Ever Wonder What Drives Hardcore Sports Fandom?

Interesting neurological perspective to remember when you can't understand why your friend or loved one is yelling at the TV during the Olympics....and....

Go Team Canada!-JR

The Unique Neurology of the Sports Fan’s Brain

Brian J. Barth

"Sports fans aren’t typically in the mood for academic research in the minutes before a big game. But Paul Bernhardt, an aspiring young behavioral scientist at Georgia State University, was determined. Armed with a bag of sterile vials, Bernhardt inched through the crowd at Atlanta’s Omni arena, politely asking anyone decked out in either University of Georgia or Georgia Tech basketball garb—the teams that were set to battle that evening—for a bit of saliva.

The year was 1991. Fans of the Bulldogs and the Yellow Jackets, the state’s two most renowned collegiate sports institutions, had been hating each other’s guts since 1893, a rivalry affectionately known as COFH: Clean, Old-Fashioned Hate. (Yes, sports rivalries can have names; COFH is historically significant enough to have a 5,000-plus word entry in Wikipedia with 50 citations.) Bernhardt wasn’t there to celebrate a century of feuding, however; he was hoping to break new ground on the scientific understanding of such fandemonium—“highly identified” fans would be the proper psychology term—to explain why being a sports nut, bitter hatred and all, feels soooo gooooood.

The fact that athletes experience a tidal rush of testosterone, a hormone associated not just with male sexuality but with self-esteem, upon winning a big game was well established. But there was a hypothesis floating around among social psychologists at the time that fans ride a similar hormonal high. Bernhardt just needed a little spit, which offers a reliable approximation of the body’s biochemistry at any given moment, to find out."

FULL ARTICLE HERE:

Updating the Map: How the Brain will be Organized in the 21st Century

Human brain mapped in unprecedented detail

Nearly 100 previously unidentified brain areas revealed by examination of the cerebral cortex 

Researchers at the Washington University School of Medicine have compiled a massive study detailing an updated map of the human brain. The implications--both scientific and clinical--have great potential for accelerating our understanding of our "control center". -JR

• By Linda Geddes, Nature magazine on July 20, 2016

Think of a spinning globe and the patchwork of countries it depicts: such maps help us to understand where we are, and that nations differ from one another. Now, neuroscientists have charted an equivalent map of the brain’s outermost layer—the cerebral cortex—subdividing each hemisphere's mountain- and valley-like folds into 180 separate parcels.

Ninety-seven of these areas have never previously been described, despite showing clear differences in structure, function and connectivity from their neighbors. The new brain map is published today in Nature.

Each discrete area on the map contains cells with similar structure, function and connectivity. But these areas differ from each other, just as different countries have well-defined borders and unique cultures, says David Van Essen, a neuroscientist at Washington University Medical School in St Louis, Missouri, who supervised the study.

FULL ARTICLE HERE:

Neuroscientists have long sought to divide the brain into smaller pieces to better appreciate how it works as a whole. One of the best-known brain maps chops the cerebral cortex into 52 areas based on the arrangement of cells in the tissue. More recently, maps have been constructed using magnetic resonance imaging (MRI) techniques—such as functional MRI, which measures the flow of blood in response to different mental tasks.

Yet until now, most such maps have been based on a single type of measurement. That can provide an incomplete or even misleading view of the brain's inner workings, says Thomas Yeo, a computational neuroscientist at the National University of Singapore. The new map is based on multiple MRI measurements, which Yeo says “greatly increases confidence that they are producing the best in vivo estimates of cortical areas”.

Study: Auditory verbal hallucinations may be due to epilepsy

A study claims that epilepsy can cause auditory verbal hallucinations in some people.

According to a new study, epilepsy patients with damage to the left temporal cortex are at risk of experiencing complex, auditory verbal hallucinations (AVHs) – suggesting there is a neurological, as well as psychiatric, origin of these phenomena.

While AVHs are well documented in people with psychiatric conditions, reports from neurological patients are rare and have not been extensively studied.

Now, though, researchers from the Swiss Federal Institute of Technology in Lausanne and University Hospital Geneva have suggested epilepsy patients with prevalent language deficits, as well as damage to posterior and basal language areas in the left temporal cortex, sometimes hallucinate voices.

The study, which is published in this month’s edition of the journal Epilepsy Behaviour, comprised an examination of more than 350 people with epilepsy.

Nine of these subjects – all of whom had drug-resistant forms of the neurological condition – were found to experience AVHs, underlining the rarity of the phenomenon. They were studied by means of a semistructured interview, neuropsychological tests and multimodal imaging. The scientists used a combination of functional and structural neuroimaging data, and surface and intracranial EEG, to locate the damaged brain tissue from which their epilepsies originated.

