Autism is a developmental neurological disorder distinguished by the presence of severe communication, language and social scarcity in affected children. Autism was not that well known 30 years ago, but in the last 2 decades it is probably the most well known of several pervasive developmental disorders which begin in early childhood (Fombonne 1999, Bailey et al, 1996). The disorder is progressive and affects all aspects of life. Individuals with autism have appropriate motor skills but their cognitive (thinking and language) and social skills are developmentally delayed compared to their normal peers. For the diagnosis of autism to be made, the children must be shown to have difficulty with social interaction, communication and behavioral (Cohen & Volkmar 1997; Russell 1997). Though all autistic individuals show similar cognitive and social impairment, the degree of the impairment is quite variable between individuals. Some individuals have only mild impairment but others have severe impairment and are difficult to manage at home.
The majority of autistic children show difficulty in social interaction at a very early age. The children simply are not able to process social and non verbal forms of communication such as eye contact and facial expression. Unlike a normal child who responds to a mother’s voice or face, an autistic child often lack the ability to appreciate faces or socially communicated gestures. The majority of Autistic children also have varying degrees of developmental delay in speech and conversational skills. Children affected with autism show peculiar and socially inappropriate behaviors. A typical feature is the indifference towards the surrounding or other humans. Many are fixated on certain objects and have repetitive behaviors. Some even find fascinating interest in the most mundane things. The movements and gestures are often stereotyped and these children prefer the need for the same order day after day. Temper tantrums are common when the order is changed. Autistic children rarely have little awareness of danger or feelings. They appear cold and withdrawn. The symptoms of autism are not present at birth but do become apparent during the latter part of the second year of life (Osterling & Dawson 1994). The majority of cases of autism are diagnosed by age 3. The disorder affects males slightly more than females but no race, culture or ethnic group is immune from the disorder. Autism is a life long disorder and its severity varies from mild to severe. Except for the very mild cases, autism interferes with normal life and the majority of the affected individuals are not able to live or work independently (Baron-Cohen et al 2000, Kanner 1943).
The cause of autism still remains a puzzle. Despite a few decades of extensive research, the disorder is poorly understood and thus treatment for the condition has been empirical. Autism is generally treated by a pediatrician who has specialty training in childhood developmental delays. These physicians understand the disorder and are generally aware of the latest treatment trends. There is no standard therapy for the condition. If you go to 10 different doctors, you will get 100 different opinions. There is no right or wrong about the treatments available for autism. Just the philosophical approach is different.
Though intervention cannot reverse the course of autism, it can result in symptom improvement and a greater capability for independence. For intervention to be maximally successful, however, it must be delivered early in the developmental process, shortly after the diagnosis of autism is first made.
There is a lot of debate whether the incidence of autism is increasing. There are some researchers who believe that the numbers have increased simply because of better recognition and awareness of the disorder. Others indicate that the actual numbers of autism children are on the increase.
What causes Autism?
Why autism occurs is not known and theories abound. Among the many theories is the hypothesis that delays in development of theory of mind may account for many of the social and communication disabilities seen in children with autism, while differences in information processing manner, in particular weak central rationality, may account for many of the non-social features of autism. Other theories have focused on emotion, perception processing, gender differences and self concentration on emotion, perceptual indulgence, and gender differences. In the last decade, another theory has attracted a lot of attention because it seems to combine the cognitive and neural aspects of the disease. This fancy hypothesis known as the “Broken Mirror” theory does explain the symptoms of the disease but not the cause (Baron-Cohen 1995).
What are mirror neurons?
Mirror neurons are thought to be a delicate collection of nerves that play a role in empathy and in learning (Metta et al 2006). The mirror neurons are distinct for one particular reason- they get activated when a certain action is performed- however, the individual observing the person performing the activity also gets activation of the same group of neurons. In this case, the neural activity is the same whether one is performing or observing (in other words it explains the adage- monkey see, monkey do). These mirror neurons have been observed in the premotor cortex and inferior parietal cortex. It is widely believed that mirror neurons are a common neurological features in most primates, possibly humans (Rizzolatti 2004, 2005). The mirror neurons strengthen the concept that seeing is believing- that perception is not just a one way street of reality but rather a complex feedback cycle between two individuals of the same species. For example when we see an individual crying from pain, we feel the same emotions and pain. Mirror neurons are thought to play a vital role in the evolutionary scale of learning, esp. among primates (Williams et al 2001, 2004).
