Chapter 12. Psychopathology: Biological Basis of Behavioral Disorders
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Claudia M. Gold At the recent gubernatorial candidates forum on mental health, Martha Coakley repeated the oft-heard phrase that depression is like diabetes. Her motivation was good, the idea being to reduce the stigma of mental illness, and to offer "parity" or equal insurance coverage, for mental and physical illness. However, I am concerned that this phrase, and its companion, "ADHD is like diabetes," will, in fact, have the exact opposite effect. A recent New York Times op ed, The Trouble with Brain Science, helped me to put my finger on what is troubling about these statements. Psychologist Gary Marcus identifies the need for a bridge between neuroscience and psychology that does not currently exist. Diabetes is a disorder of insulin metabolism. Insulin is produced in the pancreas. The above analogies disregard the intimate intertwining of brain and mind. For the pancreas, there is no corresponding "mind" that exists in the realm of feelings and relationships. While there is some emerging evidence of the brain structures involved in the collection of symptoms named by the DSM (Diagnostic and Statistical Manual of Mental Disorders,) there are no known biological processes corresponding to depression, ADHD or any other diagnosis in the DSM. There is, however, a wealth of new evidence showing how brain structure and function changes in relationships. ©2014 Boston Globe Media Partners, LLC
Link ID: 19836 - Posted: 07.16.2014
By Sharon Oosthoek, CBC News Mounting evidence that gut bacteria affect mood and behaviour has researchers investigating just how much power these tiny microbes wield over our mental health. "Many people with chronic intestinal conditions also have psychological disturbances and we never understood why," says McMaster University gastroenterologist Dr. Stephen Collins. Now, scientists such as Dr. Collins are starting to come up with answers. Our lower gastrointestinal tract is home to almost 100 trillion microorganisms, most of which are bacteria. They are, by and large, "good" bacteria that help us digest food and release the energy and nutrients we need. They also crowd out bacteria that can trigger disease. But when things go awry in our guts, they can also go awry in our brains. Up to 80 per cent of people with irritable bowel syndrome experience increased anxiety and depression. And those with autism — a syndrome associated with problems interacting with others — are more likely to have abnormal levels of gut bacteria. Dr. Collins and fellow McMaster gastroenterologist Premysl Bercik have done some of the seminal research into the bacteria-brain-behaviour connection. In a study published last year, they changed the behaviour of mice by giving them fecal transplants of intestinal bacteria. It involved giving adventurous mice bacteria from timid ones, thereby inducing timid behaviour. Before the transplant, adventurous mice placed in a dark, protected enclosure spent much of their time exploring an attached bright, wide-open area. After the transplant, they rarely ventured beyond their enclosure. © CBC 2014
|By Roni Jacobson Prozac, Paxil, Celexa, Zoloft, Lexapro. These so-called selective serotonin reuptake inhibitors (SSRIs) are among the most widely prescribed drugs in the U.S. Although they are typically used to treat depression and anxiety disorders, they are also prescribed off-label for conditions such as chronic pain, premature ejaculation, bulimia, irritable bowel syndrome, premenstrual syndrome and hot flashes. Even if you have never taken an SSRI, chances are you know someone who has. About one in every 10 American adults is being prescribed one now. For women aged 40 to 59 years old, the proportion increases to one in four. SSRIs block the body from reabsorbing serotonin, a neurotransmitter mostly found in the brain, spinal cord and digestive tract whose roles include regulation of mood, appetite, sexual function and sleep. Specifically, SSRIs bind to the protein that carries serotonin between nerve cells—called SERT, for serotonin transporter—intercepting it before it can escort the released