Links for Keyword: Schizophrenia

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By Hristio Boytchev, Believing that brains can be trained through the use of specialized computer programs, researchers are focusing on helping people with schizophrenia, which can cause them to hear imagined voices or believe that others are controlling or plotting against them. There are medications for the often-disabling disorder, but they have severe side effects and don’t get rid of all symptoms; many people will not stick with the drugs. A California company, Posit Science, is developing a computer game that it hopes will become the first to earn approval from the Food and Drug Administration for treating schizophrenia. The idea comes from Michael Merzenich, an emeritus professor of neuroscience at the University of California at San Francisco and a co-founder of Posit Science. Merzenich is something of a living legend in neuroscience, a co-inventor of cochlear implants and one of the pioneers of the theory of neuroplasticity, which asserts that the brain continues to develop throughout a lifetime. Treating schizophrenia with brain training is based on the theo­ry that the confusion and fear the disease creates may occur because the brain’s expectations about what will happen do not match up with what actually happens. That disconnect might be traced to a problem with verbal and auditory processing of information, something that brain training targets. © 1996-2013 The Washington Post

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 17826 - Posted: 02.19.2013

By Laura Sanders Psychiatry seemed poised on the edge of a breakthrough. In early 2011, after decades of no radically new drugs, a fundamentally different schizophrenia treatment promised relief from the psychotic hallucinations and delusions plaguing people with the disease. The new compound, devised by chemists at Eli Lilly and Co., hit a target in the brain that older medicines had ignored. All signs pointed to success. In mice, a similar molecule could block the schizophrenia-like effects of PCP. In people the new drug, LY2140023, appeared to curb psychotic behavior with few side effects, small pilot studies showed. In March 2011, Lilly began enrolling 1,100 people in a definitive Phase III clinical trial, the final test designed to show conclusively that the new compound worked. A year and a half later, the drug was dead. After years of work and millions of dollars of investment, the failure was crushing. People with schizophrenia were no better on the new drug than similar people taking a placebo, early results indicated. “I’m disappointed in what these results mean for patients with schizophrenia who still are searching for options to treat this terrible illness,” Jan Lundberg, president of Lilly Research Laboratories, said in a press release. Although the results were devastating, many in the field weren’t surprised. For new drugs designed to treat complex brain disorders such as schizophrenia, depression and anxiety, the odds of success are exceedingly slim. Given the current state of affairs in the drug discovery world, some would argue those odds are close to zero. Not a single drug designed to treat a psychiatric illness in a novel way has reached patients in more than 30 years, argues psychiatrist Christian Fibiger of the University of British Columbia in Kelowna, who described the problem in a 2012 Schizophrenia Bulletin editorial. “For me, the data are in,” says Fibiger, who has developed drugs at several major pharmaceutical companies. “We’ve got to change. This isn’t working.” © Society for Science & the Public 2000 - 2013

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: 17782 - Posted: 02.11.2013

By PAM BELLUCK People with mental illness are 70 percent more likely to smoke cigarettes than people without mental illness, two federal health agencies reported Tuesday. New data from the Centers for Disease Control and Prevention and the Substance Abuse and Mental Health Services Administration show that one of every three adults with mental illness smokes, compared with one in five adults without mental illness. Adults with mental illness smoke about a third of all the cigarettes in the United States, and they smoke more cigarettes per month and are significantly less likely to quit than people without mental illness, the report said. There are nearly 46 million adults with mental illness in the United States, about a fifth of the population. “Many people with mental illness are at greater risk of dying early from smoking than of dying from their mental health conditions,” said Dr. Thomas R. Frieden, director of the Centers for Disease Control, during a press briefing. The report is based on information from the National Survey on Drug Use and Health, which interviewed 138,000 adults in their homes from 2009 to 2011. People were asked 14 questions to assess psychological distress and disability, and were deemed to have mental illness if their responses indicated they had a mental, behavior or emotional disorder in the past 12 months. Those with substance abuse or developmental disorders were not considered people with mental illness. The report did not include patients in psychiatric hospitals or individuals serving in the military. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17769 - Posted: 02.06.2013

