From Cognitive and Behavioral Neurology
In September, 2011, the journal Cognitive and Behavioral Neurology published the results of a study by a group of leading researchers. Their lengthy paper was entitled, Neuropsychological Assessment: A Valuable Tool in the Diagnosis and Management of Neurological, Neurodevelopmental, Medical and Psychiatric Disorders.
Those findings have since been embraced in a position paper issued by the American Psychological Association.
Why is this of interest? Because the authors stressed the value of complete neuropsychological evaluations, which they clearly distinguished from school-based, psycho-educational and other, more limited types of assessments.
Here, for example, is its section on children and adolescents:
PEDIATRICS
"In addition to measuring the neurocognitive consequences of specific central nervous system abnormalities in children, neuropsychological assessment is widely used to evaluate complex learning and behavior problems.
Neuropsychological assessment is particularly valuable when a child presents with worsening psychiatric, family, neurodevelopmental, attention, or learning issues. Coexisting learning disabilities or attention-deficit disorder can lessen the effectiveness of interventions unless the separate but overlapping conditions are recognized and their management specifically integrated into treatment plans.
Psychiatric and complex family issues may further complicate the diagnostic picture and render checklist data or school-based psychoeducational evaluation alone ineffective for diagnostic and treatment planning purposes.
Particularly when multiple factors affect learning and behavior, a lack of specificity about a child’s cognitive strengths and weaknesses limits the utility of school-based psychoeducational evaluations for treatment planning.
Further, the neuropsychological assessment’s integrative nature is ideal for explaining the impact of psychiatric and emotional factors on cognitive and academic performance."
Tuesday, July 31, 2012
Heading Into Brain Injury – Should We Be Concerned?
From BrainBlogger.com - Neuroscience & Neurology
By Amy Wong, M.S.
July 29, 2012
"... it is recommended that proper heading techniques should be employed to minimize energy transfer to the brain."
Like any other sports fanatic, nothing else evokes a greater wave of emotional outbursts from me than a really good game. Whether I am watching a speedy game of basketball or a crawling game of baseball, feelings of celebration, anxiety, and disappointment can billow through my body within the span of a few seconds. In June, the UEFA Euro 2012 was all the rage amongst sports fans, causing many professionals to cancel work meetings, return late from lunch breaks, or simply remain home on the grounds of an “unidentified but completely legitimate sickness”.
As I was one of those many individuals crowding around a large food court flat screen, milking the last few seconds of my fifth (and very necessary) break, I could not help but cringe every time I witnessed a player heading a soccer ball.
Because I work in trauma research, I have become very familiar with cases of chronic traumatic encephalopathy (CTE) in professional athletes. CTE is a progressive neurodegenerative disease that can only be diagnosed post-mortem in individuals who have suffered from repetitive head trauma. Gross pathological findings of CTE include reduced brain weight, enlarged lateral and third ventricles, thinning of the corpus callosum, cavum septum peallucidum with fenestrations, scarring, and neuronal loss of the cerebellar tonsils. The disease has been closely tied to athletes who participate in contact sports like boxing, martial arts, American football, professional wrestling and hockey.
Although CTE cannot be verified until post-mortem, those who do suffer from the disease have been reported to lead difficult lives. Take for example, the case of Andre Waters, a retired NFL player who took his life in 2006 at the young age of 44. Prior to his untimely death, Waters manifested a history of cognitive and neuropsychiatric impairments which included chronic depression, suicide attempts, insomnia, paranoia, and impaired memory.
Even more concerning was that this was not the first reported incidence of CTE in a retired NFL player. Previous cases had also documented mental disorders in these subjects, including depression, deficits in memory and judgment, and Parkinsonian symptoms.
Despite years of mass media coverage criticizing the impact of head-jarring sports on the brain, the concern for “heading” in soccer players have only recently surfaced. Heading is a technique unique to the sport whereby players use their unprotected heads to deflect, stop, or redirect the ball for both offensive and defensive purposes.
In November, 2011, researchers from the Albert Einstein College of Medicine in New York reported that professional soccer players who frequently “head” the ball (approximately 1000-1500) times a year may develop changes in the brain analogous to those with mild traumatic brain injury (mTBI).
"...professional soccer players who frequently “head” the ball (approximately 1000-1500) times a year may develop changes in the brain that are analogous to those with mild traumatic brain injury (mTBI)."
The researchers tested two groups of soccer players: frequent headers versus non-frequent headers based on their responses to a detailed and standardized questionnaire. An advanced magnetic resonance technique known as diffusion tensor imaging (DTI) was used to measure microscopic changes in the brain’s white matter.
In healthy white matter, the direction of water movement is fairly uniform whereas previous studies have associated mTBI with disruption of this uniformity. The investigators found that frequent headers had significant disruptions in uniformity in the frontal, temporal, and occipital regions compared to infrequent headers.
In fact, there has been one publically reported case of a “formidable header” who died in 2002 from a degenerative brain disease. Jeffrey Astle, a legendary figure in England who peaked in his career in the 1960s was found to have histological changes in his brain consistent with CTE. These deformities lead the coroner to conclude that minor repetitive trauma was the cause of his death and a verdict of ‘‘death by industrial disease” was documented.
Where do these reports leave soccer moms and their maternal duty to protect their children’s mental capacity? Before anyone jumps into panic mode, let us review the evidence thus far. First, researchers have reported that frequent headers may develop changes in the brain that are similar to those with mTBI. However, this statement should be interpreted with caution as the study had a small sample size (n=38), only 25% were women with no children included, and the number of “heads” per year were based on retrospective self-report by the participants.
Second, Jeffrey Astle succumbed to a “death by industrial disease”. However, the leather balls used during his career were much heavier and could easily absorb moisture over the course of a game, adding as much as 20% extra weight. If we recall Newton’s second rule of force = mass x acceleration, then the force of impact between the ball and the player’s cranium should be dependent on the mass of the ball (i.e. the greater the mass, the greater the force impacting a player’s head). Today, the balls used are much lighter and made entirely of synthetic, hydrophobic material.
"However, there is little evidence to prove that heading in today’s soccer can lead to CTE, and the research conducted so far is certainly insufficient to support the ban of heading altogether."
There is no denying that repetitive impact to the head can have cumulative detrimental effects that may lead to long-term psychological consequences. However, there is little evidence to prove that heading in today’s soccer can lead to CTE, and the research conducted so far is certainly insufficient to support the ban of heading altogether. Until then, it is recommended that proper heading techniques should be employed to minimize energy transfer to the brain.
Still, I cannot help but twitch every time I witness the ball impact a player’s head. I fear that repetitive heading may only become clinically evident decades into the future—when it has already become too late for our generation now.
References
Omalu, B.I., DeKosky, S.T., Minster, R.L., Kamboh, M.I., Hamilton, R.L., & Wecht, C.H. (2005). Chronic traumatic encephalopathy in a National Football League player. Neurosurgery, 57 (1) PMID: 15987548
Omalu, B.I., DeKosky, S.T., Hamilton, R.L., Minster, R.L., Kamboh, M.I., Shakir, A.M., & Wecht, C.H. (2006). Chronic traumatic encephalopathy in a national football league player: part II. Neurosurgery, 59 (5) PMID: 17143242
Omalu, B.I., Hamilton, R.L., Kamboh, M.I., DeKosky, S.T., & Bailes, J. (2010). Chronic traumatic encephalopathy (CTE) in a National Football League Player: Case report and emerging medicolegal practice questions. Journal of Forensic Nursing, 6 (1), 40-6 PMID: 20201914
Radiological Society of North America (2011). ‘Heading’ A Soccer Ball Could Lead to Brain Injury. [Press release]. Retrieved from http://www2.rsna.org/timssnet/media/pressreleases/pr_target.cfm?ID=564
Saulle, M., & Greenwald, B.D. (2012). Chronic traumatic encephalopathy: a review. Rehabilitation Research and Practice, 2012 PMID: 22567320
About Amy Wong, M.S.
Amy Wong, MS, is a medical writer and conducts traumatic brain injury research in a large academic institution. She holds a Master’s of Science from the University of Toronto in the department of Pharmacology. Her studies pertained to the selective field of neuropsychopharmacology, examining the biological implications of post-stroke depression.
Related Articles
Traumatic Brain Injury: A Silent Epidemic
Brain Development and College Football
Mind-Brain Connection: PTSD and Concussions
By Amy Wong, M.S.
July 29, 2012
"... it is recommended that proper heading techniques should be employed to minimize energy transfer to the brain."
Like any other sports fanatic, nothing else evokes a greater wave of emotional outbursts from me than a really good game. Whether I am watching a speedy game of basketball or a crawling game of baseball, feelings of celebration, anxiety, and disappointment can billow through my body within the span of a few seconds. In June, the UEFA Euro 2012 was all the rage amongst sports fans, causing many professionals to cancel work meetings, return late from lunch breaks, or simply remain home on the grounds of an “unidentified but completely legitimate sickness”.
As I was one of those many individuals crowding around a large food court flat screen, milking the last few seconds of my fifth (and very necessary) break, I could not help but cringe every time I witnessed a player heading a soccer ball.
Because I work in trauma research, I have become very familiar with cases of chronic traumatic encephalopathy (CTE) in professional athletes. CTE is a progressive neurodegenerative disease that can only be diagnosed post-mortem in individuals who have suffered from repetitive head trauma. Gross pathological findings of CTE include reduced brain weight, enlarged lateral and third ventricles, thinning of the corpus callosum, cavum septum peallucidum with fenestrations, scarring, and neuronal loss of the cerebellar tonsils. The disease has been closely tied to athletes who participate in contact sports like boxing, martial arts, American football, professional wrestling and hockey.
Although CTE cannot be verified until post-mortem, those who do suffer from the disease have been reported to lead difficult lives. Take for example, the case of Andre Waters, a retired NFL player who took his life in 2006 at the young age of 44. Prior to his untimely death, Waters manifested a history of cognitive and neuropsychiatric impairments which included chronic depression, suicide attempts, insomnia, paranoia, and impaired memory.
Even more concerning was that this was not the first reported incidence of CTE in a retired NFL player. Previous cases had also documented mental disorders in these subjects, including depression, deficits in memory and judgment, and Parkinsonian symptoms.
Despite years of mass media coverage criticizing the impact of head-jarring sports on the brain, the concern for “heading” in soccer players have only recently surfaced. Heading is a technique unique to the sport whereby players use their unprotected heads to deflect, stop, or redirect the ball for both offensive and defensive purposes.
In November, 2011, researchers from the Albert Einstein College of Medicine in New York reported that professional soccer players who frequently “head” the ball (approximately 1000-1500) times a year may develop changes in the brain analogous to those with mild traumatic brain injury (mTBI).
"...professional soccer players who frequently “head” the ball (approximately 1000-1500) times a year may develop changes in the brain that are analogous to those with mild traumatic brain injury (mTBI)."
The researchers tested two groups of soccer players: frequent headers versus non-frequent headers based on their responses to a detailed and standardized questionnaire. An advanced magnetic resonance technique known as diffusion tensor imaging (DTI) was used to measure microscopic changes in the brain’s white matter.
In healthy white matter, the direction of water movement is fairly uniform whereas previous studies have associated mTBI with disruption of this uniformity. The investigators found that frequent headers had significant disruptions in uniformity in the frontal, temporal, and occipital regions compared to infrequent headers.
In fact, there has been one publically reported case of a “formidable header” who died in 2002 from a degenerative brain disease. Jeffrey Astle, a legendary figure in England who peaked in his career in the 1960s was found to have histological changes in his brain consistent with CTE. These deformities lead the coroner to conclude that minor repetitive trauma was the cause of his death and a verdict of ‘‘death by industrial disease” was documented.
Where do these reports leave soccer moms and their maternal duty to protect their children’s mental capacity? Before anyone jumps into panic mode, let us review the evidence thus far. First, researchers have reported that frequent headers may develop changes in the brain that are similar to those with mTBI. However, this statement should be interpreted with caution as the study had a small sample size (n=38), only 25% were women with no children included, and the number of “heads” per year were based on retrospective self-report by the participants.
Second, Jeffrey Astle succumbed to a “death by industrial disease”. However, the leather balls used during his career were much heavier and could easily absorb moisture over the course of a game, adding as much as 20% extra weight. If we recall Newton’s second rule of force = mass x acceleration, then the force of impact between the ball and the player’s cranium should be dependent on the mass of the ball (i.e. the greater the mass, the greater the force impacting a player’s head). Today, the balls used are much lighter and made entirely of synthetic, hydrophobic material.
"However, there is little evidence to prove that heading in today’s soccer can lead to CTE, and the research conducted so far is certainly insufficient to support the ban of heading altogether."
There is no denying that repetitive impact to the head can have cumulative detrimental effects that may lead to long-term psychological consequences. However, there is little evidence to prove that heading in today’s soccer can lead to CTE, and the research conducted so far is certainly insufficient to support the ban of heading altogether. Until then, it is recommended that proper heading techniques should be employed to minimize energy transfer to the brain.
Still, I cannot help but twitch every time I witness the ball impact a player’s head. I fear that repetitive heading may only become clinically evident decades into the future—when it has already become too late for our generation now.
