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Jon Hamilton A study of mice that hear imaginary sounds could help explain human disorders like schizophrenia, which produce hallucinations. D-Keine/Getty Images A technique that induces imaginary sounds in both mice and people could help scientists understand the brain circuits involved in schizophrenia and other disorders that cause hallucinations. The technique appears to offer "a way to study psychotic disorders in animals," says Adam Kepecs, a professor of neuroscience and psychiatry at Washington University School of Medicine in St. Louis. It also shows how levels of the brain chemical dopamine determine the likelihood that a mouse or a person will perceive something that isn't really there, Kepecs and a team report in this week's issue of the journal Science. Until now, scientists have had no good way to study precisely how hallucinations occur in the brain. "This study is valuable because it will allow us to use mice and dig into the cellular, molecular, physiological details," says Eleanor Simpson, a researcher at the New York State Psychiatric Institute. That's important, Simpson says, because it could lead to better treatments for disorders like schizophrenia. "We have drugs that treat hallucinations but they're not very good," she says. "They don't work for everybody and they have a lot of terrible side effects which prevent people from using them." The study came about because "a mouse can't tell you when it's hallucinating," Kepecs © 2021 npr

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 9: Hearing, Balance, Taste, and Smell
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 27758 - Posted: 04.03.2021

By Pam Belluck Ivan Agerton pulled his wife, Emily, into their bedroom closet, telling her not to bring her cellphone. “I believe people are following me,” he said, his eyes flaring with fear. He described the paranoid delusions haunting him: that people in cars driving into their suburban Seattle cul-de-sac were spying on him, that a SWAT officer was crouching in a bush in their yard. It was a drastic change for the 49-year-old Mr. Agerton, a usually unflappable former marine and risk-taking documentary photographer whose most recent adventure involved exploring the Red Sea for two months in a submarine. He was accustomed to stress and said that neither he nor his family had previously experienced mental health issues. But in mid-December, after a mild case of Covid-19, he was seized by a kind of psychosis that turned life into a nightmare. He couldn’t sleep, worried he had somehow done something wrong, suspected ordinary people of sinister motives and eventually was hospitalized in a psychiatric ward twice. “Like a light switch — it happened this fast — this intense paranoia hit me,” Mr. Agerton said in interviews over two months. “It was really single-handedly the most terrifying thing I’ve ever experienced in my life.” Mr. Agerton’s experience reflects a phenomenon doctors are increasingly reporting: psychotic symptoms emerging weeks after coronavirus infection in some people with no previous mental illness. Doctors say such symptoms may be one manifestation of brain-related aftereffects of Covid-19. Along with more common issues like brain fog, memory loss and neurological problems, “new onset” psychosis may result from an immune response, vascular issues or inflammation from the disease process, experts hypothesize. Sporadic cases have occurred with other viruses, and while such extreme symptoms are likely to affect only a small proportion of Covid survivors, cases have emerged worldwide. © 2021 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27740 - Posted: 03.23.2021

By Pam Belluck Almost immediately, Dr. Hisam Goueli could tell that the patient who came to his psychiatric hospital on Long Island this summer was unusual. The patient, a 42-year-old physical therapist and mother of four young children, had never had psychiatric symptoms or any family history of mental illness. Yet there she was, sitting at a table in a beige-walled room at South Oaks Hospital in Amityville, N.Y., sobbing and saying that she kept seeing her children, ages 2 to 10, being gruesomely murdered and that she herself had crafted plans to kill them. “It was like she was experiencing a movie, like ‘Kill Bill,’” Dr. Goueli, a psychiatrist, said. The patient described one of her children being run over by a truck and another decapitated. “It’s a horrifying thing that here’s this well-accomplished woman and she’s like ‘I love my kids, and I don’t know why I feel this way that I want to decapitate them,’” he said. The only notable thing about her medical history was that the woman, who declined to be interviewed but allowed Dr. Goueli to describe her case, had become infected with the coronavirus in the spring. She had experienced only mild physical symptoms from the virus, but, months later, she heard a voice that first told her to kill herself and then told her to kill her children. At South Oaks, which has an inpatient psychiatric treatment program for Covid-19 patients, Dr. Goueli was unsure whether the coronavirus was connected to the woman’s psychological symptoms. “Maybe this is Covid-related, maybe it’s not,” he recalled thinking. “But then,” he said, “we saw a second case, a third case and a fourth case, and we’re like, ‘There’s something happening.’” Indeed, doctors are reporting similar cases across the country and around the world. A small number of Covid patients who had never experienced mental health problems are developing severe psychotic symptoms weeks after contracting the coronavirus. In interviews and scientific articles, doctors described: A 36-year-old nursing home employee in North Carolina who became so paranoid that she believed her three children would be kidnapped and, to save them, tried to pass them through a fast-food restaurant’s drive-through window. © 2020 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27639 - Posted: 12.31.2020

Viviana Gradinaru Despite the wealth and quality of basic neuroscience research, there is still little we can do to treat or prevent most brain disorders. Industry efforts, meanwhile, have shied away from this field, particularly after a series of major drug candidates for the treatment of Alzheimer's disease failed to meet expectations (1). My previous research, which entailed developing and using optogenetics (2, 3) to understand how deep brain stimulation works in Parkinson's disease (PD) (4, 5), resulted in two key insights: We need to look and intervene earlier in brain disease progression, and we need to be able to access relevant cell populations with noninvasive yet precise tools to investigate, prevent, contain, or even reverse the course of disease. Accumulating evidence has highlighted a third insight: We may need to look beyond the brain to fully understand brain disorders (6, 7). My goal has been to develop an effective toolkit for neuromodulation so we can start to bridge the gap between what we know and what we can do to treat the brain. To achieve minimally invasive optogenetic-mediated modulation, we need to be able to penetrate the blood–brain barrier (BBB) so that vectors can be delivered systemically rather than through intracranial injections and address the poor reach of visible light through tissue so that large tissue volumes can be recruited without implantation of optical fibers. For early intervention, we need to get past the neuronal and brain-centric view of neurological disease. © 2020 American Association for the Advancement of Science

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27407 - Posted: 08.08.2020

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 BN: 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 BN: 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 4: Development of the Brain
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 BN: 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 BN: 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 BN: 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 BN: 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 BN: 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 BN: 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 4: Development of the Brain
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 BN: 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 BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 3: 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 BN: 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 BN: 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 BN: 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 BN: 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 4: Development of the Brain
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 BN: 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 BN: 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