Links for Keyword: Schizophrenia

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By John Horgan What is mental illness? Schizophrenia? Autism? Bipolar disorder? Depression? Since the 1950s, the profession of psychiatry has attempted to provide definitive answers to these questions in the Diagnostic and Statistical Manual of Mental Disorders. Often called The Bible of psychiatry, the DSM serves as the ultimate authority for diagnosis, treatment and insurance coverage of mental illness. Now, in a move sure to rock psychiatry, psychology and other fields that address mental illness, the director of the National Institutes of Mental Health has announced that the federal agency–which provides grants for research on mental illness–will be “re-orienting its research away from DSM categories.” Thomas Insel’s statement comes just weeks before the scheduled publication of the DSM-V, the fifth edition of the Diagnostic and Statistical Manual. Insel writes: “While DSM has been described as a ‘Bible’ for the field, it is, at best, a dictionary, creating a set of labels and defining each. The strength of each of the editions of DSM has been ‘reliability’–each edition has ensured that clinicians use the same terms in the same ways. The weakness is its lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure. In the rest of medicine, this would be equivalent to creating diagnostic systems based on the nature of chest pain or the quality of fever. Indeed, symptom-based diagnosis, once common in other areas of medicine, has been largely replaced in the past half century as we have understood that symptoms alone rarely indicate the best choice of treatment. Patients with mental disorders deserve better.” © 2013 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: 18120 - Posted: 05.06.2013

By Ferris Jabr This month the American Psychiatric Association (APA) will publish the fifth edition of its guidebook for clinicians, the Diagnostic and Statistical Manual of Mental Disorders, or DSM-5. Researchers around the world have eagerly anticipated the new manual, which, in typical fashion, took around 14 years to revise. The DSM describes the symptoms of more than 300 officially recognized mental illnesses—depression, bipolar disorder, schizophrenia and others—helping counselors, psychiatrists and general care practitioners diagnose their patients. Yet it has a fundamental flaw: it says nothing about the biological underpinnings of mental disorders. In the past, that shortcoming reflected the science. For most of the DSM's history, investigators have not had a detailed understanding of what causes mental illness. That excuse is no longer valid. Neuroscientists now understand some of the ways that brain circuits for memory, emotion and attention malfunction in various mental disorders. Since 2009 clinical psychologist Bruce Cuthbert and his team at the National Institute of Mental Health have been constructing a classification system based on recent research, which is revealing how the structure and activity of a mentally ill brain differs from that of a healthy one. The new framework will not replace the DSM, which is too important to discard, Cuthbert says. Rather he and his colleagues hope that future versions of the guide will incorporate information about the biology of mental illness to better distinguish one disorder from another. Cuthbert, whose project may receive additional funding from the Obama administration's planned Brain Activity Map initiative, is encouraging researchers to study basic cognitive and biological processes implicated in many types of mental illness. Some scientists might explore how and why the neural circuits that detect threats and store fearful memories sometimes behave in unusual ways after traumatic events—the kinds of changes that are partially responsible for post-traumatic stress disorder. Others may investigate the neurobiology of hallucinations, disruptions in circadian rhythms, or precisely how drug addiction rewires the brain. © 2013 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: 18101 - Posted: 05.01.2013

By LINDA LOGAN The last time I saw my old self, I was 27 years old and living in Boston. I was doing well in graduate school, had a tight circle of friends and was a prolific creative writer. Married to my high-school sweetheart, I had just had my first child. Back then, my best times were twirling my baby girl under the gloaming sky on a Florida beach and flopping on the bed with my husband — feet propped against the wall — and talking. The future seemed wide open. I don’t think there is a particular point at which I can say I became depressed. My illness was insidious, gradual and inexorable. I had a preview of depression in high school, when I spent a couple of years wearing all black, rimming my eyes in kohl and sliding against the walls in the hallways, hoping that no one would notice me. But back then I didn’t think it was a very serious problem. The hormonal chaos of having three children in five years, the pressure of working on a Ph.D. dissertation and a genetic predisposition for a mood disorder took me to a place of darkness I hadn’t experienced before. Of course, I didn’t recognize that right away. Denial is a gauze; willful denial, an opiate. Everyone seemed in league with my delusion. I was just overwhelmed, my family would say. I should get more help with the kids, put off my Ph.D. When I told other young mothers about my bone-wearying fatigue, they rolled their eyes knowingly and mumbled, “Right.” But what they didn’t realize was that I could scarcely push the stroller to the park, barely summon the breath to ask the store clerk, “Where are the Pampers?” I went from doctor to doctor, looking for the cause. Lab tests for anemia, low blood sugar and hypothyroidism were all negative. © 2013 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: 18085 - Posted: 04.28.2013

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.

