Sunanda Creagh, The Conversation Testosterone may trigger a brain chemical process linked to schizophrenia but the same sex hormone can also improve cognitive thinking skills in men with the disorder, two new studies show. Scientists have long suspected testosterone plays an important role in schizophrenia, which affects more men than women. Men are also more likely to develop psychosis in adolescence, previous research has shown. A new study on lab rodents by researchers from Neuroscience Research Australia analysed the impact increased testosterone had on levels of dopamine, a brain chemical linked to psychotic symptoms of schizophrenia. The researchers found that testosterone boosted dopamine sensitivity in adolescent male rodents. “From these rodent studies, we hypothesise that adolescent increases in circulating testosterone may be a driver of increased dopamine activity in the brains of individuals susceptible to psychosis and schizophrenia,” said senior Neuroscience Research Australia researcher and author of the study, Dr Tertia Purves-Tyson, who is presenting her work at the International Congress on Schizophrenia Research in Florida. Dr Philip Mitchell, Scientia Professor and Head of the School of Psychiatry at the University of NSW, said the research was very interesting. © 2013 ScienceAlert Pty Ltd.

Keyword: Schizophrenia; Aggression
Link ID: 18076 - Posted: 04.27.2013

David Adam David Kupfer is a modern-day heretic. A psychiatrist at the University of Pittsburgh in Pennsylvania, Kupfer, has spent the past six years directing the revision of a book commonly referred to as the bible of the psychiatric field. The work will reach a climax next month when the American Psychiatric Association (APA) unveils the fifth incarnation of the book, called the Diagnostic and Statistical Manual of Mental Disorders (DSM), which provides checklists of symptoms that psychiatrists around the world use to diagnose their patients. The DSM is so influential that just about the only suggestion of Kupfer's that did not meet with howls of protest during the revision process was to change its name from DSM-V to DSM-5. Although the title and wording of the manual are now settled, the debate that overshadowed the revision is not. The stark fact is that no one has yet agreed on how best to define and diagnose mental illnesses. DSM-5, like the two preceding editions, will place disorders in discrete categories such as major-depressive disorder, bipolar disorder, schizophrenia and obsessive–compulsive disorder (OCD). These categories, which have guided psychiatry since the early 1980s, are based largely on decades-old theory and subjective symptoms. The problem is that biologists have been unable to find any genetic or neuroscientific evidence to support the breakdown of complex mental disorders into separate categories. Many psychiatrists, meanwhile, already think outside the category boxes, because they see so many patients whose symptoms do not fit neatly into them. Kupfer and others wanted the latest DSM to move away from the category approach and towards one called 'dimensionality', in which mental illnesses overlap. According to this view, the disorders are the product of shared risk factors that lead to abnormalities in intersecting drives such as motivation and reward anticipation, which can be measured (hence 'dimension') and used to place people on one of several spectra. But the attempt to introduce this approach foundered, as other psychiatrists and psychologists protested that it was premature. © 2013 Nature Publishing Group

Keyword: Schizophrenia; Aggression
Link ID: 18073 - Posted: 04.25.2013

By KJ DELL'ANTONIA A cautiously worded study based on data collected in Sweden has found that “in utero exposure to both selective serotonin reuptake inhibitors (S.S.R.I.’s) and nonselective monoamine reuptake inhibitors (tricyclic antidepressants) was associated with an increased risk of autism spectrum disorders, particularly without intellectual disability.” The Swedish medical birth register (which contains data on current drug use reported by mothers early in their pregnancies), along with a system of publicly funded screenings for autism spectrum disorders and extensive national and regional registers of various health issues, make a detailed, population-based case-control study possible — one that controls for other variables like family income, parent educational level, maternal and paternal age and even maternal region of birth (all factors the authors note have been previously associated with autism). This is the second study in two years to associate antidepressant use during pregnancy with an increased incidence of autism in exposed children. An earlier, smaller study in California also found a modest increase in risk. The Sweden-based study could not (and did not) exclude the possibility that it was the severe depression, rather than the use of antidepressants, that created the association, but the smaller California study (which considered only S.S.R.I.’s) found “no increase in risk” for mothers with a history of mental health treatment in the absence of prenatal exposure to S.S.R.I.’s. © 2013 The New York Times Company

