Chapter 11. Emotions, Aggression, and Stress

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By JANE E. BRODY It’s perfectly normal for someone to feel anxious or depressed after receiving a diagnosis of a serious illness. But what if the reverse occurs and symptoms of anxiety or depression masquerade as an as-yet undiagnosed physical disorder? Or what if someone’s physical symptoms stem from a psychological problem? How long might it take before the true cause of the symptoms is uncovered and proper treatment begun? Psychiatric Times, a medical publication seen by some 50,000 psychiatrists each month, recently published a “partial listing” of 47 medical illnesses, ranging from cardiac arrhythmias to pancreatic cancer, that may first present as anxiety. Added to that was another “partial listing” of 30 categories of medications that may cause anxiety, including, ironically, popular antidepressants like selective serotonin reuptake inhibitors, or S.S.R.I.s. These lists were included in an article called “Managing Anxiety in the Medically Ill” meant to alert mental health practitioners to the possibility that some patients seeking treatment for anxiety or depression may have an underlying medical condition that must be addressed before any emotional symptoms are likely to resolve. Doctors who treat ailments like cardiac, endocrine or intestinal disorders would do well to read this article as well lest they do patients a serious disservice by not recognizing an emotional cause of physical symptoms or addressing the emotional components of a physical disease. © 2017 The New York Times Company

Keyword: Depression; Stress
Link ID: 23773 - Posted: 06.26.2017

By Alice Klein EVIDENCE that Parkinson’s disease may be an autoimmune disorder could lead to new ways to treat the illness. Parkinson’s begins with abnormal clumping of a protein called synuclein in the brain. Neighbouring dopamine-producing neurons then die, causing tremors and difficulty moving. The prevailing wisdom has been that these neurons die from a toxic reaction to synuclein deposits. However, Parkinson’s has been linked to some gene variants that affect how the immune system works, leading to an alternative theory that synuclein causes Parkinson’s by triggering the immune system to attack the brain. An argument against this theory has been that brain cells are safe from immune system attack, because most neurons don’t have antigens – the markers immune cells use to recognise a target. But by studying postmortem brain tissue samples, David Sulzer at Columbia University and his team have discovered that dopamine-producing neurons do display antigens. The team has now conducted blood tests to reveal that people with Parkinson’s show an immune response to these antigens, while people who don’t have the condition do not (Nature, DOI: 10.1038/nature22815). These findings suggest Parkinson’s may be an autoimmune disorder, in which the immune system mistakenly attacks part of the body. There have been hints before that the immune system is involved in Parkinson’s, but this is the first evidence that it plays a major pathological role, says Roger Barker at the University of Cambridge. “It would be an attractive target for therapeutic intervention,” he says. However, it isn’t clear yet if the immune response directly causes neuron death, or if it is merely a side effect of the disease. Sulzer’s team plans to try blocking the autoimmune response in Parkinson’s, to see if this can stop the disease progressing. © Copyright New Scientist Ltd.

Keyword: Parkinsons; Neuroimmunology
Link ID: 23760 - Posted: 06.22.2017

By Diana Kwon Glioblastomas, highly aggressive malignant brain tumors, have a high propensity for recurrence and are associated with low survival rates. Even when surgeons remove these tumors, deeply infiltrated cancer cells often remain and contribute to relapse. By harnessing neutrophils, a critical player in the innate immune response, scientists have devised a way to deliver drugs to kill these residual cells, according to a study published today (June 19) in Nature Nanotechnology. Neutrophils, the most common type of white blood cell, home in to areas of injury and inflammation to fight infections. Prior studies in both animals and humans have reported that neutrophils can cross the blood-brain barrier, and although these cells are not typically attracted to glioblastomas, they are recruited at sites of tumor removal in response to post-operative inflammation. To take advantage of the characteristics of these innate immune cells, researchers at China Pharmaceutical University encased paclitaxel, a traditional chemotherapy drug, with lipids. These liposome capsules were loaded into neutrophils and injected in the blood of three mouse models of glioblastoma. When the treatment was applied following surgical removal of the main tumor mass, the neutrophil-carrying drugs were able to cross the blood-brain barrier, destroy residual cancer cells, and slow the growth of new tumors. Overall, mice receiving treatment lived significantly longer than controls. © 1986-2017 The Scientist

