Links for Keyword: Schizophrenia

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By Pam Belluck Kim Victory was paralyzed on a bed and being burned alive. Just in time, someone rescued her, but suddenly, she was turned into an ice sculpture on a fancy cruise ship buffet. Next, she was a subject of an experiment in a lab in Japan. Then she was being attacked by cats. Nightmarish visions like these plagued Ms. Victory during her hospitalization this spring for severe respiratory failure caused by the coronavirus. They made her so agitated that one night, she pulled out her ventilator breathing tube; another time, she fell off a chair and landed on the floor of the intensive care unit. “It was so real, and I was so scared,” said Ms. Victory, 31, now back home in Franklin, Tenn. To a startling degree, many coronavirus patients are reporting similar experiences. Called hospital delirium, the phenomenon has previously been seen mostly in a subset of older patients, some of whom already had dementia, and in recent years, hospitals adopted measures to reduce it. “All of that has been erased by Covid,” said Dr. E. Wesley Ely, co-director of the Critical Illness, Brain Dysfunction and Survivorship Center at Vanderbilt University and the Nashville Veteran’s Administration Hospital, whose team developed guidelines for hospitals to minimize delirium. Now, the condition is bedeviling coronavirus patients of all ages with no previous cognitive impairment. Reports from hospitals and researchers suggest that about two-thirds to three-quarters of coronavirus patients in I.C.U.’s have experienced it in various ways. Some have “hyperactive delirium,” paranoid hallucinations and agitation; some have “hypoactive delirium,” internalized visions and confusion that cause patients to become withdrawn and incommunicative; and some have both. © 2020 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27336 - Posted: 06.29.2020

Michael Marshall In 2018, psychiatrist Oleguer Plana-Ripoll was wrestling with a puzzling fact about mental disorders. He knew that many individuals have multiple conditions — anxiety and depression, say, or schizophrenia and bipolar disorder. He wanted to know how common it was to have more than one diagnosis, so he got his hands on a database containing the medical details of around 5.9 million Danish citizens. He was taken aback by what he found. Every single mental disorder predisposed the patient to every other mental disorder — no matter how distinct the symptoms1. “We knew that comorbidity was important, but we didn’t expect to find associations for all pairs,” says Plana-Ripoll, who is based at Aarhus University in Denmark. The study tackles a fundamental question that has bothered researchers for more than a century. What are the roots of mental illness? In the hope of finding an answer, scientists have piled up an enormous amount of data over the past decade, through studies of genes, brain activity and neuroanatomy. They have found evidence that many of the same genes underlie seemingly distinct disorders, such as schizophrenia and autism, and that changes in the brain’s decision-making systems could be involved in many conditions. Researchers are also drastically rethinking theories of how our brains go wrong. The idea that mental illness can be classified into distinct, discrete categories such as ‘anxiety’ or ‘psychosis’ has been disproved to a large extent. Instead, disorders shade into each other, and there are no hard dividing lines — as Plana-Ripoll’s study so clearly demonstrated. © 2020 Springer Nature Limited

Related chapters from BN8e: 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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 27235 - Posted: 05.06.2020

By Kelly Servick For the first time in decades, researchers may have a new way to tweak brain signals to treat psychosis and other symptoms of schizophrenia. Results from a 245-person clinical trial hint that a compound called SEP-363856, which seems to act on neural receptors involved in dopamine signaling, might address a broader range of schizophrenia symptoms than currently available drugs do—and with fewer side effects. “If these results are confirmed, this will be big, big news,” says Jeffrey Lieberman, a psychiatrist at Columbia University. The drug’s developer, Sunovion Pharmaceuticals Inc., identified it through an unusual screening process not guided by the brain circuits and receptors already implicated in the disease, Lieberman says. “It was a big gamble on their part. This study suggests that it may pay off.” The biological basis of schizophrenia remains a puzzle, but researchers have linked patients’ hallucinations and delusions to an excess of the chemical messenger dopamine. To inhibit dopamine signaling, existing antipsychotic drugs bind to a type of dopamine receptor on neurons called D2. These drugs help control abnormal perceptions and thoughts—the “positive” symptoms of schizophrenia. But they don’t do much to address either cognitive impairments or the “negative” symptoms, including lack of motivation, dulled emotion, and social withdrawal. “Those negative symptoms are often the most devastating,” says Diana Perkins, a psychiatrist at the University of North Carolina, Chapel Hill. “A person can become, at the most extreme, robotlike.” © 2020 American Association for the Advancement of Science.

