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Social Decision-Making in Autism
By Jason von Stietz, M.A.
December 23, 2015
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It is widely believed that individuals with autism lack the capacity to read social cues. However, recent findings suggest autism affects not how social information is processed but how the information is used in decision making. The study was discussed in a recent article in MedicalXpress:  

 

Scientists at the Max Planck Institute of Psychiatry in Munich together with colleagues in Cologne and Zürich have used mathematical models to explain differences in social behaviour associated with autistic personality traits. They show that autistic traits do not – as previously thought – stop the individual from "reading" social cues, but instead affect how social information is used in making decisions. This new understanding provides a new basis for future research that will improve therapies for people with autism.

 

Autism spectrum disorder is a common psychiatric disorder that is characterized from childhood onwards by major impairments in social interaction and communication. About one half of autistic individuals are "high-functioning" as they have no intellectual impairment. However, all are severely limited in their social and professional life, which is why so many people with autism also suffer from depression. It has been suggested that autistic individuals may not "read" social cues and as a result do not respond to them properly. Alternatively, it has been suggested they are unable to empathize, thereby leading to social problems.

 

Leonhard Schilbach, consultant psychiatrist and Research Group leader at the Max Planck Institute of Psychiatry, explains "we have shown in this study that autistic trait-related differences in social behaviour are not due to a general inability to process social cues, but are related to the way social information is taken into account during decision-making".

 

It is thought that reading cues and making decisions involve an interplay between "expectations" generated in higher brain areas and signals from lower sensory brain areas. Normally, the behaviour of others that causes the sensory signal is interpreted in comparison to such "expectations". This allows individuals to regulate their behaviour in a context-sensitive and socially adequate way. In contrast to this, autism might be the result of an imbalance in this interplay, with a stronger reliance on sensory signals.

 

Computational modeling uses mathematical descriptions to characterize the variables that underlie social behaviour. Previous research has shown that humans do not only "read" the overt behaviour of others, but also the intentions that underlie and motivate the behaviour and use this information when making. Lead scientist Leonhard Schilbach explains, "we used a computational approach to investigate whether differences in social decision-making observed in people who are high or low in autistic traits are related to an inability to monitor others' intentions".

 

Schilbach and colleagues found that higher autistic traits do not impair the ability to process social information per se, but rather how this information influences decision-making. Furthermore, it was observed that individuals high in autistic traits found it harder to optimally use social information during unpredictable situations. It is hoped that this new insight into the autism spectrum will provide improved interventions for patients. Furthermore, the computational approach used in this study could also help to characterize social difficulties in other psychiatric disorders.

 

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Enhancing Experience-Dependent Neuroplasticity
By Jason von Stietz, M.A.
December 19, 2015
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Experience-dependent neuroplasticity, the brain’s capacity to change in response to environmental stimuli and learning, is a fundamental property of the brain. The impairment of this function in the brain is related to many psychiatric disorders including depression and bipolar disorder. Researchers recently studied the effect of D-cycloserine on the brain’s capacity for experience-dependent neuroplasticity (measured by EEG). The study was recently discussed in an article in MedicalXpress: 

 

In a recent study published in the Proceedings of the National Academy of Sciences, a group of researchers from various U.S. colleges have collaborated to determine if augmenting the signaling of a particular brain receptor would boost neuroplasticity in adults. During early development, experience-dependent neuroplasticity actually interacts with genetic programming in order to establish the neuronal organization and functionally connected circuits that characterize the mature brain.

 

This basic circuitry is well established by early adulthood, but throughout the lifespan, adult brains depend on experience-dependent neuroplasticity to enable new behavior patterns. Given the general acceptance of the relatively new idea that neuroplasticity endures in adults, the ability to augment its mechanisms could yield new approaches to associated psychiatric disorders. Here, the researchers sought to determine if augmenting N-methyl-D-aspartate receptor (NMDAR) signaling would promote experience-dependent plasticity. They tested a drug called D-cycloserine (DCS) on a group of participants who were monitored via a recently developed EEG paradigm for changes in plasticity.

 

The participants, divided into groups that received either DCS or placebo, engaged in three cognitive tasks: A weather prediction task, an information integration task and an n-back task, once before administration of DCS or placebo, and again 31 hours later. They determined that participants who received DCS showed greater potentiation of plasticity following the high-frequency visual stimuli of the tests than did those who received placebo. "Our findings of enhanced acquisition of the weather prediction task and the information integration task are consistent with other findings of enhanced incremental learning following DCS administration, including on category learning, motor learning, and mental rotation learning tasks," the authors write.

