Links for Keyword: Schizophrenia

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Sara Reardon Antipsychotic drugs are widely used to blunt aggressive behaviour in people with intellectual disabilities who have no history of mental illness, a UK survey of medical records finds, even though the medicines may not have a calming effect. The finding is worrisome because antipsychotic drugs can cause severe side effects such as obesity or diabetes. Psychiatry researcher Rory Sheehan and colleagues1 at University College London studied data from 33,016 people with intellectual disabilities from general-care practices in the United Kingdom over a period of up to 15 years. The researchers found that 71% of 9,135 people who were treated with antipsychotics had never been diagnosed with a severe mental illness, and that the drugs were more likely to be prescribed to those who displayed problematic behaviours. “We suspected that this would be the case, but we didn’t know the true extent,” Sheehan says. “We should be worried because the rates are high,” says James Harris, a psychiatrist at Johns Hopkins University in Baltimore, Maryland. But he adds that it is hard to determine whether treatment with antipsychotics is appropriate without knowing what other forms of treatment were available to people in the study. It is possible that medication was the only option available or that it was used to dampen a person's behaviour enough that they could participate in therapy or other types of treatment. Evidence suggests that the drugs are not effective at treating aggressive and disruptive behaviour, says psychiatrist Peter Tyrer of Imperial College London. I © 2015 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: 21376 - Posted: 09.02.2015

By Lily Hay Newman Mental health issues manifest in a number of ways, and they're not all behavioral. Increasingly, scientists are using speech analysis software to detect subtle changes in voice acoustics and patterns to detect or even predict potentially problematic conditions. A study published Wednesday in NPG-Schizophrenia by researchers at Columbia University Medical Center, the New York State Psychiatric Institute, and IBM's T. J. Watson Research Center found that digital speech analysis correctly predicted whether 34 youths at risk for mental illness (11 female, 23 male) would develop psychosis within 2.5 years. The system, which evaluated the study participants quarterly, correctly predicted all of their outcomes; five became psychotic. The algorithm evaluated transcripts for predictive "semantic and syntactic features" like coherence and phrase length. "These speech features predicted later psychosis development with 100% accuracy, outperforming classification from clinical interviews," the researchers wrote. Clinicians are able to accurately categorize patients as "at-risk," but within that subpopulation it is difficult to determine who will actually experience psychosis and potentially develop schizophrenia. If voice recognition software can help identify these individuals, they may be able to receive more effective care. "Computerized analysis of complex human behaviors such as speech may present an opportunity to move psychiatry beyond reliance on self-report and clinical observation toward more objective measures of health and illness in the individual patient," the researchers wrote. © 2015 The Slate Group LLC.

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: 21362 - Posted: 08.31.2015

Helen Thomson Serious mood disorders such as bipolar may be the price humans have had to pay for our intelligence and creativity. That’s according to new research which links high childhood IQ to an increased risk of experiencing manic bipolar traits in later life. Researchers examined data from a large birth cohort to identify the IQ of 1,881 individuals at age eight. These same individuals were then assessed for manic traits at the age of 22 or 23. The statements they provided were part of a checklist widely used to diagnose bipolar disorder. Each person was given a score out of 100 related to how many manic traits they had previously experienced. Individuals who scored in the top 10% of manic features had a childhood IQ almost 10 points higher than those who scored in the lowest 10%. This correlation appeared strongest for those with high verbal IQ. “Our study offers a possible explanation for how bipolar disorder may have been selected through generations,” said Daniel Smith of the University of Glasgow , who led the study. “There is something about the genetics underlying the disorder that are advantageous. One possibility is that serious disorders of mood - such as bipolar disorder - are the price that human beings have had to pay for more adaptive traits such as intelligence, creativity and verbal proficiency.” Smith emphasises that as things stand, having a high IQ is only an advantage: “A high IQ is not a clear-cut risk factor for bipolar, but perhaps the genes that confer intelligence can get expressed as illness in the context of other risk factors, such as exposure to maternal influenza in the womb or childhood sexual abuse.” © 2015 Guardian News and Media Limited

