Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
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By JACKIE CALMES and ROBERT PEAR WASHINGTON — The Obama administration on Friday will complete a generation-long effort to require insurers to cover care for mental health and addiction just like physical illnesses when it issues long-awaited regulations defining parity in benefits and treatment. The rules, which will apply to almost all forms of insurance, will have far-reaching consequences for many Americans. In the White House, the regulations are also seen as critical to President Obama’s program for curbing gun violence by addressing an issue on which there is bipartisan agreement: Making treatment more available to those with mental illness could reduce killings, including mass murders. In issuing the regulations, senior officials said, the administration will have acted on all 23 executive actions that the president and Vice President Joseph R. Biden Jr. announced early this year to reduce gun crimes after the Newtown, Conn., school massacre. In planning those actions, the administration anticipated that gun control legislation would fail in Congress as pressure from the gun lobby proved longer-lasting than the national trauma over the killings of first graders and their caretakers last Dec. 14. “We feel actually like we’ve made a lot of progress on mental health as a result in this year, and this is kind of the big one,” said a senior administration official, one of several who described the outlines of the regulations that Kathleen Sebelius, the secretary of health and human services, will announce at a mental health conference on Friday in Atlanta with the former first lady Rosalynn Carter. While laws and regulations dating to 1996 took initial steps in requiring insurance parity for medical and mental health, “here we’re doing full parity, and we’ve also taken steps to extend it to the people covered in the Affordable Care Act,” the senior official said. “This is kind of the final word on parity.” © 2013 The New York Times Company
Stanley Rachman. “Will these hands ne'er be clean?” In Shakespeare's play Macbeth, Lady Macbeth helps to plot the brutal murder of King Duncan. Afterwards she feels tainted by Duncan's blood and insists that “all the perfumes of Arabia” could not sweeten her polluted hands. Baffled by her compulsive washing, her doctor is forced to admit: “This disease is beyond my practise.” In the 400 years since Macbeth was first performed, other doctors, psychiatrists, neuroscientists and clinical psychologists — myself included — have also found the problem beyond the reach of their own expertise. We see compulsive washing a lot, mostly as a symptom of obsessive–compulsive disorder (OCD), but also in people who have suffered a physical or emotional trauma, for example in women who have suffered sexual assault. The events trigger a deep-seated psychological, and ultimately biological, response. We know that the driving force of compulsive washing is a fear of contamination by dirt and germs. An obsessive fear of contact with sexual fluids, for example, can drive compulsive washing in OCD and force people to restrict sexual activity to a specific room in the house. Compulsive washing fails to relieve the anxiety. Most patients with OCD continue to feel contaminated despite vigorous attempts to clean themselves. Why does repeated washing fail? There is much debate at present about the direction that psychiatric medicine and research should take. We should not underestimate what we can continue to learn from the careful observation of patients. Such observations have led my colleagues and me to diagnose a new cause of OCD and other types of compulsive washing: mental contamination. © 2013 Nature Publishing Group
By Helen Briggs BBC News Depression is the second most common cause of disability worldwide after back pain, according to a review of research. The disease must be treated as a global public health priority, experts report in the journal PLOS Medicine. The study compared clinical depression with more than 200 other diseases and injuries as a cause of disability. Globally, only a small proportion of patients have access to treatment, the World Health Organization says. Depression was ranked at number two as a global cause of disability, but its impact varied in different countries and regions. For example, rates of major depression were highest in Afghanistan and lowest in Japan. In the UK, depression was ranked at number three in terms of years lived with a disability. Dr Alize Ferrari from the University of Queensland's School of Population Health led the study. "Depression is a big problem and we definitely need to pay more attention to it than we are now," she told BBC News. "There's still more work to be done in terms of awareness of the disease and also in coming up with successful ways of treating it. "The burden is different between countries, so it tends to be higher in low and middle income countries and lower in high income countries." Policy-makers had made an effort to bring depression to the forefront, but there was a lot more work to be done, she added. BBC © 2013
Link ID: 18883 - Posted: 11.07.2013
