Megan Brooks

April 5, 2012 — A new brain imaging study shows that the human brain is wired in a simple and orderly 3-dimensional grid, akin to a checkerboard, with no diagonal paths.

"Far from being just a tangle of wires, the brain’s connections turn out to be more like ribbon cables — folding 2D sheets of parallel neuronal fibers that cross paths at right angles, like the warp and weft of a fabric," Van J. Wedeen, MD, from Massachusetts General Hospital (MGH), the Martinos Center for Biomedical Imaging, and Harvard Medical School in Boston, explained in a statement. "This grid structure is continuous and consistent at all scales and across humans and other primate species," he added.

The highly detailed images were obtained with the Connectom diffusion magnetic resonance imaging (MRI) scanner installed at MGH’s Martinos Center for Biomedical Imaging last fall. The scanner can visualize the networks of crisscrossing fibers in 10-fold higher detail than can conventional scanners.

Detail from DSI scan shows fabric-like 3-dimensional grid structure of connections in monkey brain. Van Wedeen, MD, Martinos Center and Department of Radiology, Massachusetts General Hospital and Harvard University Medical School

"This one-of-a-kind instrument is bringing into sharper focus an astonishingly simple architecture that makes sense in light of how the brain grows," Dr. Wedeen said.

Their report is published online March 30 in Science.

A Landmark in Human Neuroanatomy

In a statement, Thomas R. Insel, MD, director of the National Institutes of Mental Health said, "Getting a high resolution wiring diagram of our brains is a landmark in human neuroanatomy. This new technology may reveal individual differences in brain connections that could aid diagnosis and treatment of brain disorders."

As reported in the Science paper, Dr. Wedeen’s team scanned the brains of living humans and the postmortem brains of 4 types of monkeys: rhesus, owl, marmoset, and galago. They found that the wiring of the mature brain appears to mirror 3 primal pathways established in embryonic development.

During early development, the researchers explain, the brain’s connections form along perpendicular pathways, running horizontally, vertically, and transversely. This grid structure appears to guide connectivity as do lane markers on a highway. This structure may help enforce a more efficient, orderly way for the fibers to find their proper connections, and for the structure to adapt through evolution, the researchers say.

Obtaining highly detailed images of these pathways in the human brain has long eluded scientists, in part because the many folds, nooks, and crannies in the human cortex obscure the structure of its connections.

Dr. Wedeen’s team is part of the Human Connectome Project Harvard/MGH-University of California, Los Angeles, consortium that aims to optimize MRI technology to more accurately and precisely image the human brain.

Converging Lines of Evidence

This paper is "very interesting," Olivier Coulon, PhD, CNRS research fellow in the Laboratory for Information Science and Systems in Marseilles, France, told Medscape Medical News. "To my knowledge, it’s the first that reports such organization at the whole brain level," he pointed out.

The findings are consistent with observations made in a previous paper, he said, "although in that paper only the medial frontal cortex was studied and the orthogonal organization of fibers was described at a gross scale without any notion of the fine grid described by Wedeen et al."

"What is interesting," he added, "is the fact that it is consistent with how we think cortical sulci or folds are organized. There have been a few papers describing the cortical folds as organized according to an orthogonal grid.

"We recently published a short conference paper in which such organization becomes clearer thanks to a flat angle-preserving projection of the cortex on a rectangular domain," he added. "A longer paper should follow this year."

"All these papers," Dr. Coulon said, "are converging to propose evidence that there is a genetically-driven organization, which could help to find an invariant structure beyond the apparent great variability of the brain (cortex and fibers). Developmental studies and the improvement of fetal MRI acquisitions should help to clarify all these ideas in the future," he concluded.

Dr. Coulon is principal investigator in the BrainMorph Project, which is funded by the French Agence Nationale de la Recherche and dedicated to the development and validation of surface-based brain morphometrics methods.

Dr. Wedeen’s research was funded by grants from the National Science Foundation, the National Institutes of Health, and the Human Connectome Project. The authors have disclosed no relevant financial relationships.

Science. Published online March 30, 2012. Abstract

Medscape Medical News © 2012 WebMD, LLC
Send comments and news tips to news@medscape.net.

By Elizabeth Flock, Washington Post, January 6, 2012

Physicist, cosmologist and obsessor of black holes Stephen Hawking turns 70 Sunday, despite a diagnosis of Lou Gehrig’s disease that doctors said would kill him almost five decades ago. Many scientists are taking the birthday as a chance to reflect on what the man taught us in his brilliant career.

Stephen Hawking. (MARKUS SCHREIBER – AP)

As a professor of mathematics at the University of Cambridge, Hawking taught countless students about cosmology, gravitation and complex mathematics. As the author of “A Brief History of Time,” he instructed readers on the Big Bang, black holes and other mysteries of the universe. And despite losing his ability to speak, he continues to teach disbelieving doctors that people can live past their life expectancy if they try.

Below, six other lessons Hawking has taught us in his 70 years:

1. We will never have all the answers.

At the end of a lecture in the Royal Albert Hall in Kensington, England, in 2010, Hawking was asked: “Do you think it will come the time that people will learn everything about physics?” The scientist quickly responded: “I hope not!” And when a reader of Time magazine that same year asked him whether it felt like a huge responsibility to have all the answers, Hawking wrote back: “While physics and mathematics may tell us how the universe began, they are not much use in predicting human behavior because there are far too many equations to solve. I’m no better than anyone else at understanding what makes people tick.”

2. Knowledge is best put to use when shared.

Despite its difficult subject matter, Hawking’s “A Brief History of Time” has been read by legions of people because the physicist made it so accessible. A popular story goes that Hawking’s publisher told him readership would be cut in half for every equation in the book, so Hawking included only one: E = mc².

“The fact is that information in his mind would be useless to anyone else if he wasn’t able, somehow, to communicate it effectively,” Science blogger Mic Farris writes.

3. Learn the lessons of history.

Hawking fielded questions from the BBC this week on what might happen if humans discover other intelligent life. Hawking’s response: Know your history. “The discovery of intelligent life elsewhere in the universe would be the biggest scientific discovery ever,” he said. “But it would be very risky to attempt to communicate with an alien civilization. If aliens decided to visit us then the outcome might be similar to when Europeans arrived in the Americas. That did not turn out well for the Native Americans.”

5. Study what fuels your passion.

When the Washington Post interviewed Errol Morris, director of the film adaptation of “A Brief History of Time,” in 1992, Morris explained why he believed Hawking was so fascinated with the study of black holes: “To me, it’s like some real-life Edgar Allan Poe story, a version of the premature burial — being essentially buried alive inside of one’s self. . . . When he was 21 years old, he was given a death sentence with 2 ¹ / ₂ years to live, and in the nearly 30 years since then, he has become increasingly incapacitated. And what is the central objective of his inquiries? Black holes. Stars that collapse in on themselves, implode, become so incredibly dense that nothing can escape their gravitation field . . . To me, there’s a very close metaphorical connection.”

