I. brought to fruition by Simon Baron-Cohen. Baron-Cohen believes

I. IntroductionA. What is autism?Autism is a disorder that is becoming increasingly prevalent in today’s society. This developmental disorder ultimately impacts multiple aspects of an individual’s life. Individuals diagnosed with autism typically experience social deficits, language impairment, and repetitive behaviors. Alongside this, individuals affected with autism often experience difficulties with developing a theory of mind, which can be defined as the ability to comprehend the knowledge and desires of oneself and others (Bradford 2015). The severity of which autism appears in individuals varies, which is why the disorder is often referred to as autism spectrum disorder (ASD).B. Background ResearchSince the discovery of ASD in the 1940’s, the causes of this developmental disorder mystified researchers. Multiple theories as to what causes ASD have since been postulated and are heavily debated to this day. These theories can typically be classified into one of two categories: anatomical or psychological. One of the most current theories consists of an individual with ASD having difficulties with constructing the theory of mind, which was first brought to fruition by Simon Baron-Cohen. Baron-Cohen believes that those affected with ASD are unable to understand the thoughts, points of views, and beliefs of others, all of which is a key component of the theory of mind. Recent research has led to the discovery of mirror neurons, a specialized neuron that is believed to play a role in imitation and empathy. Mirror neurons were discovered by happenstance in the late 1980’s by neuroscientist Giacomo Rizzolatti, MD. Rizzolatti discovered a set of neurons in the ventral premotor cortex (area F5) that fired when a macaque reached for or grabbed an object. In an attempt to further understand these neurons, electrodes were placed on individual neurons in the F5 area. The researchers found that these neurons fired not just when a macaque was performing an action, such as grabbing a peanut, but also fired if the monkey watched the researcher or another macaque perform specific actions, like grab a peanut. These neurons are now referred to as mirror neurons, and due to the firing of these neurons when another individual is performing an action, it is believed that a link can be made between mirror neurons and humans ability to empathize with one another. C. Autism & Mirror NeuronsSince the theory of mind plays an important role in understanding other people’s emotions and the mirror neuron system is closely associated with empathy, it is postulated that an abnormal MNS may be the cause of the social deficits that individuals with ASD experience. This begs the question, to what extent do mirror neurons influence autism? Various viewpoints on the causes of autism will be assessed and evaluated, relying heavily upon the argument of a flawed mirror neuron system being at fault for the symptoms commonly associated with autism spectrum disorder. However, in order to fully recognize the limitations of the argument, counter arguments and opposing viewpoints will be carefully considered as well. II. Supporting Argument A. Ramachandran & Oberman V.S. Ramachandran and Lindsay Oberman of the University of California, San Diego were some of the first researchers to provide insight into the link between mirror neurons and autism. The lack of prior evidence to support the idea of mirror neurons existing within the human brain was the first obstacle Ramachandran and Oberman had to overcome. A non-invasive approach was taken to avoid the use of electrodes within a person’s brain. Ramachandran used an electroencephalogram (EEG) to measure mu waves, defined as patterns of activity in the brain that are present when the body is at rest, in children with high-functioning ASD. Typically, these mu waves are suppressed whenever a person performs a voluntary action, and are also suppressed whenever the voluntary action is watched or thought of as opposed to being performed. Typical children and children diagnosed with ASD were first instructed to perform a basic voluntary movement with their hand. As expected, both the typical and autistic children had suppressed mu waves when performing the action. Both groups of children were then shown a video of the same hand movement being performed. Ramachandran found that the mu waves in children without autism were suppressed, but the mu waves in children with high-functioning autism were not suppressed when watching the video. Ramachandran and Oberman replicated this study to increase validity with an additional 20 participants and achieved the same results.This suggests that the children with autism, while having a fully functional motor command system, have a deficient mirror neuron system due to their inability to respond to the visual stimulus of another individual moving their hand in a typical manner. B. Theoret Theoret conducted a study with 10 individuals diagnosed with high-functioning ASD, with a control of an additional 10 individuals in the control group. A transcranial magnetic stimulation (TMS), which utilises a magnetic field to induce excitability changes within the brain (Fitzgerald 2013), ¬†was placed on each participant so the researchers could observe the motor-evoked potentials (MEPs) within the participant’s primary motor cortex as the participant a hand motion. In a typical individual, the MEPs become excited when