Keyword: Autism; Aggression
Link ID: 18064 - Posted: 04.23.2013

By ABBY ELLIN Marvin Tolkin was 83 when he decided that the unexamined life wasn’t worth living. Until then, it had never occurred to him that there might be emotional “issues” he wanted to explore with a counselor. “I don’t think I ever needed therapy,” said Mr. Tolkin, a retired manufacturer of women’s undergarments who lives in Manhattan and Hewlett Harbor, N.Y. Though he wasn’t clinically depressed, Mr. Tolkin did suffer from migraines and “struggled through a lot of things in my life” — the demise of a long-term business partnership, the sudden death of his first wife 18 years ago. He worried about his children and grandchildren, and his relationship with his current wife, Carole. “When I hit my 80s I thought, ‘The hell with this.’ I don’t know how long I’m going to live, I want to make it easier,” said Mr. Tolkin, now 86. “Everybody needs help, and everybody makes mistakes. I needed to reach outside my own capabilities.” So Mr. Tolkin began seeing Dr. Robert C. Abrams, a professor of clinical psychiatry at Weill Cornell Medical College in Manhattan. They meet once a month for 45 minutes, exploring the problems that were weighing on Mr. Tolkin. “Dr. Abrams is giving me a perspective that I didn’t think about,” he said. “It’s been making the transition of living at this age in relation to my family very doable and very livable.” Mr. Tolkin is one of many seniors who are seeking psychological help late in life. Most never set foot near an analyst’s couch in their younger years. But now, as people are living longer, and the stigma of psychological counseling has diminished, they are recognizing that their golden years might be easier if they alleviate the problems they have been carrying around for decades. It also helps that Medicare pays for psychiatric assessments and therapy. Copyright 2013 The New York Times Company

Keyword: Development of the Brain; Aggression
Link ID: 18061 - Posted: 04.23.2013

By Shaunacy Ferro When David Nichols earned a Ph.D in medicinal chemistry from the University of Iowa in 1973 by studying psychedelics, he thought he would continue studying hallucinogens indefinitely. "I thought I would work on it for the rest of my life," he says. His timing was less than fortuitous. In 1970, the year after Nichols started grad school, Richard Nixon signed into law the Controlled Substances Act, designed to clamp down on the manufacture and distribution of drugs in the U.S. The act classified hallucinogenic substances like LSD, DMT, psilocybin (the psychedelic alkaloid in mushrooms) and mescaline as Schedule I substances--the most restrictive use category, reserved for drugs with high potential for abuse and no accepted medical use. Marijuana was also placed in this category, and 15 years later when ecstasy came onto the scene, MDMA was emergency-classified as a Schedule I substance as well. By contrast, cocaine, opium and morphine are Schedule II substances, meaning they can be prescribed by a doctor. Despite some promising results from trials of psychedelics in treating alcoholism, psychiatric conditions and modeling mental illness, by the early '70s, the government had tightened control of Schedule I substances, even for research. It's only now that we're starting to return to the notion that these drugs could be medicine. © 2012 Popular Science

Keyword: Depression; Aggression
Link ID: 18056 - Posted: 04.22.2013

By STEPHEN CASTLE LONDON — British antitrust authorities on Friday accused the pharmaceuticals giant GlaxoSmithKline of paying three rivals to delay the introduction of a generic version of an antidepressant drug. It is the latest so-called pay-for-delay case drawing scrutiny from regulators on both sides of the Atlantic. The Office of Fair Trading in Britain contended that Glaxo had abused its dominant position in the market, kept prices artificially high and denied “significant cost savings” to Britain’s state-run health provider, the National Health Service. The British case centers on efforts by three companies, Alpharma, Generics (U.K.) and Norton Healthcare, to market an alternative to Seroxat, GlaxoSmithKline’s brand of paroxetine. The company sells it in the United States under the brand name Paxil. In recent years, regulators in Europe and the United States have paid greater attention to pay-for-delay deals, suspecting that they may allow pharmaceutical companies to make big profits by exploiting a brief but lucrative period of monopoly over the supply of a product. “These are blockbuster drugs,” said Farasat Bokhari, a senior lecturer in economics at the University of East Anglia, “so if they are on the market without generics challenging them then companies can maintain high, monopoly profits. “As soon as generic entry takes place,” Mr. Bokhari added, “prices drop significantly, sometimes by up to 70 to 80 percent.” GlaxoSmithKline, according to British authorities, warned the three companies that their generic equivalents would infringe a patent. To resolve the dispute, each of the rivals concluded one or more agreements with GlaxoSmithKline, the Office of Fair Trading said. © 2013 The New York Times Company

