Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By Daniel Barron Earlier this month, JAMA Psychiatry published a land-breaking editorial. A group of psychiatrists led by David Ross described how and why post-traumatic stress disorder (PTSD) should be clinically evaluated from a neuroscience framework. The fact that this editorial was published in one of psychiatry’s leading journals is no small feat. Psychiatry houses a large and powerful contingency that argues neuroscience has little clinical relevance. The relevance of neuroscience to psychiatry was the subject of a recent Op-Ed debate in the New York Times: “There’s Such a Thing as Too Much Neuroscience” was rebutted with “More Neuroscience, Not Less.” This specific debate—and the dense politics as a whole—exists because competing frameworks are vying for competing funding, a conflict that pre-dates Freud’s departure from neurology. That the relevance of neuroscience to psychiatry is still questioned is blatantly outlandish: what organ do psychiatrists treat if not the brain? And what framework could possibly be more relevant than neuroscience to understanding brain dysfunction? In his editorial, Ross tactfully presented his case for neuroscience, describing the obvious choice for a clinical framework as one “perspective,” making a delicate intellectual curtsey while supporting his case with data. Ross discussed five “key neuroscience themes” (read: lines of evidence from burgeoning sub-fields) relevant to understanding and treating PTSD: fear conditioning, dysregulated circuits, memory reconsolidation, and epigenetic and genetic considerations. Each theme accounts for the diverse biological, psychological and social factors involved in PTSD—which is to say, these factors all have some affect on the brain mechanisms. Most importantly, Ross describes how a mechanistic approach allows clinicians to trace the specific causes of PTSD to specific treatments that can target those causes. © 2017 Scientific American,
By TANYA FRANK It begins in the laundry room in the early hours of the morning. I find him alone, tracing the wires of the telephone circuit board. “This is how they are monitoring us,” my son whispers. “We have to cut some stuff out, change the receiver, I can do it.” “Who?” I ask. “Who is monitoring us? And why?” He puts a finger to his lips to quiet me, and begins rifling through the tool kit. He doesn’t seem quite sure what he is looking for. He has never rerouted wires in his life, and besides, it is 2009 and we have suspended our landline. These wires that my 19-year-old is obsessing over are part of a defunct apparatus from a bygone age. I shiver in this damp afterthought of a room, but not from the concrete floor under my bare feet. I’m a Londoner with a tolerance for winter. It’s nerves that have me shaking. I am scared of my own child. My partner is in San Francisco, and we are in Los Angeles. There is no national health system here. We are unmoored, just my boy and me above a twinkling metropolis of strangers. “We can’t trust anybody,” he writes. “Our computers and phones are bugged. Listen, hear that?” I shake my head, unable to detect anything. “It’s a helicopter spying on us.” When it sinks in that this is not a delirium that can be eased with Advil and a good night’s sleep, and when I stop denying that my son is armed, I take him to the closest psychiatric hospital, where he is involuntarily held for 72 hours, considered a danger to himself or others. His symptomology is examined and classified as if he is some rare and delicate butterfly, and he emerges with a label: schizoaffective disorder. It is a complex condition with traits of both schizophrenia (a thought disorder) and bipolar (a mood disorder). Basically, my son had a psychotic break. That’s what they call it when someone disintegrates from his psyche. © 2017 The New York Times Company
Link ID: 23518 - Posted: 04.21.2017
Ian Sample Science editor Brain scans have revealed the first evidence for what appears to be a heightened state of consciousness in people who took psychedelic drugs in the name of science. Healthy volunteers who received LSD, ketamine or psilocybin, a compound found in magic mushrooms, were found to have more random brain activity than normal while under the influence, according to a study into the effects of the drugs. The shift in brain activity accompanied a host of peculiar sensations that the participants said ranged from floating and finding inner peace, to distortions in time and a conviction that the self was disintegrating. Researchers at the University of Sussex and Imperial College, London, measured the activity of neurons in people’s brains as the drugs took hold. Similar measurements have shown that when people are asleep or under anaesthetic, their neurons tend to fire in a more predictable way than when they are awake. “What we find is that under each of these psychedelic compounds, this specific measure of global conscious level goes up, so it moves in the other direction. The neural activity becomes more unpredictable,” said Anil Seth, a professor of neuroscience at the University of Sussex. “Until now, we’ve only ever seen decreases compared to the baseline of the normal waking state.”
