Links for Keyword: Schizophrenia

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 590

By Jennifer Couzin-Frankel Rachel Loewy was an undergraduate in 1995 when she answered a flyer seeking students to assist with a research study. A couple of floors up in a psychology department building, Loewy sat, clipboard in hand, interviewing teenagers whose brain health was beginning to falter. Some heard whispers. Others imagined that their teachers could read their minds, or that fellow students stared at them and wished them harm as they walked down the halls. The teenagers had been diagnosed with schizotypal personality disorder, a condition that can precede schizophrenia. Among the most debilitating and stigmatized psychiatric diseases, schizophrenia can rob sufferers of their self and their future, often in early adulthood. Although these teens didn't have schizophrenia, the researchers believed that some would later deteriorate and be diagnosed with the disorder. But when Loewy met them they were lucid and self-aware. And they were frightened that their mind sometimes spun out of control. Doctors routinely assess a patient's risk of heart attack, various cancers, and diabetes, often intervening to slow or stop disease before it strikes. But preventing psychiatric conditions, from anxiety to depression to schizophrenia, has received scant attention. © 2017 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 24336 - Posted: 11.17.2017

Hannah Devlin Science correspondent British scientists have begun testing a radically new approach to treating schizophrenia based on emerging evidence that it could be a disease of the immune system. The first patient, a 33-year old man who developed schizophrenia after moving to London from Cameroon a decade ago, was treated at King’s College Hospital in London on Thursday, marking the start of one of the most ambitious trials to date on the biology of the illness and how to treat it. During the next two years, 30 patients will receive monthly infusions of an antibody drug currently used to treat multiple sclerosis (MS), which the team hopes will target the root causes of schizophrenia in a far more fundamental way than current therapies. The trial builds on more than a decade’s work by Oliver Howes, a professor of molecular psychiatry at the MRC London Institute of Medical Sciences and a consultant psychiatrist at the Maudsley Hospital in south London. Howes’s team is one of several worldwide to have uncovered evidence that abnormalities in immune activity in the brain may lie at the heart of the illness – for some patients, at least. “In the past, we’ve always thought of the mind and the body being separate, but it’s just not like that,” said Howes. “The mind and body interact constantly and the immune system is no different. It’s about changing the way we think about mental illnesses.” Recent work by Howes and colleagues found that in the earliest stages of schizophrenia, people experience a surge in the number and activity of immune cells in the brain. As well as fighting infection, these cells, called microglia, have a “gardening” role, pruning unwanted connections between neurons. But in schizophrenia patients, the pruning appears to become more aggressive, leading to vital connections being lost. © 2017 Guardian News and Media Limited

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 24293 - Posted: 11.04.2017

Hannah Devlin Descartes’s notion of dualism – that the mind and body are separate entities – is wrong, but has proved surprisingly persistent, and until recently dominated attempts to understand mental illness. When the brain stopped working properly, a psychological origin was sought. Undoubtedly, life’s experiences and our personalities shape the way our brains function. But there is now a compelling body of evidence that brain disorders can also originate from things going awry in our basic biology. Particularly intriguing is the discovery that the brain, once thought to be separated from the immune system by the blood-brain barrier, is powerfully influenced by immune activity. The latest trial, focused on schizophrenia, is backed by converging evidence from several fields that immune cells in the brain, called microglia, play at least some role in this disease. Prof Oliver Howes, the psychiatrist leading the work, discovered that these cells appear to go into overdrive in the early stages of schizophrenia. Genetics studies have linked changes in immune system genes to increased risk for schizophrenia and anecdotal evidence, including a recent case report of a patient who developed schizophrenia after receiving a bone marrow transplant from a sibling with the illness, also triangulates on to the immune system. “It’s all challenging the idea that the brain is this separate privileged organ,” said Howes. © 2017 Guardian News and Media Limited