Keyword: Brain imaging; Neuroimmunology
Link ID: 23756 - Posted: 06.21.2017

By Timothy Revell Feeling sad? Soon your dolls will be able to tell. To demonstrate the power of a new chip that can run artificially intelligent algorithms, researchers have put it in a doll and programmed it to recognise emotions in facial images captured by a small camera. The doll can recognise eight emotions in total, including surprise and happiness, all while running on a small battery and without doing any processing in the cloud. The total cost of putting the new chip together is just €115 – an indicator of how easy it is becoming to give devices basic AI abilities. “In the near future, we will see a myriad of eyes everywhere that will not just be watching us, but trying to help us,” says project leader Oscar Deniz at the University of Castilla-La Mancha in Ciudad Real, Spain. Recent advances in AI mean we already have algorithms that can recognise objects, lip-read, make basic decisions and more. It’s only a matter of time before these abilities make their way on to little cheap chips like this one, and then put into consumer devices. “We will have wearable devices, toys, drones, small robots, and things we can’t even imagine yet that will all have basic artificial intelligence,” says Deniz. © Copyright New Scientist Ltd.

Keyword: Emotions
Link ID: 23752 - Posted: 06.20.2017

Heidi Ledford By 13 weeks of gestation, human fetuses have developed a much more unusual immune system than previously thought. A human fetus in its second trimester is extraordinarily busy. It is developing skin and bones, the ability to hear and swallow, and working on its first bowel movement. Now, a study published on 14 June in Nature finds that fetuses are also acquiring a functioning immune system — one that can recognize foreign proteins, but is less inclined than a mature immune system to go on the attack (N. McGovern et al. Nature http://dx.doi.org/10.1038/nature22795; 2017). The results add to a growing body of literature showing that the fetal immune system is more active than previously appreciated. “In general textbooks, you see this concept of a non-responsive fetus is still prevailing,” says immunologist Jakob Michaelsson at the Karolinska Institute in Stockholm. But the fetal immune system is unique, he says. “It’s not just immature, it’s special.” A developing fetus is constantly exposed to foreign proteins and cells, which are transferred from the mother through the placenta. In humans, this exposure is more extensive than in many other mammals, says immunologist Mike McCune at the University of California, San Francisco. As a result, laboratory mice have proved a poor model for studying the developing human fetal immune system. But fully understanding that development could reveal the reasons for some miscarriages, as well as explain conditions such as pre-eclampsia, which is associated with abnormal immune responses to pregnancy and causes up to 40% of premature births. © 2017 Macmillan Publishers Limited,

Keyword: Development of the Brain; Neuroimmunology
Link ID: 23746 - Posted: 06.15.2017

