Researchers identify emotions based on brain activity (fMRI Scans)

For the first time, scientists at Carnegie Mellon University have identified which emotion a person is experiencing based on brain activation. 

This image shows the average positions of brain regions used to identify emotional states. 

Credit: Carnegie Mellon University

For the first time, scientists at Carnegie Mellon University have identified which emotion a person is experiencing based on brain activity.

The study, which will be published in the June 19 issue of PLOS ONE, combines functional magnetic resonance imaging (fMRI) and machine learning to measure brain signals to accurately read emotions in individuals.

Led by researchers in CMU's Dietrich College of Humanities and Social Sciences, the findings illustrate how the brain categorizes feelings, giving researchers the first reliable process to analyze emotions.

Until now, research on emotions has been long stymied by the lack of reliable methods to evaluate them, mostly because people are often reluctant to honestly report their feelings.

Further complicating matters is that many emotional responses may not be consciously experienced.

Identifying emotions based on neural activity builds on previous discoveries by CMU's Marcel Just and Tom M. Mitchell, which used similar techniques to create a computational model that identifies individuals' thoughts of concrete objects, often dubbed "mind reading."

"This research introduces a new method with potential to identify emotions without relying on people's ability to self-report," said Karim Kassam, assistant professor of social and decision sciences and lead author of the study.

"It could be used to assess an individual's emotional response to almost any kind of stimulus, for example, a flag, a brand name or a political candidate."

One challenge for the research team was find a way to repeatedly and reliably evoke different emotional states from the participants.

Traditional approaches, such as showing subjects emotion-inducing film clips, would likely have been unsuccessful because the impact of film clips diminishes with repeated display.

The researchers solved the problem by recruiting actors from CMU's School of Drama.

Read the full article here

ADHD: Brain activity in sleep may impact emotional disturbances in children

Sleep consolidates emotional memories in healthy children but not in children with attention-deficit hyperactivity disorder (ADHD).

This is the findings of research published May 29 in the open access journal PLOS ONE by Alexander Prehn-Kristensen and colleagues from University Hospital Schleswig-Holstein.

The study suggests these deficits in sleep-related emotional processing may exacerbate emotional problems experienced in the daytime by children with ADHD.

Prehn-Kristensen

For the study, healthy adults, healthy children and children with ADHD were shown pictures that had emotional relevance, such as a scary animal, or neutral pictures showing an umbrella or lamp.

Participants were shown pictures in the evening, their brain activity was monitored as they slept, and recollections were tested the following morning.

The researchers found that during sleep, regions of the brain thought to support consolidation of emotional memories were most active in healthy children, less so in healthy adults and least active in children with ADHD.

The study states, "While several studies reported a benefit from sleep with respect to emotional memory in healthy individuals, our results showed for the first time that healthy children outperform healthy adults." 

However, the authors added that this may be, in part, attributable to the child-oriented pictures used as stimuli.

Their results support the idea that frontal brain activity is critically to the consolidation of emotional memory in sleep, and this brain region is also implicated in the emotional symptoms seen in children suffering from ADHD.

The authors add that further studies are needed to confirm whether this function of sleep in forming emotional memories develops with time in adults with ADHD, or whether the dysfunction persists in ADHD sufferers of all ages.

More information: Prehn-Kristensen A, Munz M, Molzow I, Wilhelm I, Wiesner CD, et al. (2013) Sleep Promotes Consolidation of Emotional Memory in Healthy Children but Not in Children with Attention-Deficit Hyperactivity Disorder. PLOS ONE 8(5): e65098. doi:10.1371/journal.pone.0065098

Autism: MEG Research Advances Detection from brain activity

Roberto Fernández Galán

Neuroscientists from Case Western Reserve University School of Medicine and the University of Toronto have developed an efficient and reliable method of analyzing brain activity to detect autism in children.

Their findings appear today in the online journal PLOS ONE. The researchers recorded and analyzed dynamic patterns of brain activity with magnetoencephalography (MEG) to determine the brain's functional connectivity – that is, its communication from one region to another.

MEG measures magnetic fields generated by electrical currents in neurons of the brain. Roberto Fernández Galán, PhD, an assistant professor of neurosciences at Case Western Reserve and an electrophysiologist seasoned in theoretical physics led the research team that detected autism spectrum disorder (ASD) with 94 percent accuracy.

The new analytic method offers an efficient, quantitative way of confirming a clinical diagnosis of autism.

"We asked the question, 'Can you distinguish an autistic brain from a non-autistic brain simply by looking at the patterns of neural activity?' and indeed, you can," Galán said.

"This discovery opens the door to quantitative tools that complement the existing diagnostic tools for autism based on behavioural tests."

In a study of 19 children—nine with ASD—141 sensors tracked the activity of each child's cortex.

The sensors recorded how different regions interacted with each other while at rest, and compared the brain's interactions of the control group to those with ASD.

Researchers found significantly stronger connections between rear and frontal areas of the brain in the ASD group; there was an asymmetrical flow of information to the frontal region, but not vice versa.

The new insight into the directionality of the connections may help identify anatomical abnormalities in ASD brains.

Most current measures of functional connectivity do not indicate the interactions' directionality. "It is not just who is connected to whom, but rather who is driving whom," Galán said.

Their approach also allows them to measure background noise, or the spontaneous input driving the brain's activity while at rest.

A spatial map of these inputs demonstrated there was more complexity and structure in the control group than the ASD group, which had less variety and intricacy.

