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Mirror Neuron Dysfunction in Autistic Disorder
Autistic disorder is characterized by impairments in communication and social interaction. Autistic children also often display restricted behaviors and repetitive behaviors. These signs of autism usually appear before the age of three. The inability to display empathy and imitate others in autism, a skill crucial to learning communication and social skills, has been hypothesized to result from defects in the mirror neuron system (Williams, Whiten, Suddendorf, & Perrett, 2001). The role of mirror neuron system and how dysfunctions in this system may relate to the deficits observed in autistic disorder are discussed.
Mirror neurons fire when animals or people act or observe the same action performed by another. In humans, brain activity consistent with that of mirror neurons is located the premotor cortex, the supplementary motor area, the primary somatosensory cortex, and the inferior parietal cortex (Rizzolatti & Craighereo, 2004). There are two chief hypotheses concerning the functional role of mirror neurons: (1) mirror-neuron activity mediates the imitation of actions; and (2) mirror neurons are also responsible for understanding actions. Each time an individual views an action performed by another person the neurons that represent that action are activated in the observer's premotor cortex transforming visual information into knowledge. Rizzolatti and Craighereo reported that mirror neurons are involved in multiple learning functions beside physical actions including gestural communication, speech, and semantic understanding.
The autistic spectrum disorders are described by dysfunctions with social interactions, decreased imagination, dysfunctional verbal abilities, and repetitive and restricted patterns of behavior. Williams, Whiten, Suddendorf, and Perrett, (2001) noted that recent theories of the causes of autism have centered around the lack of the so-called "theory of mind" (ToM) in autistic individuals such as understanding others' beliefs and perspectives. However, Williams Whiten, Suddendorf, and Perrett believed that the ToM was unsatisfactory as a primary explanation for autism for several reasons including: (1) the ToM is not typically observable in normal children until after their fourth year and autistic disorders are recognized earlier; (2) autistic children often imitate sounds and sayings verbatim but without the associated nonverbal aspects indicating that they may experience difficulties with the integration of visual and auditory information; (3) and clinical observation of autism indicates the their early social deficits are broader in scope than would be implied by the ToM. They also noted that deficits in imitation are associated with the earliest stages in the development of autism and that these deficits very nicely compliment and fill in most of the major gaps that the ToM leaves when explaining the possible causes of autism. In addition, imitation and attribution of mental states in others display some very important similarities such as translating perspective from another to oneself. Williams, Whiten, Suddendorf, and Perrett observed that the majority of studies of autistic children demonstrate a deficit in imitation can be observed at an early age in these children. A review of the animal model literature that demonstrates that primates with frontal and prefrontal brain lesions demonstrate poor imitation and a difficulty to assume the perspective of another as well as brain imaging studies in humans demonstrate that imitation, observation of action in others, and switching perspective produces activity in the brain regions that are believed to host mirror neurons.
Williams, Whiten, Suddendorf, and Perrett (2001) suggested several testable hypotheses based on the notion that deficits in mirror neuron functioning may explain much of the impairment observed in autism: (1) imitation deficits should be present in the earliest years in autistic children; (2) perceived sounds that are altered by viewing lip movements of others making a different sound in normal people without autism will not be present or will be different in autistic individuals (this is called the McGurk effect); (3) joint attention deficits will be observable early in autistic disorders; and (4) brain imaging and EEG studies will demonstrate altered activation or poorer developed mirror neuron brain areas in people with autism.
