Links for Keyword: Schizophrenia

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By DENISE GRADY Could pernicious anemia, a disease caused by a vitamin B12 deficiency, have explained the many strange behaviors of Mary Todd Lincoln? She was not exactly a model first lady. Historians have had a field day describing her violent temper, wild shopping sprees (she owned 300 pairs of kid gloves), depressed moods and all-consuming fears of burglars, storms and poverty. Late in life, at her son’s urging, she was committed to a mental hospital for several months. Plenty of theories, none proven, have been floated. She was bipolar. She had syphilis or that well known cause of feminine madness, menstrual trouble. She was spoiled and narcissistic. She never recovered from a road accident in which her head hit a rock. She lost her mind grieving the deaths of three of her four sons and her husband’s assassination. The latest addition to the list of possible diagnoses comes from Dr. John G. Sotos, a cardiologist, technology executive at Intel and one of the medical consultants who helped dream up the mystery diseases that afflicted patients on the television show “House.” Dr. Sotos has long been interested in difficult diagnoses, and has written a self-published book suggesting that Abraham Lincoln had a genetic syndrome that caused cancers of the thyroid and adrenal glands. In an interview, Dr. Sotos said that while he was studying President Lincoln, he came across something that intrigued him about Mrs. Lincoln: an 1852 letter mentioning that she had a sore mouth. He knew that vitamin B deficiencies could cause a sore tongue, and he began looking into her health. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22418 - Posted: 07.09.2016

By ERICA GOODE Irving Gottesman, a pioneer in the field of behavioral genetics whose work on the role of heredity in schizophrenia helped transform the way people thought about the origins of serious mental illness, died on June 29 at his home in Edina, Minn., a suburb of Minneapolis. He was 85. His wife, Carol, said he died while taking an afternoon nap. Although Dr. Gottesman had some health problems, she said, his death was unexpected, and several of his colleagues said they received emails from him earlier that day. Dr. Gottesman was perhaps best known for a study of schizophrenia in British twins he conducted with another researcher, James Shields, at the Maudsley Hospital in London in the 1960s. The study, which found that identical twins were more likely than fraternal twins to share a diagnosis of schizophrenia, provided strong evidence for a genetic component to the illness and challenged the notion that it was caused by bad mothering, the prevailing view at the time. But the findings also underscored the contribution of a patient’s environment: If genes alone were responsible for schizophrenia, the disorder should afflict both members of every identical pair; instead, it appeared in both twins in only about half of the identical pairs in the study. This interaction between nature and nurture, Dr. Gottesman believed, was critical to understanding human behavior, and he warned against tilting too far in one direction or the other in explaining mental illness or in accounting for differences in personality or I.Q. © 2016 The New York Times Company

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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 22405 - Posted: 07.07.2016

Jackie Goldstein Mental illness has been part of human society throughout recorded history, but how we care for people with mental disorders has changed radically, and not always for the better. In Colonial days, settlers lived in sparsely populated rural communities where sanctuary and community support enabled the tradition of family care brought from England. "Distracted persons" were acknowledged, but erratic behavior wasn't associated with disease. Records indicate unusual tolerance of bizarre behavior. When 18th century Pastor Joseph Moody of York, Maine, unable to face crowds, delivered sermons with a handkerchief covering his face, his behavior was tolerated for three years before he was relieved of his duties. As urban areas grew in size and number, a transient poor population with no access to family support led to almshouses, the first form of institutionalization, inspired by 18th century reforms in Europe. A Philadelphia Quaker who had visited an English retreat brought the idea to this country and in 1817 founded the Friends Asylum, a self-sufficient farm that offered a stress-free environment known as "moral treatment." Other private asylums followed, but they soon became overcrowded. By the late 19th century, this was addressed with larger state hospitals, which soon became overcrowded as well. People with mental disorders are more likely to be stigmatized owing to fear and misunderstanding when they aren't part of the community. And stigmatization can discourage those with a mental disorder from seeking or complying with treatment. © 2016 npr

