Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
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By Sara Solovitch It was November 2012 when Dennis Hartman, a Seattle business executive, managed to pull himself out of bed, force himself to shower for the first time in days and board a plane that would carry him across the country to a clinical trial at the National Institute of Mental Health (NIMH) in Bethesda. After a lifetime of profound depression, 25 years of therapy and cycling through 18 antidepressants and mood stabilizers, Hartman, then 46, had settled on a date and a plan to end it all. This clinical trial would be his last stab at salvation. For 40 minutes, he sat in a hospital room as an IV drip delivered ketamine through his system. Several more hours passed before it occurred to him that all his thoughts of suicide had evaporated. “My life will always be divided into the time before that first infusion and the time after,” Hartman says today. “That sense of suffering and pain draining away. I was bewildered by the absence of pain.” Ketamine, popularly known as the psychedelic club drug Special K, has been around since the early 1960s. It is a staple anesthetic in emergency rooms, regularly used for children when they come in with broken bones and dislocated shoulders. It’s an important tool in burn centers and veterinary medicine, as well as a notorious date-rape drug, known for its power to quickly numb and render someone immobile.
By BENEDICT CAREY A new approach to treating early schizophrenia, which includes family counseling, results in improvements in quality of life that make it worth the added expense, researchers reported on Monday. The study, published by the journal Schizophrenia Bulletin, is the first rigorous cost analysis of a federally backed treatment program that more than a dozen states have begun trying. In contrast to traditional outpatient care, which generally provides only services covered by insurance, like drugs and some psychotherapy, the new program offers other forms of support, such as help with jobs and school, as well as family counseling. The program also tries to include the patients — people struggling with a first psychotic “break” from reality, most of them in their late teens and 20s — as equals in decisions about care, including drug dosage. In a widely anticipated study last fall, called the Raise trial, researchers reported that after two years, people who got this more comprehensive care did better on a variety of measures than those who received the standard care. But the study found no evidence of related cost savings or differences in hospitalization rates, a prime driver of expense. As lawmakers in Washington are considering broad changes in mental health care, cost issues loom especially large. Outside experts said this analysis — which was based on the Raise trial data — was an important test of the new care program’s value. “This is the way cost analysis should be done,” Sherry Glied, a professor of public service and the dean of New York University’s graduate school of public service, said. “One way to think about it is to ask, if this program were a drug, would we pay for it? And the answer is yes.” © 2016 The New York Times Company
Link ID: 21842 - Posted: 02.01.2016
By CHARLES SIEBERT Nearly 30 years ago, Lilly Love lost her way. She had just completed her five-year tour of duty as an Alaska-based Coast Guard helicopter rescue swimmer, one of an elite team of specialists who are lowered into rough, frigid seas to save foundering fishermen working in dangerous conditions. The day after she left active service, the helicopter she had flown in for the previous three years crashed in severe weather into the side of a mountain, killing six of her former crewmates. Devastated by the loss and overcome with guilt, Love chose as her penance to become one of the very fishermen she spent much of her time in the Coast Guard rescuing. In less than a year on the job, she nearly drowned twice after being dragged overboard in high seas by the hooks of heavy fishing lines. Love would not formally receive a diagnosis of severe post-traumatic stress disorder for another 15 years. In that time, she was married and divorced three times, came out as transgender and retreated periodically to Yelapa, Mexico, where she lived in an isolated cabin accessible only by water. She eventually ended up living on a boat in a Los Angeles marina, drinking heavily and taking an array of psychotropic drugs that doctors at the West Los Angeles Veterans Administration Medical Center began to prescribe with increasing frequency as Love proved resistant to traditional treatments like counseling and group therapy. One night, after her fifth stay in the center’s psych ward, she crashed her boat into a sea wall. Finally, in 2006, she was in the veterans’ garden and happened to catch sight of the parrots being housed in an unusual facility that opened a year earlier on the grounds of the center. ‘‘This place is why I’m still here,’’ Love, now 54, told me one day last summer as I watched her undergo one of her daily therapy sessions at the facility, known as Serenity Park, a name that would seem an utter anomaly to anyone who has ever been within 200 yards of the place. © 2016 The New York Times Company
