Chapter 16. Psychopathology: Biological Basis of Behavior Disorders

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By Casey Schwartz Kay Redfield Jamison arrives punctually at a towering marble statue of Jesus Christ in the entrance of the old hospital building on Johns Hopkins Medical Campus. Next to it, two guest books are left open to receive the wishes and prayers of those who pass through these halls. “Dear God please help our daughter feel better. …” “Dear Lord, please heal my grandpa and let him live happily. …” This building, decorated with rows of oil paintings of Hopkins doctors and nurses through the ages, is redolent of the history of healing. The desperate, uncertain, even heroic attempt to heal is at the center of Jamison’s new book, “Fires in the Dark: Healing the Unquiet Mind,” out on May 23 from Knopf. “If I could have subtitled it ‘A Love Song to Psychotherapy,’ I would have,” she said. Jamison, 76, her blond hair cut into a bob, wears a colorful floral dress as she makes her way through hallways filled with people in scrubs to a quiet corridor reserved for psychiatry. She is the co-director of the Center for Mood Disorders and a professor of psychiatry. Her bookcase displays her many publications: her psychobiography of the poet Robert Lowell, which was nominated for the Pulitzer Prize, and her books on suicide, on exuberance and on the connection between mania and artistic genius. And, of course, her best-known work, “An Unquiet Mind,” a memoir she published in 1995 in which she went public with her own manic depression, at considerable personal cost. Jamison had been a thriving, sporty high school senior in the Pacific Palisades neighborhood of Los Angeles until suddenly, falling into a deep depression after a mild mania, “I couldn’t count on my mind being on my side,” she said. She was bewildered by what she was going through. Her high school English teacher handed her a book of poems by Robert Lowell, who had struggled all his life with manic-depression, and with whom she felt an instant connection. That same teacher also gave her “Sherston’s Progress,” by the English poet Siegfried Sassoon. More than fifty years later, Sassoon’s book would become one of the central inspirations of “Fires in the Dark.” © 2023 The New York Times Company

Keyword: Schizophrenia; Depression
Link ID: 28792 - Posted: 05.23.2023

By Claudia Lopez Lloreda Ketamine is a powerful anesthetic and sometimes recreational drug that causes people to feel dissociated from their own bodies. Recent studies suggest the drug may help treat people with depression who have tried more conventional treatments without success. But there are major questions about what makes it work. Is it the weird dissociative experience? Some molecular effect on the brain? Or just the experience of being in a clinical trial? In a new study that is yet to be peer reviewed, researchers attempted to find the answer in a unique way: They gave volunteers ketamine while they were under general anesthesia, theoretically preventing the participants from going on a trip. The approach alleviated the subjects’ depression, but not any better than a placebo did. The authors interpret this as evidence that ketamine’s effects on depression are strongly tied to a patient’s experience of being seen by medical professionals. But other experts say the study’s implications may be more complicated. Ketamine causes “dissociative” effects such as out-of-body experiences. Patients sometimes also report visual and auditory hallucinations—the voices of friends and family members who aren’t there, for example. The dissociative effects of ketamine have been linked to a stronger antidepressant response, possibly by helping patients reframe their experience from an outside perspective. But it’s a problem for researchers running double-blinded clinical trials, as participants can usually tell whether they have received ketamine or a placebo. To disentangle the subjective experience of ketamine from the biochemical effects of the drug, researchers at Stanford University recruited 40 participants who were preparing to undergo general surgery and who also had mild to moderate depression. The scientists gave the volunteers ketamine or saline as placebo right after they were put under anesthesia, but before their surgery, essentially blinding them to any psychedelic or dissociative effects. Then, for the next 3 days, the researchers surveyed the participants on their depression symptoms, scoring them on such factors as sadness, loss of appetite, and lack of sleep.

