Links for Keyword: Schizophrenia

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By Daniel Bergner Caroline Mazel-Carlton began hearing voices when she was in day care. Mornings, by the time she was in middle school, a bowl of oatmeal awaited her for breakfast next to a white saucer of colorful pills. Her voices remained vibrant. They weren’t within her head; they spoke and screamed from outside her skull. They belonged to beings she could not see. The voice who had been with her longest warned of catastrophes coming for her family in Zionsville, a town north of Indianapolis, calamities tied in some unspecified way to TV images from the gulf war: fighter planes, flashes in the sky, explosions on the ground, luminous and all-consuming. A woman’s voice castigated her at school, telling her that her clothes smelled and that she had better keep her hand down, no matter that she knew the answers to the teacher’s questions. Another voice tracked her every move, its tone faintly mocking. “She’s getting out of bed now; oh, she’s walking down the hall now.” Her mix of psychotropic pills shifted, expanded: antipsychotics, mood stabilizers, an antidepressant, a benzodiazepine for anxiety, a stimulant for attention deficit. The pileup of drugs was typical; people hearing voices or having other hallucinations rarely wind up on just one medication. Multiple chemicals are prescribed, often more than one similar antipsychotic simultaneously, in an attempt to quell the psyche. This article is adapted from “The Mind and the Moon: My Brother’s Story, the Science of Our Brains, and the Search for Our Psyches,” published this month by Ecco. At most, for Mazel-Carlton, the antipsychotics sometimes succeeded in reducing her voices to a wall of sound. This could feel more assaultive than hearing them separately. The antipsychotics caused obesity — 50 pounds of new weight — and the feeling that she was losing control of her forearms and her neck. Her hands quivered and seemed to want to flap-paddle the air. To the isolation caused by the difference of her mind, the drugs added isolation from severe side effects. Her agitation and self-disgust, her terror of being barely human, drove her to twist clusters of her hair around her fingers, to yank hard. Patches of bare scalp crept into view. Classmates taunted, asking why she shook and was going bald, calling her “fat-ass” and “crackhead.” © 2022 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: 28331 - Posted: 05.18.2022

Diana Kwon Susannah Cahalan was 24 years old when her world turned upside down. Cahalan was living a busy life as a news reporter at the New York Post when she suddenly began experiencing sensitivity to light, numbness in her limbs, and an unsettling feeling that something was not quite right in her body and her brain. One day at work, she found herself inexplicably going from crying hysterically to skipping giddily down a hall. After a seizure landed her in the hospital, her condition rapidly worsened. She started having delusions and hallucinations, believing that her father was a murderer, that she was being secretly recorded, and that she could age people using her mind. In a matter of weeks, walking, speaking, and swallowing became difficult. She eventually became immobile and unresponsive, lying in her hospital bed in a catatonic state. Despite her worsening condition, dozens of specialists from various fields—psychiatry, neurology, internal medicine—couldn’t figure out what was wrong. Numerous blood tests and brain scans failed to generate answers. To many who saw her, Cahalan’s condition looked indistinguishable from mental illnesses such as bipolar disorder or schizophrenia, in which people can experience delusions and hallucinations that make it difficult for them to distinguish what’s real and what’s not. It wasn’t until a neurologist asked Cahalan to draw a clock that the problem became clear. Cahalan had drawn all the numbers on just one side of the clock face, indicating that there was a problem in the functioning of one half of her brain. A brain biopsy confirmed what the doctor had suspected. Cahalan had anti-NMDAR encephalitis, a rare autoimmune disease in which the body produces antibodies that attack the NMDA receptor, a protein found throughout the brain. The condition had only been discovered in the early 2000s, just a few years prior to Cahalan’s diagnosis, by neurologist Josep Dalmau, then at the University of Pennsylvania. This diagnosis was much-needed good news for sufferers of the mysterious condition—their disease was treatable. After receiving immunotherapy, Cahalan was able to fully recover. © 1986–2022 The Scientist.

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: 28289 - Posted: 04.20.2022

By Lenny Bernstein Researchers have found variations in a small number of genes that appear to dramatically increase the likelihood of developing schizophrenia in some people. The interplay of a wide array of other genes is implicated for most people with schizophrenia, a severe brain disorder characterized by hallucinations, delusions and inability to function. But for some who possess mutations in the 10 genes identified in the new study, published Wednesday in the journal Nature, the likelihood of developing the disease can be 10, 20 and even 50 times greater. The discovery could one day lead to advances in diagnosis of, and therapy for, the disease, according to the lead author of the study, Tarjinder Singh, of the Broad Institute at MIT and Harvard, which led an effort that involved years of work by dozens of research institutions worldwide. “This is the biological clue that leads to better therapies,” Singh said in an interview. “But the key thing is, we haven’t had any meaningful clues for the longest time.” Ken Duckworth, chief medical officer for the National Alliance on Mental Illness, a nationwide advocacy group, said the study is an important development in the neuroscience that underlies schizophrenia. But he said it is difficult to predict how soon such basic research would pay off for people living with the disease. “This is a big step forward for science that may pay a long-term return for people with schizophrenia and the people who live with them,” Duckworth said. But, he said, “if this is a 17-inning game and they’ve gotten us from the first to the second inning, how does this help someone today?” Less than 1 percent of the U.S. population is believed to have schizophrenia, which is generally treated with an array of powerful antipsychotic medications. The disease reduces life expectancy by about 15 years, according to the new research. Scientists have long recognized a hereditary component to the disease, along with other factors such as environment. The work of isolating these genes could not have been accomplished even 10 or 15 years ago, Singh said, before the sequencing of the human genome and the spread of technology that allows such genetic detective work to be conducted in laboratories around the world. © 1996-2022 The Washington Post