5. Never lose your voice.

Because of his motor neuron disease, Hawking had to undergo a tracheotomy in 1985 that removed his ability to speak on his own. But he never stopped talking. Like movie critic Roger Ebert or the protagonist of “The Diving Bell and the Butterfly,” Hawking adopted his own way of speaking — by using a computer that picks up the twitching movements of his right cheek.

6. Genius shouldn’t always be associated with precocity.

Hawking admitted in the same Royal Albert Hall lecture that he did not learn to read until he was 8 years old. He also said he was a lazy student at Oxford University, his classwork untidy and his handwriting the “despair of my teachers.” Late bloomers, take heart.

By Elizabeth Flock  |  12:41 PM ET, 01/06/2012
Tags:  National, Stephen Hawking

First Posted: 1/5/12 , Huffington Post 

We here at HuffPost High School knew it all along (not to brag, or anything), but now there’s the research to back it up — a new study by the American Psychological Association recently found that blogging may have psychological benefits for teens.

The study, which surveyed 161 high school students in Israel, examined the teens’ self-esteem levels and daily social activities and behaviors after a 10-week blogging experiment. The researchers found that the teens who blogged — as compared to those who did nothing or kept a private diary — displayed greater improvements in self-esteem, social ease, and emotional well-being. The bloggers who wrote specifically about their social difficulties and those whose posts were open to comments showed the most improvement.

Although research on teens and social media usage have shown mixed results for the effect of social networking on well-being, with blogging, the generally encouraging comments on the blog posts may be a contributing factor in the teen bloggers’ lessened social anxiety and increased well-being.

The study’s co-author said, “Although cyberbullying and online abuse are extensive and broad, we noted that almost all responses to our participants’ blog messages were supportive and positive in nature… We weren’t surprised, as we frequently see positive social expressions online in terms of generosity, support and advice.”

Do you think blogging is good for teens? Have you found that comments on personal blog posts are generally positive? Share your thoughts in the comments below.

Study: Autistic Children Have More Brain Cells

By Alice Park Wednesday, November 9, 2011

There’s growing evidence that the brains of autistic children are very different from the brains of other youngsters. Now a new study that found an excess of brain cells in children with autism comes closer to pinpointing the origins of the condition: in utero versus in toddlerhood.

In research reported in the Journal of the American Medical Association (JAMA), scientists at the University of California, San Diego, found that autistic children have about 67% more nerve cells in a part of the brain known as the prefrontal cortex than children without autism. The prefrontal cortex is involved in processing social skills, communication, cognitive functions and language — all areas in which autistic children often show abnormal development.

Lead researcher Eric Courchesne studied the brains of seven autistic boys between the ages of 2 and 16 after their death and compared his analysis to the brains of six unaffected boys who died at similar ages. The excess of neurons was a bit of a surprise since in most cases, deficits in social skills — like the ones autistic children typically have — are linked to less, not more, nerve tissue.

“When we think of the inability to handle complicated information, we usually think of too little in the way of connections or brain cells,” he says. “But this is just the opposite.”

MORE: Risk of Autism Is Five Times Higher in Low-Birthweight Babies

Functionally, however, the autistic children may have been suffering from a dearth of proper nerve connections since the overabundance of neurons may have led to difficulty in their ability to connect and communicate with each other. That situation, says Courchesne, could "lead to pathways that slow down or prevent normal active interaction between different regions of the brain.”

Social interaction and communication, for example, require that nerves from distant portions of the brain link up. Think of too many nerves like an overgrown forest that could choke some of these critical neural bridges.

Equally significant is the fact that the excess of neurons in the prefrontal cortex aren’t formed after birth, but during early development, in utero. That suggests that the changes responsible for autism are occurring much earlier than scientists had thought.

MORE: Could the Way We Mate and Marry Boost Rates of Autism?

“Knowing that we have a specific type of defect that occurs very early in development really helps us to focus and sharpen the next steps in research to determine what caused the excess,” says Courchesne. And hopefully find new treatments that can help children and their families cope better with the symptoms of autism.

Find this article at:
http://healthland.time.com/2011/11/09/study-autistic-children-have-too-many-brain-neurons/

© 2011 Time Inc. All rights reserved

Read more: http://healthland.time.com/2011/11/09/study-autistic-children-have-too-many-brain-neurons/print/#ixzz1dDWRdOxS

http://www.sciencedaily.com/releases/2011/10/
     111020024329.htm

IQ, the standard measure of intelligence, can increase or fall significantly during our teenage years, according to research funded by the Wellcome Trust, and these changes are associated with changes to the structure of our brains. The findings may have implications for testing and streaming of children during their school years. (Credit: © lightpoet / Fotolia)

ScienceDaily (Oct. 20, 2011) — IQ, the standard measure of intelligence, can increase or fall significantly during our teenage years, according to research funded by the Wellcome Trust, and these changes are associated with changes to the structure of our brains. The findings may have implications for testing and streaming of children during their school years.

Across our lifetime, our intellectual ability is considered to be stable, with intelligence quotient (IQ) scores taken at one point in time used to predict educational achievement and employment prospects later in life. However, in a study published October 20 in the journal Nature, researchers at the Wellcome Trust Centre for Neuroimaging at UCL (University College London) and the Centre for Educational Neuroscience show for the first time that, in fact, our IQ is not constant.

The researchers, led by Professor Cathy Price, tested 33 healthy adolescents in 2004 when they were between the ages of 12 and 16 years. They then repeated the tests four years later when the same subjects were between 15 and 20 years old. On both occasions, the researchers took structural brain scans of the subjects using magnetic resonance imaging (MRI).

Professor Price and colleagues found significant changes in the IQ scores measured in 2008 compared to the 2004 scores. Some subjects had improved their performance relative to people of a similar age by as much as 20 points on the standardised IQ scale; in other cases, however, performance had fallen by a similar amount.

To test whether these changes were meaningful, the researchers analysed the MRI scans to see whether there was a correlation with changes in the structure of the subjects’ brains.

"We found a considerable amount of change in how our subjects performed on the IQ tests in 2008 compared to four years earlier," explains Sue Ramsden, first author of the study. "Some subjects performed markedly better but some performed considerably worse. We found a clear correlation between this change in performance and changes in the structure of their brains and so can say with some certainty that these changes in IQ are real."

The researchers measured each subject’s verbal IQ, which includes measurements of language, arithmetic, general knowledge and memory, and their non-verbal IQ, such as identifying the missing elements of a picture or solving visual puzzles. They found a clear correlation with particular regions of the brain.

An increase in verbal IQ score correlated with an increase in the density of grey matter — the nerve cells where the processing takes place — in an area of the left motor cortex of the brain that is activated when articulating speech. Similarly, an increase in non-verbal IQ score correlated with an increase in the density of grey matter in the anterior cerebellum, which is associated with movements of the hand. However, an increase in verbal IQ did not necessarily go hand-in-hand with an increase in non-verbal IQ.

According to Professor Price, a Wellcome Trust Senior Research Fellow, it is not clear why IQ should have changed so much and why some people’s performance improved while others’ declined. It is possible that the differences are due to some of the subjects being early or late developers, but it is equally possible that education had a role in changing IQ, and this has implications for how schoolchildren are assessed.

