Posts tagged psychology

May 9, 2012

Chronic exposure to cocaine reduces the expression of a protein known to regulate brain plasticity, according to new, in vivo research on the molecular basis of cocaine addiction. That reduction drives structural changes in the brain, which produce greater sensitivity to the rewarding effects of cocaine.

The research, led by UB’s Dietz, suggests a potential new target for development of a treatment for cocaine addiction. Credit: Douglas Levere, UB Communications

The finding suggests a potential new target for development of a treatment for cocaine addiction. It was published last month in Nature Neuroscience by researchers at the University at Buffalo and Mount Sinai School of Medicine.

"We found that chronic cocaine exposure in mice led to a decrease in this protein’s signaling," says David Dietz, PhD, assistant professor of pharmacology and toxicology in the School of Medicine and Biomedical Sciences, who did the work while at Mt. Sinai. "The reduction of the expression of the protein, called Rac1, then set in motion a cascade of events involved in structural plasticity of the brain — the shape and growth of neuronal processes in the brain. Among the most important of these events is the large increase in the number of physical protrusions or spines that grow out from the neurons in the reward center of the brain.

"This suggests that Rac1 may control how exposure to drugs of abuse, like cocaine, may rewire the brain in a way that makes an individual more susceptible to the addicted state," says Dietz.

The presence of the spines demonstrates the spike in the reward effect that the individual obtains from exposure to cocaine. By changing the level of expression of Rac1, Dietz and his colleagues were able to control whether or not the mice became addicted, by preventing enhancement of the brain’s reward center due to cocaine exposure.

To do the experiment, Dietz and his colleagues used a novel tool, which allowed for light activation to control Rac1 expression, the first time that a light-activated protein has been used to modulate brain plasticity.

"We can now understand how proteins function in a very temporal pattern, so we could look at how regulating genes at a specific time point could affect behavior, such as drug addiction, or a disease state," says Dietz.

In his UB lab, Dietz is continuing his research on the relationship between behavior and brain plasticity, looking, for example, at how plasticity might determine how much of a drug an animal takes and how persistent the animal is in trying to get the drug.

Provided by University at Buffalo

Source: medicalxpress.com

May 9, 2012

While we often think of memory as a way of preserving the essential idea of who we are, little thought is given to the importance of forgetting to our wellbeing, whether what we forget belongs in the “horrible memories department” or just reflects the minutia of day-to-day living.

Despite the fact that forgetting is normal, exactly how we forget—the molecular, cellular, and brain circuit mechanisms underlying the process—is poorly understood.

Now, in a study that appears in the May 10, 2012 issue of the journal Neuron, scientists from the Florida campus of The Scripps Research Institute have pinpointed a mechanism that is essential for forming memories in the first place and, as it turns out, is equally essential for eliminating them after memories have formed.

"This study focuses on the molecular biology of active forgetting," said Ron Davis, chair of the Scripps Research Department of Neuroscience who led the project. "Until now, the basic thought has been that forgetting is mostly a passive process. Our findings make clear that forgetting is an active process that is probably regulated."

The Two Faces of Dopamine

To better understand the mechanisms for forgetting, Davis and his colleagues studied Drosophila or fruit flies, a key model for studying memory that has been found to be highly applicable to humans. The flies were put in situations where they learned that certain smells were associated with either a positive reinforcement like food or a negative one, such as a mild electric shock. The scientists then observed changes in the flies’ brains as they remembered or forgot the new information.

The results showed that a small subset of dopamine neurons actively regulate the acquisition of memories and the forgetting of these memories after learning, using a pair of dopamine receptors in the brain. Dopamine is a neurotransmitter that plays an important role in a number of processes including punishment and reward, memory, learning and cognition.

But how can a single neurotransmitter, dopamine, have two seemingly opposite roles in both forming and eliminating memories? And how can these two dopamine receptors serve acquiring memory on the one hand, and forgetting on the other?