neurotransmitter back into the cell. This action leaves more active serotonin in the body, a chemical effect that is supposed to spur feelings of happiness and well-being. But there are hints that SSRIs are doing something other than simply boosting serotonin levels. First, people vary in their response to SSRIs: Studies have shown that the drugs are not very effective for mild to moderate depression, but work well when the disorder is severe. If low serotonin were the only culprit in depression, SSRIs would be more uniformly helpful in alleviating symptoms. Second, it takes weeks after starting an SSRI for depression and anxiety to lift even though changes in serotonin ought to happen pretty much right away. © 2014 Scientific American
By EMILY ANTHES It was love at first pet when Laurel Braitman and her husband adopted a 4-year-old Bernese mountain dog, a 120-pound bundle of fur named Oliver. The first few months were blissful. But over time, Oliver’s troubled mind slowly began to reveal itself. He snapped at invisible flies. He licked his tail until it was wounded and raw. He fell to pieces when he spied a suitcase. And once, while home alone, he ripped a hole in a screen and jumped out of a fourth-floor window. To everyone’s astonishment, he survived. Oliver’s anguish devastated Dr. Braitman, a historian of science, but it also awakened her curiosity and sent her on an investigation deep into the minds of animals. The result is the lovely, big-hearted book “Animal Madness,” in which Dr. Braitman makes a compelling case that nonhuman creatures can also be afflicted with mental illness and that their suffering is not so different from our own. In the 17th century, Descartes described animals as automatons, a view that held sway for centuries. Today, however, a large and growing body of research makes it clear that animals have never been unthinking machines. We now know that species from magpies to elephants can recognize themselves in the mirror, which some scientists consider a sign of self-awareness. Rats emit a form of laughter when they’re tickled. And dolphins, parrots and dogs show clear signs of distress when their companions die. Together, these and many other findings demonstrate what any devoted pet owner has probably already concluded: that animals have complex minds and rich emotional lives. Unfortunately, as Dr. Braitman notes, “every animal with a mind has the capacity to lose hold of it from time to time.” © 2014 The New York Times Company
By Lori Aratani The placebo effect — the idea that a treatment works because a patient believes it does — has long been a footnote to the work of finding ways to counteract disease. Some physicians have dismissed placebos as mere hokum, a trick of the mind. But researchers have found that in some people, placebos elicit similar responses in the brain to actual drug treatments. In one experiment, researchers using a PET scanner found that the brain activity in test subjects who received placebos and reported less pain mirrored that of those who received actual treatment for their pain. As Erik Vance writes in “Why Nothing Works,” published in the July/August 2014 issue of Discover magazine, the work suggests we possess an “inner pharmacy” of some sort that, if harnessed correctly, could be used as a complement to traditional treatments. But as Vance’s overview of recent research on the topic shows, it’s complicated. A placebo’s impact is not universal. Certain individuals — and certain conditions (pain and depression, for example) — seem to respond better than others to placebos. Researchers think that something in a person’s physiological makeup makes him more sensitive to placebos, while others feel little or no impact. There are ethical considerations, too, since it’s considered wrong to mislead volunteers participating in a study. But there are ways to navigate this thicket. In one small study, researchers gave placebos to a group of people with irritable bowel syndrome — after telling them that the pills were just placebos; a second group received no treatment. Surprisingly, many more of those who received the placebos reported improvements in their symptoms than did people in the no-treatment group.
