Snowdrop

Breathing is something we all take for granted because it is an automatic function, to which we do not have to pay attention. Only when something interferes with the smooth function of our respiration, such as exercising, or an adverse reaction to an allergen, or if we develop a respiratory disorder do we become all too aware of it!

Many children who have cerebral palsy, have difficulties with their breathing. Not many people are aware that the rate and depth of our breathing is subject to the forces of development and that consequently the rate and depth of a babies breathing is simply not comparable to that of an adult. For instance, the breathing rate of a newborn baby is around 40 breaths per minute, but by the time the child reaches his first birthday, this has dropped to around 35. By his second birthday the average rate has dropped to 30 and by the time he is 5 years old, it has dropped to around 25. We then see a slower decline and by the time he is 12 years old it has dropped to around 20, until finally it reaches its adult rate of around 15.

What implications does this have for a child with cerebral palsy? Well, the brain injury which adversely affects the development of the child in other areas, can also affect the development of the rate of respiration and this can have negative effects. If a child is growing physically, but his rate of respiration remains stuck at the level of a baby at around 40 shallow breaths per minute, it will create obvious consequences for the ability of that child in terms of his eating, drinking and the development of spoken language. (To test this out, try running up and down stairs until you are out of breath and then try to eat a biscuit or cake or try reciting your favourite poem. – Its difficult isn’t it)? This is the situation many of our children are faced with constantly. – Imagine the nightmare of trying to coordinate chewing, swallowing and breathing at such a rate!

Another factor which can be a worry as the child’s growing musculature demands more oxygen from a system which simply cannot provide it, is the creation of a poor physiological environment for the brain. The brain uses up 25% of all the oxygen we take in and as it develops, it not only demands more oxygen from a respiratory system which cannot deliver it, - with the consequences of brain development being slowed, but the increasing demands being made from a growing physical body provide stiff competition for the limited oxygen which is available. This can not only have the effects of limiting physical and neurological development, but can cause a child to have seizures.

So what can be done about this situation? The obvious answer seems to be the direct delivery of Oxygen, such as is seen in hyperbaric oxygen chambers, but this in turn throws up additional problems. There are sensors in the base of the brain, which are sensitive to the levels of oxygen and carbon dioxide in the bloodstream. They help regulate the rate of delivery of oxygen to the brain by widening and narrowing the arteries as is necessary. When they detect higher than normal levels of oxygen in the bloodstream, they act to constrict the arteries so that the brain is not flooded with oxygen. So in directly delivering extra oxygen, we may actually be depriving the brain of it! In the more extreme cases this has led to people experiencing a form of stroke known as an ischaemic attack!

So what do we do? At Snowdrop I find that when a child embarks on a programme of neurological rehabilitation and when we begin to make progress in developmental terms, very often the respiration makes improvements too.

Anxiety isn't a problem that you would automatically think to associate with cerebral palsy, but some children really do suffer quite badly with it. This can be due to many reasons. One reason is the discomfort produced by stiff musculature. A high muscle tone can be uncomfortable for a child and having to cope with this constantly is bound to have an anxiety raising effect.

Another possible cause can be the overproduction of norepinephrine in the brain, leaving the child on a hyper-anxiety inducing adrenaline 'high.'

Yet another cause can be sensory over-sensitivity. - A child who is unable to mask extraneous incoming sensory stimulation, but who sees, feels and / or hears too much, or whose sensory system over-amplifies incoming stimulation is likely to experience anxiety.

Another factor can be lack of sleep. Many children who have cerebral palsy have a poor sleeping pattern. We all know how we feel if we lose a night's sleep, tired, overstressed and anxious.  So for many children, anxiety can simply be part of their every day existence.

There are techniques, which Snowdrop employs within some of its programmes, which are designed to help relieve this situation, but in the most severe cases intervention can be necessary with anti – anxiety medications.

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.

I am re-posting this from my blog because I met a wonderful family today who I know will be interested in reading it, as we were discussing the issue.

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How many of our children have suffered further brain injury through the administration of 100% oxygen? There is a good preventative lesson in this report, which might mean that Snowdrop type services would not be required by so many chidren.

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The current practice of administering 100 percent oxygen to children, to prevent brain damage caused by oxygen deprivation, may actually inflict additional harm, researchers at UT Southwestern Medical Center have found.