By DAN HURLEY This couldn’t possibly be a good idea. On Friday the 13th of September, in an old brick building on 13th Street in Boston’s Charlestown neighborhood, a pair of electrodes was attached to my forehead, one over my brain’s left prefrontal cortex, the other just above my right eye socket. I was about to undergo transcranial direct-current stimulation, or tDCS, an experimental technique for delivering extremely low dose electrical stimulation to the brain. Using less than 1 percent of the electrical energy necessary for electroconvulsive therapy, powered by an ordinary nine-volt battery, tDCS has been shown in hundreds of studies to enhance an astonishing, seemingly implausible variety of intellectual, emotional and movement-related brain functions. And its side effects appear limited to a mild tingling at the site of the electrode, sometimes a slight reddening of the skin, very rarely a headache and certainly no seizures or memory loss. Still, I felt more than a bit apprehensive as I prepared to find out if a little bit of juice could amp up my cognitive reserves and make me, in a word, smarter. With the electrodes in place, J. León Morales-Quezada, senior research associate at Harvard’s Laboratory of Neuromodulation, pressed a button on his computer and I felt . . . absolutely nothing. No pain. No tingling. Not even a little muscle twitching. “Is it on?” I asked. Morales-Quezada assured me it was. For proof, he pointed to a flat-screen on the wall, displaying signals from six electroencephalogram (EEG) monitors also attached to my head. After 10 minutes of charging my brain, he turned on a computerized exercise I was supposed to practice while the current continued flowing. Called an attention-switching task, it’s used by psychologists as a measure of “executive function” or “cognitive control”: the ability to overrule your urges, to ignore distractions and to quickly shift your focus. Young adults generally do better than older people; people with greater overall cognitive abilities generally perform better than those with less. © 2013 The New York Times Company
By JOHN RUDOLF GUATEMALA CITY — DONALD RODAS, a baby-faced man in his late 20s with paranoid schizophrenia, arrived at Guatemala’s only public psychiatric hospital last year after being charged with murdering his parents. He says he often wanders freely through the sprawling facility of dilapidated one-story buildings and wooded courtyards, where detainees charged with crimes mingle with ordinary patients and the developmentally disabled. He sees ugly things. Those who refuse their medication are beaten and put in the “little room,” a barren isolation cell, he said. Desperate women sell their bodies for as little as 5 quetzales, or less than a dollar, to afford basic necessities. “I see when they have sex for money,” Mr. Rodas said in halting English. “To buy food. All they have is beans.” The United States began emptying out its vast asylum system in the 1960s, spurred by scathing reports of abuse and neglect, like a 1946 Life magazine exposé that described many institutions as “little more than concentration camps.” The transition to community-based care cut the institutionalized population by more than 90 percent by 1994. But community care resources failed to match demand in the United States, leading to widespread homelessness and an influx of the mentally ill into jails and prisons. Even so, deinstitutionalization is widely credited with ending the abuse and neglect that made mental institutions synonymous with a nightmarish netherworld. Yet this asylum-based model of mental health care remains the standard across much of the globe. In many poor and developing countries, thousands of mentally ill people are warehoused in dirty and dangerous institutions. Health experts and advocates who monitor such facilities say the picture varies little from country to country: overcrowded wards lacking in privacy; poor sanitation; physical and sexual abuse; routine use of restraints and long-term solitary confinement; and forced treatment, including electroshock without consent. The rights of patients judged to be mentally ill are easily stripped by the courts and are difficult if not impossible to regain. © 2013 The New York Times Company
Link ID: 18868 - Posted: 11.04.2013
by Bethany Brookshire In pharmacology research, it seems like one test is never enough. If you want to test a new antidepressant, reviewers (and good logic) often demand that you use more than one test. A locomotor assay to see whether the new drug depresses or increases how much a mouse moves. A forced swim test or tail suspension test to see how it stacks up against other, known antidepressants. Does it increase swimming? Or climbing? Does it decrease immobility more or less than known antidepressants? You may want to use a chronic mild stress test, which exposes mice over a long period of time to things like mild cold, noise or light to induce stress. Does chronic exposure to your new antidepressant relieve the stress like other antidepressants do? What about responses to things like chronic bullying by other mice? Does it work then? You don’t necessarily need to run all of these tests, but you usually do need to run more than one. After all, what if the drug decreases immobility in a forced swim test, like other antidepressants, but it also makes them race around the room … because it’s cocaine? These are the kind of questions that pharmacologists end up asking. Often, to find new, potential antidepressants, for example, we end up matching them against other, known antidepressants in a series of these tests. If the drug performs well in all of them, doesn’t decrease locomotor activity but keeps the mice swimming and stops them from looking stressed after bullying, we might have something new. © Society for Science & the Public 2000 - 2013.
