scholarly journals Before and below ‘theory of mind’: embodied simulation and the neural correlates of social cognition

2007 ◽  
Vol 362 (1480) ◽  
pp. 659-669 ◽  
Author(s):  
Vittorio Gallese

The automatic translation of folk psychology into newly formed brain modules specifically dedicated to mind-reading and other social cognitive abilities should be carefully scrutinized. Searching for the brain location of intentions, beliefs and desires— as such —might not be the best epistemic strategy to disclose what social cognition really is. The results of neurocognitive research suggest that in the brain of primates, mirror neurons, and more generally the premotor system, play a major role in several aspects of social cognition, from action and intention understanding to language processing. This evidence is presented and discussed within the theoretical frame of an embodied simulation account of social cognition. Embodied simulation and the mirror neuron system underpinning it provide the means to share communicative intentions, meaning and reference, thus granting the parity requirements of social communication.

2014 ◽  
Vol 37 (2) ◽  
pp. 208-209 ◽  
Author(s):  
Sheila Krogh-Jespersen ◽  
Courtney Filippi ◽  
Amanda L. Woodward

AbstractThe target article argues that developmental processes are key to understanding the mirror neuron system, yet neglects several bodies of developmental research that are informative for doing so. Infants' actions and action understanding are structured by goals, and the former lends structure to the latter. Evaluating the origins and functions of mirror neurons depends on integrating investigations of neural, social-cognitive and motor development.


2020 ◽  
Author(s):  
Soukayna Bekkali ◽  
George Joseph Youssef ◽  
Peter Donaldson ◽  
Christian Hyde ◽  
Michael Do ◽  
...  

The mirror neuron system (MNS) has been theorised to play a neurobiological role in a number of social cognitive abilities and is commonly indexed putatively in humans via interpersonal motor resonance (IMR) and mu-suppression. Though both indices are thought to measure similar neuronal populations (i.e., ‘mirror neurons’), it has been suggested that these methods are unrelated, and therefore, incompatible. However, prior studies reporting no relationships were typically conducted in small and underpowered samples. Thus, we aimed to investigate this potential association in a large sample of neurotypical adults (N = 116; 72 females). Participants underwent TMS, electromyography (EMG), and electroencephalography (EEG) during the observation of videos of actors performing grasping actions in order to index IMR and mu-suppression (in beta, lower alpha, and upper alpha bandwidths). A series of linear regressions revealed no associations between IMR and each of the mu-suppression bandwidths. Supplementary Bayesian analyses provided further evidence in favour of the null (B01 = 8.85 - 8.93), providing further support for no association between the two indices of MNS activity. Our findings suggest that these two measures may indeed be unrelated indices that perhaps assess different neurophysiological aspects of the MNS. These results have important implications for future studies examining the MNS.


2020 ◽  
Author(s):  
Mei Yan Melody Chan ◽  
Yvonne M.Y. Han

Abstract Background Impaired imitation has been found to be an important factor contributing to social communication deficits in individuals with autism spectrum disorder (ASD). It has been hypothesized that the neural correlates of imitation, the mirror neuron system (MNS), are dysfunctional in ASD, resulting in imitation impairment as one of the key behavioral manifestations in ASD. Previous MNS studies produced inconsistent results, leaving the debate of whether mirror neurons are “broken” in ASD unresolved.Methods This meta-analysis aimed to explore the differences in MNS activation patterns between typically developing (TD) and ASD individuals when they observe/imitate biological motions with/without emotional components. Effect-size signed differential mapping (ES-SDM) was adopted to synthesize the available fMRI data. Results The MNS is dysfunctional in ASD; not only the brain regions containing mirror neurons were affected, the brain regions supporting MNS functioning were also impaired. Second, MNS dysfunction in ASD is modulated by task complexity; differential activation patterns during the presentation of “cold” and “hot” stimuli might be a result of atypical functional connectivity in ASD. Third, MNS dysfunction in ASD individuals is modulated by age. MNS regions were found to show delayed maturation; abnormal lateralization development in some of the brain regions also contributed to the atypical development of the MNS in ASD. Limitations We have attempted to include a comprehensive set of original data for this analysis. However, whole brain analysis data were not obtainable from some of the published papers, these studies could not be included as a result. Moreover, the results indicating the age effect on MNS in ASD could only be generalized to individuals aged 11-37, as MNS activation remains unstudied for populations beyond this age range. Also, the ES-SDM linear regression modelling might not be ideal to illustrate the associations between age and MNS activation; the meta-regression results should be treated with caution. Conclusion There is a “global” rather than a “local” network dysfunction, which may underlie the imitation impairments in individuals with ASD. Task complexity and age modulate the functioning of the MNS, which may explain the previous peculiar results contributing to the unresolved “broken mirror neuron” debate.


