Snowdrop

The more we repeat something, the better we get at it; this much is uncontroversial. But that doesn’t mean it isn’t worth examining. The connection between repeating an action or a skill and then improving because of that repetition is a concept that is so natural and intuitive, so well accepted as common knowledge, that we often fail to appreciate the fascinating mechanics behind the process of skill acquisition. It follows the old adage, 'practice makes perfect!'

On the most basic level, learning a new skill or improving a skill involves changes in the brain. There are a few different ways that our brains adapt to picking up new skills and changing environmental conditions. The first involves a rewiring of the networks of neurons in the brain. Each skill or action that a child performs involves the activation of neural pathways. In Norman Doidge’s book on neuroplasticity, The Brain That Changes Itself, Dr. Alvaro Pascual-Leone has a beautiful little analogy for the way that these pathways relate to skilled performance (Page 209):

"The plastic brain is like a snowy hill in winter. Aspects of that hill–the slope, the rocks, the consistency of the snow–are, like our genes, a given. When we slide down on a sled, we can steer it and will end up at the bottom of the hill by following a path determined both by how we steer and the characteristics of the hill. Where exactly we will end up is hard to predict because there are so many factors in play." “But,” Pascual-Leone says, “what will definitely happen the second time you take the slope down is that you will more likely than not find yourself somewhere or another that is related to the path you took the first time. It won’t be exactly that path, but it will be closer to that one than any other. And if you spend your entire afternoon sledding down, walking up, sledding down, at the end you will have some paths that have been used a lot, some that have been used very little.”

Every action we perform, every new skill we pick up, involves beating down and refining a kind of neural trail. We are making real changes in the brain. And our brains are remarkably efficient to change in response to training. In one study, video game players who played the dark, fast-moving action-based game Call of Duty for 9 weeks were not only better at the game, but were able to see significantly more shades of gray, post-training, than a group who played a simulation strategy game that did not exercise those skills.

Over a longer time span, it is also possible to see significant structural changes in the brain. For example, the brain area associated with motor control of the right index finger in blind subjects who are braille readers has been found to be significantly larger than that of sighted individuals. Similarly, a famous study of london cabbies, famous for their ability to navigate the twisting streets of the city, found that they had greater brain volume in the hippocampus, a structure heavily involved in both memory and spatial navigation, than bus drivers who followed a predefined route every day.

With respect to the brains of children who have developmental disabilities, the brain injuries or abnormalities they suffer might slow that response to training down a little, but the response is still possible.

Evidence for neuroplasticity abounds, - from the structural differences which have been found between experienced athletes and novices, through to the Chinese study of expert divers which found increased gray matter volume in brain areas associated with skilled motor control. Along the same lines, an Australian study of skilled racket-sport players found that brain areas associated with the racket arm were larger than in a matched group of non-athletes. The evidence is irrefutable!

The overarching theme here is that the brain is malleable–it changes with training. It is an interesting concept to keep in mind, especially with respect to brain injured children and it is the overarching principle of the Snowdrop programme.

It’s easy and natural to think about training in terms of muscles, the body and physical skills. But every new skill that a child learns is accompanied also by neural changes that may be harder to see, but are equally important.

If you would like more information about the Snowdrop programme, just visit our main website on http://www.snowdrop.cc - email us at snowdrop_cdc@btinternet.com or call on 01884 38447

A baby's brain has the capacity to grow at a phenomenal rate. At birth it is only one quarter of its adult size, but by three ears of age it will be 80% the size of an adult brain. At birth it is one of the only organs which has not yet fully developed and it is sensory stimulation derived from environmental experience which drives this growth and consequently which drives the development of the child.

Billions of neurons are created throughout the primary stages of foetal development and through birth. Indeed at birth, the only brain structure which is developed to anything like its mature form is the lower brainstem. This part of the brain controls the primitive reflexes and vital functions such as respiration, cardiovascular function, etc. Immediately after birth, baby's higher brain regions begin to make billions of connections between neurons. These connections, called synapses, are used to transmit information based upon sensory experience. Stimulation through the senses of touch, hearing, vision, smell and taste, in addition to vestibular and proprioceptive experience, directly influence these neurons and help in establishing these connections.

The more frequently the neuron connections are used, the stronger and more efficient the new connections become, this is a phenomenon known as 'long term potentiation.' If some of the neural pathways are not used, they become weak and are pruned, (this is known as 'long term depression.'). This is why the repetition of the activities within a Snowdrop programme of developmental stimulation are so important.

We know that babies who are born into an impoverished environment do not develop the rich connection between neurons which develop in other babies. Children who are neglected, exposed to stress, trauma, abuse, have negative experiences which can have a detrimental effect upon brain growth and development. It has been shown, that those infants or children who are not exposed to adequate sensory stimuli because of these factors can develop brains which are smaller then those who have had those "good" sensory experiences.

So, you might ask, how does this apply to children who have suffered brain injury? Well, what effect does brain injury have on a child? It acts as a barrier between the child and his environment. It does so because it prevents the child from interacting with his sensory environment. Because he is unable to gain the necessary sensory experience from his environment, due to the 'roadblock' of the injury, or because the injury is acting to distort incoming sensory information in some way, the brain is unable to make the same number, or quality of connection as it would otherwise have done and as a consequence baby's developmental processes are either stopped, slowed, or distorted.

Is there anything which an be done to rectify this situation? Well yes, at Snowdrop we believe there is. We take children who have suffered brain injuries and as a consequence are experiencing developmental difficulties and we provide them with an 'adapted sensory environment.' Where the injury is acting as a barrier between the child and his sensory environment, the adapted environment acts to amplify the sensory stimulation to which the child is exposed, breaking through the barrier and giving the child's brain the opportunity to form connections. Where the injury is acting to distort incoming sensory information, making the child hypersensitive, or unable to selectively tune in, or to mask sensory information, our adapted environment seeks to re-tune the neurological structures which are responsible for this. Again, in this way we encourage the brain to make the appropriate number and quality of connections and to consequently improve the developmental prospects of the child.