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 24292 - Posted: 11.04.2017

Sara Reardon Human genome databases are enabling researchers to take a deeper dive into the evolution of psychiatric disorders. Psychiatric disorders can be debilitating and often involve a genetic component, yet, evolution hasn’t weeded them out. Now, recent work is beginning to reveal the role of natural selection — offering a peek at how the genetic underpinnings of mental illness has changed over time. Many psychiatric disorders are polygenic: they can involve hundreds or thousands of genes and DNA mutations. It can be difficult to track how so many genetic regions evolved, and such studies require large genome data sets. But the advent of massive human genome databases is enabling researchers to look for possible connections between mental illnesses and the environmental and societal conditions that might have driven their emergence and development. Others are looking to Neanderthal genetic sequences to help inform the picture of these disorders, as well as cognitive abilities, in humans. Several of these teams presented their findings at the American Society of Human Genetics (ASHG) meeting in Orlando, Florida, in late October. One project found that evolution selected for DNA variants thought to protect against schizophrenia. The study, led by population geneticist Barbara Stranger of the University of Chicago in Illinois, looked at hundreds of thousands of human genomes using a statistical method that identified signals of selection over the past 2,000 years1. There were no signs of selection in genetic regions associated with any other mental illness. Many of schizophrenia's symptoms, such as auditory hallucinations and jumbling sentences, involve brain regions tied to speech, says Bernard Crespi, an evolutionary biologist at Simon Fraser University in Burnaby, Canada. Over the course of hominid evolution, he says, the ability to speak could have outweighed the small, but unavoidable risk that the genes involved in language could malfunction and result in schizophrenia in a small percentage of the population. © 2017 Macmillan Publishers Limited

Related chapters from BN8e: 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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 24270 - Posted: 10.31.2017

By MARK LUKACH For my son Jonas’s first Halloween, when he was 5 months old, I dressed the two of us as matching lumberjacks. For the second, we were characters from the movie “Up.” I was Carl, the old man, my wife was Ellie, and Jonas was Russell, the enthusiastic Wilderness Explorer. We tied a dozen balloons to our bulldog’s collar, to make him the house. In our version, the wife didn’t die at the beginning of the movie, and we all lived happily ever after. The next Halloween, Jonas wanted to be an elephant. He loved the scene in “The Jungle Book” where Mowgli tries to march with the elephants. We resisted, since we like family costumes and didn’t want to buy three elephant outfits, but conceded. We displayed his elephant costume in his room the week before Halloween so he could look at it in anticipation of the big day. My wife, Giulia, wasn’t there for the lumberjack Halloween. She was in the hospital. Giulia was there for the “Up” Halloween. But as we approached the elephant Halloween, I suspected she wasn’t going to dress up. Because, once again, she was going psychotic. Giulia was 27 when the first psychotic episode happened. It came out of nowhere. She got nervous about her new job; she lost her appetite; she stopped sleeping; she began having delusions. The first delusions were encouraging. She said she spoke to God, who told her that she was going to be fine. Giulia had never been very religious, so I was alarmed, but at least she was hearing things that were comforting. But then the delusions turned on her. The voices said she wasn’t going to make it, there was no point in even trying, she was better off not being here. That’s how she ended up in the hospital the first time. They gave her medication. The delusions eventually went away. She was depressed for a long time afterward. They gave her more medication, and then she got better. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 24257 - Posted: 10.28.2017

By R. Douglas Fields BERLIN—Society’s embrace of cannabis to treat nausea, pain and other conditions proceeds apace with the drive to legalize the plant for recreational use. Pot’s seemingly innocuous side effects have helped clear a path toward making it a legal cash crop, with all of the marketing glitz brought to other consumer products. But that clean bill of health only goes so far. Marijuana’s potentially detrimental impact on the developing brains of adolescents remains a key focus of research—particularly because of the possibility teenage users could go on to face a higher risk of psychosis. New findings may fuel those worries. At the World Psychiatric Association’s World Congress in Berlin on October 9, Hannelore Ehrenreich of the Max Planck Institute of Experimental Medicine presented results of a study of 1,200 people with schizophrenia. The investigation analyzed a wide range of genetic and environmental risk factors for developing the debilitating mental illness. The results—being submitted for publication—show people who had consumed cannabis before age 18 developed schizophrenia approximately 10 years earlier than others. The higher the frequency of use, the data indicated, the earlier the age of schizophrenia onset. In her study neither alcohol use nor genetics predicted an earlier time of inception, but pot did. “Cannabis use during puberty is a major risk factor for schizophrenia,” Ehrenreich says. Other studies, although not all, support the thrust of Ehrenreich’s findings. “There is no doubt,” concludes Robin Murray, a professor of psychiatry at King’s College London, that cannabis use in young people increases the risk of developing schizophrenia as an adult. Speaking at the Berlin conference, Murray—one of the first scientists to research pot’s link to the disorder—cited 10 studies that found a significant risk of young cannabis users developing psychosis. © 2017 Scientific American

