Claudia M. Gold When Frank was a young boy, and he committed some typical toddler transgression such as having a meltdown when it was time to leave the playground, his father would slap him across the face, hurting and humiliating him in a very public way. When I spoke with Frank over 20 years later, in the context of helping him with his own son Leo's frequent tantrums in my behavioral pediatrics practice, he did not describe this experience as "trauma." Rather, he described it in a very matter-of-fact tone. But when we explored in detail his response to his son's tantrums, we discovered that, flooded by the stress of his own memories, Frank in a sense would shut down. Normally a thoughtful and empathic person, he simply told Leo to "cut it out." As we spoke he recognized how he was emotionally absent during these moments, which were increasing in frequency. It seemed as if Leo was testing Frank, perhaps looking for a more appropriate response that would help him manage this normal behavior. Once this process was brought in to awareness, Frank was able to be present with Leo- to tolerate his tantrums and understand them from his 2-year-old perspective. Soon the frequency and intensity of the tantrums returned to a level typical for Leo's developmental stage. Frank, greatly relieved, once again found himself enjoying his son. The upcoming Boston conference; Psychological Trauma: Neuroscience, Attachment, and Therapeutic Interventions, promises to offer insight in to the developmental neuroscience behind this story. What Frank experienced as a young child might be termed "quotidian" or "everyday" trauma. It was not watching a relative get shot, or having his house washed away in an avalanche. It was a daily mismatch with his father- he was looking for reassurance and containment and instead got a slap across the face. It was what leading researcher Ed Tronick would term "unrepaired mismatch." Frank, in a way that is extremely common- termed "intergenerational transmission of trauma"- was then repeating this cycle with his own child. When this dynamic was brought in to awareness, he was able to "repair the mismatch," setting his relationship with his own son on a healthier path. ©2014 Boston Globe Media Partners, LLC

Keyword: Stress; Development of the Brain
Link ID: 19656 - Posted: 05.26.2014

By JANE E. BRODY Bowels, especially those that don’t function properly, are not a popular topic of conversation. Most of the 1.4 million Americans with inflammatory bowel disease — Crohn’s disease or ulcerative colitis — suffer in silence. But scientists are making exciting progress in understanding the causes of these conditions and in developing more effective therapies. And affected individuals have begun to speak up to let others know that they are not alone. Abby Searfoss, 21, who just graduated from the University of Connecticut, shared her story not in a support group, but online. She was a high school senior in Ridgefield, Conn., when she became ill. After she researched her symptoms on the Internet, she realized that, like her father, she had developed Crohn’s disease. Her father had been very ill, losing 40 pounds, spending weeks in the hospital and undergoing surgery. Soon after Ms. Searfoss’s own diagnosis, her two younger sisters learned that they, too, had the condition. In Crohn’s disease, the immune system attacks cells in the digestive tract, most often the end of the small intestine and first part of the colon, or large intestine. Sufferers may experience bouts of abdominal pain, cramps and diarrhea, often accompanied by poor appetite, fatigue and anxiety. “You don’t go anywhere without checking where the bathroom is and how many stalls it has,” said Dr. R. Balfour Sartor, a gastroenterologist at the University of North Carolina School of Medicine and a patient himself. “The fear of incontinence is huge.” Neither Crohn’s disease nor its less common relative ulcerative colitis, which affects only the large intestine, is curable (except, in the latter instance, by removing the entire colon). But research into what predisposes people to develop these conditions has resulted in more effective treatments and has suggested new ways to prevent the diseases in people who are genetically susceptible. © 2014 The New York Times Company

