Links for Keyword: Schizophrenia

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Sara Reardon Broad population studies are shedding light on the genetic causes of mental disorders. Researchers seeking to unpick the complex genetic basis of mental disorders such as schizophrenia have taken a huge step towards their goal. A paper1 published in Nature this week ties 108 genetic locations to schizophrenia — most for the first time. The encouraging results come on the same day as a US$650-million donation to expand research into psychiatric conditions. Philanthropist Ted Stanley gave the money to the Stanley Center for Psychiatric Research at the Broad Institute in Cambridge, Massachusetts. The institute describes the gift as the largest-ever donation for psychiatric research. “The assurance of a very long life of the centre allows us to take on ambitious long-term projects and intellectual risks,” says its director, Steven Hyman. The centre will use the money to fund genetic studies as well as investigations into the biological pathways involved in conditions such as schizophrenia, autism and bipolar disorder. The research effort will also seek better animal and cell models for mental disorders, and will investigate chemicals that might be developed into drugs. The Nature paper1 was produced by the Psychiatric Genomics Consortium (PGC) — a collaboration of more than 80 institutions, including the Broad Institute. Hundreds of researchers from the PGC pooled samples from more than 150,000 people, of whom 36,989 had been diagnosed with schizophrenia. This enormous sample size enabled them to spot 108 genetic locations, or loci, where the DNA sequence in people with schizophrenia tends to differ from the sequence in people without the disease. “This paper is in some ways proof that genomics can succeed,” Hyman says. © 2014 Nature Publishing Group

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: 19864 - Posted: 07.22.2014

Dr Lucy Maddox There has been much heated debate in recent weeks about whether cognitive behavioural therapy for psychosis has been totally over-egged. One stance is that Nice (the National Institute for Clinical Excellence) has recommended a treatment with little or no evidence base. Another is that CBT is a helpful intervention for many people experiencing psychotic-like phenomena. But what is CBT for psychosis? What does it look like? And how can knowing this help us to understand the issues being argued about? Psychosis is an umbrella term for a collection of symptoms. These symptoms get classed as "positive" or "negative", which is not to infer that some are good and some are bad, but rather to capture the fact that some of the symptoms add something new and others take something away. Positive symptoms are those that add an unusual experience of some kind, eg seeing things that others can't (hallucinations) or strongly believing things that don't make sense to others (delusions). Negative symptoms involve something being taken away from the person, eg a lack of enjoyment (anhedonia), motivation (avolition), or a lack of emotion. Whilst a recent meta-analysis has shown only limited evidence for the effectiveness of CBT for psychosis and suggested that previous results are inflated, we should be cautious about using this one meta-analysis to chuck out CBT for psychosis. Among other potential holes that could be poked in its conclusions is the fact that the analysis uses psychotic symptoms as the only outcome measure for effectiveness, which might not be the best or only thing we should be looking at. Many other reviews and individual studies do report reductions in psychotic symptoms from CBT for psychosis, including delusions and hallucinations and some of the brain processing correlates of these positive symptoms (eg Kumari et al 2011). Perhaps more interestingly though, they also report benefits from CBT in domains other than the psychotic symptoms themselves. (eg Wykes et al, 2009). © 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: 19639 - Posted: 05.20.2014

by Laura Sanders An injectable form of a newer, more expensive schizophrenia drug works no better than an older drug, scientists report May 21 in the Journal of the American Medical Association. In a randomized clinical trial of 311 people with schizophrenia, injections of paliperidone palmitate failed to alleviate schizophrenia symptoms just as often as did injections of haloperidol decanoate, a drug that’s been around for decades. A single injection of paliperidone palmitate, a second-generation antipsychotic, costs about $1000 in the United States. An injection of haloperidol costs only about $35. The two drugs caused different side effects: In some patients, haloperidol led to muscle tremors and restlessness and paliperidone palmitate caused weight gain. Knowledge of these different side effects — and not differences in effectiveness — might be useful in deciding which drug a person ought to take. © Society for Science & the Public 2000 - 2013.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19638 - Posted: 05.20.2014