This is the basis of a Snowdrop developmental stimulation programme. Anyone interested in learning more about Snowdrop's work should email snowdrop_cdc@btinternet.com

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

There are two major types of autism, of which you have probably heard. Snowdrop provides treatment programmes for both. They are autism and Asperger’s syndrome. First let’s look at classical autism, how would we recognise it? Well, autism was first recognised in the mid 1940’s by a psychiatrist called Leo Kanner. He described a group of children, whom he was treating, who presented with some very unusual symptoms such as; - atypical social development, irregular development of communication and language, and recurring / repetitive and obsessional behaviour with aversion to novelty and refusal to accept change. His first thoughts were that they were suffering some sort of childhood psychiatric disorder.

At around the same time that Kanner was grappling with the problems of these children, a German scientist, Hans Asperger was caring for a group of children whose behaviour also seemed irregular. Asperger suggested that these children were suffering from what he termed ‘autistic psychopathy.’ These children experienced remarkably similar symptoms to the children described by Kanner, with a single exception. – Their language development was normal! There is still an ongoing debate as to whether autism and Asperger’s syndrome are separable conditions, or whether Asperger’s syndrome is merely a mild form of autism.

What is the cause of autism?

In the 1960s and 1970s there arose a theory that autism was caused by abnormal family relationships. This led on to the 'refrigerator mother' theory, which claimed that autism in the child was caused by cold, emotionless mothers! (Bettleheim, 1967). However the weight of evidence quickly put this theory to bed as evidence was found to support the idea that the real cause was to be found in abnormalities in the brain. This evidence was quickly followed by findings, which clearly demonstrated that the EEGs of children with autism were, in many cases, atypical and the fact that a large proportion of autistic children also suffered from epilepsy.

From this time, autism has been looked upon as a disorder, which develops as a consequence of abnormal brain development. Recently, evidence has shown that in some cases, the abnormal brain development may be caused by specific genes.

However, we should not forget that genes can only express themselves if the appropriate environmental conditions exist for them to do so and consequently, we should not rule out additional, environmental causes for autism. We should not forget that autism can also be caused by brain-injury, that an insult to the brain can produce the same effects as can abnormal development of the brain, which may have been caused by genetic and other environmental factors. I have seen too many children who have suffered oxygen starvation at birth, who have gone on to display symptoms of autism or Asperger’s syndrome. So, it is my view that autism can also be caused by brain-injury.

Difficulty in socialisation is an area, which characterises the entire concept of autism. To many parents the lack of willingness on the part of their child to share in normal social interaction is of paramount concern. One parent to whom I spoke described her child as having social amnesia.

The social impairments, which typify autism are exact, that is, the child’s social conduct is not atypical universally. It is incorrect to declare, as some do, that children who are autistic, have a deficiency in their level of curiosity in other people. What they are deficient in is the proficiency for conveying or exploiting that interest. Uninjured babies are focused on faces and voices, whereas autistic children do not seem to be able to do so. They do not turn automatically to the sound of a voice, or fix their eyes on a parent’s face, and may actively avoid making eye contact. In many cases, this is due to sensory impairments, which can block the development of these social skills.

The importance of play

One of the first signs that a toddler or preschooler has autism is their atypical play. Even the brightest youngsters with autism display highly unusual patterns of play. Classically, many children with autism over-focus their attention on visual aspects of specific toys, or noises, which their toys make. Many researchers see this as a lack of imagination in autistic individuals and it is true to say that many children with autism do lack imagination and spontaneity within their behaviour, preferring to stick rigidly to routines with which they feel comfortable and safe. What I claim though, is that many times, these problems are created as a result of the distortions of sensory processing, which they suffer. There is now evidence that the abnormal behavioural patterns produced by many children with autism and Asperger's syndrome are a response to such distortions of sensory processing. Researchers writing in the Jounal of Autism and Developmental Disorders found that young children with autistic spectrum disorders not only experienced more tactile and other sensory sensitivities, especially difficulties with auditory filtering than children with other developmental disabilities, but that their sensory difficulties were significantly correlated with their stereotyped interests and behaviours. These hard scientific findings totally support Snowdrop's approach to treating the distortions of sensory processing experienced by children with autism. More information on such sensory processing difficulties are available in our book, 'Autism.'

Checklist of Behaviours associated with autism.

• Failure to make eye contact.
• Difficulty in sharing attention with anyone.
• Difficulty in communicating with others
• Avoids interaction with others
• Failure to engage in 'pretend' play
• Lacks understanding of the emotions and / or intentions of others.
• Avoids physical contact
• Seems disconnected from the environment.
• Children with autism also suffer sensory distortions, which may cause them to display certain behaviours.
• Appear not to notice anything visually.
• Appears visually distracted as though he is looking at something which you cannot see.
• Appears visually obsessed with particular features of the environment.
• appears unable to 'switch' visual attention from one feature of the environment to another.
• Appears uncomfortable with the visual environment.
• Appears not to hear anything.
• Appears auditorily distracted as though listening to something which you cannot hear.
• Appears auditorially obsessed with particular sounds within the environment.
• Appears unable to 'switch' auditory attention from one sound within the environment to another.
• Appears uncomfortable with the auditory environment.
• Appears not to feel much sensation.
• Appears distracted by tactile stimuli of which you are not aware.
• Appears obsessed with particular tactile sensations within the environment.
• Appears unable to 'switch' tactile attention from one sensation to another.
• Appears uncomfortable with the tactile environment.

Treatment for autism.

Many of the checklist of behaviours above could feasibly have their origins in distorted sensory processing in the brain. I believe that Snowdrop's neuro - cognitive approach with its emphasis upon re-tuning the neurological structures, which are causing sensory / perceptual distortions for the child is the best approach to treatment. Anyone wanting more information should email snowdrop_cdc@btinternet.com or visit our website at http://www.snowdropcerebralpalsyandautism.com.

You can also purchase my book, ‘Autism.’ By clicking here

All visual information which enters the human brain is processed by a part of the brain known as the visual cortex. (otherwise known as the occipital cortex or occipital lobe). The visual cortex is part of the outermost layer of the brain, the cortex, and is located at the lower rear of the brain. The visual cortex obtains its information from neural pathways that extend all the way through the brain from the eyeballs. This visual pathway first passes through a stopover point in the middle of the brain, at a structure called the thalamus at an almond-like lump of brain cells known as the Lateral Geniculate Nucleus, (which are responsible for controlling the constriction and dilation of the pupils), or LGN. From there the visual pathway continues to the primary visual cortex. So when you see me test your child’s pupillary reactions, I am looking for injury between the eye and the lateral geniculate nuclei!

