Chapter 12. Psychopathology: The Biology of Behavioral Disorders

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 2908

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

Keyword: Schizophrenia
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

Keyword: Schizophrenia; Depression
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

Keyword: Schizophrenia
Link ID: 27067 - Posted: 02.24.2020

Dominique Sisley Nothing is quite as shattering as a broken heart. A bad breakup has been known to trigger a range of psychological and physical symptoms, from nausea and insomnia to clinical depression. In more extreme scenarios, broken heart syndrome – when a person’s heart stops pumping blood properly after an emotional shock – can lead to death. Fortunately, recent breakthroughs suggest we may soon be able to beat it. In March, a Spanish study found propofol, a sedative used for anaesthesia, may also be able to mute the painful memories that come with heartbreak. Participants were injected with the drug immediately after recalling a distressing story and, when asked to recount it again 24 hours later, they found the memory to be less vivid. Advertisement The principal goal of the research was to relieve the symptoms of post-traumatic stress disorder (PTSD), but it seems there may be scope for the drug to be used to suppress other upsetting memories. An unexpected loss such as heartbreak can also be traumatic, and some people report similar symptoms. Dr Bryan Strange, who led the study, says: “Combining anaesthesia with evoking an emotionally charged memory impairs its subsequent recall. We will need to derive a set of criteria that identify people for whom it works well, and where the benefit justifies the risk of anaesthesia. There may well be those for whom heartbreak is so distressing that the criteria is fulfilled.” In the past year, a wave of apps such as Mend, Rx Breakup and Break-Up Boss have been released, promising guidance, advice and distracting activities to help soothe the pain of heartbreak. It is a lofty promise, but one that appears to be rooted in logic: a study in 2017 found similar brain-training style exercises could help curb embarrassing or impulsive post-breakup behaviour and strengthen self-control. © 2020 Guardian News & Media Limited

Keyword: Depression; Sexual Behavior
Link ID: 27066 - Posted: 02.24.2020

By Jade Wu 3 Anxiety-Related Disorders You Might Not Know About Person suffering from trichotillomania, an obsessive compulsive condition where sufferers can't resist pulling their hair out. Credit: Ryan Jackson Getty Images Most people know what it’s like to feel anxious. That tension in your muscles, those butterflies in your stomach, and the drumming of your heart tells you that you’re not calm. And this is totally normal. Where would we be if genuinely dangerous situations like dark alleys at night didn’t give us the heebie-jeebies? And would we take important tasks very seriously if we didn’t get nervous in the spotlight, like when giving a wedding toast? Sometimes, anxiety goes too far and gets in the way of our everyday functioning. It can mess up our health, relationships, work, and fun. It’s not hard to imagine the pain of being plagued by non-stop worries or feeling so shy as to have trouble with dating. But sometimes, anxiety and anxiety-related processes can show up in more unusual ways, even ways that don’t seem at first to have anything to do with emotions. The Diagnostic and Statistics Manual - 5th Edition is the official American Psychiatric Association’s list of psychological disorders. It’s a huge bible detailing everything that’s considered a disorder and how it’s categorized. It takes experts years to update it in response to ongoing scientific findings. Advertisement The Anxiety Disorders section got a big makeover in the last update, which came out in 2013. It’s now split into a few different sections, including Trauma and Stress-Related Disorders and Obsessive-Compulsive Disorders. Some of the less common disorders got shuffled around, some got new names, but experts still agree that the line between categories is blurry at best. Overlapping and related to some of the most common anxiety disorders, such as generalized anxiety disorder and social anxiety disorder, are some that are less well-known.

