I Can See and Hear.

This morning was the 4th assessment of a little girl whose diagnosis is 'spastic quadriplegic cerebral palsy.' 'cortical visual impairment' and 'bilateral severe/moderate hearing loss.' When we first saw her she was 2.5 years old and in the 18 months she has been on the Snowdrop programme, she has moved to the top of the developmental profile in both visual and auditory development. Such a lovely, intelligent little girl.

West Syndrome. - A Family Fight Back on the Snowdrop Programme.

Today we saw a little boy with West Syndrome for his first reassessment and wow has he made progress in every area of development! 

When we first saw him, he was 10 months old and visually he was operating at the functional level of a 4 month old.  Now, he is 17 months old, which means he has been on the Snowdrop programme for 7 months and is operating visually at the 12 - 14 month level.  In terms of auditory development and comprehension, he has progressed from the 4 month level to the 9 month level.  Tactile perception has transformed from being grossly under-sensitive to being normal.  He has gone from sitting to crawling on all fours and also high kneeling.  He is beginning to try to pull himself to stand. His hand function has gone from basic reaching and grasping to having a sophisticated pincer grip in both hands and both hands working cooperatively. His social development is now age appropriate. 

It just goes to show that even against the flow of genetic expression, progress can be made!

ADHD and Sensory Processing Disorder.

Today, to end a busy week, we met another lovely new family to the programme with a little boy who is just much too physically active and just cannot stop.  He has extreme ADHD.  He also has huge sensory processing and attentional issues. underneath it all is a beautiful, intelligent little boy. We shall endeavour to lead him out of the world in which he is trapped into a calmer, organised world of normal sensory experience.  We have the techniques to slow him down, so that he can then develop and use his attentional abilities properly.  Only then will he join 'our world' and begin to learn the way he should.  Watch this space!

Antihistamine Promotes Remyelination

With thanks to Medscape, a fascinating piece of research about antihistamine and remyelination which will also be applicable to children on the Snowdrop programme who have myelination issues.  

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A common antihistamine available over the counter has shown evidence of remyelination in patients with multiple sclerosis (MS) in a double-blind, placebo-controlled trial.

The study showed that clemastine — at a dose just a little higher than that approved for allergies — reduced the transmission delay in the optic nerve seen in patients with MS and chronic demyelinating optic neuropathy.

"We are extremely excited about these results," lead author, Ari Green, MD, medical director, University of California San Francisco (UCSF) MS Center, commented to Medscape Medical News. "Our main message is that it appears to be possible to repair injury to nerve cells in MS by remyelination. We have been taught that the brain can't repair itself, but our results suggest that this is not true. This could have consequences for many other neurodegenerative diseases as well as MS."

The results were released April 12 in advance of their presentation at the upcoming American Academy of Neurology (AAN) 2016 Annual Meeting.

The phase 2 crossover study — which is said to be the first randomized controlled trial documenting efficacy for a candidate remyelinating agent in MS — compared twice-daily oral clemastine to placebo in 50 patients with MS and chronic demyelinating optic neuropathy. The study period was 150 days.

The primary efficacy endpoint, latency delay on visual evoked potential (VEP; the time for transmission of signal from the retina to the visual cortex), was reduced by 1.9 ms/eye for the period on treatment with clemastine (P = .003).

Dr Green explained that VEP records the speed of transmission in the optic nerve from the visual stimulus to the processing of the image in the visual cortex of the brain.

"Good myelination of the nerve enables the signal to travel faster. For example, in an unmyelinated fiber, the signal would travel at a speed of 1 m/s. In contrast, a myelinated fiber would transmit the signal at about 100 m/s, 100 times faster. Demyelination as seen in MS-related optic neuritis can delay transmission by 30 to 50 ms. Clemastine seems to restore some of this loss."

The researchers also looked at a functional endpoint — low-contrast visual acuity — and saw a strong trend for improvement, but this did not reach statistical significance (P = .089).

In terms of side effects, clemastine treatment was associated with mild worsening of fatigue on the Multidimensional Assessment of Fatigue scale (P = .017).

Reflection of Nerves Throughout the CNS

Dr Green said that although this study just focused on the optic nerve, it probably reflects what is going on throughout the central nervous system. "We are using vision as a method of testing the principle of remyelination. The optic nerve is an obvious place to start as it is logistically practicable. We believe, however, that it should reflect nerve condition generally and acts like a surrogate marker for the rest of the CNS [central nervous system]."

But he urged caution to patients with MS. "I do not want to make false promises, and I am not advocating that MS patients take clemastine on the basis of this one study. But if they chose to do so, they should have the supervision of a physician and preferably enroll in a clinical study."

Clemastine was identified as a potential remyelinating agent in a screening program developed by a UCSF team led by Jonah Chan, PhD, using precursor cells of oligodendrocytes (the cells that make myelin).

"These oligodendrocyte precursor cells are present in the brain but don't seem to mature and make oligodendrocytes," Dr Green explained. "We are looking for agents which stimulate the precursor cells to differentiate into oligodendrocytes and produce new myelin to repair the damaged neurons. Chan et al tested many different existing drugs and found that clemastine did just that."

The researchers have identified a specific muscarinic receptor at which clemastine is acting to bring about this effect. "It is probable that the drug is only partially saturating the receptor, so we may not be seeing the full effect," Dr Green said.

