by Helen Thomson ONE moment you are alive. The next you are dead. A few hours later and you are alive again. Pharmacologists have discovered a mechanism that triggers Cotard's syndrome – the mysterious condition that leaves people feeling like they, or parts of their body, no longer exist. With the ability to switch the so-called walking corpse syndrome on and off comes the prospect of new insights into how conscious experiences are constructed. Acyclovir – also known by the brand name Zovirax – is a common drug used to treat cold sores and other herpes infections. It usually has no harmful side effects. However, about 1 per cent of people who take the drug orally or intravenously experience some psychiatric side effects, including Cotard's. These occur mainly in people who have renal failure. To investigate the potential link between acyclovir and Cotard's, Anders Helldén at Karolinska University Hospital in Stockholm and Thomas Lindén at the Sahlgrenska Academy in Gothenburg pooled data from Swedish drug databases along with hospital admissions. They identified eight people with acyclovir-induced Cotard's. One woman with renal failure began using acyclovir to treat shingles. She ran into a hospital screaming, says Helldén. After an hour of dialysis, she started to talk: she said the reason she was so anxious was that she had a strong feeling she was dead. After a few more hours of dialysis she said, "I'm not quite sure whether I'm dead any more but I'm still feeling very strange." Four hours later: "I'm pretty sure I'm not dead any more but my left arm is definitely not mine." Within 24 hours, the symptoms had disappeared. © Copyright Reed Business Information Ltd.

Keyword: Attention
Link ID: 18805 - Posted: 10.17.2013

by Denise Chow, LiveScience The discovery of a fossilized brain in the preserved remains of an extinct "mega-clawed" creature has revealed an ancient nervous system that is remarkably similar to that of modern-day spiders and scorpions, according to a new study. The fossilized Alalcomenaeus is a type of arthropod known as a megacheiran (Greek for "large claws") that lived approximately 520 million years ago, during a period known as the Lower Cambrian. The creature was unearthed in the fossil-rich Chengjiang formation in southwest China. VIDEO: Bugs, Arthropods, and Insects! Oh My! Researchers studied the fossilized brain, the earliest known complete nervous system, and found similarities between the extinct creature's nervous system and the nervous systems of several modern arthropods, which suggest they may be ancestrally related. [Photos of Clawed Arthropod & Other Strange Cambrian Creatures] Living arthropods are commonly separated into two major groups: chelicerates, which include spiders, horseshoe crabs and scorpions, and a group that includes insects, crustaceans and millipedes. The new findings shed light on the evolutionary processes that may have given rise to modern arthropods, and also provide clues about where these extinct mega-clawed creatures fit in the tree of life. "We now know that the megacheirans had central nervous systems very similar to today's horseshoe crabs and scorpions," senior author Nicholas Strausfeld, a professor in the department of neuroscience at the University of Arizona in Tucson, said in a statement. "This means the ancestors of spiders and their kin lived side by side with the ancestors of crustaceans in the Lower Cambrian." © 2013 Discovery Communications, LLC.

Keyword: Evolution
Link ID: 18804 - Posted: 10.17.2013

By Christopher Wanjek and LiveScience Your liver could be "eating" your brain, new research suggests. People with extra abdominal fat are three times more likely than lean individuals to develop memory loss and dementia later in life, and now scientists say they may know why. It seems that the liver and the hippocampus (the memory center in the brain), share a craving for a certain protein called PPARalpha. The liver uses PPARalpha to burn belly fat; the hippocampus uses PPARalpha to process memory. In people with a large amount of belly fat, the liver needs to work overtime to metabolize the fat, and uses up all the PPARalpha — first depleting local stores and then raiding the rest of the body, including the brain, according to the new study. The process essentially starves the hippocampus of PPARalpha, thus hindering memory and learning, researchers at Rush University Medical Center in Chicago wrote in the study, published in the current issue of Cell Reports. Other news reports were incorrect in stating that the researchers established that obese individuals were 3.6 times more likely than lean individuals to develop dementia. That finding dates back to a 2008 study by researchers at the Kaiser Permanente Division of Research in Oakland, Calif. In another study, described in a 2010 article in the Annals of Neurology, researchers at Boston University School of Medicine found that the greater the amount of belly fat, the greater the brain shrinkage in old age. © 2013 Scientific American

