Chapter 12. Psychopathology: Biological Basis of Behavioral Disorders
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Emily Anthes Anna's life began to unravel in 2005 when her husband of 30 years announced that he had fallen in love with another woman. “It had never even occurred to me that my marriage could ever end,” recalls Anna, a retired lawyer then living in Philadelphia, Pennsylvania. “It was pretty shocking.” Over the course of several months, Anna stopped wanting to get up in the morning. She felt tired all the time, and consumed by negative thoughts. “'I'm worthless.' 'I messed up everything.' 'It's all my fault.'” She needed help, but her first therapist bored her and antidepressants only made her more tired. Then she found Cory Newman, director of the Center for Cognitive Therapy at the University of Pennsylvania, who started her on a different kind of therapy. Anna learned how to obsess less over her setbacks and give herself more credit for her triumphs. “It was so helpful to talk to someone who steered me to more positive ways of thinking,” says Anna, whose name has been changed at her request. Cognitive therapy, commonly known as cognitive behavioural therapy (CBT), aims to help people to identify and change negative, self-destructive thought patterns. And although it does not work for everyone with depression, data have been accumulating in its favour. “CBT is one of the clear success stories in psychotherapy,” says Stefan Hofmann, a psychologist at Boston University in Massachusetts. Antidepressant drugs are usually the first-line treatment for depression. They are seen as a quick, inexpensive fix — but clinical trials reveal that only 22–40% of patients emerge from depression with drugs alone. Although there are various approaches to psychotherapy, CBT is the most widely studied; a meta-analysis1 published this year revealed that, depending on how scientists measure outcomes, between 42% and 66% of patients no longer meet the criteria for depression after therapy. © 2014 Nature Publishing Group
Link ID: 20306 - Posted: 11.13.2014
Heidi Ledford If the extent of human suffering were used to decide which diseases deserve the most medical attention, then depression would be near the top of the list. More than 350 million people are affected by depression, making it one of the most common disorders in the world. It is the biggest cause of disability, and as many as two-thirds of those who commit suicide have the condition. But although depression is common, it is often ignored. Three-quarters of people with depression in the United Kingdom go undiagnosed or untreated — and even if the disorder is diagnosed, today's medications will work well for only about half of those who seek help. “It's unbelievable,” says Tom Foley, a psychiatrist at Newcastle University, UK. “If that was the case in cancer care, it would be an absolute scandal.” The comparison between depression and cancer is a common one. Cancer, too, is a terrible blight: it affects more than 32 million people and kills some 8 million a year, many more than depression. But at least in developed countries, the vast majority of people with recognized cancers do receive treatment. In research, too, depression has failed to keep up with cancer. Cancer research today is a thriving field, unearthing vast catalogues of disease-associated mutations, cranking out genetically targeted therapies and developing sophisticated animal models. Research into depression, meanwhile, seems to have floundered: once-hopeful therapies have failed in clinical trials, genetic studies have come up empty-handed. The field is still struggling to even define the disease — and overcome the stigma associated with it. © 2014 Nature Publishing Grou
Link ID: 20305 - Posted: 11.13.2014
By Julia Calderone Antidepressant use among Americans is skyrocketing. Adults in the U.S. consumed four times more antidepressants in the late 2000s than they did in the early 1990s. As the third most frequently taken medication in the U.S., researchers estimate that 8 to 10 percent of the population is taking an antidepressant. But this spike does not necessarily signify a depression epidemic. Through the early 2000s pharmaceutical companies were aggressively testing selective serotonin reuptake inhibitors (SSRIs), the dominant class of depression drug, for a variety of disorders—the timeline below shows the rapid expansion of FDA-approved uses. As the drugs' patents expired, companies stopped funding studies for official approval. Yet