The visual cortex is composed of five areas, which are labelled by neuroscientists as V1, V2, V3, V4, and V5. V1 is also known as the striate cortex because of its striped appearance. This is by far the largest and most important area of the visual cortex. It is sometimes called the primary visual cortex. The other visual areas are referred to as extrastriate cortex. V1 is one of the most extensively studied and understood areas of the human brain.

The primary visual cortex is an approximately 0.07 inch (2 mm) thick layer of brain with about the area of an index card. Because it is scrunched up, its volume is only a few cubic centimeters. The neurons in V1 are organized on both the local and global level, with horizontal and vertical organization schemes. This part of the visual cortex is tuned to pick up colour, shape, size, motion, orientation, and other visual aspects, which are more subtle. The manner in which this part of the brain is organised means that there are certain cells in the primary visual cortex, which are activated by the presence of colour A, others activated by colour B, and so on.

How does the visual pathway operate?

Raw sensory data comes from the eyes as an ensemble of nerve firings called a retinotopic map. The first series of neurons are designed to perform relatively elementary analyses of sensory data — a collection of neurons designed to detect vertical lines might activate when a critical threshold of visual "pixels" prove to be configured in a vertical pattern. Higher-level processors make their "decisions" based on preprocessed data from other neurons; for example, a collection of neurons designed to detect the velocity of an object might be dependent upon information from neurons designed to detect objects as separate entities from their backgrounds.

What happens when the visual pathway or visual cortex is damaged?

25% of the human cortex is devoted to processing visual information. With that huge amount of cortex devoted to just one sense, the chances are that any diffuse brain-injury will knock out a significant portion of brain cells dedicated to vision. Is it surprising therefore, that so many brain-injured children experience visual difficulties? Let us take a look at some ways in which those visual difficulties can express themselves. These are some of the distortions of visual processing which have been reported.

Wide spectrum tuning

Imagine a situation where everything within your visual field is competing equally for your attention. In this situation, you would not have the ability to ‘tune out’ some elements of your visual field and selectively attend to one or two elements alone. Your brain would be trying to process everything you could see AT THE SAME TIME! The result is chaos for the children who suffer this problem, causing anxiety and high stress. This type of visual oversensitivity was reported by Bruno (2006), who endured brain-injury through a car accident. She described how brain-injury propelled her into a world of psychological perplexity, double vision and incapacitating visual and auditory oversensitivity

Many parents report that the visual world is just too much for their children, indeed children have themselves reported a situation where they are unable to focus on a single visual stimulus. Indeed, it seems that apart from inappropriate activity from the brain’s tuning mechanism, damage to parts of the brain’s parietal lobes can lead to this type of visual difficulty. A child may appear to be competently scanning his visual environment, but cannot attend to particular visual features of that environment! (Carlson, 2007)

The child who suffers this problem will only relax if placed in an under-stimulating, darkened environment. He is only truly at peace when he is asleep. He rarely makes eye-contact, because he has difficulty attending to the single visual stimulus of the eyes, which are competing with other visual stimuli in the environment (does this ring any bells for parents of children diagnosed with autism?). Everything is competing for his visual attention simultaneously, so he finds it impossible to focus on any one person or object. As a consequence of his inability to cope with his visual world, the child with this problem can, in a desperate measure to protect his immature, overwhelmed sensory system, ‘withdraw’ into himself.

Narrow spectrum tuning.

In this situation, the child appears not to be aware of most of his visual environment, singling out one object and almost completely focussing his attention on it. This ‘over-focussed’ attention can appear to be obsessive behaviour to the outsider. This child plays with one toy and one toy only because he is focussed upon specific features of it. He may be fascinated with movement, such as a spinning top, or wheels moving and will spend hours just looking at this. Rizzo & Robin, (1990), describe this situation perfectly. Apart from a malfunctioning neurological tuning mechanism, injuries to the parietal / occipital lobes of both hemispheres of the brain can also create a situation whereby individuals can only pay visual attention to one object at a time. This is known as Balint’s syndrome and it is possible that some of our children who experience ‘narrow spectrum tuning’ difficulties, will have injuries in this part of the brain. However, there is also a convincing developmental explanation for ‘narrow spectrum tuning.’ Young babies have difficulty in shifting their attention, - this is well known and is a developmental phase. Infants who are less than four months of age will sometimes stare at an attractive object, being unable to shift their gaze. Occasionally this inability to shift their visual attention will make them cry out in distress, (Johnson et al, 1991). It could very well be that some children, who have ‘narrow spectrum tuning’ difficulties, never emerge from this phase of visual development.

Over-amplification

This again is a type of visual oversensitivity whereby the sensory tuning system of the child is acting to amplify the visual information, which the eyes are taking in. The child, who suffers visual over-amplification problems, is the child who hates bright lights. He particularly dislikes sunny days and hates anything moving close to his eyes.

He may not concentrate on anything at all with his central vision, preferring to view things from the less threatening position of his peripheral vision. We, as healthy individuals are allowed a small insight into the way this child feels when we have a migraine attack and our vision becomes sensitive to bright lights. What is occurring both in migraine sufferers and with our brain-injured children is that specific inhibitory systems of the tuning system within the brain are not activated sufficiently, resulting in overstimulation in the visual cortex. (Mulleners et al, 2001).

Unfortunately, this is the visual world, which this child inhabits 24/7. This child will not make eye contact, but for different reasons to the child with wide spectrum tuning difficulties; - this child literally finds eye contact to be very threatening and will avoid the situation at all costs.

Under-amplification

In this situation, the sensory tuning system of the brain is simply not exciting the visual cortex sufficiently and so it is unable to process incoming sensory information. These children are sun–worshippers; they find bright lights and visually attractive displays to be absolutely fascinating. Children with this problem, if their motor control allows, can often be found waving their hands in front of their eyes in an attempt to self-stimulate their visual system.

Children showing under-amplification problems, like those displaying over-amplification difficulties can seem hard to reach, but for the opposite reason; - they are simply unaware of much of the visual world around them.