Keyword: Depression; Drug Abuse
Link ID: 28789 - Posted: 05.21.2023

Functional neurologic disorder (FND) refers to a group of motor, sensory, or cognitive symptoms caused by an abnormality in how the brain functions. FND is distinct from other neurologic conditions such as epilepsy, stroke, and multiple sclerosis in that there is no overt structural damage in the brain. It's a dysfunction of the connections within the brain (the “software”) rather than the structure of the brain itself (the “hardware”). People with FND can experience involuntary movements, nonepileptic seizures, dizziness, blindness, numbness, fatigue, and pain. Memory and concentration also may be affected. An estimated four to 12 people per 100,000 will develop FND, according to the National Institutes of Health. Risk factors include adverse life experiences, having fibromyalgia or other disorders with no identifiable causes, and physical injury. Some people with FND have experienced abuse or neglect in their lives. FND is more common in women and occurs most frequently in people between the ages of 20 and 50, although adolescents and older people also can develop it. Symptoms can include leg and arm weakness or paralysis; nonepileptic convulsions; tremor; sudden, brief involuntary twitching or jerking of a muscle or group of muscles; tics; involuntary muscle contractions that cause slow, repetitive movements or abnormal postures; problems with walking, posture, or balance; speech or voice difficulties; persistent dizziness; and clouded thinking. To diagnose FND and distinguish it from other neurologic conditions, doctors (generally neurologists or neuropsychiatrists) conduct physical and neurologic examinations and ask questions about the person's health and medical and family histories. To evaluate for potential co-occurring conditions and to assist in developing a treatment plan, doctors also may order imaging scans and perform focused mental health and social history screenings. Other tests, which screen for other neurologic disorders, could include electromyography (to record electrical activity in muscles) and electroencephalography (to monitor the brain's electrical activity).

Keyword: Epilepsy; Muscles
Link ID: 28734 - Posted: 04.12.2023

By Z Paige L’Erario New Research Points to Causes for Brain Disorders with No Obvious Injury A picture of a human brain taken by a positron emission tomography scanner, also called PET scan, is seen on a screen on January 9, 2019, at the Regional and University Hospital Center of Brest in France. Credit: Fred Tanneau/Getty Images “Stop faking!” Imagine hearing those words moments after your doctor diagnosed you with, say, a stroke or a brain tumor. That sounds absurd but for many people diagnosed with a condition called functional neurological disorder (FND), this is exactly what happens. Although the disorder is not well known to many people, FND is actually one of the most common conditions that neurologists like myself encounter. In it, abnormal brain functioning causes symptoms to appear. FND comes in many forms, with symptoms that can include seizures, feelings of weakness and movement disorders. People may lose consciousness or their ability to move or walk. Or they may experience abnormal tremors or tics. It can be highly disabling and just as costly as structural neurological conditions such as amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, multiple sclerosis and Parkinson’s disease. Although men can develop FND, young to middle-aged women receive this diagnosis most frequently. And during the first two years of the COVID pandemic, FND briefly made international headlines when functional tic-like behaviors spread with social media usage, particularly among adolescent girls.

Keyword: Brain imaging; Stress
Link ID: 28725 - Posted: 04.01.2023

By Brian Gallagher One question for Christopher Timmermann, a cognitive neuroscientist at the Centre for Psychedelic Research at Imperial College London, where he leads the DMT Research Group and focuses on the nature of consciousness. What happens to my brain on the psychedelic DMT? The DMT experience is one in which people report going into a different dimension, an alternate reality that feels convincingly real, even more real than this everyday reality. One that has a spiritual significance. In that DMT experience, they sometimes encounter beings. In our latest study we looked at brain scans using fMRI and EEG, and found that this feeling of immersion appears to be underpinned by a dysregulation of the systems in the human brain—in the prefrontal cortex, in the temporal cortices—involved in planning, decision making, and semantics. The way in which we construct meaning, essentially. The brain usually functions in this modular, organized, hierarchical way. You have different networks and systems that crystallize as we grow older. What we see with DMT (specifically N,N-Dimethyltryptamine) is that the systems that generate complex behaviors and tasks stop working in this specialized fashion. They start to work in synchrony with the rest of the brain. The specialization is interrupted. The hierarchy is dysregulated, flattens out. What you have as a result is a more integrated connectivity in the brain. In our day-to-day lives, we have a very good demarcation of what happens inside us versus what happens outside. The sensory areas of the brain that allow us to engage with the external world are very much separated from the reflective areas of the brain that allow us to engage with ourselves. Not on DMT. What we see is that this separation, that usually divides these two poles of organization of the brain, starts to mesh together. The neurons are firing in sync. © 2023 NautilusNext Inc.,

