Chapter 12. Psychopathology: The Biology of Behavioral Disorders

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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

Keyword: Schizophrenia
Link ID: 26964 - Posted: 01.15.2020

By Eryn Brown On March 30, 1981, 25-year-old John W. Hinckley Jr. shot President Ronald Reagan and three other people. The following year, he went on trial for his crimes. Defense attorneys argued that Hinckley was insane, and they pointed to a trove of evidence to back their claim. Their client had a history of behavioral problems. He was obsessed with the actress Jodie Foster, and devised a plan to assassinate a president to impress her. He hounded Jimmy Carter. Then he targeted Reagan. In a controversial courtroom twist, Hinckley’s defense team also introduced scientific evidence: a computerized axial tomography (CAT) scan that suggested their client had a “shrunken,” or atrophied, brain. Initially, the judge didn’t want to allow it. The scan didn’t prove that Hinckley had schizophrenia, experts said — but this sort of brain atrophy was more common among schizophrenics than among the general population. It helped convince the jury to find Hinckley not responsible by reason of insanity. Nearly 40 years later, the neuroscience that influenced Hinckley’s trial has advanced by leaps and bounds — particularly because of improvements in magnetic resonance imaging (MRI) and the invention of functional magnetic resonance imaging (fMRI), which lets scientists look at blood flows and oxygenation in the brain without hurting it. Today neuroscientists can see what happens in the brain when a subject recognizes a loved one, experiences failure, or feels pain. Despite this explosion in neuroscience knowledge, and notwithstanding Hinckley’s successful defense, “neurolaw” hasn’t had a tremendous impact on the courts — yet. But it is coming. Attorneys working civil cases introduce brain imaging ever more routinely to argue that a client has or has not been injured. Criminal attorneys, too, sometimes argue that a brain condition mitigates a client’s responsibility. Lawyers and judges are participating in continuing education programs to learn about brain anatomy and what MRIs and EEGs and all those other brain tests actually show.

Keyword: Brain imaging; Aggression
Link ID: 26960 - 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

Keyword: Schizophrenia
Link ID: 26957 - Posted: 01.14.2020

By Brooke Siem The prescriptions began in the wake of my father’s sudden death when I was 15: Wellbutrin XL and Effexor XR for anxiety and depression, two separate doses of Synthroid to right a low-functioning thyroid, a morning and nighttime dose of tetracycline for acne, birth control to regulate the unpleasant side effects of womanhood, and four doses of Sucralfate to be taken at each meal and before bedtime — all given to me by the time I was old enough to vote. My general practitioner asked what Sucralfate was after I’d finished rattling off my prescriptive party mix during our first appointment. I was 22 and a recent Manhattan transplant. I had an apartment in Murray Hill and a job waiting tables at a local Italian restaurant. “It’s for something called bile reflux disease,” I said. “I used to randomly puke up bile all the time.” “Huh. Never heard of it.” He ripped off a completed prescription slip and scribbled across the new blank page. “You should really get the prescription for antidepressants from a psychiatrist, but I’ll give it to you along with all the rest since you’ve been on it for so long. And whenever you come back, maybe we should do a physical.” At the time, it never occurred to me that my medication needed monitoring or that perhaps my doctor should do a physical before sending me to the pharmacy. Not only was this five-minute exchange routine, but at no point during my years in the American mental health system did a psychiatrist, psychologist, doctor or pharmacist suggest that I consider reevaluating the decision to take antidepressants. Therefore, I believed that my only choices were to cope with depression or cope with antidepressants, and that depression would always thump inside me with the regularity of my own pulse.

Keyword: Depression; Drug Abuse
Link ID: 26939 - Posted: 01.07.2020

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?”