This feature offered better discrimination between the two groups, providing an even stronger measure of criteria than functional connectivity alone, with 94 percent accuracy.

Case Western Reserve's Office of Technology Transfer has filed a provisional patent application for the analysis' algorithm, which investigates the brain's activity at rest.

Galán and colleagues hope to collaborate with others in the autism field with emphasis on translational and clinical research.

Suppressing the Brain's Good Sense 'filter' can improve creativity

The brain's prefrontal cortex is thought to be the seat of cognitive control, working as a kind of filter that keeps irrelevant thoughts, perceptions and memories from interfering with a task at hand.

Now, researchers at the University of Pennsylvania have shown that inhibiting this filter can boost performance for tasks in which unfiltered, creative thoughts present an advantage.

Their work was published in the journal Cognitive Neuroscience.

Previous studies have shown that the prefrontal cortex -- in particular, the left prefrontal cortex -- is one important area of the brain that supports cognitive control.

Thompson-Schill

As a test of whether reduced cognitive control might be advantageous in some circumstances, Thompson-Schill's team designed an experiment that involved inhibiting the activity of the left prefrontal cortex in adults while they completed a creative task.

In this task, participants are shown pictures of everyday objects and are asked to quickly come up with uses for them that are out of the ordinary, such as using a baseball bat as a rolling pin.

Participants see a sequence of 60 objects, one every nine seconds, and the researchers measure how long it takes for them to come up with a valid response, or if they are unable to do so before the next picture appears.

The researchers hypothesized that high levels of cognitive control would be a detriment to coming up with these kinds of uncommon uses.

Evangelia Chrysikou

"When we use objects in daily life, our cognitive control helps us focus on what the object is typically used for and 'filters out' irrelevant properties," Evangelia Chrysikou said. Chrysikou is a director of the Center for Cognitive Neuroscience.

"However, to come up with the idea of using a baseball bat as a rolling pin, you have to consider things like its shape and the material it's made of."

"The real takeaway," Thompson-Schill said, "is that when you give people a task for which they do not know the goal -- such as showing them an object and asking, 'What else can you do with this thing' -- anything that they would normally do to filter out irrelevant information about the object will hurt their ability to do the task."

Experiments to test such hypotheses have been aided by new ways of non-invasively manipulating neurons in specific areas of the brain, inducing a variety of temporary changes in perception and performance.

The Method
The method Thompson-Schill's team used, called transcranial direct current stimulation, or tDCS, involves passing a weak electrical charge through the brain, aiming the charge's path so it intersects with areas thought to be associated with an ability or behaviour.

This charge can influence the electrical activity that constitutes cell-to-cell communication in those areas.

"TDCS is believed to induce incremental shifts in the electrical potential of neuronal membranes, making it more or less likely that neurons will reach their threshold for firing," Hamilton said.

"In this instance, we employed stimulation in a way that would make it harder for neurons to fire, thereby diminishing behaviorally relevant activity in that part of the brain."

Participants were first split into three groups corresponding to three experimental conditions; one group would receive TDCS to their left prefrontal cortex for the duration of the task, a second group would receive TDCS to their right prefrontal cortex and a third group would receive what amounted to a placebo.

TDCS Experiment
TDCS produces a slight tingling sensation on the scalp when it is first applied, so those in the third group received only a brief period of stimulation before the task began. They did not receive continuous stimulation throughout.

As an additional control, each of the three groups was split in half, with one set completing the uncommon-use task and the other simply stating what the object is normally used for, and all participants completed a task that involved remembering strings of numbers, (a common exercise in psychological experiments that has been shown not to require the prefrontal cortex).

"We wouldn't want to think that the stimulation affected everything," Thompson-Schill said.

"So if we found an effect when participants were remembering numbers, we'd be worried about our interpretation of the data."

As expected, none of the experimental conditions affected participants' performance when asked to recall the sequences of numbers, or when they were asked to say the common uses of the objects they saw, but there was a marked difference between those who received tDCS to their left prefrontal cortex and those who didn't when completing the uncommon-use task.

The right prefrontal cortex and placebo groups couldn't come up with uncommon uses for an average of 15 out of 60 objects, whereas those whose left prefrontal cortices were being inhibited only missed an average of eight.

The latter group was also able to provide correct responses an average of a second faster than the former two.

"A second faster difference is huge in psychology research. We're used to seeing differences measured in milliseconds," Thompson-Schill said. This is probably the biggest effect I've seen over my 20 years in research."

These results lend credence to the idea that high levels of cognitive control may be a disadvantage in some circumstances, such as in early development.

"We differ from non-human primates in having a long period of immaturity in our prefrontal cortex," Thompson-Schill said, "so we started considering whether this might not be an unfortunate accident of nature but rather a feature of our species' developmental path.

The slow development of the prefrontal cortex is one reason children fail at many attention-based tasks but excel at imaginative ones. It may also aid children in rapidly acquiring new knowledge.

"There are things that are important to not filter, in particular when you are learning," Thompson-Schill said. "If you throw out information about your environment as being irrelevant, you miss opportunities to learn about those things."

The research was supported by the US National Institutes of Health and the Robert Wood Johnson Foundation.

The above story is reprinted from materials provided by University of Pennsylvania.

The Importance of Practice and Sleep for Musicians - Molly Gebrian

Musicians v. Non-Musicians - Molly Gebrian

Most of studies on changes in neuronal activity only last a week or two at the most. 