Keyword: Drug Abuse; Depression
Link ID: 28713 - Posted: 03.23.2023

Hannah Devlin Daniela da Silva is feeling good. Lying cocooned under fleece blankets inside a medical scanner, her eyes are closed and her mind is focused and remarkably unperturbed by negative thoughts. Three hours earlier, the 39-year-old yoga teacher and neuroscience student was given a dose of the stimulant drug dextroamphetamine, which is often used to treat ADHD. “I’m having a serotonin increase. Oh definitely,” she predicts before entering the PET scanner. Da Silva is a healthy volunteer in a trial using a pioneering brain imaging technique designed to measure serotonin changes in the brains of living people. Last year, scientists used the scan to obtain what they claimed to be the first direct evidence that serotonin release is blunted in the brains of people with depression. The findings added fuel to a fiercely fought debate over the role of the brain chemical – if any – in depression. Just months earlier, a high-profile scientific review caused a stir when it reached the opposite conclusion that “after a vast amount of research, conducted over several decades, there is no convincing evidence” for the idea that depression is caused by a chemical imbalance in the brain. To many, it was news that the case for serotonin being implicated in depression was not already watertight. The idea of a chemical imbalance is embedded in public consciousness and has shaped the way we view mental illness. The main class of antidepressant drugs, selective serotonin reuptake inhibitors (SSRIs), are widely assumed to work by boosting serotonin levels. So the suggestion that the way we discuss, and treat, mental illness might be based on shaky foundations was disconcerting. But it also served as a wake-up call that this view of depression has failed to provide effective treatments for a substantial proportion of those affected. Serotonin is sometimes referred to as the “happy hormone”, conjuring up the image of a substance that swooshes through the brain leaving a warm glow of contentment in its wake. In reality, its biological role is complex and extends to basic functions like the regulation of sleep, intestinal activity and the formation of blood clots. In the brain, serotonin acts as a chemical messenger between neurons, but also as a form of volume control that alternately increases or decreases the level of communication between other neurons. “Put another way, serotonin fine-tunes the working of the brain, regulating how different parts of the brain communicate with each other,” says Dr James Rucker, a consultant psychiatrist at South London and Maudsley NHS foundation trust, whose research focuses on developing new treatments for depression. © 2023 Guardian News & Media Limited

Keyword: Depression; Emotions
Link ID: 28703 - Posted: 03.15.2023

By Joshua C. Kendall Schizophrenia has long been understood to be among the most serious and intractable of all mental disorders. The condition typically begins in early adulthood and lasts a lifetime. Its hallmark features include hallucinations, withdrawal from social situations, and serious problems in cognition, such as a highly irrational belief system and a limited attention span. In “Malady of the Mind: Schizophrenia and the Path to Prevention,” a comprehensive history of this perplexing mental disorder from the Ancient World to the present, Jeffrey A. Lieberman argues that psychiatry has finally turned a corner in determining both what causes schizophrenia and how to treat it. “Due to the progress and success of science,” he concludes, schizophrenia is “a malady of the mind no more.” BOOK REVIEW — “Malady of the Mind: Schizophrenia and the Path to Prevention,” by Jeffrey A. Lieberman (Simon & Schuster, 528 pages). It’s a bold pronouncement to make, given that Lieberman himself admits that the history of psychiatry is filled with declarations of victory over a disorder that nonetheless continues to defy efforts to pin it down. Several once-heralded treatments — say, insulin coma therapy and ice-pick lobotomies, which were both popular in the 1940s — are now dismissed as barbaric. Likewise, while antipsychotic medications, which were introduced with great fanfare in the mid-1950s and remain today’s treatment of choice, can reduce the intensity of the most troubling symptoms for some patients, they are far from a cure. The chapters on past approaches are elegantly written and are helpful in giving context to current debates about how best to address this devastating illness.