Link ID: 21839 - Posted: 01.30.2016
By BENEDICT CAREY Scientists reported on Wednesday that they had taken a significant step toward understanding the cause of schizophrenia, in a landmark study that provides the first rigorously tested insight into the biology behind any common psychiatric disorder. More than two million Americans have a diagnosis of schizophrenia, which is characterized by delusional thinking and hallucinations. The drugs available to treat it blunt some of its symptoms but do not touch the underlying cause. The finding, published in the journal Nature, will not lead to new treatments soon, experts said, nor to widely available testing for individual risk. But the results provide researchers with their first biological handle on an ancient disorder whose cause has confounded modern science for generations. The finding also helps explain some other mysteries, including why the disorder often begins in adolescence or young adulthood. “They did a phenomenal job,” said David B. Goldstein, a professor of genetics at Columbia University who has been critical of previous large-scale projects focused on the genetics of psychiatric disorders. “This paper gives us a foothold, something we can work on, and that’s what we’ve been looking for now, for a long, long time.” The researchers pieced together the steps by which genes can increase a person’s risk of developing schizophrenia. That risk, they found, is tied to a natural process called synaptic pruning, in which the brain sheds weak or redundant connections between neurons as it matures. During adolescence and early adulthood, this activity takes place primarily in the section of the brain where thinking and planning skills are centered, known as the prefrontal cortex. People who carry genes that accelerate or intensify that pruning are at higher risk of developing schizophrenia than those who do not, the new study suggests. Some researchers had suspected that the pruning must somehow go awry in people with schizophrenia, because previous studies showed that their prefrontal areas tended to have a diminished number of neural connections, compared with those of unaffected people. © 2016 The New York Times Company
Angus Chen When she was 22, Rachel Star Withers uploaded a video to YouTube called "Normal: Living With Schizophrenia." It starts with her striding across her family's property in Fort Mill, S.C. She looks across the rolling grounds, unsmiling. Her eyes are narrow and grim. She sits down in front of a deserted white cottage and starts sharing. "I see monsters. I see myself chopped up and bloody a lot. Sometimes I'll be walking, and the whole room will just tilt. Like this," she grasps the camera and jerks the frame crooked. She surfaces a fleeting grin. "Try and imagine walking." She becomes serious again. "I'm making this because I don't want you to feel alone whether you're struggling with any kind of mental illness or just struggling." At the time, 2008, there were very few people who had done anything like this online. "As I got diagnosed [with schizophrenia], I started researching everything. The only stuff I could find was like every horror movie," she says. "I felt so alone for years." She decided that schizophrenia was really not that scary. "I want people to find me and see a real person." Over the past eight years, she has made 53 videos documenting her journey with schizophrenia and depression and her therapy. And she is not the only one. There are hundreds of videos online of people publicly sharing their experiences with mental illness. © 2016 npr
Link ID: 21834 - Posted: 01.28.2016