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27200 - Posted: 04.16.2020

By Jennifer Szalai Donald Galvin was a sophomore at Colorado State when he first checked into the campus health clinic to get treated for a cat bite, offering no further explanation of what had occurred. Two years and several visits later, he arrived at the clinic with another cat bite — only this time he told a doctor what happened to the cat. “He killed a cat slowly and painfully,” the doctor recorded in his notes. “Doesn’t know why he killed the cat nor why he tormented. Got emotionally upset as he discussed the behavior.” The oldest of 12 siblings, Donald was the first to be told he was schizophrenic. Five of his brothers would eventually get the same diagnosis. Even the healthy children in the Galvin family were beset in a sense, forced to live with an affliction that inevitably shaped their relationships to their parents and to one another. As the journalist Robert Kolker writes in “Hidden Valley Road,” having just one schizophrenic family member is bound to reorient the experiences of everyone else; having six made the Galvins extraordinary, not least to the medical researchers who eventually studied them. Kolker’s previous book, “Lost Girls,” traced the lives of five murdered women on Long Island and told a story of sex work and law enforcement during a time of technological change. His new book is a comparable feat of empathy and narrative journalism, as he coaxes out the struggles of the Galvin family, showing how they embodied the roiling debates over the science of schizophrenia — not just its causes, “but what it actually is.” The Galvin children were all born between 1945 and 1965, during the two decades of the baby boom. It was a time when the psychoanalytic approach to mental illness, with its theory of the cold and domineering “schizophrenogenic mother,” reigned supreme. What began as a more holistic rejoinder to the crude biological reductionism of the early 20th century soon hardened into its own orthodoxy. According to its proponents, mental illness was a disease of nurture, not nature; as one psychiatrist put it, the schizophrenic patient “is always one who is reared by a woman who suffers from a perversion of the maternal instinct.” © 2020 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27161 - Posted: 04.02.2020

Eric Westervelt It's recreation time at a Los Angeles County jail known as the Twin Towers. Nearly a dozen disheveled young men stand docilely as they munch on sandwiches out of brown paper bags. They're half-naked except for sleeveless, thick, blanket-like restraints wrapped around them like medieval garments. All are chained and handcuffed to shiny metal tables bolted to the floor. "It's lunchtime and they're actually [in] programming right now," says a veteran guard, LA County Sheriff's Deputy Myron Trimble. Programming, in theory, means a treatment regimen. But it's difficult to determine what treatment they're actually receiving. A whiteboard nearby tracks how many days since guards on this floor had to forcibly restrain anyone: 54. These inmates haven't been violent, he says. So why are all of the men shackled to tables for recreation? "Just to make sure that they're not walking around," Trimble says. "If they don't take their medications, they could be deemed unpredictable." No one is under the illusion that shackles are helping mentally ill inmates get well. "I think everyone can agree that it's rather inhumane to have the inmate handcuffed while out," says LA Sheriff's Capt. Tania Plunkett, with the Twin Towers' Access to Care Bureau. "However, because of spacing and the lack of programming, we're not able to really focus on getting the inmate better to eventually lead to having them in a program without being handcuffed." New inmates with a mental illness arrive daily in the LA County jail system. It now holds more than 5,000 inmates with a mental illness who've had run-ins with the law. Some 3,000 are held in the jail's Twin Towers. © 2020 npr

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27073 - Posted: 02.26.2020

By Benedict Carey For years, Claire Bien, a research associate at Yale, strained to manage the gossipy, mocking voices in her head and the ominous sense that other people were plotting against her. Told she had a psychotic disorder, she learned over time to manage her voices and fears with a lot of psychotherapy and, periodically, medication. But sometime in late 1990, she tried something entirely different: She began generating her own voices, internal allies, to counter her internal abusers. “I truly felt I was channeling my father, my ancestors, a wise psychiatrist, giving me advice,” said Ms. Bien, who has written a book about her experience, “Hearing Voices, Living Fully.” She added: “Recovery for me means knowing that my mind is my own, and even when it doesn’t feel that way, I know it’s only temporary. Knowing that allows me to hold a job — a good job — and be productive, respected and even admired by the people with whom I work.” Mental-health researchers have numerous scales to track symptom relief, like the easing of depression during talk therapy, for instance, or the blunting of psychotic delusions on medication. But the field has a much harder time predicting, or even describing, what comes next. How do peoples’ lives change once they have learned to address their symptoms? Mental disorders are often recurrent, and treatment only partially effective. What does real recovery — if that’s the right word — actually look like, and how can it be assessed? This is what people in the thick of mental distress desperately want to know, and a pair of articles in a recent issue of the journal Psychiatric Services shows why good answers are so hard to come by. In one, the first study of its kind, Dutch researchers tested a standard life-quality measure, the Recovery Assessment Scale, that is typically used to rate an individual’s confidence, hope, sense of purpose, willingness to ask for help, and other features of a full, stable life. © 2020 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27071 - Posted: 02.25.2020

