JANUARY 2006
Understanding emotions in others: mirror neuron dysfunction in children with autism spectrum disorders.
Nat Neurosci. 2006 Jan;9(1):28-30. Epub
Dapretto M, Davies MS, Pfeifer JH, Scott AA, Sigman M, Bookheimer SY, Iacoboni M.
[1] Ahmanson-Lovelace Brain Mapping Center, Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles
To examine mirror neuron abnormalities in autism, high-functioning children with autism and matched controls underwent fMRI while imitating and observing emotional expressions.
Although both groups performed the tasks equally well, children with autism showed no mirror neuron activity in the inferior frontal gyrus (pars opercularis).
Notably, activity in this area was inversely related to symptom severity in the social domain, suggesting that a dysfunctional 'mirror neuron system' may underlie the social deficits observed in autism.
For a clear understanding of mirror neurons and their relationship with issues like Autism Spectrum Disorders please click onto the link here.
Tracking the recovery of visuospatial attention deficits in mild traumatic brain injury.
Brain. 2005 Dec 5
Halterman CI, Langan J, Drew A, Rodriguez E, Osternig LR, Chou LS, van Donkelaar P.
Department of Human Physiology and Institute of Neuroscience, University of Oregon,
The goal of the current investigation was to probe the deficits in the alerting, orienting and executive components of visuospatial attention in individuals who have recently suffered a mild traumatic brain injury (mTBI) and to assess the rate and degree of recovery for each of these components over a month post-injury.
A group design was employed to assess and compare the performance of participants (12 males, 8 females; mean age: 21 +/- 1.74 years) identified with mTBI relative to control subjects matched for gender, age, height, weight and activity level.
Participants performed the attentional network test, designed to isolate the constituents of attention into alerting, orienting and executive components. Reaction times (RTs) and response accuracy were the main dependent variables.
The results showed that the orienting and executive components were significantly affected by mTBI immediately after the injury, whereas the alerting component was not.
Furthermore, participants with mTBI recovered from the deficits in the orienting component of attention within a week of their injury, whereas the deficits in the executive component remained throughout the month post-injury. In addition, the RT cost to generate accurate compared with inaccurate responses was significantly larger in participants with mTBI than in controls, and this difference was maintained throughout the 1 month testing period.
These findings indicate that the regions of the brain associated with the orienting and executive components of visuospatial attention may be most susceptible to neural damage resulting from mTBI. Moreover, the lack of recovery in the executive component indicates that the degree and time course for recovery may be regionally specific.
A shift of visual spatial attention is selectively associated with human EEG alpha activity.
Eur J Neurosci. 2005 Dec;22(11):2917-26.
Sauseng P, Klimesch W, Stadler W, Schabus M, Doppelmayr M, Hanslmayr S, Gruber WR, Birbaumer N.
Department of Physiological Psychology, University of Salzburg, Austria.
Event-related potentials and ongoing oscillatory electroencephalogram (EEG) activity were measured while subjects performed a cued visual spatial attention task. They were instructed to shift their attention to either the left or right visual hemifield according to a cue, which could be valid or invalid.
Thereafter, a peripheral target had to be evaluated. At posterior parietal brain areas early components of the event-related potential (P1 and N1) were higher when the cue had been valid compared with invalid.
An anticipatory attention effect was found in EEG alpha magnitude at parieto-occipital electrode sites. Starting 200 ms before target onset alpha amplitudes were significantly stronger suppressed at sites contralateral to the attended visual hemifield than ipsilateral to it. In addition, phase coupling between prefrontal and posterior parietal electrode sites was calculated.
It was found that prefrontal cortex shows stronger phase coupling with posterior sites that are contralateral to the attended hemifield than ipsilateral sites. The results suggest that a shift of attention selectively modulates excitability of the contralateral posterior parietal cortex and that this posterior modulation of alpha activity is controlled by prefrontal regions.
New food pesticide dangerous for all Americans, three environmental groups warn
New York - December 21, 2005 -- Three environmental groups are urging the Environmental Protection Agency (EPA) to revoke their approval of sulfuryl fluoride as a pesticide fumigant on food.
EPA approved sulfuryl fluoride as an alternative food fumigant to ozone-depleting methyl bromide. The groups say additional fluoride levels in food will be harmful to the health of all Americans because fluoride is persistent and bio-accumulates in the human body.