 

They note that the performance of DCS participants on the n-back test, which was a spatial working memorytask, did not differ measurably from the performance of those receiving placebo. They note that this result is consistent with a growing body of evidence that the transient memory underlying working memory is modulated in a fundamentally different way than experience-dependent neuroplasticity.

 

While noting the limitation that the study was restricted to healthy young adults, the authors conclude that their results strongly suggest that enhancing NMDAR signaling augments experience-dependent plasticity in adult brains across a variety of tasks that leverage that ability. "These findings suggest exciting possibilities for using NMDAR agonists to help ameliorate plasticity deficits in neurodegenerative and psychiatric disorders. Our results complement a growing literature that suggests that DCS can enhance new learning during cognitive behavioral therapy interventions and cognitive training programs."

 

The researchers suggest that parallel studies in older adults and patient groups are an obligatory next step in assessing DCS as a therapeutic intervention for psychiatric disorders.

 

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Surgical Treatment of TBI in Older Adults
By Jason von Stietz, M.A.
November 30, 2015
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Researches at the Helsinki University Hospital Department of Neurosurgery investigated these use of surgery to treat acute subdural hemotomas in patients over the age of 75. Previously, older adult patients were not treated surgically, as the rates of patents who survived and recovered successfully were low. However, new findings show that older adult patients who lived independently before the accident, were not taking anticoagulants, and who arrived at the hospital conscious received were treated successfully through surgery. The study was discussed in a recent article in NeuroScientistNews: 

 

According to a study completed at the Helsinki University Hospital Department of Neurosurgery, even patients over the age of 75 may recover from severe traumatic brain injury. This is the first study to describe the results of surgically treated elderly patients with acute subdural hematomas.

 

It is generally accepted that elderly patients who suffer from an acute subdural hematoma should not be treated surgically, as few survive and even fewer recover to an independent life. However, the world's population is rapidly aging leading to an increased rate of fall accidents. In the worst case, falling may result in brain hemorrhage.

 

Age is one of the most significant outcome predictors in patients with traumatic brain injury. If the patient is young, an acute subdural hematoma is normally treated through a neurosurgical operation. However, even among young patients, mortality and significant morbidity are highly common, despite surgical treatment. In older patients, the success rate of the surgery are made worse by the fact that many patients are typically using oral anticoagulant medications to treat other cardiovascular diseases.

 

The Neurosurgical Department in Helsinki University Hospital has been an exception in its policy to also treat elderly patients with acute subdural hematomas surgically. Researchers from the University of Helsinki and Helsinki University Hospital have now determined how the patients' functional status before the injury and the use of oral anticoagulant medications influence the prognosis of patients 75 years or older operated on for an acute subdural hematoma.

 

The study showed that no patients who had been brought to hospital unconscious, who had not been independent before the trauma, or who had used anticoagulants were alive at one year after the surgery.

 

"What was surprising, however, was that patients who were conscious at presentation, who were not using anticoagulants or were independent before the operation, recovered quite well. The expected lifespan of these patients was comparable to their age-matched peers," says MD, PhD Rahul Raj, one of the main authors.

 

"One should be careful to make to strong conclusions from such a small number of patients," Raj points out, "but it seems that in approximately half of all cases, even elderly patients may benefit from surgery and recover to an independent life. It is important to note that included patients had an isolated acute subdural hematoma with no injuries to the brain tissue itself. This means that the results cannot be applied to patients with contusions or other intracranial injuries, whose treatment and prognosis are different."

 

The decision to operate should not be based on age alone

 

According to Raj, the study throws new light on the old assumption that surgical treatment of the elderly is not a sensible course of action: "The decision to treat through surgery should not be based on age alone, even though this is common."

 

Surgery of an acute subdural hematoma followed by intensive care and rehabilitation involve major costs and can cause significant suffering to patients and relatives. Thus, it is important to perform surgery on only the patients who are likely to benefit from it.

 

"But how do you define a bad prognosis? If only one in ten patients recovers sufficiently to live at home, is the treatment worthwhile? If half of the treated patients die within the year, is the treatment worthwhile? This is not a medical decision," the researchers emphasize. They believe that in the future, surgical treatment will be increasingly restricted to patients with the highest likelihood of recovering.