Heidi Ledford Addie plays hard for an 11-year-old greater Swiss mountain dog — she will occasionally ignore her advanced years to hurl her 37-kilogram body at an unwitting house guest in greeting. But she carries a mysterious burden: when she was 18 months old, she started licking her front legs aggressively enough to wear off patches of fur and draw blood. Addie has canine compulsive disorder — a condition that is thought to be similar to human obsessive–compulsive disorder (OCD). Canine compulsive disorder can cause dogs to chase their tails for hours on end, or to suck on a toy or body part so compulsively that it interferes with their eating or sleeping. Addie may soon help researchers to determine why some dogs are more prone to the disorder than others. Her owner, Marjie Alonso of Somerville, Massachusetts, has enrolled her in a project called Darwin’s Dogs, which aims to compare information about the behaviour of thousands of dogs against the animals’ DNA profiles. The hope is that genetic links will emerge to conditions such as canine compulsive disorder and canine cognitive dysfunction — a dog analogue of dementia and possibly Alzheimer’s disease. The project organizers have enrolled 3,000 dogs so far, but hope to gather data from at least 5,000, and they expect to begin analysing DNA samples in March. “It’s very exciting, and in many ways it’s way overdue,” says Clive Wynne, who studies canine behaviour at Arizona State University in Tempe. © 2016 Nature Publishing Group,
By Ellen Hendriksen This topic comes by request on the Savvy Psychologist Facebook page from listener Anita M. of Detroit. Anita works with foster kids and, too often, sees disadvantaged kids who have been on a cocktail of psychiatric medications from as early as age 6. She asks, does such early use alter a child’s brain or body? And have the effects of lifelong psychiatric medication been studied? Childhood mental illness (and resulting medication) is equally overblown and under-recognized. Approximately 21% of American kids - that’s 1 in 5 - will battle a diagnosable mental illness before they reach the age of 17, whether or not they actually get treatment. The problem is anything but simple. Some childhood illnesses - ADHD and autism, for example - often get misused as “grab-bag” diagnoses when something’s wrong but no one knows what. This leads to overdiagnosis and sometimes, overmedicating. Other illnesses, like substance abuse, get overlooked or written off as rebellion or experimentation, leading to underdiagnosis and kids slipping through the cracks. But the most common problem is inconsistent diagnosis. For example, a 2008 study found that fewer than half of individuals diagnosed with bipolar disorder actually had the illness, while 5% of those diagnosed with something completely different actually had bipolar disorder. But let’s get back to Anita’s questions: Does early psychotropic medication alter a child’s brain? The short answer is yes, but the long answer might be different than you think. © 2016 Scientific American
By PAM BELLUCK Women should be screened for depression during pregnancy and after giving birth, an influential government-appointed health panel said Tuesday, the first time it has recommended screening for maternal mental illness. The recommendation, expected to galvanize many more health providers to provide screening, comes in the wake of new evidence that maternal mental illness is more common than previously thought; that many cases of what has been called postpartum depression actually start during pregnancy; and that left untreated, these mood disorders can be detrimental to the well-being of children. It also follows growing efforts by states, medical organizations and health advocates to help women having these symptoms — an estimated one in seven postpartum mothers, some experts say. “There’s better evidence for identifying and treating women with depression” during and after pregnancy, said Dr. Michael Pignone, a professor of medicine at the University of North Carolina at Chapel Hill and an author of the recommendation, which was issued by the United States Preventive Services Task Force. As a result, he said, “we specifically called out the need for screening during this period.” Answers to questions about depression screening and maternal mental illness, following new recommendations saying that women should be screened for depression during pregnancy and after childbirth. The recommendation was part of updated depression screening guidelines issued by the panel, an independent group of experts appointed by the Department of Health and Human Services. In 2009, the group said adults should be screened if clinicians had the staff to provide support and treatment; the new guidelines recommend adult screening even without such staff members, saying mental health support is now more widely available. The 2009 guidelines did not mention depression during or after pregnancy. © 2016 The New York Times Company