They found the occurrence of AVHs in epilepsy patients was associated with the neurodevelopmental problems outlined above.

Subjects’ AVHs also followed common patterns – they heard single voices at a time, speaking in their native languages and of the same gender as the patient. The hallucinations also had consistent spatial features – most subjects reported they heard voices that seemed to come from external space, contralateral to the parts of their brain tissue that were damaged.

“We argue that the consistent location of AVHs in the contralesional external space, the prominence of associated language deficits and the prevalence of lesions to the posterior temporal language areas characterise AVHs of neurological origin, distinguishing them from those of psychiatric origin,” the report’s authors commented.

Read more here

Reasons why the NFL's new concussion rules aren't working

This article details issues with the NFL's new concussion rules and determines that the issues in football safety lie inherently within the sport.

In January, the NFL announced that, starting with the 2013 season, all games would be played with an independent neurologist on the sidelines to assist with the evaluation and treatment of head injuries. It looked like the league had done a good thing. It was establishing a new, unbiased procedure to promote player safety—an effort made all the better by the fact that it didn't involve placing the burden on the players themselves.

But the fundamental problem with football safety is football, and the league's new program is proving it.

Let's start with some background on the new rule. The players union had long demanded that the league require the presence of independent neurotrauma specialists who could evaluate players without interference or influence from any teams. To wit: On the same day the NFL made its announcement, the NFLPA cited a poll indicating that 78 percent of players didn't trust their own teams' medical staffs.

The league's decision to require these unaffiliated consultants was announced at a news conference held just before the NFLPA's annual Super Bowl week news conference. Also on that same day, NFLPA executive director DeMaurice Smith said the union had not been notified of the league's plan to make the change. And all this was at a time when the NFL was still preparing for a court battle against the concussion-related lawsuits involving thousands of former players who accused it of distorting information about the long-term effects of head trauma. Those suits have since been settled.

The two sides eventually smoothed over their differences, and soon the NFLPA was on board with the plan to have independent neurologists on the sidelines. An NFLPA spokesman told me the league and the union have since worked out an agreement by which they both have input in selecting those independent sideline consultants. Those consultants are picked from a list of experts in all 31 NFL cities. The consultants must not be affiliated with any NFL teams. TheNFL's concussion protocol also spells out that the each consultant must be "board certified or board eligible in neurology, neurological surgery, emergency medicine, physical medicine and rehabilitation or any primary care CAQ sports medicine certified physician and [have] documented competence and experience in the treatment of acute head injuries." Since last year, the protocol also mandates that an athletic trainer must be present up in the booth serve as a "spotter" for both teams by reviewing video and replay technology.

So what could go wrong? Why would there be any problems with diagnosing and handling concussions? Let's look at three situations involving three players in three games. Each one illustrates what the NFLPA spokesman told me was an "area of concern" for the players association after the first month of the new season.

The scenario: In Week 1, Jeremy Kerley of the Jets was concussed when he caught a pass over the middle toward the end of the first half against the Bucs. Kerley was hit by three different players, and Tampa's Mark Barron was flagged for unnecessary roughness:

Kerley was taken to the locker room and given the concussion tests, but he later returned to the game. The following day, he was held out of practice when he was evaluated again and diagnosed with concussion symptoms. The Jets had a short week heading into their next game, and Kerley missed their Week 2 game against the Patriots before returning to play in Week 3 against the Bills. 

The problem: Players don't always show concussion symptoms immediately.

The scenario: In Week 3, the Raiders' Terrelle Pryor took a helmet-to-helmet hit from the Broncos' Wesley Woodyard. Pryor had tucked the ball and made himself a runner, and the hit occurred inside the tackle box, so Woodyard was not penalized:Pryor lay on the turf momentarily but played two more snaps. After the Raiders turned the ball over on downs, he started showing symptoms during a sideline evaluation and was removed from the game. The next day, Pryor tweeted, "I don't remember much!" He returned to practice in a limited role later in the week and was ultimately held out of Sunday's game against the Redskins. The league's concussion protocol says that "if the occurrence of a concussion is unclear, or a player sustains a mechanism of injury ('big hit') that is reasonably expected to give rise to a concussion... the player shall be removed immediately from the field by Club medical personnel." The hit Pryor took certainly seems to fit that definition, and the NFLPA isinvestigating the Raiders' handling of Pryor to determine why he remained in the game. Per Mike Florio, the NFLPA does not want the typical sideline chaos to be used as an excuse for any failure to be properly vigilant in following the mandated protocols. The union spokesman told me that, depending on the outcome of its investigation, the NFLPA could consider filing a grievance.

The problem: A possible breakdown in protocol.