Keyword: Schizophrenia
Link ID: 28690 - Posted: 03.08.2023

By Sujata Gupta Trish Tran narrates her life in staccato notes. “I remember carrying my little sister on my back because she’s too tired and walking through the huge sunflower fields … and me feeling so tired I didn’t think I could walk another step.” “I remember being in a taxi with my mother, coming back to the man who had been violently abusive to all of us…. Her words to me were, ‘Just trust me, Trish. Just trust me.’ ” “I’m waiting at a train station … to meet my mother who I haven’t seen in many years…. Hours pass and eventually I try to call her … and she says to me, ‘I’m sorry, Trish. My neighbor was upset, and I needed to stay back with them.’ And her voice was slurring quite a lot, so I knew she had been drinking.” Tran, who lives in Perth, Australia, is dispassionate as she describes a difficult childhood. Her account lacks what are generally considered classic signs of trauma: She makes no mention of flashbacks, appears to have a generally positive outlook and speaks with relative ease about distressing events. Yet she narrates her life growing up and living in the Australian Outback as a series of disconnected events; her life story lacks connective glue. That disjointed style is not how people, at least people in the West, tend to talk about themselves, says psychologist Christin Camia. Autobiographical accounts, like any good narrative, typically contain a curation of key past experiences, transitions linking those experiences and larger arcs about where life is headed. People use these stories to make sense of their lives, says Camia, of Zayed University’s Abu Dhabi campus in the United Arab Emirates. But a growing body of evidence from fields as wide-ranging as psychology, neuroscience, linguistics, philosophy and literary studies suggests that, as with Tran, trauma can shatter the narrative coherence of one’s life. People lose the plot. © Society for Science & the Public 2000–2023.

Keyword: Stress; Attention
Link ID: 28683 - Posted: 02.25.2023

By McKenzie Prillaman Psychedelics go beneath the cell surface to unleash their potentially therapeutic effects. These drugs are showing promise in clinical trials as treatments for mental health disorders (SN: 12/3/21). Now, scientists might know why. These substances can get inside nerve cells in the cortex — the brain region important for consciousness — and tell the neurons to grow, researchers report in the Feb. 17 Science. Several mental health conditions, including depression and post-traumatic stress disorder, are tied to chronic stress, which degrades neurons in the cortex over time. Scientists have long thought that repairing the cells could provide therapeutic benefits, like lowered anxiety and improved mood. Psychedelics — including psilocin, which comes from magic mushrooms, and LSD — do that repairing by promoting the growth of nerve cell branches that receive information, called dendrites (SN: 11/17/20). The behavior might explain the drugs’ positive outcomes in research. But how they trigger cell growth was a mystery. It was already known that, in cortical neurons, psychedelics activate a certain protein that receives signals and gives instructions to cells. This protein, called the 5-HT2A receptor, is also stimulated by serotonin, a chemical made by the body and implicated in mood. But a study in 2018 determined that serotonin doesn’t make these neurons grow. That finding “was really leaving us scratching our heads,” says chemical neuroscientist David Olson, director of the Institute for Psychedelics and Neurotherapeutics at the University of California, Davis. © Society for Science & the Public 2000–2023.

Keyword: Drug Abuse; Depression
Link ID: 28673 - Posted: 02.18.2023

By Sheryl Gay Stolberg and Ellen Barry Lynn Rivers, a Democrat from Michigan, opened up about her diagnosis with bipolar disorder during a radio call-in show when she first ran for Congress. Her opponents had been hinting she had mental health problems. She decided, spur of the moment, to let it out. “Finally, I just said, ‘Are you asking me if I have depression? Yes, and so do thousands and millions of other people,’” she recalled. “I was like, ‘OK, here we go. The ball is thrown at you, just hit it.’ And so I did.” That was 1994. Ms. Rivers was elected, despite a Republican tidal wave, and served four terms. Now another Democrat, Senator John Fetterman of Pennsylvania, has announced that he has entered a hospital to be treated for clinical depression. Politicians of both parties are praising him for his openness. Mental health experts say he is a powerful symbol — especially for men, who are less likely to seek treatment for depression and suffer higher rates of suicide. Yet the stigma around mental illness remains strong — especially in politics, where questions about temperament can determine a candidate’s electability. Mr. Fetterman and others face a continuing challenge: How much do they really want to say? “We’ve come a long way; people are willing to say they have a diagnosis or that they’re going to therapy,” said Patrick J. Kennedy, a scion of the political Kennedy family, who disclosed his treatment for bipolar disorder and drug abuse when he was a congressman from Rhode Island. “But we’re still not in a place where people are comfortable saying any more than that. And really the question with Senator Fetterman is: How much is he going to disclose?” Clinical depression, also called major depression, is a severe form of the disease. Symptoms may include feelings of sadness, hopelessness or guilt; angry outbursts; loss of pleasure in ordinary activities; fatigue; anxiety; reduced appetite; and thoughts of suicide. In recent years, there have been great strides in treatment. © 2023 The New York Times Company