With regard to the first hypothesis, Receveur, Lenoir, Desombre, Roux, Barthelemy, and Malvy, (2005) explored social interaction and imitation in very young infants and children with autism. The researchers viewed family videos and films of children during medical consults of 18 children with autism. The sample was divided according to their developmental quotient level (DQ). DQ is defined as the ratio of a person's developmental age to their functional age appropriate abilities x 100. A DQ of 100 would indicate that the child functions consistently with their age, whereas lower or higher scores indicate departures from normal functioning. Receveur et al. divided their sample into two groups with one group having a DQ greater than 50 and the other with a DQ less than 50. Then an evaluation of facets of imitation and social interaction was performed by observing videos over four developmental periods: (1) between 10-12 months of age; (2) between 16-18 months of age; (3) between 24-26 months of age; and (4) beyond 4 years of age. Receveur et al.'s results revealed that the autistic children demonstrated poorer social interactions and imitational abilities s at lower DQ's compared to those with higher DQ's. Autistic children also displayed significantly lower abilities than normal children would demonstrate at the same age. These deficits were also apparent well before the age of four, supporting the hypothesis that such deficits do appear relatively early in the development of autistic children.
The second hypothesis, autistic children should show deficits with the integration of visual-auditory information, was investigated by Williams, Massaro, Peel, Bosseler, and Suddendorf (2004). In a complicated experiment groups of autistic and normal children were presented random consonant vowel syllables (CV) like ba, da, and tha. The CVs were presented via a computer animated head with a voice synthesizer in either unimodal (only auditory or visual presentation of the CV) or bimodal (integrated auditory and visual presentation) modes. The bimodal information was presented with either a consistent visual/auditory presentation of the CV or an inconsistent presentation (the McGurk effect). The autistic children were slightly poorer than controls than recognizing the stimuli in the unimodal conditions, but the effect was not significant. However, the autistic group demonstrated a reduced McGurk effect compared to the normal children; they were not confused by discrepant visual and auditory information). A statistical analysis of the data indicated that this effect was due to poor visual analysis of information by autistic children and not a result of poor visual-auditory integration as the researchers had hypothesized. The authors indicated that perhaps more research with different levels of autism would shed more light on the issue.
Regarding the hypothesis that autistic children would demonstrate deficits with joint attention, Dawson, Toth, Abbott, Osterling, Munson, Estes, and Liaw (2004) compared three to four-year-old autistic children, developmentally delayed children, and normal developing children on measures of social orienting, attention to the mother's distress, and joint attention. Joint attention is the ability to coordinate one's attention or share awareness of objects or events with interactive social partners. This was measured by standardized procedures. The autistic children displayed significantly lower joint attention than the developmentally disabled and normal children across all measures. The autistic children also displayed significantly poorer social orienting (e.g. being called by name) and attention to distress than the other groups. Difficulties with joint attention were also found to be the most sensitive discriminator of autistic children from normal and developmentally delayed children than the other measures, indicating that deficits with joint attention are particularly salient in autistic children.
The final hypothesis suggested by Williams, Whiten, Suddendorf, and Perrett, (2001) that people with autism would demonstrate differences on brain imaging studies in the brain regions associated with the presence of mirror neurons, probably has the most research support. For example, Hadjikhani, Joseph, Snyder, and Tager-Flusberg, (2006) compared the brains of high-functioning autistic adults to a group of normally-developed adults. Both groups of children were matched on gender, age, handedness, and IQ. The magnetic resonance results indicated that the cortical areas of the brain associated with imitation and empathy were thinner in the autistic subjects than in the normal subjects. The researchers also found a relation between the symptom severity of autism and the degree of cortical thinning in brain areas associated with mirror neurons, indicating that these areas may, to some degree, be responsible for the behavioral difficulties that people with autism display. There were no significant differences in the thickness of the cortex in other areas of the brains of the autistic group and the normally- developed group. The researchers also noted that subjects who had been given an inventory rating the severity of their autism in childhood demonstrated a relationship between the thinning in these brain areas and the severity of their childhood symptoms such that greater thinning was associated with more severe childhood symptoms.
These studies support three out of the four hypothesis put forth by Williams, Whiten, Suddendorf, and Perrett, (2001) regarding the notion that autistic people display deficits with the functioning of the mirror neurons in the brain. The fourth hypothesis regarding the difficulties…[continue]
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