Chapter 16. Psychopathology: Biological Basis of Behavior Disorders

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Sara Reardon When it comes to lab mice and antidepressants, it's complicated. Mouse experiments with the popular club drug ketamine may be skewed by the sex of the researcher performing them, a study suggests. The findings, presented on 14 November at the Society for Neuroscience (SfN) meeting in Washington DC, only deepen the mystery of how ketamine, which has powerful mood-lifting properties, interacts with the brain. They also raise questions about the reproducibility of behavioural experiments in mice. Ketamine is best known as a psychoactive recreational drug. But it has caught psychiatrists’ interest because of its potential to treat depression within hours. It’s unclear exactly how the drug works, however, and many researchers are using animal models to suss out the mechanism. Polymnia Georgiou, a neuroscientist at the University of Maryland in Baltimore, is one of them. In 2015, a male colleague asked her to run some experiments for him while he was out of town, including a standard way of testing antidepressants called the forced-swim test. In this assay, researchers inject healthy mice with a drug, place them into a tank of water and measure how long they swim before they give up and wait for someone to rescue them. Antidepressants can cause healthy mice to swim for longer than their untreated counterparts, which is what Georgiou’s male colleague found during his experiments using ketamine. © 2017 Macmillan Publishers Limited

Keyword: Sexual Behavior; Depression
Link ID: 24341 - Posted: 11.20.2017

By Jennifer Couzin-Frankel Rachel Loewy was an undergraduate in 1995 when she answered a flyer seeking students to assist with a research study. A couple of floors up in a psychology department building, Loewy sat, clipboard in hand, interviewing teenagers whose brain health was beginning to falter. Some heard whispers. Others imagined that their teachers could read their minds, or that fellow students stared at them and wished them harm as they walked down the halls. The teenagers had been diagnosed with schizotypal personality disorder, a condition that can precede schizophrenia. Among the most debilitating and stigmatized psychiatric diseases, schizophrenia can rob sufferers of their self and their future, often in early adulthood. Although these teens didn't have schizophrenia, the researchers believed that some would later deteriorate and be diagnosed with the disorder. But when Loewy met them they were lucid and self-aware. And they were frightened that their mind sometimes spun out of control. Doctors routinely assess a patient's risk of heart attack, various cancers, and diabetes, often intervening to slow or stop disease before it strikes. But preventing psychiatric conditions, from anxiety to depression to schizophrenia, has received scant attention. © 2017 American Association for the Advancement of Science

Keyword: Schizophrenia
Link ID: 24336 - Posted: 11.17.2017

Patricia Neighmond A study published Tuesday in the journal Clinical Psychological Science finds that increased time spent with popular electronic devices — whether a computer, cell phone or tablet — might have contributed to an uptick in symptoms of depression and suicidal thoughts over the last several years among teens, especially among girls. Though San Diego State University psychologist Jean Twenge, who led the study, agrees this sort of research can only establish a correlation between long hours of daily screen time and symptoms of alienation — it can't prove one causes the other — she thinks the findings should be a warning to parents. "One hour, maybe two hours [a day], doesn't increase risk all that much," Twenge says. "But once you get to three hours — and especially four and then, really, five hours and beyond — that's where there's much more significant risk of suicide attempts, thinking about suicide and major depression." Twenge and her colleagues took a hard look at national surveys that asked more than a half million young people, ages 13 to 18, questions that get at symptoms of depression. Twenge says the surveys asked students to respond to statements such as "Life often feels meaningless," or "I feel I can't do anything right," or "I feel my life is not very useful. Between 2010 and 2015 Twenge found the number of teens who answered "yes" to three or more of these questions increased significantly, from 16 percent in 2010 to 22 percent in 2015. © 2017 npr