By David Dobbs If you want a look at a high-profile field dealing with a lot of humbling snags, peer into #ASHG2013, the Twitter hashtag for last week’s meeting of the American Society of Human Genetics, held in Boston. You will see successes, to be sure: Geneticists are sequencing and analyzing genomes ever faster and more precisely. In the last year alone, the field has quintupled the rate at which it identifies genes for rare diseases. These advances are leading to treatments and cures for obscure illnesses that doctors could do nothing about only a few years ago, as well as genetic tests that allow prospective parents to bear healthy children instead of suffering miscarriage after miscarriage. But many of the tweets—or any frank geneticist—will also tell you stories of struggle and confusion: The current list of cancer-risk genes, the detection of which leads some people to have “real organs removed,” likely contains many false positives, even as standard diagnostic sequencing techniques are missing many disease-causing mutations. There’s a real possibility that the “majority of cancer predisposition genes in databases are wrong.” And a sharp team of geneticists just last week cleanly dismantled a hyped study from last year that claimed to find a genetic signature of autism clear enough to diagnose the risk of it in unborn children. This sample reads like an abstract of the entire field of genetics. In researching a book about genetics over the past four years, I’ve found a field that stands in a bizarre but lovely state of confusion—taken aback, but eager to advance; balanced tenuously between wild ambition and a deep but troubling humility. In the 13 years since the sequencing of the first human genome, the field has solved puzzles that 14 years ago seemed hopeless. Yet geneticists with any historical memory hold a painful awareness that their field has fallen short of the glory that seemed close at hand when Francis Collins, Craig Venter, and Bill Clinton announced their apparent triumph in June 2000. © 2013 The Slate Group, LLC
Keyword: Genes & Behavior
Link ID: 18846 - Posted: 10.29.2013
By Janet Davison, CBC News Jason Novick has seen the darkness that mental health disorders can create. The 27-year-old Toronto man has also seen how advocacy — by himself and by others — has been vital in helping him cope with bipolar disorder, general anxiety disorder, mania and depression, particular during the stressful transition from his teenage years to leaving home for post-secondary school. "Mental health awareness … is still an issue that’s largely misunderstood," he said in a recent interview. "There’s a lot of [post-secondary] administrative workers and professors and program co-ordinators and what have you who won’t know the first thing about such issues, so your best ally is probably going to be yourself a lot of the time." Another ally can also be a caring friend or family member who steps up to help others understand the larger situation. Novick remembers going with his mother to "set the record straight" with a college professor. They wanted to explain to the instructor that it was his mental health that was his problem, not any lack of interest in the course. "It was my mental health that was causing me to be so withdrawn, that was causing me to be so unmotivated. I was passionate about the subject, but I was not passionate about life and living." Novick, who says he contemplated suicide at one point and has been in closed hospital wards three times because of his disorders, is much more passionate about life and living now, particularly after having completed an inpatient program at the Centre for Addiction and Mental Health in Toronto. © CBC 2013