By ANNE SAKER CINCINNATI — The psychologist Lynda Crane found that of the many injuries inflicted by schizophrenia, the greatest could be the pain of being forgotten. Just naming the illness somehow erased the person, something she learned when her 18-year-old son’s doctors said he had schizophrenia. Six years later, he committed suicide. “It took me a long time to come to terms with it,” Dr. Crane says. “Even I had a hard time understanding it, how this bright man, with a brilliant future, could suffer like this. One thing I learned was that as soon as you mentioned the word, people stopped seeing the person. They just saw the diagnosis and a collection of symptoms. Doug, my son, was forgotten.” For years Dr. Crane, a professor at the College of Mount St. Joseph in the western hills of Cincinnati, sought a way to enlighten her students and others about the ordinary people who live with schizophrenia despite its extraordinary burdens – the confused thinking, the delusions, the hallucinations, the anxiety and fear. Then she discovered a tool more commonly used among sociologists and anthropologists: oral history. Employing the device to examine schizophrenia has shifted her own perspective about a disease she thought she knew well. “People with schizophrenia do not lose their individuality, even when the illness is very severe,” Dr. Crane says. “What I discovered through oral history is that it’s not about schizophrenia. It’s about a complexity of life that is very hard to get at any other way.” For the past three years, on their own time and with no outside money, Dr. Crane and a fellow Mount St. Joseph psychologist, Tracy McDonough, have built the Schizophrenia Oral History Project. Other oral history collections have focused on diseases like AIDS or leprosy, but this is the first to focus on schizophrenia, they say. © 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: 19593 - Posted: 05.10.2014

by Clare Wilson IMAGINE you are a doctor before the advent of modern medical tests and your patient is gasping for breath. Is it asthma, a chest injury, or are they having a heart-attack? You don't know and have no idea how best to help them. Some would argue that's what it's like for doctors trying to diagnose mental health problems today. There are no blood tests or brain scans for mental illnesses so diagnoses are subjective and unreliable. The issue came to a head one year ago this month, with the latest edition of psychiatry's "bible", the Diagnostic and Statistical Manual of Mental Disorders. The US National Institute for Mental Health (NIMH) said the DSM-5 had so many problems we effectively need to tear it up and start again. The way forward, it said, is a new research programme to discover the brain problems that underlie mental illnesses. That research is now taking off. The first milestone came earlier this year, when the NIMH published a list of 23 core brain functions and their associated neural circuitry, neurotransmitters and genes – and the behaviours and emotions that go with them (see "The mind's 23 building blocks"). Within weeks, the first drug trials conceived and funded through this new programme will begin. While just a first draft, the list arguably represents the future of neuroscience-based mental healthcare. "This is the Rosetta stone for characterising human mental function," says Andrew Krystal at Duke University in Durham, North Carolina. Criticism of psychiatry has been growing for years – existing treatments are often inadequate, and myriad advances in neuroscience and genetics have not translated into anything better. Vocal opponents are not confined to the US. Last week, the new UK Council for Evidence-based Psychiatry launched a campaign claiming that drugs such as antidepressants and antipsychotics often do more harm than good. © Copyright Reed Business Information Ltd.

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: 19588 - Posted: 05.08.2014

By Maggie Fox Treating psychiatric illnesses with antipsychotic drugs can greatly reduce the risk that a patient will commit a violent crime, researchers reported on Thursday. Their study, published in the Lancet medical journal, adds weight to the argument that severely mentally ill people need to get diagnosed and treated. Mental health experts agree that people with psychiatric illnesses such as schizophrenia are far more likely to become victims of violence than they are to hurt someone else. But Dr. Thomas Insel, director of the National Institute on Mental Health, also notes that people with severe mental illness are up to three times more likely than the general population to be violent. The question has been whether treatment lowers these risks. One high-profile case is that of Jared Loughner, a schizophrenia patient who shot and killed six people in Arizona and wounded several more, including then-congresswoman Gabrielle Giffords. Dr. Seena Fazel of Britain’s Oxford University used a Swedish national database to find out. Sweden keeps careful medical records, and has similar rates of both mental illness and violence to the United States. The only exception is homicide, where the U.S. has much higher rates than just about every other country. Fazel’s team looked at the medical records of everyone born in Sweden between 1961 and 1990. “We identified 40,937 men and 41,710 women who were prescribed any antipsychotic or mood stabilizer between Jan 1, 2006, and Dec 31, 2009,” they wrote. It worked out to about 2 percent of the population.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 19587 - Posted: 05.08.2014

