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 525

By Andrea Alfano Unexpectedly losing a loved one launched 18-year-old Debra* into an episode of major depression, triggering dangerous delusions that landed her in a hospital. Her doctor immediately started her on an antidepressant and on risperidone (Risperdal), an antipsychotic. In little more than a month, her weight shot up by 15 pounds. “Gaining weight made it even more difficult for me to want to leave my house because I felt self-conscious,” Debra says. In the medical community, antipsychotics are well known to cause significant weight gain. Gains of 20 to 35 pounds or more over the course of a year or two are not unusual. Debra's doctor never warned her, though, leaving her feeling like she was losing herself both mentally and physically. The situation is not uncommon, according to psychiatrist Matthew Rudorfer, chief of the somatic treatments program at the National Institute of Mental Health, who points out that although the U.S. Food and Drug Administration carefully tracks acute side effects such as seizures, it pays less attention to longer-term complications such as weight change. Perhaps taking their cue from the FDA, doctors tend to downplay weight-related risks that accompany many psychiatric drugs, Rudorfer says. But for Debra and many others, these side effects are not trivial. The three types of psychiatric drugs that can seriously affect body weight are reviewed below. According to a 2014 review of eight studies, as many as 55 percent of patients who take modern antipsychotics experience weight gain—a side effect that appears to be caused by a disruption of the chemical signals controlling appetite. Olanzapine (Zyprexa) and clozapine (Clozaril) are the top two offenders; studies have shown that on average these drugs cause patients to gain more than eight pounds in just 10 weeks. These two drugs also bear the highest risk of metabolic syndrome, which encompasses weight gain and other related disorders, including type 2 diabetes, according to a 2011 study of 90 people with schizophrenia. Although most antipsychotics are associated with weight gain, aripiprazole (Abilify) and ziprasidone (Geodon) stand out for their lower risk. © 2015 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 21204 - Posted: 07.23.2015

By Bret Stetka Plenty of us have known a dog on Prozac. We have also witnessed the eye rolls that come with the mention of canine psychiatry. Doting pet owners—myself included—ascribe all kinds of questionable psychological ills to our pawed companions. But in fact, the science suggests that numerous nonhuman species do suffer from psychiatric symptoms. Birds obsess; horses on occasion get pathologically compulsive; dolphins and whales, especially those in captivity, self-mutilate. And that thing when your dog woefully watches you pull out of the driveway from the window—that might be DSM-certified separation anxiety. “Every animal with a mind has the capacity to lose hold of it from time to time,” wrote science historian and author Laurel Braitman in her 2014 book Animal Madness. But at least one mental malady, while common in humans, seems to have spared other animals: schizophrenia, which affects an estimated 0.4 to 1 percent of adults. Although animal models of psychosis exist in laboratories, and odd behavior has been observed in creatures confined to cages, most experts agree that psychosis has not typically been seen in other species, whereas depression, obsessive-compulsive disorder and anxiety traits have been reported in many nonhuman species. This raises the question of why such a potentially devastating, often lethal disease is still hanging around plaguing humanity. We know from an abundance of recent research that schizophrenia is heavily genetic in origin. One would think that natural selection would have eliminated the genes that predispose to psychosis. A study published earlier this year in Molecular Biology and Evolution provides clues as to how the potential for schizophrenia may have arisen in the human brain and, in doing so, suggests possible treatment targets. It turns out that psychosis may be an unfortunate cost of having a big brain that is capable of complex cognition. © 2015 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: 21101 - Posted: 06.27.2015