By Susanne Antonetta Last September, I believed my brain was on fire. Not in some metaphorical way. It was, as far as I was concerned, on fire. I am bipolar and I was hallucinating. My hallucinations can be sensory, like the brain burn, but many are auditory — I know hallucinations are coming when I hear birds speak. I can tell you what the birds say, but what matters is how intensely personal it is, being shouted at by a fierce small crowd: persist persist persist from one, six degrees yes yes yes from another. I couldn’t sleep in all the chatter. Then I heard whispering everywhere, semi trucks coming to a halt right under my bedroom window. A small part of me sensed all this was not really happening, but most of me thought it was. There’s another hallucinatory change that’s harder to describe, one that comes every time, mild episode or intense. The world feels malleable, like felt, or soft paper. Walls rock and steady themselves. What’s around me becomes alive, air itself humming and moving. As with the birds, these changes feel intensely personal — everything around me shifts as I watch. During the six months leading up to this brain-fire time, I’d been having milder hallucinations, on and off. I took a medication that controlled my psychotic symptoms until my cholesterol skyrocketed and kept going up. The drugs used to treat people like me — atypical antipsychotics like Zyprexa and the one I take, Seroquel — have metabolic side effects. These include soaring cholesterol and triglycerides, as well as diabetes. There may be no way out of these side effects except dropping the medication, going, as I did, from one that works to one that doesn’t. Doctors, and the occasional friend, kept telling me something meant to be cheering: “This is just a disease, the same as a broken bone or a bout of pneumonia.” As though my antipsychotic could just as easily be penicillin. I’ve heard this statement in one form or another for several decades, since my diagnosis at age 29. I don’t accept this mechanistic view of the brain, which suggests that if you pump in drugs (at levels often determined by drug company-funded research), the cogs will start working smoothly again. This model dismisses patients’ individual experience of medications, which vary wildly. © 2020 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27067 - Posted: 02.24.2020

Alison Abbott Researchers studying the biological basis of mental illness have conducted the first genomic analysis of schizophrenia in an African population, and have identified multiple rare mutations that occur more frequently in people with the condition. The mutations are mainly in genes that are important for brain development and the brain’s synapses, tiny structures that coordinate communication between neurons. The genes match those identified in other similar studies of schizophrenia — but nearly all previous research has been conducted in European or Asian populations. The latest work was published1 in Science on 31 January. This research is particularly important because Africa has represented a big gap in the populations that geneticists have studied, says psychiatric geneticist Andreas Meyer-Lindenberg, director of the Central Institute of Mental Health in Mannheim, Germany. He says that the work lends support to current hypotheses about the biological origins of schizophrenia, which can cause a range of symptoms including hallucinations, delusions and disordered thinking. Researchers think that each mutation might contribute a small amount to the overall risk of developing the condition, and that disruption to synapses could be crucial to the disease’s development. Over the past decade, as studies that use genome sequencing to identify the genetic basis of diseases have flourished, geneticists have come under increasing fire for failing to sample diverse populations, largely neglecting African people. Around 80% of participants in genetic studies are of European descent, and less than 3% are of African descent. © 2020 Springer Nature Limited

Related chapters from BN8e: 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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 27016 - Posted: 02.04.2020

Hannah Devlin Science correspondent A groundbreaking brain-scanning technique has uncovered evidence that suggests schizophrenia is linked to a loss of connections between brain cells. Scientists had previously suspected a breakdown in the connections between neurons played a role in the condition, based on postmortem studies. The latest research, the first to find evidence for this in the brains of living people, could pave the way for new and better treatment. Prof Oliver Howes from the MRC London Institute of Medical Sciences, Imperial College London and King’s College London, who led the study, said: “Our current treatments for schizophrenia target only one aspect of the disease: the psychotic symptoms. “But the debilitating cognitive symptoms, such as loss of abilities to plan and remember, often cause much more long-term disability and there’s no treatment for them at the moment.” Howes believes the loss of connections, known as synapses, between brain cells, could be responsible for this broader array of symptoms. The study, published in Nature Communications, focused on measuring a protein found in synapses called SV2A, which has been shown to be a good marker of the overall density of connections in the brain. They used a tracer that binds to the protein and which emits a signal that can be picked up by a PET brain scan, which provided an indirect measure of the density of connections. The team scanned 18 adults with schizophrenia and compared them with 18 people without the condition. They found that levels of SV2A were significantly lower in the front of the brain – the region involved in planning – in people with schizophrenia. © 2020 Guardian News & Media Limited