Brain damage caused by oxygen deprivation, known as hypoxic-ischemic brain injury, is one of the most common causes of death and long-term neurological damage among infants and children. This can happen during birth trauma, near drowning and other crises.

The UT Southwestern researchers found that mice treated with less than a minute of 100 percent oxygen after a hypoxic-ischemic brain injury suffered far greater rates of brain-cell death and coordination problems similar to cerebral palsy than those allowed to recover with room air.

"This study suggests 100 percent oxygen resuscitation may further damage an already compromised brain," said Dr. Steven Kernie, associate professor of pediatrics and developmental biology and senior author of the study, which appears in the July issue of the Journal of Cerebral Blood Flow & Metabolism.

Most of the damage involved cells that create myelin, a fatty substance that insulates nerve cells and allows them to transmit electrical signals quickly and efficiently. Infants have much less myelin than adults; as myelin develops in children they become more coordinated. Areas of the brain with dense areas of myelin appear white, hence the term "white matter."

"Patients with white-matter injuries develop defects that often result in cerebral palsy and motor deficits," Dr. Kernie said.

Myelin comes from cells called glial cells, or glia, which reach out and wrap part of their fatty membranes around the extensions of nerve cells that pass electrical signals. The brain creates and renews its population of glial cells from a pool of immature cells that can develop into mature glia.

In their study, the researchers briefly deprived mice of oxygen, then gave them either 100 percent oxygen or room air, which contains about 21 percent oxygen, 78 percent nitrogen and 1 percent other gases.

After 72 hours, mice given 100 percent oxygen fared worse than those given room air. For example, they experienced a more disrupted pattern of myelination and developed a motor deficit that mimicked cerebral palsy.

The population of immature glial cells also diminished, suggesting that the animals would have trouble replacing the myelin in the long term.

"We wanted to determine whether recovery in 100 percent oxygen after this sort of brain injury would exacerbate neuronal injury and impair functional recovery, and in these animals, it did impair recovery," Dr. Kernie said. "Our research shows even brief exposure to 100 percent oxygen during resuscitation actually worsens white-matter injuries."

Dr. Kernie said adding pure oxygen to the damaged brain increases a process called oxidative stress, caused by the formation of highly reactive molecules. The researchers found, however, that administering an antioxidant, which halts the harmful oxidation process, reversed the damage in the mice given 100 percent oxygen.

"Further research is needed to determine the best possible concentration of oxygen to use for optimal recovery and to limit secondary brain injury," Dr. Kernie said. "Research is now being done to determine the best way to monitor this sort of brain damage in humans so we can understand how it correlates to the mouse models. There are many emerging noninvasive technologies that can monitor the brain."

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Interesting isn't it? I wonder if they want to know why this happens?

When we try to administer high concentrations of oxygen to the brain, we actually cut the supply of oxygen the brain actually recieves. This is because high concentrations of oxygen act to constrict the cerebral arteries and veins. Constricted veins carry less blood and as blood carries oxygen, the individual concerned, who might already be in oxygen debt, has his oxygen supply further compromised.

Exactly the same problem is seen in epilepsy, which whether caused by pathology or physiology is a reflexive response to a compromised oxygen supply. The first thing a doctor will do is to supply the individual with oxygen, which very often just produces a bigger, better and more prolonged seizure! They then have to administer massive doses of anti – epileptic medication to undo the damage they have done through administering oxygen and to bring the seizure under control.

So what should be done instead of administering oxygen?

There is a great deal of research, which suggests that carbon dioxide is a good solution to this problem. The brain reacts to higher than normal levels of CO2 by dilating the cerebral arteries and veins. Dilated arteries carry more blood and as I previously pointed out, more blood = more oxygen. Obviously the timing, level and concentration of CO2 administration would need to be carefully controlled, but there is research, particularly with regard to epilepsy that CO2 could provide answers to some serious problems. See the references to this at the end of the article.

So, in summary, the evidence suggests that we should completely review our methods for delivering oxygen to the brain. The direct route of direct administration of oxygen, actually produces the opposite effect to that which is desired and can actually make oxygen deprivation worse, thereby exacerbating the potential for brain injury and worsening neurological symptoms like epilepsy. We need to devise a treatment whereby CO2 enriched air can be administered thereby helping to turn on the brain's own natural anticonvulsant systems and in turn affecting the cerebral vascular system so that it is able to deliver oxygen as necessary. In this way we could not only prevent the occurrence of some types of brain injuries, but we could help to ameliorate the symptoms of those already suffering the consequences of neurological damage.