By ALEX WILLIAMS This past winter, Sarah Fader, a 37-year-old social media consultant in Brooklyn who has generalized anxiety disorder, texted a friend in Oregon about an impending visit, and when a quick response failed to materialize, she posted on Twitter to her 16,000-plus followers. “I don’t hear from my friend for a day — my thought, they don’t want to be my friend anymore,” she wrote, appending the hashtag #ThisIsWhatAnxietyFeelsLike. Thousands of people were soon offering up their own examples under the hashtag; some were retweeted more than 1,000 times. You might say Ms. Fader struck a nerve. “If you’re a human being living in 2017 and you’re not anxious,” she said on the telephone, “there’s something wrong with you.” It was 70 years ago that the poet W.H. Auden published “The Age of Anxiety,” a six-part verse framing modern humankind’s condition over the course of more than 100 pages, and now it seems we are too rattled to even sit down and read something that long (or as the internet would say, tl;dr). Anxiety has become our everyday argot, our thrumming lifeblood: not just on Twitter (the ur-anxious medium, with its constant updates), but also in blogger diaries, celebrity confessionals (Et tu, Beyoncé?), a hit Broadway show (“Dear Evan Hansen”), a magazine start-up (Anxy, a mental-health publication based in Berkeley, Calif.), buzzed-about television series (like “Maniac,” a coming Netflix series by Cary Fukunaga, the lauded “True Detective” director) and, defying our abbreviated attention spans, on bookshelves. With two new volumes analyzing the condition (“On Edge: A Journey Through Anxiety,” by Andrea Petersen, and “Hi, Anxiety,” by Kat Kinsman) following recent best-sellers by Scott Stossel (“My Age of Anxiety”) and Daniel Smith (“Monkey Mind”), the anxiety memoir has become a literary subgenre to rival the depression memoir, firmly established since William Styron’s “Darkness Visible” and Elizabeth Wurtzel’s “Prozac Nation” in the 1990s and continuing today with Daphne Merkin’s “This Close to Happy.” © 2017 The New York Times Company

Keyword: Depression; Stress
Link ID: 23732 - Posted: 06.12.2017

By JANE E. BRODY Hurray for the HotBlack Coffee cafe in Toronto for declining to offer Wi-Fi to its customers. There are other such cafes, to be sure, including seven of the eight New York City locations of Café Grumpy. But it’s HotBlack’s reason for the electronic blackout that is cause for hosannas. As its president, Jimson Bienenstock, explained, his aim is to get customers to talk with one another instead of being buried in their portable devices. “It’s about creating a social vibe,” he told a New York Times reporter. “We’re a vehicle for human interaction, otherwise it’s just a commodity.” What a novel idea! Perhaps Mr. Bienenstock instinctively knows what medical science has been increasingly demonstrating for decades: Social interaction is a critically important contributor to good health and longevity. Personally, I don’t need research-based evidence to appreciate the value of making and maintaining social connections. I experience it daily during my morning walk with up to three women, then before and after my swim in the locker room of the YMCA where the use of electronic devices is not allowed. The locker room experience has been surprisingly rewarding. I’ve made many new friends with whom I can share both joys and sorrows. The women help me solve problems big and small, providing a sounding board, advice and counsel and often a hearty laugh that brightens my day. © 2017 The New York Times Company

Keyword: Stress
Link ID: 23730 - Posted: 06.12.2017

By LISA SANDERS, M.D. She didn’t have any urgent medical problems, the woman told Dr. Lori Bigi. She was there because she had moved to Pittsburgh and needed a primary-care doctor. Bigi, an internist at the University of Pittsburgh Medical Center, quickly eyed her new patient. She was 31 and petite, just over five feet tall and barely 100 pounds. And she looked just as she described herself, pretty healthy. Doctors often rely on patients’ sense of their well-being, especially when their assessment matches their appearance. But as Dr. Bigi was reminded that day, patients aren’t always right. The patient did say that she had seen her old doctor for awful headaches she got occasionally. They felt like an ice pick through the top of her head, the patient explained, which, at least initially, usually came on while she was going to the bathroom. The headache didn’t last long, but it was intensely painful. Her previous doctor thought it was a type of migraine. He prescribed medication, but it didn’t help. Now her main problem was anxiety, and she saw a psychiatrist for that. Sudden Panic Anxiety is common enough, and because the patient was seeing a specialist, Bigi wasn’t planning to spend much time discussing it. But then the doctor saw that in addition to taking an antidepressant — a recommended treatment for anxiety — the patient was on a sedating medication called clonazepam. It wasn’t a first-line medication for anxiety, and this tiny woman was taking a huge dose of it. The young woman explained that for most of her life, she was not a particularly anxious person. Then, two years earlier, she started experiencing episodes of total panic for seemingly no reason. At the time she chalked it up to a new job — she worked in a research lab — and the pressures associated with a project they had recently started. But the anxiety never let up. © 2017 The New York Times Company