The study suggests that when a new memory is first formed, there also exists an active, dopamine-based forgetting mechanism—ongoing dopamine neuron activity—that begins to erase those memories unless some importance is attached to them, a process known as consolidation that may shield important memories from the dopamine-driven forgetting process.

The study shows that specific neurons in the brain release dopamine to two different receptors known as dDA1 and DAMB, located on what are called mushroom bodies because of their shape; these densely packed networks of neurons are vital for memory and learning in insects. The study found the dDA1 receptor is responsible for memory acquisition, while DAMB is required for forgetting.

When dopamine neurons begin the signaling process, the dDA1 receptor becomes overstimulated and begins to form memories, an essential part of memory acquisition. Once that memory is acquired, however, these same dopamine neurons continue signaling. Except this time, the signal goes through the DAMB receptor, which triggers forgetting of those recently acquired, but not yet consolidated, memories.

Jacob Berry, a graduate student in the Davis lab who led the experimentation, showed that inhibiting the dopamine signaling after learning enhanced the flies’ memory. Hyperactivating those same neurons after learning erased memory. And, a mutation in one of the receptors, dDA1, produced flies unable to learn, while a mutation in the other, DAMB, blocked forgetting.

Intriguing Issues

While Davis was surprised by the mechanisms the study uncovered, he was not surprised that forgetting is an active process. “Biology isn’t designed to do things in a passive way,” he said. “There are active pathways for constructing things, and active ones for degrading things. Why should forgetting be any different?”

The study also brings into a focus a lot of intriguing issues, Davis said—savant syndrome, for example.

"Savants have a high capacity for memory in some specialized areas," he said. "But maybe it isn’t memory that gives them this capacity, maybe they have a bad forgetting mechanism. This also might be a strategy for developing drugs to promote cognition and memory—what about drugs that inhibit forgetting as cognitive enhancers?"

Provided by The Scripps Research Institute

Source: medicalxpress.com

ScienceDaily (May 9, 2012) — In sports, on a game show, or just on the job, what causes people to choke when the stakes are high? A new study by researchers at the California Institute of Technology (Caltech) suggests that when there are high financial incentives to succeed, people can become so afraid of losing their potentially lucrative reward that their performance suffers.

In the study, each participant was asked to control this virtual object on a screen. The virtual object consisted of two weighted balls connected by a spring. The task was to place the object, which stretched and contracted as a weighted spring would in real life, into a square target within two seconds. (Credit: Image courtesy of California Institute of Technology)

It is a somewhat unexpected conclusion. After all, you would think that the more people are paid, the harder they will work, and the better they will do their jobs — until they reach the limits of their skills. That notion tends to hold true when the stakes are low, says Vikram Chib, a postdoctoral scholar at Caltech and lead author on a paper published in the May 10 issue of the journalNeuron. Previous research, however, has shown that if you pay people too much, their performance actually declines.

Some experts have attributed this decline to too much motivation: they think that, faced with the prospect of earning an extra chunk of cash, you might get so excited that you will fail to do the task properly. But now, after looking at brain-scan data of volunteers performing a specific motor task, the Caltech team says that what actually happens is that you become worried about losing your potential prize. The researchers also found that the more someone is afraid of loss, the worse they perform.

In the study, each participant was asked to control a virtual object on a screen by moving an index finger that had a tracking device attached to it. The virtual object consisted of two weighted balls connected by a spring. The task was to place the object, which stretched and contracted as a weighted spring would in real life, into a square target within two seconds.

The researchers controlled for individual skill levels by customizing the size of the target so that everyone would have the same success rate. That way, people who happened to be really good or bad at this task would not skew the data.

After a training period, the subjects were asked to perform the task while inside an fMRI machine, which measures blood flow in the brain — a proxy for brain activity, since wherever a brain is active, it needs extra oxygen, and thus a larger volume of blood. By monitoring blood flow, the researchers can pinpoint areas of the brain that turn on when a particular task is performed.