doctors have continued to prescribe them for more ailments. One motivating factor is that SSRIs are a fairly safe option for altering brain chemistry. Because we know so little about mental illness, many clinicians reason, we might as well try the pills already on the shelf. Doctors commonly use antidepressants to treat many maladies they are not approved for. In fact, studies show that between 25 and 60 percent of prescribed antidepressants are actually used to treat nonpsychological conditions. The most common and well-supported off-label uses of SSRIs include: Abuse and dependence ADHD (in children and adolescents) Anxiety disorders Autism (in children) Bipolar disorder Eating disorders Fibromyalgia Neuropathic pain Obsessive-compulsive disorder Premenstrual dysphoric disorder © 2014 Scientific American
Link ID: 20300 - Posted: 11.11.2014
BY Laura Sanders The first time Nathan Whitmore zapped his brain, he had a college friend standing by, ready to pull the cord in case he had a seizure. That didn’t happen. Instead, Whitmore started experimenting with the surges of electricity, and he liked the effects. Since that first cautious attempt, he’s become a frequent user of, and advocate for, homemade brain stimulators. Depending on where he puts the electrodes, Whitmore says, he has expanded his memory, improved his math skills and solved previously intractable problems. The 22-year-old, a researcher in a National Institute on Aging neuroscience lab in Baltimore, writes computer programs in his spare time. When he attaches an electrode to a spot on his forehead, his brain goes into a “flow state,” he says, where tricky coding solutions appear effortlessly. “It’s like the computer is programming itself.” Whitmore no longer asks a friend to keep him company while he plugs in, but he is far from alone. The movement to use electricity to change the brain, while still relatively fringe, appears to be growing, as evidenced by a steady increase in active participants in an online brain-hacking message board that Whitmore moderates. This do-it-yourself community, some of whom make their own devices, includes people who want to get better test scores or crush the competition in video games as well as people struggling with depression and chronic pain, Whitmore says. As reckless as it sounds to juice a brain at home with a 9-volt battery and 40 dollars’ worth of spare parts, this technology’s buzz is based on legit science. Small laboratory studies suggest that carefully controlled brain stimulation can boost a person’s memory and math abilities, hone attention and fast-track learning. The U. S. military is interested and is funding studies to test brain stimulation as a way to boost soldiers’ alertness and vigilance. The technique may even be a viable treatment for pernicious mental disorders such as major depression, according to other laboratory-based studies. © Society for Science & the Public 2000 - 2014.
By Erin Allday Stanford researchers have found some striking abnormalities in the brains of people with chronic fatigue syndrome, a frustrating and debilitating condition for which there is no known cause and no treatment that’s widely effective. The findings, published Wednesday in the journal Radiology, could improve diagnosis and spark new scientific understanding of the disease. Perhaps even more noteworthy, the results — if they can be confirmed with larger studies — could provide some of the first objective evidence that chronic fatigue syndrome is a severe illness that causes real physiological damage. That would be a major step for patients and their advocates, who still suffer under the stigma of having a condition that for decades was ignored or not taken seriously. “If this finding holds, it will be exciting because yes, we’ve found something that has never been found before. But there’s this additional layer of looking at a disease that was completely ostracized. So there’s also this component of validation,” said Dr. Jose Montoya, an infectious disease specialist who helped establish a chronic fatigue syndrome team at Stanford School of Medicine a decade ago. Montoya was the senior author of the Stanford study. For patients, Montoya said, “It’s almost like we’re saying, 'You were right all along. Hopefully this will put you where you deserve to be, in a real clinic with treatments.’” There are limitations to the study, Montoya said. Most notably, the sample size is fairly small, with 15 chronic fatigue patients and 14 healthy control subjects.
