The simulating social mind: The role of the mirror neuron system and simulation in the social and communicative deficits of autism spectrum disorders.

2007 ◽  
Vol 133 (2) ◽  
pp. 310-327 ◽  
Author(s):  
Lindsay M. Oberman ◽  
Vilayanur S. Ramachandran
2017 ◽  
Vol 4 (3) ◽  
pp. 160662 ◽  
Author(s):  
Hannah M. Hobson ◽  
Dorothy V. M. Bishop

Mu suppression studies have been widely used to infer the activity of the human mirror neuron system (MNS) in a number of processes, ranging from action understanding, language, empathy and the development of autism spectrum disorders (ASDs). Although mu suppression is enjoying a resurgence of interest, it has a long history. This review aimed to revisit mu's past, and examine its recent use to investigate MNS involvement in language, social processes and ASDs. Mu suppression studies have largely failed to produce robust evidence for the role of the MNS in these domains. Several key potential shortcomings with the use and interpretation of mu suppression, documented in the older literature and highlighted by more recent reports, are explored here.


Author(s):  
Carolina Salles de Andrade ◽  
Milena Pereira Pondé

The objective of this study was to conduct a systematic review of experimental studies performed to assess the role of mirror neurons in the pathophysiology of autism. Four papers reported that areas of mirror neurons (MN) were under-active in autistic patients, giving weight to the theory of MN as a cause of ASD. Three papers indicated that MN were activated during the proposed activities, advocating atypical activation of MN, but not necessarily hypoactivation of these areas. One of the articles reported that only part of the MN system or just those areas of interconnected neurons are dysfunctional in autism. Analysis of the selected studies showed a correlation between dysfunction of the mirror neuron system and the main symptoms of autism such as deficits in social cognition, complete absence or a reduction in the individual’s interaction with his/her social environment and a failure in the neural mechanisms of imitation.


2014 ◽  
Vol 369 (1644) ◽  
pp. 20130184 ◽  
Author(s):  
Giacomo Vivanti ◽  
Sally J. Rogers

Individuals with autism have difficulties in social learning domains which typically involve mirror neuron system (MNS) activation. However, the precise role of the MNS in the development of autism and its relevance to treatment remain unclear. In this paper, we argue that three distinct aspects of social learning are critical for advancing knowledge in this area: (i) the mechanisms that allow for the implicit mapping of and learning from others' behaviour, (ii) the motivation to attend to and model conspecifics and (iii) the flexible and selective use of social learning. These factors are key targets of the Early Start Denver Model, an autism treatment approach which emphasizes social imitation, dyadic engagement, verbal and non-verbal communication and affect sharing. Analysis of the developmental processes and treatment-related changes in these different aspects of social learning in autism can shed light on the nature of the neuropsychological mechanisms underlying social learning and positive treatment outcomes in autism. This knowledge in turn may assist in developing more successful pedagogic approaches to autism spectrum disorder. Thus, intervention research can inform the debate on relations among neuropsychology of social learning, the role of the MNS, and educational practice in autism.


Autism ◽  
2020 ◽  
Vol 24 (8) ◽  
pp. 1945-1959
Author(s):  
Luke Yates ◽  
Hannah Hobson

The mirror neuron system has been argued to be a key brain system responsible for action understanding and imitation. Subsequently, mirror neuron system dysfunction has therefore been proposed to explain the social deficits manifested within autism spectrum condition, an approach referred to as the broken mirror hypothesis. Despite excitement surrounding this hypothesis, extensive research has produced insufficient evidence to support the broken mirror hypothesis in its pure form, and instead two alternative models have been formulated: EP-M model and the social top-down response modulation (STORM) model. All models suggest some dysfunction regarding the mirror neuron system in autism spectrum condition, be that within the mirror neuron system itself or systems that regulate the mirror neuron system. This literature review compares these three models in regard to recent neuroscientific investigations. This review concludes that there is insufficient support for the broken mirror hypothesis, but converging evidence supports an integrated EP-M and STORM model. Lay abstract The mirror neuron system has been argued to be a key brain system responsible for understanding the actions of others and for imitation. It has therefore been proposed that problems within this system could explain the social difficulties experienced by people with autism spectrum condition. This idea is referred to as the broken mirror hypothesis. However, research has produced insufficient evidence to support the broken mirror hypothesis in its original form. Therefore, two other models have been suggested: EP-M model and the social top-down response modulation (STORM) model. All models suggest something is different regarding the mirror neuron system in autism spectrum condition: either within the mirror neuron system itself or within the systems that control the activity of the mirror neuron system. This literature review compares these three models in regard to recent neuroscientific investigations. This review concludes that there is insufficient support for both the broken mirror hypothesis, but converging evidence supports an integrated EP-M and STORM model.