But because clemastine also acts at many other receptors, his group is looking into developing new agents that act specifically at this receptor, which may be more appropriate for myelin repair. "We also know that there are other nonmuscarinic receptors that appear to bring about similar results, so there are a few possibilities under investigation," he added.

"The screening method has identified the biology. Now we have to fine-tune that biology," Dr Green commented.

Biogen is also developing a compound known as anti-LINGO, which has shown evidence of remyelination. Dr Green noted that the anti-LINGO study recently reported involved patients with a current episode of optic neuritis. "So they showed an acute action, whereas patients in our study had not had a recent episode of optic neuritis and so we have shown evidence of benefit in the chronic phase."

Commenting on the study for Medscape Medical News, Lily Jung Henson, MD, chief of neurology, Piedmont Healthcare, Atlanta, Georgia, said, "This is really exciting preliminary news. The results seem to suggest that clemastine may be effective in remyelination, for which we have no therapies."

She cautioned that larger studies will be needed with patients treated for longer periods of time for confirmation. "As clemastine is an anticholinergic, it will be interesting to see if it causes any worsening of some MS symptoms, such as cognitive difficulties, urinary hesitancy, or constipation," she added.

The study was funded by the University of California, San Francisco.

American Academy of Neurology (AAN) 2016 Annual Meeting. Emerging Science Abstract 008. To be presented April 19, 2016.

Case Study. - A Child with ADHD.

Today's was the 3rd reassessment of a little boy who first came to see us around 18 months ago. He was a little one lost in the tempest of his own hyperactivity. As a consequence, attentional systems had failed to develop and this in turn had affected his ability to learn, understand and produce language, to socialise and to produce sophisticated programmes for gross and fine motor development. Today, 18 months later, we still have problems with levels of physical activity, although these problems are drastically reduced. He is at the top of the developmental profile in visual and auditory cognition and in gross motor development. He has also made huge gains in language production, fine motor development and socialisation. Great to see!

How Repetition Changes the Structure of the Brain.

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

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

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

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

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

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

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

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

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

If you would like more information about the Snowdrop programme, go to our website at http://www.snowdrop.cc or email us at andrew@snowdrop.cc


Doidge, N.  The Brain that Changes itself.  Viking Press.  2007

Zuo, Y. et al. (2012). Spine tuning. Finding physical evidence of how practice rewires the brain. http://blogs.scientificamerican.com/observations/2012/04/16/spine-tuning-finding-physical-evidence-of-how-practice-rewires-the-brain/

What is Brain Plasticity?

Brain plasticity, also known as neuroplasticity, is a term that refers to the brain's ability to change and adapt as a result of experience.  In the case of brain injured children on the Snowdrop programme, that experience comes through the repetition of the developmental activities within the child's programme. 

Up until the 1960s, researchers believed that changes in the brain could only take place during infancy and childhood. By early adulthood, it was believed that the brain's physical structure was permanent. Modern research has demonstrated that the brain continues to create new neural pathways and alter existing ones in order to adapt to new experiences, learn new information and create new memories.

Psychologist William James suggested that the brain was perhaps not as unchanging as previously believed way back in 1890. In his book The Principles of Psychology, he wrote, "Organic matter, especially nervous tissue, seems endowed with a very extraordinary degree of plasticity." However, this idea went largely ignored for many years.  It is still not accepted and largely ignored by the medical community in the UK who adopt an attitude of "once a brain is injured, there is nothing which can be done," - consigning children to the 'scrapheap' of life whilst refusing to accept the evidence of plasticity and what that could mean for the child and his / her family in terms of recovery of function.  This is where the Snowdrop programme comes in, - stimulating plasticity and consequently directing the child down the correct developmental pathway. 

In the 1920s, researcher Karl Lashley provided evidence of changes in the neural pathways of rhesus monkeys. By the 1960s, researchers began to explore cases in which older adults who had suffered massive strokes were able to regain functioning, demonstrating that the brain was much more malleable than previously believed. Modern researchers have also found evidence that the brain is able to rewire itself following damage.

How Does Brain Plasticity Work?

The human brain is composed of approximately 100 billion neurons. Early researchers believed that neurogenesis, or the creation of new neurons, stopped shortly after birth. Today, it is understood that the brain possesses the remarkable capacity to reorganize pathways, create new connections and, in some cases, even create new neurons in structures such as the hippocampus.

The first few years of a child's life are a time of rapid brain growth. At birth, every neuron in the cerebral cortex has an estimated 2,500 synapses; by age of three, this number has grown to 10,000 synapses per neuron.

The average adult, however, has about half that number of synapses. Why? Because as we gain new experiences, some connections are strengthened while others are eliminated. This process is known as synaptic pruning. Neurons that are used frequently develop stronger connections and those that are rarely or never used eventually die. - 'Used frequently,' that is a key term - This is why the repetitive nature of the programme is important, so that synaptic connections associated with the developmental functions we are trying to stimulate are strengthened.  By developing new connections and pruning away weak ones in this way, the brain is able to adapt to the changing environment, - in the case of our children, the developmental environment provided by the programme.

Anyone wanting to learn more about the Snowdrop programme should email andrew@snowdrop.cc