 

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Brain's Stress Circuitry Involved in Alzheimer's Disease Treatment
By Jason von Stietz, M.A.
November 27, 2015
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Researchers at the University of San Diego School of Medicine investigated the use of a small molecule drug in preventing and treating Alzheimer’s disease in mice. Researchers found that the drug significantly reduces activity of the stress circuitry in the brains of the mice and resulted in the prevention of neurodegeneration and cognitive impairment. The study was discussed in a recent article of NeuroScientistNews:

 

The findings are described in the current online issue of the journal Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

 

The results underscore the complexity and diversity of AD, whose causes appear to be a mix of genetic, lifestyle and environmental factors. Previous research has shown a link between the brain’s stress signaling pathways and AD. Specifically, the release of a stress-coping hormone called corticotropin-releasing factor (CRF), which is widely found in the brain and acts as a neurotransmitter/neuromodulator, is dysregulated in AD and is associated with impaired cognition and with detrimental changes in tau protein and increased production of amyloid-beta—protein fragments that clump together and trigger the neurodegeneration characteristic of AD.

 

“Our work and that of our colleagues on stress and CRF have been mechanistically implicated in Alzheimer’s disease, but agents that impact CRF signaling have not been carefully tested for therapeutic efficacy or long-term safety in animal models,” said the study’s principal investigator and corresponding author Robert Rissman, PhD, assistant professor in the Department of Neurosciences and Biomarker Core Director for the Alzheimer’s Disease Cooperative Study (ADCS).

 

“The novelty of this study is two-fold: We used a preclinical prevention paradigm of a CRF-antagonist (a drug that blocks the CRF receptor in brain cells) called R121919 in a well-established AD model – and we did so in a way that draws upon our experience in human trials. We found that R121919 antagonism of CRF-receptor-1 prevented onset of cognitive impairment and synaptic/dendritic loss in AD mice.”

 

In other words, the researchers determined that modulating the mouse brain’s stress circuitry (without actually changing the normal response) mitigated generation and accumulation of amyloid plaques widely attributed with causing neuronal damage and death. As a consequence, behavioral indicators of AD were prevented and cellular damage was reduced.  The mice began treatment at 30-days-old – before any pathological or cognitive signs of AD were present – and continued until six months of age.

 

One particular challenge, Rissman noted, is limiting exposure of the drug to the brain so that it does not impact the body’s ability to response to stress. “This can be accomplished because one advantage of these types of small molecule drugs is that they readily cross the blood-brain barrier and actually prefer to act in the brain,” Rissman said. Drugs like R121919 were originally designed to treat generalized anxiety disorder, irritable bowel syndrome and other diseases, but failed to be effective in treating those disorders.

 

“Rissman’s prior work demonstrated that CRF and its receptors are integrally involved in changes in another AD hallmark, tau phosphorylation,” said William Mobley, MD, PhD, chair of the Department of Neurosciences and interim co-director of the Alzheimer’s Disease Cooperative Study at UC San Diego. “This new study extends those original mechanistic findings to the amyloid pathway and preservation of cellular and synaptic connections.  Work like this is an excellent example of UC San Diego’s bench-to-bedside legacy, whereby we can quickly move our basic science findings into the clinic for testing,” said Mobley.

 

Rissman said R121919 was well-tolerated by AD mice (no significant adverse effects) and deemed safe, suggesting CRF-antagonism is a viable, disease-modifying therapy for AD.  Rissman noted that repurposing R121919 for human use was likely not possible at this point. He and colleagues are collaborating with the Sanford Burnham Prebys Medical Discovery Institute to design new assays to discover the next generation of CRF receptor-1 antagonists for testing in early phase human safety trials.

 

“More work remains to be done, but this is the kind of basic research that is fundamental to ultimately finding a way to cure – or even prevent – Alzheimer’s disease,” said David Brenner, MD, vice chancellor, UC San Diego Health Sciences and dean of UC San Diego School of Medicine. “These findings by Dr. Rissman and his colleagues at UC San Diego and at collaborating institutions on the Mesa suggest we are on the cusp of creating truly effective therapies.”

 

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The Brain Conserves Energy By Forgetting
By Jason von Stietz, M.A.
November 11, 2015
Photo Credit: Shutterstock

 

How is it that we seem to forget information that we deem useless or unnecessary? Researchers at the Lund University in Sweden have investigated one of the brain’s mechanisms of forgetting or ignoring such information. The study was discussed in a recent article by MedicalXpress: 

 

Our brains not only contain learning mechanisms but also forgetting mechanisms that erase "unnecessary" learning. A research group at Lund University in Sweden has now been able to describe one of these mechanisms at the cellular level.

