Thursday, 29 December 2011

Autism; - It may be all in the wiring pattern.

As evidenced by my book 'Brain Injured Children. - Tapping the Potential Within.' I have long argued for the role of abnormal brain connectivity in autism, - whether that abnormal connectivity is caused by the expression of specific genes, or by brain injury.  The point i

Studying a rare disorder known as tuberous sclerosis complex (TSC), researchers at Children's Hospital Boston add to a growing body of evidence suggesting that autism spectrum disorders, which affect 25 to 50 percent of TSC patients, result from a miswiring of connections in the developing brain, leading to improper information flow. The finding may also help explain why many people with TSC have seizures and intellectual disabilities. Findings were published online in Nature Neuroscience.

TSC causes benign tumors throughout the body, including the brain. But patients with TSC may have autism, epilepsy or intellectual disabilities even in the absence of these growths. Now, researchers led by Mustafa Sahin, MD, PhD, of Children's Department of Neurology, provide evidence that mutations in one of the TSC's causative genes, known as TSC2, prevent growing nerve fibers (axons) from finding their proper destinations in the developing brain.

Studying a well-characterized axon route – between the eye's retina and the visual area of the brain – Sahin and colleagues showed that when mouse neurons were deficient in TSC2, their axons failed to land in the right places. Further investigation showed that the axons' tips, known as "growth cones," did not respond to navigation cues from a group of molecules called ephrins. "Normally ephrins cause growth cones to collapse in neurons, but in tuberous sclerosis the axons don't heed these repulsive cues, so keep growing," says Sahin, the study's senior investigator.

Additional experiments indicated that the loss of responsiveness to ephrin signals resulted from activation of a molecular pathway called mTOR, whose activity increased when neurons were deficient in TSC2. Axon tracing in the mice showed that many axons originating in the retina were not mapping to the expected part of the brain.

Although the study looked only at retinal connections to the brain, the researchers believe their findings may have general relevance for the organization of the developing brain. Scientists speculate that in autism, wiring may be abnormal in the areas of the brain involved in social cognition.
"People have started to look at autism as a developmental disconnection syndrome – there are either too many connections or too few connections between different parts of the brain," says Sahin. "In the mouse models, we're seeing an exuberance of connections, consistent with the idea that autism may involve a sensory overload, and/or a lack of filtering of information."

Sahin hopes that the brain's miswiring can be corrected by drugs targeting the molecular pathways that cause it. The mTOR pathway is emerging as central to various kinds of axon abnormalities, and drugs inhibiting mTOR has already been approved by the FDA. For example, one mTOR inhibitor, rapamycin, is currently used mainly to prevent organ rejection in transplant patients, and Sahin plans to launch a clinical trial of a rapamycin-like drug in approximately 50 patients with TSC later this year, to see if the drug improves neurocognition, autism and seizures.

In 2008, Sahin and colleagues published related research in Genes & Development showing that when TSC1 and TSC2 are inactivated, brain cells grow more than one axon – an abnormal configuration that exacerbates abnormal brain connectivity. The mTOR pathway was, again, shown to be involved, and when it was inhibited with rapamycin, neurons grew normally, sprouting just one axon.

Supporting the mouse data, a study by Sahin and his colleague Simon Warfield, PhD, in the Computational Radiology Laboratory at Children's, examined the brains of 10 patients with TSC, 7 of whom also had autism or developmental delay, and 6 unaffected controls. Using an advanced kind of MRI imaging called diffusion tensor imaging, they documented disorganized and structurally abnormal tracts of axons in the TSC group, particularly in the visual and social cognition areas of the brain (see image). The axons also were poorly myelinated – their fatty coating, which helps axons conduct electrical signals, was compromised. (In other studies, done in collaboration with David Kwiatkowski at Brigham and Women's Hospital, giving rapamycin normalized myelination in mice.)

Sahin has also been studying additional genes previously found to be deleted or duplicated in patients with autism, and finding that deletion of some of them causes neurons to produce multiple axons – an abnormality that, again, appears to be reversed with rapamycin.

"Many of the genes implicated in autism may possibly converge on a few common pathways controlling the wiring of nerve cells," says Sahin. "Rare genetic disorders like TSC are providing us with vital clues about brain mechanisms leading to autism spectrum disorders. Understanding the neurobiology of these disorders is likely to lead to new treatment options not only for TSC patients, but also for patients with other neurodevelopmental diseases caused by defective myelination and connectivity, such as autism, epilepsy and intellectual disability."

The point is that we have evidence that the brain can be encouraged to change its wiring pattern through being exposed to appropriate stimulation from the environment.  This is what the Snowdrop programme is designed to do, - to provide the appropriate environmental conditions to encourage the brain to respond by changing its wiring structure.

Friday, 23 December 2011

The Importance of Tummy Time.

When you consider the size of a newborn’s head compared to the rest of his tiny body and add the fact that for many months after birth his muscle strength is low, you can see why spending time on his tummy can be frustrating.  This is even more so for our babies who have developmental disabilities which bring additional problems with regard to muscle tone, coordination and sometimes hydrocephalus.
Nowadays we also have a fear of Sudden Infant Death Syndrome, which quite rightly keeps babies on their backs for a huge amount of time.  However, this does have developmental drawbacks because in terms of mobility development, when a baby is on his back, he is upside down. 