Keyword: Depression
Link ID: 24327 - Posted: 11.15.2017

By Elly Vintiadis The prevailing wisdom today is that addiction is a disease. This is the main line of the medical model of mental disorders with which the National Institute on Drug Abuse (NIDA) is aligned: addiction is a chronic and relapsing brain disease in which drug use becomes involuntary despite its negative consequences. The idea here is, roughly, that addiction is a disease because drug use changes the brain and, as a result of these changes, drug use becomes compulsive, beyond the voluntary control of the user. In other words, the addict has no choice and his behavior is resistant to long term change. This way of viewing addiction has its benefits: if addiction is a disease then addicts are not to blame for their plight, and this ought to help alleviate stigma and to open the way for better treatment and more funding for research on addiction. This is the main rationale of a recent piece in the New York Times, which describes addiction as a disease that is plaguing the U.S. and stresses the importance of talking openly about addiction in order to shift people’s understanding of it. And it seems like a welcome change from the blame attributed by the moral model of addiction, according to which addiction is a choice and, thus, a moral failing—addicts are nothing more than weak people who make bad choices and stick with them. Yet, though there are positive aspects to seeing addiction in this light, it seems unduly pessimistic and, though no one will deny that every behavior has neural correlates and that addiction changes the brain, this is not the same as saying that, therefore, addiction is pathological and irreversible. And there are reasons to question whether this is, in fact, the case. © 2017 Scientific American

Keyword: Drug Abuse
Link ID: 24307 - Posted: 11.09.2017

Hannah Devlin Science correspondent British scientists have begun testing a radically new approach to treating schizophrenia based on emerging evidence that it could be a disease of the immune system. The first patient, a 33-year old man who developed schizophrenia after moving to London from Cameroon a decade ago, was treated at King’s College Hospital in London on Thursday, marking the start of one of the most ambitious trials to date on the biology of the illness and how to treat it. During the next two years, 30 patients will receive monthly infusions of an antibody drug currently used to treat multiple sclerosis (MS), which the team hopes will target the root causes of schizophrenia in a far more fundamental way than current therapies. The trial builds on more than a decade’s work by Oliver Howes, a professor of molecular psychiatry at the MRC London Institute of Medical Sciences and a consultant psychiatrist at the Maudsley Hospital in south London. Howes’s team is one of several worldwide to have uncovered evidence that abnormalities in immune activity in the brain may lie at the heart of the illness – for some patients, at least. “In the past, we’ve always thought of the mind and the body being separate, but it’s just not like that,” said Howes. “The mind and body interact constantly and the immune system is no different. It’s about changing the way we think about mental illnesses.” Recent work by Howes and colleagues found that in the earliest stages of schizophrenia, people experience a surge in the number and activity of immune cells in the brain. As well as fighting infection, these cells, called microglia, have a “gardening” role, pruning unwanted connections between neurons. But in schizophrenia patients, the pruning appears to become more aggressive, leading to vital connections being lost. © 2017 Guardian News and Media Limited

Keyword: Schizophrenia; Neuroimmunology
Link ID: 24293 - Posted: 11.04.2017

Hannah Devlin Descartes’s notion of dualism – that the mind and body are separate entities – is wrong, but has proved surprisingly persistent, and until recently dominated attempts to understand mental illness. When the brain stopped working properly, a psychological origin was sought. Undoubtedly, life’s experiences and our personalities shape the way our brains function. But there is now a compelling body of evidence that brain disorders can also originate from things going awry in our basic biology. Particularly intriguing is the discovery that the brain, once thought to be separated from the immune system by the blood-brain barrier, is powerfully influenced by immune activity. The latest trial, focused on schizophrenia, is backed by converging evidence from several fields that immune cells in the brain, called microglia, play at least some role in this disease. Prof Oliver Howes, the psychiatrist leading the work, discovered that these cells appear to go into overdrive in the early stages of schizophrenia. Genetics studies have linked changes in immune system genes to increased risk for schizophrenia and anecdotal evidence, including a recent case report of a patient who developed schizophrenia after receiving a bone marrow transplant from a sibling with the illness, also triangulates on to the immune system. “It’s all challenging the idea that the brain is this separate privileged organ,” said Howes. © 2017 Guardian News and Media Limited

