Exploring the Development of the Mirror Neuron System: Finding the Right Paradigm

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 correlate of imitation, the mirror neuron system (MNS), is 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 “broken” mirror neurons in ASD are unresolved. Methods This meta-analysis aimed to explore the differences in MNS activation patterns between typically developing (TD) and ASD individuals when they observe biological motions with or without social-emotional components. Effect size signed differential mapping (ES-SDM) was adopted to synthesize the available fMRI data. Results ES-SDM analysis revealed hyperactivation in the right inferior frontal gyrus and left supplementary motor area in ASD during observation of biological motions. Subgroup analysis of experiments involving the observation of stimuli with or without emotional component revealed hyperactivation in the left inferior parietal lobule and left supplementary motor during action observation without emotional components, whereas hyperactivation of the right inferior frontal gyrus was found during action observation with emotional components in ASD. Subgroup analyses of age showed hyperactivation of the bilateral inferior frontal gyrus in ASD adolescents, while hyperactivation in the right inferior frontal gyrus was noted in ASD adults. Meta-regression within ASD individuals indicated that the right cerebellum crus I activation increased with age, while the left inferior temporal gyrus activation decreased with age. Limitations This meta-analysis is limited in its generalization of the findings to individuals with ASD by the restricted age range, heterogeneous study sample, and the large within-group variation in MNS activation patterns during object observation. Furthermore, we only included action observation studies which might limit the generalization of our results to the imitation deficits in ASD. In addition, the relatively small sample size for individual studies might also potentially overestimate the effect sizes. Conclusion The MNS is impaired in ASD. The abnormal activation patterns were found to be modulated by the nature of stimuli and age, which might explain the contradictory results from earlier studies on the “broken mirror neuron” debate.

Download Full-text

Differential Mirror Neuron System (MNS) Activation During Action Observation with and without Social-Emotional Components in Autism: A Meta-Analysis of Neuroimaging Studies

10.21203/rs.2.23748/v3 ◽

2020 ◽

Author(s):

Melody M.Y. Chan ◽

Yvonne M.Y. Han

Keyword(s):

Mirror Neuron System ◽

Action Observation ◽

Meta Analysis ◽

Inferior Frontal Gyrus ◽

Mirror Neuron ◽

Autism Spectrum ◽

Social Emotional ◽

Activation Patterns ◽

Neuron System ◽

The Right

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 correlate of imitation, the mirror neuron system (MNS), is 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 biological motions with or without social-emotional components. Effect-size signed differential mapping (ES-SDM) was adopted to synthesize the available fMRI data. Results ES-SDM analysis revealed hyperactivation in the right inferior frontal gyrus and left supplementary motor area in ASD during observation of biological motions. Subgroup analysis of experiments involving the observation of stimuli with or without emotional component revealed hyperactivation in the left inferior parietal lobule and left supplementary motor during action observation without emotional components, whereas hyperactivation of right inferior frontal gyrus was found during action observation with emotional components in ASD. Subgroup analyses of age showed hyperactivation of bilateral inferior frontal gyrus in ASD adolescents, while hyperactivation in the right inferior frontal gyrus was noted in ASD adults. Meta-regression within ASD individuals indicated that right cerebellum crus I activation increased with age, while left inferior temporal gyrus activation decreased with age. Limitations This meta-analysis is limited in its generalization of the findings to individuals with ASD by the restricted age range, heterogeneous study sample, and the large within-group variation in MNS activation patterns during object observation. Furthermore, we only included action observation studies which might limit the generalization of our results to the imitation deficits in ASD. In addition, the relatively small sample size for individual studies might also potentially overestimate the effect sizes. Conclusion The MNS is impaired in ASD. The abnormal activation patterns were found to be modulated by the nature of stimuli and age, which might explain the contradictory results from earlier studies on the “broken mirror neuron” debate.

Download Full-text

Dysfunction of the Human Mirror Neuron System in Ideomotor Apraxia: Evidence from Mu Suppression

Journal of Cognitive Neuroscience ◽

10.1162/jocn_a_00936 ◽

2016 ◽

Vol 28 (6) ◽

pp. 775-791 ◽

Cited By ~ 6

Author(s):

Silvi Frenkel-Toledo ◽

Dario G. Liebermann ◽

Shlomo Bentin ◽

Nachum Soroker

Keyword(s):