Tummy time: strength, head shape, and smarts
Placing a baby on his tummy not only gives his neck muscles a workout, it strengthens the torso and provides him with more reaching and looking practice. That’s a big boost for development; in fact, researchers have seen that more tummy time correlates to better motor skills in babies. Not only that, but, amazingly, encouraging motor skills is also known to help babies with social development, since the stimulation to motor pathways in the brain seems to encourage growth in other regions as well.  In other words, tummy time isn’t just a physical workout — it’s a boost to other areas of development too.
Seeing the world belly-down and head up also makes it easier for your baby to correlate the sounds in his surroundings with their exact location (rather than being stuck looking at the ceiling or seeing things upside-down all the time). That’s also why carrying your baby is good for the brain because it does not block his ability to turn and locate sounds as say a car seat would.

When and how much?
Most authorities agree that around two to four weeks after birth is a good window to start tummy time. Remember, at this point your baby and his large cranium are fighting an uphill gravity battle, so don’t be surprised if you don’t get far with the exercise, especially if your little one has developmental problems. Try once a day to start, and if it helps, (and if he is small enough),  place baby on your stomach (this counts) and talk to him whilst he does what could be all of a 30-second workout.  
From there, tummy time will grow in length. Recommendations range from trying for 30 minutes a day or several stints of five to 10 minutes, to a looser goal of whenever possible. But many babies don’t enjoy the exercise until they get stronger (around four months of age). Within a month or two after that, the belly becomes one of their favorite positions because it allows them to see, reach, and play more easily.  All of this will take longer with a child with say cerebral palsy because of the aforementioned difficulties which are also working against them, but keep trying, - start small and second by second work the time so that he is spending longer and longer on his tummy.

Tummy time how-to
If your baby is just starting out, you can roll up a receiving blanket and put it high on his chest, under the armpits, but don't place him so high that it restricts his movement.  Instead of plopping your baby down directly on his tummy (where he’s not used to being), start by lying him on the floor on his back. Look at him, give him a smile, and make contact first. Tell him something like: “I’m going to help you roll to your belly, okay?” (With repetition, he’ll know what’s about to happen) and roll him from the hips gently. If his arm gets stuck underneath him, lift up the hip on the same side of his body to allow him to pull his arm out. The idea is to let your baby participate in getting into the position so he’s practicing the movements and feeling more in control, instead of having you simply stick him there.
Once your baby is on his belly, get down on the floor in front of him to talk.
Put one or two toys within reaching distance or a mirror close up so he can see himself.
Once your baby can lift his head enough to see in front of him, one of his favorite things to look at might be a book of faces. Get an accordion-style baby faces book with clear, large photographs.
Use a comfortable but flat mat without too much padding so he has more control over his arms.
Your best bet is to try tummy time when your baby is fed, rested, and ready to play. His tolerance for frustration will be higher when he’s in a good mood.
Just because your baby is grunting and making noises, or kicking and struggling a bit, it doesn’t mean you have to rescue him. It’s a difficult exercise for babies, so sometimes their noises just signal effort. But when your baby truly seems unhappy or starts to cry, roll him over to his back and scoop him up to a more familiar place.
Remember that since it’s an unfamiliar position nowadays, it takes a lot of practice and repetition for some babies to like being on their bellies. But even a two-minute session counts, and it’s something to build on. Keep at it, and you’ll see your baby’s comfort, and even enjoyment, of tummy time grow.
The developmental consequences of tummy time is the development of crawling, which has profound knock - on effects upon the development of the visual system and upon cognitive development, so keep trying, but also try to make it fun.

Thursday, 22 December 2011

How Snowdrop was formed.

My name is Andrew Brereton and I was the father of a child who suffered with profound brain injuries, which caused a mixture of symptoms, - some of quadriplegic cerebral palsy and some of autism, although neither of those diagnoses do justice to the true nature and severity of his brain injuries, -suffice it to say that he was described as being in the worst 5% of possible injuries! Unfortunately, Daniel passed away eight years ago, suffering a series of brainstem strokes. We always knew that for someone with his level of disability, the length of his life would be severely limited, but unfortunately, knowing that something is going to hurt, doesn't actually stop it hurting when it happens!

Daniel was born at the North Staffordshire Maternity Hospital in Stoke –On – Trent on the 4th September 1987 and within a few short weeks was diagnosed with cerebral palsy. We were warned by the paediatrician that the fact he was able to make such an early diagnosis indicated a high degree of severity of the condition. – He was not wrong and within a few weeks it became clear that I would be forced to give up my work as a chemist in the ceramics industry, in order to help my wife, Janet look after him. - Daniel rarely slept, he could stay awake for days and nights on end. This was an impossible situation for my wife to deal with alone and soon she was struggling to cope, whilst I went out to work.

Although in the early months of Daniel’s life, I was largely at home, I became increasingly interested in Daniel's problems and in human cognitive processes, so I decided to enrol for a university degree in psychology / child development at our local college of higher education, which is part of Manchester University. The structure of my chosen courses meant that I only had to be on campus part of the time, so I was still largely available to help with Daniel's care. Three years later I passed my degree with upper second class honours, my final dissertation being on the subject of 'Programmes of rehabilitation and their effects upon brain - injured children and their families.'

The three years of my degree studies paid off in more than one way, - not only did they foster in me a greater understanding of the difficulties Daniel faced, they also highlighted some useful techniques which we could employ in treating some of those difficulties; some of these techniques really had an impact upon his quality of life. My success in my studies also further fuelled my interest in this field and so I enrolled on further courses, eventually gaining post graduate qualifications in ‘child development,’ 'language and communication impairments in children,' and ultimately an MSc based in neuroscience and child development. I was also fortunate to be involved in several research projects such as the construction of neural networks to mimic cognitive processes in children, the design and employment of sociocultural learning programmes with children who experience learning difficulties and the design and employment of various communication therapies for children who experience language and communication difficulties.