Keyword: Schizophrenia
Link ID: 24292 - Posted: 11.04.2017

By Emily Underwood In 2003, neurologist Helen Mayberg of Emory University in Atlanta began to test a bold, experimental treatment for people with severe depression, which involved implanting metal electrodes deep in the brain in a region called area 25. The initial data were promising; eventually, they convinced a device company, St. Jude Medical in Saint Paul, to sponsor a 200-person clinical trial dubbed BROADEN. This month, however, Lancet Psychiatry reported the first published data on the trial’s failure. The study stopped recruiting participants in 2012, after a 6-month study in 90 people failed to show statistically significant improvements between those receiving active stimulation and a control group, in which the device was implanted but switched off. Although that decision was “game over” for BROADEN, the story wasn’t finished for some 44 patients who asked to keep the implants in their brains, and the clinicians responsible for their long-term care, Mayberg explained last week to colleagues at a meeting on the ethical dilemmas of brain stimulation research at the National Institutes of Health (NIH) in Bethesda, Maryland. The episode highlights a tricky dilemma for companies and research teams involved in deep brain stimulation (DBS) research: If trial participants want to keep their implants, who will take responsibility—and pay—for their ongoing care? And participants in last week’s meeting said it underscores the need for the growing corps of DBS researchers to think long-term about their planned studies. © 2017 American Association for the Advancement of Science.

Keyword: Depression
Link ID: 24276 - Posted: 11.01.2017

Sara Reardon Human genome databases are enabling researchers to take a deeper dive into the evolution of psychiatric disorders. Psychiatric disorders can be debilitating and often involve a genetic component, yet, evolution hasn’t weeded them out. Now, recent work is beginning to reveal the role of natural selection — offering a peek at how the genetic underpinnings of mental illness has changed over time. Many psychiatric disorders are polygenic: they can involve hundreds or thousands of genes and DNA mutations. It can be difficult to track how so many genetic regions evolved, and such studies require large genome data sets. But the advent of massive human genome databases is enabling researchers to look for possible connections between mental illnesses and the environmental and societal conditions that might have driven their emergence and development. Others are looking to Neanderthal genetic sequences to help inform the picture of these disorders, as well as cognitive abilities, in humans. Several of these teams presented their findings at the American Society of Human Genetics (ASHG) meeting in Orlando, Florida, in late October. One project found that evolution selected for DNA variants thought to protect against schizophrenia. The study, led by population geneticist Barbara Stranger of the University of Chicago in Illinois, looked at hundreds of thousands of human genomes using a statistical method that identified signals of selection over the past 2,000 years1. There were no signs of selection in genetic regions associated with any other mental illness. Many of schizophrenia's symptoms, such as auditory hallucinations and jumbling sentences, involve brain regions tied to speech, says Bernard Crespi, an evolutionary biologist at Simon Fraser University in Burnaby, Canada. Over the course of hominid evolution, he says, the ability to speak could have outweighed the small, but unavoidable risk that the genes involved in language could malfunction and result in schizophrenia in a small percentage of the population. © 2017 Macmillan Publishers Limited

Keyword: Schizophrenia; Depression
Link ID: 24270 - Posted: 10.31.2017

Jon Hamilton People who are thinking about killing themselves appear to have distinctive brain activity that can now be measured by a computer. In these people, words like "death" and "trouble" produce a distinctive "neural signature" not found in others, scientists report in the journal Nature Human Behavior. More than 44,000 people commit suicide in the U.S. each year. "There really is a difference in the way [suicidal] people think about certain concepts," says Marcel Just, an author of the paper and the D. O. Hebb professor of cognitive neuroscience at Carnegie Mellon University. That difference allowed a computer program to distinguish people who thought about suicide from people who did not more than 90 percent of the time. It also allowed the computer program to distinguish people who had attempted suicide from people who had only thought about it. The results come from a study of just 34 young adults and will need to be replicated, says Barry Horwitz, chief of brain imaging and modeling at the National Institute on Deafness and Other Communication Disorders. But he says they hint at a future in which brain scans and computers can help assess a person's mental health. Horwitz was not involved in the study. "Just looking at behavior is probably inadequate for a lot of purposes," he says. "It's much better to be able to see what the brain is doing." © 2017 npr