Keyword: Depression; Stroke
Link ID: 28671 - Posted: 02.18.2023

By Laura Sanders You’d be forgiven for thinking that depression has a simple explanation. The same mantra — that the mood disorder comes from a chemical imbalance in the brain — is repeated in doctors’ offices, medical textbooks and pharmaceutical advertisements. Those ads tell us that depression can be eased by tweaking the chemicals that are off-kilter in the brain. The only problem — and it’s a big one — is that this explanation isn’t true. The phrase “chemical imbalance” is too vague to be true or false; it doesn’t mean much of anything when it comes to the brain and all its complexity. Serotonin, the chemical messenger often tied to depression, is not the one key thing that explains depression. The same goes for other brain chemicals. The hard truth is that despite decades of sophisticated research, we still don’t understand what depression is. There are no clear descriptions of it, and no obvious signs of it in the brain or blood. The reasons we’re in this position are as complex as the disease itself. Commonly used measures of depression, created decades ago, neglect some important symptoms and overemphasize others, particularly among certain groups of people. Even if depression could be measured perfectly, the disorder exists amid myriad levels of complexity, from biological confluences of minuscule molecules in the brain all the way out to the influences of the world at large. Countless combinations of genetics, personality, history and life circumstances may all conspire to create the disorder in any one person. No wonder the science is stuck. So here, up front, is your fair warning: There will be no satisfying wrap-up at the end of this story. You will not come away with a scientific explanation for depression, because one does not exist. But there is a way forward for depression researchers, Aftab says. It requires grappling with nuances, complexity and imperfect data. © Society for Science & the Public 2000–2023.

Keyword: Depression
Link ID: 28670 - Posted: 02.15.2023

By Veronique Greenwood It is the rare person who likes hearing their own voice on a recording. It sounds fake, somehow — like it belongs to someone else. For neuroscientists, that quality of otherness is more than a curiosity. Many mysteries remain about the origins of hallucinations, but one hypothesis suggests that when people hear voices, they are hearing their own thoughts disguised as another person’s by a quirk of the brain. Scientists would like to understand what parts of the brain allow us to recognize ourselves speaking, but studying this using recordings of people’s own voices has proved tricky. When we talk, we not only hear our voice with our ears, but on some level we feel it as the sound vibrations travel through the bones of the skull. A study published Wednesday in the journal Royal Society Open Science attempted a workaround. A team of researchers investigated whether people could more accurately recognize their voices if they wore bone-conduction headphones, which transmit sound via vibration. They found that sending a recording through the facial bones made it easier for people to tell their voices apart from those of strangers, suggesting that this technology provides a better way to study how we can tell when we are speaking. That is a potentially important step in understanding the origins of hallucinated voices. Recordings of our voices tend to sound higher than we expect, said Pavo Orepic, a postdoctoral researcher at the Swiss Federal Institute of Technology who led the study. The vibration of the skull makes your voice sound deeper to yourself than to a listener. But even adjusting recordings so they sound lower doesn’t recreate the experience of hearing your own voice. As an alternative, the team tried using bone-conduction headphones, which are commercially available and often rest on a listener’s cheekbones just in front of the ear. © 2023 The New York Times Company