My studies at university also opened our eyes to alternative therapeutic interventions which were available and consequently, over time, we not only travelled the globe to seek help for Daniel's difficulties from these approaches, but I was given the opportunity to study at various clinics. We studied and employed alternatives at clinics in the UK and internationally. Some of these approaches we found useful and productive, - others we did not. In fact, more accurately, I would say we found some techniques within most approaches to be beneficial, whilst finding many other techniques within each approach to be of no benefit. We also found the intensive philosophy of some alternatives to be detrimental to Daniel and to us as a family. I guess what I am saying is that there is an element of truth in all approaches, but no one approach has a monopoly on the facts!
Also, as we discovered, there are also people out there who are proposing preposterous, easily disproveable theories of brain function / development; - people who are not qualified to be doing what they are doing and people who are charging unjustifiable amounts of money for their preposterous, underqualified theories.

Our employment of many of these alternative approaches created a great deal of hostility within the ranks of the medical professionals who treated Daniel and over the years of his life we were subjected to a constant tirade of enmity. We arrived at the conclusion that this was as a consequence of their perceived loss of powers; - they seemed to think that any approach which we chose which was out of their circle of control, was a direct threat to their perceived competence, and they acted accordingly towards us. In truth, all we were trying to achieve was greater quality of life for Daniel by enhancing his developmental prospects. We found it amazing that we were subject to so much criticism for seeking answers to Daniel’s difficulties from a group of people who possessed no answers to those problems themselves.

Although throughout his lifetime, Daniel remained very severely handicapped, our efforts at helping him were far from fruitless. At birth, Daniel was cortically blind and deaf. This meant that although his eyes and ears were working normally, his brain was not interpreting the sensory information, which they were collecting. However gradually, through utilising our new knowledge, we were able to restore both his vision and his hearing. This may sound small beer in the global picture of overwhelming global handicap, but for Daniel it meant that he could now see his Mum and Dad; - that he could see, hear and begin to interact with his two younger brothers. – This revolutionised Daniel’s whole being.

Sadly as I say, Daniel passed away eight years ago. He had sustained injuries in his lower brainstem which were life threatening and which we knew could take him at any moment in his life. The fact that we managed to avoid this for 16 years is testament to what can be achieved through hard work. We miss him terribly and there will always be a massive hole in our lives. How do you get over the death of a child?  However, the snowball of enthusiasm and interest, which he created in me, - interest in helping to solve the problems many children face, rolls on.

Using all of the knowledge, which my son passed to me, (despite all my qualifications and research experience, he remains my most astute tutor), I have established 'Snowdrop.' It is in its infancy, but it aims to take all the knowledge and experience amassed over the years and to utilise it for the benefit of children and families like ourselves. Snowdrop provides programmes of neuroscience based therapy for children who experience a wide range of developmental disabilities. Those problems may express themselves as more global difficulties such as cerebral palsy or autism, or more specific difficulties such as dyslexia, dyspraxia, or specific language impairment. We also treat children who have a wide range of genetic disorders.

Treatment is carried out by the family in the child's own home. Our ‘programmes’ are variable in their intensity, depending upon the particular problems displayed by the child and are designed to fit in with what the family can practicably achieve without placing them under an undue burden of stress. We believe that the best environment for development to have a chance of taking place is one where both child and family are happily motivated and jointly focussed on the same objectives.

Although Snowdrop is based in the UK, in it's short life so far, it is already having an appeal internationally and we have children on our books from all over the world.  All we want to do is to be of service to children and their families. In this way, my son's life and everything he taught me about brain injury and the developmental problems children face will have not been wasted.

Please peruse our website, which can be found on

I have also published a book titled, 'Brain Injured Children. - Tapping the Potential Within.' This can be accessed through this link and through the website.

Monday, 5 December 2011

Can a Child Have Both Cerebral Palsy and Autism?

For me, the answer has to be, 'Yes,' I have seen many children who have mixed symptoms of both. There are many roads to the 'destination' of autism.  There is increasing evidence that one such road is genetic, - the gene(s) in expressing itself / themselves create an anomaly in brain development,- (the evidence points to the adoption of an abnormal wiring pattern), which produces the symptoms of autism. Another road is now thought to be methylation difficulties, another through oxygen starvation, etc. All these differing 'roads' lead to brain dysfunction, which produces what we observe as autism. So, autism consists of a set of symptoms, (distorted sensory perception, faulure of socialisation, communication and imagination, stereotypical behaviours, etc). - These symptoms, all caused by brain dysfunction, are the way in which the condition we call 'autism' expresses itself, - so autism is an expression of brain dysfunction.
There are approximately one hundred billion neurons in the human brain, each cell having the potential to create ten thousand connections to other cells to form complex groupings of connections known as neural networks. This is an unbelievably complex operating system and when it becomes injured, the pattern of injury is therefore like a fingerprint, - unique to the child. Some children may have common symptoms, but no two children will display exactly the same problems. - This is why autism is a 'spectrum disorder,' with a child at one end of the autistic spectrum, displaying totally different problems to a child at the other end of the autistic spectrum.

