Tag Archives: ADHD

Attention (is to Thinking) and Sustenance

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Stop. Listen to a song, podcast or have a conversation with a friend—for 30 seconds. That is about the length of time a child with severe attention issues is able to focus on any given piece of information coming from one sensory source at any given moment. Regardless of whether the time felt long or short, children today are required to not only pay attention, but pay_attentioncomprehend and take notes on the important information being delivered through a primarily one-dimensional sensory source for at least 5 minutes, but many times 20 or 30 minutes at a time.

Sustained attention is the ability to direct ones attention to a specified source without losing focus despite potential distractors. Children and adults greatly struggle with sustained attention today; the environment no longer demands it and, in many instances reinforces, the opposite. From the 10-second news clips, to the demands on attention from multiple sources ranging from text messages, to email, to the never-ending checklist of tasks needing to be completed. The length one is expected to pay attention has significantly decreased in the digital age of instantaneous communication and access to information. However this change has not only affected the world of adults and adult occupations. It has infested itself down to the youngest of children. Dr. Straub discusses what Dr. Dimitri Christakis found in a Baby Einstein episode “A Day on the Farm”, seven scene changes occurred in a 20 second period of time compared to no scene changes in a clip of Mister Roger’s Neighborhood. Taken one step-further, Mister Roger’s Neighborhood was the only show that had no impact on children’s attention span later in school when compared to children who watched no TV. Dr. Straub theorizes this is because the show was designed to increase attention span by requiring the sole focus to be on one person. Other television series, including Baby Einstein and Sesame Street had a negative impact on attention spans in school-aged children. The theory behind this is known as the overstimulation hypothesis, which states, “That is, prolonged exposure to rapid image changes during a child’s critical period of brain development preconditions their mind to expect high levels of stimulation, which leads to inattention in later life.” While pediatricians and child development experts dissuade children from being exposed to television, computers, etc., these changing demands on attention can be found in other modalities. Toys that light up, blink, play songs, talk, move all at the push of various buttons are not effectively aiding children in improving his/her sensory processing, but rather decreasing his/her ability to focus on any given stimulus sources for more than 30 seconds. This short snippet of required attention is reinforced throughout a child’s early development.

Then school happens. Children are suddenly required to pay attention for 5-15 minutes with major distractors—wiggly bodies, children and adults talking, chairs being pulled out and pushed in, etc. If these same children have been exposed to children’s so called educational programs, smartphones, electronic toys, they have essentially been set-up to fail. Their muscle for sustained attention has not be developed and it has little if anything to do with ADHD; the pace of learning is simply too slow. Their brains have been wired to expect and therefore perform in a near opposite way for the first 5 years of their life; therefore, like most new tasks, one needs to practice in order to become successful. Children today, need practice at sustaining their attention. Oftentimes these students with weakened sustained attention are automatically labeled and sometimes mislabeled as having Attention-Deficit-Hyperactivity Disorder (ADHD); however according to Dr. C. Thomas Gualtieri, et al “ADHD is not simply a disorder of sustained attention. Indeed, impairment in sustained attention is common to a certain extent to all children with psychiatric disorders. Neuropsychological studies of ADHD children and adults reveal subtle but clear impairments in ???????????????????????????????????????several complex functional systems: Selective attention memory; reaction time and information processing speed; motor speed and visuomotor ability; and executive control functions, like set-shifting, inhibitory control, and working memory.” Therefore, since one can have sustained attention weakness without having ADHD; it is essential for educators to be well-versed in understanding executive function skills as well as the vast array of researched and identified disorders that emerge during childhood. Quick fixes such as medication may not always be the best answer, especially if the cause is has been wrongly concluded.

Before wrongly labeling every attention-deficient student, steps to strengthen the sustained attention muscle are critical. One way to effectively do this is to incorporate state changes intentionally throughout the lessons in order to allow students to set-shift before becoming disengaged with the material because the content is being presented without a scene change and/or utilizing only one sense. State changes for all intensive purposes provide that ‘scene change’ the brain has become programmed to expect. Attention spans for elementary aged students range anywhere from 4 to 6 minutes; mini lessons are targeted at 5 minutes; however can easily go up to 15 or more. These numbers are based on what is average or typical; therefore there will be students whose sustained attention can barely make it to 3 minutes. Steve Roninette defines state changes as, “continually switching the sensory focus from visual to auditory to body kinesthetic and back again. This keeps students’ attention and gives them the opportunity to learn more as they tap into all their senses.” State changes come in a variety of forms and can become integrated into the lesson to enhance a particular point. They can be kinesthetic in nature and unrelated to any lesson, in which case it’s best to use them between lessons. Examples include: Brain Gym Activities, simple yoga poses, wiggle or dance breaks. Dr. Gerard Evanski explains the scientific reason behind the necessity and effectiveness of state changes, “The human brain does not store energy. The brain needs a constant blood supply, which brings it oxygen and nutrients. Dr. David Sousa has said that blood tends to pool in “our feet and our seat” when we sit for too long. Many of my state changes for students are designed to also energize them, and get their blood full of oxygen and flowing to the brain.” While kinesthetic state changes may be the most energizing, they are not the only option. State changes can also be verbal or auditory and related to the content, and therefore should be incorporated into the lesson right before students typically tune out. Examples include: turn and talks, think, pair, share, or any form of verbal/auditory recap of the lesson content. State changes can also be more passive and simply change the way information is being presented to students. For example, showing a video to reinforce the topic that was just presented.