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 21312 - Posted: 08.19.2015

There may finally be a way to stop people progressing beyond the first signs of schizophrenia – fish oil. When people with early-stage symptoms took omega-3 supplements for three months, they had much lower rates of progression than those who did not, according to one small-scale trial. People with schizophrenia are usually diagnosed in their teens or 20s, but may experience symptoms for years beforehand, such as minor delusions or paranoid thoughts. Only about a third of people with such symptoms do go on to develop psychosis, however, and antipsychotic drugs can cause nasty side effects, so these are rarely given as a preventative. Fish oil supplements, which contain polyunsaturated fatty acids like omega-3, may be a benign alternative. These fatty acids may normally help dampen inflammation in the brain and protect neurons from damage, and lower levels in the brain have been implicated in several mental illnesses. Tests have found that people with schizophrenia have lower levels of these fatty acids in their blood cells, suggesting the same could be true for their brain cells. Fish oil supplements have been investigated as a treatment for adults with schizophrenia, but so far results have been mixed – four trials found no benefit while another four found a small reduction in symptoms. But a study that gave omega-3 fish oil pills to younger people suggests that what matters is catching the condition in time. The trial followed 81 people aged 13 to 25 with early signs of schizophrenia. Roughly half took fish oil pills and half took placebo tablets for three months. A year later, those given fish oils were less likely to have developed psychosis. © 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: 21288 - Posted: 08.12.2015

By Nancy Szokan “This is a story of a family who made mistakes.” Thus Janet Sternburg begins her memoir of a close-knit Jewish family living in Boston. Her grandfather, Philip, was a cold, angry man who abandoned his wife and six children not long after the only son in the family, Bennie, was diagnosed as schizophrenic. As Bennie became increasingly violent and untreatable, the family — advised by a Harvard professor of psychiatry — agreed to submit him to a prefrontal lobotomy. More than a decade later, one of Bennie’s sisters, Francie, sank into a debilitating depression — relentlessly weeping, attempting suicide — and again, the solution was seen to be a lobotomy. While she was growing up, Sternburg accepted the lobotomies as her family’s normalcy. It was decades later, when she was an adult living in California, that it occurred to her to question why such terrible measures had been taken. “The years came back to me when my aunt and uncle were driven to our house” for a regular visit, she writes. As the grandmother cooked and the aunts and uncles talked and played cards, the two lobotomized siblings “sat blankly on the couch — Bennie at one end, virtually unmoving, my aunt crumpled into the far corner. . . . With the sharp return of memories came the realization that even as a child I had a slight awareness . . . that something wrong had been done.” But she also knew her relatives as good and generous people. So she set out to learn what happened, and why. “White Matter: A Memoir of Family and Medicine” is Sternburg’s tale of what she discovered, put in the context of her family’s history.

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: 21256 - Posted: 08.04.2015

Steve Connor A computer game designed by neuroscientists has helped patients with schizophrenia to recover their ability to carry out everyday tasks that rely on having good memory, a study has found. Patients who played the game regularly for a month were four times better than non-players at remembering the kind of things that are critical for normal, day-to-day life, researchers said. The computer game was based on scientific principles that are known to “train” the brain in episodic memory, which helps people to remember events such as where they parked a car or placed a set of keys, said Professor Barbara Sahakian of Cambridge University, the lead author of the study. People recovering from schizophrenia suffer serious lapses in episodic memory which prevent them from returning to work or studying at university, so anything that can improve the ability of the brain to remember everyday events will help them to lead a normal life, Professor Sahakian said. Schizophrenia affects about one in every hundred people and results in hallucinations and delusions (Rex) Schizophrenia affects about one in every hundred people and results in hallucinations and delusions (Rex) “This kind of memory is essential for everyday learning and everything we do really both at home and at work. We have formulated an iPad game that could drive the neural circuitry behind episodic memory by stimulating the ability to remember where things were on the screen,” Professor Sahakian said. © independent.co.uk

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: 21251 - Posted: 08.02.2015

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

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

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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 21101 - Posted: 06.27.2015

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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 21100 - Posted: 06.27.2015

By JAIME LOWE The manila folder is full of faded faxes. The top sheet contains a brief description of my first medically confirmed manic episode, more than 20 years ago, when I was admitted as a teenager to U.C.L.A.’s Neuropsychiatric Institute: “Increased psychomotor rate, decreased need for sleep (about two to three hours a night), racing thoughts and paranoid ideation regarding her parents following her and watching her, as well as taping the phone calls that she was making.” I believed I had special powers, the report noted; I knew ‘‘when the end of the world was coming due to toxic substances’’ and felt that I was the only one who could stop it. There was also an account of my elaborate academic sponsorship plan so I could afford to attend Yale — some corporation would pay for a year of education in exchange for labor or repayment down the line. (Another grand delusion. I was a B-plus student, at best.) After I was admitted to the institute's adolescent ward, I thought the nurses and doctors and therapists were trying to poison me. So was the TV in the rec room. I warned my one friend in the ward that its rays were trying to kill him. The generator outside my window was pumping in gas. The place, I was sure, was a death camp. I refused meds because they were obviously agents of annihilation. It took four orderlies to medicate me: They pinned me to the floor while a nurse plunged a syringe into my left hip. Over time, I became too tired to refuse medication. Or perhaps the cocktail of antipsychotics started working. The Dixie cup full of pills included lithium, which slowly took hold of my mania. After a few weeks, I stopped whispering to the other patients that we were all about to be killed. Eventually, I stopped believing it myself. Mark DeAntonio, the U.C.L.A. psychiatrist who was treating me, said I had bipolar disorder. Here’s the phrasing from the National Institute of Mental Health: ‘‘unusually intense emotional states that occur in distinct periods called ‘mood episodes.’ Each mood episode represents a drastic change from a person’s usual mood and behavior. An overly joyful or overexcited state is called a manic episode, and an extremely sad or hopeless state is called a depressive episode.’’ The generic definition doesn’t quite cover the extremes of the disease or its symptoms, which include inflated self-esteem, sleeplessness, loquaciousness, racing thoughts and doing things that, according to the Mayo Clinic, ‘‘have a high potential for painful consequences — for example, unrestrained buying sprees, sexual indiscretions or foolish business investments.’’ © 2015 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 21094 - Posted: 06.25.2015

