an individual process but as a shared experience that we can positively influence by dancing together.

Author(s):  
Yael Dai ◽  
Inge-Marie Eigsti

This chapter reviews strengths and weaknesses in executive function (EF) domains, including inhibition, working memory, flexibility, fluency, and planning, in adolescents (age 13–19) with autism spectrum disorder (ASD). Given the dramatic developmental changes in the brain regions that support EF during the period of adolescence, it is critical to evaluate which EF abilities show a distinct profile during this period. As this chapter will demonstrate, youth with ASD show deficits across all domains of EF, particularly in complex tasks that include arbitrary instructions. We describe the fundamental measures for assessing skills in each domain and discuss limitations and future directions for research, as well as clinical implications of these findings for working with youth with ASD.


2020 ◽  
Author(s):  
Bahar Tunçgenç ◽  
Carolyn Koch ◽  
Amira Herstic ◽  
Inge-Marie Eigsti ◽  
Stewart Mostofsky

AbstractMimicry facilitates social bonding throughout the lifespan. Mimicry impairments in autism spectrum conditions (ASC) are widely reported, including differentiation of the brain networks associated with its social bonding and learning functions. This study examined associations between volumes of brain regions associated with social bonding versus procedural skill learning, and mimicry of gestures during a naturalistic interaction in ASC and neurotypical (NT) children. Consistent with predictions, results revealed reduced mimicry in ASC relative to the NT children. Mimicry frequency was negatively associated with autism symptom severity. Mimicry was predicted predominantly by the volume of procedural skill learning regions in ASC, and by bonding regions in NT. Further, bonding regions contributed significantly less to mimicry in ASC than in NT, while the contribution of learning regions was not different across groups. These findings suggest that associating mimicry with skill learning, rather than social bonding, may partially explain observed communication difficulties in ASC.


2021 ◽  
Author(s):  
Pavithra Elumalai ◽  
Yasharth Yadav ◽  
Nitin Williams ◽  
Emil Saucan ◽  
Jürgen Jost ◽  
...  

Autism Spectrum Disorder (ASD) is a set of neurodevelopmental disorders that pose a significant global health burden. Measures from graph theory have been used to characterise ASD-related changes in resting-state fMRI functional connectivity networks (FCNs), but recently developed geometry-inspired measures have not been applied so far. In this study, we applied geometry-inspired graph Ricci curvatures to investigate ASD-related changes in resting-state fMRI FCNs. To do this, we applied Forman-Ricci and Ollivier-Ricci curvatures to compare networks of ASD and healthy controls (N = 1112) from the Autism Brain Imaging Data Exchange I (ABIDE-I) dataset. We performed these comparisons at the brain-wide level as well as at the level of individual brain regions, and further, determined the behavioral relevance of region-specific differences with Neurosynth meta-analysis decoding. We found brain-wide ASD-related differences for both Forman-Ricci and Ollivier-Ricci curvatures. For Forman-Ricci curvature, these differences were distributed across 83 of the 200 brain regions studied, and concentrated within the Default Mode, Somatomotor and Ventral Attention Network. Meta-analysis decoding identified the brain regions showing curvature differences as involved in social cognition, memory, language and movement. Notably, comparison with results from previous non-invasive stimulation (TMS/tDCS) experiments revealed that the set of brain regions showing curvature differences overlapped with the set of brain regions whose stimulation resulted in positive cognitive or behavioural outcomes in ASD patients. These results underscore the utility of geometry-inspired graph Ricci curvatures in characterising disease-related changes in ASD, and possibly, other neurodevelopmental disorders.


2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Seth A. Herd ◽  
Kai A. Krueger ◽  
Trenton E. Kriete ◽  
Tsung-Ren Huang ◽  
Thomas E. Hazy ◽  
...  