Matthew C Keller & Peter M Visscher Epidemiological studies and anecdotal evidence show overlap between psychiatric disorders and creativity, but why? A new study uses genome-wide association data from schizophrenia and bipolar disorder to show that genetics are part of the explanation. Thinkers contemplating the human condition have long associated creativity with psychiatric illness—the 'mad genius' archetype. According to Aristotle, “no great genius was without a mixture of insanity.” And there are the oft-repeated anecdotes: the psychotic breaks of Vincent van Gogh and John Nash, the manic and depressive episodes of Virginia Woolf and Ernest Hemingway. There is, in fact, some empirical evidence that the psychological factors underlying psychiatric disorders are linked to increased creativity. Unaffected relatives of those with bipolar disorder (BD) have greater creativity1 and are over-represented in creative professions2, and similar findings have been reported for schizophrenia (SCZ)2, 3. What these studies have not shown is whether this overlap is a result of genetic variation that influences both creativity and BD/SCZ or whether some environmental factor explains the association. For example, highly unstructured rearing environments might contribute to both creativity and risk of the disorders. Understanding whether shared gene variants are responsible for the overlap is important. It can help to elucidate the biological underpinnings of these disorders and shine light on the puzzle of why psychiatric diseases persist in the population. Power et al.4, in work reported in this issue of Nature Neuroscience, asked whether creativity and psychiatric disorders might be associated through common variation in the genome. They used a large discovery sample of 86,292 adults from Iceland and four replication samples totaling over 27,000 adults from Sweden and the Netherlands. All had genome-wide SNP genotyping and their professions were known. None of them knowingly suffered from a psychiatric illness. About 1% of them were artists, including actors, dancers, musicians and writers. © 2015 Macmillan Publishers Limited

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: 21100 - Posted: 06.27.2015

By JAIME LOWE The manila folder is full of faded faxes. The top sheet contains a brief description of my first medically confirmed manic episode, more than 20 years ago, when I was admitted as a teenager to U.C.L.A.’s Neuropsychiatric Institute: “Increased psychomotor rate, decreased need for sleep (about two to three hours a night), racing thoughts and paranoid ideation regarding her parents following her and watching her, as well as taping the phone calls that she was making.” I believed I had special powers, the report noted; I knew ‘‘when the end of the world was coming due to toxic substances’’ and felt that I was the only one who could stop it. There was also an account of my elaborate academic sponsorship plan so I could afford to attend Yale — some corporation would pay for a year of education in exchange for labor or repayment down the line. (Another grand delusion. I was a B-plus student, at best.) After I was admitted to the institute's adolescent ward, I thought the nurses and doctors and therapists were trying to poison me. So was the TV in the rec room. I warned my one friend in the ward that its rays were trying to kill him. The generator outside my window was pumping in gas. The place, I was sure, was a death camp. I refused meds because they were obviously agents of annihilation. It took four orderlies to medicate me: They pinned me to the floor while a nurse plunged a syringe into my left hip. Over time, I became too tired to refuse medication. Or perhaps the cocktail of antipsychotics started working. The Dixie cup full of pills included lithium, which slowly took hold of my mania. After a few weeks, I stopped whispering to the other patients that we were all about to be killed. Eventually, I stopped believing it myself. Mark DeAntonio, the U.C.L.A. psychiatrist who was treating me, said I had bipolar disorder. Here’s the phrasing from the National Institute of Mental Health: ‘‘unusually intense emotional states that occur in distinct periods called ‘mood episodes.’ Each mood episode represents a drastic change from a person’s usual mood and behavior. An overly joyful or overexcited state is called a manic episode, and an extremely sad or hopeless state is called a depressive episode.’’ The generic definition doesn’t quite cover the extremes of the disease or its symptoms, which include inflated self-esteem, sleeplessness, loquaciousness, racing thoughts and doing things that, according to the Mayo Clinic, ‘‘have a high potential for painful consequences — for example, unrestrained buying sprees, sexual indiscretions or foolish business investments.’’ © 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: Biological Basis of Behavioral Disorders
Link ID: 21094 - Posted: 06.25.2015

By Michael Hedrick I’ve had a little success dating in the nearly 10 years I’ve lived with schizophrenia. But there are a lot of obstacles. Schizophrenia is a terrifying word for many people. It conjures up ideas of murderous intent, lack of control and a host of other scary things. I live with this word, though; I am the word. But it is not a word you can just drop into a conversation and follow with “It’s not a big deal, though.” I seem to fall in love easily, but it’s always with girls who don’t feel the same way about me. I have seen more rejection than I care to admit, putting myself on the line like that, and it’s been a chore for me not to let my emotions get the best of me. If it’s not outright rejection, it seems to be something else that always seems to happen. I can remember one date I went on some months back. She was a big girl with blonde hair and eyes that had that squinty “I’m up to no good” look. We met over Match.com, and I was struck by how much time she spent going to Phish shows. Her profile was scattered with a number of bands that I had loved at different points in my life. She was a teacher, and she mentioned in her profile something along the lines that because of her love of sparkles, arts-and- crafts, and rainbows, she was a 6-year-old in a woman’s body. Before I knew it, I was asking if she wanted to go get a beer. She said yes, a little too eagerly I thought. I got to the restaurant about 15 minutes early and ordered a beer, apprehensive knowing that eventually I would have to tell her about my illness. Soon enough she walked in, and I was struck by the fact that she seemed a little disappointed to be there. There was no smile as she sat down to join me. © 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: Biological Basis of Behavioral Disorders
Link ID: 21051 - Posted: 06.15.2015