The scenario: In Week 2, Steelers running back Isaac Redman was injured on the opening kickoff after taking a helmet-to-helmet hit from the Bengals' Jayson DiManche. Redman was blocking on the play, and the collision happened away from the ball. Here, you can see Redman go down around the 30-yard line just as the action stops:

The problem: The tendency of players to not want to come out of the game.

These aren't rare, exotic scenarios. They're all things that come up normally in the course of play, like two-point conversions and onside kicks, and that's the issue. The new program is designed to keep concussed players from playing, yet that's not what's happening. These are problems that can't be solved via fiat and bureaucracy, and there's a simple inference to be drawn from that fact: you can't really fix football without turning it into another sport.

Read more, and see the videos referenced here

Children with sensory disorders overwhelmed with new school year

This article discusses how children with sensory processing disorders can be overwhelmed with the changes from a new school year.

Transitioning from summer to a new school year is hard for any kid, but it is particularly difficult for children who have trouble processing new sensations, according to an expert on what is known as "sensory processing disorder."

Sensory processing disorder is a neurological problem that affects behavior and learning. For kids with this disorder, too much sensory overload or the wrong kind of stimulation can lead to problems with attention, coordination and impulsiveness as the child tries to either increase or decrease the sensations they are experiencing.

Varleisha Gibbs, an assistant professor of occupational therapy at University of the Sciences in Philadelphia, explained that the transition back to school disrupts the daily routines that these children have established during the summer. She noted, however, planning ahead can help ease the stress of this transition.

"Students with sensory processing disorders typically struggle with adapting to change," Gibbs said in a university news release. "A new school year brings an abundance of changes, including new teachers and classmates, schedules and routines, classrooms and settings, as well as new demands and expectations in the classroom."

To ease the transition to a new school year for children with sensory processing disorders, Gibbs recommended that children, teachers and parents or caregivers take the following steps:

• Plan a visit. Before the first day of class, arrange a visit to the school to familiarize the child with the school setting and the teacher. If possible, take photos of the surroundings to help the child acclimate to the environment ahead of time.
• Be proactive. Reach out to the school early to inform administrators about the child's therapy schedule. A child's private occupational therapy sessions should be coordinated with any therapy offered at school so they do not overlap.
• Pack a sensory kit. Certain fidget devices may help keep children calm and focused during a stressful transition time. These objects include stress balls, seat cushions, gum and music with headphones. Teachers can also provide a variety of seating options in the classrooms, including beanbag chairs and therapy balls.
• Be open. Because not all children with sensory processing disorders are placed in special education, communicating a child's needs to teachers and school administrators can help ensure they are able to benefit from their calming strategies. For example, these children may need to chew gum in class or listen to headphones between classes.
• Shop early. Purchase backpacks and school clothes well in advance so children can try them on and identify any items that are bothersome or uncomfortable. Be sure to remove all tags, wash the clothes and find underwear that can alleviate any irritability from the fabric rubbing against the skin.
• Set an example. When parents are calm and collected, it's easier for children to feel the same way about going back to school.

Read more here

All About Obama's BRAIN Initiative

This article discusses the new BRAIN Initiative, , and how the initiative's bureaucracy is structured at the NIH.

Today at the White House, President Barack Obama unveiled the "BRAIN" Initiative -- a bold new research effort to revolutionize our understanding of the human mind and uncover new ways to treat, prevent, and cure brain disorders like Alzheimer's, schizophrenia, autism, epilepsy, and traumatic brain injury.

The NIH Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative is part of a new Presidential focus aimed at revolutionizing our understanding of the human brain. By accelerating the development and application of innovative technologies, researchers will be able to produce a revolutionary new dynamic picture of the brain that, for the first time, shows how individual cells and complex neural circuits interact in both time and space. Long desired by researchers seeking new ways to treat, cure, and even prevent brain disorders, this picture will fill major gaps in our current knowledge and provide unprecedented opportunities for exploring exactly how the brain enables the human body to record, process, utilize, store, and retrieve vast quantities of information, all at the speed of thought.

Why is the NIH BRAIN Initiative needed?

With nearly 100 billion neurons and 100 trillion connections, the human brain remains one of the greatest mysteries in science and one of the greatest challenges in medicine. Neurological and psychiatric disorders, such as Alzheimer's disease, Parkinson's disease, autism, epilepsy, schizophrenia, depression, and traumatic brain injury, exact a tremendous toll on individuals, families, and society. Despite the many advances in neuroscience in recent years, the underlying causes of most of neurological and psychiatric conditions remain largely unknown, due to the vast complexity of the human brain. If we are ever to develop effective ways of helping people suffering from these devastating conditions, researchers will first need a more complete arsenal of tools and information for understanding how the brain functions both in health and disease.

Why is now the right time for the NIH BRAIN Initiative?

