Mirror Neuron System Dysfunction Research Articles

Continuing to look in the mirror: A review of neuroscientific evidence for the broken mirror hypothesis, EP-M model and STORM model of autism spectrum conditions.

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 abstractThe 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.

From Neurons to Social Beings: Short Review of the Mirror Neuron System Research and Its Socio-Psychological and Psychiatric Implications.

The mirror neuron system (MNS) is a brain network activated when we move our body parts and when we observe the actions of other agent. Since the mirror neuron’s discovery in research on monkeys, several studies have examined its network and properties in both animals and humans. This review discusses MNS studies of animals and human MNS studies related to high-order social cognitions such as emotion and empathy, as well as relations between MNS dysfunction and mental disorders. Finally, these evidences are understood from an evolutionary perspective.

Mirror neuron system activation in children with developmental coordination disorder: A replication functional MRI study

BackgroundIt has been hypothesised that abnormal functioning of the mirror neuron system (MNS) may lead to deficits in imitation and the internal representation of movement, potentially contributing to the motor impairments associated with developmental coordination disorder (DCD). AimsUsing fMRI, this study examined brain activation patterns in children with and without DCD on a finger adduction/abduction task during four MNS activation states: observation; motor imagery; execution; and imitation. Methods and proceduresNineteen boys (8.25–12.75 years) participated, including 10 children with DCD (≤16th percentile on MABC-2; no ADHD/ASD), and nine typically developing controls (≥25th percentile on MABC-2). Outcomes and resultsEven though children with DCD displayed deficits behaviourally on imitation (Sensory Integration & Praxis Test Subtests) and motor imagery assessments prior to scanning, no differences in MNS activation were seen between the DCD and control groups at a neurological level, with both groups activating mirror regions effectively across conditions. Small clusters of decreased activation during imitation were identified in non-mirror regions in the DCD group, including the thalamus, caudate, and posterior cingulate − regions involved in motor planning and attentional processes. Conclusions and implicationsThe results of this study do not provide support for the MNS dysfunction theory as a possible causal mechanism for DCD. Further research to explore attentional and motor planning processes and how they may interact at a network level may enhance our understanding of this complex disorder.

Impact of thousand-and-one amino acid 2 kinase mediated neurodifferentiation in cerebral cortex and impairment of mirror neuron pathways on autism spectrum disorders

An understanding of how neurons develop their morphology and their distinct physiology is the key to the elucidation of the mechanisms underlying sophisticated cognitive functions in normal and disease conditions. Evidence suggests that neurodevelopmental disorders with delayed onset, such as autism spectrum disorders (ASDs) might be a consequence of aberrant dendritic arborization. This review is dedicated toward the discussion of a new pathway that specifically affects the formation of basal dendrites and axonal projections in cortical pyramidal neurons. With reference to this pathway, the function of thousand-and-one amino acid 2 kinase, in relation to dendrite morphogenesis has been elaborated. Mirror neuron system dysfunction may underlie a self-other matching impairment which has been suggested to account for autism. The hypotheses of deficit an impaired mirror neuron function in autism have now been well supported by studies employing a range of methodologies. However, underlying mechanisms require further exploration to explain how mirror neurons may be involved in attention and metalizing processes. It seems possible that different sub-populations of mirror neurons, distinct in particular anatomical regions of the brain, contribute differentially to social cognitive functions. Mirror neuron networks dysfunction in ASD-affected individuals leading to dampened imitation learning, misguided development of “egocentrism” and even failure to comprehend the intention behind a motor act. While it seems clear that autism is associated with impaired development of embodied aspects of cognition, the ways that mirror neurons contribute to these brain-behavior links are likely to be complex and demands further research.