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22393 - Posted: 07.04.2016

Angus Chen At the center of Geel, a charming Belgian town less than an hour's drive from of Antwerp, is a church dedicated to Dymphna, a saint believed to have the power to cure mental disorders. It's a medieval church with stone arches, spires and a half-built bell tower, and it has inspired an unusual centuries-old practice: For over 700 years, residents of Geel have been accepting people with mental disorders, often very severe mental disorders, into their homes and caring for them. It isn't meant to be a treatment or therapy. The people are not called patients, but guests or boarders. They go to Geel and join households to share a life with people who can watch over them. Today, there are about 250 boarders in Geel. One of them is a Flemish man named Luc Ennekans. He's slim and has green eyes, and he's 51 years old. NPR's Lulu Miller went to Geel and met him and his host family there and reported this story for Invisibilia. Like all of the guests in the town today, Ennekans first went to a public psychiatric hospital in Geel that manages the boarder program. Ennekans saw medical professionals and received treatment and an evaluation. Then he was paired with a household. His hosts, Toni Smit and Arthur Shouten, say that living with Ennekans was rough at the start. Ennekans became deeply attached to Smit. "If it were up to Luc, he would be hugging and kissing me all day," Smit says. He showered her with such affection, bringing her flowers, little kisses, linking arms with her on walks, that it began to interfere with Smit and Shouten's marriage. "You couldn't even give each other a hug or Luc is standing behind us," Shouten says. Wrinkles like this are common, according to the couple. They've had six boarders over the years, each with a unique set of challenges. © 2016 npr

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22385 - Posted: 07.01.2016

Angus Chen Rachel Star Withers runs a YouTube channel where she performs goofy stunts on camera and talks about her schizophrenia. Since 2008, when the then 22-year-old revealed her diagnosis online, tens of thousands of people have seen her videos. Some of them have a psychotic disorder or mood disorders themselves, or know people who do. They say her explanation about what a symptom like hallucinations feels like can be really helpful. So can Rachel's advice on ways to cope with them, like getting a dog or a cat. If the animal doesn't react to the hallucination, then it's probably not real, she says. We talked with people about how Withers' videos have helped them understand these diseases. What follows is a Q&A with two of these people. The interviews have been edited for length and clarity. Julia Billingsley is 22 years old and from Peoria, Ill. She learned she has schizophrenia last year, but she says her earliest encounter with the disease was back when she was very young. Her mother has schizophrenia, too, Billingsley says, and often had a delusion that their home was bugged. Julia, you started developing symptoms last year. Do you remember the first thing that happened to you? I'd just started dating my current boyfriend. And I'd be over at his house and I'd go to the bathroom. And this thought, this intrusive thought that wasn't my own at all would pop into my head like with force. And it would be like, hey. This room is bugged. And I was like, what? It made me stop. I stopped what I was doing and I didn't understand why my brain was thinking that. © 2016 npr

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22312 - Posted: 06.13.2016

By Diana Kwon A number of factors, including elements of the social environment (such as inequality and isolation) and physical stressors (such as pollution and noise) could explain how the city erodes well-being Credit: Thomas Koehler/Getty Images Life in the city can be taxing. City dwellers often face higher rates of crime, pollution, social isolation and other environmental stressors than those living in rural areas. For years studies have consistently linked the risk of developing schizophrenia to urban environments—but researchers are only beginning to understand why this association exists. Addressing the link is increasingly urgent: According to a recent U.N. report, the proportion of people living in cities will rise from 54 percent of the world’s population in 2014 to 66 percent by 2050. Researchers first suggested in the 1930s that urban living might increase schizophrenia risk. Since then many large epidemiological studies have reported an association between the two, primarily in European countries such as Sweden and Denmark. Converging evidence has revealed that growing up in the city doubles the risk of developing psychosis later in life. Studies have also begun to find that urban environments may heighten the risk of other mental health issues such as depression and anxiety. A number of factors, including elements of the social environment (such as inequality and isolation) and physical stressors (such as pollution and noise) could explain how the city erodes well-being. Conversely, people predisposed to mental illness may simply be more likely to move into urban environments. Two studies published this month shed new light on these effects and suggest both scenarios could be involved. © 2016 Scientific American, a Division