Keyword: Stress; Neuroimmunology
Link ID: 19655 - Posted: 05.26.2014

By Neuroskeptic Nothing that modern neuroscience can detect, anyway. This is the message of a provocative article by Pace University psychologist Terence Hines, just published in Brain and Cognition: Neuromythology of Einstein’s brain As Hines notes, the story of how Einstein’s brain was preserved is well known. When the physicist died in 1955, his wish was to be cremated, but the pathologist who performed the autopsy decided to save his brain for science. Einstein’s son Hans later gave his blessing to this fait accompli. Samples and photos of the brain were then made available to neuroscientists around the world, who hoped to discover the secret of the great man’s genius. Many have claimed to have found it. But Hines isn’t convinced. Some researchers, for instance, have used microscopy to examine Einstein’s brain tissue on a histological (cellular) level. Most famous amongst these studies is Diamond et al, who in 1985 reported that Einstein’s brain had a significantly higher proportion of glial cells than those of matched, normal control brains. However, Hines points out that this ‘finding’ may have been a textbook example of the multiple-comparisons problem: Diamond et al. (1985) reported four different t-tests, each comparing Einstein’s brain to the brains of the controls. Only one of the four tests performed was significant at the .05 level. Although only the results of the neuron to glial cell ratios were reported by Diamond et al. (1985), the paper makes it clear that at least six other dependent measures were examined: (1) number of neurons, (2) total number of glial cells, (3) number of astrocytes, (4) number of oligodendrocytes, (5) neuron to astrocyte ratio and (6) neuron to oligodendrocyte ratio. Thus a total of seven different dependent measures were examined in four different brain areas for a total of 28 comparisons… one p less than 0.05 result out of 28 is not surprising. Other histological studies followed from other researchers, but Hines says that they do not present a coherent picture of clear differences:

Keyword: Intelligence; Glia
Link ID: 19654 - Posted: 05.26.2014

By DOUGLAS QUENQUA It’s easy to think of fruit flies as tiny robots that simply respond reflexively to their environment. But just like humans, they take time to collect information and to deliberate when faced with a difficult choice, according to a new study. The findings, published in the journal Science, could help researchers study cognitive development and defects in humans. Scientists have long been fascinated by decision-making, said an author of the study, Dr. Gero Miesenböck, a neuroscientist at the University of Oxford. “Going back to the 19th century, psychologists have measured how long it takes humans to make up their minds,” he said. “Usually if you give people a hard perceptual choice, they take longer, because the brain needs to integrate information until it has enough to make a decision. “This is the first time in an animal as low as a fruit fly we have been able to show that similar processes occur.” To study how flies make up their minds, Oxford researchers placed the animals in bifurcated chambers filled on both sides with an odor they had been taught to avoid. When the odor was clearly more potent on one side of the chamber than the other, the flies were quick to choose which chamber to inhabit (and nearly always chose the less odorous one). But when the difference between chambers was subtle, the flies took longer to make a decision, and were more apt to make the wrong choice. “We were surprised,” Dr. Miesenböck said. “The original thought was that the flies would just act impulsively, they won’t take time to deliberate. We found that’s not true.” The process so closely mimics decision-making in humans, the researchers said, that the same mathematical models used to describe the actions of deliberating people can be used to predict a fly’s behavior. © 2014 The New York Times Company

Keyword: Attention
Link ID: 19653 - Posted: 05.24.2014

Jasmin Fox-Skelly Scientists have found a way to beat back the hands of time and fight the ravages of old age, at least in mice. A new study finds that mice bred without a specific pain sensor, or receptor, live longer and are less likely to develop diseases such as diabetes in old age. What’s more, exposure to a molecule found in chili peppers and other spicy foods may confer the same benefits as losing this pain receptor—meaning that humans could potentially benefit, too. When you touch something hot or get a nasty paper cut, pain receptors in your skin are activated, causing neurons to relay a message to your brain: “Ouch!” Although pain protects your body from damage, it also causes harm. People who experience chronic pain, for example, are more likely to have shorter lifespans, but the reason for this has remained unclear. To investigate further, researchers from the University of California (UC), Berkeley, bred mice without a pain receptor called TRPV1. Found in the skin, nerves, and joints, it’s known to be activated by the spicy compound found in chili peppers, known as capsaicin. (When you feel like your mouth is burning after eating a jalapeño, that’s TRPV1 at work.) Surprisingly, the mice without TRPV1 lived on average 14% longer than their normal counterparts, the team reports today in Cell. (Meanwhile, calorie restriction—another popular way of lengthening mouse lifespans—can make them live up to 40% longer.) When the TRPV1-less mice got old, they still showed signs of fast, youthful metabolisms. Their bodies continued to quickly clear sugar from the blood—a trait called glucose tolerance that usually declines with age—and they burned more calories during exercise than regular elderly mice. © 2014 American Association for the Advancement of Science