Internal tuning

In this phenomenon the visual system is tuned inwardly to visual phenomena, which it itself is creating. Again, it is possible to relate this to what happens to certain individuals who suffer from migraine. Many migraine sufferers, (including myself!), experience a ‘visual display’ prior to an attack, where all sorts of shapes and colours occlude the vision. Similarly, the visual system of some brain–injured children is capable of producing this effect. These children appear preoccupied with looking at something, which you cannot determine! They appear to be staring into the mid–distance and it is immensely difficult to break their concentration. As early as 1956, Beck and Guthrie were describing the internally generated visual phenomena experienced by individuals who had suffered brain-injuries, one describing seeing different coloured orbs in their visual field, floating up and down. (p. 6). Is it any wonder that some of our children are fixated upon this self – generated visual world?

Other visual problems

The development of vision and the child’s ability to use his visual skills in a meaningful way may be, as I have just described, distorted by brain-injury. Visual development therefore will most likely be stopped, or slowed to snail’s pace. Injury may interfere with the smooth operation of the visual pathways in the brain, or cause direct injury to the occipital cortex, - the processing centre for vision. Injuries such as these can take a terrible toll. They can take the visual ability of the child back to pre-birth stages, in some cases creating a neurological blindness. - This is a situation in which there is nothing at all wrong with the eyes, they are working as they should, but because of damage to the primary visual cortex and the fact that essential parts of the neural networks, which support visual ability have been damaged, the brain is simply unable to process what the eye can see.

I remember one little boy, whose parents came to me, who was totally unresponsive in visual terms. He did possess a pupillary light reflex, (his pupils dilated when in the dark and constricted when in the light). His doctors who had informed the parents that he was probably neurologically blind, were not doing anything to try to remedy the situation. It took the parents two years of patiently stimulating their son’s visual development under my direction, to bring his vision to a level where he would visually track an object across a room and visually explore his environment. The most moving moment however, was the first time he looked his mother in the eye and smiled. From there, I instituted further stimulation, which later culminated in the adoption of a reading programme. He made incredible progress!

Other visual problems, sustained by brain-injured children include visual field problems; - Each hemisphere of the brain is responsible for processing visual information from one half of the visual field, (the opposite side), so an injury to part of the occipital cortex in the right hemisphere of the brain can cause a visual deficit in the left visual field and injury to part of the left occipital cortex can cause deficits to the right visual field.

Another phenomenon, which can occur due to injury to the occipital cortex, is that the child may not notice movement within his visual environment. He may pay good visual attention to most aspects of his visual environment and yet fail to detect the sudden movement of an object close by.

Deficits in the ability to perceive colour (cerebral achromatopsia), may also be experienced due to brain-injury. Interestingly, this problem may occasionally be experienced in only one half of the visual field, if the injury to this part of the occipital cortex is only in one hemisphere. Patients with this type of injury in both hemispheres report their vision as being in black and white. (Heywood & Kentridge, 2003).

Having highlighted some of the major effects of brain-injury upon vision, we should now consider how vision develops in normal circumstances, because this is the developmental pathway, down which we wish to lead our children.

The path of visual development

When a child is born, his vision is already at a relatively sophisticated level. He can see quite well, although his vision is a little blurry and he cannot see as far or as clearly as you or I. He does have difficulty switching his focus from one point to another point at a different distance. He is however able to scan his visual field although at this point his eye movements are slow and disjointed.

By the time he is one month of age however, his eye movements are smooth and he is able to scan his visual field more effectively.

You may notice that a young baby may appear to have very big eyes in relation to the size of his head; - There is a very good reason for this. The eyes of a young baby are forming a massive number of complex attachments with the brain. If the eyes grew substantially after making those attachments, new nerve fibres, (axons) would have to be grown in order to constantly readjust the attachments between the growing eyes and the brain. This would mean that the brain would have to continually reorganise its structure as the eyes grew. Hence the eyes come ‘ready-made,’ full size!

At two months of age, baby is developing pattern discrimination and contrast sensitivity, although at this point, he prefers less complex patterns. (Such as preferring to look at a checkerboard with large squares, rather than one with small squares).

Infants are very attracted to looking at high-contrast edges and patterns. Large black and white patterns offer the maximum achievable contrast to the eye and consequently are most noticeable and eye-catching to babies.

By three months of age, baby is able to focus as well as an adult and at four months his pattern discrimination has developed to the point where he prefers to look at more complex patterns and is becoming interested in the internal detail within a shape.

At six to seven months of age, when he is starting to crawl, he is beginning to use his two eyes together and is developing an appreciation of the third dimension and depth perception (stereopsis). There is evidence that the specific neural networks, which are essential for the development of depth perception will not develop unless baby is provided the opportunity to scrutinise objects with both eyes. If baby’s eyes are not given practice in moving together properly, he may never develop fully functional depth perception, even if the eye movements are later rectified by surgery on the eye muscles .

There is also some evidence that it is crawling, which helps the development of depth perception by helping to mature the relevant areas of the brain and by affording the child, through movement, the opportunity he needs to use both eyes together properly. (Berk, 1997).

Vision continues to develop throughout the preschool years. It is essential that it does so, in order that there are continued improvements in eye/hand coordination and depth perception. There are many exercises, which can be carried out with brain-injured children to try to achieve these objectives.

One of the most important and enjoyable exercises to carry out with young children is to read to them. This encourages the development of robust visualisation proficiency as they "picture" the story in their minds. Just because a child has suffered brain-injury this is no reason to deprive him of this enjoyable activity. Although his vision, or hearing may be impaired to some degree, one never knows how much of the message is actually striking home; - so read to him!

By school age, the child’s visual acuity, (the level of fine discrimination of detail, which his vision will permit), is equal to that of an adult.

To what degree does the visual cortex have qualities of plasticity?

It was Payne and Lombar, (2002), who highlighted the plastic qualities of the visual cortex. They pointed out that the consequences of localised injury of the cerebral cortex in the brain of a child differ from the consequences elicited by corresponding damage to the brain of an adult.

“In the young brain, some distant neurons are more vulnerable to injury, whereas others survive and expand their projections to bypass damaged and degenerated structures. The net result is that visual processing can be retained. Experiments using reversible deactivation show that at least two highly localisable functions of normal visual cortex functioning are remapped across the cortical surface as a result of an early lesion of the primary visual cortex. Moreover, the redistribution of connections have spread the essential neural operations for vision from the visual parietal cortex to a normally functionally distinct type of cortex in the visual temporal system. Similar functional reorganizations can explain the retention and recovery of abilities following early lesions in other cerebral systems, and these other systems may respond well to emerging therapeutic strategies designed to enhance the sparing of functions.”