In addition to state changes, increasing sustained attention through sustaining attention is another way. Meditation or attending to guided imagery exercises offer a non-academic way to increase sustained attention while also decreasing the cortisol release and overall levels of stress. A study conducted by Dr. Stephani Sutherland at University of Southern California, found that mindfulness training and continued practice improved sustained attention when compared to no interventchildrenion or the practice of physical relaxation, whereas there was no difference between the two groups when measuring changes in concentration and inhibition of distraction. This shows that simple and easy to use interventions can be utilized in the classroom to target and increase student’s sustained attention.

Overall, the demands placed on people in the twenty-first century significantly inhibit our ability to pay attention for long periods of time; however, the very system that educates our children and many occupations in which those same children enter demand just the opposite—an ability to focus for a duration of time and internalize information despite distractors. Until one or the other changes. It is crucial to build in opportunities to help strengthen weakened or never developed abilities to attend. Most children simply cannot come to school ready-made with a skill that is not only not expected of them or naturally reinforced in their environment, but the exact opposite skill is being applied on a daily basis. If training and teaching does not occur for children during their school-day, like many other shifts in the field of education, this will be one more that sets up children for failure instead of success.

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The Article as seen in Brainblogger.com: The Fundamentals of Neuropedagogy

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Thanks to our friends at Brainblogger, here you can read the complete article. Happy reading!

Introduction

Over the past decade, we have learned that for every student who is simple to understand or figure out, there are one or two who are a conundrum. Over this same decade we as separate and collaborative professionals have also discovered that the answer to these students’ needs being met is two-fold: 1. Education looks only at symptomology not etiology 2. Education fails to integrate disciplines effectively. Special education needs to stop being about labels and start being about the whole child.

Enter the practice of Execu-Sensory and Neuropedagogy. When we look at the child as a whole: brain, body and mind, we begin to understand that more than what teachers are taught in school is at play. Take child development, for example, this class may or may not be required to earn a Masters in Educations, especially if the focus is middle childhood rather than early or elementary.  Yet, the brain is not done growing, literally, until the age of 19 or 20 and the prefrontal cortex continues to develop until the age of 25. Not to mention, the developmental surge that takes places during adolescence is akin to the one which occurs during early childhood. How then are teachers prepared to teach the ever evolving whole child if they lack the basic knowledge of brain development.  The simple answer is they most likely cannot. The brain is a vastly complex system of electrical wiring and firing that is critical to understanding, given the goal is not only to teach, but teach effectively.

However for the purposes of this blogpost, we shall focus the discussion on the fundamentals of Neuropedagogy in practice with some aspects of Execu-Sensory components.

Structure of Neuropedagogy

Neuropedagogy in its most basic state begins with the executive function skills and the developing Pre-Frontal cortex. However when we attempt discussion with other educators, the typical response is,  “Executive what in the where? Neuro?”

Understandable response, seeing as this predominantly European concept is commonly referred in the United States as Educational Neuroscience or Neuroeducation--or perhaps more commonly not discussed among educators at all. It was introduced during an educational summit in 2009 at Johns Hopkins University simultaneously with a “Learning and the Brain” wherein organizers and educators alike agreed there needed to be an interdisciplinary field that combines neuroscience, psychology and education to create improved teaching methods and curricula. It was bringing into focus new links between arts education and general learning, how learning physically alters the brain, and what goes wrong in students with learning disabilities.

Neuropedagogy however went further than Neuroeducation. The European definition of Neuropedagogy is when science and education meet and whose scientific aims are to learn how to stimulate new zones of the brain and create connections. It is targeted at stimulating the brains of all types of learners, not only those with students who have learning disabilities. Dr. Judy Willis a practicing neurologist made a conscious transition to the classroom as an educator feels that there needs be research about the brain’s neuroplasticity and the opportunities we have as educators to help students literally change their brains — and intelligence. To become a teacher without understanding the implications of brain-changing neuroplasticity is a great loss to teachers and their future students.

Based on the experience and the research we have done on current classroom structures in New York City, we have found that the most effective use of Neuropedagogy was in three sections: Brain Element Neuropedagogy, Body Element Neuropedagogy, and Mind Element Neuropedagogy. The hierarchy of training is dependent on the prior knowledge of brain function, thus beginning the discussion with the brain was the most functional and useful approach. The body then and it’s organic processes were the next step in the training and understanding connections between innervation and control, and lastly the mind which not all fields of classroom instruction fully develop or are able to reach without the clear understanding of how the brain and the body encompass the physics of the mind.

To say the least, one would need basic brain to facilitate the body and change the mind.

The Brain Element Neuropedagogy

The most obvious reason to share information is for learning, and learning can only be achieved if there is sufficient brain function. In our practice, we lay the foundation for understanding the Central Nervous System (CNS) neurotransmission, the utilization of approximate brain mapping of the cerebral hemispheres, and raise awareness of the unmistakable impact of the digital society on the organic brain.