In the last decade alone, scientists have made a number of landmark discoveries that now create the opportunity to unlock the mysteries of the brain. We have witnessed the sequencing of the human genome, the development of new tools for mapping neuronal connections, the increasing resolution of imaging technologies, and the explosion of nanoscience. These discoveries have yielded unprecedented opportunities for integration across scientific fields. For instance, by combining advanced genetic and optical techniques, scientists can now use pulses of light in animal models to determine how specific cell activities within the brain affect behavior. What's more, through the integration of neuroscience and physics, researchers can now use high-resolution imaging technologies to observe how the brain is structurally and functionally connected in living humans.

While these technological innovations have contributed substantially to our expanding knowledge of the brain, significant breakthroughs in how we treat neurological and psychiatric disease will require a new generation of tools to enable researchers to record signals from brain cells in much greater numbers and at even faster speeds. This cannot currently be achieved, but great promise for developing such technologies lies at the intersections of nanoscience, imaging, engineering, informatics, and other rapidly emerging fields of science.

How will the NIH BRAIN Initiative work?

Given the ambitious scope of this pioneering endeavor, it is vital that planning for the NIH BRAIN Initiative be informed by a wide range of expertise and experience. Therefore, NIH is establishing a high level working group of the Advisory Committee to the NIH Director (ACD) to help shape this new initiative. This working group, co-chaired by Dr. Cornelia "Cori" Bargmann (The Rockefeller University) and Dr. William Newsome (Stanford University), is being asked to articulate the scientific goals of the BRAIN initiative and develop a multi-year scientific plan for achieving these goals, including timetables, milestones, and cost estimates.

As part of this planning process, input will be sought broadly from the scientific community, patient advocates, and the general public. The working group will be asked to produce an interim report by fall 2013 that will contain specific recommendations on high priority investments for Fiscal Year (FY) 2014. The final report will be delivered to the NIH Director in June 2014.

How will the NIH BRAIN Initiative be supported?

In total, NIH intends to allocate $40 million in FY14. Given the cross-cutting nature of this project, the NIH Blueprint for Neuroscience Research -- an initiative spanning 14 NIH Institutes and Centers -- will be the leading NIH contributor to its implementation in FY14. Of course, a goal this audacious will require ideas from the best scientists and engineers across many diverse disciplines and sectors. Therefore, NIH is working in close collaboration with other government agencies, including the Defense Advanced Research Projects Agency (DARPA) and the National Science Foundation (NSF). Strong interest has also been expressed by several private foundations, including the Howard Hughes Medical Institute, the Allen Institute for Brain Science, and The Kavli Foundation, and the Salk Institute for Biological Studies. Private industries have also expressed a high level of interest in participation in this groundbreaking initiative.

Read more here

10 Important Things to Know About Epilepsy

This article discusses 10 important aspects of epilepsy that are important to know.

As a neurologist with specialty training in this field, I have been devoted to helping the plight of individuals with epilepsy find better treatments, advocate for better management and to illuminate some of the terrible misinformation that is spread about this condition.  In March 2012, the Institute of Medicine took up the topic of epilepsy and how it is handled in the United States (U.S.).  As a member of that panel, I was able to hear important testimony from public, private and government institutions about how epilepsy is managed in the U.S. and some of the major problems that affect its care and the people who have it.  The following are several important items that may help to clarify one’s knowledge about epilepsy and show that this is truly a common condition.

1. Epilepsy is the condition of having repeated, unprovoked seizures, whereas a seizure is anabnormal electrical discharge of the brain which then results in an individual losing consciousness or having a change in their neurological function. There are several types of seizures and not all are dramatic in their presentation, though they are often depicted in movies and television as a convulsion.  Some seizures manifest by one simply losing focus, but to a bystander, it may seem as daydreaming, wandering or a tremor.  Therefore, not all seizures are very dramatic in their presentations.

2. Epilepsy is very common.  According to the CDC, one in 26 people in the U.S. will develop epilepsy at some point in their lifetime.  If you think about it, that means two persons on every bus or two people in every subway car will have epilepsy.  There are 150,000 new cases of epilepsy diagnosed in the United States annually; 2.2 million people in the U.S. and more than65 million people worldwide have the condition.

3. Children and older adults are the fastest-growing segments of the population with new cases of epilepsy; however, the reason that they have epilepsy varies dramatically.  In children, we see an overabundance of genetic and infectious causes of seizures. For older adults, stroke and Alzheimer’s disease seem to be the common cause of epilepsy and seizures in this population.

4. There are numerous causes of seizures and epilepsy.  Stroke, head trauma and tumors are common causes of seizures in the U.S., yet the number one cause of seizures outside of the U.S. is an infection which is completely preventable by simply washing one’s hands. Neurocysticercosis– caused by the Taenia solium tapeworm– is one of the most common causes of epilepsy in the world and an increasing cause of seizures in the U.S.   Other preventable causes of epilepsy are head trauma from car accidents, violence or the consequences of military intervention.