By JAMES GORMAN Worldwide, 100,000 people have electrical implants in their brains to treat the involuntary movements associated with Parkinson’s disease, and scientists are experimenting with the technique for depression and other disorders. But today’s so-called deep brain stimulation only treats — it does not monitor its own effectiveness, partly because complex ailments like depression do not have defined biological signatures. The federal Defense Advanced Research Projects Agency, known as Darpa, announced Thursday that it intended to spend more than $70 million over five years to jump to the next level of brain implants, either by improving deep brain stimulation or by developing new technology. Justin Sanchez, Darpa program manager, said that for scientists now, “there is no technology that can acquire signals that can tell them precisely what is going on with the brain.” And so, he said, Darpa is “trying to change the game on how we approach these kinds of problems.” The new program, called Systems-Based Neurotechnology and Understanding for the Treatment of Neuropsychological Illnesses, is part of an Obama administration brain initiative, announced earlier this year, intended to promote innovative basic neuroscience. Participants in the initiative include Darpa, as well as the National Institutes of Health and the National Science Foundation. The announcement of Darpa’s goal is the first indication of how that research agency will participate in the initiative. The money is expected to be divided among different teams, and research proposals are now being sought. Darpa’s project is partly inspired by the needs of combat veterans who suffer from mental and physical conditions, and is the first to invest directly in researching human illness as part of the brain initiative. © 2013 The New York Times Company
Amanda Mascarelli Duplication of a single gene — and too much of the corresponding protein in brain cells — causes mice to have seizures and display manic-like behaviour, a study has found. But a widely used drug reversed the symptoms, suggesting that it could also help some people with hyperactivity who do not respond to common treatments. Smooth functioning at the synapses, the junctions between brain cells, is crucial to functions that control everything from social etiquette to everyday decision-making. It is increasingly thought that some neuropsychiatric disorders are caused by function of the synapses going awry1, and indeed researchers have found that neuropsychiatric conditions such as schizophrenia and autism can sometimes be traced to missing, mutated or duplicated copies of SHANK32, a gene that encodes one of the 'architectural' proteins that help to ensure that messages are relayed properly between cells. Some people with attention deficit hyperactivity disorder (ADHD), Asperger's syndrome or schizophrenia have an extra copy of a wider region of DNA that contains SHANK33. To explore the role of SHANK3, Huda Zoghbi, a neurogeneticist at Baylor College of Medicine in Houston, Texas, and her colleagues created mice with duplicate copies of the gene. “The mouse was remarkably hyperactive, running around like mad,” says Zoghbi. But the animals did not respond to stimulant medications typically used to treat ADHD. Instead, their hyperactivity grew much worse. “That’s when we knew this was not typical ADHD,” says Zoghbi. The study is published today in Nature4. © 2013 Nature Publishing Group
by Bruce Bower Thomas Jefferson defended the right to pursue happiness in the Declaration of Independence. But that’s so 237 years ago. Many modern societies champion everyone’s right to be happy pretty much all the time. Good luck with that, says psychologist Joseph Forgas of the University of New South Wales in Sydney. A lack of close friends, unfulfilled financial dreams and other harsh realities leave many people feeling lonely and forlorn a lot of the time. But there’s a mental and social upside to occasional downers that often goes unappreciated. “Bad moods are seen in our happiness-focused culture as representing a problem, but we need to be aware that temporary, mild negative feelings have important benefits,” Forgas says. Growing evidence suggests that gloomy moods improve key types of thinking and behavior, Forgas asserts in a new review paper aptly titled “Don’t worry, be sad!” For good evolutionary reasons, positive and negative moods subtly recruit thinking styles suited to either benign or troubling situations, he says. Each way of dealing with current circumstances generally works well, if imperfectly. New and recent studies described by Forgas in the June Current Directions in Psychological Science illustrate some of the ways in which periods of sadness spontaneously recruit a detail-oriented, analytical thinking style. Morose moods have evolved as early-warning signs of problematic or dangerous situations that demand close attention, these reports suggest. © Society for Science & the Public 2000 - 2013.