Keyword: Depression
Link ID: 18050 - Posted: 04.20.2013

By CATHERINE SAINT LOUIS Laura Ward, 41, had always attributed her excess pounds to the drugs she takes for major depression. So Ms. Ward, who is 5-foot-6 and once weighed 220 pounds, didn’t try to slim down or avoid dietary pitfalls like fried chicken. But in a clinical trial, Ms. Ward managed to lose more than 30 pounds doing low-impact aerobics three times a week. During the 18-month experiment, she was introduced to cauliflower and post-workout soreness for the first time. She and the other participants attended counseling sessions where they practiced refusing junk food and choosing smaller portions. She drank two liters of Diet Dr Pepper daily instead of eight. Eventually, Ms. Ward, who lives in Baltimore, realized her waistline wasn’t simply a drug side effect. “If it was only the medications, I would have never lost all that weight,” she said. People with serious mental illnesses, like schizophrenia, bipolar disorder or major depression, are at least 50 percent more likely to be overweight or obese than the general population. They die earlier, too, with the primary cause heart disease. Yet diet and exercise usually take a back seat to the treatment of their illnesses. The drugs used, like antidepressants and antipsychotics, can increase appetite and weight. It has been a difficult issue for mental health experts. A 2012 review of health promotion programs for those with serious mental illness by Dartmouth researchers concluded that of 24 well-designed studies, most achieved statistically significant weight loss, but very few achieved “clinically significant weight loss.” Copyright 2013 The New York Times Company

Keyword: Obesity; Aggression
Link ID: 18042 - Posted: 04.16.2013

Kristoffer Famm, et al. Imagine a day when electrical impulses are a mainstay of medical treatment. Your clinician will administer 'electroceuticals' that target individual nerve fibres or specific brain circuits to treat an array of conditions. These treatments will modulate the neural impulses controlling the body, repair lost function and restore health. They could, for example, coax insulin from cells to treat diabetes, regulate food intake to treat obesity and correct balances in smooth-muscle tone to treat hypertension and pulmonary diseases. All this is within reach if researchers from disparate disciplines in academia and industry work together. Here, we outline what needs to be done to bring about electroceuticals and unveil a public–private research initiative and an award that we hope will catalyse the field. Electrical impulses — action potentials — are the language of the body's nervous system. Virtually all organs and functions are regulated through circuits of neurons communicating through such impulses1. Two features make these circuits excellent targets for therapeutic intervention. First, they comprise discrete components — interconnected cells, fibre tracts and nerve bundles — allowing for pinpoint intervention. Second, they are controlled by patterns of action potentials, which can be altered for treatment. Already, devices that harness electrical impulses are used to treat disease. Pacemakers and defibrillators save millions of lives each year; deep-brain stimulation dramatically improves the quality of life for people with Parkinson's disease and depression; sacral-nerve stimulation restores some bladder control in people with paraplegia, and vagus-nerve stimulation shows clinical benefits in diseases ranging from epilepsy to rheumatoid arthritis2. But these devices do not target specific cells within circuits. © 2013 Nature Publishing Group