By Judy Stone We’ve touched on some of the many disturbing things that happened during the clinical trial on which Dan Markingson committed suicide. In my first post, I asked how a psychotic, homicidal patient who was involuntarily hospitalized in a psychiatric hospital could give an informed consent for participation in a clinical trial. There appeared to have been abuse of a vulnerable patient and extraordinary coercion—participate in this trial or be committed to a psych hospital seems to have been the bottom line. In my second post, we looked at investigator responsibilities, delegation of authority, and Good Clinical Practice tenets, all of which were violated with no consequences. Now we turn to the need to disclose conflicts of interest (COI), again a basic clinical research ethics principle that was violated. There are so many obvious conflicts of interest that it is hard to know quite where to start. The most obvious and egregious COI was that shown by Dr. Stephen Olson, who acted as both Dan Markingson’s treating physician and as Principle Investigator on the CAFÉ study. As Dr. Harrison Pope, a Harvard expert, concluded in his testimony, Olson “failed to meet the standards for good clinical practice both as a principal investigator and as the study physician for Mr. Markingson.” He failed his ethical responsibilities to Dan. © 2012 Scientific American

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: 17619 - Posted: 12.19.2012

by Peter Aldhous IT HAS been more than a decade in the works, but finally we know the main changes that will be introduced next May, when the American Psychiatric Association publishes the next edition of its Diagnostic and Statistical Manual of Mental Disorders, known as DSM-5. Those changes, which could influence the way millions are treated, include new definitions of autism and related conditions, and a shift in the criteria for depression to include some people grieving after bereavement. Debate over DSM-5 seems likely to rumble on. But now there is a deeper problem to ponder: while discoveries about the genes and brain circuits that underlie human behaviour are accumulating rapidly, they haven't led to major clinical advances. That's largely because these findings don't map well on to the constellation of conditions described in the DSM. When the last major revision was completed in 1994, its authors hoped that neurobiologists would soon home in on specific disruptions to brain circuitry involved in the main psychiatric disorders. "I was naive enough to think that it was just a matter of time," says Michael First of Columbia University in New York City. It hasn't worked out that way. Take schizophrenia: what was once considered to be a distinct psychotic disorder actually seems to cover a variety of disruptions to normal brain functioning. This suggests that many of psychiatry's diagnostic labels do not describe coherent conditions with common underlying causes. No wonder, then, that many conditions are so hard to treat. © 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: 17602 - Posted: 12.13.2012

In 2009, Susannah Cahalan was a healthy 24-year-old reporter for the New York Post, when she began to experience numbness, paranoia, sensitivity to light and erratic behavior. Grasping for an answer, Cahalan asked herself as it was happening, "Am I just bad at my job — is that why? Is the pressure of it getting to me? Is it a new relationship?" But Cahalan only got worse — she began to experience seizures, hallucinations, increasingly psychotic behavior and even catatonia. Her symptoms frightened family members and baffled a series of doctors. After a monthlong hospital stay and $1 million worth of blood tests and brain scans that proved inconclusive, Cahalan was seen by Dr. Souhel Najjar, who asked her to draw a clock on a piece of paper. "I drew a circle, and I drew the numbers 1 to 12 all on the right-hand side of the clock, so the left-hand side was blank, completely blank," she tells Fresh Air's Dave Davies, "which showed him that I was experiencing left-side spatial neglect and, likely, the right side of my brain responsible for the left field of vision was inflamed." As Najjar put it to her parents, "her brain was on fire." This discovery led to her eventual diagnosis and treatment for anti-NMDA receptor encephalitis, a rare autoimmune disease that can attack the brain. Cahalan says that doctors think the illness may account for cases of "demonic possession" throughout history. Cahalan's new memoir is called Brain on Fire: My Month of Madness. ©2012 NPR

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: 17494 - Posted: 11.17.2012

By Charles Q. Choi People with schizophrenia often experience the unnerving feeling that outside forces are controlling them. Other times they feel an illusory sense of power over uncontrollable events. Now scientists find these symptoms may arise from disabilities in predicting or recognizing their own actions. The findings suggest new therapies for treating schizophrenia, which afflicts an estimated 1 percent of the world population. To see where this confusion might stem from, researchers tested two ways people are known to link actions and their outcomes. We either predict the effects of our movements or retrospectively deduce a causal connection. Healthy participants and schizophrenic patients were asked to look at a clock and occasionally push a button. Most of the time the button push was followed by a tone. The participants then told researchers what time they had pushed the button and when the tone had occurred. Healthy volunteers reported later times for each button push if it was followed by a tone. This result suggests that awareness of a link between the two events causes people to perceive less time between them. Participants also tended to estimate later button pushes even in the few cases when no tone was emitted, revealing that the subjects were predicting they would hear the sound, says psychiatrist and cognitive neuroscientist Martin Voss of Charité University Hospital and St. Hedwig Hospital in Berlin. © 2012 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 14: Attention and Consciousness
Link ID: 17481 - Posted: 11.13.2012