EP 57. Biological motion perception in Parkinson‘s disease

Previous studies have suggested that action perception is linked to action execution. For example, it has been shown that perception of an action is altered by simultaneous performance of the same action ( Jacons and Shiffrar, 2005 ). Parkinson‘s disease (PD) is typically characterized by impaired motor execution. In the present study, we investigated whether PD also adversely affects biological (i.e. human) motion perception. 17 PD patients and 17 matched neurologically healthy controls participated in the study. The participants watched point-light displays of human, animal and object motion and were asked to differentiate between biomechanically plausible point-light motions and distorted versions of these motions. All participants completed two identical testing sessions. The PD patients completed the first testing session in an “OFF”-state, that is 12 hours after last taking dopaminergic medication. The second testing session was completed after the ingestion of levodopa (“ON”). Control subjects completed two identical session with a break of ∼30–60 min in between. The Unified Parkinson’s Disease Rating Score (UPDRS) was measured in OFF and ON for the PD group to ensure an effect of medication. We analyzed participants‘ sensitivity for plausible vs. distorted motion. In the OFF state, PD patients showed significantly lower sensitivity for human and animal motion than controls. Post hoc analysis revealed that the difference between PD patients and controls was significantly stronger for transitive than for intransitive human motions. Sensitivity for object motion did not differ between both groups. In the second testing session, controls showed a slight improvement of performance compared to the first session, probably due to learning effects. PD patients, however, showed no improvement of performance in the ON state (i.e., second session) compared to the OFF state. This might be due to adverse side-effects of the medication, e.g., fatigue. Our results confirm the hypothesis that PD patients who are impaired in motor execution are also impaired in the perception of human and animal motion. It has been argued that perception of actions and action execution interact in the human mirror neuron system. Mirror neurons are cells that respond to both the execution and observation of motion ( Rizzolatti and Craighero, 2004 ). We propose that human and animal motion perception deficits in patients with Parkinson‘s disease might be caused by mirror neuron system dysfunction.

Mirror neuron activation in children with developmental coordination disorder: A functional MRI study

The aim of this study was to reveal cortical areas that may contribute to the movement difficulties seen in children with Developmental Coordination Disorder (DCD). Specifically, we hypothesized that there may be a deficit in the mirror neuron system (MNS), a neural system that responds to both performed and observed actions. Using functional MRI, 14 boys with DCD (x¯=10.08 years±1.31, range=7.83−11.58 years) and 12 typically developing controls (x¯=10.10 years±1.15, range=8.33–12.00 years) were scanned observing, executing and imitating a finger sequencing task using their right hand. Cortical activations of mirror neuron regions, including posterior inferior frontal gyrus (IFG), ventral premotor cortex, anterior inferior parietal lobule and superior temporal sulcus were examined. Children with DCD had decreased cortical activation mirror neuron related regions, including the precentral gyrus and IFG, as well as in the posterior cingulate and precuneus complex when observing the sequencing task. Region of interest analysis revealed lower activation in the pars opercularis, a primary MNS region, during imitation in the DCD group compared to controls. These findings provide some preliminary evidence to support a possible MNS dysfunction in children with DCD.

Intact Automatic Imitation and Typical Spatial Compatibility in Autism Spectrum Disorder: Challenging the Broken Mirror Theory.

A lack of imitative behavior is frequently described as a core feature of Autism Spectrum Disorder (ASD), and is consistent with claims of mirror neuron system dysfunction in these individuals. Previous research has questioned this characterization of ASD however, arguing that when tests of automatic imitation are used--which do not require higher-level cognitive processing--imitative behavior is intact or even enhanced in individuals with ASD. In Experiment 1, 60 adult individuals with ASD and a matched Control group completed an automatic imitation task in which they were required to perform an index or a middle finger lift while observing a hand making either the same, or the alternate, finger movement. Both groups demonstrated a significant imitation effect whereby actions were executed faster when preceded by observation of the same action, than when preceded by the alternate action. The magnitude of this "imitation effect" was statistically indistinguishable in the ASD and Control groups. Experiment 2 utilized an improved automatic imitation paradigm to demonstrate that, when automatic imitation effects are isolated from those due to spatial compatibility, increasing autism symptom severity is associated with an increased tendency to imitate. Notably, there was no association between autism symptom severity and spatial compatibility, demonstrating the specificity of the link between ASD symptoms and increased imitation. These results provide evidence against claims of a lack of imitative behavior in ASD, and challenge the "Broken Mirror Theory of Autism."