Keyword: Learning & Memory; Development of the Brain
Link ID: 18803 - Posted: 10.17.2013

by Bob Holmes The great flowering of human evolution over the past 2 million years may have been driven not by the African savannahs, but by the lakes of that continent's Great Rift Valley. This novel idea, published this week, may explain why every major advance in the evolution of early humans, from speciation to the vast increase in brain size, appears to have taken place in eastern Africa. Anthropologists have surmised for several years that early humans, or hominins, might have evolved their unusually large, powerful brains to cope with an increasingly variable climate over the past few million years. However, studies testing this hypothesis have been equivocal, perhaps because most use global or continental-scale measures of climate, such as studying trends in the amount of airborne dust from dry earth that is blown into the ocean and incorporated into deep-sea sediments. Mark Maslin, a palaeoclimatologist at University College London, and his colleague Susanne Shultz at the University of Manchester, UK, have taken a local approach instead, by studying whether the presence or absence of lakes in the Rift Valley affected the hominins living there. Maslin's hunch is that relatively short periods of extreme variability 2.6, 1.8, and 1 million years ago – which are important periods for human evolution – corresponded to times of rapid change in the large lakes of the Great Rift Valley. Because the valley concentrates rainfall from a wide area into relatively small basins, these lakes are unusually sensitive to rainfall and swell or disappear depending on climate. © Copyright Reed Business Information Ltd.

Keyword: Evolution
Link ID: 18802 - Posted: 10.17.2013

By Jason G. Goldman Scientists love yawning. No, that’s not quite right. Scientists love doing research on yawning. It seems to be of interest to folks in fields ranging from primatology to developmental psychology to psychopathology to animal behavior. If the notion of scientifically investigation the purpose of yawning makes you, well, yawn, then you’re missing one of the more interesting debates in the social cognition literature. To understand why yawning is about more than feeling tired or bored, we have to go back a few years. Once upon a time, scientists thought that yawning might be process through which the brain keeps itself cool (PDF). Yawning is associated with increases in blood pressure, and the consequential increase in blood flow might mean that the vascular system acts as a radiator, replacing the warm blood in the brain with cooler blood. It could also be that the deep inhalation of cold air during a yawn can, through convection, alter blood temperature which in turn could cool the brain. Even if it turns out that some yawns can be explained through purely physiological means, yawning is also contagious for humans and other species. If someone watches someone else yawning, they’ll be likely to yawn as well. That means that there is social component to yawning, and it might be related to empathy. It turns out that there’s a correlation between a person’s self-reported empathy and their susceptibility to reacting to a yawn contagion, and those who are more skilled at theory of mind tasks are also more likely (PDF) to yawn contagiously. © 2013 Scientific American

Keyword: Emotions; Evolution
Link ID: 18801 - Posted: 10.17.2013

Henry Astley In the Mark Twain story The Celebrated Jumping Frog of Calaveras County, a frog named Daniel Webster "could get over more ground at one straddle than any animal of his breed you ever see." Now, scientists have visited the real Calaveras County in hopes of learning more about these hopping amphibians. They’ve found that what they see in the lab doesn’t always match the goings-on in the real world. If you wanted to know how far the bullfrog Rana catesbeiana could jump, the scientific literature would give you one answer: 1.295 meters, published in Smithsonian Contributions to Zoology in 1978. If you looked at the Guinness Book of World Records, though, you'd find a different answer. In 1986, a bullfrog called Rosie the Ribeter covered 6.55 meters in three hops. If you divide by three, at least one of those hops had to be no shorter than 2.18 meters—about four bullfrog body lengths more than the number in the scientific paper. The disparity matters. If bullfrogs can hop only 1.3 meters, they have enough power in their muscles to pull off the jump without any other anatomical help. But if they can jump farther, they must also be using a stretchy tendon to power their hops—an ability that other frogs have but that researchers thought bullfrogs had lost. These particular amphibians, scientists speculated, might have made some kind of evolutionary tradeoff that shortened their jumps but enabled them to swim better in the water, where they spend much of their lives. © 2013 American Association for the Advancement of Science

Keyword: Miscellaneous
Link ID: 18800 - Posted: 10.17.2013

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

Keyword: Prions; Alzheimers
Link ID: 18799 - Posted: 10.17.2013

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.

