Brain Science of Aspergers and Autism Pt. 4: Mirror Neurons

Mirror Neurons are the cells in the brain that allow you to feel empathy, to put yourself in someone else’s position and understand how they are feeling. It is why a smile can be contagious. Mirror neurons are the reason we flinch when we see someone get hurt, we can imagine it happening to ourselves, we know what it feels like even if we have never been in this situation.

James R Hurford, of the Linguistics Department at the University of Edinburgh defines a mirror neuron as a neuron (nerve cell) which fires both when performing an action and when observing the same action performed by another creature. Quizlet.com tells us that mirror neurons are important for “understanding actions of others (empathy, interpretation, non-verbal communication)”, which traditionally children with Aspergers and Autism have difficulty with.

Mirror neurons are also important for learning new skills, especially motor skills. A child will observe a parent engaged in a behaviour, and they will often instinctively imitate. A lack of imitative behaviour can be noted in some children with ASD (Autism Spectrum Disorder).

It has been hypothesised that people with Aspergers and Autism have a lack of mirror neuron activity (1). Most neuroscientists acknowledge that there is a dysfunction in the mirror neuron system.

When I think about my own experiences and look at my son, I believe that we do have mirror neuron activity, especially when it comes to observing pain in others. So I decided to look into this further.

Neuroscientists Lindsay M. Oberman, Edward M. Hubbard, Joseph P. McCleery, Eric L. Altschulera, Vilayanur S. Ramachandrana, Jaime A. Pinedad have done a series of studies into the role of the mirror neuron system and its link with autism.

They have discovered a dysfunction in mirror neuron activity in the sensorimotor cortex, which is involved in observing and imitating motor (movement) behaviours.  This study was undertaken with 10 males with ASD and another 10 males without as control subjects, it is not clear what ages these subjects were. A further study by the same authors discovered that the earlier observed mirror neuron dysfunction was not the case when observing familiar individuals such as family members:

“In conclusion, this study finds that the observation of actions performed by familiar individuals results in mu wave suppression [reduction in brain wave activity from the neurons] in individuals with ASD, while the actions of strangers do not. This is the first study to show normal mu wave suppression during action observation in individuals with ASD. The observation that the MNS [Mirror Neuron System] in ASD may be functioning normally under specific circumstances bodes well for therapeutic interventions aimed at improving social deficits in this population. Perhaps if one could improve the ability in children with ASD to identify with the observed unfamiliar person through behavioural, neurofeedback, or other types of training, one might improve the functioning of the MNS and alleviate some of the behavioural deficits associated with this disorder.”

The Autism Coach website has an article which discusses Mirror Neuron theory and the studies by Oberman, Ramachandrana et al and states:

“The researchers speculate that mirror neuron system may also account for the tendency of autistic individuals to interpret figures of speech literally. Which part of the human brain is involved in this skill of developing overall cognitive maps of understanding from diverse information coming from multiple sensory sources? The angular gyrus, which sits at the crossroads of the brain’s vision, hearing and touch centres, seemed to be a likely candidate because nerve cells with mirror neuron-like properties have been found there. Nonautistic subjects with damage to the angular gyrus have difficulty understanding metaphors, as do many people with autism.”

It goes on to say:

“The discovery of mirror neuron deficiencies in people with autism could be used as an early diagnostic tool.  Physicians could use the lack of mu-wave suppression as a diagnostic tool to identify children with autism in early infancy, so that  therapies can be started as quickly as possible.

The researchers also suggest that biofeedback might used to display the mu waves and then use visual feedback of the display of the mu waves to teach children how to suppress the mu waves, just as biofeedback is used enable people to manifest other brainwave patterns.  A researcher, Pineda, is pursuing this approach, and his preliminary results look promising.

Another approach is to correct chemical imbalances that disable the mirror neurons. These researchers hypothesize that specialized neuromodulators may enhance the activity of mirror neurons involved in emotional responses. According to this approach, the partial depletion of such chemicals could explain the lack of emotional empathy seen in autism, and therefore researchers should look for compounds that stimulate the release of the neuromodulators or mimic their effects on mirror neurons.”