Keyword: Pain & Touch
Link ID: 19652 - Posted: 05.24.2014

By BRUCE WEBER Dr. Gerald M. Edelman at Rockefeller University in 1972, in front of a gamma globulin model. Credit Don Hogan Charles/The New York Times Dr. Gerald M. Edelman, who shared a 1972 Nobel Prize for a breakthrough in immunology and went on to contribute key findings in neuroscience and other fields, becoming a leading if contentious theorist on the workings of the brain, died on Saturday at his home in the La Jolla section of San Diego. He was 84. The precise cause was uncertain, but Dr. Edelman had Parkinson’s disease and prostate cancer, his son David said. Dr. Edelman was known as a problem solver, a man of relentless intellectual energy who asked big questions and attacked big projects. What interested him, he said, were “dark areas” where mystery reigned. “Anybody in science, if there are enough anybodies, can find the answer,” he said in a 1994 interview in The New Yorker. “It’s an Easter egg hunt. That isn’t the idea. The idea is: Can you ask the question in such a way as to facilitate the answer? And I think the great scientists do that.” His Nobel Prize in Physiology or Medicine came in 1972 after more than a decade of work on the process by which antibodies, the foot soldiers of the immune system, mount their defense against infection and disease. He shared the prize with Rodney R. Porter, a British scientist who worked independent of Dr. Edelman. The Nobel committee cited them for their separate approaches in deciphering the chemical structure of antibodies, also known as immunoglobulins. Dr. Edelman discovered that antibodies were not constructed in the shape of one long peptide chain, as thought, but of two different ones — one light, one heavy — that were linked. © 2014 The New York Times Company

Keyword: Development of the Brain; Trophic Factors
Link ID: 19651 - Posted: 05.24.2014

By John Horgan Biologist Gerald Edelman–one of the truly great scientific characters I’ve encountered, whose work raised profound questions about the limits of science—has died. I interviewed Edelman in June 1992 at Rockefeller University in New York. Edelman subsequently left Rockefeller to head a center for neuroscience at the Scripps Institute in California. Edelman, 84, died in his home in La Jolla. The following is an edited version of my profile of Edelman in my 1996 book The End of Science. Gerald Edelman, who sought to solve the riddle of consciousness, had "the brain of an empiricist and the heart of a romantic." Gerald Edelman’s career, like that of his rival Francis Crick, has been eclectic, and highly successful. While still a graduate student, Edelman helped to determine the structure of a protein molecule crucial to the body’s immune response. In 1972 he shared a Nobel Prize for that work. Edelman moved on to developmental biology, the study of how a single fertilized cell becomes a full-fledged organism. He found a class of proteins, called cell adhesion molecules, thought to play an important role in embryonic development. All this was merely prelude, however, to Edelman’s grand project of creating a theory of mind. Edelman has set forth his theory in three books: Neural Darwinism, The Remembered Present and Bright Air, Brilliant Fire. The gist of the theory is that just as environmental stresses select the fittest members of a species, so do inputs to the brain select groups of neurons–corresponding to useful memories, for example–by strengthening the connections between them. © 2014 Scientific American

Keyword: Development of the Brain; Trophic Factors
Link ID: 19650 - Posted: 05.24.2014

