Role of Mirror Neuron System (MNS) in Autism

Role of Mirror Neuron System (MNS) in AutismMirror neuron schema (MNS) plays an important role in the specific behavioral lark abouts of people with autism. In this paper the central aspects, such as neuropathology, etiology and prevalence, of autism and related turnovers will be discussed. In addition the Empathizing-Systemizing (E-S) supposition and Theory of Mind (ToM), deuce theories linking the ill reason with the specific behavior of the disease, will be discussed. The next two chapters ar dedicated to the MNS and the consequences of its dys turn tail in autism. Important atomic number 18 the two main functions facilitated by the MNS put on and action judgment. Several studies show that dysfunction of the MNS in autism, big businessman be a reason why these abilities are underdeveloped in autistic individuals.Autism was first described in 1943 by the Austrian-Ameri rear end psychiatrist Leo Kanner. He noted 11 cases in which kids werent able to relate in usual ways t o people and showed unusual responses to the environment including stereotyped travel mannerisms, resistance to tack and decreased communicatory skills. The condition of these kids was termed Autistic disturbances of affective contact. Nowadays stricter definitions of the disorder have been proposed and clinical indications have been get along up for diagnosis.1Autism is defined by some(prenominal) clinical manifestations, including qualitative impairment in social interaction, qualitative impairment in verbal and non-verbal communication and restricted repetitive and stereotyped patterns of behavior, interests and activities.2 These characteristics of the neurological disorder begin before the age of three, although it is not always recognized at this age.Autism, along with Asperger syndrome and PDD-NOS, belongs to the family of pervasive developmental disorders (PDD). This family includes a broad range of disorders associated with underdevelopment of social and communicative skills take time officularly. These deficiencies may be caused by mental retardation (Retts syndrome) provided thats not always the case. Cases of Autism and PDD-NOS are not always linked with mental retardation and Asperger syndrome is still associated with normal level of intelligence. This shows that the members of the PDD family are very heterogeneous in their behavioral manifestations, degree of affectedness and etiology. This heterogeneity has lead to the term Autism Spectrum Disorders (ASD). ASD refers to the fact that several spooky developmental disorders (Autsim, Asperger syndrome, PDD-NOS) are linked to each separate in various ways, which makes it difficult to develop clear-cut diagnostic boundaries. This linkage is highlighted in family members of patients whom mostly do not meet the criteria for a clinical diagnosis but do show (in lesser extent) some of the manifestations present in the patient.1Figure 1 ad hoc behavior observed in persons with autism due to soc ial and communicative impairment and restricted repetitive and stereotyped patterns of behavior, interests and activities. 1 Difficulty in mingling with others. 2 Inappropriate laughing or giggling. 3 Little or no eye contact. 4 Apparent insensitivity to pain. 5 Prefers to be alone removed manner 6 Spins objects. 7 Inappropriate attachment to objects. 8 Noticeable physical over bodily function or extreme underactivity. 9 Unresponsive to normal teaching methods. 10 Insistence on comparableness resists changes in routine. 11 No real fear of dangers. 12 Sustained odd play. 13 Echolia ( restate words or phrases in place of normal language). 14 May not want cuddling or act cuddly. 15 Not responsive to verbal cues acts as deaf. 16 Difficulty in expressing needs uses gestures or pointing instead of words. 17 Tantrums displays extreme distress for no apparent reason. 18 Un however gross/fine motor skill (may not want to kick ball but stack blocks). 3There are, as mentioned above, four ma in characteristics of autistic disorders (including the age of onset). start there is qualitative impairment of social interaction. Young children learn their communicative and social cognitive skills by interaction with caregivers. Autistic kids often pay belittled attention to the smiling face or highly intonated voice of their caregiver and have more interest in the inanimate environment. This will cause a delay in the development of social interaction and also impedes the kid to get attached to a person. The social skills of patients could get better during time but even then the complexity of social interaction (e.g. showing emotions, empathy) will make it hard for the autistic person to have a normal, animated conversation. 1Another manifestation of autism is qualitative impairment in verbal and nonverbal communication and play. Around 20-30% of patients with autism never speak. There is also no attempt to let in communication or to compensate the inability to speak by nonv erbal communication. These individuals for example do not make eye contact. When autistic persons do speak, their language has often typical features. They often speak with a monotonic voice and might say things not meant for communication (i.e. non-reciprocal communication). They can show echolalia as well, which makes them repeat what is said to them or what they hear in their environment (e.g. from the radio). Next to that the social uses of language, such as humor and irony, is difficult to understand for patients with autism. Another feature typically run acrossn in individuals with autism is pronoun reversal.1A third characteristic is a markedly restricted repertoire of activities and interests. This is expressed by several stereotyped movements, including toe walking, flick flicking and body rocking. Another way in which this characteristic emerges is the interest of the individual in repetitive activities such as collecting certain objects or repeating certain words or num bers.This urge for steadiness and sameness makes it hard for autistic persons to tolerate change and variation in their daily routine and to convey with stress. 