Keyword: Schizophrenia; Hearing
Link ID: 28669 - Posted: 02.15.2023

ByEmily Underwood When two male mice meet in a confined space, the rules of engagement are clear: The lower ranking mouse must yield. But when these norms go out the window—say, when researchers rig such an encounter to favor the weakling—it sends the higher ranking male into a depressionlike spiral. That’s the conclusion of a new neuroimaging study that reveals how the mouse brain responds to an unexpected loss of social status, which has been shown to be a major risk factor for depression in humans, particularly men. The new study’s approach is “clever and powerful,” says Neir Eshel, a neuroscientist and psychiatrist at Stanford University who wasn’t involved in the work. But he cautions more work is needed to extend the results to our own species. Groups of mice live in hierarchies, both in the lab and the wild. In the lab, though, the highest ranking males form particularly despotic regimes. One or more dominant “alpha mice” will have privileged access to food and females. They can pee wherever they please, rather than in the designated corner reserved for commoners. Hailan Hu, a neuroscientist at the Zhejiang University School of Medicine, wanted to know what would happen in the brains of these mousy muckety-mucks when their pecking order was upended. She and colleagues set up a battle of wills, designed to avoid any actual fighting or bloodshed. Ten times a day, over 4 days, the researchers put a dominant mouse nose-to-nose with a subordinate in a clear, narrow tube. Then they blocked the lower ranked rodent’s exit, leaving it no choice but to advance on its superior. At first, the dominant mice resisted the upstarts and held their ground. But by the fourth day, they were retreating voluntarily from their opponents after only a few seconds. In doing so, the mouse kings also fell in social status and lost their high-ranking perks, including VIP access to a warm nest in the corner.

Keyword: Aggression; Depression
Link ID: 28651 - Posted: 02.01.2023

By Joanna Thompson People often think they know what causes chronic depression. Surveys indicate that more than 80% of the public blames a “chemical imbalance” in the brain. That idea is widespread in pop psychology and cited in research papers and medical textbooks. Listening to Prozac, a book that describes the life-changing value of treating depression with medications that aim to correct this imbalance, spent months on the New York Times bestseller list. The unbalanced brain chemical in question is serotonin, an important neurotransmitter with fabled “feel-good” effects. Serotonin helps regulate systems in the brain that control everything from body temperature and sleep to sex drive and hunger. For decades, it has also been touted as the pharmaceutical MVP for fighting depression. Widely prescribed medications like Prozac (fluoxetine) are designed to treat chronic depression by raising serotonin levels. Yet the causes of depression go far beyond serotonin deficiency. Clinical studies have repeatedly concluded that the role of serotonin in depression has been overstated. Indeed, the entire premise of the chemical-imbalance theory may be wrong, despite the relief that Prozac seems to bring to many patients. If you were still of the opinion that it was simply a chemical imbalance of serotonin, then yeah, it’s pretty damning. A literature review that appeared in Molecular Psychiatry in July was the latest and perhaps loudest death knell for the serotonin hypothesis, at least in its simplest form. An international team of scientists led by Joanna Moncrieff of University College London screened 361 papers from six areas of research and carefully evaluated 17 of them. They found no convincing evidence that lower levels of serotonin caused or were even associated with depression. People with depression didn’t reliably seem to have less serotonin activity than people without the disorder. Experiments in which researchers artificially lowered the serotonin levels of volunteers didn’t consistently cause depression. Genetic studies also seemed to rule out any connection between genes affecting serotonin levels and depression, even when the researchers tried to consider stress as a possible cofactor. All Rights Reserved © 2023

Keyword: Depression; Stress
Link ID: 28647 - Posted: 01.27.2023

Liam Drew The emergence of disease-causing bacteria that are resistant to antibiotics is often attributed to the overuse of antibiotics in people and livestock. But researchers have homed in on another potential driver of resistance: antidepressants. By studying bacteria grown in the laboratory, a team has now tracked how antidepressants can trigger drug resistance1. “Even after a few days exposure, bacteria develop drug resistance, not only against one but multiple antibiotics,” says senior author Jianhua Guo, who works at the Australian Centre for Water and Environmental Biotechnology at the University of Queensland in Brisbane. This is both interesting and scary, he says. Globally, antibiotic resistance is a significant public-health threat. An estimated 1.2 million people died as a direct result of it in 20192, and that number is predicted to climb. Early clues Guo became interested in the possible contributions of non-antibiotic drugs to antibiotic resistance in 2014, after work by his lab found more antibiotic-resistance genes circulating in domestic wastewater samples than in samples of wastewater from hospitals, where antibiotic use is higher. Guo’s group and other teams also observed that antidepressants — which are among the most widely prescribed medicines in the world — killed or stunted the growth of certain bacteria. They provoke “an SOS response”, Guo explains, triggering cellular defence mechanisms that, in turn, make the bacteria better able to survive subsequent antibiotic treatment. © 2023 Springer Nature Limited