Aimee Cunningham Taking antidepressants during pregnancy does not increase the risk of autism or attention-deficit/hyperactivity disorder, two new large studies suggest. Genetic or environmental influences, rather than prenatal exposure to the drugs, may have a greater influence on whether a child will develop these disorders. The studies are published online April 18 in JAMA. Clinically, the message is “quite reassuring for practitioners and for mothers needing to make a decision about antidepressant use during pregnancy,” says psychiatrist Simone Vigod, a coauthor of one of the studies. Past research has questioned the safety of expectant moms taking antidepressants (SN: 6/5/10, p. 22). “A mother’s mood disturbances during pregnancy are a big public health issue — they impact the health of mothers and their children,” says Tim Oberlander, a developmental pediatrician at the University of British Columbia in Vancouver. About one in 10 women develop a major depressive episode during pregnancy. “All treatment options should be explored. Nontreatment is never an option,” says Oberlander, who coauthored a commentary, also published in JAMA. Untreated depression during pregnancy creates risks for the child, including poor fetal growth, preterm birth and developmental problems. Some women may benefit from psychotherapy alone. A more serious illness may require antidepressants. “Many of us have started to look at longer term child outcomes related to antidepressant exposure because mothers want to know about that in the decision-making process,” says Vigod, of Women’s College Hospital in Toronto. |© Society for Science & the Public 2000 - 2017.
By CLYDE HABERMAN In America’s most storied political family, Rosemary Kennedy was the first in her generation to die of natural causes. Before then, a brother had been killed in war, a sister in a plane crash and two other brothers in assassinations. Not much of Ms. Kennedy’s life qualified as natural, though. Intellectually challenged from birth, she became increasingly erratic after entering womanhood. Her tempestuous mood swings troubled the family patriarch so much that he approved controversial surgery, which he was led to believe would calm her. In 1941, at age 23, Ms. Kennedy underwent a prefrontal lobotomy. It went badly. For her remaining 63 years, she led an institutionalized existence, out of public view, unable to speak clearly or walk without a limp. Retro Report, a series of video documentaries exploring major news stories of the past, harks back to that botched lobotomy and the neurologist who effectively sealed the young woman’s fate, Dr. Walter J. Freeman. The purpose is to show how the past informs the present. Psychosurgery endures, as with a procedure called a cingulotomy, which is used to treat depression and obsessive-compulsive disorder and involves severing fibers deep in the frontal lobe. But attention these days is keenly focused on stimulating discrete areas of the brain with electrical charges in the hope of easing torments like Parkinson’s disease, O.C.D. and depression. “What Walter Freeman was doing was crude and barbaric and harmful in many cases,” said Jack El-Hai, who wrote a 2005 biography of him, “The Lobotomist: A Maverick Medical Genius and His Tragic Quest to Rid the World of Mental Illness.” Referring to cingulotomies, Mr. El-Hai told Retro Report, “But what does remain is the idea that the brain can be physically manipulated, surgically manipulated, to help treat psychiatric illnesses.” The New York Times Company
Link ID: 23505 - Posted: 04.18.2017
Emily Corwin Michael Treadwell sat at the back of a courtroom in New Hampshire. He wore a windbreaker and khaki pants and leaned over his work boots with his elbows on his knees. At first it looked like he was chewing gum — a bold choice in a courtroom. But when he spoke it was clear: He wasn't chewing gum, he was chewing his own gums. Michael doesn't have any teeth. Taxpayers in Hillsborough County, N.H., have spent $63,000 over the last six years keeping Treadwell in jail for little more than trespassing. Law Investigation Into Private Prisons Reveals Crowding, Under-Staffing And Inmate Deaths For years now, his life has looked like this: Trespass in an apartment building, spend 30 days in jail; bother restaurant customers, spend 42 days in jail; panhandle aggressively, spend 30 days in jail. "When you live in a town like Nashua, there's not a lot of homelessness there, and it kinda like focuses, puts you in the spotlight," Treadwell says. "Especially if you drink alcohol and stuff." His charges all come from some combination of being homeless and getting drunk. Still, he says, jail is no worse than the streets. "People kill homeless people, violence and everything else," Treadwell says. "It can be a very dangerous life to live in. I don't suggest jail as an alternative. Ain't no kinda life." © 2017 npr