Which is why Snowdrop type programmes of developmental stimulation are so important!

If your child has visual problems which are caused by brain injury and you want to learn more about Snowdrop’s treatment, simply email snowdrop_cdc@btinternet.com

Further Reading.

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,

Berk, L. E. (1997). Child Development. (4th Edition) London. Boston. Allyn & Bacon.

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

Heywood, C. A. and Kentridge, R. W. (2003). Achromatopsia, color vision and cortex. Neurology clinics of North America. (21), 483-500.

Johnson, M. H., Posner, M. I., and Rothbart, M. K., (1991). Components of visual orienting in infancy: Contingnency learning, anticipatory looking and disengaging. Journal of Cognitive Neuroscience, 3, 335-344.

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.

Payne B, R. & Lomber S, G. Plasticity of the visual cortex after injury: what's different about the young brain? Neuroscientist. 2002 Apr;8(2):174-85.

Rizzo, M. and Robin, D. A. (1990). Simultanagnosia: A defect of sustained attention yields insights on visual information processing. Neurology, 40, 447-455.

The basal ganglia is a set of sructures, consisting of the caudate nucleus, putamen, nucleus accumbens, globus pallidus, substantia nigra, subthalamic nucleus and ventral stratium. These structures which are interconnected between the cortex, the thalamus and the brainstem, form the neural circuitry which is involved in an individual developing addiction. The key is the production of dopamine, which stimulates desire, or craving for a specific experience provided by a substance or activity.

The basal ganglia plays a role in motor function, cognitive processes, emotional processes and our ability to learn. It also provides inhibition to the thalamus, a part of the brain which mediates our sensory experiences. So, without this inhibitory role, one can imagine a thalamus in effect operating without its 'braking system' which might produce many of the sensory distortions we see in children who have brain injuries. It also acts as a 'braking system' for movement, which enables us for instance, to sit still. In order to sit still a 'brake' has to be placed on all other movements. Consequently injury at this level hampers the 'braking system' and we see children who cannot sit still and are in constant movement (athetosis, or athetoid cerebral palsy, or Parkinson's disease or Huntingdon's Chorea) and children whose sensory perception is distorted. Injury to this part of the brain also exhibits itself in many children, by retention of the primitive postural reflexes, as it is the role of the basal ganglia to suppress these in order to enable the child to move.

Children with basal ganglia/internal capsule injury are also more likely to have altered muscle tone, which can be floppy or stiff depending upon the precise location of the injury, flaccid paralysis, and persistently impaired balance and ambulation performance.

Can children with basal ganglia injury be helped? Yes, we know that "activity dependent synaptic plasticity occurs at the level of the basal ganglia, which also supports the acquisition and maintenance of certain types of learning." (Wickens, 2008, Beretta, et al, 2007).

At Snowdrop I see children with injury to this area of the brain and develop appropriate stimulatory treatment programmes. If you are interested in more information about Snowdrop's treatment programmes, should email snowdrop_cdc@btinternet.com, or call 01884 38447

Further Reading.

Berretta, N., Nisticò, R., Bernardi, G., Mercuri, N. B. Synaptic plasticity in the basal ganglia: A similar code for physiological and pathological conditions. Progress in Neurobiology. Volume 84, Issue 4, April 2008, Pages 343-362

Wickens, J. R. Synaptic plasticity in the basal ganglia. Behavioural Brain Research

Volume 199, Issue 1, 12 April 2009, Pages 119-128. Special issue on the role of the basal ganglia in learning and memory.

What do we mean when we say autism is a 'spectrum disorder?'

When the term, 'spectrum disorder' is used it means that there are a range of symptoms, which can be attributed to autism. Any one individual may display any combination of these symptoms, in differing degrees of severity. Therefore an individual at one end of the autistic spectrum may seem very different to an individual at the other end of the spectrum.

Who first discovered autism?

Autism was first recognised in the mid 1940’s by a psychiatrist called Leo Kanner. He described a group of children, whom he was treating, who presented with some very unusual symptoms such as; - atypical social development, irregular development of communication and language, and recurring / repetitive and obsessional behaviour with aversion to novelty and refusal to accept change. His first thoughts were that they were suffering some sort of childhood psychiatric disorder.

At around the same time that Kanner was grappling with the problems of these children, a German scientist, Hans Asperger was caring for a group of children whose behaviour also seemed irregular. Asperger suggested that these children were suffering from what he termed ‘autistic psychopathy.’ These children experienced remarkably similar symptoms to the children described by Kanner, with a single exception. – Their language development was normal! There is still an ongoing debate as to whether autism and Asperger’s syndrome are separable conditions, or whether Asperger’s syndrome is merely a mild form of autism.

What is the cause of autism?

In the 1960s and 1970s there arose a theory that autism was caused by abnormal family relationships. This led on to the ‘refrigerator mother’theory, which claimed that autism in the child was caused by cold, emotionless mothers! (Bettleheim, 1967). However the weight of evidence quickly put this theory to bed as evidence was found to support the idea that the real cause was to be found in abnormalities in the brain. This evidence was quickly followed by findings, which clearly demonstrated that the EEG's of children with autism were, in many cases, atypical and the fact that a large proportion of children also suffered from epilepsy. Recent findings also point to various neurological abnormailities, the most common finding seeming to be that the brains of children with autism have an abnormal wiring pattern, - a pattern of connectivity between brain cells which is not present in non - autistic individuals.

So, autism is now looked upon as a disorder, which develops as a consequence of abnormal brain development. Recently, evidence has shown that in some cases, the abnormal brain development may be caused by specific genes.

However, we should not forget that genes can only express themselves if the appropriate environmental conditions exist for them to do so and so, we should not rule out additional, environmental causes for autism. We should not forget that autism can also be caused by brain-injury, that an insult to the brain can produce the same effects as can abnormal development of the brain which may have been caused by genetic and other environmental factors. I have seen too many children who have suffered oxygen starvation at birth, who have gone on to display symptoms of autism. So, it is my view that autism can also be caused by brain-injury.

There are also other possibilities, which can ultimately produce the type of brain dysfunction, which we recognise as autism. There is a great deal of research being carried out at the moment in the area of 'oxidative stress' and 'methylation' and it's effects upon the integrity of neural networks. There is also the debate surrounding mercury levels in vaccines, which is as of yet, unresolved.