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 13: Memory and Learning
Link ID: 28274 - Posted: 04.09.2022

April Dembosky Most of the time, the voices in Keris Myrick's head don't bother her. They stay in the background or say nice things. But sometimes they get loud and mean – like when a deadly pandemic descended on the world and shut down society as we know it. "It's when things go really, really fast and they seem overwhelmingly disastrous. That's when it happens," says Myrick, who was diagnosed with schizophrenia 25 years ago. "The attacking voices were calling me stupid ... I literally had a meltdown right here in my house. Just lost it." She was able to calm herself down and quiet the voices, and as the pandemic wore on, she kept them at bay by keeping busy: She works for a foundation, hosts a podcast and wrote a children's book. She was able to manage, but she worried about others like her. "People with schizophrenia were not actually deemed as 'the priority vulnerable population' to be served or to be addressed in the same way as people who had other chronic health conditions and who were over a certain age," Myrick says. "So we kind of got left out." This omission occurred even as new data published in JAMA Psychiatry showed that people with schizophrenia are nearly three times more likely to die from COVID-19 than the general population. Their risk of death from the virus is greater than for people with diabetes, heart disease or any other condition aside from age. "People's initial reaction to this was one of disbelief," says Katlyn Nemani, a New York University School of Medicine neuropsychiatrist and the study's lead author. © 2022 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: 28255 - Posted: 03.26.2022

By Karen Brown For decades, Linda Larson has been trying to distance herself from the diagnosis she was given as a teenager: schizophrenia. She accepts that she has the mental disorder but deeply resents the term’s stigma. People hear it and think, “violent, amoral, unhygienic,” she said. Ms. Larson, 74, is part of a group trying to remove that association — by changing the name of the illness. The idea is that replacing the term “schizophrenia” with something less frightening and more descriptive will not only change how the public perceives people with the diagnosis, but also how these people see themselves. Ms. Larson is a member of the Consumer Advisory Board of the Massachusetts Mental Health Center, which is associated with Beth Israel Deaconess Medical Center in Boston. The group has been working with psychiatrists at Harvard to build momentum for a name change, most recently through a national survey published in the journal Schizophrenia Research. “That term over time has become so associated with hopelessness, with dangerousness, with volatile and erratic behavior, that doctors are afraid to use that term with people and their family members,” said Dr. Raquelle Mesholam-Gately, a Harvard psychologist and the lead author of the new paper. “And people who have the condition don’t want to be associated with that name.” As a result, she said, clinicians often avoid making such a devastating diagnosis and many patients and their families don’t seek treatment until after the illness has wreaked considerable damage. Dr. Mesholam-Gately and her team asked about 1,200 people connected to schizophrenia — including those with the disorder, their family members, mental health providers, researchers and government officials — whether it should be called something else. The survey proposed nine alternative names, based partly on the experience of people diagnosed with schizophrenia. Among them: altered perception disorder, attunement disorder, disconnectivity syndrome, integration disorder and psychosis spectrum disorder. © 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: 28124 - Posted: 12.22.2021

by Peter Hess Children born to mothers who take antipsychotic medications during pregnancy do not have elevated odds of autism or attention deficit hyperactivity disorder (ADHD), nor are they more likely to be born preterm or underweight, according to a study released this past Monday in JAMA Internal Medicine. Some women with schizophrenia, Tourette syndrome or bipolar disorder take antipsychotic drugs, such as aripiprazole, haloperidol or risperidone. Clinicians have long debated whether women should discontinue these medications during pregnancy out of concern for the drugs’ effects on the developing fetus. But children born to mothers who take antipsychotics during pregnancy and to those who do not take them have similar outcomes, the new work shows. “Our findings do not support a recommendation for women to discontinue their regular antipsychotic treatment during pregnancy,” says senior investigator Kenneth Man, research fellow at the University College London School of Pharmacy in the United Kingdom. Prescribing antipsychotics during pregnancy can help prevent potentially dangerous psychotic episodes and ensure that an expectant mother can take care of herself, says Mady Hornig, associate professor of epidemiology at Columbia University, who was not involved in the study. “We certainly don’t want to be cavalier about the use of any medication during pregnancy, but one also wants to balance out the implications of not treating.” © 2021 Simons Foundation