Link ID: 23497 - Posted: 04.17.2017
By Andy Coghlan It tastes foul and makes people vomit. But ayahuasca, a hallucinogenic concoction that has been drunk in South America for centuries in religious rituals, may help people with depression that is resistant to antidepressants. Tourists are increasingly trying ayahuasca during holidays to countries such as Brazil and Peru, where the psychedelic drug is legal. Now the world’s first randomised clinical trial of ayahuasca for treating depression has found that it can rapidly improve mood. The trial, which took place in Brazil, involved administering a single dose to 14 people with treatment-resistant depression, while 15 people with the same condition received a placebo drink. A week later, those given ayahuasca showed dramatic improvements, with their mood shifting from severe to mild on a standard scale of depression. “The main evidence is that the antidepressant effect of ayahuasca is superior to the placebo effect,” says Dráulio de Araújo of the Brain Institute at the Federal University of Rio Grande do Norte in Natal, who led the trial. Shamans traditionally prepare the bitter, deep-brown brew of ayahuasca using two plants native to South America. The first, Psychotria viridis, is packed with the mind-altering compound dimetheyltryptamine (DMT). The second, the ayahuasca vine (Banisteriopsis caapi), contains substances that stop DMT from being broken down before it crosses the gut and reaches the brain. © Copyright Reed Business Information Ltd.
Doctors trialling the use of ketamine to treat depression are calling for the treatment to be rolled out. Ketamine is licensed to be used as an anaesthetic but has a reputation as an illegal party drug. Writing in The Lancet Psychiatry, Dr Rupert McShane, who has led a trial in Oxford, since 2011 says ketamine can work on patients with depression "where nothing has helped before". However, he is calling for a national registry to monitor its use. Dr McShane says tens of thousands of people who have not responded to other treatment could be helped by the drug. But he adds there should be a national registry for those who prescribe the treatment to monitor the results and avoid misuse of the Class B substance. Of the 101 people taking part who had failed to find a successful depression treatment, 42 of them responded to the ketamine. "The first ketamine infusion literally saved my life," says one patient. "I had felt so desperate I was going to end it all. "Subsequent ketamine treatment has enabled me to return to my job full-time. I still struggle at times but being able to work again has given me such a boost." Dr McShane hopes more doctors will use it to treat depression but fears that the UK could follow the US where there are private ketamine clinics that vary in their clinical checks. © 2017 BB
By Jia Naqvi An experimental technique reduces the tics, or involuntary movements and vocal outbursts, associated with severe Tourette's syndrome in young adults, a study published Friday found. The surgical technique, called thalamic deep brain stimulation (DBS), sends electrical impulses to a specific area of the brain that reduces the tics, according to the study published in the Journal of Neurosurgery. The finding adds to the growing body of evidence about the safety and effectiveness of deep brain stimulation, which might eventually lead the Food and Drug Administration to approve the treatment for Tourette's syndrome, according to the researchers. “Our study shows that deep brain stimulation is a safe, effective treatment for young adults with severe Tourette syndrome that cannot be managed with current therapies,” said Alon Mogilner, an associate professor in the departments of neurosurgery and anesthesiology at New York University Langone and director of its Center for Neuromodulation, in a news release. “This treatment has the potential to improve the quality of life for patients who are debilitated through their teenage years and young adulthood.” Tourette's syndrome, a type of neurological disorder, according to various studies afflicts from 0.3 to 0.6 percent of children in the United States, with around 138,000 ages 6 to 17 being diagnosed with the condition. The causes for the syndrome are not well known and are thought to be largely genetic, with unidentified environmental factors increasing the likelihood of the condition. Usually the syndrome begins in childhood and the condition improves with age for some people, but for others the symptoms become more severe to the point that people become socially isolated and unable to work or attend school. © 1996-2017 The Washington Post