"We have a tendency to assess children and determine their course of education relatively early in life, but here we have shown that their intelligence is likely to be still developing," says Professor Price. "We have to be careful not to write off poorer performers at an early stage when in fact their IQ may improve significantly given a few more years.

"It’s analogous to fitness.A teenager who is athletically fit at 14 could be less fit at 18 if they stopped exercising. Conversely, an unfit teenager can become much fitter with exercise."

Other studies from the Wellcome Trust Centre for Neuroimaging and other research groups have provided strong evidence that the structure of the brain remains ‘plastic’ even throughout adult life. For example, Professor Price showed recently that guerrillas in Columbia who had learned to read as adults had a higher density of grey matter in several areas of the left hemisphere of the brain than those who had not learned to read. Professor Eleanor Maguire, also from the Wellcome Trust Centre, showed that part of a brain structure called the hippocampus, which plays an important part in memory and navigation, has greater volume in licensed London taxi drivers.

"The question is, if our brain structure can change throughout our adult lives, can our IQ also change?" adds Professor Price. "My guess is yes. There is plenty of evidence to suggest that our brains can adapt and their structure changes, even in adulthood."

"This interesting study highlights how ‘plastic’ the human brain is," said Dr John Williams, Head of Neuroscience and Mental Health at the Wellcome Trust. "It will be interesting to see whether structural changes as we grow and develop extend beyond IQ to other cognitive functions. This study challenges us to think about these observations and how they may be applied to gain insight into what might happen when individuals succumb to mental health disorders."

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The above story is reprinted from materials provided by Wellcome Trust.

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Journal Reference:

1. Sue Ramsden, Fiona M. Richardson, Goulven Josse, Michael S. C. Thomas, Caroline Ellis, Clare Shakeshaft, Mohamed L. Seghier, Cathy J. Price. Verbal and non-verbal intelligence changes in the teenage brain. Nature, 2011; DOI: 10.1038/nature10514

Wellcome Trust (2011, October 20). Brain scans support findings that IQ can rise or fall significantly during adolescence. ScienceDaily. Retrieved October 25, 2011, from http://www.sciencedaily.com­ /releases/2011/10/111020024329.htm

Special Issue: Focus on ADHD

ADHD & ODD: Confronting the Challenges of Disruptive Behavior

By CHRISTOPHER K. PETERS, MD
University of Louisville | September 9, 2009

Dr Peters is director of training in child and adolescent psychiatry and assistant professor in the division of child and adolescent psychiatry at the University of Louisville.

ABSTRACT: Disruptive behavior is the most common mental health problem seen by pediatricians. Although attention-deficit/ hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD) are both considered disruptive behavior disorders—and although about half of children with ADHD also meet the diagnostic criteria for ODD—the 2 disorders are distinct, having different etiologies and responding to different types of treatment. ADHD is generally viewed as a neurobiologically mediated problem, while ODD appears to have a stronger link to environmental risk factors and psycho- social stressors. Thus, when assessing for possible ODD in a child with disruptive behavior it is important to carefully investigate any psychosocial factors that may underlie the oppositional behavior. Treatment of ADHD clearly involves medication therapy. The 2 principal types of evidence-based treatments for children with ODD are individual therapy with a focus on problem-solving and social skills and parent management training. The latter is especially important; moreover, the provision of needed external regulation of behavior in the home has substantial benefits in the treatment of both ADHD and ODD.

A significant portion of children with attention-deficit/hyperactivity disorder (ADHD) first receive the diagnosis and subsequent treatment from their primary care pediatrician. Children with ADHD who present primarily with symptoms of inattention are often managed successfully by primary care clinicians. However, ADHD is often accompanied by symptoms such as hostility, defiance, and aggression. In fact, disruptive behaviors are the most common mental health problem seen by pediatricians,¹ and properly diagnosing and treating these problem behaviors is often a challenge.
In this article I address the diagnostic challenges posed by oppositional behavior in children with ADHD. I discuss approaches to evaluation and treatment that have proved particularly successful in these patients, and I provide tips on when referral may be warranted.
THE NATURE OF THE DISRUPTIVE DISORDERS

Disruptive behavior in children is not just a contemporary concern, as evidenced in this comment by Socrates: "Our youth now love luxury. They have bad manners and contempt for authority and disrespect for their elders. Children nowadays are tyrants."² The group of disorders that are currently classified by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, as disruptive behavior disorders include ADHD (all 3 of its subtypes—inattentive, hyperactive-impulsive, and combined), oppositional defiant disorder (ODD), conduct disorder (CD; both of childhood and adolescent onset), and disruptive behavior disorder not otherwise specified.³ These diagnoses share primary features of poor self-regulation and associated interpersonal difficulties. Although the diagnoses share "externalizing" symptoms, there are differences in how they are conceptualized. (Externalizing symptoms are negative behaviors that a patient displays as a means of managing internal distress; examples are fighting or running away.)
ADHD is generally viewed as a neurobiologically mediated problem that requires pharmacological treatment as a primary evidence-based intervention.⁴ ADHD is diagnosed in 3% to 7% of school-aged children3 and when untreated can be associated with significant morbidity (delinquency, drug use, poor academic success, increase in injuries). A number of diagnoses commonly occur comorbidly with ADHD: ODD, anxiety disorders, depressive disorders, learning disorders, and substance use disorders.
While the data for the neurobiological dysfunction in persons with ADHD have mounted, with links to the monoamine neurotransmitter systems and dysfunction in the prefrontal cortex now well established, there is a dearth of data demonstrating a clear role for neurobiological dysfunction in ODD and CD. Some studies cite information on the relationship between serotonergic dysfunction and impulsivity and aggression, while others point to the existence of an abnormality of arousal in the autonomic nervous system as evidence of catecholamine dysfunction. Nonetheless, ODD and CD remain less well understood from a biological standpoint and appear to have a stronger link to environmental risk factors and psychosocial stressors.
Despite these etiological differences, ADHD often involves more than its core features of attention deficits, impulsivity, and hyperactivity. Clinicians routinely see children whose parents are challenged by their child’s tantrum behaviors, poor frustration tolerance, and defiance.³ These behaviors are often best understood as resulting from biological vulnerabilities of the child that may be exacerbated by problematic family/parental responses. Understanding the relationship between oppositional and inattentive behaviors has critical importance for management decisions.
Although CD has been more systematically studied, the focus in this article will not be on children with this more serious disorder, who, by definition, intrude on the basic rights of others, break laws, and commit crimes. Instead, I have chosen to focus on ODD in order to help primary care clinicians better understand and intervene with children before severe conduct problems develop.