Keyword: Depression; Aggression
Link ID: 18032 - Posted: 04.13.2013

By Steven E. Hyman During the past three years the global pharmaceutical industry has significantly decreased its investment in new treatments for depression, bipolar disorder, schizophrenia, and other psychiatric disorders.1 Some large companies, such as GlaxoSmithKline, have closed their psychiatric laboratories entirely. Others, such as Pfizer, have markedly decreased the size of their research programs. Yet others, such as AstraZeneca, have brought their internal research to a close and are experimenting with external collaborations on a smaller scale. This retreat has occurred despite the fact that mental disorders are not only common worldwide, but also increasingly recognized by healthcare systems. There is, moreover, vast unmet medical need, meaning that many individuals with mental disorders remain symptomatic and often disabled despite existing treatments. For example, people suffering with the depressed phase of bipolar disorder often continue to experience severe symptoms even when they take multiple medications with serious side effects. For some significantly disabling conditions, such as the core social deficits of autism and the cognitive impairments of schizophrenia, there simply are no effective treatments. Because mental disorders are highly prevalent and our ability to treat them remains limited, these illnesses cause enormous societal burden. In aggregate, they are the world’s leading cause of disability.2 In addition, this retreat has happened despite the fact that different classes of psychiatric drugs have been among the industry’s most profitable products during the last several decades—and despite the fact that, according to Medco Health Solutions, one in five American adults now takes at least one psychiatric drug. Among the earliest commercial successes were the Valium-like benzodiazepines, used both as tranquilizers and as sleeping pills. These were followed by the Prozac-like selective serotonin reuptake inhibitor (SSRI) antidepressants. Most recently, “second-generation” antipsychotic drugs have been among the global revenue leaders for the pharmaceutical industry, serious side effects notwithstanding. That’s why it’s surprising that almost all industry research dollars are invested in cancer, metabolism, autoimmunity, and other disease areas. Copyright 2013 The Dana Foundation

Keyword: Depression; Aggression
Link ID: 18031 - Posted: 04.13.2013

By Daisy Yuhas Less than two hundred years ago, schizophrenia emerged from a tangle of mental disorders known simply as madness. Yet its diagnosis remains shrouded in ambiguity. Only now is the Diagnostics and Statistical Manual of Mental Disorders, psychiatrists’ primary guidebook, shedding the outdated, nineteenth-century descriptions that have characterized schizophrenia to this day. "There is substantial dissatisfaction with schizophrenia treated as a disease entity, it's symptoms are like a fever—something is wrong but we don't know what," says William Carpenter, a psychiatrist at the University of Maryland and chair of the manual’s Psychotic Disorder Workgroup. Psychiatrists may discover that this disorder is not a single syndrome after all but a bundle of overlapping conditions. © 2013 Scientific American,

Keyword: Schizophrenia
Link ID: 18022 - Posted: 04.11.2013

by Ed Yong The brain has hit the big time. Barack Obama has just announced $100 million of funding for the BRAIN Intitiative—an ambitious attempt to apparently map the activity of every neuron in the brain. On the other side of the Atlantic, the Human Brain Project will try to simulate those neurons with a billion euros of funding from the European Commission. And news about neuroscience, from dream-decoding to mind-melding to memory-building, regularly dominates the headlines. But while the field’s star seems to be rising, a new study casts a disquieting shadow upon the reliability of its results. A team of scientists led by Marcus Munafo from the University of Bristol analysed a broad range of neuroscience studies and found them plagued by low statistical power. Statistical power refers to the odds that a study will find an effect—say, whether antipsychotic drugs affect schizophrenia symptoms, or whether impulsivity is linked to addiction—assuming those effects exist. Most scientists regard a power of 80 percent as adequate—that gives you a 4 in 5 chance of finding an effect if there’s one to be found. But the studies that Munafo’s team examined tended to be so small that they had an average (median) power of just 21 percent. At that level, if you ran the same experiment five times, you’d only find an effect on one of those. The other four tries would be wasted. But if studies are generally underpowered, there are more worrying connotations beyond missed opportunities. It means that when scientists do claim to have found effects—that is, if experiments seem to “work”—the results are less likely to be real. And it means that if the results are actually real, they’re probably bigger than they should be. As the team writes, this so-called “winner’s curse” means that “a ‘lucky’ scientist who makes the discovery in a small study is cursed by finding an inflated effect.”