Mirror Neuron System Activity Does Not Differ Between Sporadic and Familial Cases of Schizophrenia: Preliminary Report

Schizophrenia is a heterogenous disorder, and has often been subtyped on the basis of family history of psychotic disorders. Compared to those without, a positive family history is associated with an earlier age of onset, greater structural brain abnormalities and poorer clinical course. Given recent emphasis on mirror neuron system (MNS) in attempting to explain psychopathology in schizophrenia; present analysis tried to tease out differences in MNS functioning between these two groups. With ethical approval, ten consenting right-handed patients with schizophrenia (ICD-10-DCR; M=8; Drug-naïve=2) were recruited and divided into two groups of five each (M=4,F=1): those with (age 29.40±5.85 years, duration of illness 50.80±30.84 months) and without (age 29.60±5.77 years, duration of illness 43.20±43.76 months) family history of schizophrenic illness (group difference p>0.05). MNS activity was assessed using event-related desynchronization of EEG Mu waves in response to biological motion on 192-channel EEG Neurofax EEG-1100K. On comparison, while patients had significantly lower mu suppression compared to controls (p<0.001); two schizophrenia groups did not differ between themselves, neither on MNS activity nor on psychopathology (p>0.05). Present study replicates finding of a dysfunctional MNS in schizophrenia patients, and represents a preliminary attempt at comparing two groups of symptomatic schizophrenia patients. In both these groups, MNS dysfunctions were comparable, and commensurate with respect to psychopathology. Thus, MNS dysfunction in schizophrenia might either be inherited or acquired. However, this abnormality forms a common base, and ultimate vulnerability marker, for development of psychopathology during active disease states.

Mu-wave Activity in Schizophrenia: Evidence of a Dysfunctional Mirror Neuron System from an Indian Study.

Background:The ‘mirror-neuron system’ is thought to play an important role in automatic decoding of biological motions and interpretation of socially adaptive environmental stimuli. Accordingly, a dysfunction in this system in schizophrenia has been hypothesised to mediate the psychotic manifestations.Materials and Methods:As a part of an ongoing study, we evaluated the mirror neuron system using ‘EEG mu-wave (8-13 Hz) suppression’ paradigm in 15 drug naïve/drug free patients and compared the working to 15 age, sex and education matched controls. We also correlated the psychopathology scores on PANSS with the mu wave suppression in the schizophrenia patients, at baseline. We used high (192-channel) resolution EEG to record the mu rhythm while the subjects watched alternating sequences of a socially-relevant biological motion and white visual-noise on a custom made video-clip.Results:We found a significant difference in the degree of mu wave suppression between the two groups. We also found that the degree of mu suppression over right sensorimotor cortex at presentation correlated significantly and negatively with thought disorder in the patient group, and had a strong linear relationship.Conclusion:This study replicates past findings regarding a dysfunctional mirror neuron system in schizophrenia patients, and also emphasizes the role of rMNS in schizophrenic thought disorders.

External self-representations improve self-awareness in a child with autism

We have previously suggested that the social symptoms of autism spectrum disorder (ASD) could be caused in part by a dysfunctional mirror neuron system (MNS). Since the recursive activity of a functioning MNS might enable the brain to integrate visual and motor sensations into a coherent body schema, the deficits in self-awareness often seen in ASD might be caused by the same mirror neuron dysfunction. CL is an autistic adolescent who is profoundly fascinated with his reflection, looking in mirrors at every opportunity. We demonstrate that CL’s abnormal gait improves significantly when using a mirror for visual feedback. We also show that both the fascination and the happiness that CL derives from looking at a computer-generated reflection diminish when a delay is introduced between the camera input and screen output. We believe that immediate, real-time visual feedback allows CL to integrate motor sensations with external visual ones into a coherent body schema that he cannot internally generate, perhaps due to a dysfunctional MNS.

깨진 거울인가 깨지지 않은 거울인가? : 자폐 스펙트럼 장애의 거울 뉴런 문제에 관한 고찰

The discovery of the mirror neuron system (MNS) is one of the most important neuroscientific achievements in the 20th century. Some researchers had reported that MNS dysfunction was discovered in autism spectrum disorders (ASD). Finally, the `broken mirror` theory of ASD was announced in the mid 2000`s. According to this theory, ASD cannot simulate the mind and behavior of others due to MNS dysfunction; therefore, they cannot imitate the behaviors and empathized with the mind of others. However, ASD does not always show imitation problems. The researchers who have criticized the `broken mirror` theory proposed the `social top-down response modulation (STORM)` theory. On STORM theory, the medial prefrontal cortex or temporo-parietal junction, brain areas related with mentalising, might modulate MNS according to social context. We compared the strengths and weaknesses of each theory.