5. Epilepsy is not a benign condition and can result in death. The number of people with epilepsy who die of sudden unexpected death in epilepsy (SUDEP) varies from one of every10,000 newly diagnosed to nine of every 1,000 candidates for epilepsy surgery.

6. For many people with epilepsy, seizures can be effectively reduced or eliminated by medication, surgery, devices and dietary or other therapies; however, referral to epilepsy centers for surgery can take 15 years or more.  In the Latino population, there is a considerable misinformation and lack of information; oftentimes that lack of access does not translate into meaningful care. There are 26 different drugs approved for treatment in the U.S. for epilepsy.  Moreover there is a pacemaker like device known as the vagus nerve stimulator, a diet- ketogenic or modified Atkins, and numerous surgeries.  These effective treatments are available for many types of epilepsies; however, access and referrals to these treatments fall short.

7. There is considerable stigma associated with epilepsy that sometimes overwhelms the condition itself. The word” epilepsy” is considered stigmatizing in its own right.  The long history of epilepsy is full of examples of discrimination and secrecy due to misinformation and lack of understanding by the general public.  This stigma can have a detrimental effect on people with epilepsy and continued and sustained efforts are needed to raise public awareness and convey what epilepsy is and what it is not, as well as the basic message that this is an exceedingly common condition.

8. There are significant quality of life issues associated with epilepsy and one of the most significant is driving.  Every state in the U.S. has a law that dictates whether someone with epilepsy can or cannot drive and the length of time they need to be seizure free for them to drive.  In six of these states, the law has mandatory reporting by the physician of all patients with epilepsy to a medical board.  Individuals need to be aware of these laws as there are, in some cases, criminal consequences for both physician and patients for their lack of awareness associated with it.

9. Epilepsy is more than just seizures as it often has other accompanying conditions associated with it.  Oftentimes, poor memory, mood issues, depression and anxiety walk hand in hand with issues associated with epilepsy and need to be managed and thought of when caring for the individual with epilepsy.

10. Sadly, many health professionals need to be better informed about epilepsy.  Only 20 percent of U.S. medical schools require training in neurology…and epilepsy and how to treat it.  Improvements in epilepsy care can only be made if the quality and quantity of education about epilepsy for health care professionals are improved dramatically at undergraduate and graduate levels of lifelong learning processes.  In addition, more educational efforts for patients with epilepsy and their families is needed.

It is only with a concerted effort to illuminate epilepsy and talk about the condition that one will hopefully empower individuals with knowledge so as to improve quality of life.

Read more here

Link Between Childhood Trauma and Neurological Changes

Recently, a link has been discovered between trauma during early childhood and neurological changes, a link that has been previously difficult to find.

It is well known that violent adults often have a history of childhood psychological trauma. Some of these individuals exhibit very real, physical alterations in a part of the brain called the orbitofrontal cortex. Yet a direct link between such early trauma and neurological changes has been difficult to find, until now.

Publishing in the January 15 edition of Translational Psychiatry, EPFL Professor Carmen Sandi and team demonstrate for the first time a correlation between psychological trauma in pre-adolescent rats and neurological changes similar to those found in violent humans.

"This research shows that people exposed to trauma in childhood don't only suffer psychologically, but their brain also gets altered," explains Sandi, Head of EPFL's Laboratory of Behavioral Genetics, Director of the Brain Mind Institute, and a member of the National Centers for Competence in Research SYNAPSY. "This adds an additional dimension to the consequences of abuse, and obviously has scientific, therapeutic and social implications."

The researchers were able to unravel the biological foundations of violence using a cohort of male rats exposed to psychologically stressful situations when young. After observing that these experiences led to aggressive behavior when the rats reached adulthood, they examined what was happening in the animals' brains to see if the traumatic period had left a lasting mark.

"In a challenging social situation, the orbitofrontal cortex of a healthy individual is activated in order to inhibit aggressive impulses and to maintain normal interactions," explains Sandi. "But in the rats we studied, we noticed that there was very little activation of the orbitofrontal cortex. This, in turn, reduces their ability to moderate their negative impulses. This reduced activation is accompanied by the overactivation of the amygdala, a region of the brain that's involved in emotional reactions." Other researchers who have studied the brains of violent human individuals have observed the same deficit in orbitofrontal activation and the same corresponding reduced inhibition of aggressive impulses. "It's remarkable; we didn't expect to find this level of similarity," says Sandi.

The scientists also measured changes in the expression of certain genes in the brain. They focused on genes known to be involved in aggressive behavior for which there are polymorphisms (genetic variants) that predispose carriers to an aggressive attitude, and they looked at whether the psychological stress experienced by the rats caused a modification in the expression of these genes. "We found that the level of MAOA gene expression increased in the prefrontal cortex," says Sandi. This alteration was linked to an epigenetic change; in other words, the traumatic experience ended up causing a long-term modification of this gene's expression.