Link ID: 20256 - Posted: 10.29.2014
By Michael Hedrick I have a hard time making friends. Getting to trust people well enough to call them a friend takes a lot of work. It’s especially hard when you are living with schizophrenia and think everyone is making fun of you. Schizophrenia is the devil on your shoulder that keeps whispering in your ear and, no matter what you try, the little demon won’t stop. He hasn’t stopped in the almost nine years I’ve lived with the illness, and he’s not about to stop now. He’s just quieted down a bit. I’d call him my companion but that would imply a degree of friendship, and there’s no way in hell I’m the little devil’s friend. I have plenty of acquaintances, and a couple hundred “friends” on Facebook. But real friends, mostly family, I can count on one hand. For me, making friends is like climbing a vertical rock wall with no ropes, requiring a degree of thrill-seeking, and a good deal of risk. For someone to be my friend, they have to accept that I’m crazy, and even getting to the point of telling them that is daunting when all you hear is the devil’s whispering that they’re making snap judgments about you or will be going back to their real friends and laughing about you. But interestingly, in my efforts to make friends, coffee shops have helped. The simple routine of going to get your fix of liquid energy every day provides a sort of breeding ground for community. You see these people every day,whether you like it or not and, over time, friendships form. I used to live in a small town called Niwot, about five miles down the highway from Boulder, where I now live. Every morning around 6 I would go to Winot Coffee, the small independent coffee shop, and every morning, without fail, there was a guy my age sitting outside with his computer smoking clove cigarettes. Given the regularity of seeing him every morning, and given that we were some of the only 20-somethings in town, we got to talking. © 2014 The New York Times Company
Link ID: 20240 - Posted: 10.25.2014
Scientists say they have identified the underlying reason why some people are prone to the winter blues, or seasonal affective disorder (SAD). People with Sad have an unhelpful way of controlling the "happy" brain signalling compound serotonin during winter months, brain scans reveal. As the nights draw in, production of a transporter protein ramps up in Sad, lowering available serotonin. The work will be presented this week at a neuropsychopharmacology conference. The University of Copenhagen researchers who carried out the trial say their findings confirm what others have suspected - although they only studied 11 people with Sad and 23 healthy volunteers for comparison. Using positron emission tomography (PET) brain scans, they were able to show significant summer-to-winter differences in the levels of the serotonin transporter (SERT) protein in Sad patients. The Sad volunteers had higher levels of SERT in the winter months, corresponding to a greater removal of serotonin in winter, while the healthy volunteers did not. Winter depression Lead researcher, Dr Brenda Mc Mahon, said: "We believe that we have found the dial the brain turns when it has to adjust serotonin to the changing seasons. BBC © 2014
by Amy Standen The important thing is that Meghan knew something was wrong. When I met her, she was 23, a smart, wry young woman living with her mother and stepdad in Simi Valley, about an hour north of Los Angeles. Meghan had just started a training program to become a respiratory therapist. Concerned about future job prospects, she asked NPR not to use her full name. Five years ago, Meghan's prospects weren't nearly so bright. At 19, she had been severely depressed, on and off, for years. During the bad times, she'd hide out in her room making thin, neat cuts with a razor on her upper arm. "I didn't do much of anything," Meghan recalls. "It required too much brain power." "Her depression just sucked the life out of you," Kathy, Meghan's mother, recalls. "I had no idea what to do or where to go with it." One night in 2010, Meghan's mental state took an ominous turn. Driving home from her job at McDonald's, she found herself fascinated by the headlights of an oncoming car. "I had the weird thought of, you know, I've never noticed this, but their headlights really look like eyes." To Meghan, the car seemed malicious. It wanted to hurt her. Kathy tried to reason with her. "Honey, you know it's a car, right? You know those are headlights," she recalls pressing her daughter. "You understand that this makes no sense, right?" © 2014 NPR
Link ID: 20223 - Posted: 10.21.2014