By Sandra G. Boodman, As the jet hurtled toward New York’s John F. Kennedy International Airport on New Year’s Day 2013, the clinical psychologist watched her 16-year-old daughter warily, praying there would be no recurrence of the girl’s inexplicable and bizarre behavior. The previous night, while walking down a street in Spain where the family had spent Christmas, the teenager suddenly began yelling that the traditional New Year’s Eve fireworks were actually bombs. On the flight home, the girl seemed entirely normal. Her mother thought the high school junior might have had a panic attack, stressed by her upcoming college search and impending wisdom teeth extraction. But the uneventful flight brought a short-lived relief. Five days later, the teenager was hospitalized for treatment of what appeared to be a severe psychotic break. And for the next six weeks, the news seemed to get worse as a more ominous diagnosis emerged — and with it the specter of death. “Every day seemed like a horror story,” said Carmen, a psychoanalyst who practices in New York and whose last name, along with that of her daughter, Mia, is being withheld at her request to protect her professional privacy. For Lara Marcuse, a neurologist at Mount Sinai Hospital in Manhattan who treated Mia during her hospitalization, those weeks were filled with tension and anxiety that deepened as she worried that the teenager might not survive her sudden illness. “If she was my age,” said Marcuse, who is 44, “Mia would either be dead, in a coma or in a state psychiatric center.” Instead Mia, now 18, has fully recovered. She recently had a part in her high school play, is anticipating graduation and looking forward to entering college in September. © 1996-2014 The Washington Post

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: 19548 - Posted: 04.29.2014

By BARBARA EHRENREICH MY atheism is hard-core, rooted in family tradition rather than adolescent rebellion. According to family legend, one of my 19th-century ancestors, a dirt-poor Irish-American woman in Montana, expressed her disgust with the church by vehemently refusing last rites when she lay dying in childbirth. From then on, we were atheists and rationalists, a stance I perpetuated by opting, initially, for a career in science. How else to understand the world except as the interaction of tiny bits of matter and mathematically predictable forces? There were no gods or spirits, just our own minds pressing up against the unknown. But something happened when I was 17 that shook my safely rationalist worldview and left me with a lifelong puzzle. Years later, I learned that this sort of event is usually called a mystical experience, and I can see in retrospect that the circumstances had been propitious: Thanks to a severely underfunded and poorly planned skiing trip, I was sleep-deprived and probably hypoglycemic that morning in 1959 when I stepped out alone, walked into the streets of Lone Pine, Calif., and saw the world — the mountains, the sky, the low scattered buildings — suddenly flame into life. There were no visions, no prophetic voices or visits by totemic animals, just this blazing everywhere. Something poured into me and I poured out into it. This was not the passive beatific merger with “the All,” as promised by the Eastern mystics. It was a furious encounter with a living substance that was coming at me through all things at once, too vast and violent to hold on to, too heartbreakingly beautiful to let go of. It seemed to me that whether you start as a twig or a gorgeous tapestry, you will be recruited into the flame and made indistinguishable from the rest of the blaze. I felt ecstatic and somehow completed, but also shattered. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 19452 - Posted: 04.07.2014

By LISA SANDERS, M.D. On Thursday, we challenged Well readers to solve the mystery of a 23-year-old man with episodes of aggressive, manic behavior that couldn’t be controlled. Nearly 1,000 readers wrote in with their take on this terrifying case. More than 300 of you got the right class of disease, and 21 of you nailed the precise form of the disorder. Amazing! The correct diagnosis is … Variegate porphyria The first person with the correct answer was Francis Graziano, a 23-year-old recent graduate of the University of Michigan. His major in neuroscience really gave him a leg up on this case, he told me. He recalled a case he read of a young Vietnam veteran with symptoms of porphyria. He’s a surgical technician right now, waiting to hear where he’ll be going to medical school next year. Strong work, Dr.-to-be Graziano! The Diagnosis: The word porphyria comes from the ancient Greek word for purple, “porphyra,” because patients with this disease can have purplish-red urine, tears or saliva. The porphyrias are a group of rare genetic diseases that develop in patients born without the machinery to make certain essential body chemicals, including one of the most important parts of blood known as heme. This compound makes up the core of the blood component hemoglobin. (The presence of heme is why blood is red.) Patients who can’t make heme correctly end up with too much of its chemical precursors, known as porphyrins. The excess porphyrins injure tissues throughout the body, but especially in the nervous system. The disorder is characterized by frequent episodes of debilitating back or abdominal pain and is often accompanied by severe psychiatric symptoms. Patients with porphyria do not respond to most psychiatric medications. Indeed, many of these drugs make the symptoms of porphyria worse. © 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: 19448 - Posted: 04.05.2014

