UCLA study shows brain's ability to reorganize

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

Is it possible for a child to have cerebral palsy and autism at the same time?

Yes, I have seen many children who have mixed symptoms of both. There are many roads to the 'destination' of autism. There is increasing evidence that one such road is genetic, - the gene(s) in expressing itself / themselves create an anomaly in brain development, which produces the symptoms of autism. Another road is now thought to be methylation difficulties, another through oxygen starvation, etc. All these differing 'roads' lead to brain dysfunction, which produces what we observe as autism. So, autism consists of a set of symptoms, (distorted sensory perception, faulure of socialisation, communication and imagination, stereotypical behaviours, etc). - These symptoms, all caused by brain dysfunction, are the way in which the condition we call 'autism' expresses itself, - so autism is an expression of brain dysfunction.

There are approximately one hundred billion neurons in the human brain, each cell having the potential to create ten thousand connections to other cells to form complex groupings of connections known as neural networks. This is an unbelievably complex operating system and when it becomes injured, the pattern of injury is therefore like a fingerprint, - unique to the child. Some children may have common symptoms, but no two children will display exactly the same problems. - This is why autism is a 'spectrum disorder,' with a child at one end of the autistic spectrum, displaying totally different problems to a child at the other end of the autistic spectrum.

We have already established that autism is caused by brain dysfunction, - well there are many other problems, which are also caused by brain dysfunction, one of which is cerebral palsy. CP can be caused by oxygen starvation, genetics (rarely), drug abuse, infection, jaundice, malnutrition, or one of many other causes. So it is brain dysfunction, which produces the sets of symptoms we know as CP, just as it is brain dysfunction, which produces the sets of symptoms we know as autism.

So it is correct to say that both autism and CP are caused by brain dysfunction, - indeed, they are both 'expressions' of brain dysfunction.

Now, the more severe and widespread the brain dysfunction, the more symptoms, (or expressions) will be displayed. So whilst a child who has suffered only a moderate amount of damage to the neural networks of the brain may display the symptoms or EITHER autism OR cerebral palsy, (or some other expression), the child who has suffered more severe damage, may display multiple expressions! These might include some symptoms which are considered to be on the autistic spectrum, alongside some symptoms which are considered to fall within CP (or indeed any other expression of brain dysfunction, - there are many!).

So the answer is yes, it is possible and not uncommon for a child to have a dual diagnosis of both autism and cerebral palsy. Does this mean they have two different conditions? No. They just suffer from severe brain dysfunction.

Snowdrop Rehabilitation Programmes for Adults

Adults are often the forgotten casualties of brain injury, the media and consequently the public often focussing their attention upon children. Adults suffer strokes / ischaemic attacks, they suffer head injuries, brain tumours, asphyxiation, just as children do, but what is also forgotten is that those children whose brain injuries have caused developmental disabilities grow up to be adults with developmental disabilities. So we have an entire population of adults suffering with cerebral palsy, autism, dyspraxia and a range of other neuro – developmental problems who perhaps aren't getting the attention of their younger counterparts. I believe this is a wrong which needs to be corrected and so, in response to an increasing demand for my services from adults, Snowdrop Child Development Consultants will shorten it's name simply to 'Snowdrop.' in recognition of the fact that adults suffer problems too and consequently are equally entitled to employ my services.

The brain has a high degree of plasticity, in that it is capable of reorganising it's functioning to accommodate the environment in which it finds itself, - it is capable of re-wiring itself. It is true that the younger the person the greater the degree of that plasticity, but that does not mean that as we get older, even into old age that the brain completely loses its ability to re-wire and change. Quite the opposite has been proven. Findings from studies over the past 15 years have clearly demonstrated that plasticity is not a quality which is unique to babies and children, adults and even senior citizens still possess substantial reserved plasticity, albeit more limited than their younger counterparts. (see references at the bottom of this page).

My programmes for adults, (which would consist of a few simple exercises, each lasting for a few minutes, to be repeated during the day), attempt to harness this plasticity by providing the person with an environment which is appropriately stimulating to their problem. In this way we can provide maximum opportunity to the brain to reorganise and rewire, which can lead to improved functioning in visual, auditory and tactile perception and improved functioning in mobility, language and communication, hand function, cognition and socialisation.

If you have suffered a brain injury, or care for an adult who has, or even if you simply want to maintain your brain's functioning to the maximum degree possible as you get older and you want to embark upon a programme, don't hesitate to contact us.

References.

Baltes P.B., Staudinger U.M., Lindenberger U. (1999) Lifespan psychology: theory and application to intellectual functioning. Annual Review of Psychology 50:471-507

Li S.C., Lindenberger U., Sikstrom S. (2001) Aging cognition: from neuromodulation to representation. Trends Cogn Sci. 5:479-486.