Keyword: Depression
Link ID: 24269 - Posted: 10.31.2017

By MARK LUKACH For my son Jonas’s first Halloween, when he was 5 months old, I dressed the two of us as matching lumberjacks. For the second, we were characters from the movie “Up.” I was Carl, the old man, my wife was Ellie, and Jonas was Russell, the enthusiastic Wilderness Explorer. We tied a dozen balloons to our bulldog’s collar, to make him the house. In our version, the wife didn’t die at the beginning of the movie, and we all lived happily ever after. The next Halloween, Jonas wanted to be an elephant. He loved the scene in “The Jungle Book” where Mowgli tries to march with the elephants. We resisted, since we like family costumes and didn’t want to buy three elephant outfits, but conceded. We displayed his elephant costume in his room the week before Halloween so he could look at it in anticipation of the big day. My wife, Giulia, wasn’t there for the lumberjack Halloween. She was in the hospital. Giulia was there for the “Up” Halloween. But as we approached the elephant Halloween, I suspected she wasn’t going to dress up. Because, once again, she was going psychotic. Giulia was 27 when the first psychotic episode happened. It came out of nowhere. She got nervous about her new job; she lost her appetite; she stopped sleeping; she began having delusions. The first delusions were encouraging. She said she spoke to God, who told her that she was going to be fine. Giulia had never been very religious, so I was alarmed, but at least she was hearing things that were comforting. But then the delusions turned on her. The voices said she wasn’t going to make it, there was no point in even trying, she was better off not being here. That’s how she ended up in the hospital the first time. They gave her medication. The delusions eventually went away. She was depressed for a long time afterward. They gave her more medication, and then she got better. © 2017 The New York Times Company

Keyword: Schizophrenia
Link ID: 24257 - Posted: 10.28.2017

By Alice Klein Zapping the brain to relieve depression can spark fits of fury in a small number of people, psychiatrists warn. Transcranial direct current stimulation (tDCS) is increasingly being used to treat a range of conditions, from depression and addiction to obsessive-compulsive disorder (OCD). In it, electrodes attached to the scalp emit weak currents that help strengthen electrical brain circuits. To treat depression, the current is usually applied to the left dorsolateral prefrontal cortex – a brain area involved in regulating the emotions. There is now good evidence that this lifts mood in some people. However, it also appears to trigger anger in rare cases, say Galen Chin-Lun Hung and Ming-Chyi Huang at Taipei City Hospital in Taiwan. They recently reported two people at their psychiatric facility who had uncharacteristic outbursts of fury after receiving tDCS. The first was a 39-year-old woman with severe depression, low energy and suicidal thoughts who hadn’t responded to antidepressants. Straight after tDCS treatment, she became agitated, began yelling angrily and felt the urge to “tear everything apart”. © Copyright New Scientist Ltd.

Keyword: Depression; Emotions
Link ID: 24247 - Posted: 10.27.2017

By R. Douglas Fields BERLIN—Society’s embrace of cannabis to treat nausea, pain and other conditions proceeds apace with the drive to legalize the plant for recreational use. Pot’s seemingly innocuous side effects have helped clear a path toward making it a legal cash crop, with all of the marketing glitz brought to other consumer products. But that clean bill of health only goes so far. Marijuana’s potentially detrimental impact on the developing brains of adolescents remains a key focus of research—particularly because of the possibility teenage users could go on to face a higher risk of psychosis. New findings may fuel those worries. At the World Psychiatric Association’s World Congress in Berlin on October 9, Hannelore Ehrenreich of the Max Planck Institute of Experimental Medicine presented results of a study of 1,200 people with schizophrenia. The investigation analyzed a wide range of genetic and environmental risk factors for developing the debilitating mental illness. The results—being submitted for publication—show people who had consumed cannabis before age 18 developed schizophrenia approximately 10 years earlier than others. The higher the frequency of use, the data indicated, the earlier the age of schizophrenia onset. In her study neither alcohol use nor genetics predicted an earlier time of inception, but pot did. “Cannabis use during puberty is a major risk factor for schizophrenia,” Ehrenreich says. Other studies, although not all, support the thrust of Ehrenreich’s findings. “There is no doubt,” concludes Robin Murray, a professor of psychiatry at King’s College London, that cannabis use in young people increases the risk of developing schizophrenia as an adult. Speaking at the Berlin conference, Murray—one of the first scientists to research pot’s link to the disorder—cited 10 studies that found a significant risk of young cannabis users developing psychosis. © 2017 Scientific American

Keyword: Schizophrenia; Drug Abuse
Link ID: 24226 - Posted: 10.21.2017

By Alice Klein Four genes have been identified that are linked to obsessive compulsive disorder (OCD). The genes all play a role in the same brain circuit, and may help explain why people are more likely to have OCD if they have a relative with the condition. People with OCD have intrusive thoughts and feel driven to repeat rituals, such as handwashing, to relieve their anxiety. To investigate if OCD has a genetic basis, Hyun Ji Noh at the Broad Institute of MIT and Harvard and her colleagues compared more than 600 genes across 592 people with OCD, and 560 people who don’t have it. They chose these candidate genes from several lines of evidence. Of these genes, 222 had been linked to compulsive grooming in mice, and 196 had been linked to autism in people – a condition that can involve repetitive behaviours. The team also looked at 56 genes that they had identified in a study of dogs with canine compulsive disorder, a condition in which dogs repeatedly chase their tails, pace back and forth, groom themselves or sucks things, sometimes for hours at a time. Brain safety circuit The analysis identified four genes that are different in people who have OCD. All four of these are active in a brain circuit that links the striatum, thalamus and cortex regions. © Copyright New Scientist Ltd.