by Bethany Brookshire Unless you’re in the middle of biting into a delicious Reuben sandwich, you might forget that taste is one of the fundamental senses. “It’s required for our enjoyment of food,” explains Emily Liman, a taste researcher at the University of Southern California in Los Angeles. “Without taste … people stop eating. They don’t enjoy their food.” A life without the sweet jolt of sugar or the savory delights of umami seems, well, tasteless. When you put that mouthwatering combination of corned beef, Swiss cheese, Thousand Island dressing, sauerkraut and rye in your mouth, the chemicals in the sandwich stimulate taste buds on your tongue and soft palate. Those taste buds connect to the ends of nerve fibers extending delicately into the mouth. Those nerve fibers are the ends of cells located in the geniculate ganglion, a ball of cells nestled up against the ear canal on the side of your head. From there, taste sensations head toward the brain. Chemical messengers bridge the gap between the taste bud and the end of the nerve fiber. But what chemical is involved depends on the type of cell within the bud. There are three types of taste cells (imaginatively titled I, II and III). Type I is not well-understood, but it may be a kind of support cell for other taste cells. Type II, in contrast, is better known. These taste cells sense the slight bitterness of the rye seeds, the sweet edge of the Thousand Island dressing and the savory umami of the beef. They pass that delightful message on using the chemical ATP. © Society for Science & the Public 2000 - 2016
Alison Abbott For the second time in four months, researchers have reported autopsy results that suggest Alzheimer’s disease might occasionally be transmitted to people during certain medical treatments — although scientists say that neither set of findings is conclusive. The latest autopsies, described in the Swiss Medical Weekly1 on 26 January, were conducted on the brains of seven people who died of the rare, brain-wasting Creutzfeldt–Jakob disease (CJD). Decades before their deaths, the individuals had all received surgical grafts of dura mater — the membrane that covers the brain and spinal cord. These grafts had been prepared from human cadavers and were contaminated with the prion protein that causes CJD. But in addition to the damage caused by the prions, five of the brains displayed some of the pathological signs that are associated with Alzheimer’s disease, researchers from Switzerland and Austria report. Plaques formed from amyloid-β protein were discovered in the grey matter and blood vessels. The individuals, aged between 28 and 63, were unusually young to have developed such plaques. A set of 21 controls, who had not had surgical grafts of dura mater but died of sporadic CJD at similar ages, did not have this amyloid signature. According to the authors, it is possible that the transplanted dura mater was contaminated with small ‘seeds’ of amyloid-β protein — which some scientists think could be a trigger for Alzheimer’s — along with the prion protein that gave the recipients CJD. © 2016 Nature Publishing Group,
By Anne Pycha Future doctors may ask us to say more than “Ahhh.” Several groups of neuroscientists, psychiatrists and computer scientists are now investigating the extent to which patients' language use can provide diagnostic clues—before a single laboratory test is run. Increased computing power and new methods to measure the relation between behavior and brain activity have advanced such efforts. And although tests based on the spoken word may not be as accurate as gene sequencing or MRI scans, for diseases lacking clear biological indicators, language mining could help fill the gap. Psychiatrists at Columbia University interviewed 34 young adults at risk for psychosis, a common sign of schizophrenia that includes delusions and hallucinations. Two and a half years later five of the subjects had developed psychosis, and the remaining 29 remained free of the disorder. A specially designed algorithm combed the initial interviews collectively to look for language features that distinguished the two groups and found that psychosis correlated with shorter sentences, loss of flow in meaning from one sentence to the next and less frequent use of the words “that,” “what” and “which.” When later tested on each individual interview, the computer program predicted who did and who did not develop psychosis with 100 percent accuracy. The results were recently published in Schizophrenia, and a second round of testing with another group of at-risk subjects is now under way. Parkinson's Disease Twenty-seven subjects in a study at Favaloro University in Argentina listened to recorded sentences containing verbs associated with specific hand shapes (such as “applaud” or “punch”). As soon as they understood the sentence, participants pressed a button while keeping both hands in either a flat or clenched-fist position. © 2016 Scientific American