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: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 22234 - Posted: 05.21.2016

By ERICA GOODE PORTLAND, Ore. — The 911 caller had reported a man with a samurai sword, lunging at people on the waterfront. It was evening, and when the police arrived, they saw the man pacing the beach and called to him. He responded by throwing a rock at the embankment where they stood. They shouted to him from a sheriff’s boat; he threw another rock. They told him to drop the sword; he said he would kill them. He started to leave the beach, and after warning him, they shot him in the leg with a beanbag gun. He turned back, still carrying the four-foot blade. In another city — or in Portland itself not that long ago — the next step would almost certainly have been a direct confrontation and, had the man not put down the weapon, the use of lethal force. But the Portland Police Bureau, prodded in part by the 2012 findings of a Justice Department investigation, has spent years putting in place an intensive training program and protocols for how officers deal with people with mental illness. At a time when police behavior is under intense scrutiny — a series of fatal shootings by police officers have focused national attention on issues of race and mental illness — Portland’s approach has served as a model for other law enforcement agencies around the country. And on that Sunday last summer, the police here chose a different course. At 2:30 a.m., after spending hours trying to engage the man, the officers decided to “disengage,” and they withdrew, leaving the man on the beach. A search at daylight found no signs of him. People with mental illnesses are overrepresented among civilians involved in police shootings: Twenty-five percent or more of people fatally shot by the police have had a mental disorder, according to various analyses. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22150 - Posted: 04.27.2016

Richard A. Friedman DRUG companies are eager to tell you about their newest medicines. Turn on your TV or go online and there’s a new drug — with a hefty price tag — for whatever ails you, from antidepressants to painkillers to remedies for erectile dysfunction. The pharmaceutical industry spends lavishly to get your attention: In 2014, drug makers poured $4.5 billion into so-called direct-to-consumer advertising, a 30 percent increase over two years. Drug makers claim they are educating the public with their ads, providing information that will help you make better choices about your medical care. So in the spirit of education, let’s consider a recent online ad for Latuda, a new antipsychotic medication. A young woman rides a bike off into the sun as we are told that Latuda has been shown to be effective for many people with bipolar depression, followed by that staccato recitation of potential side effects that most viewers tune out. Here’s what a helpful prescription drug label could look like, with facts that are now out of reach. These are question marks because, although many clinical trial results are published, they are difficult to find and compare. Rules should mandate that all studies are accessible. Note the same high cost for a four-fold range of Latuda doses. Often the lowest dose is just as effective; some low-dose consumers realize they can save money by ordering the higher-dose units and splitting them into pieces. The ideal label would have statistics on how many people have serious side effects. Data are not included for these drugs because they may take years to emerge, if ever. Other drugs have well-known side effects. Fair enough. But the ad omits something that most consumers would like to know: There are many older and cheaper treatments that are just as effective. In fact, Latuda is one of 10 “second generation” antipsychotic medications, many available in generic forms, that essentially work the same way. Of course, the goal of drug companies is not to educate, but to sell products. We could ban the ads, as almost every other country does, and which I’d strongly support. But such a campaign in the United States would face fierce legislative and legal challenges. Instead, let’s help the drug companies make their ads truly educational. © 2016 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: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 22140 - Posted: 04.25.2016

It was December 2012 when the country learned about the massacre at Sandy Hook Elementary School, that left 20 children dead at the hands of 20-year-old shooter Adam Lanza. After the shock and the initial grief came questions about how it could have happened and why. Reports that Adam Lanza may have had some form of undiagnosed mental illness surfaced. The tragedy drove Liza Long to write a blog post on that same day, titled "I Am Adam Lanza's Mother." She wasn't Lanza's mom, but she was raising a child with a mental disorder. Her 13-year-old son had violent rages on a regular basis. He was in and out of juvenile detention. He had threatened to kill her. She detailed all this in her essay that took off online. Now, four years later, her son is speaking out too. This week on For The Record: a mother, a son and life on the edge of bipolar disorder. Eric Walton, Liza Long's son, is now a 16-year-old high school sophomore in Boise, Idaho. After a series of misdiagnoses, he's been diagnosed with bipolar disorder. But four years ago, he didn't know much about his condition. "I knew that there were times when I would have rages, didn't like them. I knew that I wanted them to stop," Walton says. Except he felt a loss of control in those moments. He describes the onset of these rages as a "blackout" of sorts. "I would start getting angry," he says. "Then it's like being trapped inside a box inside your own head. It was like a television on the wall that shows you what you're seeing. You can feel everything, but you no longer have the video game controller to control your own body." Walton's mom says when Eric would get into those states, "he would express a lot of suicidal thoughts, and hearing him just say, 'I want to die, I just want to end it.'" Then, two days before the Newtown shooting, Eric Walton had another episode. © 2016 npr