Alison Abbott In 1965, health authorities in Camberwell, a bustling quarter of London's southward sprawl, began an unusual tally. They started to keep case records for every person in the area who was diagnosed with schizophrenia, depression, bipolar disorder or any other psychiatric condition. Decades later, when psychiatrists looked back across the data, they saw a surprising trend: the incidence of schizophrenia had more or less doubled, from around 11 per 100,000 inhabitants per year in 1965 to 23 per 100,000 in 1997 — a period when there was no such rise in the general population (J. Boydell et al. Br. J. Psychiatry 182, 45–49; 2003). The result raised a question in many researchers' minds: could the stress of city life be increasing the risk of schizophrenia and other mental-health disorders? The question is an urgent one. Back in 1950, less than one-third of the world's population lived in cities. Now, lured by the prospect of work and opportunity, more than half do. Mental illnesses already comprise the world's biggest disease burden after infectious diseases and, although global statistics do not yet show any major increase in incidence, the cost is rising. In Germany, the number of sick days taken for psychiatric ailments doubled between 2000 and 2010; in North America, up to 40% of disability claims for work absence are related to depression, according to some estimates. “It seems that cities may be making us sick,” says Jane Boydell at the Institute of Psychiatry in London, who led the Camberwell study. Anecdotally, the link between cities, stress and mental health makes sense. Psychiatrists know that stress can trigger mental disorders — and modern city life is widely perceived as stressful. City dwellers typically face more noise, more crime, more slums and more people jostling on the streets than do those outside urban areas. Those who have jobs complain of growing demands on them in the workplace, where they are expected to do much more in less time. © 2012 Nature Publishing Group

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: 17359 - Posted: 10.11.2012

By RICHARD A. FRIEDMAN, M.D. You will never guess what the fifth and sixth best-selling prescription drugs are in the United States, so I’ll just tell you: Abilify and Seroquel, two powerful antipsychotics. In 2011 alone, they and other antipsychotic drugs were prescribed to 3.1 million Americans at a cost of $18.2 billion, a 13 percent increase over the previous year, according to the market research firm IMS Health. Those drugs are used to treat such serious psychiatric disorders as schizophrenia, bipolar disorder and severe major depression. But the rates of these disorders have been stable in the adult population for years. So how did these and other antipsychotics get to be so popular? Antipsychotic drugs have been around for a long time, but until recently they were not widely used. Thorazine, the first real antipsychotic, was synthesized in the 1950s; not just sedating, it also targeted the core symptoms of schizophrenia, like hallucinations and delusions. Later, it was discovered that antipsychotic drugs also had powerful mood-stabilizing effects, so they were used to treat bipolar disorder, too. Then, starting in 1993, came the so-called atypical antipsychotic drugs like Risperdal, Zyprexa, Seroquel, Geodon and Abilify. Today there are 10 of these drugs on the market, and they have generally fewer neurological side effects than the first-generation drugs. Originally experts believed the new drugs were more effective than the older antipsychotics against such symptoms of schizophrenia as apathy, social withdrawal and cognitive deficits. But several recent large randomized studies, like the landmark Catie trial, failed to show that the new antipsychotics were any more effective or better tolerated than the older drugs. © 2012 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: 17297 - Posted: 09.25.2012

By Gary Stix Neuroscientists have devoted inordinate energy in recent years to publicize the need for, not only gene maps, but for a full wiring diagram of all brain circuits. The benefits of a connectome as it is known might yield new understanding that could eventually result in pharmaceuticals for intractable psychiatric disorders. This ultimate neural network might even divvy up intimations of the workings of consciousness. The futurist contingent, many of whom began careers hacking computers not neural circuity, has speculated that a whole brain blueprint of you or me might be copied to a hard drive so that we can live for a digital eternity like Max Headroom. Christof Koch, the chief scientist at the Allen Institute for Brain Science, the organization that produced the gene map, dismissed facile optimism about the prospects for these scenarios with a commentary in Science last month. In it, he calculated that it could take 2000 years to analyze all of the possible interactions among the 1,000 different proteins that populate a single synapse. Koch then went on to speculate about a way of reducing the complexity of such calculations. The question still remains of how we will know when we have actually started to make sense of the tangle of wiring that populates the deepest recesses inside our skulls. One plausible answer: when the FDA approves a new drug that fundamentally advances treatment of schizophrenia, the psychiatric illness that has aberrant effects on a multitude of neural pathways—an iconic example of the brain’s underlying complexity. © 2012 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: 17289 - Posted: 09.22.2012