 

The group's results, published in the international journal Proceedings of the National Academy of Sciences of the United States of America (PNAS), explain a theoretical learning phenomenon which has so far been difficult to understand.

 

The premise is that human or animal subjects can learn to associate a certain tone or light signal with a puff of air to the eye. The air puff makes the subject blink, and eventually they blink as soon as they hear the tone or see the light signal. The strange thing, however, is that if the tone and the light are presented together (and with the air puff), the learning does not improve, but gets worse.

 

"Two stimuli therfore achieve worse results than just one. It seems contrary to common sense, but we believe that the reason for it is that the brain wants to save energy", says brain researcher and professor Germund Hesslow.

 

His colleague Anders Rasmussen, who performed the present study, has previously shown that when the brain has learnt a particular association sufficiently, certain neurons that act as a brake on the learning mechanism, are activated.

 

"You could say that the part of the brain that learned the association (a part of the brain called the cerebellum) is telling its 'teacher': 'I know this now, please be quiet'. When the brain has learnt two associations, the brake becomes much more powerful. That is why it results in forgetting, usually only temporarily, however", explains Germund Hesslow.

 

Maintaining unnecessary association pathways requires energy for the brain. The researchers believe that this is the reason for the brake mechanism – even though in this case it happened to be a little too powerful.

 

The Lund researchers were able to describe how the nerve cells learn and forget through studies of animals, but believe that the mechanisms are likely to be the same in the human brain. Therefore, these findings are of fundamental interest for both brain researchers and psychologists. They could also be of practical interest to educators.

 

"Obviously, it should be important for teachers to know the mechanisms by which the brain erases the things it considers unnecessary. You do not want to accidentally activate these mechanisms", says Germund Hesslow.

 

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ADHD Improperly Diagnosed in Children
By Jason von Stietz, M.A.
October 30, 2015
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What is causing the rise in children being diagnosed with ADHD? Is it that the modern educational environment requires more of children, which makes it harder for ADHD to go unnoticed? Is it the exposure to chemicals in our environment or the processed sugar in our diet. A study by the Center for Disease Control and Prevention found that ADHD is often improperly diagnosed. The findings were discussed in an article by the Washington Post: 

 

All sorts of theories have been proposed to explain the alarming rise -- 6.4 million in 2011, a 42 percent jump from 2004 -- in schoolchildren being diagnosed with Attention-Deficit/Hyperactivity Disorder, or ADHD, requiring therapy, medicine or both to make it through their day.

 

Some believe it's simply a matter of more awareness (and paranoia) -- meaning that more parents are seeking a diagnosis. Others wonder if it's schools (they're more academic now than in the past, requiring kids to sit still for longer periods of time making those who have ADHD more obvious).

 

Still others blame the environment (all those chemicals we use). Or diet (yet another thing to blame on processed sugar).

 

The CDC report takes an in-depth look at how children with ADHD came to get the label through a survey of 2,976 families. While in the majority of cases health care providers followed American Academy of Pediatrics guidelines when making a diagnosis, there was still a large number of children for whom these practices weren't followed.

 

In 18 percent of cases, the diagnosis was done solely on the basis of family members' reports, which is inconsistent with AAP recommendations that information be collected from individuals across multiple settings -- such as a teacher, piano instructor, or sports coach. Additionally, one out of every 10 children was diagnosed without the use of a behavior rating scale that is supposed to be administered.

 

The study also shows that children are getting diagnosed at an earlier age, with half being diagnosed at age 6 or below: 17.1 percent at age 6, 14.6 percent at age 5, and 16 percent at age 4 or younger.

 

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High Connectivity Related to Positive Traits
By Jason von Stietz, M.A.
October 17, 2015
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Researchers involved in the Human Connectome Project made a surprising discovery when examining the relationship between brain connectivity during a resting state and several factors such as education, socioeconomic status, substance use, and personality traits. It was found that, overall, positive traits related to increased connectivity whereas negative traits related to decreased connectivity. Those with more highly connected brains were more likely to be more highly educated and perform better on memory tests. Those with less brain connectivity were more likely to smoke and have more aggressive personalities. The study and it’s implications were discussed in a recent article in Scientific American: 

 

The brain’s wiring patterns can shed light on a person’s positive and negative traits, researchers report in Nature Neuroscience. The finding, published on September 28, is the first from the Human Connectome Project (HCP), an international effort to map active connections between neurons in different parts of the brain.

