Links for Keyword: Depression

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|By Simon Makin For decades two very different treatments of depression have existed side by side. Medications act on molecules, cells and synapses in the brain. Psychological therapies focus on cognition and behavior, trying to alter negatively biased thinking. Now a new theory suggests that these interventions may work in more similar ways than anyone realized, providing an opportunity to better integrate the two approaches. More important, it may help provide patients faster, more reliable relief from this crippling condition. Antidepressant drugs increase the levels of certain chemical messengers in the brain, such as serotonin and norepinephrine. Yet exactly how these neurotransmitters affect mood is unknown. “There was a missing link between the cellular, molecular and synaptic bases of these drugs, on the one hand, and what they affect in humans, which is their experiences, perceptions, memories and feelings,” says Catherine Harmer, a neuroscientist at the University of Oxford. The psychological explanation, meanwhile, describes depression in terms of distorted information processing. Depressed people are thought to process perceptions, experiences and memories with a negative bias. Many studies confirm that depressed individuals show increased sensitivity to sad faces, greater memory for negative material and reduced responsiveness to rewards as compared with healthy people. Successful therapies teach patients how to correct for this clouded vision. Harmer now believes that antidepressants may also work by altering this negative emotional processing. About a decade ago she and her colleagues tested the effects of commonly prescribed antidepressants on healthy volunteers and found that many of the drugs skewed emotional processing to the positive. Previous research had shown that antidepressants also change these measures in depressed people, but studies included only patients who had been on medication for six to eight weeks because the drugs were assumed to take that long to kick in. © 2014 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 19231 - Posted: 02.10.2014

By Melissa Healy Adolescents treated with the antidepressant fluoxetine -- better known by its commercial name, Prozac -- appear to undergo changes in brain signaling that result in changed behavior well into adulthood, says a new study. Adult mice and rats who were administered Prozac for a stretch of mid-adolescence responded to daunting social and physical challenges with less despair than animals who passed their teen years unmedicated, a team of researchers found. But, even as adults long separated from their antidepressant days, the Prozac veterans reacted to stressful situations with greater anxiety than did the adult Prozac virgins. The latest research, published Wednesday in the Journal of Neuroscience, offers evidence that treatment with a selective serotonin reuptake inhibitor -- an SSRI antidepressant -- has long-lived effects on the developing brain. It also zeroes in on how and where fluoxetine effects those lasting changes: by modifying the cascade of chemical signals issued by the brain's ventral tegmentum -- a region active in mood regulation -- in stressful situations. Yet, the new research raises more questions than it answers, since the changes in adults who were treated with Prozac as adolescents seem contradictory. Sensitivity to stress appears to predispose one to developing depression. So how does a medication that treats depression in children and teens -- and that continues to protect them from depression as adults -- also heighten their sensitivity to stress?

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 19146 - Posted: 01.18.2014

By Megan Wiegand and Slate, Tips for beating the seasonal blues are as numerous as the winter night is long. Light boxes, touted to “uplift people’s spirits” and “improve mood and energy,” offer a New-Agey-seeming solution to propel us into the cold as if it’s the first beautiful day of spring. But can sitting in front of a light for a few minutes a day actually counteract the dreariest months? Yes, in many cases. Light-box therapy has been shown to alleviate symptoms in people who suffer from seasonal affective disorder, or SAD. Symptoms of this form of depression — they can include lost interest in beloved activities, overeating, loss of energy, disrupted sleep cycles and feelings of hopelessness or guilt — typically appear in late fall or early winter and dissipate in spring. Women are twice as likely as men to seek treatment for SAD, and those farther away from the equator are more likely to be diagnosed: About 11 percent of Mainers have a clinical SAD diagnosis, but only 2 percent of Floridians report the illness, according to Kathryn Roecklein, an assistant professor of psychology at the University of Pittsburgh. One tool doctors use to treat SAD is light-box therapy. Light boxes use bright white fluorescent bulbs (or sometimes blue light) that reproduce some wavelengths of the sun’s light. They contain filters to block harmful UV rays and come in various shapes, sizes, light types and price points. © 1996-2014 The Washington Post