Keyword: Brain imaging; Aggression
Link ID: 18020 - Posted: 04.11.2013

By Kathryn Doyle Despite concerns that antidepressant use during pregnancy might affect infants’ growth and development, a small new study finds no size differences in the first year of life between babies exposed and not exposed to the drugs. The medications — known as selective serotonin reuptake inhibitors, or SSRIs, which include fluoxetine (marketed as Prozac) and citalopram (Celexa) — have been tied to premature births and lower birth weight. But their effect on growth during infancy had not been studied. The agency will lift a requirement that the products carry a strict limit on how long they can be used. “It’s a reassuring finding in that when you have an illness during pregnancy, you want to know what is the impact of the illness and what is the impact of the medication,” Katherine Wisner, the study’s lead author, said. Untreated depression also didn’t seem to influence infant growth, according to Wisner, the director of Northwestern University’s Asher Center for the Study and Treatment of Depressive Disorders. That’s important because a baby’s most rapid growth happens in the first year, which sets the stage for growth patterns for the whole life span, she added. Wisner and her colleagues tracked 97 pregnant women without depression, 46 on antidepressants and 31 with depression that was not treated with medication. Their babies were measured and weighed four times over the first year of life. © 1996-2013 The Washington Post

Keyword: Depression; Aggression
Link ID: 17981 - Posted: 04.02.2013

by Niall Firth Automatic systems that analyse gestures and facial expressions may soon be helping psychologists pick up the easily missed symptoms of depression The interviewee shifts uncomfortably in his seat before stumbling over his answer. The movement, hesitation and telltale gaze aversion are noted: this person may be depressed. The probing questioner is SimSensei, a digital avatar that interviews humans to judge their state of mind. SimSensei is one of several new initiatives designed to partially automate one of the medical profession's trickiest tasks: diagnosing depression. SimSensei is more than an astute questioner. Behind the scenes, it uses face recognition technology and depth-sensing cameras built into Microsoft's Kinect to record and interpret the interviewee's body language. The animated psychologist can then respond appropriately. In work to be presented at the Automatic Face and Gesture Recognition conference in Shanghai, China, next month, Stefan Scherer of the University of Southern California and colleagues used the system to identify characteristic movements that indicate someone may be depressed. To extract the right features, his team interviewed a mixture of healthy volunteers and those who had previously been diagnosed with depression or post-traumatic stress disorder. © Copyright Reed Business Information Ltd

Keyword: Depression
Link ID: 17957 - Posted: 03.28.2013

By HARRIET BROWN Mental-health care has come a long way since the remedy of choice was trepanation — drilling holes into the skull to release “evil spirits.” Over the last 30 years, treatments like cognitive-behavioral therapy, dialectical behavior therapy and family-based treatment have been shown effective for ailments ranging from anxiety and depression to post-traumatic stress disorder and eating disorders. The trouble is, surprisingly few patients actually get these kinds of evidence-based treatments once they land on the couch — especially not cognitive behavioral therapy. In 2009, a meta-analysis conducted by leading mental-health researchers found that psychiatric patients in the United States and Britain rarely receive C.B.T., despite numerous trials demonstrating its effectiveness in treating common disorders. One survey of nearly 2,300 psychologists in the United States found that 69 percent used C.B.T. only part time or in combination with other therapies to treat depression and anxiety. C.B.T. refers to a number of structured, directive types of psychotherapy that focus on the thoughts behind a patient’s feelings and that often include exposure therapy and other activities. Instead, many patients are subjected to a kind of dim-sum approach — a little of this, a little of that, much of it derived more from the therapist’s biases and training than from the latest research findings. And even professionals who claim to use evidence-based treatments rarely do. The problem is called “therapist drift.” “A large number of people with mental health problems that could be straightforwardly addressed are getting therapies that have very little chance of being effective,” said Glenn Waller, chairman of the psychology department at the University of Sheffield and one of the authors of the meta-analysis. Copyright 2013 The New York Times Company

