Personal ViewMirror neuron dysfunction in autism spectrum disorders
Introduction
Autism spectrum disorders (ASDs) are pervasive, developmental, neurological conditions which adversely impact behaviour in three key domains: social interaction, verbal and nonverbal communication, and obsessive and/or stereotyped patterns of behaviour.1 Abnormal or impaired social interaction is characterized by deficits in joint attention, reciprocity, imitation, empathy, relationships, as well as hyperactive/impulsive behaviour and social anxiety. Communicative deficits in language include odd prosody, failure to understand metaphors or statements with implied meaning, idiosyncratic use of words and delayed speech development. Obsessive interests and stereotyped patterns of behaviour including an intense interest in a particular subject matter, preoccupation with small details as opposed to global functioning, inflexible adherence to non-functional routines and rituals, and abnormal motor and sensory functioning.2 Although presentation varies considerably across individuals, these core characteristics are defined as deviant relative to the individual’s developmental level.
The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM IV-TR),3 describes two major ASDs; Autistic disorder (AD) and Asperger’s syndrome (AS).4 Although subject to ongoing debate, AS is diagnostically differentiated from AD on the basis of normal language development, defined as expression of single words by age 2 years and communicative phrases by age 3 years.3 Where intellectual functioning is not impaired (IQ > 70–85) in AD, the condition is termed high functioning autism (HFA). A meta-analysis of 43 studies estimates the prevalence of autism (AD and HFA) to be approximately 0.13% of the population, and AS 0.03%.5
To date, an important issue confronting clinicians and researchers is the absence of definable and reliable, neurophysiological markers to the disorder. Diagnosis is made on the basis of behavioural symptoms, which reduces diagnostic clarity and limits the capacity to identify these conditions early and accurately. In 1999, two research groups independently suggested that a network of visuomotor cells known as mirror neurons (MNs) may contribute to some of the key symptoms that characterize autism.6, 7
Section snippets
Mirror neurons
MNs are activated by the performance or observation of object or goal directed actions. What distinguishes MNs from other motor neurons is they not only discharge when an individual performs a particular action (such as reaching for a piece of food), but also when an individual watches somebody else perform a similar action (such as a friend reaching for a piece of food).8
Studies in primates have identified a MN system consisting of the ventral premotor cortex (area F5) and inferior parietal
Initial theory
Prior to the discovery of MNs, a theory was penned that suggested a deficit in self-other matching may contribute to autism.17 This ability involves forming and coordinating mental representations of the self and others. Understanding others behaviours and social rules is achieved by extracting patterns of similarity between the self and other. It has now been acknowledged that this theory of autism is similar to the key role of MNs. Disruption of MN functioning may contribute to this
The case against mirror neurons
Despite this promising research base, numerous criticisms have been made toward the study of MNs in humans. Firstly, MNs have yet to be directly observed in humans.42 Secondly, MNs make up a small minority of observed cells in Macaques (approximately 6%; yet the distribution in humans remains unknown),9 which means interpretation of homologous areas in humans is not exclusively measuring suspected MN activity. Thirdly, it has been suggested that an exclusive MN explanation of imitation is too
Electroencephalograph (EEG)
One method to investigate MN activity in humans is via EEG. The mu wave measures large amplitude oscillations of the synchronized activity of sensorimotor neurons.45 Whenever a voluntary movement is made, these sensorimotor neurons are desynchronized by input from pre-motor neurons (an area believed to house MNs), which blocks the mu wave. Of interest, it has been found that the mu wave is also blocked or suppressed when a person observes another individual performing a voluntary motor action.46
Conclusions and future directions
In summary, there is evidence that brain regions believed to house MNs can be structurally and functionally disturbed in individuals with autism. Although it is premature to interpret findings with such a small research base, the current evidence suggests that MN disturbance is pronounced when information is of a social and emotional nature, or requires discrimination of different items (such as motor acts, or facial emotions). Abnormalities in MN areas have been strongly correlated to social
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Cited by (78)
Action predictability is reflected in beta power attenuation and predictive eye movements in adolescents with and without autism
2021, NeuropsychologiaCitation Excerpt :There has also been a large body of work on the neural signature of action prediction in autism. The prediction of others' actions is implemented through motor system activation (Kilner et al., 2004, 2007; Monroy et al., 2019; Schubotz, 2007), and the Mirror Neuron Dysfunction theory posits a reduction in this activation in autism (Williams et al., 2001; Perkins et al., 2010). Motor system activation can be measured with EEG over the sensorimotor cortex, and is typically seen as a decrease in power in mu and beta frequency bands.
Social brain dysfunctionality in individuals with autism spectrum disorder and their first-degree relatives: An activation likelihood estimation meta-analysis
2020, Psychiatry Research - NeuroimagingCitation Excerpt :Hypoactivation in the mPFC, the ACC, and anterior paracingulate cortex have been reported in studies with theory of mind (ToM) paradigms (Castelli et al., 2000; Wang et al., 2007), but other studies found conflicting resutls (Baron-Cohen et al., 1999). Besides, ASD-related dysfunction in the MNS have been reported in motor mimicry, emotion processing (Dapretto et al., 2006), ToM (Perkins et al., 2010) and empathy (Greimel et al., 2010). In sum, dysfunction of social brain regions were found in individuals with ASD.
Enhancement of behavioral and linguistic outcome measures in autism spectrum disorder through neuro-navigated transcranial magnetic stimulation: A pilot study
2020, Journal of Clinical NeuroscienceCitation Excerpt :The presence of corresponding deficits in ASD has given rise to the “Broken mirror theory” [10] which proposes that mirror neuron dysfunction contributes to core deficits of the disorder [11–13]. While the mechanism by which mirror neurons are impaired in ASD are not yet known, the enhancement or restoration of mirror neuron function has been promoted as one means of improving social cognition [14]. Mirror neurons are principally concentrated in the inferior frontal gyrus (IFG) and the inferior parietal lobe (IPL) in humans [12].
Insular function in autism: Update and future directions in neuroimaging and interventions
2019, Progress in Neuro-Psychopharmacology and Biological PsychiatryA transgenic monkey model of huntington’s disease
2018, Conn's Handbook of Models for Human AgingObserving and participating in social interactions: Action perception and action control across the autistic spectrum
2018, Developmental Cognitive NeuroscienceCitation Excerpt :This broken mirror neuron hypothesis of autism proposes that impaired social skills in autism are related to dysfunctions in the putative human mirror neuron system making it difficult for individuals with autism to simulate and thus understand others’ behavior (MNS; Altschuler et al., 2000; Ramachandran and Oberman, 2006). Some studies have offered supportive evidence for the involvement of the MNS (e.g. Perkins et al., 2010). However, both the validity of a broken MNS and a direct, causal relationship between the MNS and social skills in autism, have been challenged by other reports (e.g. Southgate and Hamilton, 2008).