The task began with the researchers offering the participants a randomized range of rewards — from $0 to $100 — if they could successfully place the object into the square within the time limit. At the end of hundreds of trials — each with varying reward amounts — the participant was given their reward, based on the result of just one of the trials, picked at random.

As expected, the team found that performance improved as the incentives increased — but only when the cash reward amounts were at the low end of the spectrum. Once the rewards passed a certain threshold, which depended on the individual, performance began to fall off.

Incentives are known to activate a part of your brain called the ventral striatum, Chib says; the researchers thus expected to see the ventral striatum become increasingly active as they bumped up the prizes. And if the conventional thought were correct — that the reason for the observed performance decline was over-motivation — they would expect the striatum to continue showing a lot of activation when the incentives became high enough for performance to suffer.

What they found, instead, was that when the participants were shown their potential rewards, activity in the striatum did indeed increase with rising incentives. But once the volunteers started doing the task, striatal activity decreased with rising incentives. They also noticed that the less activity they saw in a participant’s striatum, the worse that person performed on the task.

Other studies have shown that decreasing striatal activity is related to fear or aversion to loss, Chib says. “When people see the incentive that they’re being offered, they initially encode it as a gain,” he explains. “But when they’re actually doing the task, the thing that causes them to perform poorly is that they worry about losing a potential incentive they haven’t even received yet.” He adds, “We’re showing loss aversion even though there are no explicit losses anywhere in the task — that’s very strange and something you really wouldn’t expect.”

To further test their hypothesis, Chib and his colleagues decided to measure how loss-averse each participant was. They had the participants play a coin-flip game in which there was an equal chance they could win or lose varying amounts of money.

Each participant was offered varying potential win-loss amounts ($20-$20, $20-$10, $20-$5, for example), and then given the opportunity to either accept each possible gamble or decline it. The win-loss ratio at which the subjects chose to take the gamble provided a measure of how loss-averse each person was; someone willing to gamble even when they might win or lose $20 is less loss-averse than someone who is only willing to gamble if they can win $20 but only lose $5.

Once the numbers had been crunched and compared to the original experiment, it turned out that the more averse a participant was, the worse they did on the task when the stakes were high. And for a particularly loss-aversive person, the threshold at which their performance started to decline did not have to be very high. “If you’re more loss-averse, it really hurts you,” Chib says. “You’re going to reach peak performance at a lower incentive level, and your performance is also going to be worse for higher incentives.”

"Previously, it’s been shown that the ventral striatum is involved in mediating performance increases in response to rising incentives," says John O’Doherty, professor of psychology and coauthor of the paper. "But our study shows that changes in activity in this same region can, under certain situations, also lead to worsening performance."

While this study only involved a specific motor task and financial incentives, these results may well be universal, says Shinsuke Shimojo, the Gertrude Baltimore Professor of Experimental Psychology and another coauthor of the study. “The implications and applications can include any sort of decision making that contains high stakes and uncertainties, such as business and politics.”

These findings, the researchers say, might be used to develop new ways to motivate people to perform better or to train them to be less loss-averse. “This loss aversion can be an important way of deciding how to set up incentive mechanisms and how to figure out who’s going to perform well and who isn’t,” Chib says. “If you can train somebody to be less loss-averse, maybe you can help them avoid performing poorly in stressful situations.”

Source: Science Daily

May 9, 2012

How well people with newly diagnosed epilepsy respond to their first drug treatment may signal the likelihood that they will continue to have more seizures, according to a study published in the May 9, 2012, online issue ofNeurology, the medical journal of the American Academy of Neurology.

"Our research shows a pattern based on how a person responds to initial treatment and specifically, to their first two courses of drug treatment," said study author Patrick Kwan, MD, PhD, with the University of Melbourne in Australia.