Keyword: Stress; Hormones & Behavior
Link ID: 23721 - Posted: 06.08.2017

By EMILIE LE BEAU LUCCHESI Benjamin Stepp, an Iraq war veteran, sat in his graduate school course trying to focus on the lecture. Neither his classmates nor his professor knew he was silently seething. But his service dog, Arleigh, did. She sensed his agitation and “put herself in my lap,” said Mr. Stepp, 37, of Holly Springs, Miss. “I realized I needed to get out of class. We went outside, I calmed down. We breathed.” During his two deployments to Iraq, Mr. Stepp endured a traumatic brain injury and multiple surgeries on his ankle, and most days he suffers excruciating pain in his legs and lower back. He says he also returned from the war with a lot of anger, which wells up at unexpected times. “Anger kept us alive overseas,” Mr. Stepp said. “You learn that anger keeps you alive.” Now that he is back, though, that anger no longer serves a useful purpose. And Arleigh, a lab and retriever mix who came to Mr. Stepp from K9s For Warriors, a nonprofit organization that trains service dogs, has been helping him to manage it. The dog senses when his agitation and anxiety begin rising, and sends him signals to begin the controlled breathing and other exercises that help to calm him down. Pet owners and trainers have long been aware of a dog’s ability to sense a human’s emotions. In the last 10 years, researchers, too, have begun to explore more deeply the web of emotions, both positive and negative, that can spread between people and animals, said Natalia Albuquerque, an ethologist who studies animal cognition at the University of São Paulo in Brazil and the University of Lincoln in England. The spread of emotions between animals and people, or between animals — what researchers refer to as emotional contagion — is an emerging field of science. But “there are still many unanswered questions we need to address,” Ms. Albuquerque said. © 2017 The New York Times Company

Keyword: Emotions; Evolution
Link ID: 23708 - Posted: 06.05.2017

Judith Ohikuare In 2005, James Fallon's life started to resemble the plot of a well-honed joke or big-screen thriller: A neuroscientist is working in his laboratory one day when he thinks he has stumbled upon a big mistake. He is researching Alzheimer's and using his healthy family members' brain scans as a control, while simultaneously reviewing the fMRIs of murderous psychopaths for a side project. It appears, though, that one of the killers' scans has been shuffled into the wrong batch. The scans are anonymously labeled, so the researcher has a technician break the code to identify the individual in his family, and place his or her scan in its proper place. When he sees the results, however, Fallon immediately orders the technician to double check the code. But no mistake has been made: The brain scan that mirrors those of the psychopaths is his own. After discovering that he had the brain of a psychopath, Fallon delved into his family tree and spoke with experts, colleagues, relatives, and friends to see if his behavior matched up with the imaging in front of him. He not only learned that few people were surprised at the outcome, but that the boundary separating him from dangerous criminals was less determinate than he presumed. Fallon wrote about his research and findings in the book The Psychopath Inside: A Neuroscientist's Personal Journey Into the Dark Side of the Brain, and we spoke about the idea of nature versus nurture, and what—if anything—can be done for people whose biology might betray their behavior. © 2017 by The Atlantic Monthly Group.