Mirror neuron system dysfunction in autistic spectrum disorder revealed by spatial filtered magnetoencephalography

Mirror neuron system dysfunction in autistic spectrum disorder revealed by spatial filtered magnetoencephalography

Studying the Behaviour of Model of Mirror Neuron System in Case of Autism

Several experiment done by the researchers conducted that autism is caused by the dysfunctional mirror neuron system and the dysfunctions of mirror neuron system is proportional to the symptom severity of autism. In the present work those experiments were studied as well as studying a model of mirror neuron system called MNS2 developed by a research group. This research examined the behavior of the model in case of autism and compared the result with those studies conducting dysfunctions of mirror neuron system in autism. To perform this, a neural network employing the model was developed which recognized the three types of grasping (faster, normal and slower). The network was implemented with back propagation through time learning algorithm. The whole grasping process was divided into 30 time steps and different hand and object states at each time step was used as the input of the network. Normally the network successfully recognized all of the three types of grasps. The network required more times as the number of inactive neurons increased. And in case of maximum inactive neurons of the mirror neuron system the network became unable to recognize the types of grasp. As the time to recognize the types of grasp is proportional to the number of inactive neurons, the experiment result supports the hypothesis that dysfunctions of MNS is proportional to the symptom severity of autism.

Magnetoencephalography Study of Right Parietal Lobe Dysfunction of the Evoked Mirror Neuron System in Antipsychotic-Free Schizophrenia

IntroductionPatients with schizophrenia commonly exhibit deficits of non-verbal communication in social contexts, which may be related to cognitive dysfunction that impairs recognition of biological motion. Although perception of biological motion is known to be mediated by the mirror neuron system, there have been few empirical studies of this system in patients with schizophrenia.MethodsUsing magnetoencephalography, we examined whether antipsychotic-free schizophrenia patients displayed mirror neuron system dysfunction during observation of biological motion (jaw movement of another individual).ResultsCompared with normal controls, the patients with schizophrenia had fewer components of both the waveform and equivalent current dipole, suggesting aberrant brain activity resulting from dysfunction of the right inferior parietal cortex. They also lacked the changes of alpha band and gamma band oscillation seen in normal controls, and had weaker phase-locking factors and gamma-synchronization predominantly in right parietal cortex.ConclusionsOur findings demonstrate that untreated patients with schizophrenia exhibit aberrant mirror neuron system function based on the right inferior parietal cortex, which is characterized by dysfunction of gamma-synchronization in the right parietal lobe during observation of biological motion.

P27-14 Mirror neuron system dysfunction in autistic spectrum disorder revealed by spatial filtered magnetic encephalography

P27-14 Mirror neuron system dysfunction in autistic spectrum disorder revealed by spatial filtered magnetic encephalography

Post-movement beta rebound abnormality as indicator of mirror neuron system dysfunction in autistic spectrum disorder: An MEG study

The mu rhythm is regarded as a physiological indicator of the human mirror neuron system (MNS). The dysfunctional MNS hypothesis in patients with autistic spectrum disorder (ASD) has often been tested using EEG and MEG, targeting mu rhythm suppression during action observation/execution, although with controversial results. We explored neural activity related to the MNS in patients with ASD, focusing on power increase in the beta frequency band after observation and execution of movements, known as post-movement beta rebound (PMBR). Multiple source beamformer (MSBF) and BrainVoyager QX were used for MEG source imaging and statistical group analysis, respectively. Seven patients with ASD and ten normal subjects participated in this study. During the MEG recordings, the subjects were asked to observe and later execute object-related hand actions performed by an experimenter. We found that both groups exhibited pronounced PMBR exceeding 20% when observing and executing actions with a similar topographic distribution of maximal activity. However, significantly reduced PMBR was found only during the observation condition in the patients relative to controls in cortical regions within the MNS, namely the sensorimotor area, premotor cortex and superior temporal gyrus. Reduced PMBR during the observation condition was also found in the medial prefrontal cortex. These results support the notion of a dysfunctional execution/observation matching system related to MNS impairment in patients with ASD, and the feasibility of using MEG to detect neural activity, in particular PMBR abnormalities, as an index of MNS dysfunction during performance of motor or cognitive tasks.

