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

INTRODUCTION: Patients 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. METHODS: Using magnetoencephalography, we examined whether antipsychotic-free schizophrenia patients displayed mirror neuron system dysfunction during observation of biological motion (jaw movement of another individual). RESULTS: Compared 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. CONCLUSIONS: Our 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

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¯=10.02 years±1.28, range=8.33-11.17 years) and 12 typically developing controls (x¯=10.10 years±1.16, range=8.02-12 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, 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 inferior frontal gyrus, 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

Imitation, mirror neurons and autism

Various deficits in the cognitive functioning of people with autism have been documented in recent years but these provide only partial explanations for the condition. We focus instead on an imitative disturbance involving difficulties both in copying actions and in inhibiting more stereotyped mimicking, such as echolalia. A candidate for the neural basis of this disturbance may be found in a recently discovered class of neurons in frontal cortex, 'mirror neurons' (MNs). These neurons show activity in relation both to specific actions performed by self and matching actions performed by others, providing a potential bridge between minds. MN systems exist in primates without imitative and ‘theory of mind’ abilities and we suggest that in order for them to have become utilized to perform social cognitive functions, sophisticated cortical neuronal systems have evolved in which MNs function as key elements. Early developmental failures of MN systems are likely to result in a consequent cascade of developmental impairments characterised by the clinical syndrome of autism

Brain–computer interface game applications for combined neurofeedback and biofeedback treatment for children on the autism spectrum

Individuals with Autism Spectrum Disorder (ASD) show deficits in social and communicative skills, including imitation, empathy, and shared attention, as well as restricted interests and repetitive patterns of behaviors. Evidence for and against the idea that dysfunctions in the mirror neuron system are involved in imitation and could be one underlying cause for ASD is discussed in this review. Neurofeedback interventions have reduced symptoms in children with ASD by self-regulation of brain rhythms. However, cortical deficiencies are not the only cause of these symptoms. Peripheral physiological activity, such as the heart rate, is closely linked to neurophysiological signals and associated with social engagement. Therefore, a combined approach targeting the interplay between brain, body and behavior could be more effective. Brain-computer interface applications for combined neurofeedback and biofeedback treatment for children with ASD are currently nonexistent. To facilitate their use, we have designed an innovative game that includes social interactions and provides neural- and body-based feedback that corresponds directly to the underlying significance of the trained signals as well as to the behavior that is reinforced

ジヘイショウ ノ シンダン チリョウ サイゼンセン

In this paper we review the pathophysiology of autism.1）The amygdala theory of autismThe network of neural regions that comprise the social brain includes the amygdala. There isa reduction in volume of amygdala in children with autism. The concentration of N-acetylaspartateis also decreased in amygdala of autistic brain. The amygdala is therefore proposed to be one ofseveral neural regions that are abnormal in autism.2）Mirror neuron dysfunction in autismChildren with autism underwent fMRI while imitating and observing emotional expressions.They showed no mirror neuron activity in the inferior frontal gyrus（pars opercularis）. Notably,activity in this area was inversely related to symptom severity in the social domain, suggestingthat a dysfunctional mirror neuron system may underlie the social deficits observed in autism

Impaired perception of biological motion in Parkinson’s disease

OBJECTIVE: We examined biological motion perception in Parkinson’s disease (PD). Biological motion perception is related to one’s own motor function and depends on the integrity of brain areas affected in PD, including posterior superior temporal sulcus. If deficits in biological motion perception exist, they may be specific to perceiving natural/fast walking patterns that individuals with PD can no longer perform, and may correlate with disease-related motor dysfunction. METHOD: Twenty-six nondemented individuals with PD and 24 control participants viewed videos of point-light walkers and scrambled versions that served as foils, and indicated whether each video depicted a human walking. Point-light walkers varied by gait type (natural, parkinsonian) and speed (0.5, 1.0, 1.5 m/s). Participants also completed control tasks (object motion, coherent motion perception), a contrast sensitivity assessment, and a walking assessment. RESULTS: The PD group demonstrated significantly less sensitivity to biological motion than the control group (p < .001, Cohen’s d = 1.22), regardless of stimulus gait type or speed, with a less substantial deficit in object motion perception (p = .02, Cohen’s d = .68). There was no group difference in coherent motion perception. Although individuals with PD had slower walking speed and shorter stride length than control participants, gait parameters did not correlate with biological motion perception. Contrast sensitivity and coherent motion perception also did not correlate with biological motion perception. CONCLUSION: PD leads to a deficit in perceiving biological motion, which is independent of gait dysfunction and low-level vision changes, and may therefore arise from difficulty perceptually integrating form and motion cues in posterior superior temporal sulcus.Published versio

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

A Review on the Cognitive Neuroscience of Autism

With increased recognition in the media, heightened prevalence, and advances in research technologies, investigation into the causes of autism has broadened in recent years. Studies at the molecular, structural, and behavioral levels have resulted in significant findings, linking autism to qualitative differences in neurological function and an alteration of early development. Familial aggregation of autism demonstrate a strong genetic factor, although genetics can not completely account for its pathogenesis. Studies show autism having one of the most complex pathologies among neurodevelopmental disorders. Future studies applying sophisticated methodologies in new areas may shed light on current mysteries surrounding the disorder