Keyword: Aggression; Emotions
Link ID: 23707 - Posted: 06.05.2017

By Helen Thomson Life is full of decisions, and sometimes it’s difficult to know if you’re making the right one. But a drug that blocks the rush of noradrenaline through your body can boost your confidence, and may also lead to new treatments for schizophrenia and obsessive compulsive disorder. How much we trust our decisions is governed by the process we use to assess our own behaviour and abilities, known as metacognition. Our judgements shape how we’ll behave in future. For example, if you play Frisbee and you think you played badly, you might be less likely to do it again, says Tobias Hauser at University College London. Having low confidence in our actions can play a part in mental health conditions. “We see many symptoms associated with poor metacognitive judgement in schizophrenia and OCD,” says Hauser. “In OCD, for instance, people may constantly go and check whether they’ve closed a door. They are poor at judging whether they have done something correctly or not.” Little is known about the neural underpinnings of metacognition, but it is likely to involve the prefrontal cortex and the hippocampus, two brain areas modulated by the chemicals dopamine and noradrenaline. To investigate, Hauser and his colleagues asked 40 people to take a drug that blocks dopamine or noradrenaline either before or after a placebo. Another 20 people received two doses of the placebo drug. Eighty minutes after receiving the second drug, the subjects performed a task in which they had to decide whether the overall motion of a burst of randomly moving dots was directed to the left or right. © Copyright New Scientist Ltd.

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 23705 - Posted: 06.03.2017

Rebecca Hersher Emotions, the classic thinking goes, are innate, basic parts of our humanity. We are born with them, and when things happen to us, our emotions wash over us. "They happen to us, almost," says Lisa Feldman Barrett, a professor of psychology at Northeastern University and a researcher at Harvard Medical School and the Massachusetts General Hospital. She's also the author of a book called How Emotions Are Made: The Secret Life of the Brain. In it, she argues for a new theory of emotions which is featured in the latest episode of NPR's program and podcast Invisibilia. The "classical view" of emotions as innate and limited in variety, she says, "matches the way that many of us experience emotion, as if something's happening outside of our control," she tells Shots. "But the problem with this set of ideas is that the data don't support them. There's a lot of evidence which challenges this view from every domain of science that's ever studied it." Lisa Feldman Barrett spoke to Shots about her alternative theory of emotions. The interview has been edited for length and clarity. On the "classical" theory of emotions The classical view of emotion is the idea that somewhere lurking deep inside you are the animalistic engine parts of your brain. There are circuits — one each for anger, sadness, fear, disgust and so on. And that when something happens in the world to trigger one of those circuits — say, for fear — you will have a very specific facial expression, a very specific bodily response, and that these expressions and responses have universal meaning. Everyone in the world makes them and recognizes them without learning or any experience at all. © 2017 npr

Keyword: Emotions
Link ID: 23703 - Posted: 06.03.2017

Nicola Davis Being in a state of anxiety makes it harder to read the emotions of others, researchers have claimed. Difficulties in interpreting the facial expressions of others have previously been linked to a number of psychiatric disorders, while people with a greater tendency to be anxious have been found to have a greater sensitivity to faces showing fear. However, it was not clear whether such effects existed among people who experience a situation that triggers anxiety. “We were specifically trying to answer the question: how does our current level of anxiety influence how we see the world, and in particular emotions in faces?” said Marcus Munafò, professor of biological psychology at the University of Bristol and a co-author of the new study. To tackle the conundrum, Munafò and colleagues from the University of Bristol looked at the impact of an anxiety-inducing situation on the ability of 21 healthy participants to interpret emotion in facial expressions. The participants’ general tendencies to worry about situations varied, but none had anxiety disorders. The participants were each fitted with a face mask delivering either normal air, or air enriched with carbon dioxide – an approach known to induce worry and tension, as well as a raised heart rate and blood pressure. After completing each part of the study, the participants repeated the experiment breathing the alternative type of air.