Richard A. Friedman WHO among us hasn’t wanted to let go of anxiety or forget about fear? Phobias, panic attacks and disorders like post-traumatic stress are extremely common: 29 percent of American adults will suffer from anxiety at some point in their lives. Sitting at the heart of much anxiety and fear is emotional memory — all the associations that you have between various stimuli and experiences and your emotional response to them. Whether it’s the fear of being embarrassed while talking to strangers (typical of social phobia) or the dread of being attacked while walking down a dark street after you’ve been assaulted (a symptom of PTSD), you have learned that a previously harmless situation predicts something dangerous. It has been an article of faith in neuroscience and psychiatry that, once formed, emotional memories are permanent. Afraid of heights or spiders? The best we could do was to get you to tolerate them, but we could never really rid you of your initial fear. Or so the thinking has gone. The current standard of treatment for such phobias revolves around exposure therapy. This involves repeatedly presenting the feared object or frightening memory in a safe setting, so that the patient acquires a new safe memory that resides in his brain alongside the bad memory. As long as the new memory has the upper hand, his fear is suppressed. But if he is re-traumatized or re-exposed with sufficient intensity to the original experience, his old fear will awaken with a vengeance. This is one of the limitations of exposure therapy, along with the fact that it generally works in only about half of the PTSD patients who try it. Many also find it upsetting or intolerable to relive memories of assaults and other traumatizing experiences. © 2016 The New York Times Company
Link ID: 21815 - Posted: 01.23.2016
By Erin Blakemore Despite all that neurotic clucking and scratching, domestic chickens are pretty unflappable. After all, we’ve bred them to be that way, preferring chill chicks to freaked-out fowl. But the behaviors of more anxious chickens could do more than ruffle a bunch of feathers: New research suggests that studying the genome of flustered birds could shed light on human mental disorders. In a new study published in the journal Genetics, evolutionary biologist Dominic Wright and his team looked at whether there’s a genetic connection between anxious behavior in chickens, mice and humans. Despite the compact size of the chicken genome — it’s just a third of the size of a human’s — the birds’ genes share surprising similarity to those of people. There's another reason why chickens are so great for genetic research. Because there are both wild and domesticated chickens, researchers can observe their contrasting behaviors and easily pin them to genetic differences. Wright bred wild red junglefowl chickens with their calmer cousins, white leghorn chickens, for the experiment. After eight generations, his team was able to run open field tests — experiments during which the birds were put in a brightly-lit arena and assessed for how much time they spent cowering on the periphery instead of strutting through the room. These behavioral tests helped the team identify brave and anxious birds, then narrow down areas of the genome related to variations in anxiety. They identified 10 candidate genes in the hypothalamus, an area of the brain which helps regulate anxiety.
By Elizabeth Pennisi Whether foraging for food, caring for young, or defending the nest, the worker castes of carpenter ants toil selflessly for their queen and colony. Now, biologists have figured out how to make some of those worker ants labor even harder, or change their very jobs in ant society, all by making small chemical modifications to their DNA. The finding calls attention to a new source of behavioral flexibility, and drives home the idea that so-called epigenetic modifications can connect genes to the environment, linking nature to nurture. The work is “a pioneering study establishing a causal link between epigenetics and complex social behavior,” says Ehab Abouheif, an evolutionary developmental biologist at McGill University, Montreal, in Canada. “These mechanisms may extend far beyond ants to other organisms with social behavior.” Insect biologists have long debated whether the division of labor in these sophisticated species with castes is driven by colony needs or is innate. Evidence in honey bees had pointed toward a genetic difference between queens and workers. In the past several years, however, work in both honey bees and ants had indicated that epigenetic modifications—changes to DNA other than to its sequence of bases (or DNA “letters”)—influence caste choices, indicating environmental factors can be pivotal. But subsequent research about one type of change, methylation, led to contradictory conclusions. © 2016 American Association for the Advancement of Science.