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: 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

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: 18073 - Posted: 04.25.2013

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,

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: 18022 - Posted: 04.11.2013

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

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: 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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 17929 - Posted: 03.23.2013

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

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: 17902 - Posted: 03.15.2013

By NICHOLAS BAKALAR Some studies have suggested that the risk factors for violence by people with mental illness are the same as those in the general population. But a new study finds that anger, coupled with psychotic delusions, may be the most significant factor in violence committed by people with mental illness. British researchers, writing online last week in JAMA Psychiatry, studied 458 patients ages 18 to 64 who had had a first episode of psychosis. Most patients were nonviolent, 26.4 percent were involved in minor violence, and 11.8 percent in violent acts using weapons or resulting in injury. Those who were violent were more likely to be younger men and to use illicit drugs, but they did not differ from the nonviolent in social class, unemployment or alcohol use. The researchers found no difference between violent and nonviolent patients with regard to feelings of elation, fear or anxiety. People with depression were less violent. But after adjusting for other health and socioeconomic variables, the researchers found that delusions accompanied by anger were present far more often among the violent patients. “If patients are not angry, the delusions themselves don’t cause a problem,” said the lead author, Dr. Jeremy W. Coid, a professor of psychiatry at Queen Mary University of London. “An area for future research is, ‘What do you need to do to make your patient safe again? Do you treat the delusions, the anger or both?’ ” Copyright 2013 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: 17892 - Posted: 03.12.2013

By GINA KOLATA The psychiatric illnesses seem very different — schizophrenia, bipolar disorder, autism, major depression and attention deficit hyperactivity disorder. Yet they share several genetic glitches that can nudge the brain along a path to mental illness, researchers report. Which disease, if any, develops is thought to depend on other genetic or environmental factors. Their study, published online Wednesday in the Lancet, was based on an examination of genetic data from more than 60,000 people worldwide. Its authors say it is the largest genetic study yet of psychiatric disorders. The findings strengthen an emerging view of mental illness that aims to make diagnoses based on the genetic aberrations underlying diseases instead of on the disease symptoms. Two of the aberrations discovered in the new study were in genes used in a major signaling system in the brain, giving clues to processes that might go awry and suggestions of how to treat the diseases. “What we identified here is probably just the tip of an iceberg,” said Dr. Jordan Smoller, lead author of the paper and a professor of psychiatry at Harvard Medical School and Massachusetts General Hospital. “As these studies grow we expect to find additional genes that might overlap.” The new study does not mean that the genetics of psychiatric disorders are simple. Researchers say there seem to be hundreds of genes involved and the gene variations discovered in the new study confer only a small risk of psychiatric disease. Steven McCarroll, director of genetics for the Stanley Center for Psychiatric Research at the Broad Institute of Harvard and M.I.T., said it was significant that the researchers had found common genetic factors that pointed to a specific signaling system. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 17866 - Posted: 03.04.2013

by Emily Underwood No single cause has yet been discovered for schizophrenia, the devastating neuropsychiatric syndrome characterized by hallucinations, disordered thoughts, and other cognitive and emotional problems, typically beginning in early adulthood. Although schizophrenia runs in families, in many cases no genetic risk is apparent, leading many researchers to look for environmental explanations. Now, research in mice provides support for a long-held hypothesis: that the syndrome, and other neurological disorders, can emerge when multiple environmental insults such as prenatal infection and adolescent trauma combine. Environmental stressors such as infection and abuse were long ago shown to be risk factors for schizophrenia. Large studies of children whose mothers were infected with influenza during the last months of their pregnancy, for example, have a roughly twofold increase in risk of developing the syndrome compared with the general population. That doesn't explain why a few people who are exposed to an infection in the womb go on to develop schizophrenia while most don't, however, says Urs Meyer, a behavioral neurobiologist at the Swiss Federal Institute of Technology in Zurich and co-author of the study reported online today in Science. One long-held hypothesis, he says, is that early infection creates a latent vulnerability to schizophrenia that is only "unmasked" by later insults, such as physical injury or psychological trauma. Such stressors are thought to be particularly damaging during critical periods of brain development such as early puberty, he says. Although the "multiple-hit" hypothesis has been prominent in the literature for some time, it is difficult to test the idea with human epidemiology studies, he says. "You need huge, huge data sets to see anything." © 2010 American Association for the Advancement of Science.

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: 17864 - Posted: 03.02.2013

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