Right Hemisphere ◽

Mirror Neuron System ◽

Inferior Frontal Gyrus ◽

Mirror Neuron ◽

Stroke Patients ◽

Neuron System ◽

Mu Suppression ◽

Ideomotor Apraxia ◽

Manual Movements ◽

The Right

Stroke patients with ideomotor apraxia (IMA) have difficulties controlling voluntary motor actions, as clearly seen when asked to imitate simple gestures performed by the examiner. Despite extensive research, the neurophysiological mechanisms underlying failure to imitate gestures in IMA remain controversial. The aim of the current study was to explore the relationship between imitation failure in IMA and mirror neuron system (MNS) functioning. Mirror neurons were found to play a crucial role in movement imitation and in imitation-based motor learning. Their recruitment during movement observation and execution is signaled in EEG recordings by suppression of the lower (8–10 Hz) mu range. We examined the modulation of EEG in this range in stroke patients with left (n = 21) and right (n = 15) hemisphere damage during observation of video clips showing different manual movements. IMA severity was assessed by the DeRenzi standardized diagnostic test. Results showed that failure to imitate observed manual movements correlated with diminished mu suppression in patients with damage to the right inferior parietal lobule and in patients with damage to the right inferior frontal gyrus pars opercularis—areas where major components of the human MNS are assumed to reside. Voxel-based lesion symptom mapping revealed a significant impact on imitation capacity for the left inferior and superior parietal lobules and the left post central gyrus. Both left and right hemisphere damages were associated with imitation failure typical of IMA, yet a clear demonstration of relationship to the MNS was obtained only in the right hemisphere damage group. Suppression of the 8–10 Hz range was stronger in central compared with occipital sites, pointing to a dominant implication of mu rather than alpha rhythms. However, the suppression correlated with De Renzi's apraxia test scores not only in central but also in occipital sites, suggesting a multifactorial mechanism for IMA, with a possible impact for deranged visual attention (alpha suppression) beyond the effect of MNS damage (mu suppression).

Download Full-text

The Human Mirror Neuron System

Handbook of Research on Agent-Based Societies ◽

10.4018/978-1-60566-236-7.ch019 ◽

2009 ◽

pp. 275-287 ◽

Cited By ~ 1

Author(s):

David B. Newlin

Keyword(s):

Mirror Neurons ◽

Motor Behavior ◽

Mirror Neuron System ◽

Imaging Techniques ◽

Mirror Neuron ◽

Fundamental Aspect ◽

Functional Architecture ◽

Neuron System ◽

Neuro Imaging ◽

The Right

Following the discovery in Rhesus monkeys of “mirror neurons” that fire during both execution and observation of motor behavior, human studies have documented a fronto-parietal mirror neuron system (MNS) with apparently similar functions. We discuss some issues related to the human research, including measurement with neuro imaging techniques and recent neuro technologies for manipulating regional brain function. We note the remarkable overlap between several brain systems studied in people: the MNS, the Theory of Mind (ToM), the “self”-system of the brain, and the neural “default mode.” The functional architecture of these systems may have important implications for how the MNS is organized and its functions. We propose that “auto-mirroring” in which self-observation of one’s own motor behavior can be either facilitated or blocked, may be a fundamental aspect of the MNS. Finally, the implications of hemispheric asymmetry in the right and left MNS are discussed. Although MNS research is in its infancy, it bears promise to reveal basic aspects of the brain’s functional architecture.

Download Full-text

Differential Mirror Neuron System (MNS) Activation During Action Observation with and without Social-Emotional Components in autism: A Meta-Analysis of Neuroimaging Studies

10.21203/rs.2.23748/v2 ◽

2020 ◽

Author(s):

Melody M.Y. Chan ◽

Yvonne M.Y. Han

Keyword(s):

Mirror Neuron System ◽

Action Observation ◽

Meta Analysis ◽

Inferior Frontal Gyrus ◽

Mirror Neuron ◽

Social Emotional ◽

Activation Patterns ◽

Neuron System ◽

Emotional Component ◽

The Right

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 correlate of imitation, the mirror neuron system (MNS), is 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 biological motions with or without social-emotional components. Effect-size signed differential mapping (ES-SDM) was adopted to synthesize the available fMRI data. Results ES-SDM analysis revealed hyperactivation in the right inferior frontal gyrus and left supplementary motor area in ASD during observation of biological motions. Subgroup analysis of experiments involving the observation of stimuli with or without emotional component revealed hyperactivation in the left inferior parietal lobule and left supplementary motor during action observation without emotional component, whereas hyperactivation of right inferior frontal gyrus was found during action observation with emotional components in ASD. Subgroup analyses of age showed hyperactivation of bilateral inferior frontal gyrus in ASD adolescents, while hyperactivation in the right inferior frontal gyrus was noted in ASD adults. Meta-regression within ASD individuals indicated that right cerebellum crus I activation increased with age, while left inferior temporal gyrus activation decreased with age. Limitations This meta-analysis is limited in its generalization of the findings to individuals with ASD by the restricted age range, heterogeneous study sample, and the large within-group variation in MNS activation patterns during object observation. Furthermore, we only included action observation studies which might limit the generalization of our results to the imitation deficits in ASD. In addition, the relatively small sample size for individual studies might also potentially overestimate the effect sizes. Conclusion The MNS is impaired in ASD. The abnormal activation patterns were found to be modulated by the nature of stimuli and age, which might explain the contradictory results from earlier studies on the “broken mirror neuron” debate.

Download Full-text