We have already established that autism is caused by brain dysfunction, - well there are many other problems, which are also caused by brain dysfunction, one of which is cerebral palsy. 
CP can be caused by oxygen starvation, genetics (rarely), drug abuse, infection, jaundice, malnutrition, or one of many other causes. So it is brain dysfunction, which produces the sets of symptoms we know as CP just as it is brain dysfunction, which produces the sets of symptoms we know as autism.
So it is correct to say that both autism and CP are caused by brain dysfunction, - indeed, they are both 'expressions' of brain dysfunction, or if you like, 'brain injury.'
Now, the more severe and widespread the brain dysfunction, the more symptoms, (or expressions) will be displayed. So whilst a child who has suffered only a moderate amount of damage to the neural networks of the brain might display the symptoms or EITHER autism OR cerebral palsy, (or some other expression), the child who has suffered more severe damage, may display multiple expressions! These might include some symptoms which are considered to be on the autistic spectrum, alongside some symptoms which are considered to fall within CP (or indeed any other expression of brain dysfunction, - there are many!).
So the answer is yes, I believe it is possible and not uncommon for a child to have a dual diagnosis of both autism and cerebral palsy. Does this mean they have two different conditions? No. They just suffer from severe brain dysfunction. At Snowdrop we provide programmes of rehabilitation for all types of and severity of brain injury

Sunday, 27 November 2011

Dyslexia; - A failure of sensory attention?

I see this inability to 'tune out' extraneous stimuli from the environment in order to focus on a specific task or feature in children with many types of developmental disability. I talk about it in my book, where I call it 'wide spectrum tuning,' but I have never seen it in anyone with dyslexia. An interesting article apart from them going on about dyslexia having one cause! We already know of two!, - injury to part of the cerebellum and injury to parts of the 'magnocellular system.' Snowdrop provides therapy which helps to retune these attentional systems to more normal levels.
With thanks to Medical News Today. 
Dyslexia affects up to 17.5% of the population, but its cause remains somewhat unknown. A report published in the online journal PLoS ONE supports the hypothesis that the symptoms of dyslexia, including difficulties in reading, are at least partly due to difficulty excluding excess background information like noise. 

In the study of 37 undergraduate students, the researchers, led by Rachel Beattie of the University of Southern California, found that the poor readers performed significantly worse than the control group only when there were high levels of background noise. 

The two groups performed comparably at the prescribed task when there was no background noise and when the stimulus set size was varied, either a large or a small set size. 

According to Dr. Beattie, "these findings support a relatively new theory, namely that dyslexic individuals do not completely filter out irrelevant information when attending to letters and sounds. This external noise exclusion deficit could lead to the creation of inaccurate representations of words and phonemes and ultimately, to the characteristic reading and phonological awareness impairments observed in dyslexia." 

Saturday, 22 October 2011

How do Babies Learn?

So which is it? Are babies mindless beings who only eat, sleep and cry? Or are they little geniuses, ready for academic pursuits? The truth is probably half way between the two. There is no doubt that the brain of a baby is like a sponge which eagerly soaks up information and that brain plasticity in young babies is at it's peak. What we must also realise however is that young babies need a secure, loving environment in order to utilise this inherent neuroplasticity.

In evolutionary terms, babies have not changed a great deal over the last 50,000 years. However, what we know about them has changed a great deal.

Astute observers of human development have always believed that the early years were critical to developing potential and this view is supported by evidence that children exposed to highly enriched environments develop bigger, superior brains, whilst children who are exposed to impoverished environments have smaller, less well developed brains. This is a view which began as early as the Greek philosopher Aristotle and was developed in the 11th century by the Persian philosopher, Ibn Sina (known as "Avicenna" in the West. He argued that the "human intellect at birth is rather like a tabula rasa, a pure potentiality that is actualised through education and experience of the world and consequently ' “comes to know" '

While this information is exciting and hopeful, especially to the parents of children whose development has been adversely affected by brain injury or some ather retarding factor, it also poses a danger, as some professionals and parents think it means we should apply intensive and exhaustive programmes of stimulation to teaching both brain injured and 'well' children in order to maximise their potential. Enter the billion-dollar baby industrial complex to sell us videos and flash cards to make our babies "smarter and the clinics offering eight to ten hour day – long programmes of developmental stimulation to children with developmental problems.

But a number of researchers have found clear evidence that some promotion of early learning tasks can actually interfere with later learning. Not only that, but that ensuring that the child has plenty of 'downtime' actually improves the learning process. This recent study by Ellenbogen et al demonstrates that relational memory -- the ability to make logical "big picture" inferences from disparate pieces of information, and an essential part of learning - is dependent on taking plenty of breaks and even more important, getting a good night's sleep. I believe that this is where other rehabilitation centres have it worng and where Snowdrop have it right in relation to the programmes of developmental stimulation we provide for brain injured children.

So here's the dilemma: We know we're supposed to be doing something to take advantage of the early years of brain development, but what? The answers to this query may be simpler than we think. They require only the simplest understanding of how babies operate.

First, babies are wired for relationships. To paraphrase the great Russian psychologist Lev Vygotsky, everything children need to know comes to them through relationships which provide interaction with more skilled partners, relationships that mean something to them personally. From birth, they use their emerging skills to seek out those they can learn to trust. They flourish when they know they are secure. They fall apart and under-perform when they are stressed. Their behaviour is organised and meaningful. They communicate clearly when stressed if we will but pay attention to their cues. When their needs are met, they snuggle, coo and sleep. When they feel overwhelmed, they fuss, turn red and lose motor coordination.