The fact is that 'many roads lead to Rome.' - There are likely to be several factors both genetic and environmental, which can ultimately lead to the type of brain abnormality, which we call autism.

So, how do we recognise autism?

On a descriptive level, autism involves a dysfunction of the brain's systems, which control communication, socialisation, imagination and sensory perception. My theory is that it is the distortions of sensory perception, which are so characteristic of autism, which exacerbates many (but not all) of the other difficulties. Imagine a child suffering from autism who suffers distortions of sensory perception. For instance, the child who suffers distortions of visual perception, might find situations which require eye -contact to be exceptionally threatening, or on the other end of the scale might become obsessive about specific visual stimuli. The child who suffers distortions of tactile perception, might at one end of the spectrum find any situation which requires physical contact to be terrifying, whilst at the other end of the spectrum, they might be a 'sensation seeker' to the point of becoming self -injurious. The child who suffers distortions of auditory perception might at one end of the spectrum, be terrified of sounds of a certain pitch or intensity, whereas at the other end of the spectrum, they might actively seek out, or become obsessive about certain sounds.

Treatment

The question is, what can we do to help redress these distortions of sensory perception. Well, we believe we can learn from the newborn baby. When baby is born, he sleeps for most of the time, only spending short periods of time interacting with this new environment in which he finds himself; - a new environment which bombards his senses with new sights, noises and smells. So he retreats into the safe, calm environment of sleep, which provides the sensory safe haven which up until recently was the sanctuary of the womb. Very gradually, as baby adjusts his sensory system to his new environment, he spends more and more time in the waking world, interacting and learning to communicate, - but he adjusts very gradually!

There is possibly a neurological explanation for this. There are structures within the brain, which act to 'tune' sensory attention. These three structures, which allow us to tune our attention are structures, which enables us to ‘tune out’ background interference when we wish to selectively attend to something in particular. They also enables us to ‘tune in’ to another stimulus when we are attending to something completely different. They are the same mechanisms 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 these mechanisms that allow 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 these mechanisms, which allow 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 is the responsibility of three structures operating cooperatively; - these are theascending 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 faced not only by newborn babies, but the sensory difficulties our children face and yes, as the newborn shows, their performance CAN be influenced, - they can be re-tuned.

I believe the sensory system of some children with autism is experiencing similar difficulties to that of a newborn, - at one end of the autistic spectrum, the cortex is being over-excited by these structures and the person is overwhelmed and has difficulty accommodating the mass of sensory stimulation within the environment. At the other end of the autistic spectrum, the cortex is being under-excited and the person has trouble in perceiving sensory stimulation from the environment. The question is; - How do we facilitate the re-tuning of this neurological system in individuals who have autism.

The newborn retreats into sleep, a self imposed dampening of incoming sensory information. Whilst the child with autism does not do this, many children with autism attempt to withdraw from their environment because they find it so threatening.

We believe at Snowdrop that for the child at the end of the autistic spectrum who is suffering an amplification of sensory stimulation, we should create a setting where he can retreat from a world, which is overwhelming his immature sensory system. This 'adapted environment,' which should be as free as possible from all visual, auditory, tactile and olfactory stimulation will serve as a milieu where his sensory system can re-tune itself. Of course it may just be a single sense like vision, or hearing, or tactility, or any combination of senses, which are causing the difficulties and the environment may be adapted appropriately. The child suffering these difficulties will usually welcome this adapted environment, which is in effect a 'safe haven' for his immature sensory system. He should be given free access to, or placed within the adapted environment as needed and you will notice hopefully that he will relax and begin to enjoy being within its safe confines, where there are no sensory surprises.

This procedure should be continued for as long as necessary, - for several weeks or months. Indeed, some children might always need periods of time within the 'safe haven.' As the child begins to accept and be at ease in his safe haven, stimulation in whatever sensory modality is causing the difficulties, should begin to be introduced at a very low level, so low in fact that it is hardly noticeable. If the child tolerates this, then it can be used more frequently until it becomes an accepted part of the sensory environment. If the child reacts negatively in any way, then the stimulus is withdrawn and reintroduced at a later date. In this way, we can very gradually begin to build the level of tolerance, which the child has towards the stimulus.

For the child at the other end of the autistic spectrum, the child whose sensory attentional system is not exciting the cortex enough, with the consequence that he is not noticing enough of the stimulation in his sensory environment, the approach needs to be the exact opposite. These are the children who we see producing self-stimulatory behaviour. I believe that this behaviour is an attempt by the nervous system to provide itself with what it needs from the environment, - a sensory message of greater intensity! We see many children with autism 'flapping' their hands in front of their eyes, or becoming visually obsessed by certain toys, movements, colours etc. I propose that this is a reaction by the nervous system to attempt to increase the intensity, frequency and duration of the sensory stimulus due to a problem with perceiving visual stimuli from the environment.

Of course, children with autism display a far greater range of difficulties than a theory, focused upon a malfunctioning sensory – attentional system could explain. I am not attempting to claim that sensory problems on their own are an adequate explanation for every facet of autism, - that would be ridiculous! This is merely a possible explanation of a range of issues experienced by some children who have autism, which could be produced or exacerbated by the child suffering distortions of sensory perception. For instance, the following symptoms within the autistic spectrum could possibly be explained at the sensory level.

• Failure to make eye contact. 
• Difficulty in sharing attention with anyone.
• Avoiding interaction with others
• Avoiding physical contact
• Seeming disconnected from the environment.
• Appearing not to notice anything visually.
• Visual distraction, as though the child is looking at something which you cannot see.
• Visual obsession with particular features of the environment.
• Inability to 'switch' visual attention from one feature of the environment to another.
• General discomfort with the visual environment.
• Appearing not to hear anything.
• Auditory distraction, as though listening to something which you cannot hear.
• Auditory obsession with particular sounds within the environment.
• Inability to 'switch' auditory attention from one sound within the environment to another.
• Inability to 'tune out' extraneous sounds in the environment.
• General discomfort with the auditory environment.
• Appearing not to feel much sensation.
• Appearing to bee distracted by tactile stimuli of which you are not aware.
• Obsession with particular tactile sensations within the environment.
• Appears unable to 'switch' tactile attention from one sensation to another.
• General discomfort with the tactile environment.
• Difficulty in communicating with others.