By MICHAEL BEHAR One morning in May 1998, Kevin Tracey converted a room in his lab at the Feinstein Institute for Medical Research in Manhasset, N.Y., into a makeshift operating theater and then prepped his patient — a rat — for surgery. A neurosurgeon, and also Feinstein Institute’s president, Tracey had spent more than a decade searching for a link between nerves and the immune system. His work led him to hypothesize that stimulating the vagus nerve with electricity would alleviate harmful inflammation. “The vagus nerve is behind the artery where you feel your pulse,” he told me recently, pressing his right index finger to his neck. The vagus nerve and its branches conduct nerve impulses — called action potentials — to every major organ. But communication between nerves and the immune system was considered impossible, according to the scientific consensus in 1998. Textbooks from the era taught, he said, “that the immune system was just cells floating around. Nerves don’t float anywhere. Nerves are fixed in tissues.” It would have been “inconceivable,” he added, to propose that nerves were directly interacting with immune cells. Nonetheless, Tracey was certain that an interface existed, and that his rat would prove it. After anesthetizing the animal, Tracey cut an incision in its neck, using a surgical microscope to find his way around his patient’s anatomy. With a hand-held nerve stimulator, he delivered several one-second electrical pulses to the rat’s exposed vagus nerve. He stitched the cut closed and gave the rat a bacterial toxin known to promote the production of tumor necrosis factor, or T.N.F., a protein that triggers inflammation in animals, including humans. “We let it sleep for an hour, then took blood tests,” he said. The bacterial toxin should have triggered rampant inflammation, but instead the production of tumor necrosis factor was blocked by 75 percent. “For me, it was a life-changing moment,” Tracey said. What he had demonstrated was that the nervous system was like a computer terminal through which you could deliver commands to stop a problem, like acute inflammation, before it starts, or repair a body after it gets sick. “All the information is coming and going as electrical signals,” Tracey said. For months, he’d been arguing with his staff, whose members considered this rat project of his harebrained. “Half of them were in the hallway betting against me,” Tracey said. © 2014 The New York Times Company

Keyword: Robotics
Link ID: 19649 - Posted: 05.24.2014

A drug to treat a particular form of Duchenne muscular dystrophy has been given the green light by the European Medicines Agency and could be available in the UK in six months. Translarna is only relevant to patients with a 'nonsense mutation', who make up 10-15% of those affected by Duchenne. The EMA decided not to pass the drug in January, but they have since re-examined the evidence. A campaign group said the drug must reach the right children without delay. There are currently no approved therapies available for this life-threatening condition. The patients who will benefit the most are those aged five years and over who are still able to walk, the EMA said. Duchenne muscular dystrophy is a genetic disease that gradually causes weakness and loss of muscle function. Patients with the condition lack normal dystrophin, a protein found in muscles, which helps to protect muscles from injury. In patients with the disease, the muscles become damaged and eventually stop working. There are 2,400 children in the UK living with muscular dystrophy, but only those whose condition is caused by a particular 'nonsense mutation' - namely 200 children - are suitable to use Translarna. The drug, ataluren, will be known by the brand name of Translarna in the EU. It was developed by PTC Therapeutics. The next step will see the European Commission rubberstamp the EMA's scientific 'green light' within the next three months and authorise the drug to be marketed in the European Union. At that point, individual member states, including the UK, must decide how it will be funded. The Muscular Dystrophy Campaign is calling for urgent meetings with National Institute of Health of Clinical Excellence (NICE) and NHS England to discuss how Translarna can be cleared for approval and use in the UK. It said families in the UK could have access to the drug by spring 2015. Robert Meadowcroft, chief executive of the campaign, said: "This decision by the EMA is fantastic news. BBC © 2014