We address strategic cognitive sequencing, the “outer loop” of human cognition: how the brain decides what cognitive process to apply at a given moment to solve complex, multistep cognitive tasks. We argue that this topic has been neglected relative to its importance for systematic reasons but that recent work on how individual brain systems accomplish their computations has set the stage for productively addressing how brain regions coordinate over time to accomplish our most impressive thinking. We present four preliminary neural network models. The first addresses how the prefrontal cortex (PFC) and basal ganglia (BG) cooperate to perform trial-and-error learning of short sequences; the next, how several areas of PFC learn to make predictions of likely reward, and how this contributes to the BG making decisions at the level of strategies. The third models address how PFC, BG, parietal cortex, and hippocampus can work together to memorize sequences of cognitive actions from instruction (or “self-instruction”). The last shows how a constraint satisfaction process can find useful plans. The PFC maintains current and goal states and associates from both of these to find a “bridging” state, an abstract plan. We discuss how these processes could work together to produce strategic cognitive sequencing and discuss future directions in this area.


2021 ◽  
Vol 9 ◽  
Author(s):  
Rebecca J. Williams ◽  
M. Ethan MacDonald ◽  
Erin L. Mazerolle ◽  
G. Bruce Pike

Elucidating the brain regions and networks associated with cognitive processes has been the mainstay of task-based fMRI, under the assumption that BOLD signals are uncompromised by vascular function. This is despite the plethora of research highlighting BOLD modulations due to vascular changes induced by disease, drugs, and aging. On the other hand, BOLD fMRI-based assessment of cerebrovascular reactivity (CVR) is often used as an indicator of the brain's vascular health and has been shown to be strongly associated with cognitive function. This review paper considers the relationship between BOLD-based assessments of CVR, cognition and task-based fMRI. How the BOLD response reflects both CVR and neural activity, and how findings of altered CVR in disease and in normal physiology are associated with cognition and BOLD signal changes are discussed. These are pertinent considerations for fMRI applications aiming to understand the biological basis of cognition. Therefore, a discussion of how the acquisition of BOLD-based CVR can enhance our ability to map human brain function, with limitations and potential future directions, is presented.


Science ◽  
2019 ◽  
Vol 363 (6424) ◽  
pp. eaav0581 ◽  
Author(s):  
Ilaria Carta ◽  
Christopher H. Chen ◽  
Amanda L. Schott ◽  
Schnaude Dorizan ◽  
Kamran Khodakhah

The cerebellum has been implicated in a number of nonmotor mental disorders such as autism spectrum disorder, schizophrenia, and addiction. However, its contribution to these disorders is not well understood. In mice, we found that the cerebellum sends direct excitatory projections to the ventral tegmental area (VTA), one of the brain regions that processes and encodes reward. Optogenetic activation of the cerebello-VTA projections was rewarding and, in a three-chamber social task, these projections were more active when the animal explored the social chamber. Intriguingly, activity in the cerebello-VTA pathway was required for the mice to show social preference in this task. Our data delineate a major, previously unappreciated role for the cerebellum in controlling the reward circuitry and social behavior.


2009 ◽  
Vol 1 (4) ◽  
pp. 355-368 ◽  
Author(s):  
Tim Dalgleish ◽  
Barnaby D. Dunn ◽  
Dean Mobbs

The discipline of affective neuroscience is concerned with the underlying neural substrates of emotion and mood. This review presents an historical overview of the pioneering work in affective neuroscience of James and Lange, Cannon and Bard, and Hess, Papez, and MacLean before summarizing the current state of research on the brain regions identified by these seminal researchers. We also discuss the more recent strides made in the field of affective neuroscience. A final section considers different hypothetical organizations of affective neuroanatomy and highlights future directions for the discipline.


2020 ◽  
Author(s):  
Carla Esther Meyer Golden ◽  
Victoria X Wang ◽  
Hala Harony-Nicolas ◽  
Patrick R. Hof ◽  
Joseph Buxbaum