It’s not logistically feasible to have people coming into the lab for weeks or months on end to have their brains looked at, so, some neuro-scientists think musicians are an ideal population to find out what happens when you practice a motor task repeatedly for years and years.

One of the most obvious changes is that, especially in string players and keyboard players, the portion of the motor cortex devoted to the fingers is much bigger.

At the same time, the neurons in this cortical network are much more efficient.

These two things happen because, presumably, over time, lots and lots of neurons get connected by synapses that wouldn’t normally be connected, and the neuronal ensembles that result from these new connections get much better at what they do because they get to practice everyday.

A musician’s brain is so efficient at things like scales and other simple patterns that are automatic to us that entire brain areas don’t get engaged in a musician’s brain that are very active in a non-musician or amateur’s brain.

Two of these areas are the pre-motor cortex and the supplementary motor area.

These are involved in planning complex movements and coordinating timing, but when musicians play scales or simple rhythm patterns, these areas barely do anything at all.

The only other complex motor tasks that show this lack of activation are overlearned skills such as writing.

What this means is that our basic set of tools and skills as musicians are so automatic that our brain barely has to do anything to execute them.

But what this also means is that when you learn a new skill, especially something like the extended techniques used in contemporary music, there is a necessary period of days or weeks that your brain needs to rewire itself and for new neuronal ensembles and circuits to form.

The other amazing thing that happens in musicians’ brains, as new synapses form, is that our motor cortex gets connected to our auditory cortex.

Think about how strange that is. For most people, what they hear doesn’t cause them to have automatic associations with movement, and moving certainly doesn’t cause them to hear things in their heads.

But if a musician listens to a recording of a piece they know and play well, not only does their auditory cortex light up on a brain scan (fMRI), but the portion of their motor cortex devoted to their fingers does too.

Furthermore, neuroscientists have shown that the motor cortex isn’t just lighting up as a whole unit – the areas that control the individual fingers light up in the order and timing they would to execute the correct fingering (Bangert and Altenmuller, 2003).

NB: When these kinds of studies are done, measures are taken to make sure the musicians aren’t physically moving their fingers.

The opposite happens too: if you tell a pianist to play a piece silently on a tabletop, their auditory cortex lights up as it would if they were actually playing (and hearing) the piece.

These finding just serve to highlight how important it is to always keep singing in your head as you play and to be really clear about what you want to hear.

It affects what comes out of your fingers and arms and mouth, not in some strange metaphysical way, but because your auditory cortex is connected to your motor cortex.

If you aren’t clear on what you want to hear, the auditory cortex has a very limited message to send to your fingers.

The Role of Sleep in Learning

If all of these changes have to take place in your brain before you can play something fluidly and competently, is there anything you can do to speed up the process?

The answer depends on how much you want to speed it up, because it turns out that a very important component of motor (and auditory) learning is sleep.

Matthew Walker and his colleagues here in Boston have done a number of experiments on motor learning during sleep (Walker, et al, 2002, 2003, 2005).

Their basic experimental paradigm involves three groups of people. The first group gets taught a finger tapping task (4-1-2-3-4 where 4 is the pinky finger and 1 is the index finger) at 10am, which they then practice and are tested on multiple times throughout the day.

The second group gets taught and practices the same task at 10am, but they don’t get tested on it again until 10pm.

Then, they are sent home to sleep and tested the next morning at 10am. The final group is trained on the task at 10pm and has their first retest at 10am the next morning. What they found is astonishing.

The first group gets gradually better throughout the day at a rate that you can predict.

The second group shows the same linear increase during the day, but when you test them the next morning, there is a huge jump in their performance (measured by faster sequence execution without loss of accuracy).

The same goes for the group that was trained at 10pm and then retested for the first time the next day – they got much better overnight, even though all they were doing was sleeping!

NB: Everyone was instructed not to practice when they went home.

Even more surprising, there is absolutely no relationship between how much better a person got during daytime practicing and how much better they got after sleeping.

How is this possible and what does it mean? Researchers have concluded that the last result means that practice-dependent learning and sleep-dependent learning are independent processes.

This doesn’t mean, of course, that if you don’t practice, you’ll get better just by sleeping but it does mean that you shouldn’t underestimate the importance of sleep in learning, especially when it’s brand new.

Knowing this can help you use your practice time much more efficiently.

Say, for instance, you have a lot of music to learn for orchestra and not a lot of time to practice it.

You will be much better off practicing your orchestra music for 15 minutes a day until the concert, rather than “wood-shedding” the day before the concert.

Why? Because you’ll have all those nights of sleep for your brain to process the new music. So ultimately, you’ll be able to play the music better with fewer hours of actual practice.

When you’re learning a new piece that you have ample time to practice, keeping the role of sleep in mind can also help you practice more efficiently.

The primary thing that improved with sleep for the people in these studies was speed (at least that’s what the experimenters were measuring).

Since the amount of daytime improvement and learning after sleep aren’t related, spending hours and hours on a really tricky fast passage on the first few days of practicing isn’t as efficient as getting it fluent at a slower tempo and then just leaving it until the next day.

The next day, not only will you be able to play it faster, but you’ll spend much less time getting it to a faster tempo than you would’ve the day before.

No one probably would’ve guessed that just sleeping would make you better at playing your instrument, but researchers have shown that it does, over and over again.

The effects of sleep are really hard to study, but in this case, researchers think they know how it works.

Sleep is divided into two broad types: REM sleep and non-REM sleep (or NREM sleep). REM sleep is when you have dreams.

During what is called Stage 2 NREM sleep, however, electrical brain events occur that are called sleep spindles.

