Tuesday, 30 November 2010

Retraining a child's brain after injury.

When a child is labelled as having a 'learning disability' it comes with an unwanted and unwarranted stigma, which can be hurtful not only for the child, but for his / her family too.

The usual response to the diagnosis of a learning disability is to introduce supplemental learning support by way of one – to – one contact with specialist intervention or by the use of various aids. Generally, these have a minimal effect as they do not focus upon the cause of the learning disability, poor brain function in one or more areas leading to poor learning performance in specific tasks.

There is a great deal of evidence from animal experimentation that for instance, rodents who are exposed to generally stimulating environments such as mazes, etc. experience better brain growth than those who are not exposed to such environments. These findings have been mirrored in human societies with children who have been exposed to impoverished, understimulating environments having smaller, more underdeveloped brains than children who have experienced more stimulating environments, who in turn have larger, better developed brains with more connections between neurons.

Now by default, brain injured children, such as those suffering from say, cerebral palsy, have smaller, less well developed brains with less connections than their uninjured peers. This is because their brain injuries prevent them from interacting with and taking advantage of their developmental environment. However, if we could somehow ensure that they did receive enriched environmental stimulation, then we know from the previously mentioned studies that there would be an excellent chance that their brains would respond to that environment by changing its structure and functioning, ie, by brain cells forming new connections. We know that this process or brain plasticity, known as 'Long Term Potentiation' takes place in all of us, so why should children who have suffered brain injury be any different? The answer is that of course they aren't!

In the area of learning disabilities, we often need to concentrate upon developing working memory. Working memory is vital to learning and in young children, has been demonstrated to predict future academic success. When working memory is poor, it makes it difficult for children to recall the instructions given by parents or teacher, therefore making tasks difficult if not nearly impossible for them to complete. The effect of this is failure both at school and in daily life, causing lack of motivation, which further compounds an already dire situation. Children with cerebral palsy, autism, ADHD, dyslexia, dyspraxia and many more, all demonstrate poor working memory function

Fortunately, we can now address many learning difficulties by giving children appropriate training in the use of working memory and consequently encourage brain plasticity and rewiring. Many researchers have proven this to be true, most notably the Max Plank Institute for Biological Cyberneticsin Tubingen who 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 scientists were able to trace how large populations of brain cells in the human forebrain are able to reorganise and change their connections to other brain cells as a consequence of environmental stimulation. (Current Biology, March 10th, 2009)

What we do at Snowdrop, when we see a child with brain injuries, is to design a set of sensory, physical and intellectual tasks designed to gradually strengthen the child's abilities. The tasks are necessarily repetitive and demand the child's attention. This is done for several hours per week, but we do see some huge improvements. All we are doing is providing an enriched environment designed to retrain the brain of the child with brain injuries, - an environment which will encourage the plasticity and the neural rewiring that we know occurs not only in lower mammals, but in human beings too.

Research has shown that Snowdrop's approach is correct. If we train our brains we stimulate them to grow and change. By training the functions we seek to strengthen in brain injured children, we can help them to become more and more capable in those areas.

Thursday, 25 November 2010


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.  The model below, suggested by Baron – Cohen and Bolton is a reasonable working model of how autism can be caused, although a little simplistic in that it ignores several key features of the condition.  It does however ably highlight that there are many routes to the destination of autism.

diagram showing one possible pathway to autism

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

Wednesday, 24 November 2010

The brain cuts out unexpected sounds. - Unless it doesn't!

Our brains pay less attention to aspects of the world that appear to remain the same. We need this mental relief to experience life without being overwhelmed, but it can keep us from noticing when patterns change.  (I see many brain injured children, who because of the nature of their injuries have lost this ability and the sensory attentional filter attempts to pay attention to all sounds in the environment.  Consequently the child is overwhelmed).

The world is a very big, very complicated place, and your brain will take any chance it can get to simplify it. If the brain picks up on a regular pattern, it will stop looking at it as a sound in its own right and more like a natural part of the background. University of Wisconsin-Madison psychologist Keith Kluender explains:

"In perception, whether visual or auditory, sensory input has a lot of structure to it. Your brain takes advantage of the fact that the world is predictable, and pays less attention to parts it can predict."

In general, this is a good thing, but it can sometimes make us deaf to sounds our brains don't expect. To demonstrate just how powerful this effect can be, Kluender and his colleagues created an orderly set of new sounds that were somewhere between a tenor saxophone and a French horn. The noises were also on a spectrum from abrupt like a plucked string to gradual like a bowed string. They then played these noises in the background while the test subjects played with Etch-Sketches for about seven minutes.