Link ID: 23468 - Posted: 04.08.2017
MaryCatherine McDonald, Marisa Brandt, Robyn Bluhm In the wake of World War I, some veterans returned wounded, but not with obvious physical injuries. Instead, their symptoms were similar to those that had previously been associated with hysterical women – most commonly amnesia, or some kind of paralysis or inability to communicate with no clear physical cause. English physician Charles Myers, who wrote the first paper on “shell-shock” in 1915, theorized that these symptoms actually did stem from a physical injury. He posited that repetitive exposure to concussive blasts caused brain trauma that resulted in this strange grouping of symptoms. But once put to the test, his hypothesis didn’t hold up. There were plenty of veterans who had not been exposed to the concussive blasts of trench warfare, for example, who were still experiencing the symptoms of shell-shock. (And certainly not all veterans who had seen this kind of battle returned with symptoms.) We now know that what these combat veterans were facing was likely what today we call post-traumatic stress disorder, or PTSD. We are now better able to recognize it, and treatments have certainly advanced, but we still don’t have a full understanding of just what PTSD is. The medical community and society at large are accustomed to looking for the most simple cause and cure for any given ailment. This results in a system where symptoms are discovered and cataloged and then matched with therapies that will alleviate them. Though this method works in many cases, for the past 100 years, PTSD has been resisting. © 2010–2017, The Conversation US, Inc.
Link ID: 23442 - Posted: 04.04.2017
Aaron E. Carroll One of the biggest American public health victories of the last decade has been the record low reached in the teenage birthrate. Along with that have been lows in rates for teenage pregnancy and abortion. Most researchers believe that improved access to contraception is a large part of this success. But news continues to focus on the concern that hormone-based contraception — like the pill or the patch — causes depression, and that this should lead us to question its wider use. A more nuanced discussion would consider both the benefits and the harms. This issue drew widespread coverage at the end of last year with a large study published in JAMA Psychiatry. Researchers tracked all women and adolescent females (ages 15 to 34) living in Denmark from 2000 through 2014. The study found that those who used hormonal contraception had significantly higher risks of also taking an antidepressant. The study broke down the increased relative risk for each hormonal method this way: combined oral contraceptives (23 percent), progestogen-only pills (34 percent), the patch (100 percent), vaginal ring (60 percent) and levonorgestrel intrauterine system (40 percent). The risks were highest in adolescents and decreased as women aged. The risks also peaked six months after the start of contraception. Needless to say, many news outlets covered this finding widely. Some portrayed it as shocking new information that should change the way we think about hormonal birth control. Others saw it as a vindication of many women who said for years that birth control had triggered their depression while scientists and doctors ignored them. But we have to acknowledge the limitations of this type of research. It’s not a controlled trial, and it’s impossible to establish causality. Women who choose to have sex could also be more likely to consider antidepressant use. © 2017 The New York Times Company