Dow AgroSciences campaigned long and hard to get EPA's go-ahead to use sulfuryl fluoride. EPA gave Dow what they wanted in January 2004, and in so doing, approved the highest levels of fluoride in America's food basket in US history.
A December 16, 2005 submission to EPA by Fluoride Action Network (FAN), the Environmental Working Group and Beyond Pesticides, sets the basis for EPA to revoke the use of sulfuryl fluoride. For this to happen, EPA has to grant an evidentiary hearing. EPA requested the groups to refine the issues for a hearing. The December submission is in response to EPA's request. If the hearing is granted, it will be the first time a pesticide tolerance has its day in court.
When EPA approved the first-time use of sulfuryl fluoride as a food pesticide in January 2004 (on raw foods) and in July 2005 (on ALL processed foods), they approved two tolerances for residues on food: fluoride and sulfuryl fluoride. These are the tolerances the groups are seeking to revoke.
FAN has been involved in every stage of this process, which began in June 2001, because sulfuryl fluoride will be the major source of fluoride in raw and processed food.
The December 16 submission summarizes the issues and concerns of the three groups:
o Too many Americans, especially children, are currently receiving too much fluoride - even by EPA's own standards. There is, therefore, no safe room for additional exposures. Fluoride is persistent and bioaccumulates in the human body
o EPA set an allowable dosage of fluoride for infants that is five times higher than for adults. This is unprecedented in EPA's history and disregards EPA's mandate, under the Food Quality Protection Act, to be more protective of a child's exposure to pesticides, not less.
o In approving Dow's request, EPA ignored all research published after 1985, choosing to rely instead on an antiquated 20-year-old standard which considers it safe for 40% of children to develop moderate to severe dental fluorosis (a brown and black staining of teeth, with pitting and erosion of enamel).
o In all the sulfuryl fluoride animal studies performed by DOW, the major target organ was the brain. Of particular concern was the finding of holes in the brain. However EPA approved the tolerances without any developmental neurotoxicity (DNT) study. And the DNT study that EPA has asked Dow to perform is irrelevant to food exposure.
o New research indicating that low levels of fluoride can damage the brain, the bones, the kidneys, and other tissues, is currently being reviewed by the National Research Council (NRC). The NRC is expected to release its report (The Toxicologic Risk of Fluoride in Drinking Water) early in 2006. EPA rushed approval to give Dow what it wanted, without waiting for the NRC report.
If you're skilled at a physical activity like ballet, the part of your brain that controls movement activates differently than the same part in the brain of someone who's not skilled in that activity. That's what researchers at the University of College London (UCL) have found in a fascinating new study. The study has implications for helping injured athletes continue to train without moving a muscle, and perhaps even helping stroke victims regain lost movement.
Earlier studies with monkeys revealed that brain cells called mirror neurons respond both when we do something, like pick up an object, and when we simply watch someone else do it. It was known that these neurons fire when we perform an action, but it came as a surprise that the same cells also fired when we only saw that action being performed. The new study went a step further by showing that such a system operates differently depending on what you are physically expert at doing.
"Our findings suggest that once the brain has learned a skill, it may simulate the skill without even moving, through simple observation," says UCL's Patrick Haggard.
(full story)
Frontal Electroencephalogram Activation Asymmetry, Emotional Intelligence, and Externalizing Behaviors in 10-Year-Old Children.
Child Psychiatry Hum Dev. 2005 Dec
Diane Santesso L, Reker Dana L, Schmidt LA, Segalowitz SJ.
Emotional intelligence and frontal EEG asymmetry at rest are independent
predictors of child externalizing behaviors.
The purpose of the present study was to examine the relations among resting frontal brain electrical activity (EEG) (hypothesized to reflect a predisposition to positive versusnegative affect and ability to regulate emotions), emotional intelligence, and externalizing behaviors in a sample of non-clinical 10-year-old children.
We found that boys had significantly lower emotional intelligence than girls, and low emotional intelligence was associated with significantly more externalizing behaviors (i.e., aggression and delinquency), replicating previous work.
We also found that children with higher reported externalizing behaviors exhibited significantly greater relative right frontal EEG activity at rest compared with children with little to no externalizing behavioral problems. There was, however, no relation between emotional intelligence and the pattern of resting frontal EEG activity.
Thus, emotional intelligence and the pattern of frontal EEG activation at rest are independent predictors of externalizing behaviors in children.