 

The HCP, which launched in 2010 at a cost of US$40 million, seeks to scan the brain networks, or connectomes, of 1,200 adults. Among its goals is to chart the networks that are active when the brain is idle; these are thought to keep the different parts of the brain connected in case they need to perform a task.

 

In April, a branch of the project led by one of the HCP's co-chairs, biomedical engineer Stephen Smith at the University of Oxford, UK, released a database of resting-state connectomes from about 460 people between 22 and 35 years old. Each brain scan is supplemented by information on approximately 280 traits, such as the person's age, whether they have a history of drug use, their socioeconomic status and personality traits, and their performance on various intelligence tests.

 

Axis of connectivity


Smith and his colleagues ran a massive computer analysis to look at how these traits varied among the volunteers, and how the traits correlated with different brain connectivity patterns. The team was surprised to find a single, stark difference in the way brains were connected. People with more 'positive' variables, such as more education, better physical endurance and above-average performance on memory tests, shared the same patterns. Their brains seemed to be more strongly connected than those of people with 'negative' traits such as smoking, aggressive behaviour or a family history of alcohol abuse.

 

Marcus Raichle, a neuroscientist at Washington University in St Louis, Missouri, is impressed that the activity and anatomy of the brains alone were enough to reveal this 'positive-negative' axis. “You can distinguish people with successful traits and successful lives versus those who are not so successful,” he says.

 

But Raichle says that it is impossible to determine from this study how different traits relate to one another and whether the weakened brain connections are the cause or effect of negative traits. And although the patterns are clear across the large group of HCP volunteers, it might be some time before these connectivity patterns could be used to predict risks and traits in a given individual. Deanna Barch, a psychologist at Washington University who co-authored the latest study, says that once these causal relationships are better understood, it might be possible to push brains toward the 'good' end of the axis.

 

Van Wedeen, a neuroscientist at Massachusetts General Hospital in Boston, says that the findings could help to prioritize future research. For instance, one of the negative traits that pulled a brain farthest down the negative axis was marijuana use in recent weeks. Wedeen says that the finding emphasizes the importance of projects such as one launched by the US National Institute on Drug Abuse last week, which will follow 10,000 adolescents for 10 years to determine how marijuana and other drugs affect their brains.

 

Wedeen finds it interesting that the wiring patterns associated with people's general intelligence scores were not exactly the same as the patterns for individual measures of cognition—people with good hand–eye coordination, for instance, fell farther down the negative axis than did those with good verbal memory. This suggests that the biology underlying cognition might be more complex than our current definition of general intelligence, and that it could be influenced by demographic and behavioural factors. “Maybe it will cause us to reconsider what [the test for general intelligence] is measuring,” he says. “We have a new mystery now.”

 

Much more connectome data should emerge in the next few years. The Harvard Aging Brain Study, for instance, is measuring active brain connections in 284 people aged between 65 and 90, and released its first data earlier this year. And Smith is running the Developing Human Connectome Project in the United Kingdom, which is imaging the brains of 1,200 babies before and after birth. He expects to release its first data in the next few months. Meanwhile, the HCP is analysing genetic data from its participants, which include a large number of identical and fraternal twins, to determine how genetic and environmental factors relate to brain connectivity patterns.

 

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Possible "Depression Switch" to Guide Deep Brain Stimulation
By Jason von Stietz, M.A.
October 10, 2015
Photo Credit: Getty Images

 

Researchers at Emory University School of Medicine studied the impact of deep brain stimulation on chronic and treatment resistant depression. Findings may provide researchers with a structural “depression switch” that may guide the use of deep brain stimulation in the future. The study was discussed in a recent article in MedicalXpress: 

 

A "depression switch" has been mapped during intraoperative deep brain stimulation of the subcallosal cingulate, according to research published online Sept. 26 in JAMA Neurology.

 

Ki Sueng Choi, Ph.D., from the Emory University School of Medicine in Atlanta, and colleagues characterized the structural connectivity correlates of deep brain stimulation-evoked behavior effects using probabilistic tractography in depression. Data were included for nine adults undergoing deep brain stimulation implantation surgery for chronic treatment-resistant depression.