References
Omalu, B.I., DeKosky, S.T., Minster, R.L., Kamboh, M.I., Hamilton, R.L., & Wecht, C.H. (2005). Chronic traumatic encephalopathy in a National Football League player. Neurosurgery, 57 (1) PMID: 15987548
Omalu, B.I., DeKosky, S.T., Hamilton, R.L., Minster, R.L., Kamboh, M.I., Shakir, A.M., & Wecht, C.H. (2006). Chronic traumatic encephalopathy in a national football league player: part II. Neurosurgery, 59 (5) PMID: 17143242
Omalu, B.I., Hamilton, R.L., Kamboh, M.I., DeKosky, S.T., & Bailes, J. (2010). Chronic traumatic encephalopathy (CTE) in a National Football League Player: Case report and emerging medicolegal practice questions. Journal of Forensic Nursing, 6 (1), 40-6 PMID: 20201914
Radiological Society of North America (2011). ‘Heading’ A Soccer Ball Could Lead to Brain Injury. [Press release]. Retrieved from http://www2.rsna.org/timssnet/media/pressreleases/pr_target.cfm?ID=564
Saulle, M., & Greenwald, B.D. (2012). Chronic traumatic encephalopathy: a review. Rehabilitation Research and Practice, 2012 PMID: 22567320
About Amy Wong, M.S.
Amy Wong, MS, is a medical writer and conducts traumatic brain injury research in a large academic institution. She holds a Master’s of Science from the University of Toronto in the department of Pharmacology. Her studies pertained to the selective field of neuropsychopharmacology, examining the biological implications of post-stroke depression.
Related Articles
Monday, July 30, 2012
A Truly Tasty TED Talk on Prenatal Learning by "Origins" Author Annie Murphy Paul
From TED.com
What We Learn Before We're Born
Annie Murphy Paul investigates how life in the womb shapes who we become.
Why You Should Listen to Her
Science Writer Annie Murphy Paul calls it a gray zone between nature and nurture in her book Origins: How the Nine Months Before Birth Shape the Rest of Our Lives, a study of this emerging field structured around a personal narrative -- Paul was pregnant with her second child at the time. What she finds suggests a far more dynamic nature between mother and fetus than typically acknowledged, and opens up the possibility that the time before birth is as crucial to human development as early childhood.
Read Annie Murphy Paul's essay on CNN.com
What We Learn Before We're Born
Why You Should Listen to Her
Sylvia Nasar (author of A Beautiful Mind): "[Paul] combines impeccable science, extraordinary tenderness, and lyrical prose to produce a truly revolutionary chronicle of pregnancy."
To what extent do the conditions we encounter before birth influence our individual characteristics? It‘s the question at the center of fetal origins, a relatively new field of research that measures how influences outside the womb during pregnancy shape the physical, mental and even emotional well-being of the developing baby for the rest of its life.
To what extent do the conditions we encounter before birth influence our individual characteristics? It‘s the question at the center of fetal origins, a relatively new field of research that measures how influences outside the womb during pregnancy shape the physical, mental and even emotional well-being of the developing baby for the rest of its life.
Science Writer Annie Murphy Paul calls it a gray zone between nature and nurture in her book Origins: How the Nine Months Before Birth Shape the Rest of Our Lives, a study of this emerging field structured around a personal narrative -- Paul was pregnant with her second child at the time. What she finds suggests a far more dynamic nature between mother and fetus than typically acknowledged, and opens up the possibility that the time before birth is as crucial to human development as early childhood.
Read Annie Murphy Paul's essay on CNN.com
Subscribe to Annie Murphy Paul's The Brilliant Blog HERE.
Sunday, July 29, 2012
Study : Yet Another Immune System Abnormality in Autism
From the Blog Autism Jabberwocky
July 2, 2012
A new study has reported that a large number of children with autism may have an elevated level of interleukin-17A. This isn't a new result but it is interesting, because this time there appears to be an association between the level of IL-17A and the severity of autism - the more severe the case, the higher the level of IL-17A.
"This isn't a new result but it is interesting because this time there appears to be an association between the level of IL-17A and the severity of autism - the more severe the case, the higher the level of IL-17A."
Indeed. A pattern developing in many of the immune findings in the autism cohort is that as markers of inflammation increase, so too, do autism severity scores:
Of course, this could be a coincidence, but I doubt it.
.......................................................................................
From NeuroscienceNews.com
Researchers Find Evidence of Link between Immune Irregularities and Autism
By Kimm Fesenmaier
Scientists at the California Institute of Technology (Caltech) pioneered the study of the link between irregularities in the immune system and neurodevelopmental disorders such as autism a decade ago. Since then, studies of postmortem brains and of individuals with autism, as well as epidemiological studies, have supported the correlation between alterations in the immune system and autism spectrum disorder.
What has remained unanswered, however, is whether the immune changes play a causative role in the development of the disease or are merely a side effect. Now a new Caltech study suggests that specific changes in an overactive immune system can indeed contribute to autism-like behaviors in mice, and that in some cases, this activation can be related to what a developing fetus experiences in the womb.
“We have long suspected that the immune system plays a role in the development of autism spectrum disorder,” says Dr. Paul Patterson, the Anne P. and Benjamin F. Biaggini Professor of Biological Sciences at Caltech, who led the work.
“In mice, this single insult to the mother translates into autism-related behavioral abnormalities and neuropathologies in the offspring,” says Elaine Hsiao, a graduate student in Patterson’s lab and lead author of the PNAS paper.
The team found that the offspring exhibit the core behavioral symptoms associated with autism spectrum disorder—repetitive or stereotyped behaviors, decreased social interactions, and impaired communication. In mice, this translates to such behaviors as compulsively burying marbles placed in their cage, excessively self grooming, choosing to spend time alone or with a toy rather than interacting with a new mouse, or vocalizing ultrasonically less often or in an altered way compared to typical mice.
Next, the researchers characterized the immune system of the offspring of mothers that had been infected and found that the offspring display a number of immune changes. Some of those changes parallel those seen in people with autism, including decreased levels of regulatory T cells, which play a key role in suppressing the immune response. Taken together, the observed immune alterations add up to an immune system in overdrive—one that promotes inflammation.
In future studies, the researchers plan to examine the effects of highly targeted anti-inflammatory treatments on mice that display autism-related behaviors and immune changes. They are also interested in considering the gastrointestinal (GI) bacteria, or microbiota, of such mice. Co-author Sarkis Mazmanian, a professor of biology at Caltech, has shown that gut bacteria are intimately tied to the function of the immune system. He and Patterson are investigating whether changes to the microbiota of these mice might also influence their autism-related behaviors.
Notes about this Autism Research and Article
Along with Patterson, Hsiao, and Mazmanian, additional Caltech coauthors on the PNAS paper, Modeling an autism risk factor in mice leads to permanent immune dysregulation, are Mazmanian lab manager Sara McBride and former graduate student Janet Chow. The work was supported by an Autism Speaks Weatherstone Fellowship, National Institutes of Health Graduate Training Grants, a Weston Havens Foundation grant, a Gregory O. and Jennifer W. Johnson Caltech Innovation Fellowship, a Caltech Innovation grant, and a Congressionally Directed Medical Research Program Idea Development Award.
July 2, 2012
A new study has reported that a large number of children with autism may have an elevated level of interleukin-17A. This isn't a new result but it is interesting, because this time there appears to be an association between the level of IL-17A and the severity of autism - the more severe the case, the higher the level of IL-17A.
You can read the entire open-access article from the Journal of Neuroinflammation HERE.
The abstract is below.
Elevated Serum Levels of Interleukin-17A in Children with Autism
Al-Ayadhi L.Y., Mostafa, G.A. Elevated serum levels of interleukin-17A in children with autism. J Neuroinflammation. 2012 Jul 2;9(1):158. [Epub ahead of print] PubMed PMID: 22748016.
The abstract is below.
Elevated Serum Levels of Interleukin-17A in Children with Autism
By Al-Ayadhi, L.Y. and Mostafa, G.A.
BACKGROUND
The T-helper (Th)1/Th2 dichotomy dominated the field of immune regulation until interleukin (IL)-17-expressing T cells (Th17) were proposed to be a third lineage of helper T cells, the key players in the pathogenesis of autoimmune disorders. Autoimmunity to brain tissue may play a pathogenic role in autism. IL-17A is a pro-inflammatory cytokine that has been shown to play an important role in various autoimmune neuroinflammatory diseases. The aim of this study was to measure serum levels of IL-17A in relation to the degree of the severity of autism.
METHODS
Serum IL-17A levels were measured by ELISA in 45 children with autism and 40 healthy matched healthy controls.
RESULTS
Children with autism had significantly higher serum IL-17A levels than healthy controls (P <0.001), with increased serum levels of IL-17A found in 48.9% of the autism group. Patients with severe autism had significantly higher serum IL-17A levels than those with mild to moderate autism (P = 0.01), and raised serum IL-17A levels were significantly more common in children with severe autism (67.9%) than in those with mild to moderate autism (17.6%), P = 0.001.
CONCLUSIONS
Serum IL-17A levels were raised in the group with autism, and the levels correlated significantly with the severity of autism. This is the first study to measure levels of IL-17A in relation to the severity of autism, to our knowledge. Further research, with a larger subject population, is warranted to determine whether the increase of serum IL-17A levels plasma has a pathogenic role in autism, and whether anti- IL-17A therapy could be useful.
References
BACKGROUND
The T-helper (Th)1/Th2 dichotomy dominated the field of immune regulation until interleukin (IL)-17-expressing T cells (Th17) were proposed to be a third lineage of helper T cells, the key players in the pathogenesis of autoimmune disorders. Autoimmunity to brain tissue may play a pathogenic role in autism. IL-17A is a pro-inflammatory cytokine that has been shown to play an important role in various autoimmune neuroinflammatory diseases. The aim of this study was to measure serum levels of IL-17A in relation to the degree of the severity of autism.
METHODS
Serum IL-17A levels were measured by ELISA in 45 children with autism and 40 healthy matched healthy controls.
RESULTS
Children with autism had significantly higher serum IL-17A levels than healthy controls (P <0.001), with increased serum levels of IL-17A found in 48.9% of the autism group. Patients with severe autism had significantly higher serum IL-17A levels than those with mild to moderate autism (P = 0.01), and raised serum IL-17A levels were significantly more common in children with severe autism (67.9%) than in those with mild to moderate autism (17.6%), P = 0.001.
CONCLUSIONS
Serum IL-17A levels were raised in the group with autism, and the levels correlated significantly with the severity of autism. This is the first study to measure levels of IL-17A in relation to the severity of autism, to our knowledge. Further research, with a larger subject population, is warranted to determine whether the increase of serum IL-17A levels plasma has a pathogenic role in autism, and whether anti- IL-17A therapy could be useful.
References
Al-Ayadhi L.Y., Mostafa, G.A. Elevated serum levels of interleukin-17A in children with autism. J Neuroinflammation. 2012 Jul 2;9(1):158. [Epub ahead of print] PubMed PMID: 22748016.
One Very Well-Informed Reader Comments:
"This isn't a new result but it is interesting because this time there appears to be an association between the level of IL-17A and the severity of autism - the more severe the case, the higher the level of IL-17A."
Indeed. A pattern developing in many of the immune findings in the autism cohort is that as markers of inflammation increase, so too, do autism severity scores:
- http://www.sciencedirect.com/science/article/pii/S175094671100167X
- http://pediatrics.aappublications.org/content/122/2/e438.abstract
- http://www.ncbi.nlm.nih.gov/pubmed/20833247
- http://www.ncbi.nlm.nih.gov/pubmed/20302902
Of course, this could be a coincidence, but I doubt it.
.......................................................................................
From NeuroscienceNews.com
Researchers Find Evidence of Link between Immune Irregularities and Autism
By Kimm Fesenmaier
July 20, 2012
"Modeling an autism risk factor in mice leads to permanent immune dysregulation.”
Scientists at the California Institute of Technology (Caltech) pioneered the study of the link between irregularities in the immune system and neurodevelopmental disorders such as autism a decade ago. Since then, studies of postmortem brains and of individuals with autism, as well as epidemiological studies, have supported the correlation between alterations in the immune system and autism spectrum disorder.
What has remained unanswered, however, is whether the immune changes play a causative role in the development of the disease or are merely a side effect. Now a new Caltech study suggests that specific changes in an overactive immune system can indeed contribute to autism-like behaviors in mice, and that in some cases, this activation can be related to what a developing fetus experiences in the womb.
"...a new Caltech study suggests that specific changes in an overactive immune system can indeed contribute to autism-like behaviors in mice, and that in some cases, this activation can be related to what a developing fetus experiences in the womb."
The results appear in a paper this week in the Proceedings of the National Academy of Sciences (PNAS). You can read the abstract HERE.
The results appear in a paper this week in the Proceedings of the National Academy of Sciences (PNAS). You can read the abstract HERE.
“We have long suspected that the immune system plays a role in the development of autism spectrum disorder,” says Dr. Paul Patterson, the Anne P. and Benjamin F. Biaggini Professor of Biological Sciences at Caltech, who led the work.
“In our studies of a mouse model based on an environmental risk factor for autism, we find that the immune system of the mother is a key factor in the eventual abnormal behaviors in the offspring.” A new Caltech study suggests that specific changes in an overactive immune system can indeed contribute to autism-like behaviors in mice, and that in some cases, this activation can be related to what a developing fetus experiences in the womb.
The first step in the work was establishing a mouse model that tied the autism-related behaviors together with immune changes. Several large epidemiological studies—including one that involved tracking the medical history of every person born in Denmark between 1980 and 2005—have found a correlation between viral infection during the first trimester of a mother’s pregnancy and a higher risk for autism spectrum disorder in her child. To model this in mice, the researchers injected pregnant mothers with a viral mimic that triggered the same type of immune response a viral infection would.
The first step in the work was establishing a mouse model that tied the autism-related behaviors together with immune changes. Several large epidemiological studies—including one that involved tracking the medical history of every person born in Denmark between 1980 and 2005—have found a correlation between viral infection during the first trimester of a mother’s pregnancy and a higher risk for autism spectrum disorder in her child. To model this in mice, the researchers injected pregnant mothers with a viral mimic that triggered the same type of immune response a viral infection would.
“In mice, this single insult to the mother translates into autism-related behavioral abnormalities and neuropathologies in the offspring,” says Elaine Hsiao, a graduate student in Patterson’s lab and lead author of the PNAS paper.