By Adam Carter, CBC News Women who take antidepressants when they’re pregnant could unknowingly predispose their kids to type 2 diabetes and obesity later on in life, new research out of McMaster University suggests. The study, conducted by associate professor of obstetrics and gynecology Alison Holloway and PhD student Nicole De Long, found a link between the antidepressant fluoxetine and increased risk of obesity and diabetes in children. Holloway cautions that this is not a warning for all pregnant women to stop taking antidepressants, but rather to start a conversation about prenatal care and what works best on an individual basis. “There are a lot of women who really need antidepressants to treat depression. This is what they need,” Holloway told CBC. “We’re not saying you should necessarily take patients off antidepressants because of this — but women should have this discussion with their caregiver.” “Obesity and Type 2 diabetes in children is on the rise and there is the argument that it is related to lifestyle and availability of high calorie foods and reduced physical activity, but our study has found that maternal antidepressant use may also be a contributing factor to the obesity and diabetes epidemic.” According to a study out of Memorial University in St. John's, obesity rates in Canada have tripled between 1985 and 2011. Canada also ranks poorly when it comes to its overall number of cases of diabetes, according to international report from the Organization for Economic Co-operation and Development, released last year. © CBC 2014
By Brady Dennis Government warnings a decade ago about the risks associated with children and adolescents taking antidepressants appear to have backfired, causing an increase in suicide attempts and discouraging many depressed young people from seeking treatment, according to a study published Wednesday in the academic journal BMJ. Researchers said their findings underscore how even well-intentioned public health warnings can produce unintended consequences, particularly when they involve widespread media attention and sensitive topics such as depression and suicide. In 2003 and 2004, the Food and Drug Administration issued a series of warnings based on data that pointed to an increase in suicidal thinking among some children and adolescents prescribed a class of antidepressants known as selective serotonin reuptake inhibitors, or SSRIs. They included such drugs as Paxil and Zoloft. In late 2004, the agency directed manufacturers to include a “black box” warning on their labels notifying consumers and doctors about the increased risk of suicidal thoughts and behaviors in youths being treated with these medications. The FDA warnings received a flood of media coverage that researchers said focused more on the tiny percentage of patients who had experienced suicidal thinking due to the drugs than on the far greater number who benefited from them. “There was a huge amount of publicity,” said Stephen Soumerai, professor of population medicine at Harvard Medical School and a co-author of Wednesday’s study. “The media concentrated more on the relatively small risk than on the significant upside.”
Link ID: 19747 - Posted: 06.19.2014
By PAM BELLUCK Cindy Wachenheim was someone people didn’t think they had to worry about. She was a levelheaded lawyer working for the State Supreme Court, a favorite aunt who got down on the floor to play with her nieces and nephews, and, finally, in her 40s, the mother she had long dreamed of becoming. But when her baby was a few months old, she became obsessed with the idea that she had caused him irrevocable brain damage. Nothing could shake her from that certainty, not even repeated assurances from doctors that he was normal. “I love him so much, but it’s obviously a terrible kind of love,” she agonized in a 13-page handwritten note. “It’s a love where I can’t bear knowing he is going to suffer physically and mentally/emotionally for much of his life.” Ms. Wachenheim’s story provides a wrenching case study of one woman’s experience with maternal mental illness in its most extreme and rare form. It also illuminates some of the surprising research findings that are redefining the scientific understanding of such disorders: that they often develop later than expected and include symptoms not just of depression, but of psychiatric illnesses. Now these mood disorders, long hidden in shame and fear, are coming out of the shadows. Many women have been afraid to admit to terrifying visions or deadened emotions, believing they should be flush with maternal joy or fearing their babies would be taken from them. But now, advocacy groups on maternal mental illness are springing up, and some mothers are blogging about their experiences with remarkable candor. A dozen states have passed laws encouraging screening, education and treatment. And celebrities, including Brooke Shields, Gwyneth Paltrow and Courteney Cox, have disclosed their postpartum depression. © 2014 The New York Times Company
by Clare Wilson People who begin antidepressant treatment must face a gruelling wait of several weeks before they find out whether or not the drug will work for them. A new take on the causes of depression could lead to a blood test predicting who will be helped by medication – taking the guess work out of prescribing. "A test would be a major advance as at the moment millions of people are treated with antidepressants that won't have any effect," says Gustavo Turecki of McGill University in Montreal, Canada, who led the study. The research centres on miRNAs, small molecules that have an important role in turning genes on and off in different parts of the body. MiRNAs have already been implicated in several brain disorders. In the latest study, Turecki and his colleagues measured the levels of about 1000 miRNAs in the brains of people who had committed suicide. These were compared to levels in brains of people who had died from other causes. A molecule called miRNA-1202 was the most altered, being present at significantly lower levels in the brains of people who died from suicide. Crucially, this molecule seems to damp down the activity of a gene involved in glutamate signalling in the brain. That's significant because recent research has highlighted the importance of glutamate signalling in depression. © Copyright Reed Business Information Ltd.