Keyword: Stress; Emotions
Link ID: 27041 - Posted: 02.14.2020

Jon Hamilton Scientists have taken a small step toward personalizing treatment for depression. A study of more than 300 people with major depression found that brain wave patterns predicted which ones were most likely to respond to the drug sertraline (Zoloft), a team reported Monday in the journal Nature Biotechnology. If the approach pans out, it could offer better care for the millions of people in the U.S. with major depression. "This is definitely a step forward," says Michele Ferrante, who directs the computational psychiatry and computational neuroscience programs at the National Institute of Mental Health. He was not a part of the study. Right now, "one of our great frustrations is that when a patient comes in with depression we have very little idea what the right treatment for them is," says Dr. Amit Etkin, an author of the study and a professor of psychiatry at Stanford University. "Essentially, the medications are chosen by trial and error." Etkin is also the CEO of Alto Neuroscience, a Stanford-backed start-up developing computer-based approaches to diagnosing mental illness and selecting treatments. In the study, researchers used artificial intelligence to analyze the brainwave patterns in more than 300 patients who'd been diagnosed with major depression. Then they looked to see what happened when these same patients started treatment with sertraline. And one pattern of electrical activity seemed to predict how well a patient would do. "If the person scores particularly high on that, the recommendation would be to get sertraline," Etkin says. © 2020 npr

Keyword: Depression
Link ID: 27034 - Posted: 02.11.2020

Catherine Offord The first time Kees van Heeringen met Valerie, the 16-year-old girl had just jumped from a bridge. It was the 1980s and van Heeringen was working as a trainee psychiatrist at the physical rehabilitation unit at Ghent University Hospital in Belgium. As he got to know Valerie, who’d lost both legs in the jump and spent several months at the hospital, he pieced together the events leading up to the moment the teenager tried to end her life, including stressful interactions with people around her and a steady accumulation of depression symptoms. Van Heeringen, who would later describe the experience in his 2018 book The Neuroscience of Suicidal Behavior, says Valerie’s story left a permanent impression on him. “I found it very difficult to understand,” he tells The Scientist. He asked himself why anyone would do “such a horrible thing,” he recalls. “It was the first stimulus for me to start studying suicidal behavior.” In 1996, van Heeringen founded the Ghent University Unit for Suicide Research. He’s been its director ever since, helping to drive scientific research into the many questions he and others have about suicide. Many of the answers remain as elusive as they seemed that day in the rehabilitation unit. Suicide rates are currently climbing in the US and many other countries, and suicide is now the second leading cause of death among young people globally, after traffic accidents. The World Health Organization recently estimated that, worldwide, one person ends their own life every 40 seconds. © 1986–2020 The Scientist.

Keyword: Depression
Link ID: 27032 - Posted: 02.11.2020

By Chris Woolston Sometimes it takes multitudes to reveal scientific truth. Researchers followed more than 7,000 subjects to show that a Mediterranean diet can lower the risk of heart disease. And the Women’s Health Initiative enlisted more than 160,000 women to show, among other findings, that postmenopausal hormone therapy put women at risk of breast cancer and stroke. But meaningful, scientifically valid insights don’t always have to come from studies of large groups. A growing number of researchers around the world are taking a singular approach to pain, nutrition, psychology and other highly personal health issues. Instead of looking for trends in many people, they’re designing studies for one person at a time. A study of one person — also called an N of 1 trial — can uncover subtle, important results that would be lost in a large-scale study, says geneticist Nicholas Schork of the Translational Genomics Research Institute in Phoenix. The results, he says, can be combined to provide insights for the population at large. But with N of 1 studies, the individual matters above all. “People differ at fundamental levels,” says Schork, who discussed the potential of N of 1 studies in a 2017 issue of the Annual Review of Nutrition. And the only way to understand individuals is to study them. Case studies of individuals in odd circumstances have a long history in medical literature. But the concept of a clinical medicine N of 1 study gathering the same level of information as a large study goes back to an article published in the New England Journal of Medicine in 1986. Hundreds of N of 1 studies have been published since then, and the approach is gaining momentum, says Suzanne McDonald, N of 1 research coordinator at the University of Queensland in Brisbane, Australia.