By David Bornstein Shortly after the birth of her daughter, Andrea became severely depressed. She was 17 at the time and she didn’t fully understand what she was going through; she just felt like a failure. “I felt like I didn’t want to be alive,” she recalls. “I felt like I didn’t deserve to be alive. I felt like a bad person and a bad mother, and I was never going to get any better.” When her baby persisted in crying, she felt her frustration mount quickly. “I was hitting a boiling point,” she says. “I was at a point where I didn’t want to deal with anything. Sometimes I would just let her cry — but then I would feel very bad afterwards.” Depression is the most common health problem women face. In the United States, outside of obstetrics, it is the leading cause of hospitalizations among women ages 15 to 44. It’s estimated that 20 percent to 25 percent of women will experience depression during their lifetimes, and about one in seven will experience postpartum depression. For low-income women, the rates are about twice as high. As my colleague Tina Rosenberg has reported, the World Health Organization ranks depression as the most burdensome of all health conditions affecting women (as measured by lost years of productive life). Postpartum depressions are often assumed to be associated with hormonal changes in women. In fact, only a small fraction of them are hormonally based, said Cindy-Lee Dennis, a professor at the University of Toronto and a senior scientist at Women’s College Research Institute, who holds a Canada Research Chair in Perinatal Community Health. The misconception is itself a major obstacle, she adds. Postpartum depression is often not an isolated form of depression; nor is it typical. “We now consider depression to be a chronic condition,” Dennis says. “It reoccurs in approximately 30 to 50 percent of individuals. And a significant proportion of postpartum depression starts during the pregnancy but is not detected or treated to remission. We need to identify symptoms as early as possible, ideally long before birth.” © 2014 The New York Times Company
A drug being studied as a fast-acting mood-lifter restored pleasure-seeking behavior independent of — and ahead of — its other antidepressant effects, in a National Institutes of Health trial. Within 40 minutes after a single infusion of ketamine, treatment-resistant depressed bipolar disorder patients experienced a reversal of a key symptom — loss of interest in pleasurable activities — which lasted up to 14 days. Brain scans traced the agent’s action to boosted activity in areas at the front and deep in the right hemisphere of the brain. “Our findings help to deconstruct what has traditionally been lumped together as depression,” explained Carlos Zarate, M.D., of the NIH’s National Institute of Mental Health. “We break out a component that responds uniquely to a treatment that works through different brain systems than conventional antidepressants — and link that response to different circuitry than other depression symptoms.” This approach is consistent with the NIMH’s Research Domain Criteria project, which calls for the study of functions – such as the ability to seek out and experience rewards – and their related brain systems that may identify subgroups of patients in one or multiple disorder categories. Zarate and colleagues reported on their findings Oct. 14, 2014 in the journal Translational Psychiatry. Although it’s considered one of two cardinal symptoms of both depression and bipolar disorder, effective treatments have been lacking for loss of the ability to look forward to pleasurable activities, or anhedonia. Long used as an anesthetic and sometimes club drug, ketamine and its mechanism-of-action have lately been the focus of research into a potential new class of rapid-acting antidepressants that can lift mood within hours instead of weeks.
By Jane E. Brody In the 1997 film “As Good As It Gets,” Jack Nicholson portrays Melvin Udall, a middle-aged man with obsessive-compulsive disorder who avoids stepping on cracks, locks doors and flips light switches exactly five times, and washes his hands repeatedly, each time tossing out the new bar of soap he used. He brings wrapped plastic utensils to the diner where he eats breakfast at the same table every day. Though the film is billed as a romantic comedy, Melvin’s disorder is nothing to laugh about. O.C.D. is often socially, emotionally and vocationally crippling. It can even be fatal. Four years ago, John C. Kelly, 24, killed himself in Irvington, N.Y., after a long battle with a severe form of obsessive-compulsive disorder. Mr. Kelly was a devoted baseball player, and now friends hold an annual softball tournament to raise money for the foundation established in his honor to increase awareness of the disorder. Obsessive thoughts and compulsive behaviors occur in almost every life from time to time. I have a fair share of compulsive patterns: seasonings arranged in strict alphabetical order; kitchen equipment always put back the same way in the same place; two large freezers packed with foods just in case I need them. I hold onto a huge collection of plastic containers, neatly stacked with their covers, and my closets bulge with clothes and shoes I haven’t worn in years, and probably never will again — yet cannot bring myself to give away. But these common habits fall far short of the distressing obsessions and compulsions that are the hallmarks of O.C.D.: intrusive, disturbing thoughts or fears that cannot be ignored and compel the sufferer to engage in ritualistic, irrational behaviors to relieve the resulting anxiety.
Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 20208 - Posted: 10.16.2014
Patients with schizophrenia are already known to have higher rates of premature death than the general population. The study found that elevated risks of heart disease and metabolic issues such as high blood sugar in people with first episode psychosis are due to an interaction of mental illness, unhealthy lifestyle behaviors and antipsychotic medications that may accelerate these risks. Patients entered treatment with significant health concerns – including excess weight, smoking, and metabolic issues – despite an average age of only 24 years. The study identifies key opportunities for health care systems to improve the treatment of such patients with first episode psychosis. The research was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. Christoph Correll, M.D., of The Zucker Hillside Hospital, Hofstra North Shore-Long Island Jewish School of Medicine, New York, and colleagues, report their findings on Oct. 8, 2014 in JAMA Psychiatry. The study is among the first of several to report results from the Recovery After an Initial Schizophrenia Episode (RAISE) project, which was developed by NIMH to examine first episode psychosis before and after specialized treatment was offered in community settings. The researchers studied nearly 400 individuals between the ages of 15 and 40 with first episode psychosis, who presented for treatment at 34 community-based clinics across 21 states. The frequency of obesity was similar to the same age group in the general population. However, smoking and metabolic syndrome (a combination of conditions including obesity, high blood pressure, high blood sugar, and abnormal blood fats, such as cholesterol and triglycerides) were much more common.
Link ID: 20182 - Posted: 10.09.2014
By Julie Rehmeyer Eight years ago, collapsed on a neurologist’s examining table, I asked a naive question that turned out to be at the center of a long-running controversy: “So what is chronic fatigue syndrome?” I had just been diagnosed with the illness, which for six years had been gradually overtaking me. A week earlier, I had woken up barely able to walk. Fatigue hardly described what I felt. Paralysis was more like it. My legs seemed to have been amputated and replaced with tubes of liquid concrete, and just shifting them on the table made me grunt like an Olympic weightlifter. My bones hurt; my brain felt like a swollen mass. Speaking required tracking down and spearing each word individually as it scampered away from me. I felt as capable of writing an article about science — my job — as of killing a rhino with my teeth. “We don’t understand it very well,” my neurologist said, his face blank. He could recommend no tests, no treatments, no other doctors. I came to understand that, for him, the term chronic fatigue syndrome meant “I can’t help you.” My neurologist’s understanding of the illness mirrored that of many doctors, who believe two things about CFS: that it’s probably psychosomatic and that there’s nothing doctors can do for it. One survey found that nearly half of doctors thought that CFS was or might be psychosomatic, and 58 percent said there wasn’t enough information available to help them diagnose it. An examination of medical textbooks found that CFS was underrepresented, even compared with less-prevalent illnesses.
|By Brian Bienkowski and Environmental Health News On his farm in Iowa, Matt Peters worked from dawn to dusk planting his 1,500 acres of fields with pesticide-treated seeds. “Every spring I worried about him,” said his wife, Ginnie. “Every spring I was glad when we were done.” In the spring of 2011, Ginnie Peters' “calm, rational, loving” husband suddenly became depressed and agitated. “He told me ‘I feel paralyzed’,” she said. “He couldn’t sleep or think. Out of nowhere he was depressed.” A clinical psychologist spoke to him on the phone and urged him to get medical help. “He said he had work to do, and I told him if it’s too wet in the morning to plant beans come see me,” Mike Rossman said. “And the next day I got the call.” Peters took his own life. He was 55 years old. No one knows what triggered Peters’ sudden shift in mood and behavior. But since her husband’s death, Ginnie Peters has been on a mission to not only raise suicide awareness in farm families but also draw attention to the growing evidence that pesticides may alter farmers’ mental health. “These chemicals that farmers use, look what they do to an insect. It ruins their nervous system,” Peters said. “What is it doing to the farmer?” Farming is a stressful job – uncontrollable weather, physical demands and economic woes intertwine with a personal responsibility for land that often is passed down through generations. But experts say that some of the chemicals used to control pests may make matters worse by changing farmers’ brain chemistry. © 2014 Scientific American