Link ID: 21744 - Posted: 01.02.2016
Bruce Bower Craig Bryan treats military personnel who struggle with thoughts of ending their own lives, as well as those who’ve survived an actual suicide attempt. But these days he’s fighting an uphill battle. Suicide rates in the United States have been rising, especially among veterans and members of the armed forces. Traditional assumptions about why people kill themselves have not led to effective strategies for suicide prevention, Bryan says. So in recent years psychologists and others have been reconsidering basic beliefs about why people carry out the ultimate act of self-destruction. “There has been an explosion of new thinking about suicide in the past decade,” says Bryan, a clinical psychologist at the University of Utah in Salt Lake City. This shift in focus was inspired by psychologist Thomas Joiner’s introduction in 2005 of the interpersonal theory of suicide. Unlike previous theorists, Joiner, of Florida State University in Tallahassee, treated thinking about suicide and attempting suicide as separate experiences, each with its own explanations and risk factors. Joiner’s approach has inspired much new suicide research by Bryan and others. One line of work suggests that three factors render individuals especially prone to moving from suicidal thoughts to actions: a partly inborn ability to withstand pain, self-hate triggered by extremely distressing experiences and, finally, access to guns or other lethal means. © Society for Science & the Public 2000 - 2015.
Link ID: 21738 - Posted: 12.30.2015
Carl Zimmer Throughout the day, a clock ticks inside our bodies. It rouses us in the morning and makes us sleepy at night. It raises and lowers our body temperature and at the right times, and regulates the production of insulin and other hormones. From Our Advertisers The body’s circadian clock even influences our thoughts and feelings. Psychologists have measured some of its effects on the brain by having people take cognitive tests at different times of day. As it turns out, late morning turns out to be the best time to try doing tasks such as mental arithmetic that demand that we hold several pieces of information in mind at once. Later in the afternoon is the time to attempt simpler tasks, like searching for a particular letter in a page of gibberish. Another clue about the clock in our brains comes from people with conditions such as depression and bipolar disorder. People with these disorders often have trouble sleeping at night, or feel groggy during the day. Some people with dementia experience “sundowning,” becoming confused or aggressive at the end of the day. “Sleep and activity cycles are a very big part of psychiatric illnesses,” said Huda Akil, a neuroscientist at the University of Michigan. Yet neuroscientists have struggled to understand exactly how the circadian clock affects our minds. After all, researchers can’t simply pop open a subject’s skull and monitor his brain cells over the course of each day. A few years ago, Dr. Akil and her colleagues came up with an idea for the next best thing. © 2015 The New York Times Company
By BENEDICT CAREY SAN FRANCISCO — The idea was to go out in an emotional swan dive, a lunge for the afterlife that would stretch his 17-year-old imagination. He settled on a plan and shared the details with a Facebook friend: He would drop DMT, a powerful psychedelic, and then cut his throat. “Everyone was telling me what I could and couldn’t do — doctors, my parents,” said Frank, now a 19-year-old college student. “I was going to hurt myself, to show people, ‘Look, I am still in control of my life.’” And so, in time, he was. Frank, who eight months earlier had received a diagnosis of psychosis, the signature symptom of schizophrenia, and had been in and out of the hospital, gradually learned to take charge of his own recovery, in a new approach to treatment for people experiencing a first psychotic “break” with reality. At a time when lawmakers in Washington are debating large-scale reforms to the mental health care system, analysts are carefully watching a handful of new first-break programs like the one that treated Frank in New York as a way to potentially ease the cycle of hospitalization and lifetime disability that afflict so many mentally ill people. More than two million people in the United States have received a diagnosis of schizophrenia. Most are consigned to whatever treatment is available amid a hodgepodge of programs that often focus on antipsychotic drugs to blunt delusions and paranoia — medicines that can come with side effects so debilitating that many patients go off them and end up in a loop of hospitalization and despair. But over the past several years, a number of states have set up programs with a different approach, emphasizing supportive services, like sustained one-on-one therapy, school and work assistance, and family education, as well as medication. The therapists work to engage each patient as an equal partner in decisions — including about medication dosage, to make it as tolerable as possible. © 2015 The New York Times Company
Link ID: 21731 - Posted: 12.29.2015