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26964 - Posted: 01.15.2020

By Brooke N. Dulka Glutamate, arguably the most important chemical in your nervous system, is older than the brain itself. From a single cell bacterium, to mushrooms and plants, to you—every living thing on this planet relies on this tiny molecule for cellular communication. It is absolutely critical for everything we do. “The function of most, if not all, of the trillions of cells in the brain are regulated by glutamate,” neuroscientist David Baker explains to me. On November 1, 2019, neuroscientists gathered at the Harley-Davidson Museum in Milwaukee, WI to share their science. The chrome-laden motorcycle in the corner of the room was hard to ignore, but it was the presentation of Baker, a professor at Marquette University, that really caught my attention. Baker has dedicated his career to understanding how glutamate can treat disorders of the brain. Specifically, his hopes for targeting glutamate lie in a mechanism called system xc-. Glutamate is often called the “major excitatory neurotransmitter” within the brain. It is the brain’s “go” signal. Baker notes that glutamate receptors are found in every kind of brain cell, which means it is doing more than regulating the activity of neurons, it is regulating the brain’s support cells too. Glutamate is that widespread and important! But being almost everywhere increases the chances that something, somewhere, could go wrong. Thus, most disorders of the brain involve some degree of glutamate dysfunction. This includes disorders such as schizophrenia, depression, obsessive-compulsive disorder, Alzheimer’s disease and more. While one might think that this awareness provides neuroscientists with critical insights into treating disorders of the brain, actually the opposite has occurred. In fact, most psychiatric drugs weren’t even discovered through systematic drug development, as one might expect. More often than not, the drugs we commonly use today were serendipitous findings or accidental discoveries. Baker notes that almost none of the most commonly prescribed drugs for psychiatric disorders target glutamate. Given the importance of glutamate to nearly every brain function, there is a genuine, and well-reasoned, concern among both neuroscientists and psychiatrists that glutamatergic therapeutics will produce widespread impairments in the brain. © 2020 Scientific American

Related chapters from BN8e: 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: The Biology of Behavioral Disorders
Link ID: 26957 - Posted: 01.14.2020

By Christie Aschwanden When she was 24, Susannah Cahalan developed a sudden psychosis. She grew paranoid — convinced her apartment was infested with bedbugs, that people were spying on her, that her boyfriend was cheating. She started to believe she could age people with her mind. As she recounted in her 2013 bestseller, “Brain on Fire: My Month of Madness,” she received several misdiagnoses (bipolar disorder, schizoaffective disorder) before an alert doctor discovered the true culprit: autoimmune encephalitis. The moment her illness was deemed neurological, ”as in physical, in the body, real,” rather than psychiatric, “in the mind and therefore somehow less real,” the quality of her care drastically improved, Cahalan writes in her new book, “The Great Pretender.” Sympathy and understanding replaced the detached attitude that had defined her treatment as a mental patient, “as if a mental illness were my fault, whereas a physical illness was something unearned, something ‘real,’” she writes. Cahalan, a journalist, recovered from her brief psychosis, but the distinction between physical and mental illness continued to perplex her. “What does mental illness mean, anyway, and why would one affliction be more ‘real’ than another?” she asks. These questions form the backbone of “The Great Pretender.” The book centers on the work of David Rosenhan, a Stanford psychologist whose paper, “On Being Sane in Insane Places,” was an instant sensation when it was published in the journal Science in 1973. The paper begins with a question: “If sanity and insanity exist, how shall we know them?”