DIAGNOSING ODD IN CHILDREN WITH ADHD
Although some of the criteria for the diagnosis of ODD were established somewhat arbitrarily, the current ODD diagnostic criteria (Table 1) are the best method we have for identifying children who have additional difficulty with self-regulation. Between 40% and 70% of children with ADHD also meet the diagnostic criteria for ODD or CD.^4-6 In a study of preschoolers with ADHD, just over 50% were found to also have a diagnosis of ODD.⁷ To put these figures in perspective, consider that in a group of school-aged children who may or may not have ADHD, the prevalence of ODD may be between 1% and 16%,⁸ or with strict application of diagnostic criteria, between 2% and 3%.⁹

The comorbidity of ODD and ADHD seems to be bidirectional.
The clear overlap of symptoms blurs somewhat the lines of distinction between the 2 disorders and raises a number of questions for the clinician. Where does one disorder begin and the other end? Is it possible that ODD is a by-product of severe ADHD? Is there a common pathway to the evolution of disruptive behavior diagnoses? Is it possible to improve ODD symptoms simply by treating a child’s ADHD?
For primary care clinicians, the importance of identifying co-occurring disorders, such as ODD and ADHD, lies in the possibility of earlier intervention, which has a greater likelihood of having an impact than does the treatment of a more enduring pathology, which may develop if intervention is not timely.
Criteria for an ODD diagnosis.
The diagnosis of ODD requires that a child display several symptoms of antagonism and hostility, have impairment in daily function, and have symptoms/behaviors in excess of what would be expected for a developmentally matched peer—all for more than 6 months.³
The symptoms should not be better accounted for by another mental illness (eg, psychotic disorder in a paranoid child who refuses to eat, or separation anxiety disorder in a child who refuses to attend school)—nor should oppositionality and defiance be symptoms of a biologically mediated illness (eg, autism, schizophrenia).¹⁰
The ODD diagnosis from a developmental perspective.
Consideration of how children acquire self-regulation in the course of normal development can help one to better understand how disruptive behavior evolves. Toddlers, in an effort to develop some independence, display expected poor self-regulation at times (hence the expression "terrible twos"). This is a normal developmental process that assists with the acquisition of new skills for self-soothing and managing unpleasant mood states. We do not consider a diagnosis of ODD in a child who is in this developmental phase. However, if, as the child ages, he or she fails to assimilate new skills and continues to have tantrums and external expressions of emotional instability, defiance, and hostility, then it is appropriate for the family to seek assistance.
RISK FACTORS FOR ODD
A multitude of factors may affect the development of certain disorders. A child may have certain vulnerabilities that contribute to the development of a disorder—or strengths that protect against it. The risk factors and protective factors associated with ODD are summarized in Table 2.

The cases featured in this article (Case 1, Case 2, Case 3) indicate different pathways to the same end: they show how different environmental factors impinging on children with individual differences all can fuel the evolution of ODD. These cases provide a springboard for a discussion of family interactional factors that may contribute to the evolution and maintenance of disruptive behavior.
TJ’s mother (see Case 1), because of her own guilt about her failed marriage, had become an indulgent parent. She failed to maintain boundaries, limits, and expectations because of her discomfort "to see her child in distress." TJ’s internal working model of the world was thus one that reinforced immediate gratification; his acquisition of frustration tolerance and self-soothing had been thwarted. ADHD symptoms contributed to his oppositionality and defiance, probably because he needed more structure and limits to contain his impulses.

AT’s situation (see Case 2) illustrates several common reactions of parents who have exhausted their efforts to attempt to manage disruptive behavior. AT’s parents were more comfortable using authoritative approaches to effect change, and once these methods failed, they were at a loss about what to do. Her father’s frustration and sense of powerlessness were evidenced by his comment that "my father would have beat me if I acted this way, but we can’t treat kids like that anymore." AT’s parents did not err on the side of indulgence; rather, they lacked an awareness of the power of positive reinforcement and praise. Their anxiety about losing control led to their reactive, harsh parenting stance.

JS and his siblings (see Case 3) illustrate the challenges a chaotic home presents for the children who live there. Their mother’s consultation with a psychiatrist seemed to be a turning point. When she received a diagnosis of ADHD and began treatment, her parenting improved. The home became a more predictable environment, and the increased structure was associated with calming of all the children’s disruptive behavior.

These cases suggest that children’s disruptive behavior (ADHD and ODD) can arise via different pathways. However, these different paths of development share a common interactional end point: the need for familial environments that provide external regulation of behavior

EVALUATION OF A CHILD WITH DISRUPTIVE BEHAVIOR
When assessing children who exhibit negative behavior, it is important to try to understand the context of the symptoms. It would be helpful if there were a biological test or a psychological test that was reliable and valid for diagnosing any of the disruptive disorders. However, the reality is that the most important aspect of the evaluation process is the psychiatric examination. Table 3 proposes an outline for an assessment focused on understanding a child’s disruptive behavior.

When meeting with families who are dealing with severely disruptive behavior, you may find it challenging to take the time necessary to fully understand the depth and breadth of a problem. Our health care system favors rapid assessment and quick interventions; however, at times like this, these are not what is needed. When assessing younger children, it may be prudent to meet with the parents without the child to obtain additional information. Conversely, it may be important in older children or adolescents to meet separately with them to establish rapport before meeting with their parents. After the interview process, a physical examination is indicated to rule out medical causes of disruptive behavior, however rare these may be (Table 4).

Simple assessments, such as vision and hearing tests, can sometimes obviate unnecessary interventions. In older children and adolescents, it is important to assess for substance use, as well as any severe sleep-related difficulties. Exploring the influence of language and cultural factors, when appropriate, may also lead to understandable explanations for behavioral difficulties. ADHD, ODD—or both? Because so many children and adolescents with ADHD receive a diagnosis of ODD, it can be difficult to determine how distinctly separate these 2 disorders are. Newcorn and Halperin⁶ discuss the challenge of differentiating ADHD from ODD and CD because of considerable symptom overlap; however, they suggest that there is evidence that ADHD and ODD/CD do not represent variations of a single entity. Still, several studies reviewed by these researchers suggest that children with ADHD are at increased risk for the development of ODD and CD. The assessment of a child with ADHD must therefore include a careful assessment of risk factors and protective factors related to ODD and CD (see Table 2). Not only does this process result in a more accurate diagnosis, it provides a starting point for interventions.

Evaluating underlying psychosocial factors.
Although biological vulnerabilities may underlie certain disruptive symptoms (eg, aggression, impulsivity), there is currently no evidence for a unifying, valid biological explanation of the origin of oppositional and defiant behaviors.¹¹ This reality underscores the importance of a careful investigation of the psycho- social factors that underlie oppositional behavior (Table 5), as exemplified in the cases presented here.

The developmental aspects of separation-individuation are often awry in patients with ODD. The 2 periods when developmentally appropriate interpersonal antagonism is most commonly seen are the toddler years and early adolescence. An assessment must thus consider the question of whether, in some patients who present with the chief complaint of oppositionality and defiance, the behavior represents normal development. The diagnosis of ODD rests on the clinician’s determination of impairment and his or her own perception of how developmentally deviant the behavior has become.
To test or not to test?
Although the clinical interview is at the core of an evaluation for disruptive behavior, psychological testing is a valuable supplement that is designed to support clinical judgment.¹² Psychological testing can be helpful in sorting out diagnoses.
The most commonly used psychological measures in the primary care outpatient setting are rating scales. These are filled out by older patients, patients’ parents, and patients’ teachers. The Conners Rating Scales and Vanderbilt Rating Scales, which are used to evaluate for ADHD, also assess oppositional and conduct-related difficulties. The scales can be scored quickly and help with sifting through the differential diagnosis.
Further assessment is typically done when requested by a clinician having difficulty in distinguishing between multiple conditions, especially if learning difficulties are involved. When making a request for psychological testing, it is important to be specific about the nature and purpose of the assessment being sought. For example, asking for help with the differential diagnosis is different from asking, "Can you assist with evaluating for the presence of a reading disorder in this child, who has ADHD, combined type?"
Helpful components of a psychological assessment of a child with a disruptive behavior disorder may include the child behavior checklist, a learning evaluation, and projective tests (eg, Rorschach test, thematic apperception test) to evaluate for sources of oppositional behavior.