|By Tori Rodriguez The safety of football continues to be a heated topic for players and parents, with mixed evidence regarding the effect of head injuries on mental illness. Past studies on the connection have often been methodologically flawed or yielded ambiguous results. Now a paper in April in the American Journal of Psychiatry, the largest study yet to investigate the link, finds that even a single head injury indeed increases the risk of later mental illness, especially if the injury occurs during adolescence. Using Danish medical registries, researchers led by physician Sonja Orlovska of the University of Copenhagen studied 113,906 people who had been hospitalized for head injuries over a 23-year period. They discovered that in addition to cognitive symptoms caused by structural damage to the brain (such as delirium), these people were subsequently more likely than the general population to develop several psychiatric illnesses. Risk increased by 65 percent for schizophrenia and 59 percent for depression. Risk was highest in the first year postinjury but remained significantly elevated throughout the next 15 years. After the team controlled for several potential confounders, such as accident proneness and a family history of psychiatric problems, they found the strongest injury-related predictor for later onset of schizophrenia, depression and bipolar disorder was a head trauma experienced between the ages of 11 and 15. “Previous studies have shown that head injury induces inflammation in the brain, which causes several changes—for example, an increased permeability of the blood-brain barrier,” Orlovska says. Normally the barrier protects the brain from potentially harmful contents in the bloodstream, but injury-induced inflammation may allow these substances access to the brain. “For some individuals, this might initiate damaging processes in the brain,” she says. © 2014 Scientific American,
Have you ever wrongly suspected that other people are out to harm you? Have you been convinced that you’re far more talented and special than you really are? Do you sometimes hear things that aren’t actually there? These experiences – paranoia, grandiosity and hallucinations in the technical jargon – are more common among the general population than is usually assumed. But are people who are susceptible simply “made that way”? Are they genetically predisposed, in other words, or have their life experiences made them more vulnerable to these things? It’s an old debate: which is more important, nature or nurture? Scientists nowadays tend to agree that human psychology is a product of a complex interaction between genes and experience – which is all very well, but where does the balance lie? Scientists (including one of the authors of this blog) recently conducted the first ever study among the general population of the relative contributions of genes and environment to the experience of paranoia, grandiosity and hallucinations. How did we go about the research? First, it is important to be clear about the kinds of experience we measured. By paranoia, we mean the unfounded or excessive fear that other people are out to harm us. Grandiosity denotes an unrealistic conviction of one’s abilities and talents. Hallucinations are sensory experiences (hearing voices, for instance) that aren’t caused by external events. Led by Dr Angelica Ronald at Birkbeck, University of London, the team analysed data on almost 5,000 pairs of 16-year-old twins. This is the classical twin design, a standard method for gauging the relative influence of genes and environment. Looking simply at family traits isn’t sufficient: although family members share many genes, they also tend to share many of the same experiences. This is why studies involving twins are so useful. © 2014 Guardian News and Media Limited
Link ID: 20147 - Posted: 10.02.2014
By Gretchen Reynolds Exercise may help to safeguard the mind against depression through previously unknown effects on working muscles, according to a new study involving mice. The findings may have broad implications for anyone whose stress levels threaten to become emotionally overwhelming. Mental health experts have long been aware that even mild, repeated stress can contribute to the development of depression and other mood disorders in animals and people. Scientists have also known that exercise seems to cushion against depression. Working out somehow makes people and animals emotionally resilient, studies have shown. But precisely how exercise, a physical activity, can lessen someone’s risk for depression, a mood state, has been mysterious. So for the new study, which was published last week in Cell, researchers at the Karolinska Institute in Stockholm delved into the brains and behavior of mice in an intricate and novel fashion. Mouse emotions are, of course, opaque to us. We can’t ask mice if they are feeling cheerful or full of woe. Instead, researchers have delineated certain behaviors that indicate depression in mice. If animals lose weight, stop seeking out a sugar solution when it’s available — because, presumably, they no longer experience normal pleasures — or give up trying to escape from a cold-water maze and just freeze in place, they are categorized as depressed. And in the new experiment, after five weeks of frequent but intermittent, low-level stress, such as being restrained or lightly shocked, mice displayed exactly those behaviors. They became depressed. The scientists could then have tested whether exercise blunts the risk of developing depression after stress by having mice run first. But, frankly, from earlier research, they knew it would. They wanted to parse how. So they bred pre-exercised mice. © 2014 The New York Times Company