During a sleep spindle, there is a huge burst of electrical activity in a population of neurons that causes massive amounts of calcium to enter those cells.

Calcium is what causes all the changes discussed earlier, from strengthening and weakening synapses, to making new synapses, to synchronizing the firing of neuronal ensembles.

Sleep spindles reach peak intensity late in the night and have been shown to increase following motor learning during the day.

The study by Matthew Walker and his colleagues at Harvard Medical School also found that the percentage of improvement after sleeping strongly correlated with the amount of time the person spent in Stage 2 NREM sleep in the final quarter of the night, precisely when sleep spindle activity is at its peak.

This finding also highlights the importance of getting enough sleep while you’re learning something new.

A full night of sleep was defined as 8 hours in this study, and it was only the last two hours that were really important for learning.

Getting a full night’s sleep may be even more important that we realize.

Read the full article here: http://madisonjazz.files.wordpress.com/

The Developing Brain: There is no Final, Optimal state.

To reflect the ongoing structural changes in the adolescent and twenty-something brain, many journalists and scientists use words and phrases like “unfinished,” “work in progress,” “under construction” and “half-baked.”

Such language implies that the brain eventually reaches a kind of ideal state when it is “done.” But there is no final, optimal state.

The human brain is not a soufflé that gradually expands over time and finally finishes baking at age 30.

Yes, we can identify and label periods of dramatic development—or windows of heightened plasticity—but that should not eclipse the fact that brain changes throughout life.

Whether we can, at this moment in time, meaningfully link this life stage to neuroscience seems a tenuous proposition at best.

By itself, brain biology does not dictate who we are.

The members of any one age group are not reducible to a few distinguishing structural changes in the brain.

Ultimately, the fact that a twenty-something has weaker bridges between various brain regions than someone in their thirties is not hugely important—it’s just one aspect of a far more complex identity.

Organic basis for dyslexia - Max Planck Leipzig Research Study

Severe and persistent reading and spelling impairment linked with difficulties in processing speech sounds (developmental dyslexia) may be associated with under-action of an area of the brain.

Establishing an underlying organic basis for dyslexia has been a controversial area in recent years, but a team based at the Max Planck Institute Leipzig has used functional MRI scanning on dyslexic adults.

They found that there was a dysfunction in the auditory sensory thalamus, the medial geniculate body (MGB), while all other structures in the auditory pathway behaved comparably with those in control patients without dyslexia.

Furthermore, MGB activity correlated with dyslexia diagnostic scores, indicating that the task modulation of the MGB is critical for performance in dyslexics.

The authors of the research, published this week in the online Proceedings of the National Academy of Sciences of the US, suggest that 'deficits in dyslexia are associated with a failure of the neural mechanism that dynamically tunes the MGB according to predictions from cortical areas to optimise speech processing.'

This research may go some way in establishing an underlying neural framework for the various presentations of some forms of dyslexia.

Read the Abstract and get access to the full paper here; PNAS online 

Authors: Begoña Díaz, Florian Hintz, Stefan J. Kiebel and Katharina von Kriegstein

Dyslexia: Is Signal Processing in the Brain the cause?

This figure compares the situation in the brain of dyslexics and the control group. 

The blue area depicts the auditory cortices and the green area represents the medial geniculate bodies.

MPI for Human Cognitive and Brain Sciences

To participate successfully in life, it is important to be able to read and write.

Nevertheless, many children and adults have difficulties in acquiring these skills and the reason is not always obvious.

They suffer from dyslexia which can have a variety of symptoms. Thanks to research carried out by Begoña Díaz and her colleagues at the Max Planck Institute for Human Cognitive and Brain Sciences in Leipzig, a major step forward has been made in understanding the cause of dyslexia.

The scientists have discovered an important neural mechanism underlying dyslexia and shown that many difficulties associated with dyslexia can potentially be traced back to a malfunction of the medial geniculate body in the thalamus.

The results provide an important basis for developing potential treatments. People who suffer from dyslexia have difficulties with identifying speech sounds in spoken language.

For example, while most children are able to recognise whether two words rhyme even before they go to school, dyslexic children often cannot do this until late primary school age.

Those affected suffer from dyslexia their whole lives. However, there are also always cases where people can compensate for their dyslexia.

“This suggests that dyslexia can be treated. We are therefore trying to find the neural causes of this learning disability in order to create a basis for improved treatment options,” says Díaz.

Between five and ten percent of the world’s children suffer from dyslexia, yet very little is know about its causes.

Even though those affected do not lack intelligence or schooling, they have difficulties in reading, understanding and explaining individual words or entire texts.

The researchers showed that dyslexic adults have a malfunction in a structure that transfers auditory information from the ear to the cortex is a major cause of the impairment: the medial geniculate body in the auditory thalamus does not process speech sounds correctly.

“This malfunction at a low level of language processing could percolate through the entire system. This explains why the symptoms of dyslexia are so varied,” says Díaz.

Read more at: medicalxpress.com

Brain Gym/Kinesiology for Dyslexic, ADD, ADHD Kids - YouTube

For more on these exercises and others, click this link. Diana Vogel simple, quick and effective exercises to help your dyslexic/ADD/ADHD child switch their brains on for optimum learning.

These exercises are taken from Brain Gym/Kinesiology For Kids/Educational Kinesiology. http://www.TheKidWhispererSecrets.com -

Brain's Lateral Prefrontal Cortex: Images help predict how smart you are

"There is evidence that the lateral prefrontal cortex is the brain region that 'remembers' (maintains) the goals and instructions that help you keep doing what is needed when you’re working on a task," says Michael Cole. 