The team found that the offspring exhibit the core behavioral symptoms associated with autism spectrum disorder—repetitive or stereotyped behaviors, decreased social interactions, and impaired communication. In mice, this translates to such behaviors as compulsively burying marbles placed in their cage, excessively self grooming, choosing to spend time alone or with a toy rather than interacting with a new mouse, or vocalizing ultrasonically less often or in an altered way compared to typical mice.
Next, the researchers characterized the immune system of the offspring of mothers that had been infected and found that the offspring display a number of immune changes. Some of those changes parallel those seen in people with autism, including decreased levels of regulatory T cells, which play a key role in suppressing the immune response. Taken together, the observed immune alterations add up to an immune system in overdrive—one that promotes inflammation.
"Some of those changes parallel those seen in people with autism. Taken together, the observed immune alterations add up to an immune system in overdrive—one that promotes inflammation."
“Remarkably, we saw these immune abnormalities in both young and adult offspring of immune-activated mothers,” Hsiao says. “This tells us that a prenatal challenge can result in long-term consequences for health and development.”
With the mouse model established, the group was then able to test whether the offspring’s immune problems contribute to their autism-related behaviors. In the most revealing test of this hypothesis, the researchers were able to correct many of the autism-like behaviors in the offspring of immune-activated mothers by giving the offspring a bone-marrow transplant from typical mice. The normal stem cells in the transplanted bone marrow not only replenished the immune system of the host animals but altered their autism-like behavioral impairments.
The researchers emphasize that because the work was conducted in mice, the results cannot be readily extrapolated to humans, and they certainly do not suggest that bone-marrow transplants should be considered as a treatment for autism. They also have yet to establish whether it was the infusion of stem cells or the bone-marrow transplant procedure itself—complete with irradiation—that corrected the behaviors.
However, Patterson says, the results do suggest that immune irregularities in children could be an important target for innovative immune manipulations in addressing the behaviors associated with autism spectrum disorder. By correcting these immune problems, he says, it might be possible to ameliorate some of the classic developmental delays seen in autism.
“Remarkably, we saw these immune abnormalities in both young and adult offspring of immune-activated mothers,” Hsiao says. “This tells us that a prenatal challenge can result in long-term consequences for health and development.”
With the mouse model established, the group was then able to test whether the offspring’s immune problems contribute to their autism-related behaviors. In the most revealing test of this hypothesis, the researchers were able to correct many of the autism-like behaviors in the offspring of immune-activated mothers by giving the offspring a bone-marrow transplant from typical mice. The normal stem cells in the transplanted bone marrow not only replenished the immune system of the host animals but altered their autism-like behavioral impairments.
The researchers emphasize that because the work was conducted in mice, the results cannot be readily extrapolated to humans, and they certainly do not suggest that bone-marrow transplants should be considered as a treatment for autism. They also have yet to establish whether it was the infusion of stem cells or the bone-marrow transplant procedure itself—complete with irradiation—that corrected the behaviors.
However, Patterson says, the results do suggest that immune irregularities in children could be an important target for innovative immune manipulations in addressing the behaviors associated with autism spectrum disorder. By correcting these immune problems, he says, it might be possible to ameliorate some of the classic developmental delays seen in autism.
In future studies, the researchers plan to examine the effects of highly targeted anti-inflammatory treatments on mice that display autism-related behaviors and immune changes. They are also interested in considering the gastrointestinal (GI) bacteria, or microbiota, of such mice. Co-author Sarkis Mazmanian, a professor of biology at Caltech, has shown that gut bacteria are intimately tied to the function of the immune system. He and Patterson are investigating whether changes to the microbiota of these mice might also influence their autism-related behaviors.Notes about this Autism Research and Article
Along with Patterson, Hsiao, and Mazmanian, additional Caltech coauthors on the PNAS paper, Modeling an autism risk factor in mice leads to permanent immune dysregulation, are Mazmanian lab manager Sara McBride and former graduate student Janet Chow. The work was supported by an Autism Speaks Weatherstone Fellowship, National Institutes of Health Graduate Training Grants, a Weston Havens Foundation grant, a Gregory O. and Jennifer W. Johnson Caltech Innovation Fellowship, a Caltech Innovation grant, and a Congressionally Directed Medical Research Program Idea Development Award.
Saturday, July 28, 2012
Study: Adaptive Working Memory Training Can Reduce ADHD-related Off-Task Behavior
From SHARPBRAINS.com
By Dr. David Rabiner
July 18, 2012
For a number of reasons, there remains an important need to develop research supported treatments for ADHD in addition to medication and behavior therapy.
Regarding medication, not all children benefit from taking it, some experience intolerable side effects, and many continue to struggle even when medication provides some benefit.
Behavior therapy can be difficult for parents and teachers to consistently implement, and often helps but does not eliminate a child’s behavioral problems.
Furthermore, neither treatment yields positive changes that persist when the treatment is discontinued. Finally, despite numerous studies documenting the short– and intermediate term benefits of these treatments, evidence of their impact on children’s long-term success is less evident.
One relatively recent development in the realm of ADHD treatments is working memory training. Working memory (WM) refers to the ability to hold and manipulate information in mind for subsequent use and is critically important for a variety of learning activities. For example, when a child is asked questions about a story he has read, working memory allows the child to retain and review the story information in mind to answer the questions.
In doing mental math, working memory is used to hold the digits in mind and manipulate them, e.g., add or subtract, to generate the answer.
Working memory is also important in the control of attention and is a strong predictor of academic success. It is deficient in many individuals with ADHD; in fact, some researchers believe that working memory deficits are central to ADHD and underline the inattentive and hyperactive-impulsive behavior that characterizes the disorder. You can learn more about working memory and ADHD here.
Several years ago, I reviewed a study of working memory training for ADHD that yielded promising findings. Children were randomly assigned to receive either high intensity (HI) or low intensity WM training. The HI treatment involved performing computerized WM tasks, e.g., remembering the sequence in which lights appeared in different portions of a grid, recalling a sequence of numbers in reverse order, where the difficulty level was regularly adjusted to match the child’s performance by increasing or decreasing the items to be recalled.
This is described below as ‘adaptive’ training because the difficulty level adapts to match the child’s capability. In this training condition, children are consistently challenged to expand their working memory capacity.
In the LI condition, the tasks were similar but the difficulty remained low throughout, i.e., the number of items did not increase when children responded correctly. For these children, their working memory capacity was not consistently challenged and was not expected to grow as a result. This served as the control condition.
Training was conducted 5 days a week over a 5 week period; each session lasted approximately 30 to 40 minutes. Following treatment, children who received high intensity training showed stronger working memory performance than children in the control condition; these gains were evident on working memory tasks that had not been trained and remained evident 3 months after training ended.
Furthermore, only children who received high intensity training showed significant declines in parent ratings of ADHD symptoms showed significant and meaningful declines for children. These declines remained evident 3 months later.
Although these were very positive findings, a limitation was that no treatment effects were found for teacher ratings of children’s behavior. Thus, there was no indication that benefits observed by parents, and mirrored in the working memory assessments, had generalized to the classroom.
Given the need to improve behavior at school for children with ADHD, it is concerning that similar findings, i.e., training-related gains in working memory performance and in parent ratings of children’s behavior, but less observation of benefits by teachers, have emerged in subsequent studies.
Newly Published Study
A study published online recently in Neurotherapeutics [Green et. al., (2012). Will working memory training generalize to improve off-task behavior in children with attention-deficit/hyperactivity disorder? DOI 10.1007/s13311-012‑0124-y] is encouraging in that it provides that strongest evidence to date that benefits from working memory training can generalize to academic settings.
Participants were 26 children (18 males; ages 7 to 14 years old) who were randomly assigned to receive adaptive working memory training or the low intensity control training. Ten children were on medication and remained on meds during the study; this was controlled for in the analyses.
The training program used was Cogmed Working Memory training (the researchers had no affiliation with Cogmed). The standard training protocol of 5 sessions per week over 5 weeks was employed. Per standard Cogmed procedures, training was done at home and was monitored remotely by a qualified coach to help ensure the protocol was followed.
The main study outcome was children’s behavior during the Restricted Academic Situations Task (RAST). During the RAST, which takes place in a lab setting, children are instructed to complete a series of academic work sheets for 15 minutes, and not to leave their seat, or touch any of the toys or games in the room, during that time. The child is left alone to complete the work and their behavior is observed from behind a one-way mirror. The child’s behavior is coded for the amount of off task behavior, e.g., looking away from the paper, getting out of his or her seat, fidgeting, vocalizing, or playing with objects unrelated to the task.
The task thus allows for highly controlled behavioral observations and is frequently used to evaluate the effect of medication on ADHD behaviors in pharmaceutical trials. It is sensitive to moment to moment off task behavior that a teacher or parent might not detect.
The main question asked in this study was whether children who received adaptive training would show less off task behavior during the RAST than children in the control condition. If so, it would indicate a positive treatment effect of working memory training that generalized to a setting highly relevant to behavior in school. Observations of treatment and control children was made by a trained observer who did not know which group — adaptive treatment or control — each child was in.
In addition to the RAST, children’s working memory performance on tasks that differed from those used in training (the Working Memory Composite from the WISC-IV) and parent behavior ratings were obtained.
Results
Impact on Working Memory - Consistent with what has been reported in prior working memory training studies, children receiving adaptive training showed a significant increase in the working memory score on the WISC-IV after training; children in the control condition did not.
Rating Scales - Both groups showed a decline on parents’ ratings of ADHD behaviors and this did not differ between the groups. Baseline scores for children in the adaptive training group were lower than in the control group so they may have had less room for improvement.
Behavior during the RAST - The main outcome measure from the RAST was the amount of off task behavior, i.e., looking away from the work sheet rather than focusing on it, during the 15 minute seat work period. At baseline, scores for each group were equivalent. Following training, when the RAST was readmininstered, off-task behavior for children in the control group remained at their baseline level.
For the adaptive training group, there was a pronounced and statistically significant decline. Adaptively trained children were also less likely to play with objects during the task. Differences in the other behavior categories — fidgeting, leaving the seat, and vocalizing — were not significant.
Summary and Implications
This is an important study — both for Cogmed Working Memory Training specifically and the cognitive training field in general. The results strongly suggest that working memory training can yield reductions in off task behavior during academic work for children with ADHD. This has not been previously demonstrated and begins to address an important gap in the research base on working memory training for ADHD, i.e., the limited indication of training effects that generalize to the classroom.
While the RAST reflects a controlled observation setting rather than an actual classroom, behavior during the RAST does correlate with in class behavior. And, it is a frequently used and accepted measure for determining medication treatment effects for ADHD.
The study has several strengths including a carefully diagnosed sample, the use of random assignment, an appropriate control group, the use of multiple outcome measures, and observers who were blind to children’s treatment assignment. These are all key elements of a carefully designed intervention trial.
As with any single study, there are also limitations to note. Key among these is a relatively small sample size. Thus, replication with a larger sample would certainly be warranted. And, although the RAST provides a valid and highly controlled setting to observe behavior, future studies should also include observations of children’s behavior in their actual classroom. Although this makes for a more complex study, the classroom is ultimately the setting where increases in focused, on task behavior during academic work needs to occur. Finally, this study did not follow participants beyond the end of treatment so the duration of benefits observed is not known.
These limitations not withstanding, the authors have presented important new data on the potential benefits of working memory training by demonstrating generalization of training benefits to a relevant setting for academic work. Given the growing interest in working memory training — and other forms of cognitive training — it is likely that results from a number of additional studies on these approaches will become available over the next several years.
About Dr. David Rabiner
Dr. David Rabiner is a child clinical psychologist and Director of Undergraduate Studies in the Department of Psychology and Neuroscience at Duke University. His research focuses on various issues related to ADHD, the impact of attention problems on academic achievement, and attention training. He also publishes Attention Research Update, a complimentary online newsletter that helps parents, professionals, and educators keep up with the latest research on ADHD.
Previous articles by Dr. Rabiner
By Dr. David Rabiner
July 18, 2012
For a number of reasons, there remains an important need to develop research supported treatments for ADHD in addition to medication and behavior therapy.
Regarding medication, not all children benefit from taking it, some experience intolerable side effects, and many continue to struggle even when medication provides some benefit.
Behavior therapy can be difficult for parents and teachers to consistently implement, and often helps but does not eliminate a child’s behavioral problems.
Furthermore, neither treatment yields positive changes that persist when the treatment is discontinued. Finally, despite numerous studies documenting the short– and intermediate term benefits of these treatments, evidence of their impact on children’s long-term success is less evident.
One relatively recent development in the realm of ADHD treatments is working memory training. Working memory (WM) refers to the ability to hold and manipulate information in mind for subsequent use and is critically important for a variety of learning activities. For example, when a child is asked questions about a story he has read, working memory allows the child to retain and review the story information in mind to answer the questions.
In doing mental math, working memory is used to hold the digits in mind and manipulate them, e.g., add or subtract, to generate the answer.
Working memory is also important in the control of attention and is a strong predictor of academic success. It is deficient in many individuals with ADHD; in fact, some researchers believe that working memory deficits are central to ADHD and underline the inattentive and hyperactive-impulsive behavior that characterizes the disorder. You can learn more about working memory and ADHD here.
Several years ago, I reviewed a study of working memory training for ADHD that yielded promising findings. Children were randomly assigned to receive either high intensity (HI) or low intensity WM training. The HI treatment involved performing computerized WM tasks, e.g., remembering the sequence in which lights appeared in different portions of a grid, recalling a sequence of numbers in reverse order, where the difficulty level was regularly adjusted to match the child’s performance by increasing or decreasing the items to be recalled.
This is described below as ‘adaptive’ training because the difficulty level adapts to match the child’s capability. In this training condition, children are consistently challenged to expand their working memory capacity.