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 19125 - Posted: 01.14.2014

By Sandra G. Boodman, Bebe Bahnsen remembers the night, alone in her small cottage on the Alabama coast, that she felt a strong urge to drink a can of drain cleaner. For years, antidepressants combined with talk therapy had enabled Bahnsen, whose first name is Beatrice, to function well, establishing a thriving public relations business in Washington followed by a career as a newspaper reporter. But those days had been supplanted by a prolonged suicidal depression that had proved impervious to electroshock treatments, periodic hospitalizations and a raft of psychiatric drugs. The phone call in which Bahnsen confided her desire to drink poison seemed to confirm the worst fears of one of her closest friends. “I figured, well, she was one of those people who just was not ever going to get better,” said Paddy Bowman, a folklore specialist who lives in Alexandria. Bahnsen, now 73, traces the beginning of her psychological slide to the mid-1990s, when she decided that, after two decades, she’d had enough of Washington. She moved back to her home state of Georgia and her life slowly began to unravel. She felt estranged from her large and devoted circle of friends, began having problems at work, and grew restless and increasingly depressed. “I felt as though I was on a large island and everyone was slowly moving away and I was there by myself,” Bahnsen recalled. For the first time in her life, she said, she was intermittently psychotic. Periodic suicide attempts, some involving overdoses of prescribed sleeping pills, landed her in a series of mental hospitals. In November 2006 she was hospitalized in Las Vegas, where she was then living with one of her sons. Doctors, baffled by her longstanding failure to improve, decided to take a closer look at her case. What they found resulted in an entirely different treatment, one that had a rapid and dramatic effect on her mental state. © 1996-2013 The Washington Post

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 15: Language and Our Divided Brain
Link ID: 19069 - Posted: 12.24.2013

By RICHARD A. FRIEDMAN, M.D. When will we ever get depression under control? Of all the major illnesses, mental or physical, depression has been one of the toughest to subdue. Despite the ubiquity of antidepressant drugs — there are now 26 to choose from — only a third of patients with major depression will experience a full remission after the first round of treatment, and successive treatments with different drugs will give some relief to just 20 to 25 percent more. About 30 percent of people with depression have some degree of treatment resistance. And the greater the degree of resistance, the more likely a future relapse, even if the patient continues taking the drug. Although we have learned much about depression — for example, the recent research showing that the successful treatment of insomnia in depressed patients essentially doubles their response to a drug like Prozac — we still don’t understand its fundamental cause. The old idea that the disease results from a deficiency of a single neurotransmitter like serotonin or dopamine is clearly simplistic and wrong. Maybe psychiatrists and neuroscientists have something to learn from the successful hunt for the Higgs boson. Of course a debilitating disease has nothing in common with a subatomic particle, except that both are mysterious and elusive. But it was those very qualities that inspired international teams of physicists to work together for years until they finally identified the boson last year. Among biomedical scientists, who compete for the same research dollars and want to be first across the finish line with an important finding, such cooperation is hardly the norm. But there are signs that this is changing. Not long ago, I sat in at a meeting of the Hope for Depression Research Foundation. Audrey Gruss, the knowledgeable and energetic philanthropist who started the foundation, has corralled a group of senior basic and clinical neuroscientists to look for solutions. (It is not the first to try a collaborative approach; others are being sponsored by the MacArthur Foundation and the Pritzker Consortium.) Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19068 - Posted: 12.24.2013