1At last the age of onset is always before three years.1In 2006 the prevalence of autism spectrum disorder was estimated around 1 percent worldwide4, with two to four times more affected males than females5. An increase in the prevalence of autism and related conditions has been observed worldwide. The adoption of broader definitions of autism and greater awareness among clinicians and parents are most possible the main reasons for this growth. 1The etiology of autism is not always known. In most cases individuals develop autism without an identifiable cause and are diagnosed with idiopathic or non-syndromic autism. About 70% of these patients dont show any physical abnormalities and are said to have essential autism. The other 30% of the patients can suffer from dysmorphic features such as microcephaly (i.e. an abnormally small circumference of the head) and structural brain malformation.5Autism is associated with a range of other disorders and impairments. In 5-10% of cases, Individuals with Autism are also diagnosed with disorders such as Rett syndrome, Down syndrome, Fragile X syndrome and tuberous sclerosis. Epilepsy is suffered by 33% of the patients and 44,6% of children diagnosed with autism were reported to have intellectual impairment, defined by an intelligence quotient (IQ) score less than 70.5The phenotypic heterogeneity in autism patients is a major challenge in research. Individuals with autism seem to have a unique combination of symptoms and show very divergent behavior. This makes it hard for researchers to come about a cat valium cause or treatment for the syndrome. A lot of research is done to clear up the genetic background of autism. The different features of autism suggest that a set of different genes is involved with the disease.2 Alterations in gene sequence could have an impact on the function of several parts of the brain. With use of Magnetic Resonance resourcefulness (MRI) major types of pathology have been detected which, most possibly, contribute to the behavioural features of Autism patients. The abnormal brain patterns found include an abnormal acceleration of brain growth in early childhood, minicolumn (local network that contains elements for redundancy and plasticity)pathology, curtailed neuronal development and brain structure-specific delays of neuronal growth. 2 How these brain pathologies lead to the changes in the behavior described in autistic individuals is still not known. A (new) theory is proposed by Baron-Cohen to explain the connection amidst the autistic brain and the correspondent behavior of an autistic individual. This theory is called the Empathizing-Systemizing (E-S) Theory. It is found on the E-S model, which states that the social and cognitive skills of a person are based on an Empathizing Quotient (EQ) and a Syste mizing Quotient (SQ). People with autism are said to have an extreme Systemizing brain and thus show little empathy. 6The E-S theory is closely related to another theory namely the theory of mind (ToM). This theory is an innate chemical mechanism by which a person can interpret and attribute mental states to oneself and others and to understand that another person could have other intentions, desires and beliefs. It makes it possible for people to see the world through another persons eyes. It has been hypothized that a theory of mind deficit, so-called mind-blindness, is one of the main causes of the impairments in social interaction. It has been proposed that children with autism fail to employ a theory of mind, which makes it difficult for them to see things from another persons perspective.7The Mirror Neuron SystemMirror neurons were first discovered in a specific region of the premotor cortex of monkeys, the F5 area. These finicky type of neurons appeared to discharge when mo nkeys did a particular action as well as when they just observed another individual doing the same action. It didnt matter if the other individual was a human or a monkey or if the subject was rewarded afterwards responses were equally. 8Figure 2 A piece of feed is grasped by the experimenter (upper panel left), the tray is moved to the monkey and the monkey grasps the food (upper panel right). Activation of neurons in F5 area both during observation of the experimenters grasping movements, and while the same action is performed by the monkey (Lower panels). 9After the discovery of these visuomotor neurons in monkeys, research was done to find evidence for existence of the same neurons in human. By the use of neuropsychological and brain-imaging experiments some results were found that could indicate the existence of a Mirror Neuron System (MNS) in human.8First evidence for the MNS in mankind was found using electroencephalography (EEG). With this technique was demonstrated that t he mu rhythm, which is present during motor rest and disappears during motor activation and somatosensory stimulation9, disappeared during both execution and observation of hand actions10 This shows that not only by executing a task, but also by observing of someone else doing a task, motor neurons are stimulated. Although motor neurons of the observer are stimulated, no movement is made. The mechanism that prevents this unnecessary movement is still unknown. One of the possibilities