Keyword: Emotions
Link ID: 23684 - Posted: 05.31.2017

By Sharon Begley, STAT Living in a city makes people develop schizophrenia. Tell me more: The claim is not quite that stark, but it’s close. For a study published last week, researchers interviewed 2,063 British twins (some identical, some not) at age 18 about “psychotic experiences” they’d had since age 12—such as feeling paranoid, hearing voices, worrying their food might be poisoned, and having “unusual or frightening” thoughts. Among those who lived in the most densely populated large cities, 34 percent reported such experiences; 24 percent of adolescents in rural areas did. The twins are part of a long-running study that has followed them from birth in 1994-95, so the researchers— led by Helen Fisher of King’s College London and Candice Odgers of Duke University—also knew the teens’ family income, parents’ education, where they lived, and more. Conclusion: 18-year-olds raised in big cities were 67 percent more likely to have had psychotic experiences, the researchers reported in Schizophrenia Bulletin. They then used standard statistics tools to account for possible psychosis-related factors other than cities per se. Cities have more people who are poor and uneducated, which are risk factors for schizophrenia and other forms of psychosis, so they controlled for socioeconomic status. Family psychiatric history raises the risk of an individual’s developing psychosis, and since there is some evidence that people with mental illness move to cities, which have more treatment facilities, the researchers controlled for this, too. They also controlled for drug use, some forms of which are more common in urban than rural areas. These calculations brought the extra risk of psychosis among urban teens down to 43 percent. © 2017 Scientific American,

Keyword: Schizophrenia; Stress
Link ID: 23683 - Posted: 05.31.2017

Tonight, our economics correspondent, Paul Solman, explores another potential connection: whether there’s a link between risk-taking in leadership, testosterone and the perceptions around gender. It’s part of his ongoing weekly series, Making Sense, which airs every Thursday. MAN: Welcome, everybody, to this CNBC discussion on the future of banking at the World Economic Forum. PAUL SOLMAN: Financial CEOs at Davos this year. ANDREW LIVERIS, CEO, Dow Chemical: Good morning. Mr. President. Andrew Liveris, Dow Chemical. PAUL SOLMAN: Manufacturing CEOs at the White House. MARK FIELDS, CEO, Ford Motor Company: CEO of Ford. DOUGLAS OBERHELMAN, CEO, Caterpillar: Chairman of Caterpillar. PRESIDENT DONALD TRUMP: Some of the great people in the world of business. PAUL SOLMAN: CEOs now being mentioned as the next president. But, in 2017, the vast majority of CEOs, 96 percent of the Fortune 500, are still men. JENNIFER LERNER, Harvard University: I think that this is socially constructed. The differences between males and females on a wide variety of things are smaller than the differences within males and within females. PAUL SOLMAN: Psychologist Jennifer Lerner studies gender and leadership at Harvard. We will hear more from her in a bit. But, first, let’s check in with economist Andy Kim, who has made a career out of studying CEOs in intriguingly quirky ways. Now, a few of you might remember Andy Kim teaching me two years ago the equestrian dance move in the hyper-viral video sensation “Gangnam Style,” part of his offbeat research showing that CEOs who become visible, for whatever reason, can see their stock price rise irrationally. Well, he presented his brand-new research, not yet published, at this year’s annual Economics Convention. His latest hypothesis is as offbeat as ever. ANDY KIM: There is a strong linkage between your facial masculinity and your risk-taking behavior. PAUL SOLMAN: Kim is now exploring a possible link between CEO risk-taking and the hormone testosterone, which, starting with mid-19th century experiments on roosters, has been linked to male dominance and aggression throughout the animal kingdom. But how do you measure testosterone in CEOs with little time and probably even less inclination to give Korean assistant finance professors blood or saliva samples? One possible way, thought Kim, would be to study their facial bone structure. © 1996 - 2017 NewsHour Productions LLC.