In the LI condition, the tasks were similar but the difficulty remained low throughout, i.e., the number of items did not increase when children responded correctly. For these children, their working memory capacity was not consistently challenged and was not expected to grow as a result. This served as the control condition.
Training was conducted 5 days a week over a 5 week period; each session lasted approximately 30 to 40 minutes. Following treatment, children who received high intensity training showed stronger working memory performance than children in the control condition; these gains were evident on working memory tasks that had not been trained and remained evident 3 months after training ended.
Furthermore, only children who received high intensity training showed significant declines in parent ratings of ADHD symptoms showed significant and meaningful declines for children. These declines remained evident 3 months later.
Although these were very positive findings, a limitation was that no treatment effects were found for teacher ratings of children’s behavior. Thus, there was no indication that benefits observed by parents, and mirrored in the working memory assessments, had generalized to the classroom.
Given the need to improve behavior at school for children with ADHD, it is concerning that similar findings, i.e., training-related gains in working memory performance and in parent ratings of children’s behavior, but less observation of benefits by teachers, have emerged in subsequent studies.
Newly Published Study
A study published online recently in Neurotherapeutics [Green et. al., (2012). Will working memory training generalize to improve off-task behavior in children with attention-deficit/hyperactivity disorder? DOI 10.1007/s13311-012‑0124-y] is encouraging in that it provides that strongest evidence to date that benefits from working memory training can generalize to academic settings.
Participants were 26 children (18 males; ages 7 to 14 years old) who were randomly assigned to receive adaptive working memory training or the low intensity control training. Ten children were on medication and remained on meds during the study; this was controlled for in the analyses.
The training program used was Cogmed Working Memory training (the researchers had no affiliation with Cogmed). The standard training protocol of 5 sessions per week over 5 weeks was employed. Per standard Cogmed procedures, training was done at home and was monitored remotely by a qualified coach to help ensure the protocol was followed.
The main study outcome was children’s behavior during the Restricted Academic Situations Task (RAST). During the RAST, which takes place in a lab setting, children are instructed to complete a series of academic work sheets for 15 minutes, and not to leave their seat, or touch any of the toys or games in the room, during that time. The child is left alone to complete the work and their behavior is observed from behind a one-way mirror. The child’s behavior is coded for the amount of off task behavior, e.g., looking away from the paper, getting out of his or her seat, fidgeting, vocalizing, or playing with objects unrelated to the task.
The task thus allows for highly controlled behavioral observations and is frequently used to evaluate the effect of medication on ADHD behaviors in pharmaceutical trials. It is sensitive to moment to moment off task behavior that a teacher or parent might not detect.
The main question asked in this study was whether children who received adaptive training would show less off task behavior during the RAST than children in the control condition. If so, it would indicate a positive treatment effect of working memory training that generalized to a setting highly relevant to behavior in school. Observations of treatment and control children was made by a trained observer who did not know which group — adaptive treatment or control — each child was in.
In addition to the RAST, children’s working memory performance on tasks that differed from those used in training (the Working Memory Composite from the WISC-IV) and parent behavior ratings were obtained.
Results
Impact on Working Memory - Consistent with what has been reported in prior working memory training studies, children receiving adaptive training showed a significant increase in the working memory score on the WISC-IV after training; children in the control condition did not.
Rating Scales - Both groups showed a decline on parents’ ratings of ADHD behaviors and this did not differ between the groups. Baseline scores for children in the adaptive training group were lower than in the control group so they may have had less room for improvement.
Behavior during the RAST - The main outcome measure from the RAST was the amount of off task behavior, i.e., looking away from the work sheet rather than focusing on it, during the 15 minute seat work period. At baseline, scores for each group were equivalent. Following training, when the RAST was readmininstered, off-task behavior for children in the control group remained at their baseline level.
For the adaptive training group, there was a pronounced and statistically significant decline. Adaptively trained children were also less likely to play with objects during the task. Differences in the other behavior categories — fidgeting, leaving the seat, and vocalizing — were not significant.
Summary and Implications
This is an important study — both for Cogmed Working Memory Training specifically and the cognitive training field in general. The results strongly suggest that working memory training can yield reductions in off task behavior during academic work for children with ADHD. This has not been previously demonstrated and begins to address an important gap in the research base on working memory training for ADHD, i.e., the limited indication of training effects that generalize to the classroom.
While the RAST reflects a controlled observation setting rather than an actual classroom, behavior during the RAST does correlate with in class behavior. And, it is a frequently used and accepted measure for determining medication treatment effects for ADHD.
The study has several strengths including a carefully diagnosed sample, the use of random assignment, an appropriate control group, the use of multiple outcome measures, and observers who were blind to children’s treatment assignment. These are all key elements of a carefully designed intervention trial.
As with any single study, there are also limitations to note. Key among these is a relatively small sample size. Thus, replication with a larger sample would certainly be warranted. And, although the RAST provides a valid and highly controlled setting to observe behavior, future studies should also include observations of children’s behavior in their actual classroom. Although this makes for a more complex study, the classroom is ultimately the setting where increases in focused, on task behavior during academic work needs to occur. Finally, this study did not follow participants beyond the end of treatment so the duration of benefits observed is not known.
These limitations not withstanding, the authors have presented important new data on the potential benefits of working memory training by demonstrating generalization of training benefits to a relevant setting for academic work. Given the growing interest in working memory training — and other forms of cognitive training — it is likely that results from a number of additional studies on these approaches will become available over the next several years.
About Dr. David Rabiner
Dr. David Rabiner is a child clinical psychologist and Director of Undergraduate Studies in the Department of Psychology and Neuroscience at Duke University. His research focuses on various issues related to ADHD, the impact of attention problems on academic achievement, and attention training. He also publishes Attention Research Update, a complimentary online newsletter that helps parents, professionals, and educators keep up with the latest research on ADHD.Previous articles by Dr. Rabiner
Friday, July 27, 2012
Stanford Medical School Study: Non-Genetic Factors Play Surprisingly Large Role in Determining Autism in Twins
From Stanford University School of Medicine
By Erin Digitale
July 4, 2011
Joachim Hallmayer and his colleagues found that environmental factors play a larger role than previously thought in autism.
A new Stanford University School of Medicine study of twins suggests that non-genetic factors play an unexpectedly large role in determining autism risk, turning upside down recent assumptions about the cause of this common, disabling developmental disorder.
From prior studies of shared autism in twins, scientists had estimated that 90 percent of autism risk was attributable to genes and only 10 percent to non-genetic environmental factors. But the new study — the largest ever of twins in which at least one in each pair has autism — shows almost the opposite: It found that genes account for 38 percent of autism risk, with environmental factors explaining the remaining 62 percent.
"It took me a bit by surprise that the heritability of autism was so much lower than previous studies calculated," said Joachim Hallmayer, M.D., the first author of the new paper, which appears in the July 4 issue of Archives of General Psychiatry. "Our work suggests that the role of environmental factors has been underestimated." Hallmayer is an associate professor of psychiatry and behavioral sciences at Stanford. The study's senior author is Neil Risch, Ph.D., professor of biostatistics at UC-San Francisco and director of the UCSF Institute for Human Genetics.
For years, studies of non-genetic autism risk factors focused on the idea that childhood vaccines might trigger autism, a theory that extensive research did not support. But it remains an open question how much time and resources to devote to other potential environmental risks and how they interact with genetic factors.
Related News
Vaccines don't cause autism: Can we move on now?
5 questions: Hallmayer on the genetics of autism
Grappling with autism
"Our research shows us that we need to be studying both genetic and environmental factors as well as how they interact with each other," Hallmayer said. "We need to explore areas of environmental risk that are shared by both twin individuals and impact the development of the child."
Although the study does not identify specific environmental factors, they could include any non-genetic factors that influence autism risk.
The children studied were 192 pairs of twins (384 individuals) identified from a California-wide registry of children who receive services for developmental disabilities. The large size of the study and the fact that the subjects were drawn from California's entire, highly diverse population means the study's results are more reliable and apply more broadly than those from prior studies, which examined small, homogeneous groups of children in Northern European countries, Hallmayer said.
The study included 54 pairs of identical twins and 138 pairs of fraternal twins. At least one child from each pair had been diagnosed with full-blown autism or a less severe form of autism spectrum disorder. The scientists conducted standardized evaluations to verify the children's diagnoses, a step that many prior studies had omitted. Children whose autism was known to be secondary to another disease were not included in the study.
To calculate the relative contributions of genes and environment to autism risk, the researchers then examined the difference in shared autism rates between identical and fraternal twins. Identical twins share all their genes, fraternal twins share half of theirs, and both types of twins share most elements of their environment from conception through childhood. As the scientists expected for a disease that is partly explained by genes, the identical twins were more likely to share an autism diagnosis than the fraternal twins. Identical twins did not always share their diagnosis, hinting that non-genetic factors contribute to autism. The surprise came, however, in the calculation of environmental contributions to autism risk.
"The dizygotic [fraternal] twins are more similar than you would expect if you take only genetic factors into account," Hallmayer said. The higher-than-expected degree of similarity between fraternal twins confirmed that something other than genes was at work - in other words, the twins' shared environments helped explain their shared diagnoses.
To precisely calculate the genetic and environmental contributions to autism risk, the scientists employed a mathematical model that used the rate of autism in the general population to estimate the rate at which fraternal twins would have been expected to share a diagnosis if autism were purely genetic. This figure was compared with the rates of shared autism observed in the twins in the study to arrive at the scientists' final projections. Demographic factors found in previous studies to be associated with autism, such as the ages of the twins' parents, years of parental education, ethnicity, difference in birth weight between twins and gestational age at birth did not impact the rate of shared diagnosis between twin individuals.
The finding that autism risk is strongly influenced by environmental factors should alert scientists to the need to study risk factors they haven't been considering, the researchers said. In recent years, autism research has been focusing more on genetics.
"Scientists need to look for environmental factors," said Linda Lotspeich, M.D., a study author, a clinical professor of psychiatry and behavioral sciences at Stanford and a child and adolescent psychiatrist who treats children with autism at the Stanford Autism Center at Packard Children's Hospital. "But that doesn't take away the fact that autism also has a genetic component and is still caused by unknown genes."
And what might the unknown environmental risk factors be?
"That's the multimillion dollar question," Hallmayer said. "I think a lot about it." Autism's manifestation in very young children points to something that happens in early life, potentially even during pregnancy, he said.
"Our findings suggest that events during pregnancy should be a focus for future research into the origins of autism," said Lisa Croen, Ph.D., a co-author on the study. Croen is a senior research scientist and director of the Autism Research Program at the Kaiser Permanente Division of Research.
In addition to Hallmayer and Lotspeich, the Stanford researchers who contributed to the project included Jennifer Phillips, Ph.D., clinical associate professor of psychiatry and behavioral sciences; and research assistants Sue Cleveland and Andrea Torres. The Stanford team collaborated on the study with scientists at the advocacy organization Autism Speaks; the California Department of Public Health; Kaiser Permanente Northern California; UC-Davis and UCSF.
The research was funded by grants from the National Institute of Mental Health and Autism Speaks.
More information about the Department of Psychiatry and Behavioral Sciences, which also supported this work, is available at http://psychiatry.stanford.edu/.
"Random chance, plus small differences in uterine environments, give rise to divergent epigenetic patterns in identical twins. "
Scientists are still teasing out the contributions of genetic and environmental factors to epigenetic marks on the genome. Differences in DNA methylation patterns have been linked to various disease occurrences in genetically identical twins, for example, suggesting an environmental impact.
And a new study, out this week (July 15) in Genome Research, extends the influence of the environment in to the uterus by demonstrating that differences between identical twins in methylation are detectable at birth. Surprisingly, methylation patterns between some twins differ more than between unrelated individuals, also suggesting a role for random chance in the development of the epigenome.
“We already know that twins behave differently and look different, and it’s probably due to epigenetics,” said Dr. Jeffrey Craig, who led the study with Dr. Richard Saffery, both at the University of Melbourne, Australia.
Because of their identical genomes, monozygotic twins allow scientists to identify epigenetic differences that may serve as markers for disease. But it wasn’t known when differences in epigenetic patterns emerged between twins, Tadafumi Kato, who studies the molecular basis of bipolar disorder at RIKEN Brain Science Institute in Japan but was not involved in the current study, wrote in an email to The Scientist.
In order to look more closely at epigenetic differences between twins, Craig and Saffery took tissue samples when the children were born and for several months after birth, following epigenetic changes over time. They compared sets of identical twins and fraternal twins, a classic experimental setup used to separate environmental from genetic effects.
They then used a chip array to examine DNA methylation at over 27,000 sites in the human genome in each of three tissues: placenta, umbilical cord vascular endothelial cells, and cord blood mononuclear cells. The researchers also compared the newborns’ methylation patterns to those of unrelated infants.
Although DNA methylation patterns tended to be more similar for identical twins, “we were very surprised by the range” of differences, said Craig, “The distribution of monozygotic twins overlapped unrelated newborns, and some twins were more different than unrelated pairs.
The scientists also found that identical twins that shared a placenta—arguably coming as close as possible to sharing similar environments—had epigenetic patterns that differed more than identical twins that didn’t share a placenta, but did share a uterus.
This finding highlights “that sharing the same intrauterine environment does not contribute to having more similar DNA methylation patterns,” Esteban Ballestar, who studies the epigenetics of disease at the University of Barcelona, wrote in an email. “Their results would rather suggest that stochastic events could be more relevant in establishing differences between DNA methylation patterns in individuals,” added Ballestar, who was not involved in the work.