Lindenberger U., Baltes P.B. (1997) Intellectual functioning in old and very old age: Cross-sectional results from the Berlin Aging Study. Psychology and Aging 12:410-432.

Marschner A., Mell T., Wartenburger I., Villringer A., Reischies F.M., Heekeren H.R. (2005)
Reward-based decision-making and aging. Brain Research Bulletin 67:382-390.

Nicoll R.A., Schmitz D. (2005) Synaptic plasticity at hippocampal mossy fibre synapses. Nat Rev Neurosci. 6:863-76.

Taskin B., Jungehulsing G.J., Ruben J., Brunecker P., Krause T., Blankenburg F., Villringer A. (2006). Preserved Responsiveness of Secondary Somatosensory Cortex in Patients with Thalamic Stroke. Cereb Cortex 16:1431-9.

Injury to the Midbrain.

The midbrain is a small structure, which lies just above the Pons at the top of the brainstem. It is comprised of smaller structures called the tectum, the tegmentum' the substantia nigra, and the cerebral penduncles. It contains an important group of cells called the 'red nucleus.' At its top end it is connected to the Thalamus and hypothalamus.

Sensory information is processed by the midbrain on it's way to higher centres such as the thalamus. So the midbrain plays it's part in sensory functions such as in helping to control eye movement, depth perception, in addition to other visual and auditory system functions. The red nucleus and substantia nigra help to control body movement and the substantia nigra produce a neurotransmitter called 'dopamine.' Dopamine is part of the 'reward' system of the brain and is involved in motivation and the formation of the addictive process.

When the midbrain is injured, we see several effects.

• Loss of pupillary reaction
• Abnormally shaped pupils.
• Resting tremor (due to injury to dopamine producing cells)
• Extreme rigidity, (as opposed to spasticity)
• Auditory disturbances
• Parkinson's disease
• Athetosis
• Coma (if there is injury to the tegmentum).
  

Parkinson's disease is produced by degeneration in dopamine producing neurons, whilst athetoid cerebral palsy is caused by injury to the same neurons.

Can the injured Midbrain be treated?

Yes! Like all other areas of the brain the mibrain adapts it's functioning and structure to accommodate the environment in which the individual finds himself. If we can provide the correct developmental environment, this inherent plasticity can be harnessed and the individual's probems may improve. If you would like more information about Snowdrop's treatment programmes for brain injury, visit http://www.snowdrop.cc

Injury to the brain. - Absence of the Septum Pellucidum.

What is Absence of the Septum Pellucidum?

Absence of the septum pellucidum (ASP) is a rare disorder, (occuring in an estimated 2 to 3 individuals per 1 00,000 people in the general population). It is characterised by abnormal development of a thin membrane located at the midline of the brain. It runs down from the corpus callosum, the structure which connects the two cerebral hemispheres of the brain and effectively acts as a separator for the two hemispheres. The disorder usually occurs with other neurological abnormalities such as agenesis / dysgenesis of the corpus callosum.

Individuals with ASP may experience vision impairment or blindness. They may also have coordination problems and hormone deficiencies that result in short stature. Intelligence is usually affected and learning disabilities are common. The disorder usually manifests early in life, often as a consequence of discovering the other neurological abnormalities, such as corpus callosum abnormalities or septo – optic dysplasia. Symptoms include involuntary eye movements, a wasting of a part or parts of the body, and short stature. Seizures and inappropriate behaviour, such as displays of 'sham rage' may also occur. The cause of ASP is currently unknown.

What is the prognosis?

The prognosis of ASP varies depending on the severity of co-occurring abnormalities. Many cranial abnormalities are life threatening, but alone ASP is not a life-threatening disorder.

Can ASP be treated?

When a part of the brain is actually missing, - having not developed at all, then obviously no amount of treatment is going to be able to restore that missing neurology. What we can strive to do is to enable the neurology which is present to function at maximum efficiency and therefore give the child the opportunity to achieve his / her maximum potential. We believe that that at Snowdrop, we teach parents how to provide an appropriately stimulating developmental environment for this to happen. To learn more about Snowdrop programmes of developmental stimulation visit our website.

Injury to the cerebellum.

The word 'cerebellum' actually means 'little cortex' and it is not without justification, as at first site it does look like a smaller version of the cortex. It is located at the rear of the brain, behind the brainstem and it forms massive connections with the brainstem structures and with the cerebral cortex. It is the only structure within the brain which is not fully formed at birth, taking a further two years to develop to it's full complement of neurons.