By Lary C. Walker Clumps of proteins twisted into aberrant shapes cause the prion diseases that have perplexed biologists for decades. The surprises just keep coming with a new report that the simple clusters of proteins responsible for Mad Cow and other prions diseases may, without help from DNA or RNA, be capable of changing form to escape the predations of drugs that target their eradication. Prion drug resistance could be eerily similar to that found in cancer and HIV—and may have implications for drug development for Alzheimer’s and Parkinson’s, neurodegenerative diseases also characterized by misfolded proteins. Prion diseases include scrapie, chronic wasting disease and bovine spongiform encephalopathy (mad cow disease) in nonhuman species, and Creutzfeldt-Jakob disease and fatal insomnia in humans. They are unusual in that they can arise spontaneously, as a result of genetic mutations, or, in some instances, through infection. Remarkably, the infectious agent is not a microbe or virus, but rather the prion itself, a clump of proteins without genetic material. The noxious agents originate when a normally generated protein – called the prion protein – mistakenly folds into a stable, sticky, and potentially toxic shape. When the misfolded protein contacts other prion protein molecules, they too are corrupted and begin to bind to one another. In the ensuing chain reaction, the prions grow, break apart, and spread; within the nervous system, they relentlessly destroy neurons, ultimately, and invariably, leading to death. © 2013 Scientific American
Anne Trafton, MIT News Office Schizophrenia patients usually suffer from a breakdown of organized thought, often accompanied by delusions or hallucinations. For the first time, MIT neuroscientists have observed the neural activity that appears to produce this disordered thinking. The researchers found that mice lacking the brain protein calcineurin have hyperactive brain-wave oscillations in the hippocampus while resting, and are unable to mentally replay a route they have just run, as normal mice do. Mutations in the gene for calcineurin have previously been found in some schizophrenia patients. Ten years ago, MIT researchers led by Susumu Tonegawa, the Picower Professor of Biology and Neuroscience, created mice lacking the gene for calcineurin in the forebrain; these mice displayed several behavioral symptoms of schizophrenia, including impaired short-term memory, attention deficits, and abnormal social behavior. In the new study, which appears in the Oct. 16 issue of the journal Neuron, Tonegawa and colleagues at the RIKEN-MIT Center for Neural Circuit Genetics at MIT’s Picower Institute for Learning and Memory recorded the electrical activity of individual neurons in the hippocampus of these knockout mice as they ran along a track. Previous studies have shown that in normal mice, “place cells” in the hippocampus, which are linked to specific locations along the track, fire in sequence when the mice take breaks from running the course. This mental replay also occurs when the mice are sleeping. These replays occur in association with very high frequency brain-wave oscillations known as ripple events.
Link ID: 18798 - Posted: 10.17.2013
Ewen Callaway As a new study in the British Medical Journal reveals that 1 in 2000 people in the UK may harbour the infectious prion protein which causes variant Creutzfeldt–Jakob disease (vCJD), Nature explains what this means. The usually fatal condition is the human form of bovine spongiform encepalpoathy — dubbed 'mad cow disease' in the UK after an outbreak of the disease in the 1980s. Both diseases are caused by misfolded proteins called prions, which induce other proteins in the brain to clump, eventually destoying neurons. Humans are thought to contract the disease by consuming beef containing infected bovine brain or other central nervous system tissue. But it also spreads through blood transfusions, and some worry that the prion disease is transmitted via contaminated surgical instruments . The BSE outbreak in the 1980s and 1990s led to a surge in British vCJD cases, and a total of 177 have been detected in the UK to date, with just one in the last two years. Cases of vCJD peaked in 2000, leading some scientists to speculate that the disease takes about a decade to develop. Yet other studies of different forms of CJD suggest its incubation time could be much longer — indicating that many Britons may be carrying the infection without symtoms. Studies have come to varying conclusions as to just how many people harbour the abnormal prion protein (PrP) that causes vCJD. Surveys of tens of thousands of appendices and tonsil, discarded after surgery, have come up with prevalence rates ranging from 1 in 40001 to 1 in 10,0002 to 03. © 2013 Nature Publishing Group
Link ID: 18795 - Posted: 10.16.2013