One thing is certain though, no one should take it upon themselves to administer CO2 enriched air to their child or to anyone else. This should only be done under the guidance of someone who is suitably qualified.

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Online References

http://www.medicalnewstoday.com/articles/73558.php

http://books.google.co.uk/books?id=ngmo0th_2X0C&pg=PA953&lpg=PA953&dq=Carbon+dioxide+treatment+for+epilepsy&source=bl&ots=gQtQkJqNLV&sig=SzzntHyaFbq5NGFgUb-UOy61MDc&hl=en&ei=53gkTOrYEJWTjAeMkOR2&sa=X&oi=book_result&ct=result&resnum=3&ved=0CCoQ6AEwAg#v=onepage&q=Carbon%20dioxide%20treatment%20for%20epilepsy&f=false

This is a variant on a question I am frequently asked.

Question.

I am going to have my 6 year old son tested for Autism and Sensory Processing Disorder. His teachers thought that would be a good idea. What i'm concerned about, is the fact that a lot of doctors won't acknowledge that SPD is different from Autism and treat it. They treat SPD as autism and thus the treatments don't work. Of course, this is all what I have discovered, and not experienced first hand. My question I guess, would be how do they know the difference in Autism and SPD since they have such similar signs? Also, if he has SPD and is treated for Autism, or visa versa will the treatments still work since they are different. Does anyone have any insight on this subject? Thanks in advance!

Answer. -

Hi. You are quite correct to distinguish the fact that it is possible to have SPD whilst not having autism. I see many children who have 'stand alone' SPD, also children who have dyspraxia and cerebral palsy who also have SPD. I also agree with you that it is very important to treat the SPD as an individual problem, - but I believe this to be the case whether it is found alone, in Autism or in CP or dyspraxia.

The brain operates on a series of sensory - motor loops, for instance if we have distorted visual perception, - because language, hand function, socialisation and motor systems are dependent upon good visual development for their own good development, - we can expect to see these systems suffer.

If we have distorted auditory perception then we will see the dependent 'output systems,' of language and social development being adversely affected. - These are primary systems which are affected in autism, so you can see why so many professionals automatically link the SPD with autism.

If we have distorted tactile development, then the dependent motor systems of mobility, hand function and socialisation will be affected, so we again see the connection with autism.

What I am clumsily trying to say, is that the pattern of brain injury which causes SPD, displays itself many times in output terms in what we like to call 'autism.'

Now for treatment. Personally, I don't go along with the treatment methods employed by the establishment at all. They are usually symptom oriented and I prefer to address treatment to the cause, - the injured brain which is producing SPD, or what I prefer to term 'distortions of sensory processing.' These distortions are produced primarily by the malfunctioning of two systems within the brain. The first is the 'Ascending Reticular Activating System,' which is partly responsible for directing our attention towards incoming stimuli from the environment. Second is the Thalamus, which has been shown to be a relay station for sensory information, directing it to the appropriate part of the cortex for further processing. The thalamus also 'excites' the appropriate region of cortex, to enable it to process and analyse that information.

So what goes wrong? When these two structures malfunction, it results in either the attentional systems not being directed to pay attention to incoming stimuli, - so we see a child who simply does not seem to perceive the outside world sufficiently in terms of vision, hearing, or touch. We can also see a situation where a child's attention is mis-directed so that he pays too much attention to a particular stimuli. As I said, the thalamus is also responsible for exciting the cortex and it can under-excite it, or over-excite it. This results in either undersensitivity in a sensory modality or oversensitivity.

The good news is that these two structures can be re-tuned by the provision of an appropriately adapted sensory environment. In this way the brain can be taught to modulate incoming sensory stimulation at a more natural level.

This is only a brief description of some of the many distortions of sensory processing which can occur, in order to give you an example. Hope this helps.

If you need more information, contact me at snowdrop_cdc@btinternet.com

What is ataxia?