Abstract Background: Mutations and deletions in the SHANK3 synaptic gene cause the major neurodevelopmental features of Phelan-McDermid syndrome (PMS). The SHANK3 gene encodes a key structural component of excitatory synapses that is important for synaptogenesis. PMS is characterized by intellectual disability, autism spectrum disorder, cognitive deficits, physical dysmorphic features, sensory hyporeactivity, and alterations in the size of multiple brain regions. Clinical assessments and limited imaging studies have revealed a reduction in volume of multiple brain regions. They have also found white matter thinning and microstructural alterations to be persistent in patients with PMS. While many of these impairments have been replicated in mouse models of PMS, the brain structure of a rat model has not yet been studied. Methods: We assessed the brain structure of haploinsufficient and homozygous Shank3-deficient rats that model the behavioral deficits of PMS with magnetic resonance and diffusion tensor imaging, and compared their brain structure to wild type littermates.Results: Both gray and white matter structures were smaller in Shank3-deficient rats, leading to an overall reduction in brain size compared to wild type littermates. The largest region to be diminished in size was the neocortex. Some regions involved in sensory processing and white matter regions were also reduced in size. Lastly, the microstructure of two white matter tracts, the external capsule and fornix, was abnormal.Conclusions: Shank3-deficient rats replicate the reduced brain volume and altered white matter phenotypes present in individuals with PMS. Therefore, the brain regions that were altered represent potential cross-species structural biomarkers that warrant further study.


Author(s):  
Farnaz Faridi ◽  
◽  
Afrooz Seyedebrahimi ◽  
Reza Khosrowabadi ◽  
◽  
...  

Autism is a heterogeneous neurodevelopmental disorder associated with social, cognitive and behavioral impairments. These impairments are often reported along with alteration of the brain structure such as abnormal changes in the grey matter (GM) density. However, it is not yet clear whether these changes could be used to differentiate various subtypes of autism spectrum disorder (ASD). In this study, we compared the regional changes of GM density in ASD, Asperger's Syndrome (AS) individuals and a group of healthy controls (HC). In addition to regional changes itself, the amount of GM density changes in one region as compared to other brain regions was also calculated. We hypothesized that this structural covariance network could differentiate the AS individuals from the ASD and HC groups. Therefore, statistical analysis was performed on the MRI data of 70 male subjects including 26 ASD (age= 14-50, IQ= 92-132), 16 AS (age=7-58, IQ=93-133) and 28 HC (age=9-39, IQ=95-144). Results of one-way ANOVA on the GM density of 116 anatomically separated regions showed significant differences among the groups. The pattern of structural covariance network indicated that covariation of GM density between the brain regions is decreased in ASD. This attenuated structural differentiation could be considered as a reason for less efficient segregation and integration of information in the brain that could lead to cognitive dysfunctions in autism. We hope these findings could improve our understanding about the pathobiology of autism and may pave the way towards a more effective intervention paradigm.


2021 ◽  
Author(s):  
Akhil A. Vinithakumari ◽  
Piyush Padhi ◽  
Belen G. Hernandez ◽  
Susanne Je-Han Lin ◽  
Aaron Dunkerson-Kurzhumov ◽  
...  

Gastrointestinal illnesses are one of the most common comorbidities reported in patients with neurodevelopmental diseases, including autism spectrum disorders (ASD). Gut dysbiosis, overgrowth of C. difficile in the gut, and gut microbiota-associated alterations in central neurotransmission have been implicated in ASD, where the dopaminergic axis plays an important role in the disease pathogenesis. Human C. difficile strains produce a significant amount of the toxic metabolite p-cresol, an inhibitor of dopamine beta-hydroxylase (DBH), which catalyzes the conversion of dopamine (DA) to norepinephrine (NE). p-cresol is known to precipitate and exacerbate autistic behavior in rodents by increasing DA levels and altering DA receptor sensitivity in brain regions relevant to ASD. Therefore, we hypothesized that C. difficile infection dysregulates dopaminergic metabolism in the brain by increasing p-cresol levels in the gut and circulation and by inhibiting DBH, ultimately leading to elevated DA in the brain. For testing this hypothesis, we induced antibiotic-associated C. difficile in mice and determined the gut and serum p-cresol levels, serum DBH activity, and dopamine and its metabolite levels in different brain regions relevant to ASD. The results showed that C. difficile infection causes significant alterations in the dopaminergic axis in mice (p < 0.05). In addition, significantly increased circulating p-cresol levels and reduced DBH activity was observed in C. difficile infected animals (p < 0.05). Therefore, the results from this study suggest a potential link between C. difficile infection and alterations in the dopaminergic axis implicated in the precipitation and aggravation of ASD.


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