Keyword: Muscles; Movement Disorders
Link ID: 19648 - Posted: 05.24.2014

By JENEEN INTERLANDI Bessel van der Kolk sat cross-legged on an oversize pillow in the center of a smallish room overlooking the Pacific Ocean in Big Sur. He wore khaki pants, a blue fleece zip-up and square wire-rimmed glasses. His feet were bare. It was the third day of his workshop, “Trauma Memory and Recovery of the Self,” and 30 or so workshop participants — all of them trauma victims or trauma therapists — lined the room’s perimeter. They, too, sat barefoot on cushy pillows, eyeing van der Kolk, notebooks in hand. For two days, they had listened to his lectures on the social history, neurobiology and clinical realities of post-traumatic stress disorder and its lesser-known sibling, complex trauma. Now, finally, he was about to demonstrate an actual therapeutic technique, and his gaze was fixed on the subject of his experiment: a 36-year-old Iraq war veteran named Eugene, who sat directly across from van der Kolk, looking mournful and expectant. Van der Kolk began as he often does, with a personal anecdote. “My mother was very unnurturing and unloving,” he said. “But I have a full memory and a complete sense of what it is like to be loved and nurtured by her.” That’s because, he explained, he had done the very exercise that we were about to try on Eugene. Here’s how it would work: Eugene would recreate the trauma that haunted him most by calling on people in the room to play certain roles. He would confront those people — with his anger, sorrow, remorse and confusion — and they would respond in character, apologizing, forgiving or validating his feelings as needed. By projecting his “inner world” into three-dimensional space, Eugene would be able to rewrite his troubled history more thoroughly than other forms of role-play therapy might allow. If the experiment succeeded, the bad memories would be supplemented with an alternative narrative — one that provided feelings of acceptance or forgiveness or love. The exercise, which van der Kolk calls a “structure” but which is also known as psychomotor therapy, was developed by Albert Pesso, a dancer who studied with Martha Graham. He taught it to van der Kolk about two decades ago. Though it has never been tested in a controlled study, van der Kolk says he has had some success with it in workshops like this one. He likes to try it whenever he has a small group and a willing volunteer. © 2014 The New York Times Company

Keyword: Stress
Link ID: 19647 - Posted: 05.24.2014

|By Ann Graybiel and Kyle Smith For children and adults who have conditions such as obsessive-compulsive disorder (OCD), Tourette syndrome or autism, repetitive thoughts and actions can occur even if the individuals do not want them to. In OCD a thought that repeats again and again—“my hands are dirty, my hands are dirty”—can recur in a habitual way. Such conditions occur in people from different countries and cultures, suggesting that they represent a core dysfunction related to an imbalance between behaviors. These problems appear to reflect disturbances in brain circuits that are different from, but allied with, the normal habit circuits. Researchers in our group and that of Susanne Ahmari at the University of Pittsburgh have tested whether these OCD circuits can be controlled. Our lab group stimulated the neocortex and striatum in mice that were genetically engineered to have OCD-like traits. These mice groom themselves excessively, especially around the face. In the lab we mimicked a problem that people with OCD often have because they react excessively and repetitively to some trigger stimulus in the environment. We conditioned the mice to learn that after a tone sounded a drop of water would fall on their noses about a second later. We also performed the same routine with normal (“control”) mice. The OCD-like mice started by just grooming when the water drop came, but then began to start grooming in response to the tone alone, and kept grooming all the way through when the drop fell. The control mice learned to suppress this early grooming, which after all was a wasted effort because the water drop came later. The OCD-like mice groomed compulsively every time the external cue sounded. Using optogenetics—a technique that controls the activity of brain cells by shining light on them—we then excited a pathway that connects a small region in the cortex with the striatum. The pathway has been implicated in suppressing behaviors. This treatment immediately blocked the compulsive early grooming in the mutant mice! Yet when the water drop came, they could groom normally. And the optogenetic stimulation did not affect other normal behaviors such as eating; it selectively blocked the compulsive aspect of behavior. © 2014 Scientific American

Keyword: OCD - Obsessive Compulsive Disorder; Genes & Behavior
Link ID: 19646 - Posted: 05.24.2014

Kevin Loria Music was among the least of Mr. B's concerns. As a 59-year-old Dutch man living with extremely severe obsessive compulsive disorder for 46 years, he had other things on his mind. His OCD was so severe it led to moderate anxiety and mild depression. Not only was his condition extreme, but it was also resistant to traditional treatment. It got so bad that he opted to receive an implant to stimulate his brain constantly with electricity — a treatment, called deep brain stimulation (DBS), that has been shown to successfully treat OCD in the past. It worked, but had a very peculiar side effect. As researchers write in a study published in the journal Frontiers in Behavioral Neuroscience, it turned Mr. B. into a Johnny Cash fanatic, though he'd never really listened to The Man in Black before. Mr. B. had listened to the same music for decades, but was never a devout music lover. He was a Rolling Stones and Beatles fan (with a preference for the Stones), and listened to Dutch music as well. But just months after flying to Minneapolis and having two sets of electrodes tunneled into his brain for the shock therapy, he had a mind-blowing run-in with the song "Ring of Fire" playing on the radio. Something about Cash's deep bass-baritone voice resonated with him at that moment. His life had already changed. After the surgical implants and therapy, his OCD had gone from extremely severe to mild, and his depression and anxiety were at a level lower than mild. But when he heard Cash croon, another change began. Mr. B. bought all the Johnny Cash music he could find and stopped listening to anything else — no more Beatles, no more Stones, no more Nederpop. Instead, he played Cash all the time, and especially loved the songs from the '70s and '80s. "Folsom Prison Blues," "Ring Of Fire," and "Sunday Morning Come-Down" are his favorites. They make him feel like a hero, he told doctors. © 2014 Business Insider, Inc.