The proper functioning of the cerebellum ensures that any movements we make are smooth and well coordinated. It seems that the motor cortex supplies commands to the body musculature, which are then refined by the cerebellum to ensure smooth coordination. Feedback on the success of the movement is then supplied from the cerebellum back to the motor cortex where the original movement command can be refined if the movement has been unsuccessful.

One might imagine then that an injury to the cerebellum will interfere with these functions. Movement can become slow and uncoordinated, the child may display problems with balance and equilibrium, the child might experience an 'intention tremor' - (a tremor which is made worse when the child tries to move). Injury to this part of the brain causes 'Ataxia' - a form of cerebral palsy where the muscle tone is hypotonic (floppy).

Higher cognitive functions, like language and visual processing, have long been thought to reside primarily in the brain's cortex, however recent research involving premature infants is documenting an important role for the cerebellum -- previously thought to be principally involved in motor coordination -- and shows that cerebellar injury can have far-reaching developmental consequences.

This work also demonstrates that the cortex and cerebellum are tightly interconnected. Sophisticated MRI imaging of 74 pre-term infants' brains revealed that when there was injury to the cerebrum, the cerebellum failed to grow to a normal size. When the cerebral injury was confined to one side, it was the opposite cerebellar hemisphere that failed to grow normally. The reverse was also true: when injury occurred in one cerebellar hemisphere, the opposite cerebral hemisphere was smaller than normal. So, there seems to be an important developmental link between the cerebrum and the cerebellum, - it seems that the two structures modulate each other's growth and development. The way the brain forms connections between structures may be as important as the injury itself. The cerebellum has also been implicated in the development of some types of literacy problems, including dyslexia.

So the question is, can cerebellar injuries be treated? The answer has to be 'yes!' We know the brain has inherent qualities of plasticity, this is particularly so in the cerebral cortex. If we can stimulate cortical plasticity and re-wiring as a consequence of our treatment then the previous research suggests that we might well also see cerebellar development. Combined with exercises directly aimed at improving cerebellar functioning itself, we believe that Snowdrop rehabilitation programmes provide the best hope for recovery of function in children who have experienced cerebellar injuries.

If you would like to learn more about Snowdrop programmes for brain injured children, then please click here to visit our website.

Injury to the Pons.

The Pons is located in the lower brainstem, directly above the Medulla Oblongata. The word 'pons' means 'bridge' and this is an apt description as it acts as a bridge which connects the cerebellum to higher brain structures. It's involvement with the cerebellum makes it an important player in the coordination of movement and posture.

The Pons is also involved in sensory analysis... for example, information from the ear first enters the brain in the pons at the level of the Eighth cranial nerve. It is therefore easy to imagine how many of the distortions of sensory processing experienced by our children are produced by injury here!

It has parts that are important for regulating our level of consciousness and for sleep, which fits in nicely with the fact that the raphe nuclei are serotonin producing neurons. Injury to the Pons can cause coma. The pons contains the raphe nuclei which contain serotonin, a type neurotransmitter which is instrumental in mediating mood and sleep. The pons is also involved in our ability to perceive pain. Regulation of pupillary dilation and constriction is also controlled at the pons and so a good indicator of injury to this structure is the absence of a pupillary light reflex.

Another important set of nuclei in the pons is the Locus Coereleus. This area of the brain is intimately involved in REM (dream) sleep. It is these nuclei which are responsible for many stress reactions, including 'post traumatic stress disorder.' The locus ceruleus is activated by stress, and will respond by producing a neurotransmitter called 'norepinephrine,' - a form of adrenaline. Injury here is why some of our children are hyper-anxious and oversensitive in sensory terms. Norepinephrine also increases cognitive function and motivation

So injury to the Pons is capable of producing coma, causing sleep disturbances, sensory disturbances, lack of pupillary response, dysfunction in levels of arousal and attention and increases in levels of stress and anxiety. How many of our children who suffer conditions such as cerebral palsy and autism have injuries to this structure? I would suggest it is more than one would imagine.

Can an injury to the Pons be treated?

Yes! We know that the brain has a high degree of plasticity, - the ability to reorganise it's structure and functioning according to the demands of the environment in which the individual finds himself. We also know that if we can gain an improvement in functioning in one part of the brain, then we can expect 'knock - on' effects, - improvements in other parts of the brain due to the rich connectivity between all areas of the brain. What we do at Snowdrop is to provide children (and adults) with an envionment which is designed to stimulate their development by encouraging this plasticity and improved functioning.

If you are interested in learning more about Snowdrop develeopmental stimulation programmes, go to our website by clicking this link.