So babies need to be cared for by their parents and grandparents and other caregivers in a way that "listens" to what they tell us with their behaviour. Responsive care-giving gives children evidence that their needs matter. It teaches them to respect themselves and others.

They need to be cared for by people who are emotionally available to them. They need to see a smile reflect their own and a look of concern in someone's face when they cry. When they make attempts at language, they need to be heard and responded to by someone who really wants to know what they have to say. They need opportunities to play with other children and figure out what works in human interaction. They need some freedom to choose their own play activities and interact with others in their own comfortable style.

When children are confident in their safety and acceptance, they can relax and learn. According to Bjorklund and other evolutionary psychologists, learning is inhibited by fear and anxiety but facilitated by security and the opportunity to choose. Children are born learning as a natural response to their interesting world. They only need our interest and support. We adults serve as guides to help them find their way.

Anyone wanting more information on Snowdrop's work should email, or go to our website at

Friday, 21 October 2011

The Brains of People with Autism Develop More Slowly.

Yet again we see that some types of autism are clearly linked to the development of abnormal wiring patterns in the brain.  We know that the wiring pattern is largely determined by two factors, - either genetic expression, or when brain injury forces the brain to alter the normal wiring pattern.  What we also know is that environmental stimulation is the most powerful influence on that wiring pattern, which is why Snowdrop provides programmes of neurodevelopmental stimulation, which increases the normal environmental stimulus in order to try to influence the brain not to adopt an abnormal wiring pattern.

With thanks from the University of Claifornia.
Researchers at UCLA have found a possible explanation for why autistic children act and think differently than their peers. For the first time, they’ve shown that the connections between brain regions that are important for language and social skills grow much more slowly in boys with autism than in non-autistic children.
Reporting in the current on-line edition of the journal Human Brain Mapping, senior author Jennifer G. Levitt, a professor of psychiatry at the Semel Institute for Neuroscience and Human Behaviour at UCLA; first author Xua Hua, a UCLA post-doctoral researcher; and colleagues found aberrant growth rates in areas of the brain implicated in the social impairment, communication deficits and repetitive behaviours that characterize autism.
Autism is thought to affect one in 110 children in the U.S., and many experts believe the numbers are growing. Despite its prevalence, little is known about the disorder, and no cure has been discovered.
Normally, as children grow into teenagers, the brain undergoes major changes. This highly dynamic process depends on the creation of new connections, called white matter, and the elimination, or “pruning,” of unused brain cells, called gray matter. As a result, our brains work out the ideal and most efficient ways to understand and respond to the world around us.
Although most children with autism are diagnosed before they are 3 years old, this new study suggests that delays in brain development continue into adolescence.
“Because the brain of a child with autism develops more slowly during this critical period of life, these children may have an especially difficult time struggling to establish personal identity, develop social interactions and refine emotional skills,” Hua said. “This new knowledge may help to explain some of the symptoms of autism and could improve future treatment options.”
The researchers used a type of brain-imaging scan called a T1-weighted MRI, which can map structural changes during brain development. To study how the brains of boys with autism changed over time, they scanned 13 boys diagnosed with autism and a control group of seven non-autistic boys on two separate occasions. The boys ranged in age from 6 to 14 at the time of the first scan; on average, they were scanned again approximately three years later.
By scanning the boys twice, the scientists were able to create a detailed picture of how the brain changes during this critical period of development.
Besides seeing that the white-matter connections between those brain regions that are important for language and social skills were growing much slower in the boys with autism, they found a second anomaly: In two areas of the brain — the putamen, which is involved in learning, and the anterior cingulate, which helps regulate both cognitive and emotional processing — unused cells were not properly pruned away.
“Together, this creates unusual brain circuits, with cells that are overly connected to their close neighbours and under-connected to important cells further away, making it difficult for the brain to process information in a normal way,” Hua said.
“The brain regions where growth rates were found to be the most altered were associated with the problems autistic children most often struggle with — social impairment, communication deficits and repetitive behaviour,” she added.
Future studies using alternative neuroscience techniques should attempt to identify the source of this white-matter impairment, the researchers said.
“This study provides a new understanding of how the brains of children with autism are growing and developing in a unique way,” Levitt said. “Brain imaging could be used to determine if treatments are successful at addressing the biological difference. The delayed brain growth in autism may also suggest a different approach for educational intervention in adolescent and adult patients, since we now know their brains are wired differently to perceive information.”

Wednesday, 19 October 2011

UCLA Study Demonstrates the Brain's Ability to Reorganise.

Thanks to 'Scienceblog' for this report, which again clearly demonstrates just how plastic the brain actually is. It is this inherent plasticity that Snowdrop aims to direct in our programmes of rehabilitation for brain injured children.

Visually impaired people appear to be fearless, navigating busy sidewalks and crosswalks, safely finding their way using nothing more than a cane as a guide. The reason they can do this, researchers suggest, is that in at least some circumstances, blindness can heighten other senses, helping individuals adapt.

Now scientists from the UCLA Department of Neurology have confirmed that blindness causes structural changes in the brain, indicating that the brain may reorganize itself functionally in order to adapt to a loss in sensory input.

Reporting in the January issue of the journal NeuroImage (currently online), Natasha Leporé, a postgraduate researcher at UCLA's Laboratory of Neuro Imaging, and colleagues found that visual regions of the brain were smaller in volume in blind individuals than in sighted ones. However, for non-visual areas, the trend was reversed -- they grew larger in the blind. This, the researchers say, suggests that the brains of blind individuals are compensating for the reduced volume in areas normally devoted to vision.