"So it makes sense that having this region communicating effectively with other regions (the 'perceivers' and ‘doers’ of the brain) would help you to accomplish tasks intelligently." 

(Credit: Michael Cole/WUSTL)

As science has long suspected, overall brain size matters somewhat, accounting for about 6.7 percent of individual variation in intelligence.

More recent research has pinpointed the brain’s lateral prefrontal cortex, a region just behind the temple, as a critical hub for high-level mental processing, with activity levels there predicting another five percent of variation in individual intelligence.

Now, new research from Washington University in St. Louis suggests that another 10 percent of individual differences in intelligence can be explained by the strength of neural pathways connecting the left lateral prefrontal cortex to the rest of the brain.

Published in the Journal of Neuroscience, the findings establish “global brain connectivity” as a new approach for understanding human intelligence.

“Our research shows that connectivity with a particular part of the prefrontal cortex can predict how intelligent someone is,” suggests lead author Michael W. Cole, a postdoctoral research fellow in cognitive neuroscience.

The study is the first to provide compelling evidence that neural connections between the lateral prefrontal cortex and the rest of the brain make a unique and powerful contribution to the cognitive processing underlying human intelligence, says Cole, whose research focuses on discovering the cognitive and neural mechanisms that make human behaviour uniquely flexible and intelligent.

“This study suggests that part of what it means to be intelligent is having a lateral prefrontal cortex that does its job well; and part of what that means is that it can effectively communicate with the rest of the brain,” says study co-author Todd Braver, professor of psychology in Arts & Sciences and of neuroscience and radiology in the School of Medicine.

Braver is also a co-director of the Cognitive Control and Psychopathology Lab, where the research was conducted.

Read the full article at  Futurity.org or at Washington University

The seat of meta-consciousness in the brain - Sleep

This shows the brain regions activated more strongly during lucid dreaming than in a normal dream.

Credit: MPI of Psychiatry 

Studies of lucid dreamers visualize which centres of the brain become active when we become aware of ourselves. 

Which areas of the brain help us to perceive our world in a self-reflective manner is difficult to measure.

During wakefulness, we are always conscious of ourselves. In sleep, however, we are not, but there are people, known as lucid dreamers, who can become aware of dreaming during sleep.

Studies employing magnetic resonance tomography (MRT) have now been able to demonstrate that a specific cortical network consisting of the right dorsolateral prefrontal cortex, the frontopolar regions and the precuneus is activated when this lucid consciousness is attained.

All of these regions are associated with self-reflective functions. This research into lucid dreaming gives the authors of the latest study insight into the neural basis of human consciousness.

The human capacity of self-perception, self-reflection and consciousness development are among the unsolved mysteries of neuroscience.

Despite modern imaging techniques, it is still impossible to fully visualise what goes on in the brain when people move to consciousness from an unconscious state.

The problem lies in the fact that it is difficult to watch our brain during this transitional change. Although this process is the same, every time a person awakens from sleep, the basic activity of our brain is usually greatly reduced during deep sleep.

This makes it impossible to clearly delineate the specific brain activity underlying the regained self-perception and consciousness during the transition to wakefulness from the global changes in brain activity that takes place at the same time.

Scientists from the Max Planck Institutes of Psychiatry in Munich and for Human Cognitive and Brain Sciences in Leipzig and from Charité in Berlin have now studied people who are aware that they are dreaming while being in a dream state, and are also able to deliberately control their dreams.

Those so-called lucid dreamers have access to their memories during lucid dreaming, can perform actions and are aware of themselves – although remaining unmistakably in a dream state and not waking up. As author Martin Dresler explains,

"In a normal dream, we have a very basal consciousness, we experience perceptions and emotions but we are not aware that we are only dreaming. It's only in a lucid dream that the dreamer gets a meta-insight into his or her state."

By comparing the activity of the brain during one of these lucid periods with the activity measured immediately before in a normal dream, the scientists were able to identify the characteristic brain activities of lucid awareness.

"The general basic activity of the brain is similar in a normal dream and in a lucid dream," says Michael Czisch, head of a research group at the Max Planck Institute of Psychiatry.

"In a lucid state, however, the activity in certain areas of the cerebral cortex increases markedly within seconds.

The involved areas of the cerebral cortex are the right dorsolateral prefrontal cortex, to which commonly the function of self-assessment is attributed, and the frontopolar regions, which are responsible for evaluating our own thoughts and feelings.

The precuneus is also especially active, a part of the brain that has long been linked with self-perception." The findings confirm earlier studies and have made the neural networks of a conscious mental state visible for the first time.

More information: Provided by Max Planck Society

Dyslexia: 50 years old dyslexic man says "my life is a living hell"

This is a video response to a comment left under Dyslexic Brian's My Dyslexia Life Story video.

It is understandable that dyslexia can have such a negative impact on a person's life especially if they are struggling to understand and overcome it fully.

Dyslexia need not destroy your life. We all have much to do and need to reach out more.

Check out more at DyslexicBrian.com

Hearing loss may change brain structure

"In the case of tinnitus, surprisingly, there were few changes to brain structure despite changes to function, suggesting that when sensory deprivation is accompanied by self-generated noise, it may be better at preserving neural tissue," says Fatima Husain.

Researchers used two different imaging modalities in studies of people with hearing loss, normal hearing, and those with hearing loss and tinnitus (ringing in the ears).