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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 22139 - Posted: 04.25.2016

By Clare Wilson People who develop schizophrenia may have been born with brains with a different structure. The finding adds further support to the idea that genetics can play a key role in schizophrenia, which involves delusions and hallucinations and is often a lifelong condition once it develops. Schizophrenia has been the subject of a fierce nature-versus-nurture debate: childhood abuse is linked with a raised risk of the condition, but 108 genes have been implicated, too. Probing the biology of schizophrenia is difficult because brain tissue sampled from people with the condition is rarely available to study. Kristen Brennand of the Icahn School of Medicine at Mount Sinai in New York and her colleagues got around this by taking skin cells from 14 people with schizophrenia, and reprogramming them into stem cells and then nerve cells. They found that on average these nerve cells had lower levels of a signalling molecule called miR-9 than similar cells developed from people who do not have schizophrenia. A small string of nucleic acids, miR-9 can change the activity of certain genes and is known to play a role in how neurons develop in the fetus. In further experiments, Brennand’s team showed that miR-9 might also affect how neurons migrate from where they form, next to the fetal brain’s central cavities, out to their final resting place in the brain’s outer layers. © Copyright Reed Business Information Ltd.

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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 22128 - Posted: 04.23.2016

By Amy Ellis Nutt I saw it all: The beginning of Time and the end of Time. Creation and annihilation. Somehow I’d slipped through a seam in the space-time continuum, and from my privileged mental perch I'd peered into the center of the universe. I was exhilarated and drew diagrams of my visions, trying to figure out what it all meant. But when I shared those visions with friends, they were confused and concerned. I was manic, they said, and making no sense. We were at an impasse. Was I sick – or simply in search of myself? Those questions from my own past hovered in the background while I watched two very different documentaries recently. Both explore bipolar illness -- a diagnosis I received more than 25 years ago and one that 5.5 million Americans share. But the films come from very different perspectives. The first, "Ride the Tiger: A Guide Through the Bipolar Brain," was produced by Detroit Public TV and airs on PBS Wednesday. It chronicles the latest in cutting-edge research into bipolar disorder and in doing so firmly plants its flag in the biological camp: The disorder is about misfiring brain circuits, genetic mutations, neurochemical disruptions and other neurological processes not yet delineated. The result is dramatic swings in mood and behavior that affect a person's ability to think clearly. "Ride the Tiger" features appearances by former congressman Patrick Kennedy and the late actress Patty Duke, both of whom talk about their own experiences. The second documentary, "Bipolarized: Re-Thinking Mental Illness," questions the very reality of the disorder -- at least for one former psychiatric patient.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22104 - Posted: 04.14.2016

By Simon Makin Brain science draws legions of eager students to the field and countless millions in dollars, euros and renminbi to fund research. These endeavors, however, have not yielded major improvements in treating patients who suffer from psychiatric disorders for decades. The languid pace of translating research into therapies stems from the inherent difficulties in understanding mental illness. “Psychiatry deals with brains interacting with the world and with other brains, so we're not just considering a brain's function but its function in complex situations,” says Quentin Huys of the Swiss Federal Institute of Technology (E.T.H. Zurich) and the University of Zurich, lead author of a review of the emerging field of computational psychiatry, published this month in Nature Neuroscience. Computational psychiatry sets forth the ambitious goal of using sophisticated numerical tools to understand and treat mental illness. Psychiatry currently defines disorders using lists of symptoms. Researchers have been devoting enormous energies to find biological markers that make diagnosis more objective with only halting success. Part of the problem is there is usually no one-to-one correspondence between biological causes and disorders defined by their symptoms, such as those in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). A specific disorder, like depression or schizophrenia, may result from a range of different underlying causes (biological or otherwise). On the other hand, the same cause might ultimately lead to different disorders in different people, depending on anything from their genetics to their life experiences. One of the goals of computational psychiatry is to draw connections between symptoms and causes, regardless of diagnoses. © 2016 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22013 - Posted: 03.22.2016