"This study shows the exceptional plasticity of the brain and its ability to reorganize itself after a major input -- in this case, vision -- is lost," said Leporé. "In other words, it appears the brain will attempt to compensate for the fact that a person can no longer see, and this is particularly true for those who are blind since early infancy, a developmental period in which the brain is much more plastic and modifiable than it is in adulthood."

Researchers used an extremely sensitive type of brain imaging called tensor-based morphometry, which can detect very subtle changes in brain volume, to examine the brains of three different groups: those who lost their sight before the age of 5; those who lost their sight after 14; and a control group of sighted individuals. Comparing the two groups of blind individuals, the researchers found that loss and gain of brain matter depended heavily on when the blindness occurred.

Only the early-blind group differed significantly from the control group in an area of the brain's corpus callosum that aids in the transmission of visual information between the two hemispheres of the brain. The researchers suggest this may be because of the reduced amount of myelination in the absence of visual input. Myelin, the fatty sheaf that surrounds nerves and allows for fast communication, develops rapidly in the very young. When the onset of blindness occurs in adolescence or later, the growth of myelin is already relatively complete, so the structure of the corpus callosum may not be strongly influenced by the loss of visual input.

In both blind groups, however, the researchers found significant enlargement in areas of the brain not responsible for vision. For example, the frontal lobes, which are involved with, among other things, working memory, were found to be abnormally enlarged, perhaps offering an anatomical foundation for some of blind individuals' enhanced skills.

Previous studies have found that when walking down a corridor with windows, the blind are adept at detecting the windows' presence because they can feel subtle changes in temperature and distinguish between the auditory echoes caused by walls and windows.

Leporé noted that scientists and others have long been curious about whether or not blind individuals compensated for their lack of vision by developing greater abilities in their remaining senses. For example, the 18th-century French philosopher Denis Diderot wrote of his amazement with some of the abilities shown by blind individuals, in particular a blind mathematician who could distinguish real from fake coins just by touching them.

But it wasn't until the early 1990s that the suspicions of science began to be confirmed with the development of neuroimaging tools.

"That allowed researchers to probe inside the brain in a non-invasive manner, yielding insights into the impressive adaptive capacity of the brain to reorganize itself following injury or sensory deprivation," Leporé said.

Other authors included Caroline Brun, Yi-Yu Chou, Agatha D. Lee, Sarah K. Madsen, Arthur W. Toga and Paul M. Thompson, all of UCLA, and Franco Leporé, Madeleine Fortin, Frédéric Gougoux, Maryse Lassonde and Patrice Voss, of the University of Montreal.

This study was supported by the Canadian Institutes of Health Research, the Canada Research Chairs Program, the National Institute on Aging, the National Library of Medicine, the National Institute of Biomedical Imaging and Bioengineering, the National Center for Research Resources, the National Institute for Child Health and Development, and a grant from the National Institutes of Health.
The researchers report no conflicts of interest.

The UCLA Laboratory of Neuro Imaging, which seeks to improve understanding of the brain in health and disease, is a leader in the development of advanced computational algorithms and scientific approaches for the comprehensive and quantitative mapping of brain structure and function. The laboratory is part of the UCLA Department of Neurology, which encompasses more than a dozen research, clinical and teaching programs. The department has ranked No. 1 among its peers nationwide in National Institutes of Health funding for the last seven years

Sunday, 9 October 2011

Deficits in the reward system of the brains of children with ADHD found.

This is a very interesting study, with one elementary mistake! It was thought for years that the dopaminergic system was responsible for reward, - it isn't, but people, including scientists who should know better keep calling it so! The mesocorticolimbic system, which is a primary dopamine pathway, involving the stratium and the accumbens produces dopamine, but that dopamine does not produce 'reward' it produces 'desire' or what we would term 'craving.' - This 'desire' is the basis of addiction. What happens when this pathway is stimulated is that associated systems which produce opioids, - the brain's own heroin, are triggered to release those opioids, which is where the 'reward' comes in. However after a while, opioid production begins to fall and so we have desire without pleasure or reward! This is why addicts need more and more of a drug to feel the reward - to release the opioids! It is also why many addicts feel the craving to take drugs, but don't get pleasure from it! Anyway, it seems that this system might be undersensitive in some children who have ADHD and this research might lead to more effective treatments.   Indeed at Snowdrop, we use several techniques with children who have ADHD, which directly target these neural systems.


The underlying causes of Attention Deficit Hyperactivity Disorder (ADHD) have yet to be well characterized. But a new study utilizing brain imaging has found an abnormality in the pathway responsible for the motivation/reward system in patients with ADHD. The finding may lead to more effective treatments for the condition as well as a greater understanding of ADHD behavior.

A hallmark of ADHD is lack of attention. Especially seen in the classroom, both children and adults with the disorder lack the ability to focus for extended periods of time. Scientists suspected the symptom was due to a deficit in motivation and reward system--a process which can hone focus with the understanding that a reward (or at least not a punishment) will be given if successful.

Studying that pathway is a difficult task. It relies on the chemical dopamine, which can be easily affected by ADHD treatment or drug abuse which is common in adult ADHD sufferers. Tests to this point have been relatively small, but a push by lead author Nora Volkow, Director of the National Institute on Drug Abuse, finally saw a sizable cohort of participants investigated.