By organizing the hierarchy of understanding based on the processes involved from brain neurotransmission in each section of the cerebrum at any given time, we shed more light into the powerful effects of neuroplasticity, the endless ability for the brain to change itself. There are four that have been identified for learning: Acetylcholine (ACH), Serotonin, GABA, and Dopamine. Ultimately these are the communicators responsible in delivering the information to all the lobes, including the Pre-Frontal Cortex. The PFC is not currently recognized as a lobe; however, the role that it plays in learning and behavior have been measured via Executive Function Skills.

Many definitions for executive function skills exist and they all essentially make the same point. The National Center for Learning Disabilities defines executive function skills as,” mental skills that help the brain organize and act on information… [it is the ability to use] information and experiences from the past to solve current problems.” These skills are critical to understand because when they are weak or delayed in developing, they can mask themselves as an educational disability which may lay the groundwork for an Individualized Education Plan (IEP) as determined by a mutlidisciplinary team.  For example, let’s say a child is referred for an evaluation for special education services because he is showing consistent negative behavior, such as being unable to focus for more than a few minutes at a time, constantly calling out, and failing to complete homework, all of which lead to decreased academic gains.  The child will most likely be mis-classified as having ADHD or a learning disability, which ultimately leads to inefficient or worse ineffective solutions. If the interventionists applied an interdisciplinary Neuropedagogical Approach, a different and more effective outcome may have played out.

Now, let’s add a layer of dynamic complexity to Neuropedagogy. Neuroscience has looked at the brains, personalities, strengths and weaknesses of people born after 1986 and compared them with brains, personalities, strengths and weaknesses of people born before 1986. The studies show a significant difference between the two. The over-arching difference: access to the digital world.  The first group is digital natives; the second digital immigrants. Digital natives have brains that have weakened pathways for interaction, decreased activity in anterior cingulate gyrus and medial orbital frontal cortex, increased isolation, aggression, passivity, loneliness, etc, increase in cortisol due to excessive brain fatigue, decreased hippocampal size. Digital immigrants, the ones who have the capacity to hand down life experiences effectively via examples and who can communicate thoughts personally are ones who are usually comfortable with familiar technology and shy away from change in that department. They have been found to have faster PFC circuitry as they have had abilities to strengthen neuronal circuits with numerous life experiences, including delaying gratification.

WIth all of the Brain Element Neuropedagogy, one can proceed to appreciate understanding the Body and it’s unique processes.

The Body Element Neuropedagogy

In our modern society, people are perceived initially from the way they present themselves. Usually what is displayed from the external body is what immediately connects one person to the next. The body’s senses take in the physical and external world, neuronally process the input and in the cortex it’s given meaning.

From a learner’s perspective, the body is both intake and output. As interdisciplinary brain-based practitioners, we shed light into the Sensory Processing Systems, the limitless potential of a person’s Multiple Intelligences and Emotional Quotient (EQ), culminating on the influence of what we have managed to call the 3 External E’s (Ergonomics, Economics, and Environment).  The body by itself is a complete sensory organ, however it has been proven by evidence-based practice that the seven (7) senses are the checkpoints of the body: sight, sound, smell, touch, taste, movement and position in space. Research in this area was pioneered by Dr. A. Jean Ayres and current practitioners include Dr. Lucy Jane Miller and Carol Kranowitz all of who have contributed to the education and learning landscape. One simply cannot function by brain alone!

Multiple Intelligences Theory was pioneered by Howard Gardner, a developmental neuropsychologist,who played the violin well, wondered if a tool, aside from the Intelligence Quotient (IQ test), could be developed to measure additional attributes to determine a person’s complete intelligence. Another factor we considered was Daniel Goleman’s Emotional Quotient (EQ) as this too plays an important factor externally; even as the limbic system is brain centric in it’s processing of emotions, the manifestation on the outside is clearly body centric.

Education in the twentieth and now twenty first century tends to teach to two types of learners: visual and auditory. Yet, research has shown that multiple types of learners exist, not just two. Teaching methodologies need to start designing lessons, activities and classrooms not only for the typically forgotten or ever present kinesthetic learners, but for the quiet introvert and the shy extrovert and multiple combinations of them.

Simple modifications such as state changes, strategically planned brain gym breaks or yoga ball chairs have shown to improve the executive functioning skills of sustained attention and task persistence. Additionally, when inserting brief yet planned breaks of any type, students are given an opportunity to work on set-shifiting a skill in high demand in the modern digital-world.  Modifications for the introvert include quiet spaces in the classroom or projects with an option to work alone.  The shy extrovert, may benefit from group projects with assigned jobs. However, this type of differentiated instruction is believed to be fitting only to the special education population. The rest of these students, rather than adopting a label that may or may not fit, they are instructed to adapt their bodies to fit because that is what the ‘real world’ will expect of them. Meanwhile, that potential intelligence lays mostly dormant because teachers are not teaching to them, and were probably never taught how. Neuropedagogy recognizes the learning process that processes from a brain and proceeds into the body offers perspective and solutions to teaching with the body in mind.

The Mind Element Neuropedagogy

Of all of the Elements that we train, it is the Mind Element that is the most challenging to explore.The brain and the mind are used interchangeably in the realm of education; however, scientists have discovered that although they do seem to be influential of the other, the brain and mind affect each other in very different but significant ways. The psyche in psychology practice have also been associated with the mind, and pop culture usually uses the word mind loosely as choice or state of one’s mental being.