Thus, it seems that random changes and environmental factors together influence epigenetic patterns more than twins’ shared genetics. Indeed, when Craig and his colleagues statistically examined how much genetics, environmental factors, and random chance contributed to epigenetic methylation patterns, they found that slight differences in shared intrauterine environments, such as placenta size or where the umbilical cord attaches, and random changes accounted for more of the variance in epigenetic patterns than the underlying DNA sequence.
As the children aged, their methylation patterns didn’t continue to diverge, however, suggesting that environmental signals may have less of an influence on epigenetics later in life—a finding that contradicts some earlier studies.
Knowing that low birth weight has been linked to later ill health, the scientists looked more closely at the genes showing differing patterns of methylation. They found that discordantly methylated genes in sets of twins with differing birth weights were often genes encoding proteins involved in metabolism and growth, which suggests to Craig that these pathways can be “nudged” off track early by deleterious patterns of methylation even before birth.
“It’s still a very pilot experiment,” noted Arturas Petronis at the University of Toronto, who pointed out that the 27,000 sites the researchers examined represent only about 0.1 percent of possible methylation sites in the genome. More comprehensive studies will determine how well these findings apply to the whole genome, said Petronis, who did not participate in the study.
In the meantime, Craig and his colleagues are hoping to discover what subtle environmental differences within the uterus can prompt such large epigenetic differences in twins. Placement of the umbilical cord, which can regulate the number nutrients passed from mom to her babies, and even what route they take, could play a role, Craig hypothesized.
More importantly, he added, if scientists can identify early epigenetic markers of disease, it may be possible to proactively use epigenetic drugs, such as those already in cancer trials, to “nudge” their methylation patterns back on a healthy track.
Reference
L. Gordon, et al., “Neonatal DNA methylation profile in human twins is specified by a complex interplay between intrauterine environmental and genetic factors, subject to tissue-specific influence,” Genome Research, doi: 10.1101/gr.136598.111, 2012.
By Erin Digitale
July 4, 2011
Joachim Hallmayer and his colleagues found that environmental factors play a larger role than previously thought in autism.
A new Stanford University School of Medicine study of twins suggests that non-genetic factors play an unexpectedly large role in determining autism risk, turning upside down recent assumptions about the cause of this common, disabling developmental disorder.From prior studies of shared autism in twins, scientists had estimated that 90 percent of autism risk was attributable to genes and only 10 percent to non-genetic environmental factors. But the new study — the largest ever of twins in which at least one in each pair has autism — shows almost the opposite: It found that genes account for 38 percent of autism risk, with environmental factors explaining the remaining 62 percent.
"It took me a bit by surprise that the heritability of autism was so much lower than previous studies calculated," said Joachim Hallmayer, M.D., the first author of the new paper, which appears in the July 4 issue of Archives of General Psychiatry. "Our work suggests that the role of environmental factors has been underestimated." Hallmayer is an associate professor of psychiatry and behavioral sciences at Stanford. The study's senior author is Neil Risch, Ph.D., professor of biostatistics at UC-San Francisco and director of the UCSF Institute for Human Genetics.
For years, studies of non-genetic autism risk factors focused on the idea that childhood vaccines might trigger autism, a theory that extensive research did not support. But it remains an open question how much time and resources to devote to other potential environmental risks and how they interact with genetic factors.
Related News
Vaccines don't cause autism: Can we move on now?
5 questions: Hallmayer on the genetics of autism
Grappling with autism
"Our research shows us that we need to be studying both genetic and environmental factors as well as how they interact with each other," Hallmayer said. "We need to explore areas of environmental risk that are shared by both twin individuals and impact the development of the child."
Although the study does not identify specific environmental factors, they could include any non-genetic factors that influence autism risk.
The children studied were 192 pairs of twins (384 individuals) identified from a California-wide registry of children who receive services for developmental disabilities. The large size of the study and the fact that the subjects were drawn from California's entire, highly diverse population means the study's results are more reliable and apply more broadly than those from prior studies, which examined small, homogeneous groups of children in Northern European countries, Hallmayer said.
The study included 54 pairs of identical twins and 138 pairs of fraternal twins. At least one child from each pair had been diagnosed with full-blown autism or a less severe form of autism spectrum disorder. The scientists conducted standardized evaluations to verify the children's diagnoses, a step that many prior studies had omitted. Children whose autism was known to be secondary to another disease were not included in the study.
To calculate the relative contributions of genes and environment to autism risk, the researchers then examined the difference in shared autism rates between identical and fraternal twins. Identical twins share all their genes, fraternal twins share half of theirs, and both types of twins share most elements of their environment from conception through childhood. As the scientists expected for a disease that is partly explained by genes, the identical twins were more likely to share an autism diagnosis than the fraternal twins. Identical twins did not always share their diagnosis, hinting that non-genetic factors contribute to autism. The surprise came, however, in the calculation of environmental contributions to autism risk.
"The dizygotic [fraternal] twins are more similar than you would expect if you take only genetic factors into account," Hallmayer said. The higher-than-expected degree of similarity between fraternal twins confirmed that something other than genes was at work - in other words, the twins' shared environments helped explain their shared diagnoses.
To precisely calculate the genetic and environmental contributions to autism risk, the scientists employed a mathematical model that used the rate of autism in the general population to estimate the rate at which fraternal twins would have been expected to share a diagnosis if autism were purely genetic. This figure was compared with the rates of shared autism observed in the twins in the study to arrive at the scientists' final projections. Demographic factors found in previous studies to be associated with autism, such as the ages of the twins' parents, years of parental education, ethnicity, difference in birth weight between twins and gestational age at birth did not impact the rate of shared diagnosis between twin individuals.
The finding that autism risk is strongly influenced by environmental factors should alert scientists to the need to study risk factors they haven't been considering, the researchers said. In recent years, autism research has been focusing more on genetics.
"Scientists need to look for environmental factors," said Linda Lotspeich, M.D., a study author, a clinical professor of psychiatry and behavioral sciences at Stanford and a child and adolescent psychiatrist who treats children with autism at the Stanford Autism Center at Packard Children's Hospital. "But that doesn't take away the fact that autism also has a genetic component and is still caused by unknown genes."And what might the unknown environmental risk factors be?
"That's the multimillion dollar question," Hallmayer said. "I think a lot about it." Autism's manifestation in very young children points to something that happens in early life, potentially even during pregnancy, he said.
"Our findings suggest that events during pregnancy should be a focus for future research into the origins of autism," said Lisa Croen, Ph.D., a co-author on the study. Croen is a senior research scientist and director of the Autism Research Program at the Kaiser Permanente Division of Research.
In addition to Hallmayer and Lotspeich, the Stanford researchers who contributed to the project included Jennifer Phillips, Ph.D., clinical associate professor of psychiatry and behavioral sciences; and research assistants Sue Cleveland and Andrea Torres. The Stanford team collaborated on the study with scientists at the advocacy organization Autism Speaks; the California Department of Public Health; Kaiser Permanente Northern California; UC-Davis and UCSF.
The research was funded by grants from the National Institute of Mental Health and Autism Speaks.
More information about the Department of Psychiatry and Behavioral Sciences, which also supported this work, is available at http://psychiatry.stanford.edu/.
...........................................................................
From The Scientist News & Opinion
Early Epigenetic Influence
By Sabrina Richards
July 16, 2012
"Random chance, plus small differences in uterine environments, give rise to divergent epigenetic patterns in identical twins. "
Scientists are still teasing out the contributions of genetic and environmental factors to epigenetic marks on the genome. Differences in DNA methylation patterns have been linked to various disease occurrences in genetically identical twins, for example, suggesting an environmental impact.
And a new study, out this week (July 15) in Genome Research, extends the influence of the environment in to the uterus by demonstrating that differences between identical twins in methylation are detectable at birth. Surprisingly, methylation patterns between some twins differ more than between unrelated individuals, also suggesting a role for random chance in the development of the epigenome.
“We already know that twins behave differently and look different, and it’s probably due to epigenetics,” said Dr. Jeffrey Craig, who led the study with Dr. Richard Saffery, both at the University of Melbourne, Australia.Because of their identical genomes, monozygotic twins allow scientists to identify epigenetic differences that may serve as markers for disease. But it wasn’t known when differences in epigenetic patterns emerged between twins, Tadafumi Kato, who studies the molecular basis of bipolar disorder at RIKEN Brain Science Institute in Japan but was not involved in the current study, wrote in an email to The Scientist.
In order to look more closely at epigenetic differences between twins, Craig and Saffery took tissue samples when the children were born and for several months after birth, following epigenetic changes over time. They compared sets of identical twins and fraternal twins, a classic experimental setup used to separate environmental from genetic effects.
They then used a chip array to examine DNA methylation at over 27,000 sites in the human genome in each of three tissues: placenta, umbilical cord vascular endothelial cells, and cord blood mononuclear cells. The researchers also compared the newborns’ methylation patterns to those of unrelated infants.
Although DNA methylation patterns tended to be more similar for identical twins, “we were very surprised by the range” of differences, said Craig, “The distribution of monozygotic twins overlapped unrelated newborns, and some twins were more different than unrelated pairs.
The scientists also found that identical twins that shared a placenta—arguably coming as close as possible to sharing similar environments—had epigenetic patterns that differed more than identical twins that didn’t share a placenta, but did share a uterus.
This finding highlights “that sharing the same intrauterine environment does not contribute to having more similar DNA methylation patterns,” Esteban Ballestar, who studies the epigenetics of disease at the University of Barcelona, wrote in an email. “Their results would rather suggest that stochastic events could be more relevant in establishing differences between DNA methylation patterns in individuals,” added Ballestar, who was not involved in the work.
Thus, it seems that random changes and environmental factors together influence epigenetic patterns more than twins’ shared genetics. Indeed, when Craig and his colleagues statistically examined how much genetics, environmental factors, and random chance contributed to epigenetic methylation patterns, they found that slight differences in shared intrauterine environments, such as placenta size or where the umbilical cord attaches, and random changes accounted for more of the variance in epigenetic patterns than the underlying DNA sequence.
As the children aged, their methylation patterns didn’t continue to diverge, however, suggesting that environmental signals may have less of an influence on epigenetics later in life—a finding that contradicts some earlier studies.
Knowing that low birth weight has been linked to later ill health, the scientists looked more closely at the genes showing differing patterns of methylation. They found that discordantly methylated genes in sets of twins with differing birth weights were often genes encoding proteins involved in metabolism and growth, which suggests to Craig that these pathways can be “nudged” off track early by deleterious patterns of methylation even before birth.
“It’s still a very pilot experiment,” noted Arturas Petronis at the University of Toronto, who pointed out that the 27,000 sites the researchers examined represent only about 0.1 percent of possible methylation sites in the genome. More comprehensive studies will determine how well these findings apply to the whole genome, said Petronis, who did not participate in the study.
In the meantime, Craig and his colleagues are hoping to discover what subtle environmental differences within the uterus can prompt such large epigenetic differences in twins. Placement of the umbilical cord, which can regulate the number nutrients passed from mom to her babies, and even what route they take, could play a role, Craig hypothesized.
More importantly, he added, if scientists can identify early epigenetic markers of disease, it may be possible to proactively use epigenetic drugs, such as those already in cancer trials, to “nudge” their methylation patterns back on a healthy track.
Reference
L. Gordon, et al., “Neonatal DNA methylation profile in human twins is specified by a complex interplay between intrauterine environmental and genetic factors, subject to tissue-specific influence,” Genome Research, doi: 10.1101/gr.136598.111, 2012.
Thursday, July 26, 2012
Support H.4131: An Act to Reform Public School Disciplinary Procedures and Reporting
NESCA joins with organizations including Massachusetts Advocates for Children, the Education Law Task Force, Federation for Children with Special Needs, Children's Defense Fund, Massachusetts Bar Association, Disability Law Center and more than a dozen others in supporting H.4131, a bill now pending in the Mass. House of Representatives.
The new law would compel schools to maintain accurate records of all suspensions and expulsions and report them to the DESE, extend important due-process rights to students in disciplinary proceedings and afford those who are excluded from school opportunities to make up missed work or otherwise continue their educations.
These and other provisions in the bill would help to end discrimination, reduce the drop-out rate and staunch the flow through the so-called "school-to-prison pipeline."
You can read more about the bill HERE. Its best chance of passage will come if it is put to a vote prior to the end of the legislative session on July 31, 2012.
Please therefore contact your representative as soon as possible to urge immediate passage of H.4131. To identify your state legislator and to get their phone number and/or email address, contact the State House at 617-722-2000 or visit www.wheredoIvotema.com.
The new law would compel schools to maintain accurate records of all suspensions and expulsions and report them to the DESE, extend important due-process rights to students in disciplinary proceedings and afford those who are excluded from school opportunities to make up missed work or otherwise continue their educations.
These and other provisions in the bill would help to end discrimination, reduce the drop-out rate and staunch the flow through the so-called "school-to-prison pipeline."
You can read more about the bill HERE. Its best chance of passage will come if it is put to a vote prior to the end of the legislative session on July 31, 2012.
Please therefore contact your representative as soon as possible to urge immediate passage of H.4131. To identify your state legislator and to get their phone number and/or email address, contact the State House at 617-722-2000 or visit www.wheredoIvotema.com.
Special Education Students and Bullying: Research and Resources
From Psychology Today's Parenting News You Can Use
By Debbie Glasser, Ph.D.
A study published in the Journal of School Psychology followed more than 800 special and general education students aged 9 to 16 years at nine different elementary, middle and high schools. According to the results, children enrolled in special education were not only more likely to be bullied; they were more likely to bully others.
Sixty-seven percent of these students reported they had been victimized by bullies, and over a third (38.1%) admitted they had bullied other students.
Related Articles
By Debbie Glasser, Ph.D.
June 30, 2102
"Study suggests kids in special education are likely to be bullied and bully others."
Bullying can happen anywhere, to any child. But according to a new study, some children are at higher risk than others.