The author of the article gives personal experiences and suggests ways that this knowledge could help a child in the classroom.

The Mirror Neuron theory backs up my own observations over the years that the best (and usually only) way to teach my son within the autism spectrum has been to have him do the task himself.  I have found that standing behind him and using my hands to guide him through a new task was often the fastest, most effective way to teach a new skill.   Demonstrating or lecturing was almost always ineffective.  This research has wider educational implications, leading to the logical conclusion that the  typical public school model of children learning from an instructor lecturing up at the front of a room would fail to teach an autistic child.  An autistic child in a traditional classroom would be likely to be bored, frustrated and unable to learn.  However, these same children can learn if they are guided to carry out the actions of the concepts being taught, as is done in teaching them the acquisition of language through therapies such as Applied Behavioral Analysis.  This understanding of how children within the autism spectrum learn could completely redefine what constitutes an appropriate education for autistic children and best practices for teaching them in the public schools.”

Another study by Dapretto, Davies et al discovered that “high-functioning children with autism showed reduced mirror neuron activity in the brain’s inferior frontal gyrus (pars opercularis) while imitating and observing emotional expressions”, which could explain why people with ASD have more difficulty recognising emotion in facial expressions. Their study used 9 male children with ASD and 9 controls.

But there is hope for the person with ASD. Recently it has been discovered that rather than there being a lifelong dysfunction in the mirror neuron system, that it may just be delayed in developing. In an article published in Biological Psychiatry the author suggests that the mirror neuron system develops over time:

“Dr. Christian Keysers, lead author on the project, detailed their findings, “While most of us have their strongest mirror activity while they are young, autistic individuals seem to have a weak mirror system in their youth, but their mirror activity increases with age, is normal by about age 30 and unusually high thereafter.” This increase in function of mirror neuron systems may be related to increased capacity for social function or responsiveness to rehabilitative treatments among individuals with autism. The finding of late developing circuit functions could be very important. One wonders whether the recent breakthroughs in the genetics of autism could help to identify causes for the developmental delays. This type of bridge might help to identify novel treatment mechanisms for autism,” said Dr. John Krystal, Editor of Biological Psychiatry. One of the next steps in this line of research will be for researchers to examine how individuals with autism accomplish this improvement over time, and how therapeutic interventions targeting the same mechanism can help to support this important process.” (2)

It is also possible that only certain areas of the Mirror Neuron System are affected. More study is needed.

Christian Keyser on mirror neurons

References:

(1) Brain Rules for Baby by John Medina
(2) scienceblog.com

Brain Science of Aspergers and Autism Pt. 2: Anger and emotion

It is generally accepted that in Aspergers Syndrome and Autism that there is some abnormality in a primitive area of the brain called the amygdala. The name “amygdala” means almond, and there are two almond shaped structures buried deep within the medial temporal lobe. These form part of the “limbic system”, which is responsible for generating and modulating emotions, and laying down long term memories. The role of the amygdala is to coordinate information from different parts of the brain and generate the emotion.

Emotions are a response to bodily changes e.g. feeling hot, tense, sweating, or going red. The amygdala receives sensory information about a situation and the bodily changes from the nervous system, and everyday experience confirms or dismisses the threat accordingly. It is far better to interpret a stick as a snake and respond accordingly only to find out it was really a stick, than for your brain to think about it and get bitten before you realise what is going on.

According to neuroscientist Eric Kandel, emotion, such as fear and anger, has two components, conscious and unconscious. The amygdala receives information from both unconscious and conscious pathways when the brain perceives a threat.

The unconscious component of emotion is the operation of the nervous system. The stimulus is then analysed and an area of the brain called the hypothalamus regulates the emotion.

The conscious component of emotion involves evaluative functions of the cerebral cortex (the area responsible for planning, attention, language and reasoning), and the hippocampus, which is responsible for long term memories and the memory of emotion.

Central to both is the amygdala. According to Kandel, the amygdala is thought to coordinate the conscious experience of feeling and the bodily expression of emotion, particularly fear. It is also the area responsible for triggering the “fight or flight” response.