Keyword: OCD - Obsessive Compulsive Disorder; Genes & Behavior
Link ID: 24210 - Posted: 10.18.2017

By DOUGLAS QUENQUA In the days after his son was born, Rob Sandler found the thrill of becoming a new father replaced with dark feelings of dread and hopelessness. Those feelings, coupled with sleep deprivation and stress, culminated in a panic attack during his son’s bris. As a group of old friends was saying goodbye after the ceremony, “I had this feeling that they were leaving and I was stuck in this situation that would never get any better,” said Mr. Sandler, a marketing executive in Dallas. “I just felt trapped.” What followed was months of sadness, anxiety and — perhaps most worrisome of all — a feeling of acute disappointment in his own ability to be a good parent. In recent years, a growing body of research, and the increasing visibility of dads like Mr. Sandler, has given rise to the idea that you don’t have to give birth to develop postpartum depression, the so-called “baby blues.” Studies suggest that the phenomenon may occur in from 7 percent to 10 percent of new fathers, compared to about 12 percent of new mothers, and that depressed dads were more likely to spank their children and less likely to read to them. Now, a University of Southern California study has found a link between depression and sagging testosterone levels in new dads, adding physiological weight to the argument that postpartum depression isn’t just for women anymore. The study also found that while high testosterone levels in new dads helped protect against depression in fathers, it correlated with an increased risk of depression in new moms. “We know men get postpartum depression, and we know testosterone drops in new dads, but we don’t know why,” said Darby Saxbe, a professor of psychology at U.S.C. and an author of the new report. “It’s often been suggested hormones underlie some of the postpartum depression in moms, but there’s been so much less attention paid to fathers. We were trying to put together the pieces to solve this puzzle.” © 2017 The New York Times Company

Keyword: Depression; Sexual Behavior
Link ID: 24203 - Posted: 10.17.2017

By HEATHER MURPHY Can a fish be depressed? This question has been floating around my head ever since I spent a night in a hotel across from an excruciatingly sad-looking Siamese fighting fish. His name was Bruce Lee, according to a sign beneath his little bowl. There we were trying to enjoy a complimentary bloody mary on the last day of our honeymoon and there was Bruce Lee, totally still, his lower fin grazing the clear faux rocks on the bottom of his home. When he did finally move, just slightly, I got the sense that he would prefer to be dead. The pleasant woman at the front desk assured me that he was well taken care of. Was I simply anthropomorphizing Bruce Lee, incorrectly assuming his lethargy was a sign of mental distress? When I sought answers from scientists, I assumed that they would find the question preposterous. But they did not. Not at all. It turns out that not only can our gilled friends become depressed, but some scientists consider fish to be a promising animal model for developing anti-depressants. New research, I would learn, has been radically shifting the way that scientists think about fish cognition, building a case that pet and owner are not nearly as different as many assume. “The neurochemistry is so similar that it’s scary,” said Julian Pittman, a professor at the Department of Biological and Environmental Sciences at Troy University in Alabama, where he is working to develop new medications to treat depression, with the help of tiny zebrafish. We tend to think of them as simple organisms, “but there is a lot we don’t give fish credit for.” Dr. Pittman likes working with fish, in part, because they are so obvious about their depression. He can reliably test the effectiveness of antidepressants with something called the “novel tank test.” A zebrafish gets dropped in a new tank. If after five minutes it is hanging out in the lower half, it’s depressed. If it’s swimming up top — its usual inclination when exploring a new environment — then it’s not. In Dr. Pittman’s lab, researchers induce depression in a fish by keeping it drunk on ethanol for two weeks, then cutting off the supply, forcing it into withdrawal. This here is a depressed fish. Both clips, which represent a small segment of the five minute tank test, were extracted at comparable speeds. Troy University © 2017 The New York Times Company