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26920 - Posted: 12.27.2019

By Nicholas Bakalar Living with a pet dog in childhood may be linked to a reduced risk of schizophrenia in adulthood. Researchers studied adult patients at Sheppard Pratt Health System in Baltimore, 396 with schizophrenia and 381 with bipolar disorder. They compared them with 594 healthy controls. The participants reported whether they had had a dog or a cat in the household when they were children and, if so, the first and most recent time they had contact with the animal. The findings appeared this month in PLOS One. More than half of the subjects had dogs, and about a third had cats before their 13th birthdays. After adjusting for other characteristics, the scientists found that exposure to a dog at any time in childhood was associated with a 24 percent reduced risk for schizophrenia. Those exposed to dogs at birth were 55 percent less likely to have schizophrenia than people who had not been exposed at all. There was no significant effect of exposure to cats, and no effect of either animal on the risk for bipolar disorder. “We don’t know the mechanism,” said the lead author, Dr. Robert H. Yolken, a professor of pediatrics at Johns Hopkins University in Baltimore, though he noted that the microbiome, or collection of gut bacteria, of people with schizophrenia is different from that of controls. “One possibility is that having a dog in the house causes a different microbiome and changes the likelihood of developing a psychiatric disorder,” he said. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 26911 - Posted: 12.26.2019

By Nick Chrastil In May of 2016, not long after his release from a psychiatric hospital, Colby Crawford, a 23-year old black man, was booked into the Orleans Justice Center (OJC) — a new $150-million-dollar jail opened a year earlier to replace the crumbling and now shuttered Orleans Parish Prison complex, and touted as a symbol of a more progressive approach to incarceration in New Orleans. Ten months later, he was dead. Colby Crawford was diagnosed with schizophrenia, bipolar disorder, and substance use disorder. A lawsuit argues that his death at Orleans Parish jail was in part due to a profound lack of treatment for his mental illness. Visual: Courtesy of the Crawford family. Prior to Crawford’s incarceration, he had been diagnosed with schizophrenia, bipolar disorder, and substance use disorder. A psychiatrist at OJC noted that he was prone to “seeing spirits and ghosts, insomnia, anxiety, paranoia, and bad dreams,” and prescribed an antipsychotic and anticonvulsant. A month after Crawford’s arrest on allegations that he hit his mother and sister, he was transferred about an hour outside of New Orleans to a state prison called the Elayn Hunt Correctional Center — the one place he received adequate mental health care while incarcerated, according to a wrongful death suit filed by his mother. But two months later, Crawford was transferred back to OJC and placed in “disciplinary segregation” for 20 days. Upon release back into the general population, he deteriorated. He stopped taking his medications consistently and started hearing voices and seeing spirits. He couldn’t sleep and got in fights. Jail records cited in the complaint show that medical staff was aware of Crawford’s declining condition. He requested to be moved to a psychiatric tier. He never was.

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26839 - Posted: 11.21.2019

Robin McKie Major psychological disorders such as schizophrenia will continue to affect humans because men and women are continually generating genetic mutations that disrupt brain development. This will be the key conclusion of Professor Sir Michael Owen, director of Cardiff University’s centre for neuropsychiatric genetics and genomics, when he gives the annual Darwin Lecture at the Royal Society of Medicine this week. Understanding such conditions at an evolutionary level will be crucial to developing treatments, Owen believes. Thirty years ago, the new technology of DNA analysis raised hopes that schizophrenia – a condition that can track through families – would soon reveal links to one or two specific genes, said Owen. Treatments might then be relatively easy to develop, it was thought. Instead scientists found that hundreds of genes, each having a tiny effect, dictate whether or not a person will be susceptible to the condition. Characterised by profound behavioural changes, hallucinations, and delusions, these transformations in behaviour can have profound consequences, he added. For example, men with schizophrenia have – on average – only a quarter as many children as males in the general population while women with the condition have about half as many as unaffected females. That low reproduction rate should have had one clear result, Owen told the Observer last week. “Schizophrenia cases should have declined and disappeared long ago as those affected were out bred by those unaffected. This has not happened. A steady level of 1% people continue to be affected.” © 2019 Guardian News & Media Limited

Related chapters from BN8e: 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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 26831 - Posted: 11.19.2019