Keyword: Schizophrenia
Link ID: 18798 - Posted: 10.17.2013

By MICHAEL WINES NEW HOLSTEIN, Wis. — Next to their white clapboard house on a rural road here, in long rows of cages set beneath the roofs of seven open-air sheds, Virginia and Gary Bonlander are raising 5,000 minks. Or were, anyway, until two Saturdays ago, when the police roused them from bed at 5 a.m. with a rap on their door. The Bonlanders woke one recent morning to find thousands of the creatures zipping across their lawn. Outside, 2,000 minks were scampering away — up to 50 top-quality, full-length and, suddenly, free-range mink coats. “The backyard was full of mink. The driveway was full of mink,” Mrs. Bonlander recalled a few days ago. “Then, pshew” — she made a whooshing sound — “they were gone.” And not only in Wisconsin, the mink-raising capital of the United States. After something of a hiatus, the animal rights movement has resumed a decades-old guerrilla war against the fur industry with a vengeance — and hints of more to come. In New Holstein; in Grand Meadow, Minn.; in Coalville, Utah; in Keota, Iowa; and four other states, activists say, eight dark-of-night raids on mink farms have liberated at least 7,700 of the critters — more than $770,000 worth of pelts — just since late July. That is more such raids than in the preceding three years combined. Two more raids in Ontario and British Columbia freed 1,300 other minks and foxes during the same period, according to the North American Animal Liberation Press Office, which bills itself as a conduit for messages from anonymous animal rights activists. “What we’re seeing now is unprecedented,” Peter Young, a Santa Cruz, Calif., activist who was imprisoned in 2005 for his role in raids on six mink ranches, said in a telephone interview. Though still an outspoken defender of the animal rights movement and mink-ranch raids, Mr. Young says he has no contact with those who raid fur farms or commit other illegal acts and, in fact, does not know who they are. © 2013 The New York Times Company

Keyword: Animal Rights
Link ID: 18797 - Posted: 10.17.2013

by Colin Barras A part of all of us loves sums. Eavesdropping on the brain while people go about their daily activity has revealed the first brain cells specialised for numbers. Josef Parvizi and his colleagues at Stanford University in California enlisted the help of three people with epilepsy whose therapy involved placing a grid of electrodes on the surface of their brain that record activity. Neurons fired in a region called the intraparietal sulcus when the three volunteers performed arithmetic tests, suggesting they dealt with numbers. The team continued to monitor brain activity while the volunteers went about their normal activity in hospital. Comparing video footage of their stay with their brain activity (see video, above) revealed that the neurons remained virtually silent for most of the time, bursting into life only when the volunteers talked about numbers or numerical concepts such as "more than" or "less than". There is debate over whether some neural populations perform many functions or are involved in very precise tasks. "We show here that there is specialisation for numeracy," says Parvizi. Journal reference: Nature Communications, DOI: 10.1038/ncomms3528 © Copyright Reed Business Information Ltd.

Keyword: Attention
Link ID: 18796 - Posted: 10.16.2013

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

Keyword: Prions
Link ID: 18795 - Posted: 10.16.2013

Doug Greene, WVIT and NBC News staff NBC News Oreos are as addictive as cocaine, at least for lab rats, and just like us, they like the creamy center best. Eating the sugary treats activates more neurons in the brain’s “pleasure center” than drugs such as cocaine, the team at Connecticut College found. “Our research supports the theory that high-fat/ high-sugar foods stimulate the brain in the same way that drugs do,” neuroscience assistant professor Joseph Schroeder says. “That may be one reason people have trouble staying away from them and it may be contributing to the obesity epidemic.” Schroeder’s neuroscience students put hungry rats into a maze. On one side went rice cakes. “Just like humans, rats don’t seem to get much pleasure out of eating them,” Schroeder said. On the other side went Oreos. Then the rats got the option of hanging out where they liked. They compared the results to a different test. In that on, rats on one side if the maze got an injection of saline while those on the other side got injections of cocaine or morphine. Rats seems to like the cookies about as much as they liked the addictive drugs. When allowed to wander freely, they’d congregate on the Oreo side for about as much time as they would on the drug side. Oh, and just like most people - the rats eat the creamy center first.