By John Chipman, CBC News Andrew Solomon is not your typical depressive, if such a thing exists. Most people struggling with clinical depression do not like to talk about it. Depression is usually suffered in silence, because of the stigma that still clings to it. Many people still see depression as a sign of weakness, or believe that if you just cheered up or had a better attitude you'd feel so much better. Solomon has heard the wrong-headed chatter most of his life. But rather than shy away, the journalist and best-selling author wrote a book about it, detailing his own struggles with depression. It’s called The Noonday Demon: An Atlas of Depression. And he has become a vocal advocate, calling for more progressive attitudes about the disease so that people suffering from it can step out of the shadows and feel comfortable getting the help they need to survive, and to thrive. So it was with some shock and dismay that Solomon learned about Ellen Richardson, a Canadian woman turned back at the U.S. border last month because she was hospitalized last year for her depression. Richardson was told she could only enter the U.S. if a doctor — not her own, but one from a shortlist of others whom she had never met — signed a document vouching for her. She would also have to pay a fee of $500. U.S. border guards are allowed to bar anyone they deem a threat to themselves, to other Americans, or their property. They have access to police records — including even uneventful encounters with officers — but medical records are supposed to be held in the strictest confidence. © CBC 2013

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 19038 - Posted: 12.16.2013

By ROBERT PEAR WASHINGTON — Psychiatrists are significantly less likely than doctors in other specialties to accept insurance, researchers say in a new study, complicating the push to increase access to mental health care. The study, published Wednesday in the journal JAMA Psychiatry, found that 55 percent of psychiatrists accepted private insurance, compared with 89 percent of other doctors. Likewise, the study said, 55 percent of psychiatrists accept patients covered by Medicare, against 86 percent of other doctors. And 43 percent of psychiatrists accept Medicaid, which provides coverage for low-income people, while 73 percent of other doctors do. The lead author of the study, Dr. Tara F. Bishop of Weill Cornell Medical College in New York, said: “In the wake of the school killings in Newtown, Conn., and other recent mass shootings, the need for increased mental health services is now recognized. But unless patients have deep pockets, they may have a hard time finding a psychiatrist who will treat them.” Mental health care is one of 10 types of “essential health benefits” that must be provided by insurers under the new health care law. A federal rule issued last month requires insurers to cover care for mental health and addiction on the same terms as treatments for physical illnesses, without charging higher co-payments or deductibles or imposing stricter limits on services. Starting next year, Medicare will end a discriminatory policy that for decades has required people to pay a larger share of the bill for mental health care than for other outpatient services. However, the study suggests that expanding coverage may not by itself guarantee access to psychiatrists. “Even if you have good insurance that covers mental health care, you may still have a problem if there’s no doctor who accepts your insurance,” Dr. Bishop said. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19031 - Posted: 12.12.2013

By Jeanene Swanson Depression strikes some 35 million people worldwide, according to the World Health Organization, contributing to lowered quality of life as well as an increased risk of heart disease and suicide. Treatments typically include psychotherapy, support groups and education as well as psychiatric medications. SSRIs, or selective serotonin reuptake inhibitors, currently are the most commonly prescribed category of antidepressant drugs in the U.S., and have become a household name in treating depression. The action of these compounds is fairly familiar. SSRIs increase available levels of serotonin, sometimes referred to as the feel-good neurotransmitter, in our brains. Neurons communicate via neurotransmitters, chemicals which pass from one nerve cell to another. A transporter molecule recycles unused transmitter and carries it back to the pre-synaptic cell. For serotonin, that shuttle is called SERT (short for “serotonin transporter”). An SSRI binds to SERT and blocks its activity, allowing more serotonin to remain in the spaces between neurons. Yet, exactly how this biochemistry then works against depression remains a scientific mystery. In fact, SSRIs fail to work for mild cases of depression, suggesting that regulating serotonin might be an indirect treatment only. “There’s really no evidence that depression is a serotonin-deficiency syndrome,” says Alan Gelenberg, a depression and psychiatric researcher at The Pennsylvania State University. “It’s like saying that a headache is an aspirin-deficiency syndrome.” SSRIs work insofar as they reduce the symptoms of depression, but “they’re pretty nonspecific,” he adds. © 2013 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19020 - Posted: 12.11.2013