TREATING ADHD WITH COMORBID ODD
After a thorough assessment establishes the presence of ODD as a comorbid diagnosis in a child with ADHD, the next questions are "what to do?"and "what to treat first?"
Treatment of ADHD.
Recommendations for the treatment of ADHD clearly involve medication treatment, usually starting with the psychostimulants.⁴ There are also nonstimulants that can be used, such as the FDA-approved atomoxetine(Drug information on atomoxetine), as well as off-label uses of a2-agonists (guanfacine, clonidine(Drug information on clonidine)), tricyclic antidepressants (eg, imipramine(Drug information on imipramine)), and bupropion.
Whatever the initial choice, there is usually appropriate apprehension on the part of parents and some physicians about using psychoactive agents in children. There has been increasing scrutiny of the true value of medication in childhood psychiatric disorders.¹³ However, the NIMH Multimodal Treatment Study of Children with ADHD (MTA) provided strong reinforcement of the need for medication to adequately treat ADHD.
It is with this realization that clinicians treat ADHD with medication while at the same time enlisting psychosocial therapies to address a patient’s oppositional-defiant behavior. The MTA established that combining psychostimulant treatment with psychosocial interventions (ie, behavioral therapy) was helpful when treating ADHD with comorbid disorders.⁴ The combination of medication treatment and behavior therapy may have led to less decompensation when medication was not taken, as well as contributing to the use of lower doses of psychostimulants.¹⁴ Although oppositional and defiant behaviors may improve as a child’s ADHD responds to medication, the expectation that "just"medication can be used to treat the majority of children with ADHD does not acknowledge the common co-occurrence of psychosocially mediated symptoms that require psychosocial treatments.
Treatment of comorbid ODD.
When addressing the additional concerns of disruptive behavior, it is important to look beyond medication. When ADHD and ODD co-occur in the same child, a biopsychosocial etiology is implied, necessitating a multimodal treatment approach.
The primary care pediatrician plays a critical role in the inauguration of psychotherapeutic interventions. Referring a child for psychiatric consultation and/or psychotherapy invariably taps into the family’s attitudes about mental health issues. The pediatrician’s attitudes and beliefs can be powerful contributors to the perception that patients and their parents have regarding mental health care.
Be especially careful not to blame the families dealing with the disruptive behaviors. Focusing on the interventions instead may improve the likelihood of their following through with a referral. To achieve this nonblaming attitude, it is helpful to keep in mind that the problematic behaviors are interactional in nature: "problematic parenting can be elicited by a ‘difficult’ child and, at the same time, can create problems for a child."¹⁵
Given this interactional model, it is not surprising that the 2 types of evidence-based treatments for patients with ODD are individual therapy with a cognitive behavioral focus on problem-solving skills and parental intervention in the form of parent management training (PMT).
Establishing a relationship with a child and adolescent psychiatrist can facilitate treatment planning. Such a person can direct the pediatrician to therapists who are versed in both family and individual therapies.
Parent management training.
While the chief goal in working with disruptive children is to enhance their own self-confidence in their ability to manage impulses and negative emotions, this can seldom be achieved without working with the child’s family. The first step therapists typically take in working with the families of children with disruptive behavior who have been referred to them is to pursue PMT. PMT is one of the most substantiated interventions in child mental health.^8,16,17 As psychopharmacological interventions are to ADHD, so PMT is to ODD. The goal of PMT is to help parents establish a more focused approach to consistency and predictability, which promotes pro- social behavior in their child. Without a positive relationship with or attachment to the child, it becomes very difficult to establish lasting change in negative behavior. PMT teaches ways to reward children (eg, surprise rewards after desired behavior, anticipated rewards). Parents learn to value praise and their relationship with their child as powerful tools for managing disruptive behavior. Finding opportunities for the parent and child to interact in healthier ways can inject much needed positive energy into a relationship that probably has been composed solely of negative interactions.
Parents are taught about limit setting, active ignoring, consequences, and communication, as well as uses of  "time outs."
Webster-Stratton and Hancock state that "consistent limit setting and predictable responses from parents help give children a sense of stability and security . . . children who feel a sense of security regarding the limits of their environment have less need to constantly test it."¹⁸ It is important to remind parents that all children test parents’ rules and that, by upholding the rules, parents play a significant role in helping their child develop self-regulation. Parents should be reminded that much of effective limit setting is simply a matter of acquiring and practicing skills, a process not so different from that of learning a sport or a musical instrument.
It is important to discuss with parents the need for appropriate expectations regarding the timeline of their child’s response (weeks to months). Parents also need to be aware that symptoms of disruptive behavior tend to increase when the family system is changing. For example, as parents change their approach to handling inappropriate behavior, the child may become defiant to test their resolve. Preparing parents for these new stressors and helping them to view them as predictable and part of the therapeutic process is critical in maintaining their commitment to change. Some parents benefit from recommendations for adjunctive educational materials. Television shows, such as Supernanny, or parenting books, such as 1,2,3 Magic, can reinforce the skills learned in therapy.
Individual therapy for ODD. Individual work with patients with ODD is usually most effective in children of school age and older. The older the child, the more likely he will be to benefit from problem-solving skills training and social competency training. Therapy usually begins with alliance building—a challenge with children with ODD. The next step is usually to introduce a skill, to model and role-play the skill, and then to try to connect the skill to the patient’s day-to-day challenges. Patients typically are given homework assignments, such as "stop, think, and act"instructions for younger children and practice in thought monitoring for older children and adolescents.¹⁹
When PMT and individual therapy are not effective. Despite efforts to provide appropriate avenues of treatment for disruptive behavior, some families and children struggle to respond to PMT, social skills training, and problem-solving training. In such situations, a higher level of care is needed. Josephson and Serrano²⁰—and other researchers²¹—have found that when parents do not effectively use parent management techniques, it is often because of complex individual and marital dynamics—and even diagnosable disorders. In such cases, it may be necessary for the primary care clinician to refer the family to a larger mental health system (eg, an academic center or a community mental health center).
What about using medication to treat ODD? When disruptive behavior is associated with other principal diagnoses, it is clear that medication can help.⁴ However, when disruptive behavior is clearly a manifestation of ODD, medication plays no role in definitive treatment. When severe and persistent ODD develops into CD, then psychopharmacological interventions to assist with severe mood dysregulation and severe aggression may be warranted, along with referrals for higher levels of care (partial programs, inpatient treatment, and residential care).