It seems that in the brain of someone with Aspergers or Autism that the amygdala is triggered on the unconscious component of emotion. It is possible that the brain misinterprets a stimulus as threatening, possibly due to Merzenich’s undifferentiated brain maps. When the person is in this state, logic and reasoning don’t work, and they are not necessarily aware of why they feel so angry or afraid. It appears that something in this system is not working correctly. It is understood that they have an abnormality in their amygdala, but there may also be other factors at work here, such as malfunctions in the pathways to the parts of the brain that analyse the emotion.

Cognitive Behavioural Therapy is often recommended to assist a person with Aspergers or Autism in the controlling of their emotions. Often the therapist will use a visual aid such as a “thermometer” to allow the person to recognise the bodily changes described above, before the amygdala sends the message to release the hormones associated with the fight or flight reflex. It also allows them to consciously analyse their emotions. Tony Attwood has a CBT program that he has developed; further information can be found here.

Once the emotion is triggered, it is impossible to reason with the person with Aspergers, so it is best to leave them to safely calm down, or to distract them. Tony Attwood advises using their special interest as an effective distraction, or maybe giving them a sensory toy to play with.

It seems that traditional methods of meditation and relaxation do not work with someone with Aspergers. Tony Attwood notes that they prefer to be active or physical or to do something repetitive, or even listen to music of their choosing, probably very loudly and over and over again.

References: In search of Memory by Eric Kandel, The Complete Guide to Asperger’s Syndrome by Tony Attwood, The Emotional Brain by Joseph Le Doux

Autism Spectrum Disorder and Fragile X link?

Neurorocker at en.wikipedia

 

When I started to really dig into the genes behind Aspergers and Autism, it seemed that it isn’t as clear cut as I initially thought. After researching the brain science of Fragile X syndrome (and the FMR1 gene) to establish how it could cause Autism and Aspergers, I discovered that that there isn’t just one gene that causes ASD. It seems there may be a range of genes, all of which seem to have similar effects on the developing brain.

In this post I shall discuss the FMR1 gene that causes Fragile X syndrome and its link to Autism.  Fragile X Syndrome is so called because a small section of the genetic code is “repeated on a fragile area of the X chromosome” (source PubMed Health)

According to the National Fragile X Foundation:

“FXS is the most common known cause of autism or “autistic-like” behaviors [sic]”

“Fragile X syndrome can cause a child to have autism or an Autism Spectrum Disorder (ASD) though not all children with fragile X syndrome have autism or an ASD.

  • FACT: For between 2% and 6% of all children diagnosed with autism, the cause is the Fragile X gene mutation.
  • FACT: Approximately one-third of all children diagnosed with fragile X syndrome also have some degree of autism.
  • FACT: Fragile X syndrome is the most common known single gene cause of autism.”

The A.D.A.M. Medical Encyclopedia notes that the symptoms of Fragile X are very similar to those with Autism:

  • “Delay in crawling, walking, or twisting
  • Hand clapping or hand biting
  • Hyperactive or impulsive behavior
  • Mental retardation
  • Speech and language delay
  • Tendency to avoid eye contact”

The reason Fragile X caught my eye is that one of the most common symptoms or signs of Fragile X is the hypersensitivity to sensory stimuli, as outlined by an article in Science Daily:

“New research provides insight into why fragile X syndrome, the most common known cause of autism and mental retardation, is associated with an extreme hypersensitivity to sounds, touch, smells, and visual stimuli that causes sensory overload and results in social withdrawal, hyperarousal, and anxiety. The study, published by Cell Press in the February 11 issue of the journal Neuron, uncovers a previously unknown developmental delay in a critical brain circuit that processes sensory information in a mouse model of fragile X syndrome.”

This is consistent with my view that the majority of symptoms associated with Autism and Aspergers are caused by sensory overload. In response to this article the Shared Attention website notes that: “This seems to support so-called experimental therapies (e.g. sensory integration) that theorize that plasticity in sensory processing can afford lasting positive changes in neurological function and behavioral outcomes. In other words, by using natural interests of the child to harness their attention and engagement, it may be possible to use purposefully engineered activities to modify and naturalize those pathways”.