Owning a cat as a kid could put you at risk for schizophrenia and bipolar disorder later on because of parasites found in feline feces, new research says. Previous studies have linked the parasite toxoplasma gondii (T. gondii) to the development of mental disorders, and two more research papers published recently provide further evidence. Researchers from the Academic Medical Centre in Amsterdam looked at more than 50 studies and found that a person infected with the parasite is nearly twice as likely to develop schizophrenia. The other study, led by Dr. Robert H. Yolken of Johns Hopkins University School of Medicine in Baltimore, confirmed the results of a 1982 questionnaire that found half of people who had a cat as a kid were diagnosed with mental illnesses later in life compared to 42% of those who didn't grow up with a cat. "Cat ownership in childhood has now been reported in three studies to be significantly more common in families in which the child is later diagnosed with schizophrenia or another serious mental illness," the authors said in a press release. The findings were published in Schizophrenia Research and Acta Psychiatrica Scandinavica. T. gondii, which causes the disease toxoplasma, is especially risky for pregnant women and people with weak immune symptoms. The parasite can also be found in undercooked meat and unwashed fruits and vegetables.

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: 21038 - Posted: 06.10.2015

Angus Chen The genetic underpinnings of psychosis are elusive and diffuse. There are hundreds of common genetic mutations scattered throughout the human genome that each bump up by just a tiny bit the risk of developing a mental illness like schizophrenia. Many people carry some set of those genes, but most don't end up with a psychotic disorder. Instead, a study suggests, they might be getting a small creative boost. Meghan, 23, began experiencing hallucinations at 19. "Driving home, cars' headlights turned into eyes. The grills on the cars turned into mouths and none of them looked happy. It would scare the crap out of me," Meghan says. Those genetic changes may persist in human DNA because they confer benefits, according Dr. Kári Stefánsson, a neurologist and CEO of a biological research company called deCODE Genetics, which conducted the study published in Nature Neuroscience Monday. "They are found in most of us, and they're common because they either confer or in the past conferred some reproductive advantage," he says. The advantage of having a more creative mind, he suggests, might help explain why these genes persist, even as they increase the risk of developing debilitating disorders, such as schizophrenia. It's an idea from the ancients. The philosopher Aristotle famously opined that genius and madness go hand in hand. Psychiatric studies have to some degree supported the adage. Studies of more than 1 million Swedish people in 2011 and 2013 found that people who had close relatives with schizophrenia or bipolar disorder were much more likely to become creative professionals. (The patients with mental illness were not themselves more creative, with the exception of some who had bipolar disorder.) What's more, studies that looked at healthy people who carry genetic markers associated with a psychotic disorder found their brains work slightly differently than others who lack those genetic markers. © 2015 NPR

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: 21032 - Posted: 06.09.2015

Steve Connor Scientists have linked the condition with variations in the DNA of genes known to be involved in stimulating or inhibiting the passing of chemical messages across the tiny gaps or “synapses” between nerve cells in the brain. They said the findings are part of a wider body of evidence pointing to the genetic causes of schizophrenia which is known to have a strong inherited component as well as being influenced by a person’s environment and upbringing. “We’re finally starting to understand what goes wrong in schizophrenia. Our study marks a significant step towards understanding the biology underpinning schizophrenia, which is an incredible complex condition and has up until very recently kept scientists largely mystified as to is origins,” said Andrew Pocklington of Cardiff University. “We now have what we hope is a pretty sizeable piece of the jigsaw puzzle that will help us to develop a coherent model of the disease, while helping us to rule out some of the alternatives,” said Dr Pocklington, the lead author of the study published in the journal Neuron. “A reliable model of disease is urgently needed to direct future efforts in developing new treatments, which haven’t really improved a great deal since the 1970s,” he said. © independent.co.uk

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: 21021 - Posted: 06.06.2015