Amy Maxmen Before his 33-year-old son became bedridden with chronic fatigue syndrome, biochemist Ronald Davis created technologies to analyse genes and proteins faster, better and more cheaply. Now he aims his inventions at a different target: the elusive inner workings of his son’s malady. In his office at the Stanford Genome Technology Center in Palo Alto, California, Davis holds a nanofabricated cube the size of a gaming die. It contains 2,500 electrodes that measure electrical resistance to evaluate the properties of human cells. When Davis exposed immune cells from six people with chronic fatigue syndrome to a stressor — a splash of common salt — the cube revealed that they couldn’t recover as well as cells from healthy people could. Now his team is fabricating 100 more devices to repeat the experiment, and testing a cheaper alternative — a paper-thin nanoparticle circuit that costs less than a penny to make on an inkjet printer. Davis’s findings, although preliminary, are helping to propel research on chronic fatigue syndrome, also called myalgic encephalomyelitis (ME/CFS), into the scientific mainstream. Physicians used to dismiss the disease as psychosomatic, but studies now suggest that it involves problems in the chemical reactions, or pathways, within cells. “We now have a great deal of evidence to support that this is not only real, but a complex set of disorders,” says Ian Lipkin, an epidemiologist at Columbia University in New York City. “We are gathering clues that will lead to controlled clinical trials.” © 2017 Macmillan Publishers Limited,
By Melissa Banigan Twenty years ago, I started experiencing what turned into a long list of seemingly unrelated health issues. Headaches, depression, insomnia, peripheral neuropathy, fatigue, joint pain, chest pain, shortness of breath, a lesion on my spine and a variety of uncomfortable gastrointestinal ailments. Over the past five years, things went from bad to worse as I also became lactose-intolerant, developed mild vitiligo (a condition that leads to loss of skin pigmentation) and major vertigo, experienced a series of low-grade fevers and started to have some memory loss that I referred to as brain fogs. Doctors told me that as an overworked single mother of 40, I might just need to figure out ways to get more sleep and relax. Some of what was happening, they said, might be attributed to the normal processes of aging. What was happening, however, didn’t feel normal. Always a voracious reader and a writer by profession, I could no longer focus on work, read even a page of a book or grip a pen long enough to write a grocery list. I often felt too exhausted to keep plans with friends. When I did pull myself off my couch to see them, I couldn’t concentrate on conversations, so I sequestered myself in my apartment and let my friendships fade. I had been a runner, a swimmer and a hiker, but just walking up a flight of stairs made me lose my breath so completely that I succumbed to inactivity. I did everything the doctors asked me to do. I changed my diet and sleep schedule, went to a physical therapist and saw specialists in neurology and rheumatology and even a mental-health therapist. I then also turned to massage therapists, herbalists and an acupuncturist. © 1996-2017 The Washington Post
By Anil Ananthaswamy People who have chronic pain are more likely to experience mood disorders, but it’s not clear how this happens. Now a study in mice has found that chronic pain can induce genetic changes in brain regions that are linked to depression and anxiety, a finding that may lead to new treatments for pain. “At least 40 per cent of patients who suffer from severe forms of chronic pain also develop depression at some point, along with other cognitive problems,” says Venetia Zachariou of the Icahn School of Medicine at Mount Sinai in New York. To see if there might be a genetic link between these conditions, Zachariou and her team studied mice with damage to their peripheral nervous system. These mice show symptoms similar to chronic pain in people – they become hypersensitive to harmless touch, and avoid other situations that might also cause them pain. Until now, pain behaviour in mice had only been studied for at most a week at a time, says Zachariou, whose team monitored their mice for 10 weeks. “At the beginning, we saw only sensory deficits and pain-like symptoms. But several weeks later, the animals developed anxiety and depression-like behaviours.” The team then examined gene activity in three regions in the mouse brains we know are associated with depression and anxiety. Analysing the nucleus accumbens, medial prefrontal cortex, and periaqueductal gray, they found nearly 40 genes where activity was significantly higher or lower than in mice without the nervous system damage. © Copyright Reed Business Information Ltd.