And it seems that treatment for a child with Fragile X is similar to those with Autism and Aspergers. Source: Medicine.net:

  • Know the learning style of the individual.
  • Develop a consistent daily schedule or routine.
  • Use visual signs (pictures, sign language, logos, words) and concrete examples or materials to present ideas, concepts, steps, etc.
  • Prepare the individual for any changes in routine by explaining them ahead of time, possibly using visual signs.
  • Include functional goals with academic goals; for instance, teaching the individual the names of different pieces of clothing as well as how to dress him/herself.
  • Provide opportunities for the child to be active and move around.
  • Use computers and interactive educational software.
  • Provide a quiet place where the child can retreat and regroup.

So how does the Fragile X gene lead to symptoms similar to Autism?

This from the A.D.A.M. Medical Encyclopedia.

“Normally, the FMR1 gene makes a protein needed for your brain to grow properly. A defect in this gene makes your body produce too little of the protein, or none at all.” The link between the FMR1 gene and the hypersensitivity displayed in Aspergers and Autism has been established (see academic paper)  . The nerve cells in the brain initially grow extra branches, which could explain the hypersensitivity to various sensory stimuli. This could lead to the premature turning off of the “critical period” as discovered by Merzenich. The nerve cells eventually “prune” the branches so that the nerve cells appear normal, but at this stage it could already be too late, as the brain is left with the “undifferentiated brain maps” discovered by Merzenich.

According to the A.D.A.M. Medical Encyclopedia:

“Boys and girls can both be affected, but because boys have only one X chromosome, a single fragile X is likely to affect them more severely. You can have Fragile X syndrome even if your parents do not have it.

Fragile X syndrome can be a cause of autism or related disorders, although not all children with fragile X syndrome have these conditions.”

The symptoms are more likely to be pronounced in boys, girls may only exhibit behaviours such as shyness.

But the FMR1 gene cannot be the only cause of ASD. The main issue with this as an umbrella answer to ASD is that males with Fragile X cannot pass it onto their sons, due to the fact that they only transmit the Y chromosome, and not the X. (source: Autism Help)  But it seems that many boys with Aspergers and Autism have a father who also has it. In addition the IQ of a person with Fragile X Syndrome is highly likely to be below average, although this is not always true for girls. Although the research in this area may be slightly inaccurate, as medicine.net points out:

“Attention disorders, hyperactivity, anxiety, and language processing problems can interfere with test-taking skills and learning. Because many people with Fragile X have these problems, a person with Fragile X may have more capabilities than his or her IQ score suggests”

So the search for the common cause continues…

Academic Papers on Fragile X:

http://www.fragilex.org/pdf/kaufmann-et-al_autismandfragileX.pdf

http://www.ncbi.nlm.nih.gov/pubmed/19441123

Brain Science of Aspergers and Autism Pt. 1: Sensory Overload

Shiny Brain by Artem Chernyshevych http://www.sxc.hu/photo/1254880

In this first post on the brain science of Aspergers I want to talk about the theory of neuroscientist Michael Merzenich. Merzenich is one of the world’s leading experts on brain plasticity, and his studies into the causes of Autism and his work on the Fast ForWord software program has revolutionised the lives of many young autistics.

Merzenich discovered that early in a child’s life when the brain is making its early connections, what neuroscientists call the “critical period”, a nerve growth factor (a protein called BDNF or Brain Derived Neurotropic Factor, which is responsible for growing nerve fibres in the brain) is released. Read more of this post

Brain Science of Aspergers and Autism: Introduction

A friend recently asked me what happens in the brain of someone with Aspergers or Autism. There are many studies that have been undertaken by neuroscientists to discover the causes and brain functions that characterise Aspergers.

It has been discovered that it affects not just one area of the brain, but there are various areas that contribute to the features and cognitive functions of Aspergers and Autism. Read more of this post