Olfactory bulb dysgenesis, mirror neuron system dysfunction, and autonomic dysregulation as the neural basis for autism

Autism is a disorder characterized by social withdrawal, impoverished language and empathy, and a profound inability to adopt another's viewpoint - a failure to construct a "theory of mind" for interpreting another person's thoughts and intentions. We previously showed that these symptoms might be explained, in part, by a paucity of mirror neurons. Prompted by an MRI report of an individual with autism, we now suggest that there may be, in addition, a congenital aplasia/dysplasia of the olfactory bulbs with consequent reduction of vasopressin and oxytocin receptor binding. There may also be sub-clinical temporal lobe epilepsy affecting the recently discovered third visual system that is rich in "empathy" related mirror neurons (MNS) and projects (via the TOP junction - just below the inferior parietal lobule) to limbic structures that regulate autonomic outflow. This causes deranged autonomic feedback, resulting in additional deficiencies in MNS with loss of emotional empathy and introspection.

EEG study of the mirror neuron system in children with high functioning autism

Individuals with Autism Spectrum Disorder (ASD) are characterised by an impaired imitation, thought to be critical for early affective, social and communicative development. One neurological system proposed to underlie this function is the mirror neuron system (MNS) and previous research has suggested a dysfunctional MNS in ASD. The EEG mu frequency, more precisely the reduction of the mu power, is considered to be an index for mirror neuron functioning. In this work, EEG registrations are used to evaluate the mirror neuron functioning of twenty children with high functioning autism (HFA) between 8 and 13 years. Their mu suppression to self-executed and observed movement is compared to typically developing peers and related to age, intelligence and symptom severity. Both groups show significant mu suppression to both self and observed hand movements. No group differences are found in either condition. These results do not support the hypothesis that HFA is associated with a dysfunctional MNS. The discrepancy with previous research is discussed in light of the heterogeneity of the ASD population.

Motor–auditory–visual integration: The role of the human mirror neuron system in communication and communication disorders

The mirror neuron system (MNS) is a trimodal system composed of neuronal populations that respond to motor, visual, and auditory stimulation, such as when an action is performed, observed, heard or read about. In humans, the MNS has been identified using neuroimaging techniques (such as fMRI and mu suppression in the EEG). It reflects an integration of motor–auditory–visual information processing related to aspects of language learning including action understanding and recognition. Such integration may also form the basis for language-related constructs such as theory of mind. In this article, we review the MNS system as it relates to the cognitive development of language in typically developing children and in children at-risk for communication disorders, such as children with autism spectrum disorder (ASD) or hearing impairment. Studying MNS development in these children may help illuminate an important role of the MNS in children with communication disorders. Studies with deaf children are especially important because they offer potential insights into how the MNS is reorganized when one modality, such as audition, is deprived during early cognitive development, and this may have long-term consequences on language maturation and theory of mind abilities. Learning outcomes: Readers will be able to (1) understand the concept of mirror neurons, (2) identify cortical areas associated with the MNS in animal and human studies, (3) discuss the use of mu suppression in the EEG for measuring the MNS in humans, and (4) discuss MNS dysfunction in children with (ASD).

Does Joe influence Fred's action? Not if Fred has autism spectrum disorder

It has been proposed that the deficits in social interaction seen in autism spectrum disorder (ASD) arise from problems in action perception stemming from a dysfunction of the mirror neuron system (MNS) — a neural network that becomes active during the performance and observation of action. A dysfunction of this system could have a cascading effect leading to deficits in social cognition because poor activation of the MNS during action observation may lead to an incomplete understanding of another person's actions, intentions and, ultimately, mental states. The present study tested the MNS dysfunction explanation by determining if people with ASD demonstrate a between-person inhibition of return (BP-IOR) effect. The BP-IOR effect, longer reaction times to targets presented at the location of another person's previous response relative to an unresponded-to location, has been hypothesized to be the result of the MNS co-representing the observed response and subsequently activating the mechanisms that cause IOR when individuals respond on their own (within-person IOR [WP-IOR]). Consistent with the MNS dysfunction hypothesis, participants with ASD did not demonstrate a BP-IOR effect in a condition in which they only observed the movement of the partner. The participants with ASD did demonstrate a WP-IOR effect suggesting that the mechanisms underlying IOR are intact in ASD. The contrast between the BP- and WP-IOR effects in the participants with ASD provides significant behavioural evidence for MNS dysfunction in ASD and has important implications for understanding this disorder.