By Rachael Rettner and LiveScience Mathematician John Nash, who died May 23 in a car accident, was known for his decades-long battle with schizophrenia—a struggle famously depicted in the 2001 Oscar-winning film "A Beautiful Mind." Nash had apparently recovered from the disease later in life, which he said was done without medication. But how often do people recover from schizophrenia, and how does such a destructive disease disappear? Nash developed symptoms of schizophrenia in the late 1950s, when he was around age 30, after he made groundbreaking contributions to the field of mathematics, including the extension of game theory, or the math of decision making. He began to exhibit bizarre behavior and experience paranoia and delusions, according to The New York Times. Over the next several decades, he was hospitalized several times, and was on and off anti-psychotic medications. But in the 1980s, when Nash was in his 50s, his condition began to improve. In an email to a colleague in the mid-1990s, Nash said, "I emerged from irrational thinking, ultimately, without medicine other than the natural hormonal changes of aging," according to The New York Times. Nash and his wife Alicia died, at ages 86 and 82, respectively, in a crash on the New Jersey Turnpike while en route home from a trip on which Nash had received a prestigious award for his work. © 2015 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: 21018 - Posted: 06.06.2015

By Melissa Healy contact the reporter Schizophrenia is one of psychiatry's most puzzling afflictions, with a complex of symptoms that goes far beyond its hallmark hallucinations and delusional thinking. But new research has found connections among several of schizophrenia's peculiar collection of symptoms -- including agitation and memory problems -- and linked them to a single genetic variant among the hundreds thought to heighten risk of the disorder. The findings offer new insights into the molecular basis for schizophrenia and could lead to treatments for the disease that are more targeted and more comprehensive. Published Monday in the journal Nature Neuroscience, the study looks at how a gene variant called Arp2/3 contributes to psychosis, agitation and problems of short- and long-term memory. Mice that were genetically modified to lack the Arp2/3 gene variant showed all three symptoms (although to measure psychosis in mice, scientists looked instead for an abnormal startle response that is also seen in humans in the grips of psychosis). The study's authors, led by Duke University neurobiologist Scott Soderling, then dug below those behaviors to see whether brain abnormalities linked to such behaviors had anything in common. Mice that lacked the Arp2/3 gene variant, they discovered, had not only symptoms of schizophrenia, but also several of the underlying brain abnormalities most closely linked to psychosis, agitation and memory problems seen in those with schizophrenia.

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: 20895 - Posted: 05.06.2015

By KATIE THOMAS Last fall, an article in the American Journal of Psychiatry caught the attention of specialists who treat borderline personality disorder, an intractable condition for which no approved drug treatment exists. The article seemed to offer a glimmer of hope: The antipsychotic drug Seroquel XR reduced some of the disorder’s worst symptoms in a significant number of patients. “It was an exciting development,” recalled Mark F. Lenzenweger, a professor at Binghamton University and Weill Cornell Medical College and an expert in borderline personality disorder. In the realm of clinical trials, however, reality is sometimes far messier than the tidy summaries in medical journals. A closer look at the Seroquel XR study shows just how complicated things can get when a clinical trial involves psychiatric disorders and has its roots in intersecting and sometimes competing interests: a drug company looking to hold onto sales of a best-selling drug, a prominent academic with strong ties to the pharmaceutical industry and a university under fire for failing to protect human study subjects. The trial was paid for by AstraZeneca, the maker of Seroquel XR, and was conducted by Dr. S. Charles Schulz, the head of psychiatry at the University of Minnesota. Two of the study participants were living in a residential treatment facility for sex offenders and may have lied about their diagnosis to qualify for the trial. One of those men slipped the drugs to unwitting treatment center residents and staff, an alarming development that nevertheless did not seem to ruffle the university oversight board that is charged with looking into such episodes. The University of Minnesota’s clinical trial practices are now under intense scrutiny. In February, a panel of outside experts excoriated the university for failing to properly oversee clinical trials and for paying inadequate attention to the protection of vulnerable subjects. The review, commissioned by the university after years of criticism of its research practices, singled out Dr. Schulz and his department of psychiatry, describing “a culture of fear” that pervaded the department. © 2015 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: 20814 - Posted: 04.18.2015