Keyword: Depression
Link ID: 17952 - Posted: 03.26.2013

Arran Frood Two studies have decoded the structure of two of the brain's serotonin receptors. Here shown is a receptor known as 1B with the migraine drug ergotamine (pink) locked into one of its binding pockets. Researchers have deciphered the molecular structures of two of the brain's crucial lock-and-key mechanisms. The two molecules are receptors for the natural neurotransmitter serotonin — which regulates activities such as sleep, appetite and mood — and could provide targets for future drugs to combat depression, migraines or obesity. “This is huge,” says Bryan Roth, a neuropharmacologist at the University of North Carolina Chapel Hill Medical School, and a co-author of the two studies published in Science today1, 2. “Before this there was no crystal structure for any serotonin receptor. A lot of what was theoretical is now known with a great degree of certainty,” he says. Scientists have been trying to decipher serotonin receptors for years. Armed with information on the atomic level, they might now be able to make breakthroughs in drug discovery and in understanding how the physical structures of the brain produce consciousness, says Roth. Christoph Anacker, a neuropharmacologist at King's College London, agrees that the findings are important for drug discovery. “These receptors are involved in so many conditions, especially depression, and knowing the molecular structures will help to develop more specific drugs and avoid the expression of undesired side effects.” © 2013 Nature Publishing Group,

Keyword: Depression
Link ID: 17937 - Posted: 03.23.2013

Joshua P. Johansen Anxiety does not arise from a single neural circuit. An interplay between neighbouring, yet opposing, circuits produces anxiety, and outputs from these circuits regulate specific anxiety responses. We all know anxiety. We might have experienced it while waiting to hear about a promotion at work, or on our way to see the doctor because she wants to talk about test results in person. A diffuse uneasiness, sometimes accompanied by perspiration and subtle changes in breathing, anxiety ebbs and flows depending on life's circumstances, and can even occur for no apparent reason. The condition can be healthy and adaptive, but research in the United States1 shows that, for roughly one-third of people, anxiety is a debilitating disorder at some point in their lives. Nevertheless, answers to important questions — such as how different neuronal populations represent anxiety, and how the various components of the anxious state are constructed and represented in neural circuits — remain elusive. In two papers published on Nature's website today, Jennings et al.2 and Kim et al.3 address these questions using optogenetics to manipulate distinct neuronal subpopulations in mice and so dissect out the contribution of intermixed but functionally distinct cell groups. Both teams analysed a large, diffuse brain region called the bed nucleus of the stria terminalis (BNST). Previous studies4, 5, 6, 7 have found that lesions of the BNST reduce anxiety and fear of specific environments. Other work has discovered8, 9 distinct subregions and subpopulations of BNST neurons, and has found that the region has connections with several other brain areas that are involved in motivated behaviour and stress responses. However, the functions of the various BNST subpopulations and subregions, as well as the significance of these connections, have remained unclear. © 2013 Nature Publishing Group,

Keyword: Emotions; Aggression
Link ID: 17936 - Posted: 03.23.2013

by Emily Underwood Hallucinations and paranoia aren't the only symptoms that make life difficult for people with schizophrenia. Problems with memory and other cognitive functions also interfere with daily tasks, such as remembering the way to the office or balancing a checkbook. Now, by dampening the activity of a small group of neurons deep within the mouse brain, researchers have produced cognitive deficits similar to those found in those with schizophrenia, a discovery that they say could potentially lead to new treatments for the disorder, which affects roughly 24 million people worldwide. There's an ongoing debate over how much mice can mirror human psychiatric diseases, ranging from autism to depression. Still, neuroscientists often turn to rodents to study specific features of these human conditions. One abnormality that researchers have observed in functional magnetic resonance imaging scans of the brains of people with schizophrenia is an unusually low level of activity from a specific group of neurons near the brain stem. Called the mediodorsal thalamus (MD), the region appears to work with the prefrontal cortex—an area associated with planning and decision-making—to carry out tasks that require us to remember and process multiple pieces of information at once. (Going to the kitchen to fetch something, while remembering what it was you needed, for example.) In the past, scientists have studied the effects of low brain activity in the MD by cutting it out in mice—an extreme measure that didn't accurately mimic the "mild" reduction in activity seen in schizophrenia, says Columbia University psychiatrist Joshua Gordon. To create a more realistic mouse model of low MD activity, the team devised a new method that uses a virus to embed into the surface of MD neurons receptors that block cellular activity in the presence of a compound called clozapine-N-oxide. The beauty of this approach is its "exquisite specificity," Gordon says—it targets only neurons in the MD, and you can control how many neurons get shut down. © 2010 American Association for the Advancement of Science