Keyword: Schizophrenia
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

Keyword: Schizophrenia; Stress
Link ID: 26911 - Posted: 12.26.2019

By Diana Kwon MDMA, or ecstasy, once had the reputation of exclusively being an illicit party drug popular at raves and dance clubs. That view has changed in recent years. The substance, known for its ability to produce feelings of euphoria and affection for others, has developed a new identity as a promising therapeutic tool. Researchers are currently investigating MDMA-assisted therapy as a potential treatment for post-traumatic stress disorder in late-stage clinical trials. The drug’s capacity to enhance sociability has also led to studies investigating its benefits for other conditions, such as social anxiety in individuals with autism spectrum disorder. Despite the promise of its therapeutic benefits, concern persists among some scientists that MDMA could be abused because its pleasurable effects can make it addictive. “By no means [does the drug] have the addictive liability of methamphetamine or certain opioids,” says Robert Malenka, a professor of psychiatry and behavioral sciences at Stanford University. “But it does have abuse potential.” A new study by Malenka and his team suggests it may be possible to circumvent this risk. The findings, published today in Science Translational Medicine, reveal that MDMA’s sociability-enhancing abilities and its pleasurable properties are controlled by distinct pathways in the brain—at least in mice. That insight opens the possibility of developing a safer version of the drug. Previous research by Malenka’s group and others had revealed that MDMA stimulated the release of both serotonin and dopamine in the brain. The existing evidence suggested the drug’s effects on sociability were linked to serotonin and its addictive potential to dopamine, but the extent to which these pathways were distinct was unknown. “Separating out the prosocial from the addictive effects has tremendous implications for drug development,” says Boris Heifets, an anesthesiologist at Stanford and lead author of the latest study. A key question is, “Can we make something with the same kind of prosocial effect that maybe isn’t as prone to abuse?” © 2019 Scientific American

Keyword: Drug Abuse; Depression
Link ID: 26891 - Posted: 12.12.2019

By Andrea Petersen Anne Firmender, 74, was working with her psychologist to come up with a list of her positive attributes. “I cook for others,” said Ms. Firmender. “It’s giving,” encouraged the psychologist, Dimitris Kiosses. “Good kids,” continued Ms. Firmender, who has four grown children and four grandchildren. “And great mother,” added Dr. Kiosses. Ms. Firmender smiled. Dr. Kiosses typed up the list and handed a printout to Ms. Firmender to take home. “When you’re feeling down and hard on yourself, you can remind yourself of your strengths,” he told her. Ms. Firmender, who has a history of mental health problems, was in therapy for depression. But she also has mild cognitive impairment and can have trouble remembering what day it is. So Dr. Kiosses was treating her with a novel approach called Problem Adaptation Therapy, or PATH. The therapy, developed at Weill Cornell Medicine in New York City and White Plains, N.Y., focuses on solving tangible problems that fuel feelings of sadness and hopelessness. It incorporates tools, like checklists, calendars, signs and videos, to make it accessible for people with memory issues. A caregiver is often involved. The approach is one of several new psychotherapies to treat anxiety and depression in people with cognitive impairments, including early to moderate dementia. Another, the Peaceful Mind program, developed by researchers at Baylor College of Medicine and elsewhere for patients with anxiety and dementia, simplifies traditional cognitive behavioral therapy and focuses on scheduling pleasurable activities and skills, like deep breathing. Therapy sessions are short and take place in patients’ homes. A program designed by researchers at University College London gives cards to patients to take home to remind them of key strategies. One that says “Stop and Think” prompts them to pause when they have panicky and unhelpful thoughts to help keep those thoughts from spiraling and creating more anxiety. © 2019 The New York Times Company

Keyword: Alzheimers; Depression
Link ID: 26884 - Posted: 12.09.2019

By Laura Sanders “Does the pill cause depression?” the news headline asked. Prompted by a recent study that described a link between taking birth control pills as a teenager and depression in adulthood, the news got some doctors hopping mad. Early research hints that there are reasons to look more closely at hormonal birth control’s side effects. But so far, the link is less than certain. “This is a premature connection,” says pediatrician Cora Breuner of Seattle Children’s Hospital. Putting too much stock in preliminary evidence may lead to fewer teenagers getting birth control and, in turn, more unwanted pregnancies among teens — a situation that can upend young lives, Breuner says. Headlines that frighten teens, their families and doctors are “yet another barrier in place for accessing a completely effective way to prevent unplanned pregnancies.” Ob-gyn and contraception researcher Katharine O’Connell White agrees. “Birth control gets all of the worry and concern,” says White, of Boston University School of Medicine. “But we know that other things are much more dangerous.” Teen pregnancy, for instance. Access to effective birth control is vital for sexually active teenagers, the doctors say. “I don’t think the evidence is there right now to say that this is a threat,” adds epidemiologist and public health researcher Sarah McKetta of Columbia University, who has studied birth control use in teens. Still, she sees value in more research on the issue. “Women deserve good medication … that’s not giving them problems.” If there are risks that come with the pill, then scientists ought to get a handle on them. © Society for Science & the Public 2000–2019

Keyword: Depression; Hormones & Behavior
Link ID: 26864 - Posted: 12.02.2019

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.