In referencing the brain, it  is the material organic matter that has the physical manifestation of the neuronal processes while the mind is where consciousness and active thinking occur. However a thought may occur from consciousness which may alter the neuronal process that was intended to happen and vice versa. The mind discussion includes: theory of mind, the belief-desire reasoning in learners, and neuroplasticity in the habit loop, Behavior Modification and Habit Routine change that can have both positive and negative effects.

Neuropedagogy of the mind starts with the premise that the mind of a child is complex. The Belief-Desire Reasoning from H.M. Wellman’s The Child’s Theory of Mind Mechanism shows just that.  Thinking, perception, sensations, beliefs, cognitive emotions, physiology, basic emotions are all interconnected and simultaneously interacting to produce desires, intentions, actions and inevitably reactions. Actions are merely the tip of the iceberg to the ongoings of a child’s, and ultimately a learner’s mind. Educators who understand and teach with Executive Function Skills such as Metacognition, Emotional Control and Response Inhibition in mind, essentially have x-ray vision, which provides them the insight to ask the questions that will reveal the iceberg. Intention is marked by a WHOLE person, a product of perception, inception and conclusions.

Conclusion: The Neuropedagogy Synthesis

ESNP's Unique Neuropedagogy Synthesis
ESNP’s Unique Neuropedagogy Synthesis

When science and education meet it is called Neuropedagogy, whose scientific aims are to learn how to stimulate new zones of the brain and create connections. The information that is presented here may appear overwhelming and less comprehensive in practice however it the changing the lens and perspective that allow best practices to occur, to remind those involved in direct service that people are not formulaic in their learning.

The Neuropedagogy synthesis demonstrates just that. One of our current partnerships, The Teaching Firms of America Professional Charter School in Brooklyn, New York applies these principles by tying choice and action to their basis in the brain, Theory of Mind, and most importantly, the brain has the ability to change.  They empower their scholars to be thinkers and owners of their actions and choices by giving them knowledge from the world of neuroscience.  Finally, the utilize the principles of Neuropedagogy to guide and inform their instruction, interactions and interventions. It is a common occurrence to hear students say, “I can change my brain.” From initial classroom set-up to end of day classroom clean up, they created and continue an atmosphere of curiosity and intellect, which always seems to start and end with the brain.

Brain Molecular Connections in Neurodevelopmental Disorders: The Interventions

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With the findings from the latest local and international research cited in our previous post, it is without a doubt that there would be a direct intervention that could bridge and ultimately correct the molecular genetic brain protein aberrations and eliminate neuronal misfiring. Current methods available however continue to border on the traditional drug therapies, behavioral therapies, and recently, an upsurge for use of adjunct and alternative therapies.

Just like any treatment however, we STRONGLY recommend to check with your physician or medical professional before embarking on any therapy or regimen. In spite of efficacy studies on these treatments, results may vary from person to person.

Adjunct therapies for neurodevelopmental disorders range from lifestyle changes to alternative therapies and diet manipulation. According to the Autism Centre in the UK, published information in 2009 suggests that a Magnesium deficiency in the electroyte serum, resulting from a magnesium deficient diet, or a diet high in sugar, salt, and saturated fats, can have an effect on neural efficiency- neuronal homeostasis-, leading to conditions on the Autism Spectrum Disorder. In view of this apparent relationship there is justification to consider supplementing the diet of newly pregnant mothers and those contemplating pregnancy with easily digestible magnesium compounds where deficient. It is in the same relationship that folic acid supplementation is proven to be efficient in reducing neural tube defects.

Other Adjunct Therapies, also called Complimentary and Alternative Therapies by the University of Maryland Medical Center, recommend Diets, Vitamins and Minerals, and even Herbs have been seen to alleviate Attention-Deficit Hyperactivity in children alongside the traditional Drug Therapies.

The Medical Center discusses in detail the different dietary options people with neurodevelopmental disorders may try, including the Feingold diet. The Feingold diet was developed in the 1970s by Benjamin Feingold. He believed that artificial colors, flavors, and preservatives, as well as naturally-occurring salicylates (chemicals similar to aspirin that are found in many fruits and vegetables), were a major cause of hyperactive behavior and learning disabilities in children. Studies examining the diet’s effect have been mixed. Most show no benefit, although there is some evidence that salicylates may play a role in hyperactivity in a small number of children.

Other dietary therapies may concentrate on eating foods that are high in protein and complex carbohydrates, and eliminating sugar and artificial sweeteners from the diet. One study found increased hyperactivity among children after eating foods with artificial food coloring and additives. However, there are no conclusive studies show no relation between sugar and ADHD as there were results that children whose diets were high in sugar or artificial sweeteners behaved no differently than children whose diets were free of these substances. This was true even among children whose parents described them as having a sensitivity to sugar.  However, there are some researchers believe that chronic excessive sugar intake leads to alterations in brain signaling, which would contribute to the symptoms associated with ADHD.

Some of Vitamins and Minerals recommended by The University of Maryland Medical Center:

Magnesium (200 mg per day) — Symptoms of magnesium deficiency include irritability, decreased attention span, and mental confusion. Some experts believe that children with ADHD may be showing the effects of mild magnesium deficiency. In one preliminary study of 75 magnesium-deficient children with ADHD, those who received magnesium supplements showed an improvement in behavior compared to those who did not receive the supplements. Too much magnesium can be dangerous and magnesium can interfere with certain medications, including antibiotics and blood pressure medications.