Keyword: Depression
Link ID: 28645 - Posted: 01.27.2023

Hannah Devlin Science correspondent Widely used antidepressants cause “emotional blunting”, according to research that offers new insights into how the drugs may work and their possible side-effects. The study found that healthy volunteers became less responsive to positive and negative feedback after taking a selective serotonin reuptake inhibitor (SSRI) drug for three weeks. The “blunting” of negative emotions could be part of how the drugs help people recover from depression, but could also explain a common side-effect. The work’s senior author, Prof Barbara Sahakian of the University of Cambridge, said: “In a way, this may be in part how they work. They take away some of the emotional pain that people who experience depression feel, but unfortunately it seems that they also take away some of the enjoyment.” The findings could help patients make better informed choices about their medication, she said, but added “there is no doubt that antidepressants are beneficial” for many patients. According to the NHS more than 8.3 million patients in England received an antidepressant drug in 2021-22. SSRIs are among the most widely used, and are effective for the majority of, although not all, patients. Some people on the medication report feeling emotionally dull or no longer finding things as pleasurable, with one study suggesting this applied to 40-60% of people taking the drug. However, it has been unclear whether this symptom is a drug side-effect or a symptom of depression. The latest work suggests that the drug alone can produce emotional blunting. In the study, published in the journal Neuropsychopharmacology, 66 volunteers were given either the SSRI drug, escitalopram, or a placebo for at least 21 days before doing a set of cognitive tests. © 2023 Guardian News & Media Limited

Keyword: Depression; Emotions
Link ID: 28641 - Posted: 01.25.2023

By Andrew Jacobs PORTLAND, Ore. — The curriculum was set, the students were enrolled and Oregon officials had signed off on nearly every detail of training for the first class of “magic” mushroom facilitators seeking state certification. But as the four-day session got underway inside a hotel conference room in early December, an important pedagogical tool was missing: the mushrooms themselves. That’s because state officials, two years after Oregon voters narrowly approved the adult use of psilocybin, were still hammering out the regulatory framework for the production and sale of the tawny hallucinogenic fungi. Instead, the students, most of them seasoned mental health professionals, would have to role play with one another using meditation or intensive breathing practices that could lead to altered states of consciousness — the next best thing to the kind of psychedelic trip they would encounter as licensed guides. Not that anyone was complaining. Like many of the two dozen students who paid nearly $10,000 for the course, Jason Wright, 48, a hospital psychiatric nurse in Portland, said he was thrilled to be part of a bold experiment with national implications. “It’s incredible to be on the front lines of something that has the potential to change our relationship with drugs that should never have been criminalized in the first place,” he said. On Jan. 1, Oregon became the first state in the nation to legalize the adult use of psilocybin, a naturally occurring psychedelic that has shown significant promise for treating severe depression, post-traumatic stress disorder and end-of-life anxiety among the terminally ill, among other mental health conditions. © 2023 The New York Times Company

Keyword: Drug Abuse; Depression
Link ID: 28617 - Posted: 01.04.2023

By Sandra G. Boodman The 23-year-old patient arrived in the back of a police car and was in four point restraints — hands and feet strapped to a gurney — when emergency physician Elizabeth Mitchell saw her at a Los Angeles hospital early on March 17. Chloe R. Kral was being held on a 5150, shorthand in California for an emergency psychiatric order that allows people deemed dangerous to themselves or others to be involuntarily confined for 72 hours. She had spent the previous six months at a private treatment center receiving care for bipolar disorder and depression. Chloe had improved and was set to move to transitional housing when she suddenly became combative and threatened to harm staff and kill herself. Police had taken her to the emergency room at Cedars-Sinai Marina del Rey Hospital before a planned transfer to a mental hospital. Chloe, Mitchell recalled, was “mumbling about Rosa Parks” when they met. She managed to tell the doctor that she hadn’t used drugs or alcohol, but was otherwise incoherent. “We get a lot of psychiatric patients, and they’re just waiting for placement,” Mitchell said. But something indefinable — Mitchell characterized it as “maybe gut instinct” honed by nearly two decades of practice — prompted her to order a CT scan of Chloe’s head to better assess her mental status. When she pulled up the image, Mitchell gasped. “I had never seen anything like it,” she said. She rounded up her colleagues and “made everyone in the whole ER come look.” “I was speechless,” she said. “All I could think was ‘How did no one figure this out?’ ”