By BENEDICT CAREY Dr. Robert L. Spitzer, who gave psychiatry its first set of rigorous standards to describe mental disorders, providing a framework for diagnosis, research and legal judgments, as well as a lingua franca for the endless social debate over where to draw the line between normal and abnormal behavior, died on Friday. He was 83. From Our Advertisers Dr. Spitzer died from complications of heart disease at the assisted living facility where he lived in Seattle, his wife, Janet Williams, said. The couple had moved to Seattle from Princeton, N.J., this year. Dr. Spitzer’s remaking of psychiatry began with an early interest in one of the least glamorous and, historically, most ignored corners of the field: measurement. In the early 1960s, the field was fighting to sustain its credibility, in large part because diagnoses varied widely from doctor to doctor. For instance, a patient told he was depressed by one doctor might be called anxious or neurotic by another. The field’s diagnostic manual, at the time a pamphlet-like document rooted in Freudian ideas, left wide latitude for the therapist’s judgment. Dr. Spitzer, a rising star at Columbia University, was himself looking for direction, increasingly frustrated with Freudian analysis. A chance meeting with a colleague working on a new edition of the manual — the Diagnostic and Statistical Manual of Mental Disorders, or the D.S.M. for short — led to a job taking notes for the committee debating revisions. There, he became fascinated with reliable means for measuring symptoms and behavior — i.e., assessment. “At the time, there was zero interest in assessment,” said Dr. Michael First, a professor of clinical psychiatry at Columbia. “He saw how important it was, and his whole career led to assessment being taken seriously.” © 2015 The New York Times Company
Jon Hamilton Taking antidepressants during the second or third trimester of pregnancy may increase the risk of having a child with autism spectrum disorder, according to a study of Canadian mothers and children published Monday in JAMA Pediatrics. But scientists not involved in the research say the results are hard to interpret and don't settle the long-running debate about whether expectant mothers with depression should take antidepressants. "This study doesn't answer the question," says Bryan King, program director of the autism center at Seattle Children's Hospital and a professor of psychiatry and behavioral sciences at the University of Washington. "My biggest concern is that it will be over-interpreted," says King, who wrote an editorial that accompanied the study. "It kind of leaves you more confused," says Alan Brown, a professor of psychiatry and epidemiology at Columbia University who studies risk factors for autism. "Mothers shouldn't get super worried about it," he says. One reason it's confusing is that there's strong evidence that mothers with depression are more likely than other women to have a child with autism, whether or not they take antidepressants during pregnancy. King and Brown say that makes it very hard to disentangle the effects of depression itself from those of the drugs used to treat it. © 2015 npr
By ALAN SCHWARZ Andrew Rios’s seizures began when he was 5 months old and only got worse. At 18 months, when an epilepsy medication resulted in violent behavior, he was prescribed the antipsychotic Risperdal, a drug typically used to treat schizophrenia and bipolar disorder in adults, and rarely used for children as young as 5 years. From Our Advertisers When Andrew screamed in his sleep and seemed to interact with people and objects that were not there, his frightened mother researched Risperdal and discovered that the drug was not approved, and had never even been studied, in children anywhere near as young as Andrew. “It was just ‘Take this, no big deal,’ like they were Tic Tacs,” said Genesis Rios, a mother of five in Rancho Dominguez, Calif. “He was just a baby.” Cases like that of Andrew Rios, in which children age 2 or younger are prescribed psychiatric medications to address alarmingly violent or withdrawn behavior, are rising rapidly, data shows. Many doctors worry that these drugs, designed for adults and only warily accepted for certain school-age youngsters, are being used to treat children still in cribs despite no published research into their effectiveness and potential health risks for children so young. Almost 20,000 prescriptions for risperidone (commonly known as Risperdal), quetiapine (Seroquel) and other antipsychotic medications were written in 2014 for children 2 and younger, a 50 percent jump from 13,000 just one year before, according to the prescription data company IMS Health. Prescriptions for the antidepressant fluoxetine (Prozac) rose 23 percent in one year for that age group, to about 83,000. The company’s data does not indicate how many children received these prescriptions (many children receive several prescriptions a year), but previous studies suggest that the number is at least 10,000. IMS Health researched the data at the request of The New York Times. © 2015 The New York Times Company