by Colin Barras What a nerve! Skin cells taken from people with bipolar disorder have been turned into brain cells. These in turn are offering up clues about the changes in the brain that drive the disorder, and may also provide a way to test new treatments. About three in every 100 people develop bipolar disorder – a mental illness characterised by episodes of depression and euphoria. But the condition remains poorly understood. That's because it would be too invasive to obtain and study viable nerve cells from the brains of people with the condition. There are also no good animal models, because bipolar disorder – although highly heritable – has, for the most part, not been linked to any specific genes that can be studied using animals. "People say the condition is probably the result of a lot of small contributions by multiple genes," says Sue O'Shea at the University of Michigan in Ann Arbor. Now O'Shea and her colleagues may have found an ethical way to make a genetic model of the condition. First, they took skin samples from 22 people with bipolar disorder and 10 healthy volunteers. They induced these adult skin cells to return to a stem-cell-like state, creating what are called induced pluripotent stem cells (iPSCs) and then encouraged these cells to mature into neurons. O'Shea was surprised to find that neurons derived from people with bipolar disorder grew differently from those from people without the condition. "I was expecting it would take decades of careful science before we would find any real differences," she says. © Copyright Reed Business Information Ltd.

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: 19412 - Posted: 03.26.2014

Sara Reardon Thomas Insel, the director of the US National Institute of Mental Health (NIMH), has had enough of shooting in the dark. He thinks that if a clinical trial of a psychiatric therapy fails, scientists should at least learn something about the brain along the way. Now Insel is translating that belief into action: the NIMH, based in Bethesda, Maryland, has decided to stop funding clinical trials that aim merely to ease patients’ symptoms. “Future trials will follow an experimental medicine approach in which interventions serve not only as potential treatments, but as probes to generate information about the mechanisms underlying a disorder”, he wrote in a 27 February blog post announcing the move. This funding switch, which will affect grants due to be made in a few months’ time, intensifies the NIMH’s apparent shift in emphasis from abstract psychiatry to the neurobiological roots of disease. “It’s a totally new departure for us,” says Bruce Cuthbert, a clinical psychologist and director of the institute’s adult translational-research division. Insel notes that the NIMH spent about US$100 million on clinical trials in 2013, and says that more than half of recipient projects received funding without any requirement to examine the biological processes involved in a disease. In many cases, “if you get a negative result you have no idea why, and you have to try something else at random”, Cuthbert says. “It’s an incredible waste of money.” The new rules, which will apply to the grant cycle that begins in June, also seek to increase transparency by requiring faster online registration of trials and stricter guidelines for reporting results. Insel acknowledges that researchers may have to rework their studies to satisfy the new guidelines. “I think this will be really unpopular,” he says. © 2014 Nature Publishing Group

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: 19367 - Posted: 03.15.2014