Keyword: Depression; Schizophrenia
Link ID: 28603 - Posted: 12.21.2022

By Ellen Barry BETHESDA, Md. — The psychiatrist E. Fuller Torrey is 85 years old and has Parkinson’s disease, the tremors at times so strong that his hand beats like a drum on the table. Still, every morning when he reads the newspapers, he looks for accounts of violent behavior by people with severe mental illness, to add to an archive he has maintained since the 1980s. His records include reports of people who, in the grip of psychosis, assaulted political figures or pushed strangers into the path of subway trains; parents who, while delusional, killed their children by smothering, drowning or beating them; adult children who, while off medication, killed their parents with swords, axes or hammers. Dr. Torrey, who has done pioneering research into the biological basis of schizophrenia, has used these stories in service of an argument: that it was a mistake for the United States to shut down its public psychiatric hospitals without adequate follow-up care. And that to remedy this, the government should create systems to compel seriously mentally ill people in the community to get treatment. For much of his career, Dr. Torrey was a lonely voice on this issue, disavowed by patient advocacy groups and by organized psychiatry. But his ideas are now animating major policy shifts, including the announcement by Mayor Eric Adams of New York last month that city officials would send people with untreated mental illnesses to hospitals, even if they posed no threat to others. Dr. Torrey’s influence on New York City’s policy is profound. The mayor’s adviser on this matter is Brian Stettin, who was thrust into mental health policy in 1999 when, as a lawyer in the office of Attorney General Eliot Spitzer of New York, he was asked to draft Kendra’s Law, named for a woman who was pushed in front of a subway train by a man with schizophrenia. The law allows a court to order a person with mental illness to comply with an outpatient treatment plan, risking involuntary commitment if the person refuses. © 2022 The New York Times Company

Keyword: Schizophrenia
Link ID: 28593 - Posted: 12.13.2022

By Ingrid Wickelgren  Recurrent intrusive memories lie at the heart of certain mental illnesses, including post-traumatic stress disorder and obsessive-compulsive disorder. Clinicians often treat these conditions with “exposure therapy.” They gradually and gently re-expose patients to feared stimuli or simulations—from reminders of active combat to germs on a toilet—teaching the brain to become accustomed to the stimuli and to decouple them from danger. But exposure therapy has drawbacks. “Facing these traumatic memories is painful to patients,” says Yingying Wang, a cognitive psychologist at Zhejiang University in China. “These treatments suffer from a very high dropout rate.” Wang and her colleagues have taken a first step toward developing a more benign way to dim traumatic memories. Their proof-of-concept study involves subliminal exposure to cues to those memories after putting the brain in a state in which it is likely to forget. The new findings present a new spin on a form of active forgetting in which people learn to suppress memories by practicing not thinking about them in the presence of reminders. In various studies, participants have memorized pairs of words such as needle-doctor or jogger-collie and then practiced either thinking or not thinking about the second word when the first word (the reminder) appears. Practicing not thinking about the second word has led to forgetting. The mechanism for this effect centers on the brain’s main memory hub, the hippocampus. Psychologists have discovered that suppressing memory retrieval puts the hippocampus in a degraded functional state. This state lasts for a small window of time—at least 10 seconds but potentially much longer—casting what researchers have dubbed an “amnesic shadow” that leads to poor memory for other things that happen within it. So when people suppress neutral word pairs, they put their brain into a state in which they are likely to forget new experiences. © 2022 Scientific American,

Keyword: Stress; Learning & Memory
Link ID: 28586 - Posted: 12.10.2022