By ABIGAIL ZUGER, M.D. On an early summer night in 1944, on the wooded shoulder of a rural Massachusetts highway, a man in a rumpled brown suit wandered in the shadows. Whenever a car passed, he dropped to the ground and lay flat. His hair was matted, his face smeared with mud. He was a respectable Boston doctor on the lam, hungry, lost and ill. He was Mimi Baird’s father, Dr. Perry Baird, a Texas-born, Harvard-trained physician whose severe bipolar disease ultimately destroyed his life and scarred his family with the usual wide-ranging cruelties of mental illness. Dr. Baird vanished from Ms. Baird’s life when she was a little girl. She saw him once, briefly, when she was a teenager, then never again. He died in his mid-50s, in 1959. More than 30 years later, when Ms. Baird herself was in her 50s, a large package arrived on her doorstep and her father re-entered her world. The box contained a manuscript long forgotten in a relative’s garage, written in smudged pencil on onionskin paper, a memoir her father had composed of five terrible months in his life. The story began the very day Dr. Baird said goodbye to 5-year-old Mimi and her sister, and permanently left the household. Stunned and bereft all over again, Ms. Baird then spent two decades chasing down the rest of the story, talking to neighbors, colleagues and relatives about long-ago events and obtaining her father’s medical records. Now in her late 70s, a retired medical administrator, she has, with the help of a co-author, woven all this material into “He Wanted the Moon,” an extraordinary Möbius strip of a book. (Read an excerpt.) Its core is the full text of her father’s manuscript, deftly annotated and explained. Around it she layers the voices of caretakers, friends, relatives and medical authorities. Events are revisited and reframed, turned inside out, then right side up again. The book is autobiography, biography, science, history and literature all in one, as instructive as any textbook and utterly impossible to put down. © 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: Biological Basis of Behavioral Disorders
Link ID: 20600 - Posted: 02.24.2015

By Kate Baggaley A buildup of rare versions of genes that control the activity of nerve cells in the brain increases a person’s risk for bipolar disorder, researchers suggest in a paper posted online the week of February 16 in Proceedings of the National Academy of Sciences. “There are many different variants in many different genes that contribute to the genetic risk,” says coauthor Jared Roach, a geneticist at the Institute for Systems Biology in Seattle. “We think that most people with bipolar disorder will have inherited several of these…risk variants.” The bulk of a person’s risk for bipolar disorder comes from genetics, but only a quarter of that risk can be explained by common variations in genes. Roach’s team sequenced the genomes of 200 people from 41 families with a history of bipolar disorder. They then identified 164 rare forms of genes that show up more often in people with the condition. People with bipolar disorder had, on average, six of these rare forms, compared with just one, on average, found in their healthy relatives and the general population. The identified genes control the ability of ions, or charged particles, to enter or leave nerve cells, or neurons. This affects neurons’ ability to pass information through the brain. Some of the gene variants probably increase how much neurons fire while others decrease it, the researchers say. Future research will need to explain what role these brain changes play in bipolar disorder. Citations S.A. Ament et al. Rare variants in neuronal excitability genes influence risk for bipolar disorder. Proceedings of the National Academy of Sciences. Published online the week of February 16, 2015. doi:10.1073/pnas.1424958112. © Society for Science & the Public 2000 - 2015

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: 20588 - Posted: 02.18.2015

By Neuroskeptic | An important new study could undermine the concept of ‘endophenotypes’ – and thus derail one of the most promising lines of research in neuroscience and psychiatry. The findings are out now in Psychophysiology. Unusually, an entire special issue of the journal is devoted to presenting the various results of the study, along with commentary, but here’s the summary paper: Knowns and unknowns for psychophysiological endophenotypes by Minnesota researchers William Iacono, Uma Vaidyanathan, Scott Vrieze and Stephen Malone. In a nutshell, the researchers ran seven different genetic studies to try to find the genetic basis of a total of seventeen neurobehavioural traits, also known as ‘endophenotypes’. Endophenotypes are a hot topic in psychiatric neuroscience, although the concept is somewhat vague. The motivation behind interest in endophenotypes comes mainly from the failure of recent studies to pin down the genetic cause of most psychiatric syndromes: endophenotypes_A Essentially an endophenotype is some trait, which could be almost anything, which is supposed to be related to (or part of) a psychiatric disorder or symptom, but which is “closer to genetics” or “more biological” than the disorder itself. Rather than thousands of genes all mixed together to determine the risk of a psychiatric disorder, each endophenotype might be controlled by only a handful of genes – which would thus be easier to find.