Link ID: 19731 - Posted: 06.14.2014
By ANEMONA HARTOCOLLIS Dozens of Whole Foods stores in the Northeast and a restaurant in New York received beef over an eight-month period that may not have been properly slaughtered to reduce the threat of mad cow disease, federal officials said on Thursday. The producer of the beef, Fruitland American Meat, in Jackson, Mo., recalled thousands of pounds of bone-in grass-fed rib eyes, and two quartered beef carcasses, after federal officials reviewing slaughtering logs found that certain precautions had not been followed. The beef in question was processed between Sept. 5 and April 25, and the meat has the number 2316 inside the Agriculture Department inspection mark. The federal government said the beef posed only a “remote” health hazard, and the cows themselves had shown no evidence of the disease. Fruitland American denied on Thursday that the meat had been improperly handled. The company said the government’s finding was based on a clerical error, in which the age of the cattle had been documented as 30 months or more, when rules on mad cow must be followed, because older cows are believed to be at greater risk. But birth records showed that the cows were in fact no more than 28 months old, a spokesman said. A spokeswoman for the Agriculture Department, Alexandra Tarrant, said the agency was looking into the chance that a clerical error had occurred. The meat was shipped to 34 Whole Foods stores in northern Connecticut, Maine, Massachusetts and Rhode Island. Michael Sinatra, a spokesman for the company, said none of the meat was currently in the stores. © 2014 The New York Times Company
Link ID: 19726 - Posted: 06.14.2014
The financial crisis has been linked to a 4.5 per cent increase in Canada’s suicide rate, according to a study that estimates at least 10,000 extra suicides could be connected to economic hardship in EU countries and North America. Researchers compared suicide data from the World Health Organization before and after the onset of the recession in 2007. "A crucial question for policy and psychiatric practice is whether these suicide rises are inevitable," Aaron Reeves of Oxford University’s sociology department and his co-authors said in Wednesday’s issue of the British Journal of Psychiatry. Given that the rise in suicides exceeded what would be expected and the large variations in suicide rates across countries, the researchers suspect some of the suicides were "potentially avoidable." In Canada, the suicides rose by 4.5 per cent or about 240 suicides more than expected between 2007 and 2010. In the U.S.A, the rate increased by 4.8 per cent over the same period. Before 2007 in Europe, suicide rates had been falling, but the trend reversed, rising by 6.5 per cent by 2009 and staying elevated through 2011. Two countries, Sweden and Finland, bucked the trend in the early 1990s. Job loss, home repossession and debt are the main risk factors leading to suicide during economic downturns, previous studies suggest. © CBC 2014
By Chris Wodskou, CBC News For the past 25 years, people suffering from depression have been treated with antidepressant drugs like Zoloft, Prozac and Paxil — three of the world’s best-selling selective serotonin reuptake inhibitors, or SSRIs. But people are questioning whether these drugs are the appropriate treatment for depression, and if they could even be causing harm. The drugs are designed to address a chemical imbalance in the brain and thereby relieve the symptoms of depression. In this case, it’s a shortage of serotonin that antidepressants work to correct. In fact, there are pharmaceutical treatments targeting chemical imbalances for just about every form of mental illness, from schizophrenia to ADHD, and a raft of anxiety disorders. Hundreds of millions of prescriptions are written for antipsychotic, antidepressant and anti-anxiety medications every year in the United States alone, producing billions of dollars in revenue for pharmaceutical companies. But what if the very premise behind these drugs is flawed? What if mental illnesses like depression aren’t really caused by chemical imbalances, and that millions of the people who are prescribed those drugs derive no benefit from them? And what if those drugs could actually make their mental illness worse and more intractable over the long term? Investigative journalist Robert Whitaker argued that psychiatric drugs are a largely ineffective way of treating mental illness in his 2010 book called Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs and the Astonishing Rise of Mental Illness in America. Whitaker maintains that the foundation of modern psychiatry, the chemical imbalance model, is scientifically unproven. © CBC 2014
Link ID: 19712 - Posted: 06.09.2014