Someday, a smart phone app that asks what you’re feeling 10 times a day may be able to tell you if you’re edging closer to depression—and recommend that you seek preventive therapy or drugs. Scientists have discovered that how quickly someone bounces back from negative feelings, over hours or days, can predict whether that person is at risk of an episode of major depressive disorder. “The holy grail of depression epidemiology is that we want to intervene early to prevent people from having depressive episodes,” says social scientist Stephen Gilman of Harvard University, who was not involved in the study. “Where this work is headed is making an advance in that direction, toward early detection and therefore early intervention.” Researchers asked more than 600 people—some healthy and some with a diagnosis of depression—to track their emotions for 5 or 6 days. Ten times a day, at random intervals, a watch would beep and the subjects would record how strongly they identified with each of four emotions: cheerful, content, sad, and anxious. Six to 8 weeks later, participants filled out a more detailed questionnaire that rated their levels of clinical depression. By the end of the follow-up period, about 13% of the subjects had experienced a shift toward being more depressed, a number consistent with what would be expected in the general population. Trends in the daily mood records, the team discovered, could predict whether a previously healthy person would make that shift toward depression. © 2013 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19015 - Posted: 12.10.2013

By Jason Tetro For millennia, the human race has sought to combat psychological disorders through the intervention of natural – and eventually synthetic – chemicals. Originally, the sources for these psychoactive substances were the various fruits and flowers, including the Areca tree (betel nut), the poppy (opium), and the coca plant (cocaine). But in the 20th Century, new actives were being created in the lab thanks in part to the discovery of lysergic acid, better known as LSD, in 1938. By the middle of the 1950s, the psychiatric community was fascinated by the idea that mental health could be restored through the direct use of drugs or in combination with traditional psychotherapy. The idea took off in the 1960s as research continued to elucidate the biology of psychiatry. It essentially created a new avenue for psychiatric treatment: psychopharmacology. This inevitably led to the synthesis of a new compound, 3-(p-trifluoromethylphenoxy)-N-methyl-3-phenylpropylamine, which eventually became known as fluoxetine, and then, as we have all come to know it, Prozac. By the late 1980s, it was known by another name: the wonder drug. Today, pharmacologic compounds for psychiatric treatment are numerous and up to 20% of all Americans are taking some type of psychotropic medication totalling some $34 billion dollars annually. While there have been calls for a reduction in use of these chemicals, primarily due to the fact that many are ineffective, there is a constant pressure from the public to have all their problems solved by a pill.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18952 - Posted: 11.21.2013

By BENEDICT CAREY Curing insomnia in people with depression could double their chance of a full recovery, scientists are reporting. The findings, based on an insomnia treatment that uses talk therapy rather than drugs, are the first to emerge from a series of closely watched studies of sleep and depression to be released in the coming year. A student demonstrating equipment at Colleen Carney’s sleep lab at Ryerson University. Dr. Carney is the lead author of a new report about the effects of insomnia treatment on depression. The new report affirms the results of a smaller pilot study, giving scientists confidence that the effects of the insomnia treatment are real. If the figures continue to hold up, the advance will be the most significant in the treatment of depression since the introduction of Prozac in 1987. Depression is the most common mental disorder, affecting some 18 million Americans in any given year, according to government figures, and more than half of them also have insomnia. Experts familiar with the new report said that the results were plausible and that if supported by other studies, they should lead to major changes in treatment. “It would be an absolute boon to the field,” said Dr. Nada L. Stotland, professor of psychiatry at Rush Medical College in Chicago, who was not connected with the latest research. “It makes good common sense clinically,” she continued. “If you have a depression, you’re often awake all night, it’s extremely lonely, it’s dark, you’re aware every moment that the world around you is sleeping, every concern you have is magnified.” The study is the first of four on sleep and depression nearing completion, all financed by the National Institute of Mental Health. They are evaluating a type of talk therapy for insomnia that is cheap, relatively brief and usually effective, but not currently a part of standard treatment. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 18945 - Posted: 11.19.2013