For the study, 1,098 people from Scotland between the ages of nine and 93 with newly diagnosed epilepsy were followed for as long as 26 years after being given their first drug therapy. Participants were considered seizure-free if they had no seizures for at least a year without changes in their treatment. If they had further seizures, a second drug was chosen to be given alone or to be added to the first. If seizures continued, a third drug regimen was selected, and the process continued for up to nine drug regimens.

The study found that 50 percent of the people were seizure-free after the first drug tried, 13 percent were seizure-free after the second drug regimen tried and 4 percent were seizure-free after the third drug regimen tried. Less than two percent of the participants stopped having seizures on additional drug treatment courses up to the seventh one tried, and none became seizure-free after that.

The research also found that 37 percent of people in the study became seizure-free within six months of treatment. Another 22 percent became seizure-free after more than six months of starting treatment. Both groups continued to be seizure-free. However, 16 percent had fluctuating periods of seizure freedom and relapses, and 25 percent were never seizure-free for one year.

At the end of the study, 749 people (68 percent) were seizure-free and 678 people (62 percent) were on only one drug. The results were independent of the age when the person had the first seizure or the type of epilepsy.

"A person who doesn’t respond well to two courses of epilepsy drug treatment should be further evaluated to verify an epilepsy diagnosis and to identify whether surgery is the best next step," said Patricia E. Penovich, MD, with the Minnesota Epilepsy Group PA and the University of Minnesota School of Medicine in St. Paul, Minn., and a Fellow with the American Academy of Neurology, who wrote an accompanying editorial on the study.

Provided by American Academy of Neurology

Source: medicalxpress.com

May 9, 2012

In 1619, the pioneering astronomer Johannes Kepler published Harmonices Mundi in which he analyzed data on the movement of planets and asserted that the laws of nature governing the movements of planets show features of harmonic relationships in music. In so doing, Kepler provided important support for the, then controversial, model of the universe proposed by Copernicus.

In the latest issue of Biological Psychiatry, researchers at the University of California in San Diego suggest that careful analyses of the electrical signals of brain activity, measured using electroencephalography (EEG), may reveal important harmonic relationships in the electrical activity of brain circuits.

The underlying premise is a simple one - that brain function is expressed by circuits that fire, and therefore generate oscillating EEG signals, at different frequencies.

High frequency EEG activity called gamma, for example, might reflect the activity of fast-spiking cells which are often a subclass of inhibitory nerve cells containing parvalbumin. Represented musically, this would be a high pitch, i.e., toward the right side of the piano.

Lower frequency EEG activity, called theta, might come from cells that fire with a lower frequency.

As circuits interact with each other, one would see different “musical combinations”, like the chords of music, emerging in the EEG signal. Abnormalities in the structure and function of brain circuits would be reflected in cacophonous music, chords where the musical “voices” are firing at the wrong rate (pitch), volume (amplitude), or timing.

It is increasingly evident that schizophrenia is a disorder characterized by disturbances in the “music of the brain hemispheres.” This new report describes relationships between low- and high-frequency EEG oscillations in the human brain produced when high frequency auditory stimuli are presented to a research subject. The authors observed relatively slower oscillations and reduced cross-phase synchrony (for example, peak of theta coinciding with peak of gamma) in schizophrenia patients compared to healthy study participants.

Dr. John Krystal, Editor of Biological Psychiatry, commented, “The new findings highlight the importance of understanding the relationships between different circuits. It seems that cortical abnormalities in schizophrenia disturb brain function, in part, by disturbing the ‘tuning’ of brain circuits in relation to each other.”

Provided by Elsevier

Source: medicalxpress.com

May 9th, 2012

This family comprises a cluster of six genes that may be altered in neurological conditions, such as Parkinson’s and Charcot-Marie-Tooth disease.

A team headed by Eduardo Soriano at the Institute for Research in Biomedicine (IRB Barcelona) has published a study in Nature Communications describing a new family of six genes whose function regulates the movement and position of mitochondria in neurons. Many neurological conditions, including Parkinson’s and various types of Charcot-Marie-Tooth disease, are caused by alterations of genes that control mitochondrial transport, a process that provides the energy required for cell function.