 

The researchers recorded 72 active and 36 sham trials among the patients. Stereotypical behavior patterns included changes in interoceptive and in exteroceptive awareness. For all nine patients, the best response was a combination of exteroceptive and interoceptive changes at a single left contact. The best response contacts had a pattern of connections to the bilateral ventromedial frontal cortex (via forceps minor and left uncinate fasciculus) and to the cingulate cortex (via left cingulum bundle); only cingulate involvement was seen in behaviorally salient but non-best contacts.

 

"This analysis of transient behavior changes during intraoperative deep brain stimulation of the subcallosal cingulate and the subsequent identification of unique connectivity patterns may provide a biomarker of a rapid-onset depression switch to guide surgical implantation and to refine and optimize algorithms for the selection of contacts in long-term stimulation for treatment-resistant depression," the authors write.

 

Two authors disclosed financial ties to medical device companies, including Medtronic and St. Jude Medical, both of which develop products related to the research in this article. St. Jude Medical also donated the study device.

 

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Study Links Optimism, Anxiety, and Orbitifrontal Cortex Size
By Jason von Stietz, M.A.
October 3, 2015
Photo Credit: Getty Images

 

Can optimism be traced to a structure in the brain? Researchers at the University of Illinois have linked optimism, anxiety, and the orbitofrontal cortex (OFC). Their study found that those with a larger OFC tend to report more optimism and less anxiety. The study was discussed in a recent article in MedicalXpress: 

 

The new analysis, reported in the journal Social, Cognitive and Affective Neuroscience, offers the first evidence that optimism plays a mediating role in the relationship between the size of the OFC and anxiety.

 

Anxiety disorders afflict roughly 44 million people in the U.S. These disorders disrupt lives and cost an estimated $42 billion to $47 billion annually, scientists report.

 

The orbitofrontal cortex, a brain region located just behind the eyes, is known to play a role in anxiety. The OFC integrates intellectual and emotional information and is essential to behavioral regulation. Previous studies have found links between the size of a person's OFC and his or her susceptibility to anxiety. For example, in a well-known study of young adults whose brains were imaged before and after the colossal 2011 earthquake and tsunami in Japan, researchers discovered that the OFC actually shrank in some study subjects within four months of the disaster. Those with more OFC shrinkage were likely to also be diagnosed with post-traumatic stress disorder, the researchers found.

 

Other studies have shown that more optimistic people tend to be less anxious, and that optimistic thoughts increase OFC activity.

 

The team on the new study hypothesized that a larger OFC might act as a buffer against anxiety in part by boosting optimism.

 

Most studies of anxiety focus on those who have been diagnosed with anxiety disorders, said University of Illinois researcher Sanda Dolcos, who led the research with graduate student Yifan Hu and psychology professor Florin Dolcos. "We wanted to go in the opposite direction," she said. "If there can be shrinkage of the orbitofrontal cortex and that shrinkage is associated with anxiety disorders, what does it mean in healthy populations that have larger OFCs? Could that have a protective role?"

 

The researchers also wanted to know whether optimism was part of the mechanism linking larger OFC brain volumes to lesser anxiety.

 

The team collected MRIs of 61 healthy young adults and analyzed the structure of a number of regions in their brains, including the OFC. The researchers calculated the volume of gray matter in each brain region relative to the overall volume of the brain. The study subjects also completed tests that assessed their optimism and anxiety, depression symptoms, and positive (enthusiastic, interested) and negative (irritable, upset) affect.

 

A statistical analysis and modeling revealed that a thicker orbitofrontal cortex on the left side of the brain corresponded to higher optimism and less anxiety. The model also suggested that optimism played a mediating role in reducing anxiety in those with larger OFCs. Further analyses ruled out the role of other positive traits in reducing anxiety, and no other brain structures appeared to be involved in reducing anxiety by boosting optimism.

 

"You can say, 'OK, there is a relationship between the orbitofrontal cortex and anxiety. What do I do to reduce anxiety?'" Sanda Dolcos said. "And our model is saying, this is working partially through optimism. So optimism is one of the factors that can be targeted."

 

"Optimism has been investigated in social psychology for years. But somehow only recently did we start to look at functional and structural associations of this trait in the brain," Hu said. "We wanted to know: If we are consistently optimistic about life, would that leave a mark in the brain?"