Vitamin B6 — Adequate levels of vitamin B6 are needed for the body to make and use brain chemicals, including serotonin, dopamine, and norepinephrine, the chemicals affected in children with ADHD. One preliminary study found that B6 pyridoxine was slightly more effective than Ritalin in improving behavior among hyperactive children. However, the study used a high dose of B6, which could cause nerve damage (although none occurred in the study). Other studies have shown that B6 has no effect on behavior.

Zinc (35 mg per day) — Zinc regulates the activity of brain chemicals, fatty acids, and melatonin, all of which are related to behavior. Several studies show that zinc may help improve behavior, slightly.

Essential fatty acids — Fatty acids, such as those found in fish and fish oil (omega-3 fatty acids) and evening primrose oil (omega-6 fatty acids), are “good fats” that play a key role in normal brain function. The results of studies are mixed, but research continues. Omega-3 fatty acids are also good for heart health in adults, but high doses may increase the risk of bleeding.

L-carnitine — L-carnitine is formed from an amino acid and helps cells in the body produce energy. One study found that 54% of a group of boys with ADHD showed improvement in behavior when taking L-carnitine, but more research is needed to confirm any benefit. Because L-carnitine has not been studied for safety in children, talk to your doctor before giving a child L-carnitine. L-carnitine may make symptoms of hypothyroid worse, and may increase the risk of seizures in people who have had seizures before.

Recommending herbs for ADHD may help strengthen and tone the body’s systems. As per the University of Maryland Medical Center Resource Center,  the use of herbs as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, make teas with 1 tsp. herb per cup of hot water. Steep covered 5 – 10 minutes for leaf or flowers, and 10 – 20 minutes for roots. Drink 2 – 4 cups per day. Tinctures alone may be used or in combination as noted.

Several herbal remedies for ADHD are sold in the United States and Europe. Only a handful of scientific studies have investigated whether these herbs improve symptoms of ADHD. Some of the more popular herbs and teas in the United States are as follows (Please note the interactions that the UMMC have indicated below):

  • Roman chamomile (Chamaemelum nobile). Chamomile may cause an allergic reaction in people sensitive to Ragweed. Chamomile may have estrogen-like effects in the body and therefore should be used with caution in people with hormone-related conditions, such as breast, uterine, or ovarian cancers, or endometriosis. Chamomile can also interact with certain medications.
  • Valerian (Valerian officinalis). Valerian can potentially interact with certain medications. Since valerian can induce drowsiness, it may interact with sedative medications.
  • Lemon balm (Melissa officinalis). Lemon balm may interact with sedative medications.
  • Passionflower (Passiflora incarnata). Passionflower may interact with sedative medications.

Other herbs commonly contained in botanical remedies for ADHD include:

  • Gingko (Gingko biloba) — used to improve memory and mental sharpness. Gingko needs to be used with caution in patients with a history of diabetes, seizures, infertility, and bleeding disorders. Gingko can interact with many different medications, including but not limited to, blood-thinning medications.
  • American ginseng (Panax quinquefolium) and gingko — One study suggests that gingko in combination with ginseng may improve symptoms of ADHD. American ginseng should be used with caution in patients with a history of diabetes, hormone-sensitive conditions, insomnia, or schizophrenia. It can interact with several medications, including but not limited to, blood-thinning medications.

Relaxation techniques and massage can reduce anxiety and activity levels in children and teens. It was determined in one study that teenage boys with ADHD who received 15 minutes of massage for 10 consecutive school days showed significant improvement in behavior and concentration compared to those who were guided in progressive muscle relaxation for the same duration of time.

Also in a study of 43 children with ADHD, those who received an individualized homeopathic remedy showed significant improvement in behavior compared to children who received placebo. The homeopathic remedies found to be most effective included:

  • Stramonium — for children who are fearful, especially at night
  • Cina — for children who are irritable and dislike being touched; whose behavior is physical and aggressive
  • Hyoscyamus niger — for children who have poor impulse control, talk excessively, or act overly exuberant

Brain Molecular Protein Connections in Neurodevelopmental Disorders: The Research

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It is not news to us in the field that researchers looking to determine causation of Neurodevelopmental Disorders have zeroed in on Molecular Proteins in the brains. To be specific, these disorders (namely Epilepsy, Intellectual Disability, Autism Spectrum Disorder, and Attention Deficit Hyperactivity Disorder) are being hailed as brain-based disorders due to the surging evidence in the last 2 years that indeed, some molecular proteins are atypical in both brain origin and development.

Let’s begin the survey in August 2013 where genetic studies were initiated in large scale. An international study on the genes involved in Epilepsy Disorder had uncovered 25 new mutations on 9 key genes behind a devastating form of epilepsy disorder during childhood. Among those were two genes never before associated with this form of epilepsy. One of these genes previously had been linked to autism and a rare neurological disorder, for which an effective therapy had previously been developed. With the findings of this research, the direction for developing genome-wide diagnostic screens for newborns to identify who is at risk for epilepsy improves potentially development of precise therapies for the condition.