Imagine that, after feeling unwell for a while, you visit your GP. "Ah," says the doctor decisively, "what you need is medication X. It's often pretty effective, though there can be side-effects. You may gain weight. Or feel drowsy. And you may develop tremors reminiscent of Parkinson's disease." Warily, you glance at the prescription on the doctor's desk, but she hasn't finished. "Some patients find that sex becomes a problem. Diabetes and heart problems are a risk. And in the long term the drug may actually shrink your brain … " This scenario may sound far-fetched, but it is precisely what faces people diagnosed with schizophrenia. Since the 1950s, the illness has generally been treated using antipsychotic drugs – which, as with so many medications, were discovered by chance. A French surgeon investigating treatments for surgical shock found that one of the drugs he tried – the antihistamine chlorpromazine – produced powerful psychological effects. This prompted the psychiatrist Pierre Deniker to give the drug to some of his most troubled patients. Their symptoms improved dramatically, and a major breakthrough in the treatment of psychosis seemed to have arrived. Many other antipsychotic drugs have followed in chlorpromazine's wake and today these medications comprise 10% of total NHS psychiatric prescriptions. They are costly items: the NHS spends more on these medications than it does for any other psychiatric drug, including antidepressants. Globally, around $14.5bn is estimated to be spent on antipsychotics each year. Since the 1950s the strategy of all too many NHS mental health teams has been a simple one. Assuming that psychosis is primarily a biological brain problem, clinicians prescribe an antipsychotic medication and everyone does their level best to get the patient to take it, often for long periods. There can be little doubt that these drugs make a positive difference, reducing delusions and hallucinations and making relapse less likely – provided, that is, the patient takes their medication. © 2014 Guardian News and Media Limited

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: 19336 - Posted: 03.08.2014

Ian Sample, science correspondent Children born to fathers over the age of 45 are at greater risk of developing psychiatric problems and more likely to struggle at school, according to the findings of a large-scale study. The research found that children with older fathers were more often diagnosed with disorders such as autism, psychosis, attention deficit hyperactivity disorder (ADHD), schizophrenia and bipolar disorder. They also reported more drug abuse and suicide attempts, researchers said. The children's difficulties seemed to affect school performance, leading to worse grades at the age of 15 and fewer years in education overall. "We were shocked when we saw the comparisons," said Brian D'Onofrio, the first author of the study at Indiana University in the US. But he added that it was impossible to be sure that older age was to blame for the problems. Scientists have reported links between fathers' age and children's cognitive performance and health before but this study suggests the risks may be more serious than previously thought. The increased risks might be caused by genetic mutations that build up in sperm as men age. Researchers at Indiana University and the Karolinska Institute in Stockholm studied medical and educational records of more than 2.6 million babies born to 1.4 million men. The group amounted to nearly 90% of births in Sweden from 1973 and 2001. Using the records, the scientists added up diagnoses for psychiatric disorders and educational achievements and compared the figures for children born to fathers of different ages. © 2014 Guardian News and Media Limited

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: 19303 - Posted: 02.27.2014

By MICHAEL HEDRICK I still remember the first group therapy session I went to after I got out of the hospital. I was 20 and had been diagnosed as schizophrenic after a road trip that took me from Colorado to the United Nations building in New York City, my mind riddled with notions of good and evil, demons and angels, and a determination to save the world. Now I was in something of a state of shock, having come to understand that amid the delusions and paranoia that swarmed through my head I was, in reality, insane. A constant need to move felt like ants crawling over my skin, a side effect of the antipsychotic medications I had been prescribed. Every second of every day, I felt like clawing out my eyes and tearing out my hair because I just couldn’t sit still. I held up my front, though. I smiled when I thought I had to and tried to be nice to people. Laughter, however, was not something that was possible, and wouldn’t be for a long time. The group was a dual-functioning therapy technique to address both mental health issues and drug abuse. I had been assigned to it after disclosing that I had a marijuana habit. The doctors had told me that therapy groups were an integral part of my getting better. I agreed to go only to get out of the hospital prison and back home to my warm bed. I sat in a circle with a melting pot of people. There was the construction worker still wearing dusty boots and clothes splattered with mud, and the depressed sorority girl, makeup and hair still impeccable. The two had formed a friendship over their history with methamphetamine. There was the quiet bipolar Hispanic man who spoke only in short staccato sentences, and the rotund marketing guy who introduced himself by saying his drugs of choice were food, cocaine and marijuana. © 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: 19302 - Posted: 02.27.2014