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: 20396 - Posted: 12.06.2014

Daniel Freeman and Jason Freeman “Although it is a waste of time to argue with a paranoid patient about his delusions, he may still be persuaded to keep them to himself, to repress them as far as possible and to forgo the aggressive action they might suggest, in general to conduct his life as if they did not exist.” This quote from Clinical Psychiatry, a hugely influential textbook in the 1950s and 1960s, epitomises the way in which unusual mental states were generally understood for much of the 20th century. Delusions (such as paranoid thoughts) and hallucinations (hearing voices, for example) were of interest purely as symptoms of psychosis, or what used to be called madness. Apart from their utility in diagnosis, they were deemed to be meaningless: the incomprehensible effusions of a diseased brain. Or in the jargon: “empty speech acts, whose informational content refers to neither world nor self”. There’s a certain irony here, of course, in experts supposedly dedicated to understanding the way the mind works dismissing certain thoughts as unworthy of attention or explanation. The medical response to these phenomena, which were considered to be an essentially biological problem, was to eradicate them with powerful antipsychotic drugs. This is not to say that other strategies weren’t attempted: in one revealing experiment in the 1970s, patients in a ward for “paranoid schizophrenics” in Vermont, US, were rewarded with tokens for avoiding “delusional talk”. These tokens could be exchanged for items including “meals, extra dessert, visits to the canteen, cigarettes, time off the ward, time in the TV and game room, time in bedroom between 8am and 9pm, visitors, books and magazines, recreation, dances on other wards.” (It didn’t work: most patients modified their behaviour temporarily, but “changes in a patient’s delusional system and general mental status could not be detected by a psychiatrist”.) © 2014 Guardian News and Media Limited

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: 20369 - Posted: 11.29.2014

By Michael Hedrick I have a hard time making friends. Getting to trust people well enough to call them a friend takes a lot of work. It’s especially hard when you are living with schizophrenia and think everyone is making fun of you. Schizophrenia is the devil on your shoulder that keeps whispering in your ear and, no matter what you try, the little demon won’t stop. He hasn’t stopped in the almost nine years I’ve lived with the illness, and he’s not about to stop now. He’s just quieted down a bit. I’d call him my companion but that would imply a degree of friendship, and there’s no way in hell I’m the little devil’s friend. I have plenty of acquaintances, and a couple hundred “friends” on Facebook. But real friends, mostly family, I can count on one hand. For me, making friends is like climbing a vertical rock wall with no ropes, requiring a degree of thrill-seeking, and a good deal of risk. For someone to be my friend, they have to accept that I’m crazy, and even getting to the point of telling them that is daunting when all you hear is the devil’s whispering that they’re making snap judgments about you or will be going back to their real friends and laughing about you. But interestingly, in my efforts to make friends, coffee shops have helped. The simple routine of going to get your fix of liquid energy every day provides a sort of breeding ground for community. You see these people every day,whether you like it or not and, over time, friendships form. I used to live in a small town called Niwot, about five miles down the highway from Boulder, where I now live. Every morning around 6 I would go to Winot Coffee, the small independent coffee shop, and every morning, without fail, there was a guy my age sitting outside with his computer smoking clove cigarettes. Given the regularity of seeing him every morning, and given that we were some of the only 20-somethings in town, we got to talking. © 2014 The New York Times Company

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: 20240 - Posted: 10.25.2014

by Amy Standen The important thing is that Meghan knew something was wrong. When I met her, she was 23, a smart, wry young woman living with her mother and stepdad in Simi Valley, about an hour north of Los Angeles. Meghan had just started a training program to become a respiratory therapist. Concerned about future job prospects, she asked NPR not to use her full name. Five years ago, Meghan's prospects weren't nearly so bright. At 19, she had been severely depressed, on and off, for years. During the bad times, she'd hide out in her room making thin, neat cuts with a razor on her upper arm. "I didn't do much of anything," Meghan recalls. "It required too much brain power." "Her depression just sucked the life out of you," Kathy, Meghan's mother, recalls. "I had no idea what to do or where to go with it." One night in 2010, Meghan's mental state took an ominous turn. Driving home from her job at McDonald's, she found herself fascinated by the headlights of an oncoming car. "I had the weird thought of, you know, I've never noticed this, but their headlights really look like eyes." To Meghan, the car seemed malicious. It wanted to hurt her. Kathy tried to reason with her. "Honey, you know it's a car, right? You know those are headlights," she recalls pressing her daughter. "You understand that this makes no sense, right?" © 2014 NPR

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: 20223 - Posted: 10.21.2014