Keyword: Schizophrenia
Link ID: 17935 - Posted: 03.23.2013

By Meghan Rosen Shushing neural chitchat in mouse brains can spark schizophrenia-like symptoms, a new study suggests. The findings are the first to demonstrate — at least in mice — that curbing communication among neurons in certain parts of the brain can cause some of the cognitive problems associated with schizophrenia. By muzzling neurons in the mediodorsal thalamus, or MD — a cell cluster that sends signals to the brain’s outer layer — researchers hindered mouse memory and learning in much the same way that schizophrenia seems to do in humans, scientists report March 20 in Neuron. Cognitive problems in schizophrenia have long been a mystery to scientists and a troubling symptom for people with the condition. The findings suggest that the problems stem from the thalamus, says neuropsychologist Neil Woodward of Vanderbilt University in Nashville, who was not involved with the new work. People with schizophrenia suffer from a range of debilitating symptoms: hallucinations, delusions and social disorders, says study coauthor Christoph Kellendonk of Columbia University. Patients also have problems with short-term memory and learning. Unlike other symptoms, these cognitive problems have been nearly impossible to treat. Brain imaging of people with schizophrenia had previously linked cognitive defects to changes in the MD — part of a walnut-sized chunk of gray matter snuggled above the brain stem. Normally, the MD relays information to and from the prefrontal cortex, the brain region behind the forehead that controls complex thought. In people with schizophrenia, the imaging showed, the MD is unusually quiet. © Society for Science & the Public 2000 - 2013

Keyword: Schizophrenia; Aggression
Link ID: 17929 - Posted: 03.23.2013

By Neuroskeptic When does sadness cease to be a normal emotional response, and become a mental disorder? Can psychiatrists ‘draw the line’ between healthy and sick moods, and if so, where? An important new study offers an answer: When does depression become a disorder? Using recurrence rates to evaluate the validity of proposed changes in major depression diagnostic thresholds (free pdf). The authors, Jerome Wakefield and Mark Schmitz of New York, made use of the ECA survey, a 1980s study of almost 20,000 American adults. Participants were surveyed twice each, approximately one year apart. On each occasion, they were asked questions about their mood, emotions, and mental health symptoms. Some people reported a history of depression at the first visit. Wakefield & Schmitz wanted to find a way of predicting which of those people were most likely to end up depressed at the time of the second interview, a year later – the recurrence rate. To do this, they examined the particular patterns of symptoms reported at the first visit. It turned out that there was a strong predictor of recurrence, which the authors call “complicated” depression. People with a history of complicated depression had a 15% chance of being depressed at follow up. Only 3.4% of those who’d had “uncomplicated” symptoms, however, were depressed a year later. Given that 1.7% of people with no depression history had become unwell by Time 2, this means that “uncomplicated” depression was almost never recurrent.

Keyword: Depression
Link ID: 17911 - Posted: 03.18.2013

By NICHOLAS BAKALAR Compared with the rest of the population, people with mental illness may be at sharply increased risk of dying by homicide, a new study has found. Researchers used Swedish government registries to determine psychiatric diagnoses and causes of death among the entire adult population of 7.2 million from 2001 to 2008. There were 615 murders in the period, 141 of them of people with mental disorders. (The homicide rate in Sweden is about one-fifth that of the United States.) After controlling for age, education level, income and other factors, they found that people with mental illness were almost five times as likely to be a victim of murder as a person without a psychiatric diagnosis. The study appeared online last week in the journal BMJ. The risk was highest among those with substance use disorders — nine times that of the general population. Those with personality disorders had three times the risk, people with depression two and a half times, and those with anxiety or schizophrenia about twice the risk of being murdered, compared with people without mental illness. The lead author, Dr. Casey Crump, a clinical assistant professor of medicine at Stanford, said the findings were consistent with those from smaller studies done in the United States. Interestingly, he said, “these results extended to all the most common mental disorders.” Copyright 2013 The New York Times Company

Keyword: Schizophrenia
Link ID: 17902 - Posted: 03.15.2013