These fascinating neural structures were first discovered in rhesus macaques nearly 20 years ago. Since their discovery mirror neurons have been implicated in almost all brain functions- some factual and many hypothetical. It is now widely believed that for some unknown reason there is an absence or under functioning of these mirror neurons in autistic children. Some call it “Mind Blindness”. Mirror neurons not only explain the behavior in autistic children but also help explain how we normal humans visualize the world (Whiten & Brown 1999).
The ‘broken mirror’ hypothesis
One of the classic features of autism is the lack of imitation (Williams et al 2004). Children with autism show a decrease in spontaneous imitation, diminished precision of intentional imitation, and reduced automatic imitation compared to normal children of same age. This is a common feature at all ages and functioning levels of autistic children. Some researchers believe that this lack of imitation is central to autism and occurs chiefly due to failure of the mirror neuron system. This lack of imitation is perhaps the first clinical observation by parents that something is wrong with the child. While the reduced imitation is mild as a child, it does not disappear and in many cases does worsen over time. The mirror neural network is believed to have several important functions. Besides being part of the motor system, it is also important for the coordination of vision-hand directed functions (e.g. hitting a nail with a hammer). Damage to the Mirror group of nerves can lead to apraxia. Secondly this system is widely believed to have an integral role in our social perception (Iacoboni et al 2001).
It is widely believed that the lack of automatic imitation of facial and postural movements may be a factor in the blunted emotional and social responses seen in autism. Individuals with autism do not have any visible anatomical or pathological defects but now it is believed that there are some mirror networks that may under function (Castelli et al 2002). There are some recent observations that these mirror networks may have blunted responses both when observing others and when imitating others. Further, there is belief that the degree of atypical mirror neuron activation is directly related to the severity of autism symptoms. Thus, the mirror neuron system may be an important part of the biological foundation for the behavioral impairments seen in autism (Smith & Bryson 1994).
With the recent availability of newer brain recording technology, scientists have been able to image the brain and perform some exciting experiments. Experiments in monkeys either performing or observing simple activities have shown activation of the same mirror neurons in both groups of animals. While there are visual mirror neurons one should be aware that there are also non visual neurons which are only activated in the performer and not the observer. The majority of these mirror neurons have been observed in Boca’s area which is important for the acquisition of mutual movements and meaning (Iacoboni et al 2001, 1999, Makuuchi 2005)). Over the past few years, many experimental studies using functional magnetic resonance imaging (fMRI), positron emission tomography (PET), electroencephalography (EEG), magnetoencephalography (MEG) and transcranial magnetic stimulation (TMS) have been utilized to discover the human ‘mirror system’ homologue.
Unfortunately in humans the studies are not as straight forward like in primates. Gross EEG recordings from motor areas reveal suppression of activity when normal children watch other humans move around or perform some type of activity. The scientists believe that this is human homologue of Mirror Network of neurons. The same recordings in autistic children do not reveal any suppression of this motor activity. Also, children with autism have less activity in mirror neuron regions of the brain when imitating.
Finally, anatomical differences have been found in the mirror neuron related brain areas in adults with autism spectrum disorders, compared to non-autistic adults. All these cortical areas were thinner and the degree of thinning was correlated with autism symptom severity, a correlation nearly restricted to these brain regions And based on these vague non specific recordings the researchers believe that they have discovered the mysterious missing link in Autism. The crude experiments which have never been unanimously repeated by other researchers are now at the center piece of autism research. Some researchers claim that autism is caused by a lack of mirror neurons, leading to disabilities in social skills, imitation, empathy and theory of mind. However, there are also studies showing that children with autism can do tasks which require mirror neurons. There are just as many studies which reveal absoluelty nothing in autistic children and so this Mirror theory remains just speculation (Goldenberg & Hagman 1997).
Research on mirror neuron systems’ impact on autistic social functioning is only just beginning. It is not possible to say that mirror neuron system dysfunction is the ’cause’ of autistic people’s problems at this time, but it certainly appears that mirror neurons play an important role in creating autistic problems. As is usually the case, more research is necessary, and time will tell.