by Clare Wilson AS MANY as 1 in 10 cases of schizophrenia may be triggered by an autoimmune reaction against brain cells, according to early trial results shared with New Scientist. The finding offers the possibility of gentler treatments for this devastating mental illness. Last month, doctors at a conference at the Royal Society of Medicine in London were told to consider an autoimmune cause when people first show symptoms of schizophrenia. People with schizophrenia experience symptoms of psychosis, such as hallucinations, delusions and paranoia. It affects 1 per cent of people in the West and is thought to be caused by overactive dopamine signalling pathways in the brain. Anti-psychotic drugs don't always work wellMovie Camera and have serious side effects. Previous studies had found that antibodies that target the NMDA receptor on neurons trigger brain inflammation, leading to seizures, comas – and sometimes psychosis (Annals of Neurology, doi.org/fdgnpc). In the past few years, these antibodies have also been found in the blood of people whose only symptom is psychosis. In 2010, Belinda Lennox at the University of Oxford tested 46 people with recent onset of psychosis for antibodies known to target neurons. Three people – about 6 per cent – tested positive (Neurology, doi.org/chs532). "The question is whether a larger percentage of cases might have other antibodies which we cannot yet detect," says Robin Murray at the Institute of Psychiatry in London, who wasn't involved in the research. Now Lennox is conducting a larger trial. Early results suggest other antibodies could well be involved. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 19251 - Posted: 02.15.2014

Schizophrenia and related mental illnesses can have a devastating effect on people who suffer from them, often making it impossible for them to work or maintain normal social relationships. Antipsychotic drugs are usually the first line of defense, but they can have serious side effects. A new study concludes that psychological approaches could be an alternative for patients who either can’t or won’t take medication, although some critics continue to question the effectiveness of these interventions. Schizophrenia, which can involve hallucinations, delusions, paranoia, emotional problems, and severe difficulty focusing on daily tasks, affects about 1% of populations worldwide. More than 20 antipsychotic medications, such as risperidone, haloperidol, and clozapine, are now on the market, and they are often effective in temporarily relieving the worse symptoms. But when taken for extended periods, such drugs can cause uncontrollable muscle movements, serious weight gain, and higher risk of heart attacks. In recent years, a number of psychiatrists and psychologists have begun to advocate psychological approaches, including an approach called cognitive behavioral therapy (CBT), as an adjunct to antipsychotic drugs. With CBT, which has long been shown to be effective for depression and anxiety disorders, a therapist takes the subject through a series of guided steps designed to explore alternative interpretations and explanations of what he or she is experiencing, with the goal of changing both outlook and behavior. A schizophrenic patient who is having hallucinations might be encouraged to stop trying to fight them off or suppress them, for example, or to stop engaging with voices in his or her head, to test how strong such symptoms really are and how much control they exert over the subject’s life. The technique also involves what practitioners call “normalization”: The patient might be reassured that hearing voices and seeing things that are not there is an experience that many normal people have from time to time, thus reducing some of the anxiety that makes sufferers feel distressed and isolated. © 2014 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19227 - Posted: 02.08.2014

By James Gallagher Health and science reporter, BBC News Changing the way people think about and deal with schizophrenia could be as effective as drugs, say researchers. Cognitive behavioural therapy is an officially recommended treatment, but is available to less than 10% of patients in the UK with schizophrenia. A study published in the Lancet indicates CBT could help the many who refuse antipsychotic medication. Experts say larger trials are needed. About four-in-10 patients benefit from taking antipsychotic medication. But the drugs do not work for the majority and they cause side-effects such as type 2 diabetes and weight gain. Up to half of patients with schizophrenia end up not taking the drugs. The study looked at cognitive behaviour therapy in 74 people. The therapy works by identifying an individual patient's problem - such as hearing voices, paranoid thinking or no longer going out of the house - and developing techniques to deal with them. Prof Tony Morrison, director of the psychosis research unit at Greater Manchester West Mental Health Foundation Trust, said: "We found cognitive behavioural therapy did reduce symptoms and it also improved personal and social function and we demonstrated very comprehensively it is a safe and effective therapy." It worked in 46% of patients, approximately the same as for antipsychotics - although a head-to-head study directly comparing the two therapies has not been made. Douglas Turkington, professor of psychiatry at Newcastle University, said: "One of our most interesting findings was that when given the option, most patients were agreeable to trying cognitive therapy." BBC © 2014

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: 19212 - Posted: 02.06.2014