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 24226 - Posted: 10.21.2017

David Dobbs By the time Nev Jones entered DePaul University's esteemed doctoral program in philosophy, she had aced virtually every course she ever took, studied five languages and become proficient in three, and seemed to have read and memorized pretty much everything. Small and slightly built, with a commanding presence that emerged when she talked, she was the sort of student that sharp teachers quickly notice and long remember: intellectually voracious, relentlessly curious, endlessly capable, and, as one of her high school teachers put it, "magnificently intense." Her mind drew on a well-stocked, seemingly flawless memory with a probing, synthesizing intelligence. With astounding frequency she produced what one doctoral classmate called "genius-level reflections." So Jones grew alarmed when, soon after starting at DePaul in the fall of 2007, at age 27, she began having trouble retaining things she had just read. She also struggled to memorize the new characters she was learning in her advanced Chinese class. She had experienced milder versions of these cognitive and memory blips a couple times before, most recently as she’d finished her undergraduate studies earlier that year. These new mental glitches were worse. She would study and draw the new logograms one night, then come up short when she tried to draw them again the next morning. These failures felt vaguely neurological. As if her synapses had clogged. She initially blamed them on the sleepless, near-manic excitement of finally being where she wanted to be. She had wished for exactly this, serious philosophy and nothing but, for half her life. Now her mind seemed to be failing. Words started to look strange. She began experiencing "inarticulable atmospheric changes," as she put it—not hallucinations, really, but alterations of temporality, spatiality, depth perception, kinesthetics. Shimmerings in reality's fabric. Sidewalks would feel soft and porous. Audio and visual input would fall out of sync, creating a lag between the movement of a speaker's lips and the words' arrival at Jones' ears. Something was off. © 2017 The Social Justice Foundation

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 24148 - Posted: 10.05.2017

By JAIME LOWE WHEN I was 16, I was admitted to U.C.L.A.’s neuropsychiatric institute. I’d been suffering from increasing paranoia (I thought war was imminent; I thought I would be called into battle) and lack of sleep (I paced our staircase into the early hours of morning). Most profoundly, I thought my parents were actually secret agents, wearing masks, sent to monitor my behavior. My hallucinations encompassed a wide range of cultural references — Michael Jackson, the Muppets, the Night Stalker, Bob from “Twin Peaks” and the clown from “It.” My parents told the doctors at U.C.L.A. that my behavior had been erratic for two months — I was obsessing over odd things, I wasn’t eating and I was convinced that the end of the world was on its way. In short, I was manic. I was hospitalized for almost a month, and I left the institute with a diagnosis of bipolar disorder. My cure came in the form of three pink pills: 900 milligrams of lithium. It worked when I was on it. But a few years ago, my general practitioner had discovered heart-attack-level blood pressure and high creatinine measures — side effects that I couldn’t feel but were serious enough to warrant a visit to the E.R. As a result of my taking lithium, my kidneys were breaking down — I basically had a 60-year-old’s kidneys in my 37-year-old body. I was given a choice: I could stay on the lithium and get a kidney transplant eventually, or I could switch medication and risk having mania return. I chose to try a new medication. No drug could ever be as cool as lithium, a mysterious element that was present during the Big Bang and lingers throughout the galaxy as primordial stardust. Lithium has a medicinal history that dates to the Greeks and Romans, yet no doctor or researcher knows exactly how or why it works. It just does. It’s on the periodic table of elements, unpatentable and therefore cheap. Depakote, a drug officially approved for bipolar patients in the United States in the mid-1990s, has none of this cachet, and yet it’s known to be as effective as lithium in bipolar cases like mine. So my psychiatrist prescribed it to replace my pink pills. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 24141 - Posted: 10.03.2017