By Karen Weintraub Dr. Steven E. Hyman, a neuroscientist and former Harvard provost, now directs the Stanley Center for Psychiatric Research at the Broad Institute, which is trying to better understand and develop treatments for conditions like depression, anxiety, schizophrenia, bipolar disorder, ADHD, obsessive-compulsive disorder, and autism. Q. There haven’t been a lot of drugs developed recently to treat these conditions. A. The modern era of neuropsychopharmacology began brilliantly in the early 1950s. There has been enormous progress in making drugs safer and more tolerable. [But effectiveness has not improved substantially.] We’ve reached a fairly unsatisfactory place in the treatment of these devastating illnesses. Q. Big drug companies are now getting out of the business of developing new medications for these conditions. A. The pharmaceutical industry is basically giving up and throwing in the towel. Their exit is both a symptom of the difficulty and a problem. Q. What does this mean for someone with one of these conditions? A. I don’t want to be inappropriately negative. If somebody has OCD or panic disorder or depression, the combination of cognitive behavioral therapy and a well chosen SSRI-like drug [like Prozac] will, for a reasonable fraction of those patients, markedly improve their lives, although there will be side effects and residual symptoms. © 2012 NY Times Co.

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: 17154 - Posted: 08.13.2012

By Scott O. Lilienfeld and Hal Arkowitz Imagine an eight-year-old boy whom we will call Eric. He is irritable and talks incessantly. Unable to sit still and concentrate, he does poorly at school. Nevertheless, he claims to be one of the smartest kids in the world and blames his poor academic performance on his “horrible” teachers. There are periods when his mood changes abruptly from euphoria to depression and then swings back again. Eric's symptoms qualify him for a diagnosis of bipolar disorder, which is characterized by episodes of full-blown mania or a less severe form called hypomania. These moods usually alternate with periods of depression [see box on opposite page]. Until about 1980 most mental health professionals believed that bipolar disorder did not occur in children. Although a few still hold this view, the general opinion of the psychiatric community has drastically shifted over the past 30 years, a period in which diagnoses of the disorder in kids have skyrocketed. In a study published in 2007 psychiatrist Carmen Moreno, then at Gregorio Marañón University General Hospital in Madrid, and her colleagues found a 40-fold increase between 1994 and 2003 in the number of visits to a psychiatrist in which a patient younger than 19 was given this diagnosis. By 2003, the researchers reported, the number of office visits resulting in a bipolar diagnosis in these youths had risen from 25 per 100,000 people to 1,003 per 100,000 people, a rate almost as high as that for adults. Such data have sparked widespread concern that the condition is egregiously overdiagnosed, perhaps contributing to the use of ineffective and even harmful medical treatments. In this column, we discuss controversies regarding the overdiagnosis of bipolar disorder in children and recent attempts to remedy this situation. © 2012 Scientific American

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: 17001 - Posted: 07.05.2012

By Laura Sanders New details about how some drugs for schizophrenia accumulate in the brain may help explain why patients often must wait for weeks for the medications to work. Because many commonly used antipsychotics such as haloperidol and clozapine quickly latch onto their targets, it would seem that the drugs should bring fast relief. “But there’s always a side story,” says neuroscientist Michael Cousin of the University of Edinburgh in Scotland. “There’s another layer of complexity.” Researchers led by Teja Groemer of Friedrich-Alexander University of Erlangen-Nürnberg in Germany illuminate this process in the June 7 Neuron by describing how the buildup of certain drugs in the brain may have underappreciated consequences for their effectiveness. The idea that drugs accumulate in the brain isn’t totally new; other scientists have suggested that antipsychotic drugs can pile up in certain places, Groemer says. But most people have assumed such accumulation is inconsequential. Not so, Groemer and his team found. Stockpiled drugs may actually squelch nerve cells’ behavior in a highly selective way by being released only when needed most. Using a proxy compound that could be seen with a microscope (because making the drugs themselves visible would have changed their behavior), the researchers watched the chemical build up in small pockets, called synaptic vesicles, inside nerve cells that were growing in a dish. © Society for Science & the Public 2000 - 2012