Keyword: Depression; Evolution
Link ID: 24201 - Posted: 10.17.2017

By James Gallagher Health and science reporter, BBC News website A hallucinogen found in magic mushrooms can "reset" the brains of people with untreatable depression, raising hopes of a future treatment, scans suggest. The small study gave 19 patients a single dose of the psychedelic ingredient psilocybin. Half of patients ceased to be depressed and experienced changes in their brain activity that lasted about five weeks. However, the team at Imperial College London says people should not self-medicate. There has been a series of small studies suggesting psilocybin could have a role in depression by acting as a "lubricant for the mind" that allows people to escape a cycle of depressive symptoms. But the precise impact it might be having on brain activity was not known. Image copyright Getty Images The team at Imperial performed fMRI brain scans before treatment with psilocybin and then the day after (when the patients were "sober" again). The study, published in the journal Scientific Reports, showed psilocybin affected two key areas of the brain. The amygdala - which is heavily involved in how we process emotions such as fear and anxiety - became less active. The greater the reduction, the greater the improvement in reported symptoms. The default-mode network - a collaboration of different brain regions - became more stable after taking psilocybin. Dr Robin Carhart-Harris, head of psychedelic research at Imperial, said the depressed brain was being "clammed up" and the psychedelic experience "reset" it. He told the BBC News website: "Patients were very ready to use this analogy. Without any priming they would say, 'I've been reset, reborn, rebooted', and one patient said his brain had been defragged and cleaned up." © 2017 BBC

Keyword: Depression; Drug Abuse
Link ID: 24195 - Posted: 10.16.2017

Haroon Siddique Magic mushrooms may effectively “reset” the activity of key brain circuits known to play a role in depression, the latest study to highlight the therapeutic benefits of psychadelics suggests. Psychadelics have shown promising results in the treatment of depression and addictions in a number of clinical trials over the last decade. Imperial College London researchers used psilocybin – the psychoactive compound that occurs naturally in magic mushrooms – to treat a small number of patients with depression, monitoring their brain function, before and after. Images of patients’ brains revealed changes in brain activity that were associated with marked and lasting reductions in depressive symptoms and participants in the trial reported benefits lasting up to five weeks after treatment. Dr Robin Carhart-Harris, head of psychedelic research at Imperial, who led the study, said: “We have shown for the first time clear changes in brain activity in depressed people treated with psilocybin after failing to respond to conventional treatments. “Several of our patients described feeling ‘reset’ after the treatment and often used computer analogies. For example, one said he felt like his brain had been ‘defragged’ like a computer hard drive, and another said he felt ‘rebooted’. “Psilocybin may be giving these individuals the temporary ‘kick start’ they need to break out of their depressive states and these imaging results do tentatively support a ‘reset’ analogy. Similar brain effects to these have been seen with electroconvulsive therapy.” © 2017 Guardian News and Media Limited

Keyword: Depression; Drug Abuse
Link ID: 24189 - Posted: 10.13.2017

By Simon Makin About 10 years ago David Adam scratched his finger on a barbed wire fence. The cut was shallow, but drew blood. As a science journalist and author of The Man Who Couldn't Stop: OCD and the True Story of a Life Lost in Thought, a book about his own struggles with obsessive-compulsive disorder, Adam had a good idea of what was in store. His OCD involved an obsessive fear of contracting HIV and produced a set of compulsive behaviors revolving around blood. In this instance he hurried home to get some tissue and returned to check there was not already any blood on the barbed-wire. “I looked and saw there was no blood on the tissue, looked underneath the fence, saw there was no blood, turned to walk away, and had to do it all again, and again and again,” he says. “You get stuck in this horrific cycle, where all the evidence you use to form judgments in everyday life tells you there’s no blood. And if anyone asked, you’d say ‘no.’ Yet, when you ask yourself, you say ‘maybe.’” Such compulsive behaviors, and the obsessions to which they are typically linked are what define OCD. Far from merely excessive tidiness, the mental disorder can have a devastating impact on a person’s life. Adam's story illustrates a curious feature of the condition. Sufferers are usually well aware their behavior is irrational but cannot stop themselves from doing whatever it is they feel compelled to do. Advertisement A new study published September 28 in Neuron uses mathematical modeling of decision-making during a simple game to provide insight into what might be going on. The game looked at a critical aspect of the way we perceive the world. Normally, a person's confidence about their knowledge of the surrounding environment guides their actions. “If I think it’s going to rain, I'm going to take an umbrella,” says lead author Matilde Vaghi. The study shows this link between belief and action is broken to some extent in people with OCD. As a consequence, what they do conflicts with what they know. This insight suggests compulsive behaviors are a core feature rather than merely a consequence of obsessions or a result of inaccurate beliefs. © 2017 Scientific America