By Julianne Chiaet Kate wanted to die. She remembers the moment the psychiatrist said “the antidepressant isn’t going to work right away. Can you promise to be here next week and not kill yourself?” “I told her no,” Kate says. “I couldn’t promise my doctor I’d make it a week. That’s how bad my life had to be before I got help. When you’re struggling to stay alive every single day, and then your doctor tells you it’s going to take two to six weeks before the medications they give you are going to work, it’s devastating.” To make matters worse, after those weeks, the drug didn’t work. Kate went through five different anti-depressants over the course of six months before confirming that none of them worked. The debilitating disorder kept her out of school for extended periods of time. The National Center for Health Statistics estimates more than 1 in 10 Americans over the age of 12 took antidepressants between 2005 and 2008, the last time period for which the data are available. The rate of antidepressant use increased 400 percent from 1998 to 2008. Traditional antidepressants go after serotonin neurotransmitters, which sit in the membrane of the brain. Some antidepressants also target norepinephrine and dopamine. The drug keeps the transmitters from performing their normal function of transporting serotonin from the outside to the inside of the brain cells. People with depression have a normal amount of serotonin inside of their brain cells, however they have an insufficient amount on the outside of their cells. Thus by inhibiting the transmitter, the drug blocks the transportation of serotonin being taken into the cell, thus building up the serotonin outside of the cell. © 2013 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18919 - Posted: 11.13.2013

By Michelle Roberts Health editor, BBC News online Depression can make us physically older by speeding up the ageing process in our cells, according to a study. Lab tests showed cells looked biologically older in people who were severely depressed or who had been in the past. These visible differences in a measure of cell ageing called telomere length couldn't be explained by other factors, such as whether a person smoked. The findings, in more than 2,000 people, appear in Molecular Psychiatry. Experts already know that people with major depression are at increased risk of age-related diseases such as cancer, diabetes, obesity and heart disease. This might be partly down to unhealthy lifestyle behaviours such as alcohol use and physical inactivity. But scientists suspect depression takes its own toll on our cells. To investigate, Josine Verhoeven from the VU University Medical Centre in the Netherlands, along with colleagues from the US, recruited 2,407 people to take part in the study. More than one third of the volunteers were currently depressed, a third had experienced major depression in the past and the rest had never been depressed. The volunteers were asked to give a blood sample for the researchers to analyse in the lab for signs of cellular ageing. The researchers were looking for changes in structures deep inside cells called telomeres. BBC © 2013

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18913 - Posted: 11.12.2013

By JACKIE CALMES and ROBERT PEAR WASHINGTON — The Obama administration on Friday will complete a generation-long effort to require insurers to cover care for mental health and addiction just like physical illnesses when it issues long-awaited regulations defining parity in benefits and treatment. The rules, which will apply to almost all forms of insurance, will have far-reaching consequences for many Americans. In the White House, the regulations are also seen as critical to President Obama’s program for curbing gun violence by addressing an issue on which there is bipartisan agreement: Making treatment more available to those with mental illness could reduce killings, including mass murders. In issuing the regulations, senior officials said, the administration will have acted on all 23 executive actions that the president and Vice President Joseph R. Biden Jr. announced early this year to reduce gun crimes after the Newtown, Conn., school massacre. In planning those actions, the administration anticipated that gun control legislation would fail in Congress as pressure from the gun lobby proved longer-lasting than the national trauma over the killings of first graders and their caretakers last Dec. 14. “We feel actually like we’ve made a lot of progress on mental health as a result in this year, and this is kind of the big one,” said a senior administration official, one of several who described the outlines of the regulations that Kathleen Sebelius, the secretary of health and human services, will announce at a mental health conference on Friday in Atlanta with the former first lady Rosalynn Carter. While laws and regulations dating to 1996 took initial steps in requiring insurance parity for medical and mental health, “here we’re doing full parity, and we’ve also taken steps to extend it to the people covered in the Affordable Care Act,” the senior official said. “This is kind of the final word on parity.” © 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18901 - Posted: 11.09.2013