/ By Katie Rose Quandt One afternoon in 2013, after swimming and playing outside, 9-year-old Taylor Johnson, from outside Atlanta, began sneezing incessantly. The fit lasted days before stopping abruptly, only to return months later. For a year, her violent sneezing fits came and went, to the bewilderment of a series of doctors. For families, the diagnosis can seem like an answer to their prayers. But there’s a catch: Most doctors won’t treat the diseases — and many don’t believe they even exist. “She was making this noise with her mouth at times 140 to 150 times a minute,” said her mother, Lori Johnson. “She was frantic, she couldn’t eat, she couldn’t sleep.” And “when she wasn’t sneezing, she was very depressed… She lost all interest in anything. Her whole personality just dissolved into nothing.” Then an otolaryngologist (an ear, nose, and throat doctor) realized Taylor wasn’t sneezing at all — the behavior was a repetitive, sneeze-like tic. That prompted a round of visits to neurologists, psychologists, and other specialists, until an allergist finally suggested a set of diagnoses unfamiliar to the Johnsons: PANS and PANDAS. These disorders, a specialist told them, can arise in certain predisposed children when the immune system responds to an infection like strep throat by attacking the brain. The resulting inflammation can lead to violent body tics and OCD-like symptoms. Copyright 2017 Undark
By Daisy Yuhas, Spectrum on March 22, 2017 In children with a deletion on chromosome 22, having autism does not boost the risk of developing schizophrenia later in life, according to a new study1. The children in the study have 22q11.2 deletion syndrome, which is linked to a 25-fold increase in the risk of developing a psychotic condition such as schizophrenia. A deletion in the region is also associated with an increased risk of autism. Some researchers have suggested that the relatively high autism prevalence in this population is the result of misdiagnoses of early signs of schizophrenia. The new findings, published 21 January in Schizophrenia Research, support an alternate theory: Autism and schizophrenia are independent outcomes of the same genetic syndrome. If there is a relationship between the two conditions, “that can only be a very small, probably negligible effect,” says lead investigator Jacob Vorstman, assistant professor of child psychiatry and genetics at the University Medical Center Utrecht in the Netherlands. The new findings could help guide clinical care, says Opal Ousley, assistant professor of psychiatry at the Emory Autism Center in Atlanta. If prenatal testing picks up the 22q11.2 deletion, for instance, clinicians could discuss the risk of both autism and schizophrenia with parents. © 2017 Scientific American
As the father of two sons with schizophrenia, author Ron Powers is familiar with the pain and frustration of dealing with a chronic, incurable disease of the brain. Powers' younger son, Kevin, was a talented musician whose struggles with schizophrenia began at age 17. Just before his 21st birthday, in 2005, Kevin took his own life. A few years later, Powers' older son, Dean, started experiencing symptoms of schizophrenia and had a psychotic break. "There is no greater ... feeling of helplessness than to watch two beloved sons deteriorate before [your] eyes, not knowing what to do to bring them back," Powers tells Fresh Air's Terry Gross. Powers' new book, No One Cares About Crazy People, is both a memoir about his sons and a history of how the mentally ill have been treated medically, legally and socially. Although Dean is now medicated and doing well, Powers notes that many people with schizophrenia don't receive the treatment they need — in part because they often don't believe they are ill. "This unwillingness to believe that one is afflicted has led to tremendous problems," Powers says. "To force that person into being helped is a violation of his or her civil rights ... and the law may penalize the care workers who give [people with schizophrenia] medications or admit them to a hospital against their will. ... That is the great reigning Catch-22 of the way our society deals — or fails to deal — with schizophrenia." © 2017 npr
Link ID: 23383 - Posted: 03.21.2017