“The limitations of what we currently can do for epilepsy patients are completely overwhelming,” said Daniel Lowenstein, MD, a UCSF neuroscientist and epilepsy expert. Along with Ruben Kuzniecky, MD from New York University, the pair was overseeing the Epilepsy Phenome/Genome Project (EPGP). “More than a third of our patients are not treatable with any medication, so the idea of finding specific drug targets, instead of a drug that just bathes the brain and may cause problems with normal brain function, is very appealing.”

“We knew there was something happening that was unique to these kids, but we had no idea what that was,” said Elliott Sherr, MD, PhD. He a pediatric neurologist at UCSF Benioff Children’s Hospital, and is the principal investigator of the Epi4K Epileptic Encephalopathy (EE) project. He was responsible for the development of this group of the target research patients within EPGP.

The team identified in in their research children with two classic forms of EE – infantile spasms and Lennox-Gastaut Syndrome – in which no other family member was affected. They excluded children who had identifiable causes of epilepsy, such as strokes at birth, which are a known risk for this group of disorders. Of the 4,000 patients whose genomes are being analyzed in the Epi4K, 264 children fit that description. The Epi4K sequencing team, led by David Goldstein, PhD from Duke University ran a genetic scan on the children and their parents.  They compared their scans to thousands of people of similar heritage without epilepsy,  used a cutting-edge new technique called exome sequencing. This method focuses on the exome, which is the 2 percent of our genetic code that represents active, protein-making genes. Those 25,000 genes are considered to be the code for what makes us unique, and is also responsible for disease mutations.

The genetic analysis revealed 439 new mutations in the children, with 181 of the children having at least one. Nine of the genes that hosted those mutations appeared in at least two children with EE and five of those had shown up in previous, smaller EE studies. Of the four other genes included, two may have been coincidental, the researchers found. But two new genes never before associated with EE – known scientifically as GABRB3 and ALG13 – each appeared with less than a one-in-40-billion statistical chance (p = 4.1×10-10) of being connected to EE by coincidence.

The findings implicated GABRB3, for the first time, as a single-gene cause of EE, and offered the strongest evidence to date for the gene’s role in any form of epilepsy, Sherr said. Knowing this about GABRB3, which is also involved with Angelman’s Syndrome, also offers the possibility that children with mutations only in this gene might benefit from the existing therapy for Angelman’s.

Another new gene, ALG13, is key to putting sugars on proteins, which points to a new way of thinking about the causes of and treatment for epilepsy.

‘The take-home is that a lot of these kids have genetic changes that are unique to them,” Sherr said. “Most of these genes have been implicated in these or other epilepsies – others were genes that have never been seen before – but many of the kids have one of these smoking guns.”

From GABRB3 and ALG13 genes in Epilepsy to misfiring neurons in the ADHD brain, the evidence continues to mount on how one size results do not fit all.  In June 2104, Neuroscientists collaborating from the Mayo Clinic in Florida and  rom Aarhus University in Denmark have shed light on why neurons in the brain’s reward system can be miswired, potentially contributing to disorders such as attention deficit hyperactivity disorder (ADHD).

In their study, scientists looked at dopaminergic neurons, which regulate pleasure, motivation, reward, and cognition, and have been implicated in development of ADHD. Together they unveiled a receptor system that is critical for correct wiring of the dopaminergic brain area during embryonic development. However they also discovered that after brain maturation, a cut in the same receptor, SorCS2, produces a two-chain receptor that induces cell death following damage to the peripheral nervous system.

It is the SorCS2 receptor that functions as a molecular switch between apparently opposing effects in proBDNF. ProBDNF is a neuronal growth factor that helps select cells that are most beneficial to the nervous system, while eliminating those that are less favorable in order to create a finely tuned neuronal network. The reserchers also found that some cells in mice deficient in SorCS2 are unresponsive to proBDNF and have dysfunctional contacts between dopaminergic neurons.

“This miswiring of dopaminergic neurons in mice results in hyperactivity and attention deficits. A number of studies have reported that ADHD patients commonly exhibit miswiring in this brain area, accompanied by altered dopaminergic function. We may now have an explanation as to why ADHD risk genes have been linked to regulation of neuronal growth,” says the study’s senior investigator, Anders Nykjaer, M.D., Ph.D., a neuroscientist at Mayo Clinic in Florida and at Aarhus University in Denmark.

On the other hand, a study published by Cell Press in the October 2014 issue of  The American Journal of Human Genetics shows that Neurodevelopmental Disorders caused by distinct genetic mutations produce similar molecular effects in cells. This suggests a unique perspective in that a one-size-fits-all therapeutic approach could be effective for conditions, ranging from seizures to attention-deficit hyperactivity disorder.

“Neurodevelopmental disorders are rare, meaning trying to treat them is not efficient,” says senior study author Carl Ernst of McGill University. “Once we fully define the major common pathways involved, targeting these pathways for treatment becomes a viable option that can affect the largest number of people.”