By ERICA CROMPTON I’ve been fired more times than I care to admit. I have even more resignation letters to my name. Work and paranoid schizophrenia aren’t exactly a recipe for success. At one job I had, on the ground floor of a city office, there were bars on the windows. The bars were no doubt put in for security reasons, like all the other shops and offices on the street. But I grew increasingly convinced that they were placed there just for me as part of a grand conspiracy. I have always felt that people are setting me up for heinous crimes or that I’ve committed one that I can’t remember and that the police are spying on me to gather evidence. With the windows I felt they’d been fitted by a stranger who knew of me, sometime before I started work, to send me the message that I would soon “be behind bars.” Seeing a policeman on the street outside the office or hearing a helicopter fly by would set my heart racing. I was convinced they’d finally come for me. I didn’t last long in that office. The sedative effects of my medications also mean I often oversleep and get into the office late. Really late. Sometimes 90 minutes late. The head of my department at another job I had didn’t seem to mind, as I always made the time up in the evening. But colleagues did mind, others in the office told me, including the girl who sat next to me. Back then, I wasn’t open about having schizophrenia. I didn’t want to stigmatize myself by giving reasons for my tardiness. So I assume people just thought I was lazy. Far too often, I would regard an off-the-cuff remark by a work colleague, a roll of the eyes when I offered an idea at a meeting, or a sigh when I arrived late, as aggressive and threatening, an insult directed toward me. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 24113 - Posted: 09.26.2017

By Michael Nedelman, CNN (CNN)Emily Gavigan was convinced that a nearby truck was following her. Someone was after her. She was a sophomore at the University of Scranton in January 2009 when the "bizarre" behavior began, said her father, Bill. Her parents noticed that she had been rambling, not making any sense. At one point, she called her family and friends to warn them: Something terrible was going to happen to all of them. "Emily was like a different person. We didn't know who she was," Bill Gavigan said. "We had gone from having this daughter who was perfectly normal, happy, vibrant ... with a bright future ahead. "All of a sudden, this all came crashing down." Then, one day, Gavigan disappeared. "We didn't know where she was for more than 24 hours," her father said. She had gotten in her car and driven from Pennsylvania to New Jersey with no money. She went right through toll booths without paying. But she eventually found her way back to her grandparents' house, still convinced that she was being followed. Her grandfather peered out the window, looking for something suspicious. But they soon realized there was no one after her. "I get emotional when I think about it," said Gavigan's grandfather Joseph Chiumento. Her parents showed up and took her to the hospital. Emily Gavigan began exhibiting odd behavior when she was 19, which doctors mistook for a mental illness. Emily Gavigan began exhibiting odd behavior when she was 19, which doctors mistook for a mental illness. Say, 'I love you, dad' Doctors initially thought Gavigan had a mental illness. She spent time in different psychiatric facilities, which made her family uneasy. One in particular reminded her father of the movie "One Flew Over the Cuckoo's Nest." "They just kept trying medication after medication after medication, and none of it worked," Bill Gavigan said. Things kept getting worse. There was some numbness in her face and hands, and she would develop seizures. © 2016 Cable News Network.

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 24011 - Posted: 08.30.2017

By Diana Kwon Sometimes our brains are on acid—literally. A main source of these temporary surges is the carbon dioxide that is constantly released as the brain breaks down sugar to generate energy, which subsequently turns into acid. Yet the chemistry in a healthy human brain tends to be relatively neutral, because standard processes including respiration—which expels carbon dioxide—help maintain the status quo. Any fleeting acidity spikes usually go unnoticed. But a growing body of work has suggested that for some people, even slight changes in this balance may be linked with certain psychiatric conditions including panic disorders. New findings this month provide additional evidence that such links are real—and suggest they may extend to schizophrenia and bipolar disorder. There were earlier hints that this was the case: Post-mortem studies of dozens of human brains revealed lower pH (higher acidity levels) in patients with schizophrenia and bipolar disorder. Multiple studies in the past few decades have found that when people with panic disorders are exposed to air with a higher-than-normal concentration of carbon dioxide—which can combine with water in the body to form carbonic acid—they are more likely to experience panic attacks than healthy individuals are. Other research has revealed that the brains of people with panic disorders produce elevated levels of lactate—an acidic source of fuel that is constantly produced and consumed in the energy-hungry brain. © 2017 Scientific American