By Meeri Kim, Many of us find ourselves swimming along in the tranquil sea of life when suddenly a crisis hits — a death in the family, the loss of a job, a bad breakup. Some power through and find calm waters again, while others drown in depression. Scientists continue to search for the underlying genes and neurobiology that dictate our reactions to stress. Now, a study using mice has found a switch-like mechanism between resilience and defeat in an area of the brain that plays an important role in regulating emotions and has been linked with mood and anxiety disorders. (Bo Li/Cold Spring Harbor Laboratory) - Researchers at Cold Spring Harbor Laboratory identify the neurons in the brain that determine if a mouse will learn to cope with stress or become depressed. These neurons, located in a region of the brain known as the medial prefrontal cortex (top, green image) become hyperactive in depressed mice. The bottom panel is close-up of above image - yellow indicates activation. The team showed that this enhanced activity causes depression. After artificially enhancing the activity of neurons in that part of the brain — the medial prefrontal cortex — mice that previously fought to avoid electric shocks started to act helpless. Rather than leaping for an open escape route, they sat in a corner taking the pain — presumably out of a belief that nothing they could do would change their circumstances. “This helpless behavior is quite similar to what clinicians see in depressed individuals — an inability to take action to avoid or correct a difficult situation,” said study author and neuroscientist Bo Li of the Cold Spring Harbor Laboratory in New York. The results were published online May 27 in the Journal of Neuroscience. © 1996-2014 The Washington Post
Link ID: 19704 - Posted: 06.06.2014
by Bethany Brookshire We all respond to stress in different ways. Some of us work harder. Others drink more or eat our feelings. Sometimes we experience sleep loss, heart palpitations or sweats. When the stress dissipates, many of us go back to our daily lives, none the worse for wear. We are resilient. But some people find that stress is a first step on the way to a major depressive episode. It’s not quite clear what’s different between people who go back to normal after stress, and those who descend into depression. “One of the most important questions is, how do the brains of resilient animals (or humans) differ from those that are vulnerable to depression following stress?” asks John Morrison, a neuroscientist at the Icahn School of Medicine at Mount Sinai in New York. A new study from Minghui Wang and colleagues at Cold Spring Harbor Laboratory in New York provides a new hint. Mice with a depressive-like response to stress have stronger connections between neurons in the medial prefrontal cortex of the brain following the stress. Resilient mice show weaker connections. The mechanism could help scientists understand why some people respond to stress with depression, while others are able to shake it off. The prefrontal cortex is best known for its role in executive function — thought, memory, prediction and other tasks. But dysfunction in some areas of the cortex, particularly one called Brodmann area 25, has been linked with recurring major depressive disorder. Scientists have been electrically stimulating this area to relieve depression in patients. But researchers still don’t understand what makes this brain area important in depression, and how dysfunctions might occur. “I’ve had a long interest in the mechanism of human diseases like depression,” says study coauthor Bo Li, a cellular and behavioral neuroscientist at Cold Spring Harbor. “The idea has been to identify an area that is responsible, to link a mechanism in the brain to a behavior.” Wang, Li and their colleagues were especially interested in changes to the mouse prefrontal cortex following stress. © Society for Science & the Public 2000 - 2013.
Joy Jernigan TODAY contributor Depression is a serious medical condition that affects millions of Americans — and nearly twice as many women as men. Symptoms can include persistent feelings of sadness or hopelessness and loss of interest in activities that were once pleasurable, according to the National Institute of Mental Health. Other symptoms include feelings of guilt or worthlessness, irritability, changes in appetite, increased fatigue, difficulty concentrating — even recurrent thoughts of suicide. About 12 million American women suffer from depression each year, women like Debi Lee. Although depression is treatable, most commonly with medications or counseling, many never seek help, often because they are too embarrassed or ashamed. "Depression is really a physical illness," said Dr. Andrew Leuchter, a psychiatrist at the Semel Institute for Neuroscience and Human Behavior at University of California, Los Angeles. It's a disorder that even can be seen in brain scans, with images clearly showing the difference between a normal functioning brain and the brain of someone suffering from depression. "When you show this image to a person who's struggling with depression and you show them that their brain looks different than the quote so-called healthy person, what's their reaction?" Shriver asked. "It's commonly one of relief," Leuchter said. Now, Dr. Leuchter says there's an innovative new treatment called synchronized transcranial magnetic stimulation, or sTMS, that may have the potential to provide relief. Dr. Leuchter, a consultant and stockholder in the company behind sTMS, says it syncs to each patient's brain, then stimulates it with low levels of magnetic energy, 30 minutes a day for several weeks.