People in the hearing loss group showed structural changes in their brains.

“This suggests that functional changes due to sensory deprivation may result in long-term structural changes,” says Fatima Husain, a Beckman Institute faculty member at the University of Illinois.

The goal of the study was to investigate structural gray and white matter changes related to tinnitus and hearing loss and try to dissociate them from changes due only to hearing loss. (Credit: Fatima Husain)

“However, in the case of tinnitus, surprisingly, there were few changes to brain structure despite changes to function, suggesting that when sensory deprivation is accompanied by self-generated noise, it may be better at preserving neural tissue.”

Husain and her collaborators on the study measured neuroanatomical changes in gray and white matter in the brains of participants with only bilateral hearing loss (HL), participants who had HL and tinnitus (TIN), and a control group with normal hearing (NH) without tinnitus.

Their study, reported in the journal Brain Research, looked at neuroanatomical alterations associated with hearing loss and tinnitus.

Read the original study DOI: 10.1016/j.brainres.2010.10.095

The researchers used structural magnetic resonance imaging (MRI) scans and voxel-based morphometry (VBM) to examine changes in gray matter, and diffusion tensor imaging (DTI), to identify changes in white matter tract orientation.

While tinnitus is often accompanied by hearing loss, not everyone with hearing loss experiences tinnitus.

The goal of the study was to investigate structural gray and white matter changes related to tinnitus and hearing loss and try to dissociate them from changes due only to hearing loss.

“We observed that the HL group had the most profound changes in both white and gray matter relative to the other groups,” Husain says. The gray matter decreases seen in the HL group relative to the NH group were in the anterior cingulate, putamen, and middle frontal gyrus.

Two of these regions, the anterior cingulate and frontal cortex, were “also implicated in our companion study that studied functional response of the brain in the same group of subjects and points to involvement of the attention processing network.”

By dissociating the effect of tinnitus from hearing loss, the researchers concluded that “hearing loss rather than tinnitus had the greatest influence on gray and white matter alterations.”

Husain directs the Auditory Cognitive Neuroscience Lab in the Department of Speech and Hearing Science.

More news from the University of Illinois: http://www.beckman.illinois.edu/index.aspx

Brain Potential Institute: Brain-Training Treatment for Learning Disabilities

Several years after launching its online one-on-one brain-training program that treats people with learning disabilties and concentration problems, Brain Potential Institute claims it has affirmative evidence that the program is equally as successful when completed online as at its onsite center.

The Institute believes that Results of the online treatment program indicate a significant increase in IQ, attention, focusing, and memory for those with ADD, ADHD, central auditory processing issues, autism and memory loss.

Jane Davis, P.T., M.S.H.P founded Brain Potential Institute in 2002 as Kid Potential Inc. The company expanded its services to provide brain training to teens, adults and seniors, which required rebranding itself as Brain Potential Institute.

Brain Potential Institute is dedicated to optimizing through cognitive training, the human brain to reach its highest intellectual potential for optimum performance at school and work, and to preserve brain function at all ages. Brain Potential Institute accepts students ages 3 through 90. Screenings are free

Brain Potential Institute claims to be one of the few companies able to increase a persons IQ by significant numbers. Its program is aimed to help with concentration issues, math and reading problems, development disorders and a litany of other cognitive and learning disabilities.

The foundation on which Brain Potential Institute has based its program is neurogenesis the brains ability to create new neuro-pathways.

Jane Davis, P.T., M.S.H.P, CEO and founder, Brain Potential Institute states that many students have gained three grade levels in reading and experienced up to a 30-point IQ increase.

Scientists Link Rare Gene Mutations to Heightened Risk of Autism

Three teams of scientists working independently to understand the biology of autism have for the first time homed in on several gene mutations that they agree sharply increase the chances that a child will develop the disorder, and have found further evidence that the risk increases with the age of the parents, particularly the father.

The gene mutations are extremely rare and together account for a tiny fraction of autism cases, suggesting that the search for therapies will be a long one, and that what is loosely known as autism may represent a broad category of related but biologically distinct conditions.

There are likely hundreds, perhaps thousands, of rare mutations that could disrupt brain development enough to result in social and developmental delays.

But experts said that the overlapping results, reported in three papers posted online Wednesday in the journal Nature, give scientists working on the genetics of autism something they have not had: a clear strategy for building a real understanding of the disease’s biological basis.

Researchers hope to find more similar, rare mutations in the next year or so that they estimate could account for 10 percent to 20 percent of all cases.

Biologists have been groping in vain for a reliable, verifiable foothold from which to investigate the underlying genetics of so-called autism spectrum disorders, including Asperger syndrome and related social difficulties that are being diagnosed at alarmingly high rates — on average, in one of 88 children, according to a government estimate released last week.

Previous studies have produced a scattering of gene findings but little consensus or confidence in how to proceed.

The new work provides a measure of both, as well as strong backing for earlier studies linking autism to the age of new fathers.

“These studies aren’t so much a breakthrough, because we knew this was coming,” said Jonathan Sebat, a geneticist at the University of California, San Diego, who was not a part of the research teams.

“But I’d say it’s a turning point. We now have a reliable way forward, and I think it’s fair to expect that we will find 20, 30, maybe more such mutations in the next year.”

Other researchers were more cautious, saying that the genetics of rare mutations was not yet well enough understood to make conclusive statements about their effect on the behavior of specific genes.