by Simon Makin A drug similar to ketamine has been shown to work as an antidepressant, without the psychosis-like side effects associated with the party drug. In 2000, ketamine was seen to alleviate depression almost immediately in people for whom other treatments had failed. Larger clinical trials have since corroborated the findings. The drawback is that ketamine can cause hallucinations and other psychotic symptoms, making it unsuitable for use as a treatment. These effects also make it difficult to conduct randomised, placebo-controlled trials – the gold standard in clinical medicine – as it is obvious which participants have been given the drug. This meant that there was a possibility that the beneficial effects seen in previous trials were inflated. So a team led by Gerard Sanacora of Yale University and Mike Quirk of pharmaceutical firm AstraZeneca looked for an alternative compound. They decided to test lanicemine, a drug originally developed to treat epilepsy that targets the same brain receptors as ketamine. The team gave 152 people with moderate-to-severe depression and a history of poor response to antidepressants either lanicemine or a placebo three times a week, for three weeks. They were allowed to continue taking any medications they were already on. Before and after the trial the participants' level of depression was rated on a 60-point scale. After three weeks, those taking lanicemine were less depressed by an average of 13.5 points – 5.5 points better than those who took the placebo. The improvement was still statistically significant up to two weeks after the treatment ended. Dizziness was the only common side effect. © Copyright Reed Business Information Ltd.
Mind over matter. New research explains how abstract benefits of exercise—from reversing depression to fighting cognitive decline—might arise from a group of key molecules. While our muscles pump iron, our cells pump out something else: molecules that help maintain a healthy brain. But scientists have struggled to account for the well-known mental benefits of exercise, from counteracting depression and aging to fighting Alzheimer’s and Parkinson’s disease. Now, a research team may have finally found a molecular link between a workout and a healthy brain. Much exercise research focuses on the parts of our body that do the heavy lifting. Muscle cells ramp up production of a protein called FNDC5 during a workout. A fragment of this protein, known as irisin, gets lopped off and released into the bloodstream, where it drives the formation of brown fat cells, thought to protect against diseases such as diabetes and obesity. (White fat cells are traditionally the villains.) While studying the effects of FNDC5 in muscles, cellular biologist Bruce Spiegelman of Harvard Medical School in Boston happened upon some startling results: Mice that did not produce a so-called co-activator of FNDC5 production, known as PGC-1α, were hyperactive and had tiny holes in certain parts of their brains. Other studies showed that FNDC5 and PGC-1α are present in the brain, not just the muscles, and that both might play a role in the development of neurons. © 2013 American Association for the Advancement of Science.
Link ID: 18781 - Posted: 10.12.2013
Children whose mothers are depressed during pregnancy have a small increased risk of depression in adulthood, according to a UK study. Medical treatment during pregnancy could lower the risk of future mental health problems in the child, say researchers at Bristol University. The study followed the offspring of more than 8,000 mothers who had postnatal or antenatal depression. The risk is around 1.3 times higher than normal at age 18, it found. The study is published in JAMA Psychiatry. Lead researcher Dr Rebecca Pearson told the BBC: "Depression in pregnancy should be taken seriously and treated in pregnancy. It looks like there is a long-term risk to the child, although it is small." She said it was an association, not a causal link, and needed further investigation. Prof Carmine Pariante of King's College London's Institute of Psychiatry said the development of an individual's mental health did not start at birth but in the uterus. "The message is clear - helping women who are depressed in pregnancy will not only alleviate their suffering but also the suffering of the next generation." Prof Celso Arango of Gregorio Maranon General University Hospital, Madrid, said stress hormones may affect the child's development in the womb. "Women with depression would ideally be treated before getting pregnant, but if they are already pregnant when diagnosed with depression it is even more important that they are treated as it will impact on the mother and child." The researchers think different factors may be involved in antenatal and postnatal depression, with environmental factors such as social support having a bigger impact in postnatal depression. BBC © 2013