Link ID: 19689 - Posted: 06.04.2014
By Lara Salahi A team of researchers at Massachusetts General Hospital have embarked on a new project to create an implantable device in the brain that would read and alter the emotions of someone with a mental illness. The team is working in collaboration with researchers at the University of California, San Francisco, on a new program funded by the Department of Defense’s Defense Advanced Research Projects Agency (DARPA). The researchers are working to create an implantable device that can sense abnormal activity in the brain using algorithms, and then deliver electrical impulses to certain parts of the brain that would suppress the abnormal signals. “Imagine if I have an addiction to alcohol and I have a craving,” Jose Carmena, a researcher at the University of California, Berkeley, who is involved in the project, told MIT Technology Review. “We could detect that feeling and then stimulate inside the brain to stop it from happening.” Mental illness and suicide rates among the US military have spiked over the past decade, the National Institute of Mental Healthreports. The current research is part of DARPA’s emerging neurotechnology therapy program which investigates new approaches to treat neuropsychological illnesses among military servicemembers and veterans. Their goal is to treat at least seven psychiatric conditions, including depression, post-traumatic stress disorder, addiction, and fibromyalgia.
Jyoti Madhusoodanan Most people handle stress well, but some find it difficult to cope and as a result develop depression and other mood disorders. Researchers have previously been able to identify the part of the brain that controls this response, but not exactly how it does so. Now, a study in mice identifies a small group of neurons that could be responsible. The research might also help elucidate the mechanism of deep brain stimulation, a therapy that uses electrical impulses to treat depression and other neurological disorders. How an animal deals with stress is controlled by a part of the brain known as the prefrontal cortex, and the neurons in this part of the brain are known to change in structure and function in response to stressful situations1. To look at the cellular basis of the responses, neuroscientist Bo Li of Cold Spring Harbor Laboratory in New York and his colleagues subjected mice to small electric shocks at random intervals to produce stress. Most of the mice tried to avoid the shocks, but just over one-fifth did not. They also started to avoid other animals or failed to choose tasty foods over plain ones — typical signs of depressive behaviour. The researchers then looked at the animals' brains and found that a specific set of neurons in the prefrontal cortex were easily excitable in depressed mice, but much harder to excite in those resilient to the stress. Furthermore, artificially increasing the activity of these neurons caused mice that were once resilient to become susceptible to depressive behaviours. “We were surprised that we were able to see a difference between depressed and resilient animals at the level of synaptic transmission,” says Li. © 2014 Nature Publishing Group,
By NICHOLAS BAKALAR The hormone estrogen is the recommended treatment for menopausal night sweats and hot flashes, but some women are unable or unwilling to use it. Now a clinical trial suggests that the antidepressant venlafaxine, often used as an alternative, is equally effective. In an eight-week placebo-controlled double-blind study, researchers randomly assigned 339 perimenopausal and postmenopausal women to one of three treatments: 0.5 milligrams a day of estrogen (in the form of estradiol), 75 milligrams a day of the antidepressant venlafaxine (a generic form of Effexor), or a placebo. Before the start of the study, all the women had had symptoms at least 14 times a week. Compared to the rate before the study — an average of 8.1 episodes a day — the frequency of hot flashes and night sweats declined by 52.9 percent in the estradiol group, 47.6 percent in the Effexor group, and 28.6 percent among those who took a placebo. Both Effexor and estradiol were effective treatments, but the study, published online in JAMA Internal Medicine, was not large enough to show that one was significantly better than the other. “Women have important choices of different medications to discuss with their doctors,” said the lead author, Dr. Hadine Joffe, an associate professor of psychiatry at Harvard. “They should know, as they think about these options, that both are effective.” © 2014 The New York Times Company
Keyword: Hormones & Behavior
Link ID: 19673 - Posted: 05.31.2014
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
Link ID: 19647 - Posted: 05.23.2014
|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