Findings also suggest that individual differences in emotional intelligence may not be based on differences in levels of emotional regulation or the generation of positive affect as reflected in frontal EEG asymmetries, but rather other social and cognitive competencies required for adaptive behavior.
Functional plasticity or vulnerability after early brain injury?
Anderson V, Catroppa C, Morse S, Haritou F, Rosenfeld J.
Traumatic brain injury (TBI) is a common, acquired, childhood disability that may be used as a model to understand more completely the impact of early brain injury on both brain structure and day-to-day function.
Contrary to previously held views of the "plasticity" of the young brain, recent research suggests that such early insults may have a profound impact on development. To date, these suggestions remain largely untested.
OBJECTIVES: To plot changes in cognitive abilities after childhood TBI over the 30 months after injury and to examine the impact of age at injury on cognitive outcomes.
DESIGN: Prospective longitudinal study.
SETTING: Royal Children's Hospital, Victoria, Australia. MAIN OUTCOME
MEASURES: Global intellectual ability, verbal and nonverbal skills, attention, and processing speed. PARTICIPANTS: A total of 122 children admitted to the hospital with a diagnosis of TBI were divided according to injury age, ie, young (age: 3-7 years) or old (age: 8-12 years), and injury severity (mild, moderate, or severe) and were evaluated acutely and at 12 and 30 months after injury. An additional sample of children injured before 3 years of age (n = 27) was compared with these groups with respect to global intellectual ability only.
RESULTS: A clear relationship was documented between injury severity and cognitive performance. For children who sustained severe injury, younger age at injury was associated with minimal, if any, recovery after injury, but better outcomes were observed after severe TBI among older children. Age at injury was not predictive of outcomes for children with mild or moderate TBI, although infants (age: 0-2.11 years) with moderate TBI showed poorer outcomes than did older children with injury of similar severity.
CONCLUSIONS: Findings support a "double-hazard" model for severe and early brain insults and add to the ongoing debate regarding cerebral plasticity, suggesting that, contrary to traditional views, young children who sustain severe TBI in early childhood or moderate or severe TBI in infancy may be particularly vulnerable to significant residual cognitive impairment. From a clinical perspective, results indicate that long-term follow-up monitoring and management should be targeted to this high-risk group.
Neurodegeneration from mitochondrial insufficiency: nutrients, stem cells, growth factors, and prospects for brain rebuilding using integrative management.
Altern Med Rev. 2005 Dec;10(4):268-293.
University of California, Berkeley,
Degenerative brain disorders (neurodegeneration) can be frustrating for both conventional and alternative practitioners. A more comprehensive, integrative approach is urgently needed. One emerging focus for intervention is brain energetics.
Specifically, mitochondrial insufficiency contributes to the etiopathology of many such disorders. Electron leakages inherent to mitochondrial energetics generate reactive oxygen free radical species that may place the ultimate limit on lifespan. Exogenous toxins, such as mercury and other environmental contaminants, exacerbate mitochondrial electron leakage, hastening their demise and that of their host cells.
Studies of the brain in Alzheimer's and other dementias, Down syndrome, stroke, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, Huntington's disease, Friedreich's ataxia, aging, and constitutive disorders demonstrate impairments of the mitochondrial citric acid cycle and oxidative phosphorylation (OXPHOS) enzymes.
Imaging or metabolic assays frequently reveal energetic insufficiency and depleted energy reserve in brain tissue in situ. Orthomolecular nutrients involved in mitochondrial metabolism provide clinical benefit.
Among these are the essential minerals and the B vitamin group; vitamins E and K; and the antioxidant and energetic cofactors alpha-lipoic acid (ALA), ubiquinone (coenzyme Q10; CoQ10), and nicotinamide adenine dinucleotide, reduced (NADH).
Recent advances in the area of stem cells and growth factors encourage optimism regarding brain regeneration. The trophic nutrients acetyl L-carnitine (ALCAR), glycerophosphocholine (GPC), and phosphatidylserine (PS) provide mitochondrial support and conserve growth factor receptors; all three improved cognition in double-blind trials.
The omega-3 fatty acid docosahexaenoic acid (DHA) is enzymatically combined with GPC and PS to form membrane phospholipids for nerve cell expansion. Practical recommendations are presented for integrating these safe and well-tolerated orthomolecular nutrients into a comprehensive dietary supplementation program for brain vitality and productive lifespan.
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