Here's where it gets strange. The subjects were asked to identify which of three sounds was different from the others. If the odd sound was different in the same way the background noises had been - say, it varied in its instrument and the length of the noise - then they had no problem. But if the different sound didn't fit the pattern - like, say, it didn't have enough saxophone in the noise - the test subjects were lost, incapable of telling the difference between the sounds.

If the subjects hadn't spent the last several minutes establishing a pattern of sounds, they likely wouldn't have had as much trouble. Without the newly built-in expectations, they would have just evaluated the sounds in isolation and, in all likelihood, figured out the odd one out. But their brains had taken those noises for granted, and so they couldn't do it. It's mental efficiency gone overboard.

This finding fits well with previous theoretical descriptions of how an efficient brain should work, although this is the first time it's been demonstrated this clearly in people. Most of the time, our ability to predict noises is very useful, as fellow researcher Christian Stilp explains:

"The world around us isn't random. If you have an efficient system, you should take advantage of that in the way you perceive the world around you. That's never been demonstrated this clearly with people."

Indeed, despite the subjects' inability to identify the sound, this effect is far more helpful than not, as Kluender explains with a rather nefarious example:

"That's part of why people can understand speech even in really terrible conditions. You can press your ear to the wall in a cheap apartment and make out a conversation going on next door even though the wall removes two-thirds of the acoustic information. From just small pieces of sounds, your brain can predict the rest."

It is often that in many of the children I see who have problems of auditory development, their brains have lost this ability to predict, - to isolate patterns, therefore they do not pick up on the ‘beat’ or pattern of speech.  Consequently, they not only have a great deal of trouble understanding spoken language, - but because speech comprehension and speech production are the input and output variables of a neurological sensory – motor loop, they don’t produce spoken language either.

Fortunately, this sensory – attentional filter, which tunes into speech sounds can often be re-tuned simply by consistently exposing the child to an adapted auditory environment.  We can then begin to train the filter to pick out speech sounds and the whole process of language comprehension and development can begin.

Anyone wanting more information about language development in children and Snowdrop’s approach to developing language should email snowdrop_cdc@btinternet.com or visit http://www.snowdropcerebralpalsyandautism.com

Tuesday, 23 November 2010

Discovery could rejuvenate the brain

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!
In Medicine & Health / Research

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 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 mature central nervous system is restricted in reorganising 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 inhibition from doing so by the protein calpain.   So If we were in some way able to block the mechanism by which this protein works, then theoretically neurons should again be able to sprout new connections, therefore enabling the brain 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.

Monday, 22 November 2010

Plasticity within the visual system. - Learning without conscious awareness.

A team of researchers from the University of Minnesota's College of Liberal Arts and College of Science and Engineering have discovered that a part of the visual cortex is capable of  rewiring itself when people are trained to perceive visual stimuli, and have demonstrated for the first time that this neural learning appears to be independent of higher order conscious visual processing.   (This evidence supports many of Snowdrop's techniques for stimulating visual development.)

The researchers' discovery could help shape training programs for people who must learn to detect subtle stimuli quickly, such as doctors reading X-rays or air traffic controllers monitoring radars. In addition, they appear to offer a resolution to a long-standing controversy surrounding the learning capabilities of the brain's early (or low-level) visual processing system.  (What they don't seem to appreciate however are the important ramifications this research has for the stimulation of visual abilities in brain injured children).

The study by lead author Stephen Engel, a psychology professor in the College of Liberal Arts, is published in the Nov. 10 issue of the Journal of Neuroscience. 

"We've basically shown that learning can happen in the earliest stages of visual processing in the brain," Engel said. 

The researchers studied how well people could identify a visual stimuli on a computer screen which continuously became more and more faint. They discovered that over a period of 30 days, subjects were able to recognise visual stimuli which was more and more faint. Before and after this training, they measured brain responses using EEG, which records electrical activity along the scalp produced by the firing of neurons within the brain. 

"We discovered that learning actually increased the strength of the EEG signal," Engel said. "Critically, the learning was visible in the initial EEG response that arose after a subject saw one of these patterns. Even a tiny fraction of a second after a pattern was flashed, subjects showed bigger responses in their brain." 

In other words, this part of the brain shows local "plasticity," which seems independent of  conscious higher order processing, with no changes in the visual attention of the individual. Such higher order processing would take time to occur and so its effects would not be seen in the earliest part of the EEG response.

This research supports many of Snowdrop's techniques for stimulating visual abilities in brain injured children.  Anyone wanting more information on Snowdrop's programmes should email snowdrop_cdc@btinternet.com  or visit the website at http://www.snowdropcerebralpalsyandautism.com 

Monday, 15 November 2010

Injury to the visual system of the brain.

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.


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.


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, or visit our website at http://www.snowdropcerebralpalsyandautism.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.

Tuesday, 9 November 2010

Injury to the basal ganglia.

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, visit the website, 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 NeurobiologyVolume 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.