“We have identified a set of new genes that are highly expressed in the nervous system and have a specific function in a biological process that is crucial for the activity and viability of the nervous system”, explains Eduardo Soriano, head of the Neurobiology and Cell Regeneration group at IRB Barcelona and full professor at the University of Barcelona (UB).

By means of comparative genomic analyses, the scientists have discovered that these genes are found only in more evolved mammals, the so-called Eutharia, these characterized by internal fertilization and development. “This finding indicates the relevance of mitochondrial biology. When the brain evolved in size, function and structure, the mitochondrial transport process also became more complex and probably required additional regulatory mechanisms”, says Soriano. “Likewise, given the origin of the gene cluster, in the transition between primitive mammals, such as marsupials (kangaroos) and the remaining placental mammals, it is tempting to propose that the cluster is linked to the increased complexity of the cerebral cortex in the lineage that leads to humans”, adds the full UB professor Jordi Garcia-Fernàndez, collaborator in the study.

In the image, red indicates the localization of mitochondria in a neuron. The new proteins described help to regulate their positions in the cell. Image adapted from IRB Barcelona press release image.

Correct brain function is highly energy-demanding. However, this energy must be finely distributed throughout neurons —cells that have ramifications that can reach up to tens of centimetres in length, from the brain to the limbs. This cluster of genes forms part of the “wheel” machinery of mitochondria and regulates the localization of each cell on the basis of its energy requirements. “These genes would be like an extra control in cellular mitochondrial trafficking and they interact with the major proteins associated with the regulation of mitochondrial transport”, explains Soriano.

Another striking characteristic of these new proteins is that they are found both in mitochondria, the function of which has already been described, and in the cell nucleus, where their function is unknown. “They may also be involved in the regulation of gene expression, a possibility that we are now studying”. In addition to their potential involvement in brain pathologies, the researchers believe that these proteins may be related to metabolic diseases and cancer.

Source: Neuroscience News

May 9, 2012

Researchers have developed a new technique which allows them to measure brain activity in large populations of nerve cells at the resolution of individual cells. The technique, reported today in the journal Nature, has been developed in zebrafish to represent a simplified model of how brain regions work together to flexibly control behaviour.

Our thoughts and actions are the product of large populations of nerve cells, called neurons, working in harmony, often millions at a time. Measuring brain activity during behaviour at detailed resolution in these groups of cells has proved extremely challenging. Currently, scientists are restricted to measuring their activity in individual brain areas of, for example, moving rats, typically in less than a few hundred neurons.

Dr Misha Ahrens, a Sir Henry Wellcome Postdoctoral Fellow based at Harvard University and the University of Cambridge, worked with colleagues to develop a technique which allows neuroscientists to study as many as 2,000 neurons simultaneously, anywhere in the brain of a transparent zebrafish. Their work was funded by the Wellcome Trust and the National Institutes of Health.

Dr Ahrens and colleagues created a virtual environment for zebrafish, which allowed them to measure activity in the neurons as the fish ‘moved’. In reality, the zebrafish was paralysed to allow the researchers to image its brain; the fish perceived to ‘move’ through the virtual environment by activating their motor neuron axons, the cells responsible for generating movement.

Zebrafish are often used as a simple organism to study genetics and characteristics of the nervous system that are conserved in humans . They are genetically modifiable, so by manipulating the fish’s genetic make-up, Dr Ahrens and colleagues created a fish in which all neurons contained a particular protein that increases its fluorescence when the cells are active. The fish are transparent and so the team were able to use a laser-scanning microscope, to see activity in any neuron in the brain of the fish, and up to 2,000 neurons simultaneously.