Keyword: Sexual Behavior; Aggression
Link ID: 23663 - Posted: 05.26.2017

By Jack Turban We all know that person. Her Instagram is covered with more pictures of feline friends than human companions. Not an insignificant number of these pictures feature mini cat-sized lattes with the caption “Fluffy simply adores her morning coffee.” And let us not forget that the archetype of crazy cat man may be just as prevalent. When you look at these pictures, you probably wonder: is he like this because of the cat? Or does he have the cat because he is like this? It turns out that cats have a mischievous and somewhat dark reputation in neuroscience. There is research to suggest that a cat’s proximity to other mammals can cause them to behave strangely. This feline power has been attributed to a protozoan that lives in their stool, called Toxoplasma gondii (or Toxo for short). In one classic story, researchers showed that Toxo can travel into a rat’s brain and cause the rat to no longer avoid areas where cats live. The rats, in fact, become attracted to the smell of cat urine. Previously repulsed by the smell, these brain-infected rodents run joyously through urine-laden environments. They walk right through the cat’s trap, until their young rodent lives come to an end under a forceful paw. These same protozoans can affect the brains of humans. Immuno-compromised patients, like those with AIDS, can contract the infection from a litter box and develop dangerous brain abscesses. We treat these patients with powerful antibiotics and frequently recommend that they give away their cats. Pregnant women are also advised not to handle cat litter, as a fetus does not yet have the immune system needed to fight Toxo. Fetuses exposed to the protozoan can suffer from seizures, cognitive problems, and blindness. But what about your immunocompetent and decidedly non-pregnant Instagram friend; is she under the influence of this cat’s protozoan minion? . © 2017 Scientific American,

Keyword: Emotions
Link ID: 23651 - Posted: 05.24.2017

By GRETCHEN REYNOLDS Mice do not, so far as we know, practice meditation. But in order to study how that activity affects human brains at the cellular level, researchers at the University of Oregon managed to put murine brains into a somewhat equivalent state. Their experiments, reported in March in the Proceedings of the National Academy of Sciences, suggest new ways of investigating how a person’s brain can constantly reshape itself. Past studies have suggested that people who meditate tend to have more white matter in and around the anterior cingulate cortex, a part of the brain involved in regulating emotions. Meditation also seems to intensify theta-wave activity, a type of rhythmic electrical pulsation often associated with a state of calm. Psychologists at Oregon speculated that the surge in theta waves stimulated the production of cells in the white matter. But they needed to develop an animal model of this activity; they obviously couldn’t examine the living brain tissue in meditating humans. So the psychologists asked colleagues in the university’s neuroscience department if they could increase theta-wave activity in mice, which were already being used to study brain states and neural plasticity, or the brain’s ability to rewire itself. Could the neuroscientists create a comparable effect in mice? Yes, it turned out, using a brain-research technique known as optogenetics, which uses light to turn on and off neurons, and mice that have been bred with specific genes responsive to light. The Oregon group, by pulsing the light at the same frequency found in human theta waves (eight hertz), were able to switch on the neurons in the anterior cingulate cortexes of the mice. They also exposed some mice to light at higher and lower frequencies and left others alone. Each treated mouse received 30 minutes of light therapy for 20 days, in an attempt to mimic the amount of meditation done in earlier human studies. Afterward, those mice exposed to the eight-hertz, thetalike light waves proved to be relatively calm in behavioral tests: they lingered in lighted portions of a special cage, while their twitchier counterparts ran for the shadows. © 2017 The New York Times Company