 

Florin Dolcos said future studies should test whether optimism can be increased and anxiety reduced by training people in tasks that engage the orbitofrontal cortex, or by finding ways to boost optimism directly.

 

"If you can train people's responses, the theory is that over longer periods, their ability to control their responses on a moment-by-moment basis will eventually be embedded in their brain structure," he said.

 

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Football Player Enhances Performance with Neurofeedback
By Jason von Stietz, M.A.
September 27, 2015
Photo Credit: Getty Images

 

Washington Redskins quarterback Kirk Cousins has revitalized his career through not only hard work and a change in outlook but also through the use of neurofeeback training. Cousins first utilized neurofeedback  during his senior year at Michigan state and again this February as he revamped his approach to his craft. Cousins new approach and experience with neurofeedback was recently discussed in an article in the Washington Post: 

 

From the moment the Washington Redskins drafted him three rounds behindRobert Griffin III in 2012, Michigan State’s Kirk Cousins was reduced to a fallback plan. He was the football equivalent of a college applicant’s “safety school” or the friend who fills in as a prom date after true love fails.  

 

Handed the chance to prove he could be more, Cousins stumbled last season, undercutting his 10 touchdowns passes with nine grievously timed interceptions while filling in for the injured Griffin. Even Cousins’s body language conceded defeat as he trudged off the field in Week 7, head bowed, following that ninth errant throw. He was replaced by Colt McCoy and relegated to scout-team duty the rest of the year.

 

Less than 11 months later, Redskins Coach Jay Gruden stepped to a microphone at Redskins Park and uttered the improbable.

 

“It’s Kirk’s team,” Gruden said, announcing Aug. 31 that Cousins would be the team’s starting quarterback in 2015.

 

Cousins hadn’t played a down in a regular season game since his benching last fall. But after a solid showing in training camp, followed by a productive preseason performance, he convinced Gruden that he represents the best hope of turning around a team with back-to-back losing seasons.

 

But is Cousins simply the Redskins’ best available fallback plan? Or has Cousins, at 27, learned to leverage his strengths and minimize his shortcomings after a three-year NFL apprenticeship of waiting, watching and too often short-circuiting in the limited opportunities he has had?

 

At first glance, little has changed about the 6-foot-3, 202-pound Cousins entering Year 4, apart from a beard that hints at a new steeliness.

 

Washington Redskins quarterback Kirk Cousins practiced at Estero High School near Fort Myers this winter with members of the school's varsity football team. 

 

The overhaul of consequence, Gruden believes, is Cousins’s mental game.

 

His offseason work included copious film study and tutoring from a private throwing coach, as is common among NFL quarterbacks. But it included unlikely assists from a few dozen high school receivers who ran pass patterns and caught balls during Cousins’s winter vacations in Georgia and Florida and a Michigan-based company called Neurocore that Cousins said “retrained” his brain to operate in a “sweet spot” best suited to peak athletic performance.

 

“It’s kind of an abstract thing, but I call it brain performance,” Cousins said of his training with Neurocore Brain Performance Center, which he intensified after getting benched last fall. “I see it as the next frontier because you look at weightlifting in the 1950s and ’60s, not every football player was lifting weights; they weren’t sure about the benefit it would give you. Now everybody has a strength coach; everybody lifts weights. And I see brain training kind of being that next thing. I just want to maximize what I’ve got.”

 

The son of a minister and a man of deep faith, Cousins conceded that dark times followed his benching in October. The NFL career he had labored for seemed at hand after he took over for Griffin and led five touchdown drives in a 41-10 rout of Jacksonville in Week 2.

 

The next week, he threw for 427 yards at Philadelphia. The Redskins lost, and Cousins’s play deteriorated from there. After a 45-14 loss to the New York Giants in which he threw four second-half interceptions, Giants defenders said Cousins was telegraphing his throws.

 

“Anytime you have a job to do and you feel like you didn’t get the job done, it’s going to eat at you if you care about it,” Cousins said this week when asked about his mind-set after his Oct. 19 benching. “For me, I deeply care about it, and so it was eating at me.”

 

The turning point came, Cousins said, when he quit berating himself.

 

“What do I do now?” he asked himself. “What can I do to get better and deliberately practice, whatever that is.”

 

Once Griffin was back in the starting job and McCoy named the No. 2 quarterback, Cousins was ruled inactive. With no need to prepare for the upcoming opponent, he devoted his film-study to poring over footage of the NFL’s better quarterbacks and taking a hard look at his own footage.