Alison Abbott In a sign that psychiatric-disease research is entering a new era, the pharmaceutical giant Novartis has hired an expert in neural circuitry, rather than pharmacology, to head its relaunched neuroscience division. The appointment of 42-year-old Ricardo Dolmetsch, who has spent his entire career in academic research, signifies a radical policy shift for the company, as it moves away from conventional neurotransmitter research to concentrate on analysing the neural circuitry that causes brain diseases. The decision suggests Novartis is confident that after years of fruitless research in the field, revolutionary advancements in, for example, genetic and stem-cell technologies will pay dividends. The company intends to hire 100 new staff members for the department over the next 3 years. But the move is risky: even if it pans out, new drugs for common disorders such as schizophrenia could be decades away from reaching the market. Dolmetsch, a former senior director at the Allen Institute for brain Science in Seattle, Washington, who has also worked at Stanford University School of Medicine in California, says that his new role gives him access to previously unimaginable resources. “I had this idea that big pharma was a slow, plodding, conservative giant,” he says. “I was surprised by the depth of science at Novartis.” An expert in autism spectrum disorder, he was also attracted by the prospect of contributing to the development of therapies — something that academic institutions are poorly equipped to do — particularly because one of his own sons has autism. There was “not much enthusiasm” for studying disease at the Allen Institute, which focuses instead on basic research into brain science, he says. © 2013 Nature Publishing Group
by Linda Geddes There's little doubt that smoking during pregnancy is bad for the baby. But besides stunting growth and boosting the risk of premature birth, it seems that tobacco smoke leaves a lasting legacy on the brain. Children whose mothers smoked during pregnancy have altered brain growth, which may put them at greater risk of anxiety and depression. Hanan El Marroun at Erasmus Medical Center in Rotterdam, the Netherlands, and her colleagues had previously seen impaired brain growth in babies born to women who smoked throughout their pregnancy, although no differences were seen if women stopped smoking soon after learning that they were pregnant. The question was whether these changes were permanent, or would correct themselves as the child developed. So El Marroun's team used MRI to look at the brains of 113 children aged between 6 and 8 years old whose mothers smoked during pregnancy, and another 113 children whose mums did not. The children's behavioural and emotional functioning was also tested. Depression link Those whose mothers smoked throughout pregnancy had smaller total brain volumes and reduced amounts of grey and white matter in the superior frontal cortex, an area involved in regulating moods. What's more, these structural differences correlated with symptoms of depression and anxiety in the children. Not every child whose mother smoked showed these symptoms, and the study could not definitively prove cause and effect. However, because we already know that smoking is bad for babies, pregnant women should continue to be advised not to smoke, El Marroun says. © Copyright Reed Business Information Ltd.
By Gary Stix Psychological depression is more than an emotional state. Good evidence for that comes from emerging new uses for a technology already widely prescribed for Parkinson’s patients. The more neurologists and surgeons learn about the aptly named deep brain stimulation, the more they are convinced that the currents from the technology’s implanted electrodes can literally reboot brain circuits involved with the mood disorder. Thomas Schlaepfer, a psychiatrist from the University of Bonn Hospital and a leading expert in researching deep brain stimulation, describes in the interview that follows the workings of the technique and why it may help the severely depressed. Can you explain what deep brain stimulation is and what it is currently used for? Deep brain stimulation refers to the implantation of very small electrodes in both hemispheres of the brain, which are connected to a neurostimulator, usually placed under the skin on the right chest. This device is in size and function very similar to a heart pacemaker. It allows stimulations of different pulse width and frequency. Depending on the chosen stimulation parameters the electrodes in the brain are able to “neuromodulate” – to reversibly alter the function – of the surrounding brain tissue. Deep brain stimulation has gained widespread acceptance as a successful treatment for tremor associated with Parkinson’s disease. More than 80,000 patients worldwide have been treated with this method. Some see deep brain stimulation as a much less invasive and fully reversibly alternative to historical neurosurgical interventions, which require tiny amounts of brain tissue to be destroyed in order to have clinical effects. © 2013 Scientific American
Link ID: 18747 - Posted: 10.05.2013