Ernst and his team used human fetal brain cells to study the molecular effects of reducing the activity of genes that are mutated in two distinct autism-spectrum disorders. Changes in transcription factor 4 (TCF4) cause 18q21 deletion syndrome, which is characterized by intellectual disability and psychiatric problems. Mutations in euchromatic histone methyltransferase 1 (EHMT1) cause similar symptoms in a condition known as 9q34 deletion syndrome.  “Our study suggests that one fundamental cause of disease is that neural stem cells choose to become full brain cells too early. This could affect how they incorporate into cellular networks, for example, leading to the clinical symptoms that we see in kids with these diseases,” Ernst says.

So far, we have learned about breakthroughs in genetic studies in Epilepsy, discoveries of misfiring of neurons in ADHD and in long lasting effects of mutations of certain brain cells leading to Intellectual Disability or psychiatric problems. Now let’s take a closer look at Austism Spectrum Disorder. Would we find some molecular or genetic aberration? Stanford University researchers in December 2014 mapped an entire molecular network of crucial protein interactions that contribute to autism.

While “much work remains to be done,” Dr. Charles Auffray of Université de Lyon who collaborated with the researchers, states this  is “a bold attempt to leverage a number of rich sources of data and knowledge and to complement them with relevant additional measurements to unravel the molecular networks of ASD.”

Though further research is needed to fully understand autism’s origins, this study “contributes to the development of an openly shared methodological framework and tools for data analysis and integration that can be used to explore the complexity underlying many other rare or common diseases,” Auffray said.

In this current study of autism, the scientists did not just look at genes, they also looked at gene expression — the protein interactions — in patients with autism. After they had identified a “protein interaction module,” the researchers sequenced the genomes of 25 patients to confirm its involvement in autism.  They then validated these findings with data from 500 additional patients. In the next step, the team examined gene expression within the module, partly by using the Allen Human Brain Atlas.

It was in this stage that the researchers discovered the brain’s corpus callosum and oligodendrocyte cells  made important contributions to ASD. Developmentally, the oligodendrocyte cells help form myelin, the insulating sheath of brain cells necessary for high velocity nerve conduction. And for patients with autism, for instance, these cells exhibited extensive gene mis‐expression in the corpus callosum, the bundle of nerve fibers connecting left and right brain hemispheres.

The findings from the Stanford University study were not only supported in 2014 by the Heidelberg University but also given more specificity in the mutations not only for those with ASD, but for neurodevelopmental disorders in general.  These German Researchers posited that generally, these disorders are multi-faceted and can lead to intellectual disability, autism spectrum disorder and language impairment. Mutations in the Forkhead box FOXP1 gene have been linked to all these disorders, suggesting that it may play a central role in various cognitive and social processes.

Dysfunction of motor, social, sensory and cognitive aspects play a major role in autism spectrum disorder (ASD) and intellectual disability (ID). A high comorbidity is often observed between these disorders, suggesting that mutations in critical genes can cause a spectrum of neuropsychiatric phenotypes. The Forkhead box transcription factor FOXP1, for example, has been linked to various cognitive disorders. FOXP1-specific deletions, mutations and chromosomal breakpoints interrupting the gene have been reported in patients with Intellectual Disability, Autism Spectrum Disorder, speech and language deficits, and motor development delay.

They were interested to examine the behavioral phenotype of our Foxp1 KO mice, as FOXP1 mutations are associated with various behavioral deficits in humans, including social unattainability, hyperactivity, altered learning and memory, and specific obsessions.Results showed:  Foxp1 KO mice have a reduced ability for short-term recognition memory and memory for spatial contexts, which have been described before in ASD patients and in mouse models of ASD. The effect on spatial memory may be explained by the CA1 hippocampal deficits we observed in Foxp1 KO as the hippocampus is important for spatial memory. The disruption of the striatal region in Foxp1 KO mice may also contribute to the deficits in learning and memory. It has been shown that striatal lesions and infusion of the striatum with a dopaminergic antagonist results in impaired performance in spatial learning tests, while object recognition is impaired by administration of glutamate antagonists to the striatum. Interestingly, the striatum has previously been associated with the pathology of ASD in both mice and humans.

Foxp1 KO mice also displayed a higher occurrence of repetitive behaviours, in accordance with previous findings in mouse models of autism. Repetitive motor behavior is associated with abnormal activation of dopaminergic cortical-basal ganglia circuitry and therefore might partially be explained by the morphological disruption we observed in the striatal region.

They also recorded a striking reduction of social interest  in Foxp1 KO mice. Difficulties communicating and interacting with other people is a key feature of human ASD, and reduced social interaction as well as hyperactivity has been reported in mouse models of ASD before. A strong PPI deficit was observed in Foxp1 KO mice, indicating impaired abilities for sensorimotor integration. Reduced PPI has been previously reported in ASD patients. This effect on PPI in Foxp1 KO mice may be partly explained by the reduction in the striatal region as a cortico-limbic-striatopallidal circuit is involved in the circuit regulating PPI.

Excitatory and inhibitory imbalance is a hallmark brain feature of Autism Spectrum Disorder. Several studies have reported that ASD-related mutations selectively impact glutamatergic or GABAergic synapses without affecting the other, leading to an imbalance of excitatory and inhibitory inputs. WIth their research, they have ultimately shown that the amplitude of miniature excitatory postsynaptic currents but not miniature inhibitory postsynaptic currents is larger in Foxp1 KO CA1 hippocampal neurons. This suggests that  Foxp1 KO neurons receive a disproportionate magnitude of excitatory to inhibitory input. In addition, excitability of CA1 pyramidal cells was reduced in Foxp1 KO mice.