By Jane E. Brody There‌ are‌ ‌some‌ ‌crimes‌ ‌that‌ ‌are‌ almost‌ ‌impossible‌ ‌to‌ ‌forget. ‌ ‌ For‌ me, ‌they‌ ‌include‌ ‌the‌ ‌death‌ ‌in‌ ‌1999‌ ‌of‌ ‌Kendra‌ ‌Webdale, ‌an‌ ‌aspiring‌ ‌young‌ ‌journalist‌ ‌who‌ ‌was‌ ‌pushed‌ ‌in‌ ‌front‌ ‌of‌ ‌a‌ ‌New‌ ‌York‌ ‌subway‌ ‌train‌ ‌by‌ ‌a‌ ‌29-year-old‌ ‌man‌ ‌with‌ ‌schizophrenia‌ ‌who‌ ‌had‌ ‌stopped‌ ‌taking‌ ‌his‌ ‌medication. ‌That‌ ‌same‌ ‌year, ‌two‌ ‌mentally‌ ‌ill‌ ‌teenage‌‌‌ ‌boys‌ ‌massacred‌ ‌12‌ ‌students‌ ‌and‌ ‌one‌ ‌teacher‌ ‌at‌ ‌Columbine‌ ‌High‌ ‌School‌ ‌in‌ ‌Colorado. ‌ ‌ Thirteen‌ ‌years‌ ‌later, ‌a‌ ‌seriously‌ ‌emotionally‌ ‌disturbed‌ ‌20-year-old‌ ‌man‌ ‌murdered‌ ‌20‌ ‌young‌ ‌children‌ ‌and‌ ‌six‌ ‌adults‌ ‌at‌ ‌Sandy‌ ‌Hook‌ ‌Elementary‌ ‌School‌ ‌in‌ ‌Connecticut. ‌This‌ ‌year, ‌a‌ ‌homeless‌ ‌24-year-old‌ ‌man‌ ‌bludgeoned‌ ‌four‌ ‌men‌ ‌to‌ ‌death‌ ‌while‌ ‌they‌ ‌slept‌ ‌on‌ ‌the‌ ‌streets‌ ‌of‌ ‌my‌ ‌city. ‌ ‌ Although‌ ‌New York is now far‌ ‌safer‌ ‌than‌ ‌when‌ ‌I‌ ‌was‌ ‌a‌ ‌child‌ ‌in‌ ‌the‌ ‌1940s‌ ‌and‌ ‌’50s‌ ‌who‌ ‌walked‌ ‌to‌ ‌and‌ ‌from‌ ‌school‌ ‌unescorted, ‌like‌ ‌most‌ ‌big‌ ‌cities, ‌it still‌ ‌harbors‌ ‌untold‌ ‌numbers‌ ‌of‌ ‌men‌ ‌and‌ ‌women‌ ‌with‌ ‌known‌ ‌or‌ ‌undiagnosed‌ ‌severe‌ ‌mental‌ ‌illness‌ ‌that‌ ‌can‌ ‌and‌ ‌should‌ ‌be‌ ‌treated‌ ‌before‌ ‌yet‌ ‌another‌ ‌personal‌ ‌or‌ ‌societal‌ ‌tragedy‌ ‌occurs. ‌ ‌ What, ‌I‌ ‌wondered, ‌is‌ ‌or‌ ‌can‌ ‌be‌ ‌done‌ ‌to‌ ‌help‌ ‌them‌ ‌and‌ ‌avert‌ ‌further‌ ‌disasters? ‌ ‌ Contrary‌ ‌to‌ ‌politically‌ ‌motivated‌ ‌claims, ‌I‌ ‌learned‌ ‌that‌ ‌people‌ ‌with‌ ‌serious‌ ‌mental‌ ‌ills‌ ‌are‌ ‌not‌ ‌necessarily‌ ‌prone‌ ‌to‌ ‌commit‌ ‌violent‌ acts‌ ‌ — ‌they‌ ‌are‌ ‌far‌ ‌more‌ ‌likely‌ ‌to‌ ‌become‌ ‌‌victims‌‌ ‌of‌ ‌crime. ‌Rather, ‌the‌ ‌issue‌ ‌is‌ ‌that‌ ‌treatments‌ ‌known‌ ‌to‌ ‌be‌ ‌effective‌ ‌are‌ ‌underfunded‌ ‌or‌ ‌wrongly‌ ‌dismissed‌ ‌as‌ ‌ineffective‌ ‌or‌ ‌too‌ ‌dangerous; ‌basic‌ ‌research‌ ‌in‌ ‌university‌ ‌and‌ ‌government‌ ‌laboratories‌ ‌into‌ ‌new‌ ‌and‌ ‌better‌ ‌drugs‌ ‌is‌ ‌limited‌ ‌and‌ ‌also‌ ‌underfunded; ‌and‌ ‌pharmaceutical‌ ‌companies‌ ‌have‌ ‌shown‌ ‌little‌ ‌interest‌ ‌in‌ ‌developing‌ ‌and‌ ‌testing‌ ‌treatments‌ ‌for‌ ‌severe‌ ‌mental‌ ‌illness. ‌ ‌ Also‌ ‌at‌ ‌issue‌ ‌is‌ ‌that, ‌as‌ ‌was‌ true‌ for‌ ‌cancer‌ ‌until‌ ‌recently, ‌acknowledgment‌ ‌of‌ ‌mental‌ ‌illness‌ ‌carries‌ ‌a‌ ‌stigma‌ ‌that‌ ‌impedes‌ ‌its‌ ‌early‌ ‌recognition, ‌when‌ ‌it‌ ‌can‌ ‌be‌ ‌most‌ ‌effectively‌ ‌treated‌ ‌or‌ ‌reversed. ‌ ‌ © 2019 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 26829 - Posted: 11.18.2019