Dr Ahrens explains: “Our behaviour is determined by thousands, possibly millions, of nerve cells working in harmony. The zebrafish performs complex behaviors, with a brain of about 100,000 neurons, almost all of which are accessible to optical recording of neural activity. Our new technique will help us examine how large networks mediate behaviour, while at the same time telling us what each individual cell is doing.”

Using the technique, Dr Ahrens and colleagues asked the question: dozebrafish adapt their behaviour in response to changes in their environment? To do this, they manipulated the virtual environment to simulate the fish suddenly becoming more “muscular”. This served as a simplified version of what happens when the brain needs to adapt the way it drives behavior, for example, when water temperature changes the efficacy of the muscles, or when the fish gets injured.

Dr Ahrens adds: “The paralyzed fish in the virtual world do indeed adapt their behaviour, by adjusting the amount of impulses the brain sends to the muscles. They also ‘remember’ this change for a while. Imaging the brain everywhere during this behaviour, we identified certain brain regions that were involved, most notably the cerebellum and related structures. This technique opens the possibility that eventually, the behaviour may be used to gain insights into human motor control and motor control deficits.

"Our own motor control is continuously recalibrating itself in a similar way to the fish’s to cope with ever changing conditions of our body and environment, such as when we injure a leg, or if we’re walking on a slippery floor or carrying a heavy bag. The zebrafish’s behaviour is an ultra-simplified version of this and we have been able to gain some insight into how its brain structures drive behaviour. This might someday help us understand how damage to certain brain regions in humans affects the way in which the brain integrates sensory information to control body movements."

Understanding the brain is one of the Wellcome Trust’s five strategic challenges.

Provided by Wellcome Trust

Source: medicalxpress.com

May 9, 2012

Research published in the May 10 issue of the journal Neuron, describes a potential new therapeutic approach for improving memory and modifying disease progression in patients with amnestic mild cognitive impairment. The study finds that excess brain activity may be doing more harm than good in some conditions that cause mild cognitive decline and memory impairment.

Elevated activity in specific parts of the hippocampus, a brain region involved in memory, is often seen in disorders associated with an increased risk for Alzheimer’s disease. Amnestic mild cognitive impairment (aMCI), where memory is worse than would be expected for a person’s age, is one such disorder. “In the case of early aMCI, it has been suggested that the increased hippocampal activation may serve a beneficial function by recruiting additional neural resources to compensate for those that are lost,” explains senior study author, Dr. Michela Gallagher, from Johns Hopkins University. “However, animal studies have raised the alternative view that this excess activation may be contributing to memory impairment.”

Dr. Gallagher and colleagues tested how a reduction of hippocampal activity would impact human patients with aMCI. The researchers used a low dose of a drug used clinically to treat epilepsy, for the purpose of reducing hippocampal activity in subjects with aMCI to levels that were similar to activity levels in healthy, age-matched subjects in a control group. The researchers found that treatment with the drug improved performance on a memory task. These findings point to the therapeutic potential of reducing excess activation in the hippocampus in aMCI.

The results also have broader significance as elevated activity in the hippocampus is also observed in other conditions that are thought to precede Alzheimer’s disease, and may be one of the underlying mechanisms of neurodegeneration. “Apart from a direct role in memory impairment, there is concern that elevated activity in vulnerable neural networks could be causing additional damage and, possibly, widespread disease-related degeneration that underlies cognitive decline and the conversion to Alzheimer’s disease,” concludes Dr. Gallagher. “Therefore, reducing the elevated activity in the hippocampus may help to restore memory and protect the brain.”

Provided by Cell Press

More information: Bakker et al.: “Reduction of hippocampal hyperactivity improves cognition in amnestic mild cognitive impairment.”,DOI:10.1016/j.neuron.2012.03.023

Source: medicalxpress.com

Released: 5/9/2012 11:20 AM EDT

Newswise — After completing the first study of its kind, researchers at McMaster University have discovered that very early musical training benefits children even before they can walk or talk.

They found that one-year-old babies who participate in interactive music classes with their parents smile more, communicate better and show earlier and more sophisticated brain responses to music.