Keyword: Stress
Link ID: 23646 - Posted: 05.22.2017

By LISA SANDERS, M.D. The woman woke to the sound of her 57-year-old husband sobbing. They’d been married for 30 years, and she had never heard him cry before. “I hurt so much,” he wailed. “I have to go back to the hospital.” The symptoms started two weeks earlier. One afternoon, coming home from his job as a carpenter, he felt hot and tired. He shook with shivers even though the day was warm. He drank a cup of tea and went to bed. The next day he felt fine, until the end of the day, when he felt overwhelmed by the heat and chills again. The day after that was the same. When he woke one morning and saw that his body was covered with pale pink dots — his arms, his face, his chest and thighs — he started to worry. His wife took him to the Griffin Hospital emergency room in Derby, Conn. The first doctor who saw him thought he probably had Lyme disease. Summer had just started, and he’d already seen a lot of cases. He sent the patient home with an antibiotic and steroid pills for the rash. The man took the medications but didn’t get any better. Soon everything started to hurt. His muscles, his joints and his back felt as if he’d been beaten. He dragged himself back to the E.R. He was given pain pills. A few days later, he went to the E.R. a third time and was given more pain meds. After waking up crying, he went yet again, and this time, the doctors admitted him. By then the patient had had several blood tests, which showed no sign of Lyme or other tick-borne diseases. A CT scan was equally uninformative. The next day, the man was walking to the bathroom when his legs gave out and he fell down. The doctor in charge of his care came and examined him once again. The man looked fit and healthy, despite the now-bright-red rash, but his legs were extremely weak. If the doctor applied even light pressure to the raised leg, it sagged back down to the bed. And his feet felt numb. He had a sensation of tingling in his hands, as if they had gone to sleep. That was how the weakness and numbness in his legs started, he told the doctor. And the next day, his hands were so weak he had to use both just to drink a cup of water. © 2017 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 23644 - Posted: 05.22.2017

Jon Hamilton It took an explosion and 13 pounds of iron to usher in the modern era of neuroscience. In 1848, a 25-year-old railroad worker named Phineas Gage was blowing up rocks to clear the way for a new rail line in Cavendish, Vt. He would drill a hole, place an explosive charge, then pack in sand using a 13-pound metal bar known as a tamping iron. But in this instance, the metal bar created a spark that touched off the charge. That, in turn, "drove this tamping iron up and out of the hole, through his left cheek, behind his eye socket, and out of the top of his head," says Jack Van Horn, an associate professor of neurology at the Keck School of Medicine at the University of Southern California. Gage didn't die. But the tamping iron destroyed much of his brain's left frontal lobe, and Gage's once even-tempered personality changed dramatically. "He is fitful, irreverent, indulging at times in the grossest profanity, which was not previously his custom," wrote John Martyn Harlow, the physician who treated Gage after the accident. This sudden personality transformation is why Gage shows up in so many medical textbooks, says Malcolm Macmillan, an honorary professor at the Melbourne School of Psychological Sciences and the author of An Odd Kind of Fame: Stories of Phineas Gage. "He was the first case where you could say fairly definitely that injury to the brain produced some kind of change in personality," Macmillan says. © 2017 npr

Keyword: Attention; Emotions
Link ID: 23643 - Posted: 05.22.2017

By DAVE PHILIPPS Three-fifths of troops discharged from the military for misconduct in recent years had a diagnosis of post-traumatic stress disorder, traumatic brain injury or another associated condition, according to a report released Tuesday by the Government Accountability Office. The report, mandated by Congress, for the first time combined military medical and staffing data, as well as data from the Department of Veterans Affairs, to show that tens of thousands of wounded troops were kicked out of the armed forces and severed from benefits designed to ease their transition from service in war. “It is everything many of us believed for years” said Kristopher Goldsmith, a veteran who served in Iraq and was discharged for misconduct after a suicide attempt. He is now an assistant director for policy at Vietnam Veterans of America, a veterans advocacy group based in Washington. “Many people didn’t believe that the problem could be this big. Now I hope Congress will direct the resources to making it right.” From 2011 to 2015, according to the report, nearly 92,000 troops were discharged for misconduct — the military equivalent of being fired. Troops can be discharged for reasons like testing positive for drugs or repeatedly showing up late. And in recent years, as the military was downsized, misconduct discharges surged. Of those discharged, 57,000 had a diagnosis of PTSD, traumatic brain injury (known as T.B.I.) or a related condition. About 9,000 were found to have PTSD or T.B.I. But a majority had a personality disorder or an adjustment disorder — diagnoses that count as pre-existing conditions, not war wounds. Critics of the military’s handling of mental health have long accused the military of using such diagnoses to sidestep safeguards put in place for troops with PTSD. © 2017 The New York Times Company

Keyword: Brain Injury/Concussion; Stress
Link ID: 23626 - Posted: 05.17.2017