By Jonathan Leo Last week, according to many media accounts, scientists from Harvard Medical School, Boston Children’s Hospital, and the Broad Institute discovered the genetic basis of schizophrenia. The researchers reported in Nature that people with schizophrenia were more likely to have the overactive forms of a gene called complement component 4, or C4, which is involved in pruning synapses during adolescence. However, suggesting a biologic mechanism for a small subset of those diagnosed with schizophrenia is not the same as confirming the genetic theory of schizophrenia. Benedict Carey, science reporter for the New York Times, delved into the details and reported the all-important fact that having the C4 variant would increase a person’s risk by about 25 percent over the 1-percent base rate of schizophrenia—that is, to 1.25 percent. Genes for schizophrenia and depression have been discovered before, and in those cases, the subsequent enthusiastic headlines were shortly followed by retractions and more sober thinking. There are so many open questions (for instance, why do many people with the problematic variant not develop schizophrenia, and why do many people who don’t have the variant develop schizophrenia?) that the same may occur with the C4 discovery. The idea that mental illness is the result of a genetic predisposition is the foundation for modern-day psychiatry and has been the driving force for how research money is allocated, how patients are treated, and how society views people diagnosed with conditions identified in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition. Schizophrenia holds a unique spot in the annals of mental health research because of its perceived anatomical underpinnings and is often cited as evidence in favor of a genetic predisposition to other conditions.

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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 21863 - Posted: 02.06.2016

By BENEDICT CAREY A new approach to treating early schizophrenia, which includes family counseling, results in improvements in quality of life that make it worth the added expense, researchers reported on Monday. The study, published by the journal Schizophrenia Bulletin, is the first rigorous cost analysis of a federally backed treatment program that more than a dozen states have begun trying. In contrast to traditional outpatient care, which generally provides only services covered by insurance, like drugs and some psychotherapy, the new program offers other forms of support, such as help with jobs and school, as well as family counseling. The program also tries to include the patients — people struggling with a first psychotic “break” from reality, most of them in their late teens and 20s — as equals in decisions about care, including drug dosage. In a widely anticipated study last fall, called the Raise trial, researchers reported that after two years, people who got this more comprehensive care did better on a variety of measures than those who received the standard care. But the study found no evidence of related cost savings or differences in hospitalization rates, a prime driver of expense. As lawmakers in Washington are considering broad changes in mental health care, cost issues loom especially large. Outside experts said this analysis — which was based on the Raise trial data — was an important test of the new care program’s value. “This is the way cost analysis should be done,” Sherry Glied, a professor of public service and the dean of New York University’s graduate school of public service, said. “One way to think about it is to ask, if this program were a drug, would we pay for it? And the answer is yes.” © 2016 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 21842 - Posted: 02.01.2016