Finally, the researchers tested the efficacy of an MAOA gene inhibitor, in this case an anti-depressant, to see if it could reverse the rise in aggression induced by juvenile stress, which it did. Going forward, the team will explore treatments for reversing physical changes in the brain, and above all, attempt to shed light on whether some people are more vulnerable to being effected by trauma based on their genetic makeup.

"This research could also reveal the possible ability of antidepressants -- an ability that's increasingly being suspected -- to renew cerebral plasticity," says Sandi.

Read more here

Study shows why resolutions about physical activity are difficult to keep

An interesting study shows a neurological basis of why New Years Resolutions regarding physical activity are difficult to keep.

Physical inactivity is a major public health problem that has both social and neurobiological causes. According to the results of an Ipsos survey published on December 31, the French have put "taking up a sport" at the top of their list of good resolutions for 2013. However, Francis Chaouloff, research director at Inserm's NeuroCentre Magendie (Inserm Joint Research Unit 862, Université Bordeaux Ségalen), Sarah Dubreucq, a PhD student and François Georges, a CNRS research leader at the Interdisciplinary Institute for Neuroscience (CNRS/Université Bordeaux Ségalen) have just discovered the key role played by a protein, the CB1 cannabinoid receptor, during physical exercise. In their mouse studies, the researchers demonstrated that the location of this receptor in a part of the brain associated with motivation and reward systems controls the time for which an individual will carry out voluntary physical exercise. These results were published in the journal Biological Psychiatry.

The collective appraisal conducted by Inserm in 2008 highlighted the many preventive health benefits of regular physical activity. Such activity is limited, however, by our lifestyle in today's industrial society. While varying degrees of physical inactivity may be partly explained by social causes, they are also rooted in biology.

"The inability to experience pleasure during physical activity, which is often quoted as one explanation why people partially or completely drop out of physical exercise programmes, is a clear sign that the biology of the nervous system is involved," explains Francis Chaouloff.

But how exactly? The neurobiological mechanisms underlying physical inactivity had yet to be identified.

Francis Chaouloff (Giovanni Marsicano's team at the NeuroCentre Magendie; Inserm joint research unit, Université Bordeaux Ségalen) and his team have now begun to decipher these mechanisms. Their work clearly identifies the endogenous cannabinoid (or endocannabinoid) system as playing a decisive role, in particular one of its brain receptors. This is by no means the first time that data has pointed to interactions between the endocannabinoid system, which is the target of delta9-tetrahydrocannabinol (the active ingredient of cannabis), and physical exercise. It was discovered ten years ago that physical exercise activated the endocannabinoid system in trained sportsmen, but its exact role remained a mystery for many years. Three years ago, the same research team in Bordeaux observed that when given the opportunity to use a running wheel, mutant mice lacking the CB1 cannabinoid receptor, which is the principal receptor of the endocannabinoid system in the brain, ran for a shorter time and over shorter distances than healthy mice. The research published in Biological Psychiatry this month seeks to understand how, where and why the lack of CB1 receptor reduces voluntary exercise performance (by 20 to 30%) in mice allowed access to a running wheel three hours per day.

The researchers used various lines of mutant mice for the CB1 receptor, together with pharmacological tools. They began by demonstrating that the CB1 receptor controlling running performance is located at the GABAergic nerve endings. They went on to show that the receptor is located in the ventral tegmental area of the brain (see diagram below), which is an area involved in motivational processes relating to reward, whether the reward is natural (food, sex) or associated with the consumption of psychoactive substances.

VTA: Ventral tegmental area/NAcc: nucleus accumbens/PFC: prefrontal cortex/DA: dopamine

Based on the results of this study and earlier work, the Bordeaux team suggests the following neurobiological explanation: at the beginning and for the duration of physical exercise, the CB1 receptor is constantly simulated by the endocannabinoids, lipid molecules that naturally activate this receptor in response to pleasant stimuli (rewards) and unpleasant stimuli (stress). Endocannabinoid stimulation of the CB1 receptor during physical exercise inhibits the release of GABA, an inhibitory neurotransmitter that controls the activity of the dopamine neurons associated with the motivation and reward processes. This stimulation of the CB1 receptor "inhibits inhibition," in other words, it activates the dopaminergic neurons in the ventral tegmental area. The CB1 receptor must therefore be stimulated before the exercise can go on for longer and the body must receive the necessary motivation.

Conversely, without these CB1 receptors, the "GABAergic brake" continues to act on the dopaminergic neurons in the ventral tegmental area, leading to the reduced performance levels observed above.