This is encouraging, but even though the brain might be encouraged to produce new neurons, we will still need to provide an appropriately enriched environment in order to allow those new cells to 'bed down' into neural networks and to function efficiently. This is what Snowdrop's 'neuro-cognitive therapy' programmes are designed to do!

-----------------------------------------------------

Researchers at The University of British Columbia have discovered why the brain loses its capacity to re-grow connections and repair itself, knowledge that could lead to therapeutics that “rejuvenate” the brain.

The study, published today in The EMBO Journal, identified a set of proteins -- calpain and cortactin, which regulate and control the sprouting of neurons -- a mechanism known as neural plasticity.

Neurons, or nerve cells, process and transmit information by electrochemical signalling and are the core components of the brain and spinal cord. During development, growing neurons are relatively plastic and can sprout new connections, however their plasticity levels drop rapidly as they mature and become integrated into neuronal networks.

This process is the mechanism by which the brain regulates these networks from uncontrolled growth, however; as a consequence, the central nervous system is unable to reorganize itself in response to injury or disease.

“This discovery is exciting because we now know that neurons haven’t lost their capacity to re-grow connections, but instead are under constant repression by the protein calpain,” says Ana Mingorance-Le Meur, postdoctoral fellow in UBC’s Department of Cellular and Physiological Sciences, who has led the investigation along with UBC Professor Timothy O’Connor. “If we can target therapies that block this mechanism, then neurons should be able to sprout new connections, therefore stimulating the brain’s ability to repair its wiring network.”

The research reveals that the loss of plasticity is due to the protein calpain actively blocking the protein cortactin, which is responsible for the sprouting of new connections. The researchers reduced calpain activity in animal models to unlock the sprouting potential of neurons and found that when calpain activity is reduced neural plasticity is enhanced.

“The maintenance of neuronal connections is an active process that requires constant repression of the formation of nerve sprouts by the protein calpain to avoid uncontrolled growth,” says Mingorance-Le Meur, who is also a member of the Brain Research Centre at UBC and VCH Research Institute. “But a consequence of this role is that calpain limits neural plasticity and the brain’s ability to repair itself. The next step is to find a way to enhance neural plasticity without interfering with the good connections that are already in place. The next step is to find a way to enhance neural plasticity without interfering with the good connections that are already in place.”

According to Mingorance-Le Meur, who is also a member of International Collaboration on Repair and Discovery (ICORD), the results are very promising because they help us understand how neural plasticity is regulated. Drugs that could promote neural plasticity could potentially treat a wide range of neurological disorders, as well as boost the effects of other treatments under investigation.

Provided by University of British Columbia

The approach to the treatment of cerebral palsy and other neuro-developmental disabilities which is used by Snowdrop is known as 'neuro-cognitive therapy.'   The question is, why do I believe it offers the best chance for children to make developmental progress and what evidence can be provided to support it's use?

My approach is based upon certain irrefutable facts concerning brain function, which I apply to the treatment of children's developmental difficulties. The most important of these is brain plasticity.

What is Brain Plasticity?

It is the ability of the brain to respond to changes in the environment to enable the person to function as efficiently as possible within that environment.  It is led by environmental demand.  It is the repeated sensory demands produced by the environment which produce function in the child, - because the brain responds to those sensory demands by building the neural architecture to support the function necessary for the child to function.   How do we know this?  Because we know that the developmental function of children who have been exposed to poorly stimulating, impoverished environments, is poor, - as is their brain development.  We also know that children who are raised in highly stimulating, enriched environments have superior developmental function and superior brain development.

Now think about it for a moment, - what is the effect of a brain injury in terms of a child's ability to interact with the sensory environment all around him?  That's right, it impeded his ability to interact with that environment!  It does this in several ways. - It might have injured the neural systems responsible for detecting, passing on or interpreting the sensory information coming from outside.  The injury might result in the child percieving the environment in distorted ways, which is quite common in children who have autism.  It might have injured the motor areas of the brain so that even if the child has normal perceptual abilities to begin with, they will not develop and mature appropriately because he cannot physically interact.  So, because of these impaired sensory messages coming into the brain, - brain plasticity is driven in directions which are unhelpful to the child and his / her development.  So we see the neural architecture being built to support hypersensitive hearing, stiff muscle tone, tactile undersensitivity, etc.

What can we do about this?  What I try to do is to manipulate the sensory environment to which the child is exposed in order to encourage the natural plasticity in the regions of the brain, which are responsible for processing the sensory stimuli, (the sensory - attentional filter of the brain, - the ascending reticular activating system and the thalamus), to re-tune the structures and to process information more normally. Evidence that it is the thalamus and reticular system which carry out these functions is widely available. (Carlson, 2007).

We encourage these systems to re-tune by providing an adapted sensory environment which is tailored to the individual perceptual problems the child is facing.   In this way, (because as we know brain plasticity involves, the brain growing new synapses and pruning disused ones), we can influence not only brain function, but the development of it's structure.  The aim being that the synapses which have been built to support the problems which the child is displaying are pruned and that synapses supporting more normal functioning are built.

Evidence that these structures can be re-tuned can be seen in all human beings, but a good examples is in a mother who is lying asleep and is blissfully ignorant of the traffic passing by outside, - the neural systems in question being used to 'tuning out' this noise. However, the instant her newborn baby makes a sound, she is awake! - Her tuning system has re-tuned to classify this sound as one (within her changed environment), which requires immediate attention and consequently, she wakes!  

Sensory impairments such as these, which our children commonly display in varying degrees of severity, can have wide ranging effects upon the areas of development which produce our 'output' functions, for instance, language, mobility and social development are all heavily dependent upon sensory processing abilities, as is the development of hand function. It is often the case that as sensory abilities begin to improve due to our efforts to directbrain plasticity in morepositive directions, so do these abilities!

Another aspect of our approach is aimed at any learning difficulties the child might have and is informed by research from Vygotskian psychology. Recent research has provided ample evidence concerning how children learn. (unfortunately, often children do not learn in the manner by which schools teach) (Rogoff 1990. Rogoff, B., Mosier, C., Mistry, J., & Goncu, A. 1993. Wood, 1998).