Patients with schizophrenia are already known to have higher rates of premature death than the general population. The study found that elevated risks of heart disease and metabolic issues such as high blood sugar in people with first episode psychosis are due to an interaction of mental illness, unhealthy lifestyle behaviors and antipsychotic medications that may accelerate these risks. Patients entered treatment with significant health concerns – including excess weight, smoking, and metabolic issues – despite an average age of only 24 years. The study identifies key opportunities for health care systems to improve the treatment of such patients with first episode psychosis. The research was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. Christoph Correll, M.D., of The Zucker Hillside Hospital, Hofstra North Shore-Long Island Jewish School of Medicine, New York, and colleagues, report their findings on Oct. 8, 2014 in JAMA Psychiatry. The study is among the first of several to report results from the Recovery After an Initial Schizophrenia Episode (RAISE) project, which was developed by NIMH to examine first episode psychosis before and after specialized treatment was offered in community settings. The researchers studied nearly 400 individuals between the ages of 15 and 40 with first episode psychosis, who presented for treatment at 34 community-based clinics across 21 states. The frequency of obesity was similar to the same age group in the general population. However, smoking and metabolic syndrome (a combination of conditions including obesity, high blood pressure, high blood sugar, and abnormal blood fats, such as cholesterol and triglycerides) were much more common.

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: 20182 - Posted: 10.09.2014

Have you ever wrongly suspected that other people are out to harm you? Have you been convinced that you’re far more talented and special than you really are? Do you sometimes hear things that aren’t actually there? These experiences – paranoia, grandiosity and hallucinations in the technical jargon – are more common among the general population than is usually assumed. But are people who are susceptible simply “made that way”? Are they genetically predisposed, in other words, or have their life experiences made them more vulnerable to these things? It’s an old debate: which is more important, nature or nurture? Scientists nowadays tend to agree that human psychology is a product of a complex interaction between genes and experience – which is all very well, but where does the balance lie? Scientists (including one of the authors of this blog) recently conducted the first ever study among the general population of the relative contributions of genes and environment to the experience of paranoia, grandiosity and hallucinations. How did we go about the research? First, it is important to be clear about the kinds of experience we measured. By paranoia, we mean the unfounded or excessive fear that other people are out to harm us. Grandiosity denotes an unrealistic conviction of one’s abilities and talents. Hallucinations are sensory experiences (hearing voices, for instance) that aren’t caused by external events. Led by Dr Angelica Ronald at Birkbeck, University of London, the team analysed data on almost 5,000 pairs of 16-year-old twins. This is the classical twin design, a standard method for gauging the relative influence of genes and environment. Looking simply at family traits isn’t sufficient: although family members share many genes, they also tend to share many of the same experiences. This is why studies involving twins are so useful. © 2014 Guardian News and Media Limited

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: 20147 - Posted: 10.02.2014

By MICHAEL HEDRICK I can remember the early days of having schizophrenia. I was so afraid of the implications of subtle body language, like a lingering millisecond of eye contact, the way my feet hit the ground when I walked or the way I held my hands to my side. It was a struggle to go into a store or, really, anywhere I was bound to see another living member of the human species. With a simple scratch of the head, someone could be telling me to go forward, or that what I was doing was right or wrong, or that they were acknowledging the symbolic crown on my head that made me a king or a prophet. It’s not hard to imagine that I was having a tough time in the midst of all the anxiety and delusions. Several months after my diagnosis, I took a job at a small town newspaper as a reporter. I sat in on City Council meetings, covering issues related to the lowering water table and interviewing local business owners for small blurbs in the local section, all the while wondering if I was uncovering some vague connections to an international conspiracy. The nights were altogether different. Every day, I would come home to my apartment and smoke pot, then lay on my couch watching television or head out to the bar and get so hammered that I couldn’t walk. It’s hard to admit, but the only time I felt relaxed was when I was drunk. I eventually lost my newspaper job, but that wasn’t the catalyst for change. It all came to a head one night in July. I had been out drinking all night and, in a haze, I decided it would be a good idea to drive the two miles back to my apartment. This is something I had done several times before, but it had never dawned on me that it was a serious deal. I thought I was doing well, not swerving and being only several blocks from my house, when I saw flashing lights behind me. What started as a trip to the bar to unwind ended with me calling my parents to bail me out of jail at 3 a.m. © 2014 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: 20045 - Posted: 09.08.2014