By Helen Briggs BBC News Depression is the second most common cause of disability worldwide after back pain, according to a review of research. The disease must be treated as a global public health priority, experts report in the journal PLOS Medicine. The study compared clinical depression with more than 200 other diseases and injuries as a cause of disability. Globally, only a small proportion of patients have access to treatment, the World Health Organization says. Depression was ranked at number two as a global cause of disability, but its impact varied in different countries and regions. For example, rates of major depression were highest in Afghanistan and lowest in Japan. In the UK, depression was ranked at number three in terms of years lived with a disability. Dr Alize Ferrari from the University of Queensland's School of Population Health led the study. "Depression is a big problem and we definitely need to pay more attention to it than we are now," she told BBC News. "There's still more work to be done in terms of awareness of the disease and also in coming up with successful ways of treating it. "The burden is different between countries, so it tends to be higher in low and middle income countries and lower in high income countries." Policy-makers had made an effort to bring depression to the forefront, but there was a lot more work to be done, she added. BBC © 2013

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18883 - Posted: 11.07.2013

By DAN HURLEY This couldn’t possibly be a good idea. On Friday the 13th of September, in an old brick building on 13th Street in Boston’s Charlestown neighborhood, a pair of electrodes was attached to my forehead, one over my brain’s left prefrontal cortex, the other just above my right eye socket. I was about to undergo transcranial direct-current stimulation, or tDCS, an experimental technique for delivering extremely low dose electrical stimulation to the brain. Using less than 1 percent of the electrical energy necessary for electroconvulsive therapy, powered by an ordinary nine-volt battery, tDCS has been shown in hundreds of studies to enhance an astonishing, seemingly implausible variety of intellectual, emotional and movement-related brain functions. And its side effects appear limited to a mild tingling at the site of the electrode, sometimes a slight reddening of the skin, very rarely a headache and certainly no seizures or memory loss. Still, I felt more than a bit apprehensive as I prepared to find out if a little bit of juice could amp up my cognitive reserves and make me, in a word, smarter. With the electrodes in place, J. León Morales-Quezada, senior research associate at Harvard’s Laboratory of Neuromodulation, pressed a button on his computer and I felt . . . absolutely nothing. No pain. No tingling. Not even a little muscle twitching. “Is it on?” I asked. Morales-Quezada assured me it was. For proof, he pointed to a flat-screen on the wall, displaying signals from six electroencephalogram (EEG) monitors also attached to my head. After 10 minutes of charging my brain, he turned on a computerized exercise I was supposed to practice while the current continued flowing. Called an attention-switching task, it’s used by psychologists as a measure of “executive function” or “cognitive control”: the ability to overrule your urges, to ignore distractions and to quickly shift your focus. Young adults generally do better than older people; people with greater overall cognitive abilities generally perform better than those with less. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 14: Attention and Consciousness
Link ID: 18870 - Posted: 11.04.2013

by Bethany Brookshire In pharmacology research, it seems like one test is never enough. If you want to test a new antidepressant, reviewers (and good logic) often demand that you use more than one test. A locomotor assay to see whether the new drug depresses or increases how much a mouse moves. A forced swim test or tail suspension test to see how it stacks up against other, known antidepressants. Does it increase swimming? Or climbing? Does it decrease immobility more or less than known antidepressants? You may want to use a chronic mild stress test, which exposes mice over a long period of time to things like mild cold, noise or light to induce stress. Does chronic exposure to your new antidepressant relieve the stress like other antidepressants do? What about responses to things like chronic bullying by other mice? Does it work then? You don’t necessarily need to run all of these tests, but you usually do need to run more than one. After all, what if the drug decreases immobility in a forced swim test, like other antidepressants, but it also makes them race around the room … because it’s cocaine? These are the kind of questions that pharmacologists end up asking. Often, to find new, potential antidepressants, for example, we end up matching them against other, known antidepressants in a series of these tests. If the drug performs well in all of them, doesn’t decrease locomotor activity but keeps the mice swimming and stops them from looking stressed after bullying, we might have something new. © Society for Science & the Public 2000 - 2013.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18859 - Posted: 10.31.2013