2014 ◽  
Vol 37 (2) ◽  
pp. 212-213 ◽  
Author(s):  
Lindsay M. Oberman ◽  
Edward M. Hubbard ◽  
Joseph P. McCleery

AbstractCook et al. argue that mirror neurons originate from associative learning processes, without evolutionary influence from social-cognitive mechanisms. We disagree with this claim and present arguments based upon cross-species comparisons, EEG findings, and developmental neuroscience that the evolution of mirror neurons is most likely driven simultaneously and interactively by evolutionarily adaptive psychological mechanisms and lower-level biological mechanisms that support them.


2019 ◽  
Vol 30 (4) ◽  
pp. 243-249
Author(s):  
Ronja Weiblen ◽  
Melanie Jonas ◽  
Sören Krach ◽  
Ulrike M. Krämer

Abstract. Research on the neural mechanisms underlying Gilles de la Tourette syndrome (GTS) has mostly concentrated on abnormalities in basal ganglia circuits. Recent alternative accounts, however, focused more on social and affective aspects. Individuals with GTS show peculiarities in their social and affective domain, including echophenomena, coprolalia, and nonobscene socially inappropriate behavior. This article reviews the experimental and theoretical work done on the social symptoms of GTS. We discuss the role of different social cognitive and affective functions and associated brain networks, namely, the social-decision-making system, theory-of-mind functions, and the so-called “mirror-neuron” system. Although GTS affects social interactions in many ways, and although the syndrome includes aberrant social behavior, the underlying cognitive, affective, and neural processes remain to be investigated.


2021 ◽  
Author(s):  
Stephanie N. L. Schmidt ◽  
Joachim Hass ◽  
Peter Kirsch ◽  
Daniela Mier

2011 ◽  
Vol 26 (S2) ◽  
pp. 2113-2113 ◽  
Author(s):  
A.M. Borghi ◽  
F. Binkofski

The ability to understand intentions of actions performed by others is one of the prerequisites for social interaction. This ability has been attributed to our capacity to mentalize others’ behaviour, by simulating or predicting their mental states that would cause that behaviour and make it comprehensible. Brain imaging studies revealed the so called “mentalizng network” including the pSTS/TPJ, the temporal poles and the medial prefrontal cortex. This network gets constantly activated anytime we try to take the perspective of others or try to simulate their state of mind. On the other hand the discovery of mirror neurons has provided an additional explanation for understanding of the content of actions. The functional properties of these neurons point out that action understanding is primarily based on a mechanism that directly matches the sensory representation of perceived actions with one's own motor representation of the same actions. We provide evidence that both systems interact closely during the processing of intentionality of actions. Thus mentalizing is not the only form of intentional understanding and motor and intentional components of action are closely interwoven. Both systems play an important role in the pathophysiology of schizophrenia.


Author(s):  
Vittorio Gallese ◽  
Corrado Sinigaglia

Mental simulation was claimed to provide a distinctive way of gaining knowledge about others’ actions and thoughts since the late 1980s. A decade later, the discovery of mirror neurons in macaque monkeys and the evidence of mirror brain areas in humans presented a new angle on this claim, suggesting also an embodied approach to simulation. The aim of the present chapter is to introduce and discuss this embodied approach and its role in basic social cognition. In doing this, we shall start by characterizing the distinctive features of embodied simulation (ES), especially in relation to its its motor aspects. Then, we shall provide evidence for the claim that ES may be critically involved in understanding others’ actions. Finally, we shall explore the conjecture that ES might involve a common ground for action execution and observation not only at the functional but also at the phenomenological level.


2020 ◽  
Author(s):  
Rhideeta Jalal ◽  
Aarti Nair ◽  
Amy Lin ◽  
Ariel Eckfeld ◽  
Leila Kushan ◽  
...  