Keyword: Schizophrenia
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

Keyword: Schizophrenia; Genes & Behavior
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

Keyword: Schizophrenia; Aggression
Link ID: 26829 - Posted: 11.18.2019

National Institutes of Health researchers found that a single, low-dose ketamine infusion was relatively free of side effects for patients with treatment-resistant depression. Elia Acevedo-Diaz, M.D., Carlos Zarate, M.D., and colleagues at the NIH’s National Institute of Mental Health (NIMH) report their findings in the Journal of Affective Disorders. Studies have shown that a single, subanesthetic-dose (a lower dose than would cause anesthesia) ketamine infusion can often rapidly relieve depressive symptoms within hours in people who have not responded to conventional antidepressants, which typically take weeks or months to work. However, widespread off-label use of intravenous subanesthetic-dose ketamine for treatment-resistant depression has raised concerns about side effects, especially given its history as a drug of abuse. “The most common short-term side effect was feeling strange or loopy,” said Acevedo-Diaz, of the Section on the Neurobiology and Treatment of Mood Disorders, part of the NIMH Intramural Research Program (IRP) in Bethesda, Maryland. “Most side effects peaked within an hour of ketamine administration and were gone within two hours. We did not see any serious, drug-related adverse events or increased ketamine cravings with a single-administration.” The researchers compiled data on side effects from 163 patients with major depressive disorder or bipolar disorder and 25 healthy controls who participated in one of five placebo-controlled clinical trials conducted at the NIH Clinical Center over 13 years. While past studies have been based mostly on passive monitoring, the NIMH IRP assessment involved active and structured surveillance of emerging side effects in an inpatient setting and used both a standard rating scale and clinician interviews. In addition to dissociative (disconnected, unreal) symptoms, the NIMH IRP assessment examined other potential side effects — including headaches, dizziness, and sleepiness. The study did not address the side effects associated with repeated infusions or long-term use.

Keyword: Depression
Link ID: 26822 - Posted: 11.16.2019

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

Keyword: Schizophrenia; Depression
Link ID: 26815 - Posted: 11.12.2019

Maheen Mausoof Adamson, Ph.D. The 1982 science fiction film classic Blade Runner is a gritty detective story set in the dystopian future that raises questions about what it means to be human. In the film, Harrison Ford plays Rick Deckard, a police officer turned bounty hunter searching the streets of Los Angeles for a replicant (human-like androids) rebellion leader Roy Batty. Batty is presented as a technologically perfected being fitted with a human-template brain completely rewired to create an enemy to be deathly feared. Fear of the perfect altered brain is prominent in science fiction—and may be particularly prevalent today, amid growing concerns about genetic editing and artificial intelligence. The prospect of a fully artificial human brain remains very distant. However, we are in the midst of a neuromodulation revolution that will increase our ability to treat disease and optimize human performance. We must, however, carefully consider the benefits and risks of these techniques in fully evaluating their potential for society as well as the individual. A large number of patients suffering from neurological or psychiatric disorders—depression, pain, and post-traumatic stress disorder among them—are resistant to or can develop resistance to standard medication and psychotherapy, suggesting the need for new approaches. Neuromodulation may possibly be such an approach. The term (aka neurostimulation) refers to direct stimulation and modification of the nervous system through the use of electrical, chemical, or mechanical signals. Neuromodulation therapy is already used to treat many brain disorders, most commonly movement disorders, chronic pain, and depression. © 2019 The Dana Foundation.

Keyword: Parkinsons; Depression
Link ID: 26797 - Posted: 11.07.2019

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

Keyword: Schizophrenia
Link ID: 26784 - Posted: 11.02.2019

Ricardo F. Muñoz I have been convinced of the importance of prevention in addressing mental-health problems since the early 1970s, when I began my doctorate in clinical psychology. But only now is there sufficient evidence from clinical trials of the effectiveness of preventive interventions, using approaches derived from interpersonal and cognitive behavioural therapy, to justify deploying them. And only now are the tools available to make such interventions available to people worldwide. Two recent reports underline this conclusion. In February, the US Preventive Services Task Force, an independent panel of experts in evidence-based medicine, urged clinicians to “provide or refer pregnant and postpartum persons who are at increased risk of perinatal depression to counseling interventions”1. And last month, the US National Academies of Sciences, Engineering, and Medicine (NASEM) released a report2 calling on various stakeholders, from educators to policymakers, to prevent mental-health disorders and to promote healthy mental, emotional and behavioural development in the under 25s. (I was a member of the committees that prepared this document and two previous NASEM reports in 1994 and 2009 on preventive interventions3,4.) The latest NASEM call to action2 is so all-encompassing, it is hard to know where to begin. I propose that initial efforts focus on preventing depression in pregnant women or in women who have recently given birth (perinatal depression). There is substantial evidence for the effectiveness of providing such women with basic skills in mood management5. These interventions could have an impact across generations, because better maternal mental health is linked to babies’ healthier development2. And if researchers and health-care systems were to monitor and compare the epidemiology of depression in thousands of mothers and their children in areas that have or have not deployed preventive interventions, stakeholders could measure their effect on entire communities. © 2019 Springer Nature Limited