The findings were published recently in the scientific journals Developmental Science and Annals of the New York Academy of Sciences.

“Many past studies of musical training have focused on older children,” says Laurel Trainor, director of the McMaster Institute for Music and the Mind. “Our results suggest that the infant brain might be particularly plastic with regard to musical exposure.”

Trainor, together with David Gerry, a music educator and graduate student, received an award from the Grammy Foundation in 2008 to study the effects of musical training in infancy. In the recent study, groups of babies and their parents spent six months participating in one of two types of weekly music instruction.

One music class involved interactive music-making and learning a small set of lullabies, nursery rhymes and songs with actions. Parents and infants worked together to learn to play percussion instruments, take turns and sing specific songs.

In the other music class, infants and parents played at various toy stations while recordings from the popular Baby Einstein series played in the background.

Before the classes began, all the babies had shown similar communication and social development and none had previously participated in other baby music classes.

“Babies who participated in the interactive music classes with their parents showed earlier sensitivity to the pitch structure in music,” says Trainor. “Specifically, they preferred to listen to a version of a piano piece that stayed in key, versus a version that included out-of-key notes. Infants who participated in the passive listening classes did not show the same preferences. Even their brains responded to music differently. Infants from the interactive music classes showed larger and/or earlier brain responses to musical tones.”

The non-musical differences between the two groups of babies were even more surprising, say researchers.

Babies from the interactive classes showed better early communication skills, like pointing at objects that are out of reach, or waving goodbye. Socially, these babies also smiled more, were easier to soothe, and showed less distress when things were unfamiliar or didn’t go their way.

While both class types included listening to music and all the infants heard a similar amount of music at home, a big difference between the classes was the interactive exposure to music.

“There are many ways that parents can connect with their babies,” says study coordinator Andrea Unrau. “The great thing about music is, everyone loves it and everyone can learn simple interactive musical games together.”

Released: 5/9/2012 11:00 AM EDT 

Newswise — “Practice makes perfect,” the saying goes. Optimal performance, however, can require more than talent, effort, and repetition. Training the brain to reduce stress through neurofeedback can remove barriers and enhance one’s innate abilities.

An article in the journal Biofeedback presents the narrative of a young cellist who was able to realize the potential of his talent and eliminate debilitating migraine headaches. This case study is part of a special section in the Spring 2012 issue focusing on optimal functioning.

Enhancing people’s performance in business, performing and visual arts, academia, and sports can be realized through biofeedback and neurofeedback training. Tools of stress reduction, mental imagery training, psychology, and psycho-physiological technology are combined to help people reach their goals.

The author and practitioner in this case study has combined her work and study in the fields of theater, social work, and neurofeedback. In her practice, she coaches clients to achieve outstanding performances. For example, a singer can better understand and interpret a musical selection, allowing that singer to better convey the emotion of the music, resulting in a noticeably improved performance.

William, the young musician, sought relief from migraine headaches that were affecting him almost daily. His therapy, however, did not take the approach of treating the headaches, but of focusing on William as a person and as a performer. By improving his functionality, working through moments of obsessiveness, self-criticism, fear, and anxiety, the headaches could also be resolved.

William’s therapist conducted neurofeedback — using sensors to read his brainwaves, analyzing these with NeuroOptimal™ software, and then giving feedback to the brain through a visual display and sound. With this information, the brain can learn to self-correct. This technology assists in getting people past that moment when they obsess over whether they have given the correct answer or hit the right note.

NeuroOptimal feedback, guided imagery, and coaching about decisions regarding his music helped William move beyond the difficulties he encountered. During his senior recital at his college, he was able to give a relaxed, confident performance that was met with a standing ovation.

Full text of the article, “William’s Story: A Case Study in Optimal Performance,” Biofeedback, Volume 40, Issue 1, Spring 2012, is available at http://www.aapb-biofeedback.com/

Source: newswise