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: 16884 - Posted: 06.07.2012

By Kay Lazar, Globe Staff Federal regulators announced a multi-year initiative Wednesday to slash the inappropriate use of antipsychotic drugs in nursing home residents, saying that nearly 40 percent of residents with dementia were receiving the powerful sedatives though they didn’t have a condition that would warrant it. The US Centers for Medicare & Medicaid Services said it was aiming to reduce the use of antipsychotic drugs in nursing home residents by 15 percent by the end of this year, through training of nursing home staff and state inspectors to use alternative methods instead of relying on antipsychotics to quell agressive and agitated behavior among people with dementia. Alice Bonner, director of the agency’s nursing home division, said in an interview that the 15 percent reduction is just the first step. “In 2013 we will set another goal,” Bonner said. “At that point, we will be looking at even more significant reductions.” Another agency official said during a conference call with reporters that between July and September of 2010, almost 40 percent of nursing home residents with signs of dementia were receiving antipsychotic drugs even though they had not been diagnosed with a psychosis. The drugs have sometimes-lethal side effects, prompting the US Food and Drug Administration to issue two warnings since 2005 against using them in elderly patients with dementia. © 2012 NY Times Co

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: 16855 - Posted: 05.31.2012

By Laura Sanders Schizophrenia’s elusive genetic roots may finally be within grasp. A new, wide-ranging effort has uncovered a set of DNA signatures that are shared by people with the disease consistently enough that the set can be used to reliably predict whether someone has the disease. If replicated, the results may point out ways to diagnose schizophrenia and suggest new targets for treatment. By analyzing a battery of 542 genetic variants, researchers could predict who had schizophrenia in a group of European Americans and African Americans. The confirmation of the result in people of varying ancestry suggests that the set of genes truly does detect the core features of the disorder, scientists report online May 15 in Molecular Psychiatry. “Genetic studies in psychiatry tend to produce initial excitement but are then not reproduced in independent populations, which is the most important proof that a finding is solid and real,” says study coauthor Alexander Niculescu of the Indiana University School of Medicine in Indianapolis. Niculescu and his colleagues created their gene panel by assessing a slew of earlier studies on schizophrenia: Data from humans and animals on gene variation and gene behavior all fed into the team’s analysis. If a gene popped out of several different datasets, the reasoning went, it is probably important to schizophrenia. Niculescu compares this method — called convergent functional genomics — to an Internet search: “The more links to a web page, the higher it comes up on your search list.” © Society for Science & the Public 2000 - 2012

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: 16803 - Posted: 05.16.2012

By John Horgan When I teach history of science at Stevens Institute of Technology, I devote plenty of time to science’s glories, the kinds of achievements that my buddy George Johnson wrote about in The Ten Most Beautiful Experiments (Alfred A. Knopf, 2008). George helps us appreciate what Galileo did with inclined planes, Newton with prisms, Pavlov with dogs, Galvani with frogs, Millikan with oil drops, Faraday with a magnet and coil of wire. (When George demonstrated Faraday’s experiment on Comedy Central’s The Colbert Report, Stephen Colbert found the experiment so shocking that he blurted out, “Mother——!”) But I tell my students about science’s missteps, too, to remind them that scientists can be as flawed as the rest of us mortals. In that negative spirit, here are five experiments that I consider to be especially hideous, horrible, immoral—in short, ugly. Walter Freeman and Transorbital Lobotomies In 1949, the Portuguese neurologist Egas Moniz won a Nobel Prize for inventing the lobotomy, a treatment for mental illness that called for inserting a sharp instrument into holes drilled through the skull and destroying tissue in the frontal lobes. By then, physician Walter Freeman Jr., (father of neuroscientist Walter Freeman III, a leading consciousness researcher) had already begun carrying out lobotomies in the United States. In 1941 Freeman lobotomized the unruly, 23-year-old sister of John F. Kennedy; Rosemary Kennedy was so severely disabled after her lobotomy that she required care for the rest of her life. Freeman later invented the transorbital lobotomy, which involved slipping an ice pick past the eyeball, thrusting it through the rear of the eye socket and swishing it back and forth in the brain. © 2012 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 16795 - Posted: 05.15.2012