With all this information, it is possible to hypothesize that treatment protocol will also change to a more direct, molecular level based on the genetic misfiring or aberration. In the next post, we will discuss the current therapeutic interventions available for these disorders.

Is it Negative Behavior or ADHD Sensory Overload? An Educator’s Quick Reference

Brain Bits, , , , , , , , , , , ,

How many times have students been pigeon-holed into the category of displaying bad or negative behavior when opposing class work or during transitions from a state of play or break back to the classroom and vice versa?

When the body appears like this during an overt meltdown:

What May Look Like This May Actually Not Be...
What May Look Like This May Actually Not Be…

The Brain Actually looks like this:

The Amygdala and Hypothalamus Fired Up in Fight or Flight State
The Amygdala and Hypothalamus Fired Up in Fight or Flight State

The Emotional Brain that is highlighted are two specific parts of the limbic system, the amygdala and the hypothalamus. The amygdala controls the brain’s ability to coordinate many responses to emotional stimuli, including endocrine, autonomic, and behavioral responses. Stress, anxiety, and fear are primary stimuli that produce responses. Mediation by the amygdala allows control among the stimuli.

The hypothalamus plays a significant role in the endocrine system and are effected by the amygdala. It is responsible for maintaining your body’s internal balance, which is known as homeostasis. This includes the  heart rate, blood pressure, fluid and electrolyte balance, appetite, sleep cycles and is the key connector between the endocrine system (glands and hormones) and the nervous system.

Now we are painting this picture of the brain developing at a functionally optimal manner; without aberrations from either genetic means or environmental factors. However, when faced with students who have underlying imaging differences in brain imaging due to the said factors and manifest a type of negative behavior that can easily be mistaken and categorized as a regular tantrum, the subtle elevations in amygdala and hypothalamic responses are now pushed to abnormally erratic levels in these brains.

For example, take the Attention Deficit Hyperactivity Brain in comparison to the Normal Brain:

We see clearly that the shape alone of the cerebrum of the ADHD brain is not elongated or similar to a normal brain’s saddle

Imaging of the Normal Brain in Contrast to the ADHD brain
Imaging of the Normal Brain in Contrast to the ADHD brain

type shape. It is oblong and with heavy concentration on temporal and occipital real estate versus the butterfly formation of the normal brain. What is also fascinating is the corpus callosum (where part of the amygdala and hypothalamus are housed) is lighter in the ADHD brain. What that means is that there is no clear path of communication between both hemispheres as compared to that of a normal brain. The blues indicate calm sections of the brains and the greens are considered to be the brain in an even keeled state, balanced and not in fight-flight mode.

Here’s also an image of a person with and without ADHD medication:

Brain Chemical Responses with Adderall Versus Without Adderall
Brain Chemical Responses with Adderall Versus Without Adderall

With Adderall, the brain is utilized in full functional capacity, the chemical connections between neurotransmitters is efficient and there are little if any underutilized processing areas. When Adderall is wearing off, the results are unimaginable: the only sections  of the brain that have any residual function left are the orbitofrontal area of the Pre Frontal Cortex (responsible for sensory integration and some decision making), and spotty areas across the 4 lobes. What is fascinating to mention here is the loss of Adderall effects are from back to front of the cerebrum.

These images provide a very clear picture of the typical versus atypical brain, especially the differences between one with ADHD and one without.   If ony it were that easy as a classroom teacher to distinguish a student with ADHD from a student with  sensory overload.  The list below is not as ‘yellow’ and ‘red’ as the brains above, but hopefully it will provide clarity and a concrete direction for you to take in order to best meet the needs of your students.

First, it crucial to note that boys and girls with ADHD display different symptoms; therefore, they are distinguished below.  Second, students with meltdowns as a result of negative behavior, will most likely present with similar symptoms; therefore, it is an undertaking for teachers to take quantitative data on the targeted behaviors. Forms like the one below:

TRUE ABC Chart For Objective DATA Collection
TRUE ABC Chart For Objective 5 Session DATA Collection (click for printable image)

BOYS

  • Fidgety while sitting
  • Talk nonstop
  • Constant motion, may include touching items in their path
  • Difficulty sitting still
  • extreme impatience
  • Always “bored”
  • Lack verbal filter
    Sensory Overload or Negative Behavior?
  • Interrupt others’

GIRLS

  • Spacey
  • Unfocused
  • Inattentive
  • Trouble with organization
  • Forget directions
  • Forget or incomplete homework
  • Lose or misplace papers, books, personal belongings
  • Much Less Likely
    • hyperactive
    • impulsive

For students with ADHD, these symptoms as well as sensory overload meltdowns will be manifested consistently throughout the day across environments, unless the student is highly engaged in a preferred activity. Students presenting with negative behaviors will have meltdowns at specific yet intermittent periods of the day or throughout the day as will be shown in the ABC Chart above. For example, when the medication is wearing off, one may see a spike in ADHD symptoms in any combination. Once you can answer when, where, how long and make valid hypotheses as to why students are displaying the behaviors below, you should be able to have a pretty strong understanding as to whether your student is having a meltdown because of learned negative behaviors or as a result of having an ADHD brain on sensory overload.