TREATMENT OUTCOMES IN 3 CASES
In Case 1, adequately treating TJ’s ADHD did very little to mitigate the indulgent strategies that his mother used to assuage her own guilt and coercively minimize acute problems. She did not realize that she was impeding TJ’s development of self-regulation. Through PMT and individual therapy to help her see the role her own thoughts and emotions played in maintaining her son’s behavior, TJ’s mother was able to make strides in creating more appropriate limits and boundaries. Although TJ continues to have challenges, he is showing progress.
In Case 2, AT’s parents had been struggling with a lack of confidence in their parenting methods, and they responded well to PMT.

In Case 3, JS engaged well with the therapist and began to try out new ways of self-managing his anger and frustration. He also benefited from his mother’s response to her own treatment for ADHD.
Although not every case is a success story, with better understanding of the interactional components of ODD, primary care pediatricians can provide more appropriate interventions and will be more likely to elicit the needed change. While the major goal of working with disruptive patients is to enhance their own self-confidence in managing impulses and negative emotions, this cannot occur without working with the context within which these children live—that is, their families.

REFERENCES

1. Fravenglass S, Routh DK. Assessment of the disruptive behavior disorders: dimensional and categorical approaches. In: Quay HC, Hogan AE, eds. Handbook of Disruptive Behavior Disorders: Dimensional and Categorical Approaches. New York: Kluwer Academic/Plenum Publishers; 1999:49-71.

2. Finch AJ Jr, Nelson WM III, Hart KJ. Conduct disorder: description, prevalence and etiology. In: Nelson WM III, Finch AJ Jr, Hart KJ, eds. Conduct Disorders: A Practitioner’s Guide to Comparative Treatments. New York: Springer Publishing; 2006: 1-13.

3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Arlington, VA: American Psychiatric Publishing, Inc; 2000:83-103.

4. The MTA Cooperative Group. A 14-month randomized clinical trial of treatment strategies for attention-deficit/hyperactivity disorder. Multimodal Treatment Study of Children with ADHD. Arch Gen Psychiatry. 1999;56:1073-1086.

5. Perepletchikova F, Kazdin AE. Oppositional defiant disorder and conduct disorder. In: Cheng K, Myers KM, eds. Child and Adolescent Psychiatry: The Essentials. Philadelphia: Lippincott Williams & Wilkins; 2005:73-88.

6. Newcorn JH, Halperin JM. Attention-deficit disorders with oppositionality and aggression. In: Brown TE, ed. Attention-Deficit Disorders and Comorbidities in Children, Adolescents, and Adults. Washington, DC: American Psychiatric Press, Inc; 2000:171-207.

7. Greenhill L, Kollins S, Abikoff H, et al. Efficacy and safety of immediate-release methylphenidate treatment for preschoolers with ADHD [published correction appears in J Am Acad Child Adolesc Psychiatry. 2007;46:141]. J Am Acad Child Adolesc Psychiatry. 2006;45:1284-1293.

8. Steiner H, Remsing L; Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with oppositional defiant disorder. J Am Acad Child Adolesc Psychiatry. 2007;46:126-141.

9. Angold A, Costello EJ. Toward establishing an empirical basis for the diagnosis of oppositional defiant disorder. J Am Acad Child Adolesc Psychiatry. 1996;35:1205-1212.

10. McHugh PR. Striving for coherence: psychiatry’s efforts over classifications. JAMA. 2005;293: 2526-2528.

11. Burke JD, Loeber R, Birmaher B. Oppositional defiant disorder and conduct disorder: a review of the past 10 years, part II. J Am Acad Child Adolesc Psychiatry. 2002;41:1275-1293.

12. Quinlan DM. Assessment of attention-deficit/ hyperactivity disorder and comorbidities. In: Brown TE, ed. Attention-Deficit Disorders and Comorbidities in Children, Adolescents, and Adults. Washington, DC: American Psychiatric Press, Inc; 2000:455-507.

13. Mayes R, Bagwell C, Erkulwater J. Medicating Children: ADHD and Pediatric Mental Health. Cambridge, MA: Harvard University Press; 2009.

14. Pappadopulos E, Jensen PS, Chait AR, et al. Medication adherence in the MTA: saliva methylphenidate samples versus parent report and mediating effect of concomitant behavioral treatment. J Am Acad Child Adolesc Psychiatry. 2009;48:501-510.

15. Peters CK, Josephson AM. Understanding and managing adolescent disruptive behavior: a developmental family perspective. Psychiatr Times. 2009; 26(2):42-47.

16. Kazdan AE. Parent Managed Training: Treatment for Oppositional, Aggressive, and Antisocial Behavior in Children and Adolescents. New York: Oxford University Press; 2005.

17. Mabe PA, Turner MK, Josephson AM. Parent management training. Child Adolesc Psychiatr Clin N Am. 2001;10:451-464.

18. Webster-Stratton C, Hancock L. Training for parents of young children with conduct problems: content, methods, and therapeutic processes. In: Briesmeister JM, Schaefer CE, eds. Handbook of Parent Training: Parents as Co-Therapists for Children’s Behavior Problems. 2nd ed. Hoboken, NJ: John Wiley & Sons; 1989:99-152.

19. Bloomquist ML, Schnell SV. Social competence training. In: Bloomquist ML, Schnell SV, eds. Helping Children With Aggression and Conduct Problems: Best Practices for Intervention. New York: Guilford Press; 2002:117-143.

20. Josephson AM, Serrano A. The integration of individual therapy and family therapy in the treatment of child and adolescent psychiatric disorders. Child Adolesc Psychiatr Clin N Am. 2001;10:431-450.

21. Weissman MM, Pilowsky DJ, Wickramaratne PJ, et al; STAR*D-Child Team. Remissions in maternal depression and child psychopathology: a STAR*D-child report [published correction appears in JAMA. 2006;296:1234]. JAMA. 2006;295:1389-1398.

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Study Shows Toddlers With Autism Have Abnormal Synchronization in Brain’s Communication Area

By Kathleen Doheny
WebMD Health News

Reviewed by Laura J. Martin, MD

June 22, 2011 — A brain that is out of sync may be an early clue of autism, researchers suggest.

Toddlers with autism are more likely to have abnormal synchronization between certain brain areas than other kids the same age, even those with language delays, according to a new study.

”There seems to be impaired or reduced synchronization between the right and left hemispheres, specifically the areas involved in language and communication,” says researcher Ilan Dinstein, PhD, a postdoctoral fellow at the Weizmann Institute of Science in Rehovot, Israel.

The study was done at the University of California, San Diego. It is published in the journal Neuron.

The researchers found only a link between the abnormality and autism, not cause and effect, Dinstein says. Still, the discovery may someday help experts develop tools to diagnose the condition earlier, he says.

Autism and autism spectrum disorder are a range of neurodevelopmental disorders marked by difficulties in social and communication skills and repetitive behavior. About one in 110 U.S. children are affected, according to CDC estimates.

Coordination of Brain’s Tasks

Synchronization helps coordinate the brain’s different tasks, Dinstein says. “Your brain is set up to do specific tasks.” Some involve vision, for instance, or motor skills or decision making.