53 adults with ADHD who had never received treatment were subjected to a PET scan along with 44 healthy controls. Researchers looked at both ends of the dopamine pathway--"dopamine receptors, to which the chemical messenger binds to propagate the "reward" signal, and dopamine transporters, which take up and recycle excess dopamine after the signal is sent."

The study showed those with ADHD had lower levels of both receptors and transporters. This was especially clear in the acumbens and midbrain, both of which are regions important to the motivation/reward process.

Understanding the deficit in dopamine can help change the way ADHD patients interact with the world. Volkow stated, "[The pathway's] involvement in ADHD supports the use of interventions to enhance the appeal and relevance of school and work tasks to improve performance."

Though the dopamine problems have not been a solid fact until this moment, the medication that has been used for decades were on the right track. "Our results also support the continued use of stimulant medications — the most common pharmacological treatment for ADHD — which have been shown to increase attention to cognitive tasks by elevating brain dopamine," Volkow said.

The team also hopes that this study will help adults with ADHD who tend towards drug abuse and obesity. The lack of dopamine makes the rewards system difficult to trigger, so overeating and over use of stimulant drugs may be seen as a dangerous form of compensation, an unconscious move to help bolster the feeling of reward. Developing therapies that help attenuate the need for drugs and binge eating will greatly improve quality of life. Thanks to the examiner

Monday, 26 September 2011

Sensory Processing Difficulties.

Although the sensory system is very complex and its correct development is vital, this post is only able to provide a brief guide. I will however highlight the major problems, which children who suffer brain injury face in the developmental areas of vision, hearing and touch.

We take in information about our environment through our senses. This is something, which we cannot help but do. The amount of sensory information our brains are processing at any one moment is phenomenal. As I sit here typing for instance, I am aware of several sensory stimuli. Visually I see the computer keyboard, with the letters printed on the keys; I can see my hands, the desk, the computer screen and more. In my peripheral vision, I am aware of the window, my dog, the sofa and other items in the room. Auditorially (hearing), I can hear the kettle beginning to boil, I hear my fingers tapping on the keys of the keyboard and I hear my cat mewing. In terms of touch (tactility), I can feel the keys of the keyboard; feel the wooden floor beneath my feet etc. These are merely the things of which I am aware and these sensory stimuli are all being processed simultaneously, in a fraction of a second.

As an example of this processing, consider the complexity of my typing this text, which hopefully you are reading with enjoyment! The front part of my brain (the frontal cortex) is sending out messages to the motor parts of my brain (the motor cortex), which control my hands,
instructing it which keys on the keyboard I need to hit next in order for the written words on this page to make sense. The motor cortex then instructs the hands to move in order to hit those keys. Parts of the brain known as the basal ganglia and cerebellum then become involved in
order to attempt to execute the necessary movements of the hands in a fluent and accurate manner. When the movements have been executed, feedback signals are then sent back to the frontal cortex, via the ‘cerebellum’ and ‘basal ganglia’ to inform it how successful the hands
were at hitting the correct keys on the keyboard and whether the movements were accurate and fluent. If necessary, the frontal cortex then issues new instructions, to correct any errors.

In a healthy, uninjured brain, this grossly oversimplified description of events all takes place within a fraction of a second whilst the brain simultaneously takes care of many other complex tasks. It is a phenomenal feat.

Also, consider how the brain decodes the various sounds we call language and how it regulates its own attention. Imagine you are sitting in your lounge holding a conversation with a visiting friend. There you are, happily chatting away; - you are attending to your friend’s voice
so that your auditory system is able to process the constant stream of noise, which we call speech. Your brain is able to take this constant stream of sound, break it down into recognisable chunks and attribute meaning to it so that you understand what it is your friend is saying. At
the same time, your brain is tuning out extraneous sounds in the background, such as traffic passing outside your window, so that you are able to focus on the task at hand. Your brain does all of this and much more, (this again is actually a gross oversimplification), with the
minimum of effort, without you even being conscious of the processes involved.

Now consider a brain, which is not healthy; - a brain, which has suffered injury and try to imagine the chaos, which might ensue for a child whose sensory processing system has been impaired. Imagine this child’s ability to ‘tune out’ noises, which he does not wish to pay attention to, has been impaired. What havoc would that child experience?

I believe that the sensory problems, which are faced by brain-injured children can be assigned to five categories, which we shall discuss later. Fundamentally it seems to me that many brain-injured children experience difficulties in correctly modulating incoming sensory information, their sensory system processing incoming stimuli in a distorted manner.’ I have applied these theories (which are all supported by evidence), to differing patterns of brain-injury: - And there are many patterns of brain-injury to which they can be applied! A particular pattern rarely has absolute, identifiable boundaries and symptoms from another. There is often a great deal of ‘overlap’ in the symptoms which differing patterns of brain-injury display. Allow me to explain.

A good example is my proposition that cerebral palsy, autism and ADHD are not distinct separable conditions, but are a continuum; they are overlapping expressions of brain–injury and consequently it is possible to have some symptoms of autism, or ADHD within what is termed cerebral palsy. It is also possible to have some symptoms of cerebral palsy within what is known as autism or ADHD.

I can already hear the howls of indignation over the fact that I have referred to autism as brain-injury! Have you not seen all the recent evidence, they will say, which points to the cause of autism as being genetic? Yes, I have seen this evidence and I accept that some forms
of autism have genetic causes. However, I have seen too many children with brain-injuries, who display amongst their repertoire of symptoms, many autistic qualities. Thus, I cannot ignore the fact that some forms of autism also have environmental causes. In other words, they are produced by brain-injury. I am also aware that genes can only express themselves in the correct environmental conditions!