Jon Hamilton Gerard Sanacora, a professor of psychiatry at Yale University, has treated hundreds of severely depressed patients with low doses of ketamine, an anesthetic and popular club drug that isn't approved for depression. This sort of "off-label" prescribing is legal. But Sanacora says other doctors sometimes ask him, "How can you be offering this to patients based on the limited amount of information that's out there and not knowing the potential long-term risk?" Sanacora has a simple answer. "If you have patients that are likely to seriously injure themselves or kill themselves within a short period of time, and they've tried the standard treatments, how do you not offer this treatment?" he says. Dozens of clinics now offer ketamine to patients with depression. And a survey of providers in the U.S. and Canada showed that "well over 3,000" patients have been treated so far, Sanacora says. A number of small studies have found that ketamine can do something no other drug can: it often relieves even suicidal depression in a matter of hours in patients who have not responded to other treatments. Ketamine's potential as an antidepressant was recognized more than a decade ago. And studies done since then provide "compelling evidence that the antidepressant effects of ketamine infusion are both rapid and robust, albeit transient," according to a consensus statement from a task force of the American Psychiatric Association. Sanacora is one of the task force members. © 2017 npr
By Taylor Beck LSD, “magic” mushrooms and mescaline have been banned in the U.S. and many other countries since the 1970s, but psychedelic medicine is making a comeback as new therapies for depression, nicotine addiction and anxiety. The drugs have another scientific use, too: so-called psychotomimetics, or mimics of psychosis, may be useful tools for studying schizophrenia. By creating a brief bout of psychosis in a healthy brain, as indigenous healers have for millennia, scientists are seeking new ways to study—and perhaps treat—mental illness. “We think that schizophrenia is a group of psychoses, which may have different causes,” says Franz Vollenweider, a psychiatrist and neuroscientist at the University of Zurich. “The new approach is to try to understand specific symptoms: hearing voices, cognitive problems, or apathy and social disengagement. If you can identify the neural bases of these, you can tailor the pharmacology.” Vollenweider and his colleagues have found an existing drug for anxiety that blocks specific effects of psilocybin, the psychoactive ingredient in magic mushrooms. When healthy people were given the drug before tripping, they did not report visual hallucinations and other common effects, according to a study published in April 2016 in European Neuropsychopharmacology. The effort is part of a burgeoning movement in pharmacology that seeks to induce psychosis to learn how to treat it. And schizophrenia desperately needs new treatments. Seventy-five percent of afflicted patients have cognitive problems. And most commonly used drugs do not treat the disorder's “negative” symptoms—apathy, social withdrawal, negative thinking—nor the cognitive impairments, which best predict how well a patient will fare in the long term. © 2017 Scientific American
By JULIE REHMEYER and DAVID TULLER What are some of the treatment regimens that sufferers of chronic fatigue syndrome should follow? Many major medical organizations cite two: psychotherapy and a steady increase in exercise. There’s just one problem. The main study that has been cited as proof that patients can recover with those treatments overstated some of its results. In reality, the claim that patients can recover from these treatments is not justified by the data. That’s the finding of a peer-reviewed preliminary re-analysis of previously unpublished data from the clinical trial, the largest ever for chronic fatigue syndrome. Nicknamed the PACE trial, the core findings of the British study appeared in The Lancet in 2011 and Psychological Medicine in 2013. Patients battled for years to obtain the underlying data, and last spring, a legal tribunal in Britain, the General Regulatory Chamber, directed the release of some of the study’s information. The impact of the trial on treatment options for the estimated one million chronic fatigue patients in the United States has been profound. The Mayo Clinic, Kaiser Permanente, WebMD, the American Academy of Family Physicians and others recommend psychotherapy and a steady increase in exercise. But this approach can be harmful. According to a 2015 report from the Institute of Medicine, now the National Academy of Medicine, even minimal activity can cause patients prolonged exhaustion, muscle pain, cognitive problems and more. In severe cases, a short conversation or a trip to the bathroom can deplete patients for hours, days or more. In surveys, patients routinely report deterioration after a program of graded exercise. The psychotherapeutic intervention also encourages patients to increase their activity levels. Many patients (including one of us) have remained ill for years or decades with chronic fatigue syndrome, also known as myalgic encephalomyelitis, or ME/CFS. It can be triggered by a viral infection, resulting in continuing or recurring immunological and neurological dysfunction. The Institute of Medicine dismissed any notion that it is a psychiatric illness. © 2017 The New York Times Company