“While all these different parts are doing different things, they have to be coordinated,” he says. For normal brain development, this coordination seems to be very important, he tells WebMD.

Other recent research on adults and teens with autism has found problems in this coordination, too, Dinstein says. That led them to look at younger subjects. 

The researchers used functional MRIs (fMRIs) to evaluate 72 toddlers, ages 1 to 3.5, during sleep. Of the 72 participants, 29 had autism, 30 were typically developing, and 13 had language delays. The fMRIs were done while the children were in similar stages of sleep.

Compared to both other groups, those who had a diagnosis of autism had weaker correlations between hemispheres in two areas commonly linked with language production and comprehension. These areas are the inferior frontal gyrus and superior temporal gyrus.

The abnormal synchronization was evident in 70% of those with autism. However, just a handful of the other children had it.

The researchers also found that the weaker the synchronization, the more severe the communication problems for the autistic children.

This suggests that the poor synchronization is found at the earliest stages of the disorder and could be linked to the severity, the researchers say.

If the findings bear out, earlier diagnosis may be possible, Dinstein says. That would make earlier intervention possible, of course.

It’s possible that the reduced synchronization is a by-product of something else causing the autism, he says. ”The fact that this phenomenon is evident in 70% of kids [with autism] does not mean it is the biology causing the autism,” he says. “There could be a different biological mechanism causing both the autism and the reduced synchronization.”

However, even if the the abnormality is a by-product of something else causing the condition, he says, that would still be useful information for making a diagnosis.

Typically, a child is age 3 or older before a diagnosis of autism is made, he says.

Connection Failure in the Brain

The study reinforces some research and breaks some new ground, according to Geraldine Dawson, PhD, chief science officer for Autism Speaks. She reviewed the report but did not participate in the research.

“Some have described autism as a ‘developmental disconnection syndrome’ because several studies have found that there is a failure of long-range connectivity between different brain regions in autism,” she says. “This helps explain why people with autism have trouble with complex behaviors, such as social interaction and language, which require coordinated activity across several brain regions.”

It is the first study, she believes, ”to show reduced functional connectivity in very young children with autism.” The study, she says, suggests this abnormality is an early characteristic of the disorder. It helps explain some symptoms seen early on, she says. “Even early gestures and social games require coordinated activity among several brain regions.”

4 Must-See Articles

• What It’s Like to Have Autism
• Gluten-Free Diets for Autism
• On a Mission to Get My Son Better
• Join the Discussion in the Autism Community

SOURCES:

Ilan Dinstein, PhD, postdoctoral fellow, Weizmann Institute of Science, Rehovot, Israel.

Geraldine Dawson, PhD, chief science officer, Autism Speaks.

Dinstein, I. Neuron, June 23, 2011; vol 70: pp 1218-1225.

© 2011 WebMD, LLC. All rights reserved.

©2005-2007 WebMD, Inc. All rights reserved.

Autism is a national health emergency, now affecting nearly 1% of America’s children

NIXA, Mo., April 2, 2011 /PRNewswire-USNewswire/ — The National Autism Association (NAA) joins with organizations worldwide in recognizing April as Autism Awareness month.  With one in 110 children now diagnosed with autism, and autism mortality rates doubling that of the general population,(1) NAA is once again calling upon legislators and government health agencies to declare autism a national health emergency. Parents of children diagnosed with autism are asking for more research funding, better services, and wider access to safety equipment including tracking devices.

"If you don’t have a family member affected by autism, chances are you have a friend or neighbor who does," said NAA board chair Lori McIlwain. Citing a 2007 Harvard study(2)putting the lifetime care cost at $3.2 million per individual with autism needing round the clock care, Ms. McIlwain observed, "If we don’t find better treatments and services, it will fall upon taxpayers to address the needs of an overwhelming number of children whose parents will one day be unable to care for them."

NAA points out the following critical areas that need to be addressed on behalf of children and families affected by autism:

Prevention:

• Genetics alone cannot explain the rise in autism. Proper study into environmental exposures should be a top priority among our government, researchers and Interagency Autism Coordinating Committee (IACC).
• Recent studies(3), (4), (5) indicate an association between the hepatitis B vaccine and brain damage.
• A new study(6) confirms the relationship between vaccines and autism, stating that "autism is the result of genetic defects and/or inflammation of the brain." The study also points out the implications of the increasing number of vaccines given in a short period of time.
• Parents have consistently stated that regression in their child occurred following immunizations. Further research on the increased use of vaccines is warranted and should be conducted with significant stakeholder input. Obvious research that has been ignored, such as health outcomes in vaccinated versus non-vaccinated populations must be undertaken.  
• Certain subgroups may be more susceptible to environmental regression, including those with a family history of autoimmune disorders, premature infants, and children that are ill at the time of vaccination. Researching ways to decrease adverse vaccine reactions while increasing the safety of vaccines benefits the overall health of the general public.

Treatment:

• Children with autism have underlying medical conditions that often go missed, dismissed or misunderstood. These conditions deserve the full attention of our government health agencies and medical community.
• Physicians should listen to each caregiver’s account of any medical issues their child with autism may have and not presume all symptoms to be behavioral.
• Treatment, services and therapies should be available to all individuals with autism. Insurance coverage for co-morbid medical conditions should be mandated nationwide.
• Studies on children that significantly progressed or completely lost a classic autism diagnosis should be conducted to uncover biological underpinnings.  
• Clinical studies on promising treatments are necessary.

Support: 

• Wandering-related deaths are on the rise among children diagnosed with autism.  So far this year, four children with autism have died from wandering away from safe environments. A wandering prevention protocol should be in the hands of every pediatrician to share with families.
• School systems are overwhelmed by increased autism rates. Our community is in critical need of additional and properly trained special education personnel.
• Federal legislation, The Preventing Harmful Restraint & Seclusion in Schools Act, was introduced last year to address rising abuse and unsafe practices within school systems nationwide, but was stalled in Congress, never making it to a vote before the session ended.  Legislation to protect our children should be a priority in the current Congress.  Cameras in special education classrooms are warranted, as well as stiffer penalties for those who abuse schoolchildren.
• Families are often unable to pay for basic speech and occupational therapies. Government aid is needed for these struggling families.
• We will soon be faced with a disproportionate number of diagnosed adults in need of housing, job assistance, and lifetime care. Preparation should begin immediately and resources allocated accordingly. 
• The Combating Autism Act of 2006 will sunset in September. The reauthorization of this legislation is currently being drafted under the leadership of Senator Menendez. Parents and advocates need to contact their legislators and insist that the new legislation will include provisions for desperately needed research and services that will make a difference in the lives of families affected by autism.

"Autism is a national health emergency. Our hope is that the government will finally declare it as such so that proper prevention, treatments and resources will be put in place," says NAA Executive Director Rita Shreffler. "Immediate action is necessary for our community and for the public in general. The numbers are so huge now that autism really does impact each and every one of us."

For more information about autism, visit www.nationalautismassociation.org.