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 24008 - Posted: 08.29.2017

By Bianca Datta Hallucinations are often distressing—a suggestion that something is amiss in our brains. But new research suggests we’re all susceptible to hallucinations, and that may not be such a bad thing. In a paper released last week in Science, a team from Yale University set out to understand how we interpret the world around us—in short, how we determine what’s real and what’s not. They suspected that people who regularly hallucinate perceive the world based on what they expect to happen, while others, who don’t hallucinate, would rely more what their senses are telling them is happening in the world. Even healthy participants experienced conditioned hallucinations. The mechanism that causes auditory hallucinations is related to those used in normal perception. To determine that, authors Phil Corlett and Al Powers began by conditioning participants to hear a tone when they were shown a checkerboard pattern. Then they slowly removed the actual sound and asked people when they heard it. Participants who regularly heard voices were five times more likely to say they heard a tone when there wasn’t one, and they were 25-30% more confident in their choice. But they weren’t alone in hearing things. In fact, all of the participants experienced some induced hallucinations during the experiment. “I did not expect that people who did not have a psychotic illness would perform so similarly to people who did hear voices,” Powers says. “They were very, very alike.” © 1996-2017 WGBH Educational Foundation

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 23981 - Posted: 08.22.2017

By Knvul Sheikh At his psychiatric clinic in the Connecticut Mental Health Center, Albert Powers sees people every day who experience hallucinations. The condition is often a hallmark of psychosis, occurring in an estimated 60 to 70 percent of people with schizophrenia, and in a subset of those diagnosed with bipolar disorder, dementia and major depression. Auditory hallucinations are the most common type experienced. Some patients report hearing voices; others hear phantom melodies. But increasing evidence over the past two decades suggests hearing imaginary sounds is not always a sign of mental illness. Healthy people also experience hallucinations. Drugs, sleep deprivation and migraines can often trigger the illusion of sounds or sights that are not there. Even in the absence of these predisposing factors, approximately one in 20 people hear voices or see visual hallucinations at least once in their lifetimes, according to mental health surveys conducted by the World Health Organization. Whereas most researchers have focused on the brain abnormalities that occur in people suffering at an extreme end of this spectrum, Powers and his colleagues have turned their attention to milder cases in a new study. “We wanted to understand what’s common and what’s protecting people who hallucinate but who don’t require psychological intervention,” he says. Normally when the brain receives sensory information, such as sound, it actively works to fill in information to make sense of what it hears—its location, volume and other details. “The brain is a predictive machine,” explains Anissa Abi-Dargham, a psychiatrist at Stony Brook University School of Medicine, who was not involved in the new work. “It is constantly scanning the environment and relying on previous knowledge to fill in the gaps [in] what we perceive.” Because our expectations are usually accurate, the system generally works well. For example, we are able to hear the sound of running water or the murmur of a friend talking across the room and then react in an instant, Abi-Dargham says. © 2017 Scientific American,

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 23950 - Posted: 08.11.2017

By Sharon Begley, STAT Lab mice whose brains were injected with cells from schizophrenia patients became afraid of strangers, slept fitfully, felt intense anxiety, struggled to remember new things, and showed other signs of the mental disorder, scientists reported on Thursday. The latest advance in “chimeras,” animals created by transplanting cells from one species into another, demonstrated the value of the technique, scientists not involved in the study said, but is likely to draw renewed attention to a controversial field that opponents see as deeply immoral and undermining the natural order. Under a 2015 moratorium, the National Institutes of Health does not fund research that transplants human stem cells into early embryos of other animals. When the NIH asked for public comment on lifting the moratorium, it received nearly 20,000 responses, almost all objecting to “grossly unethical research”; many mentioned Frankenstein. But the new study, in Cell Stem Cell, injected human cells into newborn mice, not embryos. It received funding from the NIH as well as private foundations, to unravel how brain development goes off the rails to cause schizophrenia. Although the prevailing idea has been that the devastating disease, which strikes some 1 percent of U.S. adults, is primarily caused by something going wrong with neurons, the scientists suspected the brain’s support cells, called glia. © 2017 Scientific American,