Abstract Background: 22q11.2 deletion syndrome (22q11DS) is a common recurrent neurogenetic condition associated with elevated risk for developmental neuropsychiatric disorders and intellectual disability. Children and adults with 22q11DS often exhibit marked social impairment as well as neurocognitive deficits, and have elevated rates of both autism spectrum disorder (ASD) and psychosis. However, the relationship between the basic processes of social cognition and cognitive ability has not been well studied in 22q11DS. Here, we examined differences in social cognition in 22q11DS, relative to multiple groups of idiopathic neuropsychiatric disorders, and typically developing healthy controls (HC). Additionally, we examined differences in intellectual functioning and its relationship to social cognitive abilities. Finally, we examined the relationship between social cognitive abilities and real-world social behavior. Methods: We examined social cognition and intellectual functioning in 273 participants (mean age = 17.74+/-5.18% female = 44.3%): 50 with 22q11DS, 49 youth with first episode psychosis (FEP), 48 at clinical high-risk (CHR) for psychosis, 24 participants with ASD, and 102 HC. Social cognition was assessed using The Awareness of Social Inference Test (TASIT), while reciprocal social behavior was assessed via parent/caregiver ratings on the Social Responsiveness Scale (SRS). Participants were also administered the Wechsler Abbreviated Scale of Intelligence, 2 nd edition (WASI-II) to assess intellectual functioning. Results: The 22q11DS group exhibited significantly lower social cognitive abilities compared to all other groups, even after controlling for intellectual functioning. Significant positive correlations were found between social cognition, as measured by the TASIT, and IQ across groups. In contrast, no significant relationships were found between TASIT and real-world social behavior (SRS) for any group. Conclusions: Our findings indicate social cognitive deficits are more prominent in 22q11DS than idiopathic neuropsychiatric conditions across the age range, even after adjusting for global intellectual function. These results contribute to our understanding of the intellectual and social vulnerabilities of 22q11DS in comparison to idiopathic neuropsychiatric disorders. Our findings of robust associations between intellectual ability and social cognition emphasizes the importance of accounting for neurocognitive deficits in social skills interventions and tailoring these existing treatment models for 22q11DS and other populations with intellectual impairment.


2020 ◽  
Author(s):  
Rhideeta Jalal ◽  
Aarti Nair ◽  
Amy Lin ◽  
Ariel Eckfeld ◽  
Leila Kushan ◽  
...  

Abstract Background 22q11.2 deletion syndrome (22q11DS) is a common recurrent neurogenetic condition associated with elevated risk for developmental neuropsychiatric disorders and intellectual disability. Children and adults with 22q11DS often exhibit marked social impairment as well as neurocognitive deficits, and have elevated rates of both autism spectrum disorder (ASD) and psychosis. However, the relationship between the basic processes of social cognition and cognitive ability has not been well studied in 22q11DS. Here, we examined differences in social cognition in 22q11DS, relative to multiple groups of idiopathic neuropsychiatric disorders, and typically developing healthy controls (HC). Additionally, we examined differences in intellectual functioning and its relationship to social cognitive abilities. Finally, we examined the relationship between social cognitive abilities and real-world social behavior. Methods We examined social cognition and intellectual functioning in 306 participants (mean age = 16.63+/-4.59; % female = 44.8%): sixty-eight with 22q11DS, 49 youth with first episode psychosis (FEP), 48 at clinical high-risk (CHR) for psychosis, 24 participants with ASD, and 117 HC. Social cognition was assessed using The Awareness of Social Inference Test (TASIT), while reciprocal social behavior was assessed via parent/caregiver ratings on the Social Responsiveness Scale (SRS). Participants were also administered the Wechsler Abbreviated Scale of Intelligence, 2 nd edition (WASI-II) to assess intellectual functioning. Results The 22q11DS group exhibited significantly lower social cognitive abilities compared to all other groups, even after controlling for intellectual functioning. Significant positive correlations were found between social cognition, as measured by the TASIT, and IQ across groups. In contrast, no significant relationships were found between TASIT and real-world social behavior (SRS) for any group. Conclusions Our findings indicate social cognitive deficits are more prominent in 22q11DS than idiopathic neuropsychiatric conditions across the age range, even after adjusting for global intellectual function. These results contribute to our understanding of the intellectual and social vulnerabilities of 22q11DS in comparison to idiopathic neuropsychiatric disorders. Our findings of robust associations between intellectual ability and social cognition emphasizes the importance of accounting for neurocognitive deficits in social skills interventions and tailoring these existing treatment models for 22q11DS and other populations with intellectual impairment.


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