Ataxia is caused by injury to a part of the brain called the 'cerebellum,' a structure low down in the back of the brain. The functions of the cerebellum are to help control balance and coordination via it's connection with the vestibular system and the eighth cranial nerve. It also has a function in regulation of muscle tone, smooth movement, proprioception and depth perception.  Injury to the cerebellum produces many symptoms such as poor balance, coordination, low muscle tone, (hypotonia),  jerky, uncontrolled movements, poor depth perception, wide based gait (walking or standing with the feet an unusual distance apart), poor proprioception, reading difficulties and a tremor which appears when the individual tries to move a limb.  These symptoms are seen in many conditions such as the cerebellar ataxia, cerebral palsy, multiple sclerosis and Friedreich's ataxia to name just a few.

The question is, can these problems be treated?   The answer is 'yes, they can.' At Snowdrop we believe the answer to improvement of these difficulties lies in those important connections between the cerebellum and the vestibular system and consequently the pons, medulla and the eighth cranial nerve.

Let's take a look at where this neurological system begins, with the first order vestibular afferents (afferent nerves are nerves travelling into the brain from a sensory 'end system' in this case the ear). These nerves are bundled with others to become the Eighth cranial nerve. This nerve then enters the brainstem at the level between the pons and medulla, where the fourth ventricle is at its widest. A few of these vestibular nerves split off here and travel directly into the cerebellum through a part of that structure called the 'inferior cerebellar peduncle.The eighth cranial nerve is actually three separate nerves in one bundle.

One part is concerned with transmitting sensory information about hearing and the other two with sending sensory information about balance and proprioception from the middle ear to the cerebellum and brainstem. This is why, very often when we see a child who is suffering from injury to this system, we also see that the child is suffering a distortion of sensory processing with regards to their hearing. This distortion might result in the child experiencing oversensitive hearing, undersensitive hearing, or experiencing some other distortion to the perception of hearing.At Snowdrop we have developed techniques to help ameliorate these symptoms and to help restart children's developmental processes.

What is Cortical Visual Impairment?

Cortical visual impairment occurs when a part of the brain responsible for vision is damaged and therefore not functional. The eye is working perfectly well, but because of damage or lack of maturation, the brain is unable to process the information being sent from the eye. There are three categories into which cortical visual impairment can be separated, they are cortical visual impairment, delayed visual maturation and cortical blindness. These distinctions are made according to what area of the brain has been damaged.

Corticalvisual impairment (CVI) has a range of causes, including, but not limited to, lack of oxygen before, during, and after birth, viral or bacterial illness such as meningitis and cytomegalovirus, or traumatic brain injury.

CVI can affect vision in a number of ways and causes a variation of visual loss that can range from mild to severe, it can also be temporary or permanent. There is no way to predict how a child's vision will mature but many children who experience CVI do show some improvement in their visual ability. Fluctuating vision is also experienced by many children, this being experienced more commonly by children who also suffer epilepsy, or who are taking specific medications such as Dilantin, Tegretol, or Phenobarbital. This means a child may be able to see an object one day and be completely unable to the next.

Another common feature in children who have CVI is that they may have better peripheral than central vision and thus look at objects out of the side of their eye. They may also experience problems with visual field loss which may not be symmetrical (one eye may be worse than the other).

Children with CVI commonly experience problems with specific types of visual tasks. They have difficulty with figure-ground (seeing an object instead of the background), and with complex visual displays such as cluttered pictures (a picture of five different animals instead of two). Spatial confusion is also commonly experienced; for example being unable to locate their chair even though they can see it. They may also be visually inattentive, not wanting to look at objects, and may prefer their sense of touch. It is common to see a child turn his/her head away as they explore an object with their hands. Seeing with CVI can be compared with trying to listen to one voice in a noisy room or to speaking a foreign language.

Can CVI be treated?

Yes, but with varying degrees of success. Snowdrop has treated children and completely restored their visual ability, but we have also treated children and seen little or no progress. Visual stimulation is proven to help most children with CVI as with other visual impairments and this can lead to improvments in the way they are able to perceive and use their vision. For visual stimulation to be effective it needs to be dramatic. We may not only be stimulating vision in the child, but also the way in which a child is able to use and switch his visual attention. This can only be done by giving the correct stimulation at the correct frequency, intensity and duration,in the correct therapeutic environment