“This is a great beginning, and I’m impressed with the work, but we don’t know the cause of these rare mutations, or even their levels in the general population,” said Dr. Aravinda Chakravarti, of the Institute of Genetic Medicine at the Johns Hopkins University Medical School, who was not involved in the studies.

“I’m not saying it’s not worth it to follow up these findings, but I am saying it’s going to be a hard slog.”

The three research teams took a similar approach, analyzing genetic material taken from blood samples of families in which parents who have no signs of autism give birth to a child who develops the disorder.

This approach gives scientists the opportunity to spot the initial mutations that accompany the condition, rather than trying to work though possible genetic contributions from maternal and paternal lines.

In all three studies, the researchers focused on rare genetic glitches called de novo mutations.

De novo mutations are not inherited but occur spontaneously near or during conception. Most people have at least one and the overwhelming majority of them are harmless.

Read more here: Scientists Link Rare Gene Mutations to Heightened Risk of Autism - NYTimes.com

Autism: Why Some Children ‘Bloom’ and Overcome Their Disabilities

A new study offers some good news for families with autism. Most children affected by the disorder do not have intellectual disabilities, the study finds, and even among the severely low-functioning, about 10% may improve dramatically over time, with some growing out of their diagnosis by their teens.

The study tracked nearly 7,000 autistic children born in California between 1992 and 2001. The group included most of the children who received an autism diagnosis in the state during that time period.

The kids were followed from diagnosis to age 14 or the oldest age they had reached by the time the data collection was concluded.

The researchers found that 63% of the children did not have intellectual disabilities. Although autism is known to cause cognitive deficits in some children, it is also associated with certain enhanced intellectual abilities, and some affected children have extremely high IQs.

About one-third of the study group were considered low- to low/medium-functioning in terms of communication and social skills, meaning that they may have trouble talking, interacting with others or socializing and making friends with peers.

High-functioning kids with autism, meanwhile, can communicate effectively with others, maintain friendships and are willing to engage in social pursuits.

While the highest-functioning children tended to show the most improvement over time in the California study, about 10% of those who started out in the low-functioning group also moved into the highest group by age 14.

“The critical finding is that when you look at those children that this study refers to as ‘bloomers’, the children who seemed very low-functioning at the beginning and then did extremely well, they [tend not to] have any intellectual disabilities,” says Rahil Briggs, assistant professor of pediatrics at Albert Einstein College of Medicine, she was not associated with the research.

Low-functioning children without intellectual disabilities were twice as likely to “bloom” as those who had cognitive deficits.

Briggs adds that another “very key” factor is that the mothers of the kids who bloomed tended to be more educated and not minorities.

This suggests that low-income immigrant or minority families may not be receiving the services and support for their children that educated, affluent parents are able to access more easily.

With developmental disorders, the earlier a child receives help, the more likely he or she is to overcome disabilities.

Early intervention matters because the brain is remarkably vulnerable early in life, built to shape itself to the environment it initially faces. “The young brain is disproportionately receptive to input, whether positive or negative,” says Briggs.

“That’s why young children can learn a second language easily and why early exposure to domestic violence and toxic stress are so incredibly damaging.”

If autistic children receive intervention before such coping mechanisms as repetitive behaviours and extreme social withdrawal are firmly entrenched, for example, their innate oversensitivity to their environment is far less likely to become or remain disabling, and their other abilities and gifts can flourish.

If these children are reached early enough, “we can actually start to change brain functioning if we provide the right kind of repetitive and focused intervention,” Briggs says.

Parents Need to be Aggressive Champions
The American Academy of Pediatrics currently recommends that doctors screen children for autism at their 18-month well-child visit. Briggs adds that parents must become aggressive champions for their children.

“So much can depend on how good that parent is at advocating for the child,” says Briggs, noting that parents need to be aware not only of what services are available, but also which ones are best, which are not helpful and how to get the best care.

“That puts an incredible burden on parents,” she acknowledges. With the Centers for Disease Control and Prevention reporting last week that autism now affects 1 in 88 children, it is becoming a burden shared by more and more American families.

Briggs says that the findings in the new study reflect the types of developmental trajectories she sees in children in her practice as director of the Healthy Steps program at Montefiore Hospital in the Bronx (NY), which helps disadvantaged families access numerous services, including autism therapies, through their pediatricians’ office visits.

She describes working with a 5-year-old autistic boy and his family. The family said he would come home from kindergarten crying, but they couldn’t figure out what was wrong.

Finally, he described how he felt while he waited for his mother to pick him up in the school’s cafeteria:
“There were so many echoes bouncing off the walls that it felt like people were having a party in my head and they wouldn’t turn down the music,” he said.

Identifying the problem led Briggs to enroll the boy in listening therapy, which helped him cope with his sensitivity to sounds.

When such sensory issues, which are common in autism, can be mitigated, children become far less stressed and far better able to learn other skills like social interaction and communication.

Most children from disadvantaged backgrounds aren’t able to get these kinds of services, however. “If we still see these huge differences in children with autism based on socioeconomic factors, we clearly don’t have enough programs or haven’t made them available enough,” Briggs says.

The research was published in Pediatrics.

Autism: Defective Genes May Explain Uncontrolled Brain Growth

As a baby grows inside the womb, its brain does not simply expand like a dehydrated sponge dropped in water.

Early brain development is an elaborate procession. Every minute some 250,000 neurons bloom, squirming past one another like so many schoolchildren rushing to their seats at the sound of the bell.

Each neuron grows a long root at one end and a crown of branches at the other, linking itself to fellow cells near and far.