By BENEDICT CAREY Scientists reported on Wednesday that they had taken a significant step toward understanding the cause of schizophrenia, in a landmark study that provides the first rigorously tested insight into the biology behind any common psychiatric disorder. More than two million Americans have a diagnosis of schizophrenia, which is characterized by delusional thinking and hallucinations. The drugs available to treat it blunt some of its symptoms but do not touch the underlying cause. The finding, published in the journal Nature, will not lead to new treatments soon, experts said, nor to widely available testing for individual risk. But the results provide researchers with their first biological handle on an ancient disorder whose cause has confounded modern science for generations. The finding also helps explain some other mysteries, including why the disorder often begins in adolescence or young adulthood. “They did a phenomenal job,” said David B. Goldstein, a professor of genetics at Columbia University who has been critical of previous large-scale projects focused on the genetics of psychiatric disorders. “This paper gives us a foothold, something we can work on, and that’s what we’ve been looking for now, for a long, long time.” The researchers pieced together the steps by which genes can increase a person’s risk of developing schizophrenia. That risk, they found, is tied to a natural process called synaptic pruning, in which the brain sheds weak or redundant connections between neurons as it matures. During adolescence and early adulthood, this activity takes place primarily in the section of the brain where thinking and planning skills are centered, known as the prefrontal cortex. People who carry genes that accelerate or intensify that pruning are at higher risk of developing schizophrenia than those who do not, the new study suggests. Some researchers had suspected that the pruning must somehow go awry in people with schizophrenia, because previous studies showed that their prefrontal areas tended to have a diminished number of neural connections, compared with those of unaffected people. © 2016 The New York Times Company

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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 21835 - Posted: 01.28.2016

Angus Chen When she was 22, Rachel Star Withers uploaded a video to YouTube called "Normal: Living With Schizophrenia." It starts with her striding across her family's property in Fort Mill, S.C. She looks across the rolling grounds, unsmiling. Her eyes are narrow and grim. She sits down in front of a deserted white cottage and starts sharing. "I see monsters. I see myself chopped up and bloody a lot. Sometimes I'll be walking, and the whole room will just tilt. Like this," she grasps the camera and jerks the frame crooked. She surfaces a fleeting grin. "Try and imagine walking." She becomes serious again. "I'm making this because I don't want you to feel alone whether you're struggling with any kind of mental illness or just struggling." At the time, 2008, there were very few people who had done anything like this online. "As I got diagnosed [with schizophrenia], I started researching everything. The only stuff I could find was like every horror movie," she says. "I felt so alone for years." She decided that schizophrenia was really not that scary. "I want people to find me and see a real person." Over the past eight years, she has made 53 videos documenting her journey with schizophrenia and depression and her therapy. And she is not the only one. There are hundreds of videos online of people publicly sharing their experiences with mental illness. © 2016 npr

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 21834 - Posted: 01.28.2016

By Erin Blakemore Despite all that neurotic clucking and scratching, domestic chickens are pretty unflappable. After all, we’ve bred them to be that way, preferring chill chicks to freaked-out fowl. But the behaviors of more anxious chickens could do more than ruffle a bunch of feathers: New research suggests that studying the genome of flustered birds could shed light on human mental disorders. In a new study published in the journal Genetics, evolutionary biologist Dominic Wright and his team looked at whether there’s a genetic connection between anxious behavior in chickens, mice and humans. Despite the compact size of the chicken genome — it’s just a third of the size of a human’s — the birds’ genes share surprising similarity to those of people. There's another reason why chickens are so great for genetic research. Because there are both wild and domesticated chickens, researchers can observe their contrasting behaviors and easily pin them to genetic differences. Wright bred wild red junglefowl chickens with their calmer cousins, white leghorn chickens, for the experiment. After eight generations, his team was able to run open field tests — experiments during which the birds were put in a brightly-lit arena and assessed for how much time they spent cowering on the periphery instead of strutting through the room. These behavioral tests helped the team identify brave and anxious birds, then narrow down areas of the genome related to variations in anxiety. They identified 10 candidate genes in the hypothalamus, an area of the brain which helps regulate anxiety.

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: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 21763 - Posted: 01.08.2016