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 13: Memory and Learning
Link ID: 27954 - Posted: 08.21.2021

By Jane E. Brody I was doing research and interviews on bipolar disorder when notices appeared in my Brooklyn neighborhood about a 21-year-old man who had been missing for a week. He was described as “bipolar” and “may be experiencing a manic episode.” It took me back nearly seven decades when the state police in Texas called my father to say they had found his brother, my favorite uncle, wandering on a highway. How he got there from Brooklyn we never learned. He had apparently suffered a psychotic break and ended up in a New York State mental hospital that administered electric shock treatments but did little else to help him re-enter society effectively. Not until decades later did he receive a correct diagnosis of manic depression, now known as bipolar disorder. Characterized by extreme shifts in mood, “manic-depressive illness” was officially recognized by the American Psychiatric Association in 1952. But it would be many years before an effective treatment, the drug lithium, which acts on the brain to help stabilize debilitating episodes of severe mania and depression, was available to help my brilliant uncle resume a reasonably normal life. Bipolar disorder typically runs in families, with different members experiencing symptoms to a greater or lesser degree. If a parent has the disorder, a child’s risk can rise to 10 percent. My uncle’s only child displayed some minor behavioral characteristics of bipolar disorder, like very rapid speech and frenetic activity, but was able to complete two advanced degrees, marry, be a parent and succeed in an intellectually demanding career. Bipolar disorder is most often diagnosed in the later teen years or young adulthood, affecting some 4 percent of people at some point in their lives. But in recent decades, diagnosis of the disorder has soared in children and adolescents, although some experts believe the condition is overdiagnosed or overtreated with potent psychiatric drugs. © 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: 27893 - Posted: 07.06.2021

By Diana Kwon Long before the earliest animals swam through the water-covered surface of Earth’s ancient past, one of the most important encounters in the history of life took place. A primitive bacterium was engulfed by our oldest ancestor — a solo, free-floating cell. The two fused to form a mutually beneficial relationship that has lasted more than a billion years, with the latter providing a safe, comfortable home and the former becoming a powerhouse, fueling the processes necessary to maintain life. That’s the best hypothesis to date for how the cellular components, or organelles, known as mitochondria came to be. Today, trillions of these bacterial descendants live within our bodies, churning out ATP, the molecular energy source that sustains our cells. Despite being inextricably integrated into the machinery of the human body, mitochondria also carry remnants of their bacterial past, such as their own set of DNA. The DNA that constitutes the human genome is contained within the nucleus of our cells. But mitochondria possess their own set of circular DNA, which is likely a remnant of their ancient bacterial past. These features make mitochondria both a critical element of our cells and a potential source of problems. Like the DNA inside the nuclei of our cells that makes up the human genome, mitochondrial DNA can harbor mutations. Age, stress and other factors may disrupt mitochondria’s many functions. On top of that, mitochondrial injury can release molecules that, due to their similarities to those made by bacteria, can be mistaken by our immune system as foreign invaders, triggering a harmful inflammatory response against our own cells. © 2021 Annual Reviews, Inc

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 13: Memory and Learning
Link ID: 27863 - Posted: 06.19.2021

By Judith Warner Dr. Benjamin Rush, the 18th-century doctor who is often called the “father” of American psychiatry, held the racist belief that Black skin was the result of a mild form of leprosy. He called the condition “negritude.” His onetime apprentice, Dr. Samuel Cartwright, spread the falsehood throughout the antebellum South that enslaved people who experienced an unyielding desire to be free were in the grip of a mental illness he called “drapetomania,” or “the disease causing Negroes to run away.” In the late 20th century, psychiatry’s rank and file became a receptive audience for drug makers who were willing to tap into racist fears about urban crime and social unrest. (“Assaultive and belligerent?” read an ad that featured a Black man with a raised fist that appeared in the “Archives of General Psychiatry” in 1974. “Cooperation often begins with Haldol.”) Now the American Psychiatric Association, which featured Rush’s image on its logo until 2015, is confronting that painful history and trying to make amends. In January, the 176-year-old group issued its first-ever apology for its racist past. Acknowledging “appalling past actions” on the part of the profession, its governing board committed the association to “identifying, understanding, and rectifying our past injustices,” and pledged to institute “anti-racist practices” aimed at ending the inequities of the past in care, research, education and leadership. This weekend, the A.P.A. is devoting its annual meeting to the theme of equity. Over the course of the three-day virtual gathering of as many as 10,000 participants, the group will present the results of its yearlong effort to educate its 37,000 mostly white members about the psychologically toxic effects of racism, both in their profession and in the lives of their patients. © 2021 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 1: Introduction: Scope and Outlook
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 27797 - Posted: 05.01.2021

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