Keyword: Depression
Link ID: 26778 - Posted: 11.01.2019

Terry Gross Ever since childhood, author Kevin Wilson has lived with disturbing images that flash through his mind without warning. "I've always had this kind of agitation and looping thoughts and small tics," he says. "Falling off of tall buildings, getting stabbed, catching on fire — they were these just quick, kind of violent bursts in my head." Not that Wilson would ever harm anyone else — the harm in these quick, intrusive thoughts was strictly internal. The images fed off of his own anxiety, and left him feeling terrified. It wasn't until Wilson was diagnosed with Tourette's syndrome as an adult that he began to understand what he was seeing. At first, he was skeptical of the diagnosis; Tourette's is a neurological disorder often characterized by involuntary vocal or motor tics, and Wilson's version wasn't what he'd seen portrayed on TV or in books. "Mine is so much more internal," he says. "Those images and looping tics are in my head. And so a lot of the work that I'm doing is just keeping it in there." One way that Wilson helps control the images is to include them through his writing. His new novel, Nothing to See Here, is about a woman who takes over the care of twin children who burst into flames when they're afraid or angry. "Writing is, I think, the thing that saved me — being able to transfer what was in my head onto the page," he says. "There's this freedom that once it ... goes out into the world and you publish it, you're kind of free of it for a little while — at least it's somebody else's problem." © 2019 npr

Keyword: Tourettes
Link ID: 26774 - Posted: 10.31.2019

By Nicholas Bakalar A healthy diet may help relieve the symptoms of depression. There is good evidence from observational studies that diet can affect mood, and now a randomized controlled trial suggests that healthy eating can modestly improve clinical levels of depression. The study, in PLOS One, randomized 76 college students with poor diet and depression symptoms to two groups. One group was put on a Mediterranean-style diet high in fruits, vegetables, fish, olive oil, nuts and seeds, and low in refined carbohydrates, sugar and saturated fat. The other continued their usual eating habits. At the beginning and end of the three-week trial, all participants were assessed with well-validated scales measuring depression, anxiety, current mood, memory and self-efficacy (confidence in one’s ability to exert control over behavior). Symptoms of depression improved, on average, in the diet group, shifting from the moderate severity range to the normal range. Depressive symptoms among the controls, meanwhile, remained stable, staying within the moderate severity range. On tests of anxiety and stress, the diet group had significantly lower scores than the controls, after controlling for levels of anxiety and stress at the start of the study. There were no differences between the two groups in memory or self-efficacy scores. The study controlled for smoking, physical activity, B.M.I. and other factors. © 2019 The New York Times Company

Keyword: Depression; Obesity
Link ID: 26772 - Posted: 10.31.2019

Sarah Boseley Health editor The use of cannabis medicines to treat people with depression, anxiety, psychosis or other mental health issues cannot be justified because there is little evidence that they work or are safe, according to a major new study. A review of evidence from trials conducted over nearly 40 years, published in the journal Lancet Psychiatry, concludes that the risks outweigh the benefits. And yet, say the authors, they are being given to people with mental health problems in Australia, the US and Canada, and demand is likely to grow. Prof Louisa Degenhardt of the National Drug and Alcohol Research Centre at UNSW Sydney, Australia, lead author of the study, said the findings had important implications in countries where medical use was allowed. “There is a notable absence of high-quality evidence to properly assess the effectiveness and safety of medicinal cannabinoids compared with placebo, and until evidence from randomised controlled trials is available, clinical guidelines cannot be drawn up around their use in mental health disorders,” she said. “In countries where medicinal cannabinoids are already legal, doctors and patients must be aware of the limitations of existing evidence and the risks of cannabinoids. These must be weighed when considering use to treat symptoms of common mental health disorders. Those who decide to proceed should be carefully monitored for positive and negative mental health effects of using medicinal cannabinoids.” © 2019 Guardian News & Media Limited

Keyword: Drug Abuse; Schizophrenia
Link ID: 26769 - Posted: 10.30.2019