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 23863 - Posted: 07.22.2017

By Aaron Reuben, Jonathan Schaefer Most of us know at least one person who has struggled with a bout of debilitating mental illness. Despite their familiarity, however, these kinds of episodes are typically considered unusual, and even shameful. New research, from our lab and from others around the world, however, suggests mental illnesses are so common that almost everyone will develop at least one diagnosable mental disorder at some point in their lives. Most of these people will never receive treatment, and their relationships, job performance and life satisfaction will likely suffer. Meanwhile the few individuals who never seem to develop a disorder may offer psychology a new avenue of study, allowing researchers to ask what it takes to be abnormally, enduringly, mentally well. Epidemiologists have long known that, at any given point in time, roughly 20 to 25 percent of the population suffers from a mental illness, which means they experience psychological distress severe enough to impair functioning at work, school or in their relationships. Extensive national surveys, conducted from the mid-1990s through the early 2000s, suggested that a much higher percentage, close to half the population, would experience a mental illness at some point in their lives. These surveys were large, involving thousands of participants representative of the U.S. in age, sex, social class and ethnicity. They were also, however, retrospective, which means they relied on survey respondents’ accurate recollection of feelings and behaviors months, years and even decades in the past. Human memory is fallible, and modern science has demonstrated that people are notoriously inconsistent reporters about their own mental health history, leaving the final accuracy of these studies up for debate. Of further concern, up to a third of the people contacted by the national surveys failed to enroll in the studies. Follow-up tests suggested that these “nonresponders” tended to have worse mental health. © 2017 Scientific American

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23837 - Posted: 07.14.2017

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

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 23683 - Posted: 05.31.2017

Nicola Davis People from ethnic minorities have up to a five times greater risk of psychotic disorders than the white British population, researchers say. A new study reveals that the trend holds in both urban and rural settings, with first-generation migrants who arrive in the UK in childhood among those at increased risk. The team behind the study say a number of factors could be at play, including stresses related to the migration process, discrimination and issues related to isolation and integration. James Kirkbride, a psychiatric epidemiologist from University College London and co-author of the research, described the figures as shocking. It’s time to tackle mental health inequality among black people “If this was any other disorder we would be horrified and up in arms and we would be campaigning from a public health perspective on how we could reduce this level of suffering,” he said. “There is a massive health inequality and it hasn’t got much attention.” While psychosis is rare – rates in England stand at about 30 cases per 100,000 people per year – Kirkbride says more should be done to offer services to those in need and to unpick drivers behind raised risks. “In the present climate when issues about migration are at the forefront of the public’s mind, people from ethnic minority backgrounds may face additional stresses that could potentially contribute to mental health problems,” he added. Writing in the journal Schizophrenia Bulletin, Kirkbride and colleagues from the University of Cambridge and a collection of NHS foundation trusts describe how they looked at trends among 687 people in the east of England.

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23678 - Posted: 05.30.2017

By Daniel Barron Earlier this month, JAMA Psychiatry published a land-breaking editorial. A group of psychiatrists led by David Ross described how and why post-traumatic stress disorder (PTSD) should be clinically evaluated from a neuroscience framework. The fact that this editorial was published in one of psychiatry’s leading journals is no small feat. Psychiatry houses a large and powerful contingency that argues neuroscience has little clinical relevance. The relevance of neuroscience to psychiatry was the subject of a recent Op-Ed debate in the New York Times: “There’s Such a Thing as Too Much Neuroscience” was rebutted with “More Neuroscience, Not Less.” This specific debate—and the dense politics as a whole—exists because competing frameworks are vying for competing funding, a conflict that pre-dates Freud’s departure from neurology. That the relevance of neuroscience to psychiatry is still questioned is blatantly outlandish: what organ do psychiatrists treat if not the brain? And what framework could possibly be more relevant than neuroscience to understanding brain dysfunction? In his editorial, Ross tactfully presented his case for neuroscience, describing the obvious choice for a clinical framework as one “perspective,” making a delicate intellectual curtsey while supporting his case with data. Ross discussed five “key neuroscience themes” (read: lines of evidence from burgeoning sub-fields) relevant to understanding and treating PTSD: fear conditioning, dysregulated circuits, memory reconsolidation, and epigenetic and genetic considerations. Each theme accounts for the diverse biological, psychological and social factors involved in PTSD—which is to say, these factors all have some affect on the brain mechanisms. Most importantly, Ross describes how a mechanistic approach allows clinicians to trace the specific causes of PTSD to specific treatments that can target those causes. © 2017 Scientific American,