Keyword: OCD - Obsessive Compulsive Disorder; Attention
Link ID: 19645 - Posted: 05.24.2014

By GRETCHEN REYNOLDS A new study found subtle differences in the brains of college football players when compared to other students.Tim Larsen for The New York TimesA new study found subtle differences in the brains of college football players when compared to other students. The brains of college football players are subtly different from the brains of other students, especially if the players have experienced a concussion in the past, according to an important new brain-scan study that, while restrained in its conclusions, adds to concerns that sports-related hits to the head could have lingering effects on the brain, even among the young and healthy. Almost all of us have heard by now that concussions are more injurious than was once believed. It’s been widely reported that the autopsied brains of some professional football and hockey players who experienced repeated hits to the head showed signs of severe and progressive brain damage. Meanwhile, recent studies with living animals suggest that the brain may respond to even mild concussive blows with inflammatory and other reactions that, while designed to spur healing, could also contribute to tissue damage. But many fundamental questions about the long-term impacts of blows to the head during sports remain unanswered, including which portions of the brain are most affected, whether any brain changes also affect the ability to think, and if playing a contact sport might alter the structure and function of the brains of athletes, even ones who have never experienced a confirmed concussion. So, for a study published last week in JAMA, researchers at the Laureate Institute for Brain Research and the University of Tulsa, both in Tulsa, Okla., and other institutions, started delving into those issues by turning to the university’s Division I football team. Tulsa is, of course, in the heart of football country. But the researchers say they met no resistance from the school, team or players. © 2014 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 19644 - Posted: 05.22.2014

Four common chronic pain conditions share a genetic element, suggesting they could - at least in part - be inherited diseases, say UK researchers. The four include irritable bowel syndrome, musculoskeletal pain, pelvic pain and dry eye disease. The study of more than 8,000 sets of twins found the ailments were common in identical pairs sharing the same DNA. The King's College London team say the discovery could ultimately help with managing these debilitating diseases. While environmental factors probably still play a role in the four conditions, genes could account for as much as two-thirds of someone's chances of developing the disease, they believe. They told the journal Pain that more research is needed to pinpoint the precise genes involved. Chronic pain - pain which persists or recurs for months on end - is common and has many different causes, which can make it difficult to diagnose and treat. While the pain can be related to other medical conditions, it is thought to be caused by problems with the nervous system, sending pain signals to the brain despite no obvious tissue damage. Experts are keen to understand more about chronic pain to improve the quality of life of the millions of people who have to endure it. Some have suspected that some people may have a genetic predisposition to chronic pain since many sufferers share similar symptoms and often have more than one of the different types of chronic pain conditions. The team at King's College London decided to study identical and non-identical twins because these two groups provide an ideal comparison for investigating inherited genes - identical twins share the same DNA while non-identical twins do not. BBC © 2014