By Ferris Jabr* In the offices of psychiatrists and psychologists across the country you can find a rather hefty tome called the Diagnostic and Statistical Manual for Mental Disorders (DSM). The current edition of the DSM, the DSM-IV, is something like a field guide to mental disorders: the book pairs each illness with a checklist of symptoms, just as a naturalist’s guide describes the distinctive physical features of different birds. These lists of symptoms, known as diagnostic criteria, help psychiatrists choose a disorder that most closely matches what they observe in their patients. Every few decades, the American Psychiatric Association (APA) revises the diagnostic criteria and publishes a brand new version of the DSM. The idea is to make the criteria more accurate, drawing on what psychologists and psychiatrists have learned about mental illness since the manual’s last update. In May 2013, the APA plans to publish the fifth and newest edition of the DSM, which it has been preparing for more than 11 years. On its DSM-5 Development website, the APA states that the motivation for the ongoing revisions was an agreement to “expand the scientific basis for psychiatric diagnosis and classification.” The website further states that “over the past two decades, there has been a wealth of new information in neurology, genetics and the behavioral sciences that dramatically expands our understanding of mental illness.” © 2012 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: 16769 - Posted: 05.09.2012

Daniel Cressey With the official opening of a £5.4-million (US$8.7-million) facility at its UK base on 30 April, pharmaceutical giant Eli Lilly says it is reaffirming its commitment to neuroscience research at a time when other drug firms are mostly avoiding the field. The site, at Erl Wood in Windlesham, Surrey, will house around 130 scientists working on the early phases of clinical drug development, making it Lilly's second-largest research site worldwide, after the company’s headquarters in Indianapolis, Indiana. Researchers will work on conditions ranging from cancer and diabetes to Alzheimer's disease and schizophrenia, says Sarah Chatham, managing director of the centre. The investment contrasts with lay-offs at other pharma companies. Many have turned their attention to acquiring smaller firms to get new drugs, instead of using large in-house research teams. Lilly’s focus on neuroscience is also unusual, with Novartis, GlaxoSmithKline and AstraZeneca all bailing out of much brain work in recent years (see 'Novartis to shut brain research facility'). The centre was welcomed by UK science minister David Willetts, not least because policy-makers have grown anxious that Britain is no longer perceived as a good place to do medical research. Academics are concerned that their research environment is overburdened with red tape, especially because of what they see as the bureaucratic way the United Kingdom implemented the European Union Clinical Trials Directive in 2004 (see 'UK health research to be rehabilitated'). © 2012 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: 16742 - Posted: 05.03.2012

Horrific crimes, such as the Anders Breivik case, illustrate the misconceptions the public has about mental illness, a leading expert says. Professor Simon Wessely, of King's College London, said the simplest responses to mass killings were that the perpetrators "must be mad". But he said the way Breivik carried out the killings suggested otherwise. He said the idea a psychiatric diagnosis could help people avoid punishment was wrong too. Writing in the Lancet medical journal, Professor Wessely said putting forward a mental illness defence in the UK could lead a person to spending more time behind bars than less. "The forensic psychiatry system is not a soft or popular option," he added. The psychiatrist also said the Breivik case highlighted another misconception - that outrageous crimes must mean mental illness. "For schizophrenia to explain Breivik's actions, they would have to be the result of delusions." But he added: "The meticulous way in which he planned his attacks does not speak to the disorganisation of schizophrenia." BBC © 2012

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: 16728 - Posted: 04.30.2012

By Brian Vastag So-called atypical antipsychotic drugs have been blockbusters for the drug industry, pulling in $16 billion in 2010. Developed to treat schizophrenia and related disorders, physicians also prescribe these drugs “off label” for bipolar disorder, insomnia, and other problems the drugs are not approved to treat, as Sandra Boodman wrote in the Post on March 12. But a new report finds that psychiatrists have not been given a full picture of these drugs, which include big sellers like Abilify (aripiprazole), Zyprexa (olanzapine), Risperdal (risperidone), and Seroquel (quetiapine). When seeking approval for eight atypical antipsychotic drugs, drug companies performed 24 studies, according to a Food and Drug Administration database. But four of the studies were never published in professional journals — and all four were unflattering for the drug in question. Three of the unpublished studies showed that the new drug did not perform better than a sugar pill. The fourth study showed that while the antipsychotic drug helped patients more than a placebo, older, less expensive drugs helped patients even more. “That’s bad if you’re marketing the drug,” said Erick Turner, the psychiatrist at Oregon Health & Science University who conducted the new analysis, which was published Tuesday in the journal PLoS Medicine . © 1996-2012 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: 16560 - Posted: 03.22.2012