one individual observes another individual performing an action. The participants in Theoret’s study were shown a video of finger movements, allowing Theoret to examine if MEPs differentiated between individuals with ASD and the control group. The excitability of the MEPs within the primary motor cortex was found to be significantly lower in those diagnosed with ASD as opposed to the excitability of the MEPs within the control group. The lack of MEP excitability for the individuals diagnosed with autism spectrum disorder gives merit to the idea of a broken mirror neuron system existing within those affected with ASD. The MNS system is assumed to be closely associated with imitation, and if the individuals highlighted in the above study were unable to excite neurons within the motor cortex when observing finger movements, then it can be assumed a disconnect between the sender and receiver, therefore resulting in an impaired ability to imitate the actions of others. III. Counter Argument CourchesneEric Courchesne of the University of California, San Diego, is a researcher amongst the group of anatomists whom of which believes structural changes in the brain are at fault for the cause of autism. Courchesne’s research studied the postmortem tissue of the prefrontal cortex, an area of the brain that assists in regulating emotional and behavioral aspects of an individual, from male children with ages ranging from 2-16, 7 of which whom were diagnosed with ASD and 6 in the control group. Stereological methods, defined as the ability to estimate the quantitative amount of neurons from a cross-section of the brain, were utilised to quantify the amount of neurons in the dorsolateral prefrontal cortex (DL-PFC) and medial prefrontal cortex (M-PFC) of the sampled tissue. The research showed that the mean number of neurons in the DL-PFC in the children diagnosed with ASD was approximately 1.57 billion, and in the control group was 0.88 billion. Alongside this, the mean number of neurons in the M-PFC region for children diagnosed with ASD was 0.36 billion, while the mean number of neurons in the M-PFC region for the control group was approximately 0.28 billion neurons. From this data, Courchesne drew the conclusion that this influx in neurons in those children diagnosed with ASD may be due to prenatal circumstances, due to the fact that cortical neurons are not formed after birth. The lack of apoptosis and/or excessive proliferation in the prenatal stage may account for the excess amount of cortical neurons found in the children diagnosed with ASD.Courchesne’s research supports the idea that structural abnormalities within the brain are the source of ASD, specifically an increased number of neurons within the M-PFC, as well as the DL-PFC. Though it is ultimately unknown how this excess amount of neurons may causes the common symptoms of ASD, assumptions can be drawn as to how this phenomenon may be linked with social deficits. While the prefrontal cortex is associated with the mechanisms involved with self-awareness, specifically DL-PFC is thought to be involved with “actively maintaining information in working memory, changing behavior according to task demands or representing past events, current goals, and future predictions” (Siddiqui 2008). Alongside this, the M-PFC is thought to be involved with controlling the influence of body arousal, spatial memory, bimanual coordination, and self-initiated movement (Siddiqui 2008). With this knowledge in mind, it can presumed that structural abnormalities, like those seen in Courchesne’s research, would have detrimental effects on B. HamiltonAn additional study was performed by Antonia F. de C. Hamilton, provoked by her skepticism regarding the broken MNS theory. The study consisted of 25 children diagnosed with ASD and 31 children in the control group. All children were given tasks to test their ability on various action representation tasks. The results of the study showed that children diagnosed with ASD had a superior performance on a specific gesture recognition task, and there was no statistically significant difference between the performances of the typical children and the children diagnosed with ASD. Hamilton also believes that the MNS should also be associated with one’s ability to predict actions or the understanding of action goals (Hamilton 2013). IV. Conclusion A. Answering the Question To answer the question “To what extent do mirror neurons influence autism,” one must consider both supporting and counter arguments. The above research gives both of these aspects and it appears that an impaired MNS system does impact one’s social behavior, and in turn may create symptoms that is often seen in individuals with autism spectrum disorder. B. Future of MNS Theory While the research highlighted above is quite compelling and gives merit to the claim that autism is a product of a broken mirror neuron system, it is quite evident the amount of research that is still necessary in regards to this specific topic. It is undeniable that the link between the mirror neuron system and autism spectrum disorder prompts for further research of this topic. This room for further investigation is extremely well-known and understood within the field of psychology, however. Dr. Matthew Mosconi, the Director of the Kansas Center for Autism Research and Training, noted “MNS dysfunction may contribute to some aspects of ASD for some individuals, but clearly more research is needed in this area.”