Keyword: Genes & Behavior; Schizophrenia
Link ID: 27027 - Posted: 02.10.2020

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

Keyword: Schizophrenia; Genes & Behavior
Link ID: 27016 - Posted: 02.04.2020

Rhitu Chatterjee One in seven women experiences depression during or after pregnancy. The good news is that perinatal depression is treatable. Here are five things to know about perinatal depression, its symptoms and treatment options. Loveis Wise for NPR Shortly after she gave birth to her son last May, Meghan Reddick, 36, began to struggle with depression. "The second I had a chance where I wasn't holding [my son], I would go to my room and cry," says Reddick, who lives with her son and husband. "And I probably couldn't count how many hours a day I cried." Reddick is among the many women who suffer from depression during pregnancy and after childbirth. "There's this kind of myth that women couldn't possibly be depressed during pregnancy, [that] this is such a happy time," says Jennifer Payne, a psychiatrist and the director of the Women's Mood Disorders Center at Johns Hopkins University. "The reality is that a lot of women struggle with anxiety and depression during pregnancy as well as during the postpartum period." An estimated one in seven women experiences depression during or after pregnancy. Among some groups, such as teenage moms and women with a history of trauma, the rate can be even higher. Left untreated, depression during this time can have serious consequences on the health of the mother, the baby and the entire family. © 2020 npr

Keyword: Depression; Sexual Behavior
Link ID: 27005 - Posted: 01.29.2020

A fast acting ketamine-like anti-depressant spray that can lift mood within hours has been rejected by the NHS healthcare watchdog. The National Institute for Health and Care and Excellence (NICE) says there are too many uncertainties about the correlation between the price and clinical benefits of esketamine. It is licensed as a therapy for people with hard-to-treat depression. But it costs about £10,000 per patient for a single course of treatment. Mixed reactions Some people already prescribed it - as part of a trial, for example - will be able to continue on the treatment if their doctor says it is appropriate to do so, the NICE's draft recommendation for England and Wales says. Scotland is yet to issue guidance. Experts have expressed mixed reactions to NICE's decision. Dr Sameer Jauhar, at the Institute of Psychiatry, Psychology and Neuroscience, King's College London, said NICE had made the call because there was not yet enough long-term evidence to support the use of nasal esketamine alongside another anti-depressant. Consultant psychiatrist Dr Paul Keedwell, at Cardiff University, said patients would be disappointed by a decision based largely on cost rather than lack of effectiveness. Marjorie Wallace, chief executive of mental health charity Sane, said: "People with depression are currently relying on medications that are 30 years old. "Although these drugs can be life-saving for some people, they can have unpleasant side-effects and do not work for everyone. "It is therefore deeply disappointing that the first new compound that works in a fundamentally different way on the brain should not have passed this hurdle. "This is especially so because people can take as much as six to eight weeks to feel the full effects of most anti-depressants. "We hope this setback will serve only to inspire pharmaceutical companies, researchers and others to discover new ways of treating serious depression." Recreational misuse Ketamine is used in medicine to numb the body or induce sleep and sometimes prescribed for depression. © 2020 BBC.

Keyword: Depression; Drug Abuse
Link ID: 27004 - Posted: 01.29.2020

By Laura Sanders After taking a compound found in magic mushrooms, people with cancer had less anxiety and depression, even years later, a new study suggests. The evidence isn’t strong enough yet to pin these lasting improvements on the hallucinatory episode itself, as opposed to other life changes. But the findings leave open the possibility that the compound, called psilocybin, may be able to profoundly reshape how people handle distress and fear (SN: 9/26/06). Research published in 2016 suggested that a dose of psilocybin in combination with therapy could quickly ease anxiety and depression in people with cancer. But scientists wanted to know whether these effects lasted. Surveys conducted about three and 4½ years after the psilocybin dose showed that a majority of the 15 people still had fewer signs of anxiety and depression compared with before they took the compound, the team reports January 28 in the Journal of Psychopharmacology. (By the second follow-up, about a third of the participants still had active cancer; the rest were in partial or complete remission.) All the participants said they had “moderate,” “strong” or “extreme” positive changes in their behavior that they attribute to their experience, which many described as one of the most personally meaningful events of their lives. © Society for Science & the Public 2000–2020