By Janet Davison, CBC News Jason Novick has seen the darkness that mental health disorders can create. The 27-year-old Toronto man has also seen how advocacy — by himself and by others — has been vital in helping him cope with bipolar disorder, general anxiety disorder, mania and depression, particular during the stressful transition from his teenage years to leaving home for post-secondary school. "Mental health awareness … is still an issue that’s largely misunderstood," he said in a recent interview. "There’s a lot of [post-secondary] administrative workers and professors and program co-ordinators and what have you who won’t know the first thing about such issues, so your best ally is probably going to be yourself a lot of the time." Another ally can also be a caring friend or family member who steps up to help others understand the larger situation. Novick remembers going with his mother to "set the record straight" with a college professor. They wanted to explain to the instructor that it was his mental health that was his problem, not any lack of interest in the course. "It was my mental health that was causing me to be so withdrawn, that was causing me to be so unmotivated. I was passionate about the subject, but I was not passionate about life and living." Novick, who says he contemplated suicide at one point and has been in closed hospital wards three times because of his disorders, is much more passionate about life and living now, particularly after having completed an inpatient program at the Centre for Addiction and Mental Health in Toronto. © CBC 2013

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 18842 - Posted: 10.28.2013

By JAMES GORMAN Worldwide, 100,000 people have electrical implants in their brains to treat the involuntary movements associated with Parkinson’s disease, and scientists are experimenting with the technique for depression and other disorders. But today’s so-called deep brain stimulation only treats — it does not monitor its own effectiveness, partly because complex ailments like depression do not have defined biological signatures. The federal Defense Advanced Research Projects Agency, known as Darpa, announced Thursday that it intended to spend more than $70 million over five years to jump to the next level of brain implants, either by improving deep brain stimulation or by developing new technology. Justin Sanchez, Darpa program manager, said that for scientists now, “there is no technology that can acquire signals that can tell them precisely what is going on with the brain.” And so, he said, Darpa is “trying to change the game on how we approach these kinds of problems.” The new program, called Systems-Based Neurotechnology and Understanding for the Treatment of Neuropsychological Illnesses, is part of an Obama administration brain initiative, announced earlier this year, intended to promote innovative basic neuroscience. Participants in the initiative include Darpa, as well as the National Institutes of Health and the National Science Foundation. The announcement of Darpa’s goal is the first indication of how that research agency will participate in the initiative. The money is expected to be divided among different teams, and research proposals are now being sought. Darpa’s project is partly inspired by the needs of combat veterans who suffer from mental and physical conditions, and is the first to invest directly in researching human illness as part of the brain initiative. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 5: The Sensorimotor System
Link ID: 18835 - Posted: 10.26.2013

by Simon Makin A drug similar to ketamine has been shown to work as an antidepressant, without the psychosis-like side effects associated with the party drug. In 2000, ketamine was seen to alleviate depression almost immediately in people for whom other treatments had failed. Larger clinical trials have since corroborated the findings. The drawback is that ketamine can cause hallucinations and other psychotic symptoms, making it unsuitable for use as a treatment. These effects also make it difficult to conduct randomised, placebo-controlled trials – the gold standard in clinical medicine – as it is obvious which participants have been given the drug. This meant that there was a possibility that the beneficial effects seen in previous trials were inflated. So a team led by Gerard Sanacora of Yale University and Mike Quirk of pharmaceutical firm AstraZeneca looked for an alternative compound. They decided to test lanicemine, a drug originally developed to treat epilepsy that targets the same brain receptors as ketamine. The team gave 152 people with moderate-to-severe depression and a history of poor response to antidepressants either lanicemine or a placebo three times a week, for three weeks. They were allowed to continue taking any medications they were already on. Before and after the trial the participants' level of depression was rated on a 60-point scale. After three weeks, those taking lanicemine were less depressed by an average of 13.5 points – 5.5 points better than those who took the placebo. The improvement was still statistically significant up to two weeks after the treatment ended. Dizziness was the only common side effect. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18793 - Posted: 10.16.2013