Keyword: Pain & Touch; Genes & Behavior
Link ID: 19643 - Posted: 05.22.2014

André Aleman & Damiaan Denys According to the World Health Organization, almost 1 million people kill themselves every year. That is more than the number that die in homicides and war combined. A further 10 million to 20 million people attempt it. Suicide is one of the three leading causes of death in the economically most productive age group — those aged 15–44 years — and rates have risen since the economic crisis triggered by the banking crash in 2008 (see 'Suicide rates in Europe'). For example, the number of suicides per year in the Netherlands rose by 30% between 2008 and 2012, from 1,353 to 1,753. In the United States, the average suicide costs society US$1.06 million according to the US Centers for Disease Control and Prevention. Despite its enormous societal impact, little progress has been made in the scientific understanding or treatment of suicidal behaviour. We do know that up to 90% of suicides occur in people with a clinically diagnosable psychiatric disorder1. Large epidemiological studies have shown mental disorders, particularly depression and alcohol addiction, to be major risk factors2. And there is compelling evidence that adequate prevention and treatment of such disorders can reduce suicide rates2. But psychiatry has long neglected the topic. Other than as symptoms of borderline personality disorder and mood disorders, suicide, suicide attempts and suicidal thoughts were not listed in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). The DSM-5 (published last year) does not code suicidal behaviour — the most prominent emergency in psychiatry in primary care. Suicidality is perceived as a medical complication rather than as a disorder in its own right. © 2014 Nature Publishing Group

Keyword: Depression
Link ID: 19642 - Posted: 05.22.2014

By JAMES GORMAN If an exercise wheel sits in a forest, will mice run on it? Every once in a while, science asks a simple question and gets a straightforward answer. In this case, yes, they will. And not only mice, but also rats, shrews, frogs and slugs. True, the frogs did not exactly run, and the slugs probably ended up on the wheel by accident, but the mice clearly enjoyed it. That, scientists said, means that wheel-running is not a neurotic behavior found only in caged mice. They like the wheel. Two researchers in the Netherlands did an experiment that it seems nobody had tried before. They placed exercise wheels outdoors in a yard garden and in an area of dunes, and monitored the wheels with motion detectors and automatic cameras. They were inspired by questions from animal welfare committees at universities about whether mice were really enjoying wheel-running, an activity used in all sorts of studies, or were instead like bears pacing in a cage, stressed and neurotic. Would they run on a wheel if they were free? Now there is no doubt. Mice came to the wheels like human beings to a health club holding a spring membership sale. They made the wheels spin. They hopped on, hopped off and hopped back on. “When I saw the first mice, I was extremely happy,” said Johanna H. Meijer at Leiden University Medical Center in the Netherlands. “I had to laugh about the results, but at the same time, I take it very seriously. It’s funny, and it’s important at the same time.” Dr. Meijer’s day job is as a “brain electrophysiologist” studying biological rhythms in mice. She relished the chance to get out of the laboratory and study wild animals, and in a way that no one else had. © 2014 The New York Times Company

Keyword: Emotions; Biological Rhythms
Link ID: 19641 - Posted: 05.21.2014

Puffing on a battery-powered, electronic cigarette to satisfy nicotine cravings could help longtime smokers quit their tobacco addiction. The evidence supporting that claim has been thin in the past, but researchers have now reported that adults in England who used the devices were 60% more likely to remain smoke-free than those who turned to nicotine patches or went cold turkey. Some public health researchers, though, still worry that’s not enough to cancel out the negative effects of e-cigarettes, which might keep other smokers hooked on nicotine or prevent them from seeking out more effective ways to quit. “This is an important study because, until now, the data on quitting smoking with e-cigarettes has been mostly anecdotal,” says Neal Benowitz, a physician at the University of California, San Francisco (UCSF), who studies tobacco addiction and was not involved in the work. E-cigarettes produce a nicotine-rich vapor that’s free of many of the toxins and carcinogens that make tobacco cigarettes so unhealthy. Their popularity has skyrocketed since they hit the market in the early 2000s; a 2012 survey found that 30% of adult smokers in the United States had tried e-cigarettes. But studies attempting to establish both the risks and benefits of the devices have had varied conclusions. One recent review of the scientific literature, which included Benowitz as an author, reported that smokers who used e-cigarettes were less likely to quit smoking than those who didn’t use the devices. The results were based on broad surveys of all smokers, however, not just those attempting to quit. Another paper concluded that e-cigarettes are about as effective as nicotine patches at helping people stop smoking. Since 2006, researchers in England have run an ongoing surveillance program, in conjunction with the government’s research bureau, called the Smoking Toolkit Study. Every month, they survey a new sample of 1800 random adults about their smoking behavior. © 2014 American Association for the Advancement of Science.