Researchers at the University of Nebraska discovered that students receiving special education services for behavioral disorders, as well as kids with more obvious disabilities (like language or hearing impairments), are more likely than general-education students to be victims of bullying. What’s more, these children may be more likely to bully others.
"Study suggests kids in special education are likely to be bullied and bully others."
Bullying can happen anywhere, to any child. But according to a new study, some children are at higher risk than others.
Researchers at the University of Nebraska discovered that students receiving special education services for behavioral disorders, as well as kids with more obvious disabilities (like language or hearing impairments), are more likely than general-education students to be victims of bullying. What’s more, these children may be more likely to bully others.
A study published in the Journal of School Psychology followed more than 800 special and general education students aged 9 to 16 years at nine different elementary, middle and high schools. According to the results, children enrolled in special education were not only more likely to be bullied; they were more likely to bully others.
Sixty-seven percent of these students reported they had been victimized by bullies, and over a third (38.1%) admitted they had bullied other students.
Related Articles
- Nature-Deficit Disorder Redux: Kids Need To Get Off Their Butts
- Education: Getting Schooled
- A Brief History Lesson—Back to the Basics—Teach Spelling!
The authors indicate that children with observable disabilities may be more likely to be bullied because they seem easy to victimize. They also suggest that these kids may subsequently act as bullies towards others in an effort to seek revenge.
According to the study findings, students who receive special education services are also more likely than others to be sent to the school office for discipline issues.
Another finding: Bullying behavior isn’t limited to one gender. The authors discovered that bullying impacts boys and girls equally.
Potential Effects of Bullying
We’ve all read the tragic headlines about children and teens ending their lives after chronic, destructive bullying. In addition to the heartbreaking stories in the news, there are many other outcomes of bullying. These may be less likely to appear in the headlines, but they’re critically important to address. For example, children who are victimized may experience anxiety, depression, and various health concerns.
Warning Signs
Parents, school staff, and other professionals need to be aware of risk factors and warning signs. Some signs that may suggest your child is being bullied include:
According to the study findings, students who receive special education services are also more likely than others to be sent to the school office for discipline issues.
Another finding: Bullying behavior isn’t limited to one gender. The authors discovered that bullying impacts boys and girls equally.
Potential Effects of Bullying
We’ve all read the tragic headlines about children and teens ending their lives after chronic, destructive bullying. In addition to the heartbreaking stories in the news, there are many other outcomes of bullying. These may be less likely to appear in the headlines, but they’re critically important to address. For example, children who are victimized may experience anxiety, depression, and various health concerns.
Warning Signs
Parents, school staff, and other professionals need to be aware of risk factors and warning signs. Some signs that may suggest your child is being bullied include:
- Difficulty sleeping or frequent nightmares
- Changes in eating habits
- Looking for excuses to avoid attending school
- Unexplainable injuries
- Lost or destroyed items of value (i.e., money, iPod, cell phone)
- Decreased self-esteem
- Increased physical symptoms (i.e., headaches, stomachaches)
- Sudden decline in grades
The presence of these behaviors doesn’t necessarily suggest that your child is being bullied. However, if you have concerns about your child, seek professional guidance.
Recommendations
The authors offer several suggestions in response to their findings. They recommend that anti-bullying programs promoting prosocial skills should be implemented for students in both special and general education classes. They are hopeful that these programs will encourage socially skilled students to serve as positive role models for other students.
In addition, they suggest that teachers and school staff help those students with observable disabilities become better integrated into general-education classes in an effort to prevent bullying behavior.
Ideally, meaningful anti-bullying programming will be introduced to all children, in all grades, as part of a comprehensive curriculum.
"...the foundation of respect, acceptance and kindness begins at home. It’s up to us, as parents, to teach our children to treat all people with dignity and compassion."
Of course, the foundation of respect, acceptance and kindness begins at home. It’s up to us, as parents, to teach our children to treat all people with dignity and compassion. It’s also up to all of the adults in children’s lives to advocate for effective anti-bullying programs and interventions to promote a peaceful, tolerant and respectful environment in our schools and communities.
Additional Information
To learn more about how to talk with your child about bullying, and to advocate on behalf of promoting effective anti-bullying programs in schools, here are some resources:
Web
Recommendations
The authors offer several suggestions in response to their findings. They recommend that anti-bullying programs promoting prosocial skills should be implemented for students in both special and general education classes. They are hopeful that these programs will encourage socially skilled students to serve as positive role models for other students.
In addition, they suggest that teachers and school staff help those students with observable disabilities become better integrated into general-education classes in an effort to prevent bullying behavior.
Ideally, meaningful anti-bullying programming will be introduced to all children, in all grades, as part of a comprehensive curriculum.
"...the foundation of respect, acceptance and kindness begins at home. It’s up to us, as parents, to teach our children to treat all people with dignity and compassion."
Of course, the foundation of respect, acceptance and kindness begins at home. It’s up to us, as parents, to teach our children to treat all people with dignity and compassion. It’s also up to all of the adults in children’s lives to advocate for effective anti-bullying programs and interventions to promote a peaceful, tolerant and respectful environment in our schools and communities.
Additional Information
To learn more about how to talk with your child about bullying, and to advocate on behalf of promoting effective anti-bullying programs in schools, here are some resources:
Web
- AbilityPath.org
- Education.com/topic/school-bullying-teasing/
- Specialneeds.thebullyproject.com/
- StopBullying.gov
Books
- Bullying Prevention and Intervention: Realistic Strategies for Schools, by Susan M. Swearer, Ph.D., Dorothy L. Espelage, Ph.D., Scott A. Napolitano, Ph.D.
- Bullyproof Your Child for Life: Protect Your Child from Teasing, Taunting and Bullying for Good, by Joel Haber and Jenna Glatzer
- Perfect Targets: Asperger Syndrome and Bullying -- Practical Solutions for Surviving the Social World, by Rebekah Heinrichs
- Why Good Kids Act Cruel: The Hidden Truth about the Pre-Teen Years, by Carl Pickhardt, Ph.D.
About Dr. Glasser
Debbie Glasser, Ph.D. is a licensed clinical psychologist, author and speaker specializing in parenting and child development. She is past chairwoman of the National Parenting Education Network (NPEN) and, in her clinical work, she has developed programs and provided services on sleep challenges and single parenting.
Dr. Glasser has appeared in Associated Press, Parenting, Family Circle, Redbook, First for Women, Parents, Family Circle, Baby Talk, USA Today, Media Tracks, and on CNN Headline News, CNN.com, PBS Public Television, Scholastic Online, and iParenting. For ten years, she penned "Positive Parenting," a weekly column in The Miami Herald.Dr. Glasser was also the on-air expert for South Florida's WSVN weekly Parent-to-Parent segment.
Debbie Glasser, Ph.D. is a licensed clinical psychologist, author and speaker specializing in parenting and child development. She is past chairwoman of the National Parenting Education Network (NPEN) and, in her clinical work, she has developed programs and provided services on sleep challenges and single parenting.Dr. Glasser has appeared in Associated Press, Parenting, Family Circle, Redbook, First for Women, Parents, Family Circle, Baby Talk, USA Today, Media Tracks, and on CNN Headline News, CNN.com, PBS Public Television, Scholastic Online, and iParenting. For ten years, she penned "Positive Parenting," a weekly column in The Miami Herald.Dr. Glasser was also the on-air expert for South Florida's WSVN weekly Parent-to-Parent segment.
Wednesday, July 25, 2012
Save the Dates: College Success Boot Camp at NESCA Monday - Tuesday, August 13 - 14th
Co-Sponsored by
Thinking Outside the
Classroom and College
Solutions, in Cooperation with NESCA
This 6-hour, highly-interactive course is recommeded for anyone eager to succeed at the college level, whether going for the first time or returning to campus in September.
This 6-hour, highly-interactive course is recommeded for anyone eager to succeed at the college level, whether going for the first time or returning to campus in September.
When: 1st Session: 6:30 - 9:30pm Monday, August 13
2nd Session: 6:30 - 9:30pm Tuesday, August
14
Where: NESCA, 55 Chapel
Street, 2nd Floor, Newton, MA
Cost: $400 per person; enrollment limited to
12!
Participants will learn how to:
- Create a personalized planning and motivational system;
- Select a major that fits your interests and goals;
- Take effective notes and prepare for exams;
- Master test taking strategies and anxiety;
- Research and write college-level papers;
- Tap into online and mobile tools for student success;
- Build positive relationships and networking skills;
- Develop career interests and an action plan for maximizing early career success.
- Identify the challenges and pressures faced by today’s college student and strategies to overcome them;
- Assess your current expectations about college, personal strengths, and areas needing improvement;
- Use planning and prioritizing tools to enhance your academic and early career success;
- Use motivational techniques to persist in college when things get tough and achieve academic goals;
- Communicate more effectively with faculty, staff, and peers;
- Discover campus resources that can support your academic and co-curricular interests and goals;
- Appreciate the importance of personal branding and maintaining a positive online image.
For additional information and to register, please call NESCA at
617-658-9800, or email nesca@nesca-newton.com.
When Diagnosing ADHD, Consider Possibility of Giftedness in Some Children
From SENG - Supporting Emotional Needs of the Gifted
By Erik von Hahn, M.D., FAAP
July, 2012
Parents and teachers often ask whether a child might have attention-deficit/hyperactivity disorder (ADHD). But when a child is gifted, a diagnosis is not always clearcut.
Although gifted children generally do well, they may show behaviors that mimic ADHD. For example, they may appear hyperactive because they ask many questions and are so excited about learning. Or, they may fail to participate in age-expected activities because of their over-focus on an area of interest. Finally, boredom can lead to inattention as well as feelings of depression.
In such cases, the child does not have ADHD or another disability, and the appropriate intervention is to provide needed stimulation. Otherwise, the child is at risk for academic and social failure despite superior potential.
‘Twice-Exceptional’ Children
Although atypical behaviors in gifted children do not necessarily indicate the presence of a disability, gifted children can have ADHD or another behavioral or mental health condition even when they are provided with appropriate levels of stimulation.
"This concept of dual diagnosis, or twice-exceptional children, can be difficult. Adults may not accept that a student can be gifted and have a disability."
This concept of dual diagnosis, or twice-exceptional children, can be difficult for parents, teachers and clinicians to accept. Adults who work with children often seek one explanation for the child’s behaviors and may not accept that a student can be gifted and have a disability.
Identifying giftedness and an accompanying disability such as ADHD is not hard to do if one considers the possibility that both might be present in the same child. As is the case for any child who may have ADHD, criteria from the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV), must be fulfilled to make the diagnosis.
The clinician also needs to consider whether symptoms listed in the DSM-IV are due to giftedness (and the result of excitement, boredom or over-focus on other interests); if they are due to the executive dysfunctions believed to cause ADHD; or if they are due to a combination of the two.
Ask These Questions
These questions can help clinicians identify a gifted child:
• Do the parents believe the child might be gifted? Most of the time, parents are accurate in their assessment of their child’s giftedness. They will give a good description of their child’s advanced skills and will state that their child complains of boredom or completes his/her work much more quickly than peers, etc.
• Does the child have strong academic or cognitive skills, unexpected for his or her age? These are identified through formal intelligence measures but also should be evident from the student’s school performance (past or present). Examples include advanced reading, writing or math skills. Detailed questioning may be needed to identify advanced academic skills in students who may also show academic failure due to boredom.
• Does the child show non-academic abilities unexpected for his or her peer group? Exceptional skills are those valued by society, such as advanced skills in drawing, dance, sports or music.
• Does inattention occur in only one setting or with certain types of tasks? Can the child explain why she or he is not paying attention? More importantly, is the child attentive, focused and productive when engaged in his or her area of interest?
The following questions might help pediatricians identify a gifted child who also might have ADHD:
• Do symptoms of inattention persist even though the gifted student participates in classroom and other activities that provide the appropriate level of stimulation (i.e., enrichment activities and/or activities with similarly abled peers)?
• Does the child complain of not being able to focus successfully or of being forgetful? These complaints are especially pertinent if they interfere with the tasks that the child wishes to complete.
• Does the inattention interfere with academic and social success, and also with managing daily routines? The child has to show symptoms of inattention during different types of tasks and across settings, and has to require significant adult supervision/supports to manage routines of the day.
Although these lists are not complete, the take-home message is that giftedness can look like ADHD and can co-exist with ADHD. If clinicians consider both conditions, they will be able to gather the necessary information or make the appropriate referrals to establish an accurate diagnostic picture.
Resources
• Webb J.T., et al., Misdiagnosis and Dual Diagnoses of Gifted Children and Adults. Great Potential Press, 2005
• National Association for Gifted Children, www.nagc.org
• Supporting the Emotional Needs of the Gifted, www.sengifted.org
• The Association for the Gifted, Division of the Council for Exceptional Children, www.cectag.org
• Davidson Institute for Talent Development, www.ditd.org
About Dr. Erik von Hahn
Dr. von Hahn is a developmental and behavioral pediatrician at the Floating Hospital for Children, at Tufts Medical Center in Boston. He works collaboratively with schools at the interface between the health care
system and the educational system.
By Erik von Hahn, M.D., FAAP
July, 2012
Parents and teachers often ask whether a child might have attention-deficit/hyperactivity disorder (ADHD). But when a child is gifted, a diagnosis is not always clearcut.
Although gifted children generally do well, they may show behaviors that mimic ADHD. For example, they may appear hyperactive because they ask many questions and are so excited about learning. Or, they may fail to participate in age-expected activities because of their over-focus on an area of interest. Finally, boredom can lead to inattention as well as feelings of depression.
In such cases, the child does not have ADHD or another disability, and the appropriate intervention is to provide needed stimulation. Otherwise, the child is at risk for academic and social failure despite superior potential.