By BENEDICT CAREY SAN FRANCISCO — The idea was to go out in an emotional swan dive, a lunge for the afterlife that would stretch his 17-year-old imagination. He settled on a plan and shared the details with a Facebook friend: He would drop DMT, a powerful psychedelic, and then cut his throat. “Everyone was telling me what I could and couldn’t do — doctors, my parents,” said Frank, now a 19-year-old college student. “I was going to hurt myself, to show people, ‘Look, I am still in control of my life.’” And so, in time, he was. Frank, who eight months earlier had received a diagnosis of psychosis, the signature symptom of schizophrenia, and had been in and out of the hospital, gradually learned to take charge of his own recovery, in a new approach to treatment for people experiencing a first psychotic “break” with reality. At a time when lawmakers in Washington are debating large-scale reforms to the mental health care system, analysts are carefully watching a handful of new first-break programs like the one that treated Frank in New York as a way to potentially ease the cycle of hospitalization and lifetime disability that afflict so many mentally ill people. More than two million people in the United States have received a diagnosis of schizophrenia. Most are consigned to whatever treatment is available amid a hodgepodge of programs that often focus on antipsychotic drugs to blunt delusions and paranoia — medicines that can come with side effects so debilitating that many patients go off them and end up in a loop of hospitalization and despair. But over the past several years, a number of states have set up programs with a different approach, emphasizing supportive services, like sustained one-on-one therapy, school and work assistance, and family education, as well as medication. The therapists work to engage each patient as an equal partner in decisions — including about medication dosage, to make it as tolerable as possible. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 21731 - Posted: 12.29.2015

By ALAN SCHWARZ Andrew Rios’s seizures began when he was 5 months old and only got worse. At 18 months, when an epilepsy medication resulted in violent behavior, he was prescribed the antipsychotic Risperdal, a drug typically used to treat schizophrenia and bipolar disorder in adults, and rarely used for children as young as 5 years. From Our Advertisers When Andrew screamed in his sleep and seemed to interact with people and objects that were not there, his frightened mother researched Risperdal and discovered that the drug was not approved, and had never even been studied, in children anywhere near as young as Andrew. “It was just ‘Take this, no big deal,’ like they were Tic Tacs,” said Genesis Rios, a mother of five in Rancho Dominguez, Calif. “He was just a baby.” Cases like that of Andrew Rios, in which children age 2 or younger are prescribed psychiatric medications to address alarmingly violent or withdrawn behavior, are rising rapidly, data shows. Many doctors worry that these drugs, designed for adults and only warily accepted for certain school-age youngsters, are being used to treat children still in cribs despite no published research into their effectiveness and potential health risks for children so young. Almost 20,000 prescriptions for risperidone (commonly known as Risperdal), quetiapine (Seroquel) and other antipsychotic medications were written in 2014 for children 2 and younger, a 50 percent jump from 13,000 just one year before, according to the prescription data company IMS Health. Prescriptions for the antidepressant fluoxetine (Prozac) rose 23 percent in one year for that age group, to about 83,000. The company’s data does not indicate how many children received these prescriptions (many children receive several prescriptions a year), but previous studies suggest that the number is at least 10,000. IMS Health researched the data at the request of The New York Times. © 2015 The New York Times Company

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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 21696 - Posted: 12.12.2015

By Jonathan Webb Science reporter, BBC News A study of 153 brain scans has linked a particular furrow, near the front of each hemisphere, to hallucinations in schizophrenia. This fold tends to be shorter in those patients who hallucinate, compared with those who do not. It is an area of the brain that appears to have a role in distinguishing real perceptions from imagined ones. Researchers say the findings, published in Nature Communications, might eventually help with early diagnosis. The brain wrinkle, called the paracingulate sulcus or PCS, varies considerably in shape between individuals. It is one of the final folds to develop, appearing in the brain only just before birth. "The brain develops throughout life, but aspects such as whether the PCS is going to be a particularly prominent fold - or not -may be apparent in the brain at an early stage," said Jon Simons, a neuroscientist at the University of Cambridge, UK. "It might be that a reduction in this brain fold gives somebody a predisposition towards developing something like hallucinations later on in life." If further work shows that the difference can be detected before the onset of symptoms, for example, Dr Simons said it might be possible to offer extra support to people who face that elevated risk. But he stressed that schizophrenia is a complicated phenomenon. Hallucinations are one of the main symptoms, but some patients are diagnosed on the basis of other irregular thought processes. "We've known for some time that disorders like schizophrenia are not down to a single region of the brain. Changes are seen throughout various different areas. "To be able to pin such a key symptom to a relatively specific part of the brain is quite unusual." © 2015 BBC.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 21644 - Posted: 11.18.2015