Author(s):  
Giuseppe Di Fede

After several years of researches to identify possible neurochemical alterations, at present it is known that autism is characterized and induced by at least three neuroendocrine deficiencies, involving the pineal function and the secretion of its most investigated hormone, melatonin (MLT), brain cannabinoid system, and the neurohypophyseal production of oxytocin (OT). Because of the fundamental role of MLT in sleep regulation, brain cannabinoid system in pleasure perception and control of anxiety, and OT in the affective life, these three neuroendocrine deficiencies might explain at least in part the symptomatology of autism. Therefore, autism-related neurochemical anomalies would involve the same main brain structures responsible for the conscious and the affective life, as well as for pleasure perception. On these bases, a preliminary study was performed to evaluate the influence of a progressive neuroendocrine. Substitutive treatment in autistic children. The study included 30 consecutive patients, by treating the first 12 subjects with the only MLT (100 mg/day in the dark period), the next 12 subjects with MLT plus cannabidiol. (CBD) (10 mg twice/day), and the remaining 6 subjects with MLT plus CBD plus OT (2 mg twice/day). All therapies were orally administered. MLT alone was mainly active in the treatment of sleep disorders. The association with CBD improved the control of anxiety. Finally, the further association with OT was also effective in improving the social and affective relationships. These preliminary results would suggest the possibility to treat the autism spectrum disorders by correcting their main neuroendocrine deficiencies through an exogenous administration.


2021 ◽  
Author(s):  
Lei Xu ◽  
Xiaoxiao Zheng ◽  
Shuxia Yao ◽  
Jialin Li ◽  
Meina Fu ◽  
...  

The amygdala is a core node in the social brain which exhibits structural and functional abnormalities in Autism spectrum disorder and there is evidence that the mirror neuron system (MNS) can functionally compensate for impaired emotion processing following amygdala lesions. In the current study, we employed an fMRI paradigm in 241 subjects investigating MNS and amygdala responses to observation, imagination and imitation of dynamic facial expressions and whether these differed in individuals with higher as opposed to lower autistic traits. Results indicated that individuals with higher compared to lower autistic traits showed reduced left amygdala responses to imitation and enhanced responses in the left superior temporal sulcus (STS) of the MNS to observation, imagination and imitation. Additionally, functional connectivity between the left amygdala and the left STS as well as some other MNS regions was increased in individuals with higher autistic traits, especially during imitation of fearful expressions. The amygdala-MNS connectivity significantly moderated autistic group differences on recognition memory for fearful faces and real-life social network indices, indicating that increased amygdala-MNS connectivity could diminish the social behavioral differences between higher and lower autistic trait groups. Overall, findings demonstrate decreased imitation-related amygdala activity in individuals with higher autistic traits in the context of increased cortical MNS activity and amygdala-MNS connectivity which may functionally compensate for amygdala dysfunction and social deficits. Training targeting the MNS may capitalize on this compensatory mechanism for therapeutic benefits in Autism spectrum disorder.


2020 ◽  
Vol LXXXI (4) ◽  
pp. 273-282
Author(s):  
Maja Jędruszczak ◽  
Danuta Al-Khamisy

This article looks at the findings of a study whose aim was to explore the difference in the social functioning of a student with autism spectrum disorders before biomedical treatment was introduced and during the treatment. It provides information on changes in the participant’s social behaviors collected with the use of the case study method and a short description of biomedical treatment guidelines and elements. Analysis of the information gathered shows that after 12 months from the beginning of biomedical treatment for autism, positive changes occurred in the participant's social functioning. He made the most progress in fulfilling the role of a friend and the least progress in social behaviors toward his family.


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