‘Twice-Exceptional’ Children
Although atypical behaviors in gifted children do not necessarily indicate the presence of a disability, gifted children can have ADHD or another behavioral or mental health condition even when they are provided with appropriate levels of stimulation.
"This concept of dual diagnosis, or twice-exceptional children, can be difficult. Adults may not accept that a student can be gifted and have a disability."
This concept of dual diagnosis, or twice-exceptional children, can be difficult for parents, teachers and clinicians to accept. Adults who work with children often seek one explanation for the child’s behaviors and may not accept that a student can be gifted and have a disability.
Identifying giftedness and an accompanying disability such as ADHD is not hard to do if one considers the possibility that both might be present in the same child. As is the case for any child who may have ADHD, criteria from the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV), must be fulfilled to make the diagnosis.
The clinician also needs to consider whether symptoms listed in the DSM-IV are due to giftedness (and the result of excitement, boredom or over-focus on other interests); if they are due to the executive dysfunctions believed to cause ADHD; or if they are due to a combination of the two.
Ask These Questions
These questions can help clinicians identify a gifted child:
• Does the child have strong academic or cognitive skills, unexpected for his or her age? These are identified through formal intelligence measures but also should be evident from the student’s school performance (past or present). Examples include advanced reading, writing or math skills. Detailed questioning may be needed to identify advanced academic skills in students who may also show academic failure due to boredom.
• Does the child show non-academic abilities unexpected for his or her peer group? Exceptional skills are those valued by society, such as advanced skills in drawing, dance, sports or music.
• Does inattention occur in only one setting or with certain types of tasks? Can the child explain why she or he is not paying attention? More importantly, is the child attentive, focused and productive when engaged in his or her area of interest?
The following questions might help pediatricians identify a gifted child who also might have ADHD:
• Do symptoms of inattention persist even though the gifted student participates in classroom and other activities that provide the appropriate level of stimulation (i.e., enrichment activities and/or activities with similarly abled peers)?
• Does the child complain of not being able to focus successfully or of being forgetful? These complaints are especially pertinent if they interfere with the tasks that the child wishes to complete.
• Does the inattention interfere with academic and social success, and also with managing daily routines? The child has to show symptoms of inattention during different types of tasks and across settings, and has to require significant adult supervision/supports to manage routines of the day.
Although these lists are not complete, the take-home message is that giftedness can look like ADHD and can co-exist with ADHD. If clinicians consider both conditions, they will be able to gather the necessary information or make the appropriate referrals to establish an accurate diagnostic picture.
Resources
• Webb J.T., et al., Misdiagnosis and Dual Diagnoses of Gifted Children and Adults. Great Potential Press, 2005
• National Association for Gifted Children, www.nagc.org
• Supporting the Emotional Needs of the Gifted, www.sengifted.org
• The Association for the Gifted, Division of the Council for Exceptional Children, www.cectag.org
• Davidson Institute for Talent Development, www.ditd.org
About Dr. Erik von Hahn
Dr. von Hahn is a developmental and behavioral pediatrician at the Floating Hospital for Children, at Tufts Medical Center in Boston. He works collaboratively with schools at the interface between the health care
system and the educational system.Tuesday, July 24, 2012
Social Brain Circuits Disrupted in Autism
From the National Institute of Mental Health (NIMH)
July 19, 2012 Science Update
In a study of high-functioning adolescents with an autism spectrum disorder, scientists using functional brain imaging have found reduced connectivity selectively affecting parts of the brain that form circuits supporting social behavior.
The findings sharpen the focus of previous reports suggesting disruptions in connectivity across the brain in autism, and offer a target for future studies to search for the genes that shape the development of these circuits and how they become disrupted in the disorder.
Background
Difficulties with communication and social interactions are central features of autism spectrum disorders (ASD), and are universally present in those with an ASD. To determine how brain function is disrupted in autism, scientists have used noninvasive functional brain imaging to explore connectivity in the brain—the extent to which patterns of activity in functionally related parts of the brain correlate with each other. Scientists increasingly see the brain and its disorders in terms of circuits, with a given behavior engaging multiple centers across the brain, functioning together.
Functional imaging of people with an ASD has suggested that there are disruptions in connectivity across the brain. Narrowing the search to determine if losses in connectivity affect only specific circuits has been difficult, however.
Mapping which centers of the brain are tightly connected in most people but disrupted in illness potentially involves comparisons in activity between thousands of points in different brain regions. Accordingly, previous studies have focused on a predetermined, small handful of regions to evaluate connectivity differences in ASD.
This Study
Stephen Gotts, Alex Martin and colleagues at the National Institute of Mental Health developed an approach to identify regions throughout the entire brain for which connectivity was reduced in ASD, and measure the magnitude of the reductions. The scans were done on 31 adolescents with ASD and 29 without the disorder, while they were at rest, not engaged in any task. Scan results revealed decreases in connectivity among those with ASD compared to individuals without ASD, concentrated in areas of the brain involved in social functions.
In particular, the greatest decreases occurred between a cluster of brain regions involved in the emotional aspects of social behavior (the limbic brain) and two other clusters: one involved in language and communication and the other in the interplay between visual perception and movement. Moreover, participants in the study who had the greatest difficulties with social interactions were those in whom the decreases in connectivity were the most marked.
Significance
These data offer evidence in terms of brain activity to confirm what scientists have suspected but have been unable to examine systematically, that disruptions in connectivity in autism are concentrated in social centers of the brain.
"The limbic brain is composed of structures that mediate emotional and affective components of our social interactions, so you can understand the rules about how other people are behaving and acting. These brain regions are active in autism spectrum disorders, but they are not interacting appropriately with the rest of the social brain.”
According to Dr. Gotts, what they found was not that this circuit was inactive, but that, among participants with ASD, patterns of activity in the three clusters of brain centers did not correlate with each other. “So a circuit that is normally in sync with the rest of the social brain has become decoupled."
"The limbic brain is composed of areas and structures that mediate emotional and affective components of our social interactions, so you can understand the social rules about how other people are behaving and acting. These brain regions are active in autism spectrum disorders and are coordinated amongst themselves, but they are not interacting appropriately with the rest of the social brain.”
The clusters of brain centers identified in the study as functionally connected are also anatomically connected circuits. One of the most exciting aspects of the research, says Gotts, is that in humans, this brain circuit shows a different developmental growth trajectory relative to the rest of the brain's cortex during typical development. Since genes are responsible for guiding growth during development, these findings provide a target for searching for genes that drive abnormal growth and limbic circuit functioning in ASD.
"The differences in connectivity also offer the possibility of a 'systems-level' marker—an indicator reflecting function across the brain—to use in developing and testing possible treatment."
The differences in connectivity also offer the possibility of a “systems-level” marker—an indicator reflecting function across the brain—to use in developing and testing possible treatment. Local abnormalities in cell signaling or, alternatively, loss of longer range neuronal connections could explain the differences reported. If the differences can be traced to more local dynamics, it may be possible to identify new medications or behavioral therapies; variations in circuit activity as shown by functional brain imaging could be used as markers of whether therapy was effective.
Brain regions showing decreases in connectivity in high functioning adolescents with an autism spectrum disorder (ASD) are shown above: Limbic-related regions involved in emotional/affective aspects of social behavior (shown in red), regions involved in social communication and comprehension (shown in blue), and regions involved in visual, somatosensory and motor aspects of social behavior (shown in green). In typically developing adolescents, these circuits are interactive and coordinated, exhibiting correlated patterns of brain activity over time (traces of neural activity would appear as illustrated in upper right plot).
In adolescents with an ASD, the activity in the limbic circuit has become decoupled from the other social brain regions (see red activity trace in lower right plot). Activity within the limbic circuit itself remains coordinated but no longer interacts appropriately with the other two circuits.
Reference
Gotts, S.J., Simmons, W.K., Milbury, L.A., Wallace, G.L., Cox, R.W., and Martin, A. Fractionation of Social Brain Circuits in Autism Spectrum Disorders. Brain 2012 doi:10.1093/brain/aws160.
July 19, 2012 Science Update
In a study of high-functioning adolescents with an autism spectrum disorder, scientists using functional brain imaging have found reduced connectivity selectively affecting parts of the brain that form circuits supporting social behavior.
The findings sharpen the focus of previous reports suggesting disruptions in connectivity across the brain in autism, and offer a target for future studies to search for the genes that shape the development of these circuits and how they become disrupted in the disorder.
Background
Difficulties with communication and social interactions are central features of autism spectrum disorders (ASD), and are universally present in those with an ASD. To determine how brain function is disrupted in autism, scientists have used noninvasive functional brain imaging to explore connectivity in the brain—the extent to which patterns of activity in functionally related parts of the brain correlate with each other. Scientists increasingly see the brain and its disorders in terms of circuits, with a given behavior engaging multiple centers across the brain, functioning together.
Functional imaging of people with an ASD has suggested that there are disruptions in connectivity across the brain. Narrowing the search to determine if losses in connectivity affect only specific circuits has been difficult, however.
Mapping which centers of the brain are tightly connected in most people but disrupted in illness potentially involves comparisons in activity between thousands of points in different brain regions. Accordingly, previous studies have focused on a predetermined, small handful of regions to evaluate connectivity differences in ASD.
This Study
Stephen Gotts, Alex Martin and colleagues at the National Institute of Mental Health developed an approach to identify regions throughout the entire brain for which connectivity was reduced in ASD, and measure the magnitude of the reductions. The scans were done on 31 adolescents with ASD and 29 without the disorder, while they were at rest, not engaged in any task. Scan results revealed decreases in connectivity among those with ASD compared to individuals without ASD, concentrated in areas of the brain involved in social functions.In particular, the greatest decreases occurred between a cluster of brain regions involved in the emotional aspects of social behavior (the limbic brain) and two other clusters: one involved in language and communication and the other in the interplay between visual perception and movement. Moreover, participants in the study who had the greatest difficulties with social interactions were those in whom the decreases in connectivity were the most marked.
Significance
These data offer evidence in terms of brain activity to confirm what scientists have suspected but have been unable to examine systematically, that disruptions in connectivity in autism are concentrated in social centers of the brain.
"The limbic brain is composed of structures that mediate emotional and affective components of our social interactions, so you can understand the rules about how other people are behaving and acting. These brain regions are active in autism spectrum disorders, but they are not interacting appropriately with the rest of the social brain.”
According to Dr. Gotts, what they found was not that this circuit was inactive, but that, among participants with ASD, patterns of activity in the three clusters of brain centers did not correlate with each other. “So a circuit that is normally in sync with the rest of the social brain has become decoupled."
"The limbic brain is composed of areas and structures that mediate emotional and affective components of our social interactions, so you can understand the social rules about how other people are behaving and acting. These brain regions are active in autism spectrum disorders and are coordinated amongst themselves, but they are not interacting appropriately with the rest of the social brain.”
The clusters of brain centers identified in the study as functionally connected are also anatomically connected circuits. One of the most exciting aspects of the research, says Gotts, is that in humans, this brain circuit shows a different developmental growth trajectory relative to the rest of the brain's cortex during typical development. Since genes are responsible for guiding growth during development, these findings provide a target for searching for genes that drive abnormal growth and limbic circuit functioning in ASD.
"The differences in connectivity also offer the possibility of a 'systems-level' marker—an indicator reflecting function across the brain—to use in developing and testing possible treatment."
The differences in connectivity also offer the possibility of a “systems-level” marker—an indicator reflecting function across the brain—to use in developing and testing possible treatment. Local abnormalities in cell signaling or, alternatively, loss of longer range neuronal connections could explain the differences reported. If the differences can be traced to more local dynamics, it may be possible to identify new medications or behavioral therapies; variations in circuit activity as shown by functional brain imaging could be used as markers of whether therapy was effective.
Brain regions showing decreases in connectivity in high functioning adolescents with an autism spectrum disorder (ASD) are shown above: Limbic-related regions involved in emotional/affective aspects of social behavior (shown in red), regions involved in social communication and comprehension (shown in blue), and regions involved in visual, somatosensory and motor aspects of social behavior (shown in green). In typically developing adolescents, these circuits are interactive and coordinated, exhibiting correlated patterns of brain activity over time (traces of neural activity would appear as illustrated in upper right plot).
In adolescents with an ASD, the activity in the limbic circuit has become decoupled from the other social brain regions (see red activity trace in lower right plot). Activity within the limbic circuit itself remains coordinated but no longer interacts appropriately with the other two circuits.
Reference
Gotts, S.J., Simmons, W.K., Milbury, L.A., Wallace, G.L., Cox, R.W., and Martin, A. Fractionation of Social Brain Circuits in Autism Spectrum Disorders. Brain 2012 doi:10.1093/brain/aws160.
Monday, July 23, 2012
Nine Signs that Neuroscience Has Entered the Classroom
From Edudemic.com
By Terry Heick
June 29, 2012
There is often a big divide between what happens in the laboratory and the way laboratory findings are practically applied. The relationship between neuroscience research and education is no exception. While there are numerous educational products that claim to be based on neuroscience research (often quite dubiously so), the real impact of brain-based research on education has been much more subtle. While neuroscience hasn’t yet radically changed the way we think about teaching and learning, it is helping to shape educational policies and influencing new ways of implementing technology, improving special education, and streamlining day-to-day interactions between teachers and students.
While there is still a long way to go before we truly understand the science of learning and how to use those findings in the real world classroom, it’s important to highlight some of the key ways that neuroscience is changing the classroom of today for the better.
1.) Cognitive Tutoring
Cognitive tutoring is still in its infancy, but it is looking to be one of the most promising products of the intersection of neuroscience and education. Researchers at Carnegie Mellon are using their expertise in neuroscience and programming along with help and input from teachers to build software that’s both innovative and practical for everyday use. The first tutor created by the team focuses on algebra and has so far had promising results in helping students raise their math test scores.