 

When February came, Cousins and his wife, Julie, traveled to Florida’s Gulf Coast for vacation. But he wanted to keep working on his game, so he phoned a local high school near Fort Myers. He introduced himself, explained that he had his cleats and a couple footballs with him and asked whether the football coach could round up some receivers to throw to and let them use the Estero High field for a workout.

 

Cousins’s throwing coach, former NFL quarterback Jeff Christensen, flew in from Chicago to supervise. And for three days, Cousins threw to teenagers.

 

“He was dead on every time,” Estero Coach Jeff Hanlon recalled in a phone interview. “There was never a bad throw. Sometimes there was something he wasn’t happy with — maybe the height on the ball — and he wanted to adjust it. . . .

 

“And with every throw, he said something encouraging to the kids. Even if it was a dropped pass, he’d say, ‘Hey, great route!’ Whatever it was, he found something positive in every single rep that gave that motivation and encouragement to the kids.”

 

While in Florida, Cousins, joined by Redskins running back Alfred Morris, also worked with Gruden’s brother, Super Bowl champion coach turned ESPN analyst Jon Gruden, who mentors young quarterbacks in the offseason.

 

And while in Atlanta visiting his wife’s family, he also tracked down high school receivers to throw to.

 

Also in February, he ramped up his training with Neurocore, which he had begun his senior season at Michigan State.

 

Neurocore was founded roughly 10 years ago to help children with attention-deficit disorders through “neurofeedback” rather than medication and expanded to applications for people with sleep and anxiety disorders as well as elite athletes. Its brain-training system starts with electroencephalograms to measure the electrical activity in the brain. If the data suggests the brain is running faster or slower than is ideal, conditioning exercises are developed to help train the brain to run at what Tim Royer, the company’s founder, describes as “a sweet spot.”

 

According to Royer, Cousins’s data revealed that his brain was running faster than it should, relying on adrenaline much of the time. Readings of his cardiovascular system and respiratory system suggested a similar, over-stimulated condition that Royer likened to “somebody running from a lion.”

 

“When you try to play sports at an elite level and the body and brain are doing that, it makes it difficult over time,” Royer said in a telephone interview.

 

So he devised a training system to help Cousins regulate that speed and outfitted the quarterback with home-based gear to practice the exercises on his own.

 

In one such exercise, Cousins attaches the EEG leads to his scalp and connects it to a computer that displays the speed of his brain, heart and breathing as if it’s the dashboard of a car. Then comes the “reward system” that affirms when he has relaxed or conditioned his brain to operate in the sweet spot.

 

As Royer explains it, Cousins puts a movie in the computer, and a program driven by the electrical activity in the brain will play the movie only when the reading confirms that his brain is running in the optimum range.

 

In the early going, Royer said, Cousins might have been able to watch “Iron Man” for 20 seconds of a one-minute exercise. With practice, that period of time — time in which the brain is operated at an optimal speed — increased to 30 seconds, then 40.

 

On Sunday against Miami, Cousins will find himself staring at Iron Men of a different sort — lined up across from a Dolphins defensive line that Hall of Fame quarterback Dan Fouts believes is the best in the NFL.

 

“It’s a great opportunity for Cousins and an unbelievable challenge with that Dolphins front four,” said Fouts, who will provide commentary for the CBS broadcast. “He has to start fast and have success right away.”

 

Pro Bowl left tackle Trent Williams will protect Cousins’s blind side. But rookie Brandon Scherff and second-year player Morgan Moses must fend off the heart of Miami’s pass rush, sack-specialists Ndamukong Suh and Cameron Wake.

 

Cousins has the quickest release of the Redskins’ trio of quarterbacks, which should help. He also understands protections, Dolphins Coach Joe Philbin noted, able to bark out last-second adjustments. And he knows there’s no need for high-risk heroics after he makes a mistake, whether interception, fumble or sack.

 

Noting the gifted receiving and running back corps around him, Cousins said this week: “It’s my job to get them the football, then let them go do the jaw-dropping stuff.”

 

If boos rain down from a restive fan base, Cousins has heard them before. If he falls short of his own expectation, he has been there.

 

This year, if the offseason lessons stick, Cousins will take a deep breath. He will acknowledge to himself that, yes, it is a huge game, but he won’t let the magnitude paralyze him or send him into panic mode.

 

He will breathe deeply, settle his mind and call the next play.

 

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