By Kristopher Nielsen Have you ever heard of a condition known as “general paresis of the insane”? Probably not. In the 19th century general paresis was one of the most commonly diagnosed mental disorders. Its symptoms included odd social behaviors, impaired judgment, depressed mood and difficulty concentrating. Around the turn of the 20th century, though, we figured what it really was—a form of late-stage syphilis infecting the brain and disrupting its function. A few decades later we discovered a highly effective treatment: penicillin. Although general paresis is now very rare, its example is still instructive. Any honest researcher will tell you we don’t currently have good explanations for most mental disorders. Depression, obsessive-compulsive disorder, schizophrenia—we don’t really know how these patterns of disrupted thought, behavior and emotion develop or why they stick around. Yet the hope remains that, much like with general paresis, we may soon discover the root causes of these illnesses, and this knowledge may tell us how to treat them. An example of this hope can be seen in the popular notion that a “chemical imbalance” causes depression. This might turn out to be true, but the truth is we don’t know. Some researchers are starting to think that for many mental disorders, such hope might be based on incorrect assumptions. Instead of having one root cause, as general paresis did, mental disorders might be caused by many mechanisms acting together. These mechanisms might be situated in the brain, but they could also be located in the body and even in the external environment, interacting with one another in a network to create the patterns of distress and dysfunction we currently recognize and label as varieties of mental illness. In this more complex view, patterns such as depression and generalized anxiety arise as tendencies in the human brain-body-environment system. Once the patterns are established, they are hard to change because the network continues to maintain them. © 2019 Scientific American

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26815 - Posted: 11.12.2019

By Emily Eakin Ten years ago, Susannah Cahalan was hospitalized with mysterious and terrifying symptoms. She believed an army of bedbugs had invaded her apartment. She believed her father had tried to abduct her and kill his wife, her stepmother. She believed she could age people using just her mind. She couldn’t eat or sleep. She spoke in gibberish and slipped into a catatonic state. Had it not been for an ingenious doctor brought in to consult on her case, Cahalan might well have ended up in a psychiatric ward. Instead, as she recounted in “Brain on Fire,” her best-selling 2012 memoir about her ordeal, she was eventually found to have a rare — or at least newly discovered — neurological disease: anti-NMDA-receptor autoimmune encephalitis. In plain English, Cahalan’s body was attacking her brain. She was only the 217th person in the world to be diagnosed with the disorder and among the first to receive the concoction of steroids, immunoglobulin infusions and plasmapheresis she credits for her recovery. Cahalan’s condition is what in medicine is called a “great pretender”: a disorder that mimics the symptoms of various disorders, confounding doctors and leading them astray. “The Great Pretender” also happens to be the title of Cahalan’s new book, which comes out on Tuesday. It, too, is a medical detective story, only this time at the heart of the mystery is not a patient or a disease but a member of the profession: David Rosenhan, a Stanford psychologist and the author of “On Being Sane in Insane Places,” a landmark 1973 study that, by questioning psychiatrists’ ability to diagnose mental illness, plunged the field into a crisis from which it has still not fully recovered. Cahalan, 34, learned about Rosenhan six years ago, while on tour for the paperback edition of “Brain on Fire.” She was inundated with letters, hundreds a week, from desperate patients and their families, convinced that they too might have a neurological condition masquerading as mental illness. She was haunted by the idea that sheer luck had allowed her to escape a similar fate. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26784 - Posted: 11.02.2019