It is already known that CB1 receptors play a regulatory role in the motivation to consume rewards, whether natural or not. What is original about this research is that it shows that physical exercise can be added to the array of natural rewards regulated by the endocannabinoid system. "If confirmed, this motivational hypothesis would imply that the role played by the CB1 receptor has more to do with 'staying power' in the exercise than with actual physical performance levels" explain the researchers.

This work reveals that the endocannabinoid system plays a major role in physical exercise performance through its impact on motivational processes. It thus opens up new avenues of research into the mediators of pleasure -- and even addiction -- associated with regular physical exercise. "After endorphins, we now need to consider endocannabinoids as another potential mediator of the positive effects that physical exercise has on our mood," the researchers conclude.

Read more here

Bálint's Syndrome: Her Vision Is 20/20, but She Can't Make Sense of What She Sees

This article discusses two cases of Bálint's Syndrome where a person has perfect vision, but they can't make sense of what they see.

It was a quiet Thursday afternoon when AS, a 68-year-old woman from a suburb of Chicago, awakened from a nap to the realization that something was terribly wrong.

Thus begins a Loyola University Medical Center paper on a rare and baffling neurological disorder called Balint's syndrome, which badly impairs a patient's ability to make sense of what he or she sees.

The article describes, in novelistic detail, the difficult adjustments two patients have had to make in their lives. The article is published in the Sept. 11, 2012, issue of Neurology®, the medical journal of the American Academy of Neurology. The paper was written by Jose Biller, MD, Murray Flaster, MD, and first author Jason Cuomo. Biller and Flaster are neurologists and Cuomo is a fourth-year medical student at Loyola University Chicago Stritch School of Medicine.

The authors note that amid the rigors of clinical practice, physicians can content themselves with understanding the phenomenon of disease to the exclusion of understanding the patient's experience. Their article "is an attempt to inform both our clinical and subjective understandings of Balint's syndrome through narratives of two patients suffering from this rare and unique neurological disorder."

Balint's syndrome is named after Austro-Hungarian neurologist Rezső Bálint, who first described it. The condition is caused by one or more strokes in certain regions of the brain. It causes three deficits: Difficulty initiating voluntary eye movements (such as following a physician's finger); inaccurate arm pointing (a patient can see an object, but is unable to pick it up); and constriction of the visual field (ask a patient to look at a parking lot, and all she sees is a lamp post or a car.)

When AS woke from her nap, she couldn't find where doors or cabinets were. She couldn't name or distinguish familiar household objects. She couldn't read a book or the numbers on her telephone. She couldn't see where the bedroom wall ended and the door began. Yet when she saw an ophthalmologist, her vision with glasses was 20/20. She and her husband left the ophthalmologist's office with a referral to see a neurologist, and "wondering what sort of ailment could rob her of her ability to see the bathroom sink, while leaving her with what we typically think of as perfect vision."

The second patient, JD, was a robust, hard-working owner of a trucking business. While driving to his son's house for Thanksgiving, he began to swerve. And at Thanksgiving dinner, he held the spoon upside down. He then experienced left-sided weakness and facial drooping, before losing consciousness. Doctors believe he had suffered a massive stroke, followed by a series of mini strokes.

AD has made many adjustments. For example, while getting ready in the morning, she must touch the sink at all times to remain oriented. While showering, she has to keep her hand on the shower bar. Before brushing her teeth, she puts the toothpaste directly in her mouth, then moves the toothbrush by trial and error to meet it. She has stopped driving. And because she can no longer read, she listens to audio books.

JD has suffered depression, a first for him. "He never once cried before," his wife said, "but now he cries often."

AD said she would not wish Balint's syndrome on anyone, "because not only is this a life-change, it's a mind change."

AD hopes her story will motivate physicians to seek better treatments and therapies.

Read more here

Q and A on West Nile Virus including Neurological Complications

This article discusses common questions and answers on West Nile Virus due to the rise in cases recently. This is important due to the neurological complications in serious cases of West Nile Virus.

The outbreak of West Nile virus this year has spread to nearly every state and is shaping up to be the largest one on record since the first human cases were reported in the United States in 1999.

But for all the fear and concerns in some parts of the country, health officials say the reality is that most people who become infected will not have any symptoms, and of those who do, only a fraction will develop severe illness. To find out more about the disease and the factors fueling the current outbreak, we spoke with Dr. Erin Staples, a medical epidemiologist at the Centers for Disease Control and Prevention.

Q.

Is it true that many of the symptoms of West Nile are easily overlooked? How many people probably have it and don’t know it?

A.

From studies we know that only about one in every five people who get infected with West Nile will actually develop symptoms. The most common ones are fever, headaches, body ache, joint pain, vomiting, diarrhea and rash. A lot of people who develop symptoms usually just wait it out at home. Or they’ll go to a medical doctor and end up recovering from their illness and feeling much better within several weeks. Sometimes, people will complain of fatigue or report feeling not quite themselves for several months.