Our approach to learning dfficulties utilises Vygotky's concept of the 'zone of proximal development.' We look at the child's current developmental level in terms of his / her cognitive development and we reinforce these abilities. We then look at the next stage of development for the child (his proximal development) and in recognition that learning is a social activity, we provide support to enable him to attain that ability (this support encompasses Bruner's concept of 'scaffolding' and Rogoff's concept of 'apprenticeship.') This may also entail breaking the developmental task down into smaller, simpler sub-components thus enabling the child to succeed. As the child improves his functioning at the desired cognitive / developmental task, the scaffolding (support) is gradually removed until he is performing the desired task automaically. This is not just the way in which children learn, - this is the way we all learn. (Mercer, 1995. Hughes & Westgate, 1997).

Anyone who wants more information should email on snowdrop_cdc@btinternet.com or visit the website at http://www.snowdropcerebralpalsyandautism.com

References and Further Reading.

Brereton. A. (2010).  Brain Injured Children.  Tapping the Potential Within.  Snowdrop Publications. Exeter

Carlson, N. R., (2007). Physiology of Behaviour. (9th Ed). Pearson. London. 

Hughes, M. and Westgate, D. (1997). Teachers and other adults as talk partners for pupils in nursery and reception classes. Education. 3-13. (1997) March.  In Woodhead, M.; Faulkner, D., and Littleton , K. (1998). Cultural worlds of early childhood. London & Milton Keynes. Routledge & Open University Press.

Kolb, B & Wishaw, I. Q. Brain plasticity and behaviour. Annual Review of Psychology. Vol. 49: 43-64

­

Mercer, N. (1995). The Guided Construction of Knowledge: Talk amongst teachers and learners. Clevedon. Multilingual Matters.

Moll, L. C., & Whitmore, K. F. (1993). Contexts for learning: sociocultural dynamics in children’s development. Oxford . Oxford University Press.  In.Faulkner, D., Littleton , K. and Woodhead, M. (2003). Learning relationships in the classroom. London . Routledge. 

Rogoff, B. (1990). Apprenticeship in Thinking: Cognitive Development in Social Context. Oxford Oxford University Press. 

Rogoff, B., Mosier, C., Mistry, J., & Goncu, A. (1993). Toddlers’ guided participation with their caregivers in cultural activity.   In Woodhead, M.; Faulkner, D., and Littleton , K. (1998). Cultural worlds of early childhood. London & Milton Keynes. Routledge & Open University Press. 

Tizard, B., & Hughes, M. (1984). Young children Learning: Talking and Thinking at Home and School. London . Fontana .  In Woodhead, M.; Faulkner, D., and Littleton , K. (1998). Cultural worlds of early childhood. London & Milton Keynes. Routledge & Open University Press.

Vygotsky, L. S. Mind in Society. Development of Higher Psychological Processes. Harvard University Press.

Vygotsky, L. S. (1986) Ed )Thought and Language. MIT Press.

Wood, D. (1986). Aspects of teaching and learning. In Woodhead, M.; Faulkner, D., and Littleton , K. (1998). Cultural worlds of early childhood. London & Milton Keynes. Routledge & Open University Press. 

For twenty years now, many people working in the field of neuroscience, including myself have been saying that the brain is capable of re-wiring itself. Twenty years ago, the medical professionals I said it to laughed at me and gave me the sort of looks, which are usually reserved for those who are 'not quite right in the head.'  Ten years ago, they smiled and looked in disbelief.   Today, we have actual evidence. Snowdrop has been utilising this principle within it's programmes for children with cerebral palsy, autism and other developmental disabilities, since it was established. Read on.

---------------------------------------------------

Scientists in Tübingen have proven for the first time that widely-distributed networks of nerves in the brain can fundamentally reorganize as required

Scientists at the Max Planck Institute for Biological Cybernetics in Tübingen have succeeded in demonstrating for the first time that the activities of large parts of the brain can be altered in the long term. The breakthrough was achieved through the experimental stimulation of nerve cells in the hippocampus.

Using a combination of functional magnetic resonance tomography, microstimulation and electrophysiology, the scientists were able to trace how large populations of nerve cells in the forebrain reorganise. This area of the brain is active when we remember something or orient ourselves spatially. The insights gained here represent the first experimental proof that large parts of the brain change when learning processes take place.

Scientists refer to the characteristic whereby synapses, nerve cells or entire areas of the brain change depending on their use as neuronal plasticity. It is a fundamental mechanism for learning and memory processes. The explanation of this phenomenon in neuronal networks with shared synapses reaches as far back as the postulate of Hebbian learning proposed by psychologist Donald Olding Hebb in 1949: when a nerve cell  'A' permanently and repeatedly stimulates another nerve cell 'B', the synapse is altered in such a way that the signal transmission becomes more efficient. The membrane potential in the recipient neuron increases as a result. This learning process, whose duration can range from a few minutes to an entire lifetime, was intensively researched in the hippocampus.

A large number of studies have since shown that the hippocampus plays an important role in memory capacity and spatial orientation in animals and humans. Like the cortex, the hippocampus consists of millions of nerve cells that are linked via synapses. The nerve cells communicate with each other through so-called "action potentials": electrical impulses that are sent from the transmitter cells to the recipient cells. If these action potentials become more frequent, faster or better coordinated, the signal transmission between the cells may be strengthened, resulting in a process called long-term potentiatation (LTP), whereby the transmission of the signal is strengthened permanently. The mechanism behind this process is seen as the basis of learning.

Although the effects of long-term potentiation within the hippocampus have long been known, up to now it was unclear how synaptic changes in this structure can influence the activities of entire neuronal networks outside the hippocampus, for example cortical networks. The scientists working with Nikos Logothetis, Director at the Max Planck Institute for Biological Cybernetics, have researched this phenomenon systematically for the first time. What is special about their study is the way in which it combines different methods: while the MRI scanner provides images of the blood flow in the brain and, therefore, an indirect measure of the activity of large neuronal networks, electrodes in the brain measure the action potentials directly, and therefore the strength of the nerve conduction. It emerged from the experiments that the reinforcement of the stimulation transmission generated in this way was maintained following experimental stimulation. 

"We succeeded in demonstrating long-term reorganization in nerve networks based on altered activity in the synapses," explains Dr. Santiago Canals. 

The changes were reflected in better communication between the brain hemispheres and the strengthening of networks in the limbic system and cortex. While the cortex is responsible for, among other things, sensory perception and movement, the limbic system processes emotions and is partly responsible for the emergence of instinctive behavior.