It was Delacato in the 1970’s, who first claimed that children suffer distortions of sensory processing, separating them into the categories of ‘hyper-sensory,’ hypo-sensory’ and white noise. I have managed to identify five categories of sensory difficulties, which children display,
(other researchers may find more!) and I see these as symptoms of a malfunctioning ‘tuning mechanism’ in the brain. This ‘tuning’ mechanism is the structure which enables us to ‘tune out’ background interference when we wish to selectively attend to something in particular; it also enables us to ‘tune in’ to another stimulus when we are attending to something completely different. It is the same mechanism of the brain, which allows us to listen to what our friend is saying to us, even when we are standing in the midst of heavy traffic on a busy road. It is this mechanism that allows us, even though we are in conversation in a crowded room, to hear our name being spoken by someone else across that room. It is this mechanism, which allows a mother to sleep though various loud, night-time noises such as her husband snoring, or an aeroplane passing overhead and yet the instant her new baby stirs, she is woken. It is a remarkable feature of the human brain and it seems to be the responsibility of three structures operating cooperatively; - these are the ascending reticular activating formation, the thalamus and the limbic system.

Having made such a bold claim, allow me to furnish you with the evidence to support it. The three structures just mentioned receive sensory information from the sense organs and relay the information to specific areas of the cortex. The thalamus in particular is responsible
for controlling the general excitability of the cortex (whether that excitability tunes the cortex up to be overexcited, tunes it down to be under excited, or tunes it inwardly to selectively attend to it’s own internal sensory world.) (Carlson, 2007). The performance of these neurological structures, or in the case of our children, their distorted performance seems to be at the root of the sensory problems our children face.

I would label the five categories of sensory distortion, which I have witnessed in brain-injured children as follows: -

1. Sensory over-amplification. The particular sensory modality, (vision, hearing, touch, etc) can become oversensitive to stimuli from the environment. It is my belief that in this case, the thalamus, limbic system and reticular formation, which are acting as the brain’s ‘tuning
system’ are malfunctioning and are not effectively regulating the level of incoming sensory stimuli. Indeed, in this case they would appear to be acting to over-excite the cortex, which would have the effect of amplifying the sensory stimuli. This could possibly cause the child to
overreact, or to withdraw into himself as a defensive strategy from a world, which in sensory terms is simply overwhelming.

2. Sensory under-amplification. The particular sensory modality can appear to become under sensitive to incoming stimuli from the environment. In this case, I believe the thalamus and other two brain structures, acting as the tuning system, are acting to under-excite the cortex, which is having the effect of appearing to dampen down incoming sensory stimuli. This could influence the child to act as though he cannot see, hear or feel; - he may be deficient in this way, in one or more sensory modalities.

3. Internally focussed sensory tuning. In this case, the particular sensory modality appears to be ‘inwardly tuned.’. In this case the three brain structures, acting as the brain’s tuning system are exciting the cortex to attend to sensory information of the sensory system’s own making, or from within the child’s own body. Consequently, the child may have difficulties perceiving the ‘outside’ sensory world through this haze of internal stimulation. We see this effect ourselves in the visual aura of a migraine, or when we have 'pins and needles.'

4. Wide spectrum tuning. In this case, the three neurological structures are exciting the cortex and attempting to tune its attention to many incoming stimuli simultaneously. They seem unable to filter out background noise, sights, etc in order to allow the child to focus on one aspect of the environment. For this child, the world is absolute chaos and again, he often withdraws into himself.

5. Narrow spectrum tuning. In this case, the neurological structures are only exciting the cortex selectively, allowing the cortex to attend to limited, isolated sensory stimuli. This child may often seem ‘over-focussed’ on one particular aspect of his environment. He can for instance, become intensely interested with a spinning top or the particular features of one toy and will not play with anything else, to the point of seeming obsession. For this child, it appears his sensory tuning system is focussed too narrowly and he cannot spread his attention to incorporate several features of his environment simultaneously.

Can these problems be addressed? Yes they can. As part of its programme for children with sensory processing issues, Snowdrop creates an individually tailored 'adapted sensory environment' for the child to encourage his sensory system to begin to process stimuli on a much more normal level. Are we experiencing success with children who have sensory processing problems? Yes we are.

Anyone requiring more information should contact


Beck, A. T., and Guthrie, T. (1956). Psychological significance of visual auras: Study of three cases with brain damage and seizures. Psychosomatic Medicin, Vol XVIII, no 2,

Carlson, N. R. (2007). Physiology of Behavior. London. Allyn and Bacon.

Haist, F., Adamo, M., Westerfield, W., Courchesne,E., and Townsend, J., (2005). The functional neuroanatomy of spatial attention in autistic spectrum disorder. Developmental Neuropsychology, 27, 3, 425-458.

Mulleners, W. M., Chronicle, E. P., Palmer, J, E., Koehler, P. J., and Vredeveld, J. W. (2001), Suppression of perception in migraine: Evidence for reduced inhibition in the visual cortex, Neurology, January 23, 2001; 56(2): 178 - 183.

Yang, T., and Maunsell, J. H. R.. (2004) The effect of perceptual learning on neuronal responses in monkey visual area V4. Journal of Neuroscience, 24, 1617 – 1626.