While the Mirror neurons may explain some behaviors in autism children, there are many other behaviors which have no relation to dysfunction of MN. For example, some individuals with autism are often either supersensitive or hyposensitive to certain sensory stimulation of the auditory, olfactory, gustatory or tactile sensations. It is not only difficult to understand how a simple mirror neuron can explain all these phenomenon without the presence of any real pathology. The link between Autism and the ‘human mirror system’ becomes even more dubious when the physiological features associated with the disorder are taken into account. There have been several studies that have observed anatomical difference between brain organelles and neurotypical observations. Some scientists have noticed that there is altered cell morphology or changes in volume and or thickness of the cortex and overall size in brain locations not associated with the ‘human mirror system’ . However, one has to remember that there are just as many studies which have not seen any type of anatomical or pathological differences in brain of autistic children. While the Mirror nerves may account for a few isolated phenomenon, they are definitely not the missing link capable of explaining the entire subject of Autism
For the moment, the mirror neuron dysfunction and autism is based more on speculation than factual evidence. The improbability that a multitude of behavioral and physiological variations can be accounted for by a tiny population of visuomotor neurons that encompass only ~10% of the neurons in only two cortical areas. Furthermore, one should not discount the presence of other theories that may also partially account for the behaviors seen in autism (Byrne & Russon 1998).
So what happens now?
A deficit in the development of the MNs system whether inappropriate development of some segments or links between those segments might be present in autism, and manifest the clinical symptoms. Lack of functionality of the MNs system may cause an impaired formation of specific self-other representation which is the root of the autistic disorder. It can explain the inability to understand others mimics, beliefs, lack of understanding of language, lack of social skills and even speech delay. The MNs can’t explain the whole autistic disorder but can defiantly contribute to the understanding of the mechanisms underlying some of the autistic symptoms (Pennington & Ozonoff 1996).
Executive functions such as planning are also damaged in the autistic disorder. Planning is a product of developmental processes but it is also possible that simple planning strategies are acquired through observation and then are generalized to different situations. In this case the MNs system has a role in the development of planning capability and thus a poor MNs system may contribute to a planning disorder.
The mirror nerve theory is just a hypothesis and nothing more than that, it does not explain the cause of autism nor does it change how we treat the disorder. And while there has been a lot of hype about this theory, this is nothing special. Hype is common in science, numbers are thrown around, figures are enlarged, facts are juggled, explanations are always available for all observations and the boundary between fact and function often become blurred. Autism is not the only disorder which has no explanation- the majority of medicine is like that. The brain is much more complex to understand and we are still grappling with the very basic knowledge about nerves. Even though we do understand basic concepts, we are a long ways to solving the mysteries in medicine.
Mirror neurons are fascinating and may underlie certain social capabilities in both animals and humans. However, the study of mirror neurons and the ‘human mirror system’ in particular is fraught with technical difficulty, intense speculation and little solid evidence. Placing a small electrical wire blindly onto or inside the brain and recording electrical activity is a naÃ¯ve way of interpreting the complex brain with its billion neurons. The brain is unlike any other organ and a casual link between some facial gesture and a firing of a neuron has little meaning. Until we develop more selective 3-D imaging with superb resolution, the testing is non selective and will only confuse what little we know. MRI and all other brain imaging techniques are useful in detecting large anatomical or structural defects in the brain, but these techniques can not isolate a single nerve cell and determine its function. There is no technique available today which can non invasively determine neuronal function, its location or its precise behavior.
There is no disorder which has more myths and misconceptions surrounding it than autism. Autism is a complex illness and every few years a new theory comes along which claims to be the Pandora’s box. Like most brain disorders, the solution to autism is not likely to be forth coming in the near future. The theories do not help with treatment nor do they provide any evidence of a cause.
The eventual outlook for a child with autism depends on the severity of the autistic features and when treatment was started. Without any treatment, most children regress. Even with treatment, some core features of the disorder remain. And despite all the knowledge we have gathered, we still have difficulty in predicting the course of the disorder. The disorder has just too many variable- the symptoms are vast and range from no concentration ability to bizarre motor movements. The severity may be intense, their may or not be familial pathology, the environment may not be conducive to treatment and the types of treatment are just too many. The one feature which has been used a predictor of the prognosis of the child is the verbal IQ. A decent verbal IQ is a good indicator of future functioning. A few children with autism are able to develop some type of communication and social skills that allows them a certain degree of independence. Others do learn behaviors skills but can not communicate. However, despite the isolated reports of success, the majority of autistic children grow up to be adults and require life long support from their families.
As far as using the MN to treat the child, there are some who advocate that perhaps the MN can be revived or restored with repetitive motor or imitation skills. Perhaps these same researchers should understand that when a mirror is broken, a new reflection of YOU can only be obtained by getting a new mirror not patching the mirror with scotch tape- in other words- these individuals need a new brain.
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