By BENEDICT CAREY BETHESDA, Md. — The police arrived at the house just after breakfast, dressed in full riot gear, and set up a perimeter at the front and back. Not long after, animal rights marchers began filling the street: scores of people, young and old, yelling accusations of murder and abuse, invoking Hitler, as neighbors stepped out onto their porches and stared. It was 1997, in Decatur, Ga. The demonstrators had clashed with the police that week, at the Yerkes National Primate Research Center at nearby Emory University, but this time, they were paying a personal call — on the house of the center’s director, inside with his wife and two teenage children. “I think it affected the three of them more than it did me, honestly,” said Dr. Thomas R. Insel, shaking his head at the memory. “But the university insisted on moving all of us to a safe place for a few days, to an ‘undisclosed location.’ “I’ll say this. I learned that if you’re going to take a stand, you’re going to make some people really angry — so you’d better believe in what you’re doing, and believe it completely.” For the past 11 years, Dr. Insel, a 62-year-old brain scientist, has run an equally contentious but far more influential outfit: the National Institute of Mental Health, the world’s leading backer of behavioral health research. The job comes with risk as well as power. Patient groups and scientists continually question the agency’s priorities, and politicians occasionally snipe at its decisions. Two previous directors resigned in the wake of inflammatory statements (one on marijuana laws, one comparing urban neighborhoods to jungles), and another stepped down after repeatedly objecting to White House decisions. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 1: Biological Psychology: Scope and Outlook
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 1: An Introduction to Brain and Behavior
Link ID: 19202 - Posted: 02.04.2014

By RICHARD A. FRIEDMAN, M.D. “How the Federal Government Destroyed the Mental Illness Treatment System”: That subtitle is the opening shot across the bow in this jeremiad of a book by the psychiatrist Dr. E. Fuller Torrey. It could just as well have read: “How a group of well-intentioned, starry-eyed idealists made a hash of mental health care.” You could hardly blame them for trying, though. The care of people with serious mental illness was long a national disgrace. By the 1950s, slightly more than half a million psychiatric patients resided in overcrowded and underfunded state mental hospitals, often under appalling conditions. Related Coverage Enter a group of high-minded psychiatrists with a vision to “create a brave new world, a mentally healthy America,” in Dr. Torrey’s words. Armed with little more than optimism, they helped start the National Institute of Mental Health and set in motion an ambitious agenda for the next half-century: closing the state mental hospitals, initiating a federal takeover of the mental health system, and creating a nationwide network of community mental health centers. Reform was well underway when President John F. Kennedy endorsed this new era in mental health in a 1963 speech, calling for a “bold new approach” in which “reliance on the cold mercy of custodial isolation will be supplanted by the open warmth of community concern and capability.” Those were heady days in American psychiatry, when psychoanalysis and the mental hygiene movement held sway and promised to cure all manner of ills by early intervention and improving the social environment. In hindsight, the therapeutic zeal of these professionals was impressively naïve: They were certain that severely mentally ill patients in state hospitals — many living there for decades — would magically adjust to the community and do well with outpatient treatment. How wrong they proved to be. © 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: 19127 - Posted: 01.14.2014

By Tia Ghose and LiveScience Neurons derived from schizophrenic patients. Image: Dr. Kristen Brennand, Salk Institute for Biological Studies. Some so-called jumping genes that copy and paste themselves throughout the genome may be linked to schizophrenia, new research suggests. The new study, published Jan. 2 in Neuron, suggests these jumping genes may alter how neurons (or nerve cells in the brain) form during development, thereby increasing the risk of schizophrenia, study co-author Dr. Tadafumi Kato, a neurobiologist at the RIKEN Brain Science Institute in Japan, wrote in an email. Jumping genes, or retrotransposons, are mobile genetic elements that copy and paste themselves at different places throughout the genome. About half of the human genome is made of these mysterious elements, compared with the 1 percent of genes that actually code for making proteins, Kato said. Earlier studies had found that a certain type of jumping gene, known as long interspersed nuclear element-1 (LINE-1), was active in human brain cells. Kato and his colleagues wondered whether they might play a role in mental illness. To find out, the team conducted a post-mortem analysis of 120 human brains, 13 from patients who had been diagnosed with schizophrenia. The team found a higher number of LINE-1 copies in the brains of schizophrenics compared with other groups. © 2014 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: 19098 - Posted: 01.04.2014