By Michael Hedrick I’ve had a little success dating in the nearly 10 years I’ve lived with schizophrenia. But there are a lot of obstacles. Schizophrenia is a terrifying word for many people. It conjures up ideas of murderous intent, lack of control and a host of other scary things. I live with this word, though; I am the word. But it is not a word you can just drop into a conversation and follow with “It’s not a big deal, though.” I seem to fall in love easily, but it’s always with girls who don’t feel the same way about me. I have seen more rejection than I care to admit, putting myself on the line like that, and it’s been a chore for me not to let my emotions get the best of me. If it’s not outright rejection, it seems to be something else that always seems to happen. I can remember one date I went on some months back. She was a big girl with blonde hair and eyes that had that squinty “I’m up to no good” look. We met over Match.com, and I was struck by how much time she spent going to Phish shows. Her profile was scattered with a number of bands that I had loved at different points in my life. She was a teacher, and she mentioned in her profile something along the lines that because of her love of sparkles, arts-and- crafts, and rainbows, she was a 6-year-old in a woman’s body. Before I knew it, I was asking if she wanted to go get a beer. She said yes, a little too eagerly I thought. I got to the restaurant about 15 minutes early and ordered a beer, apprehensive knowing that eventually I would have to tell her about my illness. Soon enough she walked in, and I was struck by the fact that she seemed a little disappointed to be there. There was no smile as she sat down to join me. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 21051 - Posted: 06.15.2015

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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 21038 - Posted: 06.10.2015

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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 21032 - Posted: 06.09.2015

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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 21021 - Posted: 06.06.2015

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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 21018 - Posted: 06.06.2015

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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20895 - Posted: 05.06.2015

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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20814 - Posted: 04.18.2015

By ABIGAIL ZUGER, M.D. On an early summer night in 1944, on the wooded shoulder of a rural Massachusetts highway, a man in a rumpled brown suit wandered in the shadows. Whenever a car passed, he dropped to the ground and lay flat. His hair was matted, his face smeared with mud. He was a respectable Boston doctor on the lam, hungry, lost and ill. He was Mimi Baird’s father, Dr. Perry Baird, a Texas-born, Harvard-trained physician whose severe bipolar disease ultimately destroyed his life and scarred his family with the usual wide-ranging cruelties of mental illness. Dr. Baird vanished from Ms. Baird’s life when she was a little girl. She saw him once, briefly, when she was a teenager, then never again. He died in his mid-50s, in 1959. More than 30 years later, when Ms. Baird herself was in her 50s, a large package arrived on her doorstep and her father re-entered her world. The box contained a manuscript long forgotten in a relative’s garage, written in smudged pencil on onionskin paper, a memoir her father had composed of five terrible months in his life. The story began the very day Dr. Baird said goodbye to 5-year-old Mimi and her sister, and permanently left the household. Stunned and bereft all over again, Ms. Baird then spent two decades chasing down the rest of the story, talking to neighbors, colleagues and relatives about long-ago events and obtaining her father’s medical records. Now in her late 70s, a retired medical administrator, she has, with the help of a co-author, woven all this material into “He Wanted the Moon,” an extraordinary Möbius strip of a book. (Read an excerpt.) Its core is the full text of her father’s manuscript, deftly annotated and explained. Around it she layers the voices of caretakers, friends, relatives and medical authorities. Events are revisited and reframed, turned inside out, then right side up again. The book is autobiography, biography, science, history and literature all in one, as instructive as any textbook and utterly impossible to put down. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20600 - Posted: 02.24.2015

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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 20588 - Posted: 02.18.2015

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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20396 - Posted: 12.06.2014