So, how is it different from other tutoring programs? The cognitive tutoring programs allow students to learn by doing and are based on cognitive psychology theory, employing an AI system to adjust to student needs as well as to track student progress and thought processes so teachers can better help them learn. Read more about the tutoring system here, and learn how schools can tailor it to their individual needs as well.
2.) High Schools Starting Later
Neuroscience research has demonstrated that sleep patterns change, often significantly, as individuals age. Multiple studies have found that adolescents need more sleep than other age groups and are unlikely to function at peak cognitive capacity early in the morning. In addition to needing more sleep, teens also simply have different circadian rhythms, which often makes them drowsy and moody in the morning. Many schools are starting to use this data to make changes, pushing back start times to allow students to sleep in a little later.
Surprisingly, as little as 30 minutes of difference can have a major impact on mood and attentiveness, and schools that have chosen to take this neuroscience research into account when making policies are reaping the benefits, reporting fewer students showing up late, skipping breakfast, and feeling sleepy throughout the day.
3.) Offering More Variety
Repetition can be a valuable learning tool, no matter what you’re trying to learn, but neuroscience research has pinpointed a “spacing effect,” demonstrating that students learn more when episodes of learning are spaced out over time rather than pushed into one single episode. One of the ways this manifests itself is by bringing greater variety into the classroom, with lessons extending over the course of a semester rather than being fit into a few days or weeks.
Researchers have also found that variety is key in learning because, simply put, the brain craves it, boosting levels of both attention and retention in students. So how is this being put into practice? Teachers are presenting information in unique ways or asking students to solve a problem using multiple methods, not just memorizing a single way to do so.
This same research has also debunked the idea that there are individual learning styles, suggesting that presenting information in a variety of ways is helpful to all students, not just those who enjoy more visual or auditory content.
4.) Individualized Education
While our general brain anatomy is similar, neuroscience is showing that no two brains work exactly alike. Personal experiences actually determine where information is stored in the brain, developing unique neuron structures for each person. Because we’re all wired a little bit differently, learning tools that are adaptable to individual needs are especially valuable in the classroom. New, highly plastic digital tools are filling part of that role, but neuroscience and education are taking this information in another direction as well. Teachers are being encouraged to expose students to novel experiences when presenting information to build entirely new neural connections or to connect new information to previous experiences students have had to take advantage of existing brain pathways.
5.) Understanding Use It or Lose It
When it comes to knowledge, you either use it or you lose it. Anyone who has ever tried to remember lessons from grade school decades later can attest to this, but neuroscience backs it up, demonstrating that people who read more challenging books often have a greater variety and number of neural connections. This research also has practical applications for modern education aside from simply encouraging students to read.
Research has shown that the more time students spend outside of school, the more they’ll forget, leading to more work to regain lost information. As a result, many schools are shortening summer breaks or going to a year-round schedule in order to reduce the amount of time students are away from their studies.
6.) Better Identification and Intervention for Learning Disorders
Neuroscience research is making it easier to identify which students have learning disabilities and to get those students interventions that can significantly help their academic performance. Through neuroscience research, new biomarkers and diagnostic strategies for disabilities like ADHD and dyslexia have been identified, in turn leading to more successful early interventions for students and some potentially amazing tools to help students learn.
One example is a neuroscience-based reading program for dyslexic students called Fast ForWord, which helps students compensate for the difficulties they have with auditory processing. The scientists behind the software are experimenting to see if it can also help other students without dyslexia build their cognitive “muscles” and take advantage of brain plasticity in the same way that it does for dyslexic students.
7.) Making Learning Fun
Increasingly, neuroscience is demonstrating the importance of making learning a fun and positive experience. Pleasurable experiences cause the body to release dopamine, which in turn helps the brain remember facts. One great example of how this is making it into the classroom is Khan Academy, an online learning portal that challenges students to complete games and problem sets in order to win badges. Many students report feeling an affinity for subjects like math and science that they didn’t have before the game-based learning program was implemented in their schools. Even when students didn’t have a marked increase in test scores after using Khan, they reported a more positive attitude about learning, which can often be a major hurdle for educators.
Recent research has also shown just how much of an emotional experience learning can be, with negative emotional states like fear, anxiety, shame, or worry making it difficult or impossible for students to reason, learn, or store new memories. This data further stresses the need for developing learning environments that are not just fun but are also positive, safe places for students.
8.) Making Learning Social
Human beings are highly social creatures, so it should come as no surprise that neuroscience would point to a positive effect from social learning experiences. A study by teacher and neurologist Judy Willis in 2011 found that students who worked on writing in positive, supportive groups experienced a surge in dopamine (which we’ve already discussed the positive effects of), as well as a redirection and facilitation of information through the amygdala into the higher cognitive brain, allowing students to better remember information over the long term.
She also found that learning in groups reduced anxiety, which can frequently be a major roadblock to effective learning. Some schools have used this study and others like it as the basis for allowing students to do more group work or even to help struggling peers grasp a new concept.
9.) Focus on Neuroeducation
We’ve already discussed neuroscience research that has shown us how diverse our brains can be, but research also demonstrates that they are incredibly dynamic. Through practice, it’s actually possible to change the way our brains are structured, adding more brain connections and changing neural pathways through neuroplasticity afforded by our brain cells.
Education is just beginning to acknowledge that successful learning isn’t just a process of taking in facts; it’s also about strengthening and developing the brain itself. These developments can not only help to improve learning in those with disabilities but can also improve memory and language skills in all students, regardless of ability.
Educators are increasingly encouraging administrators to move away from memorization-based learning to programs that ask students to solve problems, think critically, and explore creativity, as these methods not only build knowledge but also enhance and build brain pathways themselves, prepping the brain for future experiences.
About Terry Heick
Terry Heick is editor of, and a principal contributor to the provocative educational website TeachThought.com, which describes itself as "a fluid platform dedicated to the progression of learning forms and resources."
Heick says, "TeachThought was developed initially as a pure curriculum design group with the goal of innovating reading and writing instruction in secondary schools (i.e., English Literature), but since has broadened its scope to helping educators uncover and implement innovative learning tools for their classroom. This includes tools (e.g., iPads, apps, and smartphones) and trends (e.g., flipped classrooms, social media, and online learning), to resources (e.g., curricula, models, and thought leadership) and learning models (e.g., Connected Learning from DML, the “Inside Out School” and dozens of others).
Above all else, TeachThought is interested in supporting the innovation of the learning process–not simply how we learn, but our reasons for learning."
By Terry Heick
June 29, 2012
There is often a big divide between what happens in the laboratory and the way laboratory findings are practically applied. The relationship between neuroscience research and education is no exception. While there are numerous educational products that claim to be based on neuroscience research (often quite dubiously so), the real impact of brain-based research on education has been much more subtle. While neuroscience hasn’t yet radically changed the way we think about teaching and learning, it is helping to shape educational policies and influencing new ways of implementing technology, improving special education, and streamlining day-to-day interactions between teachers and students.
While there is still a long way to go before we truly understand the science of learning and how to use those findings in the real world classroom, it’s important to highlight some of the key ways that neuroscience is changing the classroom of today for the better.
1.) Cognitive Tutoring
Cognitive tutoring is still in its infancy, but it is looking to be one of the most promising products of the intersection of neuroscience and education. Researchers at Carnegie Mellon are using their expertise in neuroscience and programming along with help and input from teachers to build software that’s both innovative and practical for everyday use. The first tutor created by the team focuses on algebra and has so far had promising results in helping students raise their math test scores.
So, how is it different from other tutoring programs? The cognitive tutoring programs allow students to learn by doing and are based on cognitive psychology theory, employing an AI system to adjust to student needs as well as to track student progress and thought processes so teachers can better help them learn. Read more about the tutoring system here, and learn how schools can tailor it to their individual needs as well.
2.) High Schools Starting Later
Neuroscience research has demonstrated that sleep patterns change, often significantly, as individuals age. Multiple studies have found that adolescents need more sleep than other age groups and are unlikely to function at peak cognitive capacity early in the morning. In addition to needing more sleep, teens also simply have different circadian rhythms, which often makes them drowsy and moody in the morning. Many schools are starting to use this data to make changes, pushing back start times to allow students to sleep in a little later.
Surprisingly, as little as 30 minutes of difference can have a major impact on mood and attentiveness, and schools that have chosen to take this neuroscience research into account when making policies are reaping the benefits, reporting fewer students showing up late, skipping breakfast, and feeling sleepy throughout the day.
3.) Offering More Variety
Repetition can be a valuable learning tool, no matter what you’re trying to learn, but neuroscience research has pinpointed a “spacing effect,” demonstrating that students learn more when episodes of learning are spaced out over time rather than pushed into one single episode. One of the ways this manifests itself is by bringing greater variety into the classroom, with lessons extending over the course of a semester rather than being fit into a few days or weeks.
Researchers have also found that variety is key in learning because, simply put, the brain craves it, boosting levels of both attention and retention in students. So how is this being put into practice? Teachers are presenting information in unique ways or asking students to solve a problem using multiple methods, not just memorizing a single way to do so.
This same research has also debunked the idea that there are individual learning styles, suggesting that presenting information in a variety of ways is helpful to all students, not just those who enjoy more visual or auditory content.
4.) Individualized Education
While our general brain anatomy is similar, neuroscience is showing that no two brains work exactly alike. Personal experiences actually determine where information is stored in the brain, developing unique neuron structures for each person. Because we’re all wired a little bit differently, learning tools that are adaptable to individual needs are especially valuable in the classroom. New, highly plastic digital tools are filling part of that role, but neuroscience and education are taking this information in another direction as well. Teachers are being encouraged to expose students to novel experiences when presenting information to build entirely new neural connections or to connect new information to previous experiences students have had to take advantage of existing brain pathways.
5.) Understanding Use It or Lose It
When it comes to knowledge, you either use it or you lose it. Anyone who has ever tried to remember lessons from grade school decades later can attest to this, but neuroscience backs it up, demonstrating that people who read more challenging books often have a greater variety and number of neural connections. This research also has practical applications for modern education aside from simply encouraging students to read.
Research has shown that the more time students spend outside of school, the more they’ll forget, leading to more work to regain lost information. As a result, many schools are shortening summer breaks or going to a year-round schedule in order to reduce the amount of time students are away from their studies.
6.) Better Identification and Intervention for Learning Disorders
Neuroscience research is making it easier to identify which students have learning disabilities and to get those students interventions that can significantly help their academic performance. Through neuroscience research, new biomarkers and diagnostic strategies for disabilities like ADHD and dyslexia have been identified, in turn leading to more successful early interventions for students and some potentially amazing tools to help students learn.
One example is a neuroscience-based reading program for dyslexic students called Fast ForWord, which helps students compensate for the difficulties they have with auditory processing. The scientists behind the software are experimenting to see if it can also help other students without dyslexia build their cognitive “muscles” and take advantage of brain plasticity in the same way that it does for dyslexic students.
7.) Making Learning Fun
Increasingly, neuroscience is demonstrating the importance of making learning a fun and positive experience. Pleasurable experiences cause the body to release dopamine, which in turn helps the brain remember facts. One great example of how this is making it into the classroom is Khan Academy, an online learning portal that challenges students to complete games and problem sets in order to win badges. Many students report feeling an affinity for subjects like math and science that they didn’t have before the game-based learning program was implemented in their schools. Even when students didn’t have a marked increase in test scores after using Khan, they reported a more positive attitude about learning, which can often be a major hurdle for educators.
Recent research has also shown just how much of an emotional experience learning can be, with negative emotional states like fear, anxiety, shame, or worry making it difficult or impossible for students to reason, learn, or store new memories. This data further stresses the need for developing learning environments that are not just fun but are also positive, safe places for students.
8.) Making Learning Social
Human beings are highly social creatures, so it should come as no surprise that neuroscience would point to a positive effect from social learning experiences. A study by teacher and neurologist Judy Willis in 2011 found that students who worked on writing in positive, supportive groups experienced a surge in dopamine (which we’ve already discussed the positive effects of), as well as a redirection and facilitation of information through the amygdala into the higher cognitive brain, allowing students to better remember information over the long term.
She also found that learning in groups reduced anxiety, which can frequently be a major roadblock to effective learning. Some schools have used this study and others like it as the basis for allowing students to do more group work or even to help struggling peers grasp a new concept.
9.) Focus on Neuroeducation
We’ve already discussed neuroscience research that has shown us how diverse our brains can be, but research also demonstrates that they are incredibly dynamic. Through practice, it’s actually possible to change the way our brains are structured, adding more brain connections and changing neural pathways through neuroplasticity afforded by our brain cells.
Education is just beginning to acknowledge that successful learning isn’t just a process of taking in facts; it’s also about strengthening and developing the brain itself. These developments can not only help to improve learning in those with disabilities but can also improve memory and language skills in all students, regardless of ability.
Educators are increasingly encouraging administrators to move away from memorization-based learning to programs that ask students to solve problems, think critically, and explore creativity, as these methods not only build knowledge but also enhance and build brain pathways themselves, prepping the brain for future experiences.
About Terry Heick
Terry Heick is editor of, and a principal contributor to the provocative educational website TeachThought.com, which describes itself as "a fluid platform dedicated to the progression of learning forms and resources."Heick says, "TeachThought was developed initially as a pure curriculum design group with the goal of innovating reading and writing instruction in secondary schools (i.e., English Literature), but since has broadened its scope to helping educators uncover and implement innovative learning tools for their classroom. This includes tools (e.g., iPads, apps, and smartphones) and trends (e.g., flipped classrooms, social media, and online learning), to resources (e.g., curricula, models, and thought leadership) and learning models (e.g., Connected Learning from DML, the “Inside Out School” and dozens of others).
Above all else, TeachThought is interested in supporting the innovation of the learning process–not simply how we learn, but our reasons for learning."
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