Q.

How does a person know if he or she has a more serious form of the illness? What symptoms should prompt you to see a doctor?

A.

Symptoms of severe neurological disease due to West Nile virus infection can include high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, vision loss, numbness and paralysis. These symptoms may last several weeks, and neurological effects may be permanent.

Less than 1 percent of people who are infected will develop such symptoms of more serious neurological illness, like encephalitis or meningitis, which is inflammation of the brain or surrounding tissue.

But people with the serious neurological symptoms are more likely to seek treatment and find out that they have it. With the serious neurological symptoms, about 10 percent of people will die as a result.

Q.

How do you find out if you have West Nile? Is there a test?

A.

People who have symptoms that concern them should see a health care provider. If they think they have West Nile, they can have their blood tested for the presence of antibodies or, in more severe cases that affect the central nervous system, a doctor can take samples of the cerebrospinal fluid that surrounds the brain and spinal cord.

Usually people are hospitalized if they have more serious symptoms.

Q.

Are certain groups at higher risk?

A.

Anyone who is outdoors during times when mosquitoes are active is at a higher risk — so that means people who go outside at dusk and dawn who haven’t done anything to prevent getting bitten, like using repellents or wearing pants and long sleeves.

We do know that there are certain groups that are also at risk of having more severe disease. The groups we’ve identified include people over the age of 50, and people who have medical conditions like cancer, diabetes, hypertension, kidney disease and organ transplants.

We know this from data we’ve collected from state health departments. For a lot of these high-risk groups, it probably deals with their ability to fight infection. You may have people with cancer, for example, who are receiving drugs that inhibit their immune cells. Someone with diabetes may not be able to fight the infection as well as an otherwise healthy person.

With people over the age of 50, it’s most likely that as you age your immune cells are not as robust. We do have a larger proportion of people with encephalitis in the older age group. But anybody who’s out there and not using measures to prevent mosquito bites could be at risk for getting West Nile.

Q.

How widespread is the outbreak, and how are you keeping track of it?

A.

The C.D.C. reports numbers once a week. We take a snapshot, and the states know to report to us by Tuesday morning at 3 a.m.So as of Tuesday we knew that there were 1,118 cases of West Nile being reported from throughout the United States, and that included 41 deaths.

Right now, we have received reports of West Nile virus infections or activity in people, birds or mosquitoes in 47 states. It’s pretty much widespread in the continental United States. The states that have not reported any are Hawaii and Alaska, which have never reported any West Nile activity, and then Vermont. Vermont has previously reported cases, just none so far this year.

Q.

What is the regional breakdown of cases? Are most in Texas?

A.

Almost half of our cases have been reported in Texas, so that is the most affected region at this point. But about 75 percent of our cases have been reported from five states. The first is Texas, the next is Mississippi, Louisiana, then South Dakota and Oklahoma. The central region of the United States is the main area reporting the most cases, but most states are being affected, just to varying degrees.

Q.

How does this compare with other West Nile outbreaks?

A.

We definitely have received reports from state health departments of earlier and greater West Nile activity, particularly in the central states. It’s more than we’ve seen in recent years, and we’re not quite sure why. Essentially there are several factors that play a role, including the weather, the number and types of mosquitoes that spread the virus, birds that also spread the virus, what people are doing to prevent it, and whether there’s community-based spraying. All of those things may determine the size and location of an outbreak. So it makes it very difficult to predict from year to year where we may see West Nile virus outbreaks, because these things change.

Q.

Why is this outbreak so severe? Is it the biggest?

A.

There is some thought that the unusual mild winter we had, the early spring and the hot summer, may have fostered some conditions that are favorable to breeding mosquitoes that spread West Nile virus.

What we can say right now is this is the biggest outbreak. If we look at the number of cases reported to the C.D.C. over the last 10 years, through the third week of August, we’ve had an average of 390 West Nile cases reported each year, and that ranged from a low last year of 77 cases to a high in 2004 of 832 cases.

So now, having more than 1,000 cases reported to us this year through the third week of August, we’re up from what we’ve traditionally seen in the past. However, we don’t know how this is going to translate in the end of the year, for instance, if there’s going to be significant changes. Let’s say New York goes into an early frost this year. That could truncate transmissions.

Q.

What steps can people take to protect themselves?

A.

Use insect repellents when you go outdoors. Wear long sleeves and pants to prevent mosquito bites at dusk and dawn. Install or repair screens or windows to prevent mosquitoes from getting inside your home. Empty any containers of standing water around your home — things like flower pots, kiddie pools, buckets and sometimes even gutters, which can have standing water in them.

Read more here