Keyword: Drug Abuse
Link ID: 19640 - Posted: 05.21.2014

Dr Lucy Maddox There has been much heated debate in recent weeks about whether cognitive behavioural therapy for psychosis has been totally over-egged. One stance is that Nice (the National Institute for Clinical Excellence) has recommended a treatment with little or no evidence base. Another is that CBT is a helpful intervention for many people experiencing psychotic-like phenomena. But what is CBT for psychosis? What does it look like? And how can knowing this help us to understand the issues being argued about? Psychosis is an umbrella term for a collection of symptoms. These symptoms get classed as "positive" or "negative", which is not to infer that some are good and some are bad, but rather to capture the fact that some of the symptoms add something new and others take something away. Positive symptoms are those that add an unusual experience of some kind, eg seeing things that others can't (hallucinations) or strongly believing things that don't make sense to others (delusions). Negative symptoms involve something being taken away from the person, eg a lack of enjoyment (anhedonia), motivation (avolition), or a lack of emotion. Whilst a recent meta-analysis has shown only limited evidence for the effectiveness of CBT for psychosis and suggested that previous results are inflated, we should be cautious about using this one meta-analysis to chuck out CBT for psychosis. Among other potential holes that could be poked in its conclusions is the fact that the analysis uses psychotic symptoms as the only outcome measure for effectiveness, which might not be the best or only thing we should be looking at. Many other reviews and individual studies do report reductions in psychotic symptoms from CBT for psychosis, including delusions and hallucinations and some of the brain processing correlates of these positive symptoms (eg Kumari et al 2011). Perhaps more interestingly though, they also report benefits from CBT in domains other than the psychotic symptoms themselves. (eg Wykes et al, 2009). © 2014 Guardian News and Media Limited

Keyword: Schizophrenia
Link ID: 19639 - Posted: 05.21.2014

by Laura Sanders An injectable form of a newer, more expensive schizophrenia drug works no better than an older drug, scientists report May 21 in the Journal of the American Medical Association. In a randomized clinical trial of 311 people with schizophrenia, injections of paliperidone palmitate failed to alleviate schizophrenia symptoms just as often as did injections of haloperidol decanoate, a drug that’s been around for decades. A single injection of paliperidone palmitate, a second-generation antipsychotic, costs about $1000 in the United States. An injection of haloperidol costs only about $35. The two drugs caused different side effects: In some patients, haloperidol led to muscle tremors and restlessness and paliperidone palmitate caused weight gain. Knowledge of these different side effects — and not differences in effectiveness — might be useful in deciding which drug a person ought to take. © Society for Science & the Public 2000 - 2013.

Keyword: Schizophrenia
Link ID: 19638 - Posted: 05.21.2014

Dr. Mark Saleh Bell's palsy is a neurological condition frequently seen in emergency rooms and medical offices. Symptoms consist of weakness involving all muscles on one side of the face. About 40,000 cases occur annually in the United States. Men and women are equally affected, and though it can occur at any age, people in their 40s are especially vulnerable. The facial weakness that occurs in Bell's palsy prevents the eye of the affected side from blinking properly and causes the mouth to droop. Because the eyelid doesn't close sufficiently, the eye can dry and become irritated. Bell's palsy symptoms progress fairly rapidly, with weakness usually occurring within three days. If the progression of weakness is more gradual and extends beyond a week, Bell's palsy may not be the problem, and other potential causes should be investigated. Those with certain medical conditions, such as diabetes or pregnancy, are at greater risk of developing Bell's palsy, and those who have had one episode have an 8 percent chance of recurrence. Bell's palsy is thought to occur when the seventh cranial (facial) nerve becomes inflamed. The nerve controls the muscles involved in facial expression and is responsible for other functions, including taste perception, eye tearing and salivation. The cause of the inflammation is unknown, although the herpes simplex virus and autoimmune inflammation are possible causes. © 2014 Hearst Communications, Inc.

Keyword: Movement Disorders
Link ID: 19637 - Posted: 05.21.2014