By Jocelyn Kaiser HOUSTON, TEXAS—Schizophrenia tends to run in families, which suggests it’s largely inherited. But a long-running search for genes underlying this severe psychiatric condition has yielded only indirect clues. Now, by scouring the DNA of tens of thousands of people, gene hunters have for the first time nabbed a handful of rare genes that, when mutated, appear to be direct contributors to the disease—and may shed light on what goes awry in a schizophrenia patient’s brain. “These are concrete genes with mutations with a clear molecular mechanism,” says Mark Daly of the Broad Institute in Cambridge, Massachusetts, and the University of Helsinki, who is principal investigator for a consortium that presented the work last week at the annual meeting of the American Society of Human Genetics (ASHG) here. “It was a fabulous talk,” says Jennifer Mulle of Emory University in Atlanta, who studies the genetics of psychiatric disorders. “We don’t understand anything about the biological pathways [in schizophrenia]. Now, these genes give us an avenue.” People with schizophrenia, which afflicts about 0.7% of the U.S. population, have a distorted sense of reality and confused thinking; they may have hallucinations and delusions. Some patients share similar genetic abnormalities, such as missing specific chunks of DNA, but how those gaps may contribute to disease isn’t known. © 2019 American Association for the Advancement of Science

Related chapters from BN8e: 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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 26756 - Posted: 10.26.2019

Researchers have discovered in mice how one of the few genes definitively linked to schizophrenia, called SETD1A, likely confers risk for the illness. Mice genetically engineered to lack a functioning version of the enzyme-coding gene showed abnormalities in working memory, mimicking those commonly seen in schizophrenia patients. Restoring the gene’s function corrected the working memory deficit. Counteracting the gene’s deficiencies also repaired neuronal circuit deficits in adult mice – suggesting clues for potential treatment strategies. A team of scientists led by Joseph Gogos, M.D., Ph.D., of Columbia University, New York City, reported on their research – supported by the National Institutes of Health – in Neuron. “You could call SETD1A a master regulator,” explained David Panchision Ph.D., of the NIH’s National Institute of Mental Health (NIMH), which co-funded the study. “This schizophrenia risk gene codes for an enzyme that influences the expression of many other genes. In mice, a hobbled version of SETD1A disrupted gene expression in a network harboring other genomic suspects in schizophrenia. Remarkably, the resulting abnormalities were reversible.” Researchers have identified both common and rare genetic variations that contribute to risk for schizophrenia. Mutant SETD1A is one of just a few rare genes known to unequivocally confer risk for schizophrenia. While common genetic variations linked to schizophrenia individually exert only tiny effects on risk, having just one mutant copy of SETD1A is sufficient to confer a large increase in disease risk. SETD1A plays a key role in epigenomic regulation – the switching on-and-off of genes in response to experience – a molecular process widespread in the brain. Mutations in SETD1A have primarily been found in people with schizophrenia, suggesting that this rare gene variation might hold important clues to the underlying disease process.

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26750 - Posted: 10.25.2019

By Liz Eavey My brother Roland’s Facebook post set off a flurry of concern throughout his social network. He’d been assaulted, he wrote, by “old-world mentality Agent Smiths who are threatening our ability to bring natural plant-based Medicine and intelligent health care to the world.” In caps, he told his followers to ALERT THE PRESS AND BRING SIGNS OF PROTEST. The yogis sent positive vibes; the rebels cried fight the man; the good Samaritans offered to jump in their cars and rescue him. Except that Roland hadn’t exactly been assaulted. He’d been placed under an involuntary psychiatric hold and forcibly subdued in an emergency room at the same institution where he was training to become a psychiatrist. And, with that, four years ago, Facebook snitched our big family secret: Roland, the literary prodigy, the tenderhearted musician, the Ivy League grad, was bipolar. Roland — who read and approved this essay — is the effortlessly brilliant middle child who takes up a disproportionate amount of space in a room, with a booming voice and the charisma of a megachurch pastor. After college, he moved to Hollywood and landed, with zero experience or connections, a coveted job with an A-list director. Then, he decided to become a doctor, enrolling in a top-tier M.D./M.B.A. program. Everything about my brother is superlative, including his demons: crippling insomnia, legendary alcoholism and a chemical imbalance that has repeatedly imploded his life. I, the firstborn, am diplomatic and obedient, less concerned with standing out than blending in. Just 17 months apart, Roland and I constantly butted heads trying to assert our individuality growing up. In seventh grade, I wrote “An Older Sister’s Guide to Having Younger Brothers,” which began: “A smart idea, which would prevent use of this guide, would be to just not have younger brothers.” Yet, when we weren’t vying for sibling dominance, we were always looking out for each other. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26652 - Posted: 09.27.2019