Link ID: 20145 - Posted: 10.01.2014
by Bethany Brookshire Isaac Newton famously showed that in physics, every action has an equal and opposite reaction. A similar push-and-pull of positive and negative inputs also exists in our brains. Brain cells can send out excitatory chemical signals, and they can also receive inhibitory chemical signals, putting the brakes on further signaling. This delicate balance of excitation and inhibition allows our brains to function normally and to react to the world around us. A new study shows that the same neurons contribute excitatory and inhibitory chemical signals in a brain area linked with how we process disappointment, and that antidepressants might be able to change this delicate molecular dance and stop some of the negative thought cycles associated with depression. But while the work finds an association, it’s not yet proof that the balance of these chemicals holds the key to relieving depressive symptoms. The study, published September 19 in Science, focuses on the lateral habenula. This tiny area makes up the “stalk” connecting the pineal gland to the rest of the brain. It receives inputs from areas of the brain important in reward and emotional processing, including the basal ganglia. Some areas of the brain appear to specialize in predicting rewards, showing increases in activity in response to enjoyable things such as food, sex or drugs. Activity in these areas lets us know when things are about to get good. But for every high there is a low. The lateral habenula is thought to play a role in how we process negative events: Getting a lemon on the slot machine again or the empty inbox on your dating site. Studies in monkeys and other animals have shown that increased activity in the habenula is linked to depressive behaviors, and treatment with antidepressants decreases this activity. In addition, a study in rats and a 2009 case study in a human patient showed that deep-brain stimulation in the lateral habenula could relieve symptoms of depression. © Society for Science & the Public 2000 - 2014.
Link ID: 20125 - Posted: 09.27.2014
By Dick Miller, CBC News Dan Campbell felt the bullets whiz past his head. The tracer rounds zipped between his legs. It was his first firefight as a Canadian soldier in Afghanistan. "I was completely frightened and scared like I’d never been before in my life,” he says. As the attack continued, the sights, sounds and smells started to form memories inside his brain. The fear he felt released the hormone norepinephrine, and in the complex chemistry of the brain, the memories of the battle became associated with the fear. 'I think one day, hopefully in the not-too-distant future, we will be able to delete a memory.'- Dr. Sheena Josselyn, senior scientist, Hospital For Sick Children Research Institute Six years later, a sight or sound such as a firecracker or car backfiring can remind him of that night in 2008. The fear comes back and he relives rather than remembers the moments. "It can be hard. Physically, you know, there’s the tapping foot, my heart beating,” he says. Like so many soldiers and victims of assault or people who have experienced horrific accidents, Campbell was diagnosed with post traumatic stress disorder. Now a newspaper reporter in Yellowknife, Campbell thinks one day he may get therapy. But for now he is working on his own to control the fear and anger the memories bring. © CBC 2014
|By Simon Makin The Claim Casual cannabis use harms young people's brains. The Facts A study found differences in the brains of users and nonusers, but it did not establish that marijuana use caused the variations or that they had any functional significance. The Details Researchers at Northwestern University and Harvard Medical School conducted MRI scans of two groups of 20 young adults ages 18 to 25. One group reported using marijuana at least once a week, smoking 11 joints a week on average, whereas the other had used it less than five times total and not at all during the last year. Neither group had any psychiatric disorders, and the users were psychiatrically assessed as not dependent on the drug. The study focused on two brain regions involved in processing rewards, the nucleus accumbens and the amygdala. These areas create pleasurable experiences of things such as food and sex, as well as the high associated with drugs, and have been shown to change in animals given THC, the main psychoactive component of cannabis. The researchers found that cannabis users had more gray matter density in the left nucleus accumbens and left amygdala, as well as differences in the shape of the left nucleus accumbens and right amygdala. The left nucleus accumbens also tended to be slightly larger in users. They concluded that recreational cannabis use might be associated with abnormalities in the brain's reward system. News reports have proclaimed that scientists have shown that even casual cannabis use harms young people's brains. The Caveats The most obvious problem with leaping to that conclusion is that the scans were conducted at only one point. © 2014 Scientific American