might be the existence of regulatory reverberate neurons or super reflect neurons.11After this first evidence for the existence of a MNS in humans, more clues were found using other techniques such as Transcranial Magnetic Stimulation (TMS) and functional Magnetic Insoncance Imaging (fMRI). These studies showed that during action observation, cortical areas of the brain involved in motor control were activated.9 Activation was particularly observed in posterior outclassed frontal gyrus (IFG), also k nown as pars opercularis, and adjacent ventral premotor cortex (PMC). In addition mirror neurons were found in the rostral part of the middle-level parietal lobule. Activation was also found in the superior temporal sulcus (STS), which is believed to be the region responsible for visual input to the MNS (figure 3).11Figure 3 schematic overview of the neural circuitry for imitation. Visual input enters via the posterior superior temporal sulcus (STS). Visual information is passed on to the rostral inferior parietal lobule(IPL) (orange arrow). The red arrow represents the information flow rate from the parieral lobule to the ventral MNS, i.e the ventral premotor cortex (PMC) and inferior frontal gyrus (IFG), concerned with the goal of action. Efference copies of moter imitative commands that are sent back to the STS are represented by black arrows. This allows matching between the senory predictions of imitative motor plans and the visual description of the observed action.11Based on these findings, two hypotheses have been proposed that give the possible function of mirror neurons. The first scheme states that mirror-neuron activity mediates imitation 12 Humans are one of the few species that can learn by imitation. Studies show that 12-month-old infants can imitate facial and hand gestures and by this mechanism learn these movements themselves.13 Next to that the infants were also able to predict the action of goals by other people. This introduces the second hypothesis that says that mirror neurons are the basis of action catch.9 For people to interact with each other, they must be able to understand the actions of another person. So action understanding plays a key role in the organization of social behavior of humans. An interesting experiment has been done by Umilta et al, showing that mirror neurons became activated even when visual stimuli were hidden.14So different studies show that most likely both hypotheses are true, although there is still some discussion by which mechanism the mirror neurons execute these functions.9Autism and the Mirror Neuron SystemRecently it has been proposed that dysfunction of the mirror neuron system could have an influence on the development of autism.15 Defects of these neurons early in development are believed to interfere with the development of normal social actions such as imitation, theory of mind and language. 11Several studies are done to testify this hypothesis. Testing the IQ of children with autism shows a negative relationship between the activity of the mirror neurons and the scores of the children on the social subscales. This means that a higher activity in de mirror neuron system is accompanied with a high score on the social domain. This gives one of the first indications of a link between the dysfunction of the MNS and the development autism.11One of the functions that is thought to be impaired by the dysfunction of the MNS is imitation. Imitation is one of the most important m echanism by which green children learn their social and communicative skills. Different experiments demonstrated that children with autism have difficulties performing imitation.17Studies using fMRI supported the hypothesis by showing a reduced MNS activity in children with autism during imitation and observation of facial emotional expression. These results all suggest that mirror neurons play indeed an important role in imitation and early dysfunction of MNS may be at the core of the social limitations observed in children with autism. 16Rizzolatti and Arbib have proposed that the part of the monkey brain which contains mirror neurons dealing with hand actions, has evolved to subserve speech in humans. 17 This would suggest that hand gestures and mouth gestures are linked in humans. A defect in this specific part of the MNS could result in an inability to speak, like some of the persons with autism do. However, to date no research is done to prove this possibility.Another possibl e loading of mirror neuron dysfunction could be underdevelopment of ToM. It has been demonstrated that children with autism have difficulties perceiving the world from another persons eyes, suggesting that they have a reduced ToM. However, a study showing a correlation between the dysfunction of the MNS and ToM has still to be done.15ConclusionAlthough the discovery of mirror neuron system is just recently done, already a lot of research is dedicated to this interesting part of the brain. The specific neurons first found in monkeys, are most probably also an important part of the human brain forming a basis for functions such as imitation and action understanding. In autistic persons, who show to have difficulties with these abilities, reduced activity of mirror neurons has been found. This would suggest that the MNS is a key factor that influences the degree of social and communicative impairments in these individuals. Still a lot of research has to be done to find strong evidence for the dysfunction of the MNS and its relationship with reduced speech, social interaction skills and theory of mind.Referenties1 Kiln A (2006) Autism and Asperger syndrome an overview. Rev. 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