Keyword: Depression; Drug Abuse
Link ID: 27003 - Posted: 01.29.2020

By Nicholas Bakalar People with depression are at increased risk for dementia, researchers report, and the risk may persist for decades. Using the Swedish National Patient Register, scientists identified 119,386 people over 50 with depression and matched them with an equal number of people without that diagnosis. Dementia developed in 5.7 percent of those with depression, compared to only 2.6 percent of those without depression, over an average follow-up of more than 10 years. Those with depression were more than 15 times as likely to develop dementia in the first six months after their depression diagnosis as their peers who were not depressed. That rate decreased rapidly but was still evident after 20 years. The researchers also studied 25,322 sibling pairs older than 50 in which one sibling had depression and the other did not. A sibling with a depression diagnosis was more than 20 times as likely as his brother or sister without depression to be diagnosed with dementia in the first six months after the diagnosis. Again, the risk declined over time, but persisted for more than 20 years. The study is in PLOS Medicine. “This is an observational study that does not prove causation,” said the lead author, Peter Nordstrom, a professor of geriatrics at Umea University in Sweden. “If you are diagnosed with depression, that doesn’t mean that you are bound to have dementia.” © 2020 The New York Times Company

Keyword: Depression; Alzheimers
Link ID: 26988 - Posted: 01.24.2020

Edward Bullmore Unlikely as it may seem, #inflammation has become a hashtag. It seems to be everywhere suddenly, up to all sorts of tricks. Rather than simply being on our side, fighting infections and healing wounds, it turns out to have a dark side as well: the role it plays in causing us harm. It’s now clear that inflammation is part of the problem in many, if not all, diseases of the body. And targeting immune or inflammatory causes of disease has led to a series of breakthroughs, from new treatments for rheumatoid arthritis and other auto-immune diseases in the 1990s, through to the advent of immunotherapy for some cancers in the 2010s. Even more pervasively, low-grade inflammation, detectable only by blood tests, is increasingly considered to be part of the reason why common life experiences such as poverty, stress, obesity or ageing are bad for public health. Advertisement The brain is rapidly emerging as one of the new frontiers for inflammation. Doctors like myself, who went to medical school in the 20th century, were taught to think that there was an impermeable barrier between the brain and the immune system. In the 21st century, however, it has become clear that they are deeply interconnected and talk to each other all the time. Medical minds are now opening up to the idea that inflammation could be as widely and deeply implicated in brain and mind disorders as it is in bodily disorders. Advances in treatment of multiple sclerosis have shown the way. Many of the new medicines for MS were designed and proven to protect patients from brain damage caused by their own immune systems. The reasonably well-informed hope – and I emphasise those words at this stage – is that targeting brain inflammation could lead to breakthroughs in prevention and treatment of depression, dementia and psychosis on a par with the proven impact of immunological medicines for arthritis, cancer and MS. Indeed, a drug originally licensed for multiple sclerosis is already being tried as a possible immune treatment for schizophrenia. © 2020 Guardian News & Media Limited

Keyword: Alzheimers; Neuroimmunology
Link ID: 26975 - Posted: 01.21.2020

By Donna Jackson Nakazawa More than a decade ago, I was diagnosed with a string of autoimmune diseases, one after another, including a bone marrow disorder, thyroiditis, and then Guillain-Barré syndrome, which left me paralyzed while raising two young children. I recovered from Guillain-Barré only to relapse, becoming paralyzed again. My immune system was repeatedly and mistakenly attacking my body, causing the nerves in my arms, legs, and those I needed to swallow to stop communicating with my brain, leaving me confined to — and raising my children from — bed. As I slowly began to recover and learn to walk again, I noticed that along with residual physical losses I had experienced shifts in my mood and clarity of mind. Although I’d always been an optimistic person, I felt a bleak unshakable dread, which didn’t feel like the “old me.” I also noticed cognitive glitches. Names, words, and facts were hard to bring to mind. I can still recall cutting up slices of watermelon, putting them in a bowl, and staring down at them thinking, “What is this again?” I knew the word but couldn’t remember it. I covered my lapse by bringing the bowl to the table and waiting for my children to call out, “Yay! Watermelon!” And I thought, “Yes. Of course. Watermelon.” As a science journalist whose niche spans neuroscience, immunology, and human emotion, I knew at the time that it didn’t make scientific sense that inflammation in the body could be connected to — much less cause — illness in the brain. At that time, scientific dogma held that the brain was the only organ in the body not ruled by the immune system. The brain was considered to be “immune privileged.” © 2020 STAT

Keyword: Glia; Alzheimers
Link ID: 26971 - Posted: 01.20.2020

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

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