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

Walking After 11 Months on the Snowdrop Programme

This young man from the United States has hemiplegic cerebral palsy.  He has been on the Snowdrop 'distance programme' (a programme where the child is assessed remotely via questionnaire and video footage), for just 11 months.  When he first started the programme he wasn't even crawling, but he has made incredible progress and here he is demonstrating his new found skill of walking.

Max's Story.

This post was written a couple of days ago by a mum from Australia who has a little boy on our distance programme.  Max has been on the Snowdrop programme for around 12 months and in that time he has made incredible progress.  Although your kind words are much appreciated Faith, you are the real star here, having worked incessantly to rescue your little boy from the depths of brain injury.

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Wake up Sleepyhead

 

I started writing this blog, about 2 weeks after Max's stroke. A good friend suggested it might be cathartic to write about our experiences. It's also been a good way to disseminate information everyone wanted to know. In the first few weeks of writing, I wrote furiously to get all the facts down on paper before I forgot them. My early posts are pretty crappy and straight to the point. Over time, I've written a few 'flashback' posts, and talked about certain events in more detail. Which is exactly what this post is going to be....

Max spent about 2 days officially, in a medically induced coma. It was the only way, they could stop the seizures which was causing his brain to dangerously swell. It probably sounds strange, but I was grateful for those 2 comatose days. It gave me a chance to process everything which was going on. Every medical professional I spoke to in those 2 days, uttered the same phrase "we'll know more about his prognosis, once he's out of the coma". I was in no hurry for him to wake up, I was petrified of the reality we were going to face. 

In those 2 days, I sat with him, with every intention of reading him stories and singing his favourite songs. I never did either of those things because I couldn't find the strength. Instead, I cleaned his eyes when they got mucky, I cleaned his mouth and kept his lips moist. Occasionally, I changed his nappy, although there wasn't much point because he had a catheter and his bowels were essentially 'paralyzed'. 

The thing I did most of all, during those days, was think. I had no idea who my son would be when he woke up. By that stage, we knew he had permanent brain damage but didn't know how it would affect him. Would he be permanently paralyzed? Would he be dependent on me for the rest of his life? Would he be mentally handicapped? Would he ever do those 'normal' things that other parents take for granted? I feel a little ashamed, but the one thought which had the most air time, was 'I never signed up for this sh*t'.

Coming out of a coma is nothing like you see in the movies. On TV, the (beautifully made up) comatose patients eyelids flutter before they slowly open, they look at the person sitting lovingly by their bedside and stutter "wh-wh-at happened?". 

In reality, the process is very long and extremely tedious. For 2 days, I'd basically seen, no signs of life from my baby. No twitching, no eyelid flutters, no response to anything. 100% of his breathing was done by a life support machine. Slowly, we started to see little twitches, his eyes started moving behind closed eyelids and every now and then, he breathed for himself. His eyes didn't flutter open like they do in the movies. They opened millimeter by millimeter, over the course of 24 hours. Once they were open, his gaze was vacant. 

There's one particular photo, I look at fairly often which tells the story of how far we've come since last June. It was taken by my mother on the day Max started coming out of the coma. I don't think I took any photos on that day, because it hurt like hell. When I think back to that day, I still feel the stabbing pain in my heart. 




It took days, maybe even weeks for the Thiopental (aka Coma drug), to wash out of his body. The doctors explained in laymans terms, Thiopental literally soaks into every fat and muscle cell of the body. It was going to take his little body awhile to rid itself of the drug (Incidentally, I later discovered, Thiopental is the first of the 3 lethal injections given in executions- I'm glad I didn't know that at the time). 

Even after the Thiopental and pain killers were out of his system, Max was still a space cadet. He would've been happy lying in his cot all day and staring at the wall. Not once did I let him do that. When Max was awake, Max's brain was being stimulated somehow. We played music, read stories and took him for walks around the hospital. I was the crazy mummy, who took her baby to the Starlight room and joined in the art groups. Despite all of this, he was still pretty vague. I could bang saucepans only meters away from him and he wouldn't respond. Yet, we knew, his hearing was perfect. 




After months of (slightly obsessive) researching, I started Max on the Snowdrop Program. He literally 'woke up' after only one day of the program. On Monday, I could carry him into the shops easy peasy. On Tuesday, he was a humanoid Octopus who tried to grab everything off the shelves. 

Looking at him now, it's almost impossible to believe he's the same child. Check out these recent pictures, he is alert, hyperactive and incredibly mischievous. 




















From a physical perspective, we still have a long way to go, but that's a whole other post. I have days, when the cheeky little sod is driving me batty and I have to remind myself of how far he's come. There aren't enough ways to say thank you to Andrew and the Snowdrop Program. It's my greatest wish, for us to travel to the UK, because there's one thing I really need to say to him in person. "Thank you for bringing my son back". 

This isn't a sponsored post but for anyone wanting to know more about the program, here's the link- 

Snowdrop for Brain Injured Children