1 Mouridsen SE, Bronnum-Hansen H, Rich B, Isager T.Mortality and causes of death in ASD: an update Department of Child and Adolescent Psychiatry, Bispebjerg University Hospital, Copenhagen, Denmark. July 2008

2 Ganz, ML. The lifetime distribution of the incremental societal costs of autism. Archives of Pediatric and Adolescent Medicine. 2007 April 16. 

3 Hewitson L, Houser LA, et al. Delayed acquisition of neonatal reflexes in newborn primates receiving a thimerosal-containing Hepatitis B vaccine: Influence of gestational age and birth weight. 2009 Oct 2.  Department of Obstetrics and Gynecology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, United States; Thoughtful House Center for Children, Austin, TX 78746, United States

4 Gallagher, C., Goodman, M. Hepatitis B Triple series vaccine and developmental disability in US children aged 1-9 years. Toxicological & Environmental Chemistry, Vol. 90, No. 5, September-October 2008, 997-1008.

5 Gallagher, C., Goodman, M. Vaccination of Male Neonates and Autism. Annals of Epidemiology, Volume 19, Issue 9, Pages  659-659

6 Ratajczak ,HV.Theoretical aspects of autism: causes–a review.Journal of Immunotoxicology, 2011 Jan-Mar;8(1):68-79.

Contacts:
Rita Shreffler (Nixa, MO) 417-818-9030
Wendy Fournier (Portsmouth, RI) 401-835-5828

SOURCE National Autism Association

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By Mary Agnes Welch, Winnipeg Free Press , March 1, 2011

New research by an Israeli scientist suggests vitamin A could act almost like an antidote to the effects of alcohol on very early embryos during the critical development of the head and central nervous system. That’s when the worst effects of FASD start.

WINNIPEG — It’s too early to call it a cure, but plain old vitamin A could curb the devastating effects of fetal alcohol spectrum disorder.

New research by an Israeli scientist suggests vitamin A could act almost like an antidote to the effects of alcohol on very early embryos during the critical development of the head and central nervous system. That’s when the worst effects of FASD start.

"Scientifically, this is a very interesting story," said Abraham Fainsod, a professor of genetics and biochemistry at the Hebrew University of Jerusalem. "If we can continue our research, we could do some good."

On Monday, Manitoba pledged $750,000 to help set up a joint FASD research consortium between the Hebrew University and the University of Manitoba. Sorting through the vitamin A issue will be among the projects earmarked for funding.

"This has the possibility of being a relatively simple solution," said Geoff Hicks, Fainsod’s counterpart at the University of Manitoba. "That’s why everyone is so excited."

What research Fainsod has done on frogs, Hicks will now try to reproduce using mice, which are the model for mammals.

They’ll be looking at retinoic acid, one of the main biological forms of vitamin A and a critical element in cell development and revitalization. That’s why so many wrinkle creams tout vitamin A as a key ingredient.

Alcohol prevents the conversion of vitamin A to retinoic acid because both compete for one particular enzyme and the alcohol usually wins. While the body is processing alcohol, it’s not making any new retinoic acid, which, in embryos, interrupts the normal development of the head and brain cells.

Fainsod’s research suggests adding more vitamin A to the equation — rebalancing the amount of alcohol and retinoic acid — can reverse or curb brain defects caused by alcohol.

But Fainsod is quick to say vitamin A can never be seen as a licence to drink while pregnant. Too much vitamin A can cause birth defects that mimic the effects of alcohol. And scientists haven’t yet figured out what the correct balance might be.

But vitamin A could one day be added to food as folic acid was added to white flour to reduce birth defects like spina bifida.

Or it could be given to at-risk populations or chronic alcoholics who are unable to quit drinking but who risk having multiple children with FASD.

© Copyright (c) Winnipeg Free Press

New research by an Israeli scientist suggests vitamin A could act almost like an antidote to the effects of alcohol on very early embryos during the critical development of the head and central nervous system. That’s when the worst effects of FASD start.

Photograph by: Ian Waldie, Getty Images

Moderate exercise increases the size of part of the brain that controls memory, researchers suggest

By Peter Russell
WebMD Health News, February 1, 2011

Reviewed by Dr Rob Hicks

Article Link: http://www.webmd.boots.com/healthy-ageing/news/20110201/exercise-reverses-memory-loss

1^st February 2011 – Exercising for 40 minutes three times a week can boost memory in older people, a new study suggests.

Researchers in the US say a year’s worth of moderate physical activity was enough to increase the size of the brain’s hippocampus, leading to the improvement in spatial memory.

820,000 people in the UK have dementia, a number forecast to rise as our population ages. Although the study did not look at people with the condition, it could have important implications for an ageing society.

Exercise regime

Teams led by scientists from the University of Pittsburgh and the University of Illinois recruited 120 inactive people aged between 55 and 80 without dementia and assigned them at random to two groups. Half began an exercise regime in which they walked around a track for 40 minutes a day, three times a week. The remainder acted as a ‘control’ group for the experiment and were limited to stretching and toning exercises.

Magnetic resonance images of the brains of all those taking part were collected before the experiments began, after six months and at the end of the one year study.

The researchers found that in the aerobic exercise group they were able to measure an increase in volume of the left and right hippocampus of 2.12% and 1.97%, respectively.

The same regions of the brain in those who did stretching exercises decreased in volume by 1.40 and 1.43 percent, respectively.

Reversing age-related loss

Writing in Proceedings of the National Academy of Sciences, the authors note that the size of the Hippocampus shrinks by 1-2% each year in older adults who do not have dementia, and that this loss of volume increases the risk of losing brain function. They write, “Exercise training increased hippocampal volume by 2%, effectively reversing age-related loss in volume by one to two years.”

Spatial memory tests were carried out on all participants at the three intervals. Those in the aerobic exercise group showed improved memory function, when measured against their performance at the start of the study, the researchers report.

"We think of the atrophy of the hippocampus in later life as almost inevitable," Kirk Erickson, professor of psychology at the University of Pittsburgh and the paper’s lead author said in a statement. "But we’ve shown that even moderate exercise for one year can increase the size of that structure. The brain at that stage remains modifiable."

Art Kramer from the University of Illinois, and lead author of the research, said in a statement: "The results of our study are particularly interesting in that they suggest that even modest amounts of exercise by sedentary older adults can lead to substantial improvements in memory and brain health."

Never too late to exercise: Dementia charity

Dr Simon Ridley, Head of Research at the Alzheimer’s Research Trust, said in an emailed statement: “Although this study doesn’t look at memory loss in Alzheimer’s or dementia, it suggests it’s never too late to start exercising to help keep our brains healthy. Even modest exercise may improve memory and help protect the brain from normal decline caused by ageing.”

“Increasing evidence suggests regular exercise and a healthy diet may help reduce our risk of developing dementia as well as reaping numerous other benefits from living a healthy lifestyle.”

View Article Sources

SOURCES:

Press release, University of Pittsburgh.

‘Exercise training increases size of hippocampus and improves memory’, Arthur F Kramer et al, Proceedings of the National Academy of Sciences, doi/10.1073/pnas.1015950108.

Dr Simons Ridley, Alzheimer’s Research Trust.

© 2011 WebMD, LLC. All rights reserved.