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 14: Attention and Consciousness
Link ID: 23536 - Posted: 04.26.2017

By TANYA FRANK It begins in the laundry room in the early hours of the morning. I find him alone, tracing the wires of the telephone circuit board. “This is how they are monitoring us,” my son whispers. “We have to cut some stuff out, change the receiver, I can do it.” “Who?” I ask. “Who is monitoring us? And why?” He puts a finger to his lips to quiet me, and begins rifling through the tool kit. He doesn’t seem quite sure what he is looking for. He has never rerouted wires in his life, and besides, it is 2009 and we have suspended our landline. These wires that my 19-year-old is obsessing over are part of a defunct apparatus from a bygone age. I shiver in this damp afterthought of a room, but not from the concrete floor under my bare feet. I’m a Londoner with a tolerance for winter. It’s nerves that have me shaking. I am scared of my own child. My partner is in San Francisco, and we are in Los Angeles. There is no national health system here. We are unmoored, just my boy and me above a twinkling metropolis of strangers. “We can’t trust anybody,” he writes. “Our computers and phones are bugged. Listen, hear that?” I shake my head, unable to detect anything. “It’s a helicopter spying on us.” When it sinks in that this is not a delirium that can be eased with Advil and a good night’s sleep, and when I stop denying that my son is armed, I take him to the closest psychiatric hospital, where he is involuntarily held for 72 hours, considered a danger to himself or others. His symptomology is examined and classified as if he is some rare and delicate butterfly, and he emerges with a label: schizoaffective disorder. It is a complex condition with traits of both schizophrenia (a thought disorder) and bipolar (a mood disorder). Basically, my son had a psychotic break. That’s what they call it when someone disintegrates from his psyche. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23518 - Posted: 04.21.2017

By CLYDE HABERMAN In America’s most storied political family, Rosemary Kennedy was the first in her generation to die of natural causes. Before then, a brother had been killed in war, a sister in a plane crash and two other brothers in assassinations. Not much of Ms. Kennedy’s life qualified as natural, though. Intellectually challenged from birth, she became increasingly erratic after entering womanhood. Her tempestuous mood swings troubled the family patriarch so much that he approved controversial surgery, which he was led to believe would calm her. In 1941, at age 23, Ms. Kennedy underwent a prefrontal lobotomy. It went badly. For her remaining 63 years, she led an institutionalized existence, out of public view, unable to speak clearly or walk without a limp. Retro Report, a series of video documentaries exploring major news stories of the past, harks back to that botched lobotomy and the neurologist who effectively sealed the young woman’s fate, Dr. Walter J. Freeman. The purpose is to show how the past informs the present. Psychosurgery endures, as with a procedure called a cingulotomy, which is used to treat depression and obsessive-compulsive disorder and involves severing fibers deep in the frontal lobe. But attention these days is keenly focused on stimulating discrete areas of the brain with electrical charges in the hope of easing torments like Parkinson’s disease, O.C.D. and depression. “What Walter Freeman was doing was crude and barbaric and harmful in many cases,” said Jack El-Hai, who wrote a 2005 biography of him, “The Lobotomist: A Maverick Medical Genius and His Tragic Quest to Rid the World of Mental Illness.” Referring to cingulotomies, Mr. El-Hai told Retro Report, “But what does remain is the idea that the brain can be physically manipulated, surgically manipulated, to help treat psychiatric illnesses.” The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23505 - Posted: 04.18.2017