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 24150 - Posted: 10.05.2017

David Dobbs By the time Nev Jones entered DePaul University's esteemed doctoral program in philosophy, she had aced virtually every course she ever took, studied five languages and become proficient in three, and seemed to have read and memorized pretty much everything. Small and slightly built, with a commanding presence that emerged when she talked, she was the sort of student that sharp teachers quickly notice and long remember: intellectually voracious, relentlessly curious, endlessly capable, and, as one of her high school teachers put it, "magnificently intense." Her mind drew on a well-stocked, seemingly flawless memory with a probing, synthesizing intelligence. With astounding frequency she produced what one doctoral classmate called "genius-level reflections." So Jones grew alarmed when, soon after starting at DePaul in the fall of 2007, at age 27, she began having trouble retaining things she had just read. She also struggled to memorize the new characters she was learning in her advanced Chinese class. She had experienced milder versions of these cognitive and memory blips a couple times before, most recently as she’d finished her undergraduate studies earlier that year. These new mental glitches were worse. She would study and draw the new logograms one night, then come up short when she tried to draw them again the next morning. These failures felt vaguely neurological. As if her synapses had clogged. She initially blamed them on the sleepless, near-manic excitement of finally being where she wanted to be. She had wished for exactly this, serious philosophy and nothing but, for half her life. Now her mind seemed to be failing. Words started to look strange. She began experiencing "inarticulable atmospheric changes," as she put it—not hallucinations, really, but alterations of temporality, spatiality, depth perception, kinesthetics. Shimmerings in reality's fabric. Sidewalks would feel soft and porous. Audio and visual input would fall out of sync, creating a lag between the movement of a speaker's lips and the words' arrival at Jones' ears. Something was off. © 2017 The Social Justice Foundation

Keyword: Schizophrenia
Link ID: 24148 - Posted: 10.05.2017

By JAIME LOWE WHEN I was 16, I was admitted to U.C.L.A.’s neuropsychiatric institute. I’d been suffering from increasing paranoia (I thought war was imminent; I thought I would be called into battle) and lack of sleep (I paced our staircase into the early hours of morning). Most profoundly, I thought my parents were actually secret agents, wearing masks, sent to monitor my behavior. My hallucinations encompassed a wide range of cultural references — Michael Jackson, the Muppets, the Night Stalker, Bob from “Twin Peaks” and the clown from “It.” My parents told the doctors at U.C.L.A. that my behavior had been erratic for two months — I was obsessing over odd things, I wasn’t eating and I was convinced that the end of the world was on its way. In short, I was manic. I was hospitalized for almost a month, and I left the institute with a diagnosis of bipolar disorder. My cure came in the form of three pink pills: 900 milligrams of lithium. It worked when I was on it. But a few years ago, my general practitioner had discovered heart-attack-level blood pressure and high creatinine measures — side effects that I couldn’t feel but were serious enough to warrant a visit to the E.R. As a result of my taking lithium, my kidneys were breaking down — I basically had a 60-year-old’s kidneys in my 37-year-old body. I was given a choice: I could stay on the lithium and get a kidney transplant eventually, or I could switch medication and risk having mania return. I chose to try a new medication. No drug could ever be as cool as lithium, a mysterious element that was present during the Big Bang and lingers throughout the galaxy as primordial stardust. Lithium has a medicinal history that dates to the Greeks and Romans, yet no doctor or researcher knows exactly how or why it works. It just does. It’s on the periodic table of elements, unpatentable and therefore cheap. Depakote, a drug officially approved for bipolar patients in the United States in the mid-1990s, has none of this cachet, and yet it’s known to be as effective as lithium in bipolar cases like mine. So my psychiatrist prescribed it to replace my pink pills. © 2017 The New York Times Company

Keyword: Schizophrenia
Link ID: 24141 - Posted: 10.03.2017