By the end of the second trimester, neurons in the baby's brain have formed trillions of connections, many of which will not survive into adulthood—the least traveled paths will eventually wither.

Sometimes, the developing brain blunders, resulting in "neuro-developmental disorders," such as autism.

But exactly why or how early cellular mistakes cause autism has eluded medical science. Now, Eric Courchesne of the University of California, San Diego, thinks he has linked atypical gene activity to excessive growth in the autistic brain.

With the new data, he has started to trace a cascade of genetic and cellular changes that he thinks define autism.

Although intrigued by Courchesne's work, other researchers caution that explosive neural growth is not necessarily a defining feature of all autistic brains.

Since 1998 Courchesne has been searching autistic brains for unusual structural features.

His studies suggest that while in the womb, the autistic brain sprouts an excess of neurons and continues to balloon during the first five years of life, as all those extra neurons grow larger and form connections.

Sometime after age four or five, Courchesne has also found, autistic brains actually start to lose neural connections, faster than typical brains.

In a study published November 2011 in JAMA, The Journal of the American Medical Association, Courchesne reported that children with autism have 67 percent more neurons in their prefrontal cortex (PFC) than typical children.

Located in the area of the brain just behind the eyes, the PFC is responsible for what psychologists call "executive functions"—high-level thinking, such as planning ahead, inhibiting impulses and directing attention. In his 2011 study Courchesne sliced up brain tissue from six autistic children and seven typical children who had passed away and counted the number of cell bodies in the sections to estimate the total number of neurons in their PFCs.

Now, Courchesne and his colleagues have analyzed DNA and RNA in 33 cubes of brain tissue from people who passed away, 15 of whom were autistic (nine children and six adults) and 18 who had typical brains (seven children and 11 adults).

Looking at the order of DNA's building blocks reveals whether individual genes have mutations; measuring levels of RNA indicates how often those genes were translated into proteins.

Such gene expression, Courchesne and his colleagues found, varied between autistic and typical brains.

In brain tissue from both autistic children and autistic adults, genes coding for proteins that identify and repair mistakes in DNA were expressed at unusually low levels.

Additionally, all autistic brains demonstrated unusual activity levels for genes that determine when neurons grow and die and how newborn neurons migrate during early development.

Some genes involved in immune responses, cell-to-cell communication and tissue repair, however, were expressed at unusual levels in adult autistic brains, but not in autistic children's brains.

The results appear in the March 22 issue of PLoS Genetics.

You can also Read More of this article here at Scientific American: The Ballooning Brain

Serotonin Levels: Protein in overdrive links to Autism (ASD)

Early disruptions in serotonin signaling in the brain may contribute to Autism Spectrum Disorder (ASD) and other “enduring effects on behavior,” researchers report.

Serotonin is a brain chemical that carries signals across the synapse, or gap between nerve cells. The supply of serotonin is regulated by the serotonin transporter (SERT).

In 2005, a team of researchers from Vanderbilt University led by Randy Blakely and James Sutcliffe identified rare genetic variations in children with ASD that disrupt SERT function.

In a new study published this week in the Proceedings of the National Academy of Sciences (PNAS), the researchers report the creation of a mouse model that expressed the most common of these variations.

The change is a very small one in biochemical terms, yet it appears to cause SERT in the brain to go into “overdrive” and restrict the availability of serotonin at synapses.

“The SERT protein in the brain of our mice appears to exhibit the exaggerated function and lack of regulation we saw using cell models,” says Blakely, director of the Vanderbilt Silvio O. Conte Center for Neuroscience Research.

“Remarkably, these mice show changes in social behavior and communication from early life that may parallel aspects of ASD,” notes first author Jeremy Veenstra-VanderWeele, assistant professor of psychiatry, pediatrics and pharmacology.

The researchers conclude that a lack of serotonin during development may lead to long-standing changes in the way the brain is “wired.”

In 1961, investigators at Yale University discovered that as many as 30 percent of children with autism have elevated blood levels of serotonin, a finding described as “hyperserotonemia.”

Since then, these findings have been replicated many times. Indeed, hyperserotonemia is the most consistently reported biochemical finding in autism, and is a highly inherited trait. Yet, the cause or significance of this biomarker has remained shrouded in mystery.

Until now. In the current study, Veenstra-VanderWeele, Blakely and their colleagues showed that they could produce hyperserotonemia in mice that express a variant of a human SERT gene associated with autism.

Because the genetic change makes the transporter more active, higher levels of serotonin accumulate in platelets and therefore in the bloodstream.

In the brain, overactive transporters should have the opposite effect—lowering serotonin levels at the synapse and producing behavioural changes relevant to autism. That’s exactly what the researchers observed.

Of course, no mouse model can completely explain or reproduce the human condition. Neither does a single genetic variation cause autism. Experts believe the wide spectrum of autistic behaviours represents a complex web of interactions between many genes and environmental factors.

But animal models are critical to exploring more deeply the basis for the developmental changes that are observed in ASD.

The scientists are using these mice to explore how altered brain serotonin levels during development may produce long-lasting changes in behaviour and impact the risk for autism.

Scientists from the National Institute of Mental Health, the Medical University of South Carolina and the University of Texas Health Science Center in San Antonio contributed to the study.

The research was supported by the National Institutes of Health, the advocacy organisation Autism Speaks (UK), and the American Academy of Child and Adolescent Psychiatry.

More news from Vanderbilt University: news.vanderbilt.edu/research