Keyword: Drug Abuse; Obesity
Link ID: 18794 - 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.

Keyword: Depression; Drug Abuse
Link ID: 18793 - Posted: 10.16.2013

By Emilie Reas Think back to your first childhood beach vacation. Can you recall the color of your bathing suit, the softness of the sand, or the excitement of your first swim in the ocean? Early memories such as this often arise as faded snapshots, remarkably distinct from newer memories that can feel as real as the present moment. With time, memories not only lose their rich vividness, but they can also become distorted, as our true experiences tango with a fictional past. The brain’s ability to preserve or alter memories lies at the heart of our basic human experience. The you of today is molded not only by your personal history, but also by your mental visits to that past, prompting you to laugh over a joke heard yesterday, reminisce about an old friend or cringe at the thought of your awkward adolescence. When we lose those pieces of the past we lose pieces of our identity. But just where in the brain do those old memories go? Despite decades studying how the brain transforms memories over time, neuroscientists remain surprisingly divided over the answer. Some of the best clues as to how the brain processes memories have come from patients who can’t remember. If damage to a particular brain area results in memory loss, researchers can be confident that the region is important for making or recalling memories. Such studies have reliably shown that damage to the hippocampus, a region nestled deep inside the brain, prevents people from creating new memories. But a key question, still open to debate, is what happens to a memory after it’s made. Does it stay in the hippocampus or move out to other areas of the brain? To answer this, scientists have studied old memories formed before brain damage, only to discover a mix of inconsistent findings that have given rise to competing theories. © 2013 Scientific American

Keyword: Learning & Memory
Link ID: 18792 - Posted: 10.16.2013

Brian Owens Bats that nest inside curled-up leaves may be getting an extra benefit from their homes: the tubular roosts act as acoustic horns, amplifying the social calls that the mammals use to keep their close-knit family groups together. South American Spix’s disc-winged bats (Thyroptera tricolor) roost in groups of five or six inside unfurling Heliconia and Calathea leaves. The leaves remain curled up for only about 24 hours, so the bats have to find new homes almost every day, and have highly specialized social calls to help groups stay together. When out flying, they emit a simple inquiry call. Bats inside leaves answer with a more complex response call to let group members know where the roost is. Gloriana Chaverri, a biologist at the University of Costa Rica in Golfito, took curled leaves into the lab and played recorded bat calls through them, to see how the acoustics were changed by the tapered tubular shape of the leaves. “The call emitted by flying bats got really amplified,” she says, “while the calls from inside the leaves were not amplified as much.” Sound system The inquiry calls from outside the roost were boosted by as much as 10 decibels as the sound waves were compressed while moving down the narrowing tube — the same thing that happens in an amplifying ear trumpet. Most response calls from inside the leaf were boosted by only 1–2 decibels, but the megaphone shape of the leaf made them highly directional. The results are published today in Proceedings of the Royal Society B1. © 2013 Nature Publishing Group

Keyword: Hearing; Animal Communication
Link ID: 18791 - Posted: 10.16.2013

By ELISABETH ROSENTHAL The barrage of advertisements targets older men. “Have you noticed a recent deterioration of your ability to play sports?” “Do you have a decrease in sex drive?” “Do you have a lack of energy?” If so, the ads warn, you should “talk to your doctor about whether you have low testosterone” — “Low T,” as they put it. In the view of many physicians, that is in large part an invented condition. Last year, drug makers in the United States spent $3.47 billion on advertising directly to consumers, according to FiercePharma.com. And while ever-present ads like those from AbbVie Pharmaceuticals have buoyed sales of testosterone gels, that may be bad for patients as well as the United States’ $2.7 trillion annual health care bill, experts say. Sales of prescription testosterone gels that are absorbed through the skin generated over $2 billion in American sales last year, a number that is expected to more than double by 2017. Abbott Laboratories — which owned AbbVie until Jan. 1 — spent $80 million advertising its version, AndroGel, last year. Once a niche treatment for people suffering from hormonal deficiencies caused by medical problems like endocrine tumors or the disruptive effects of chemotherapy, the prescription gels are increasingly being sold as lifestyle products, to raise dipping levels of the male sex hormone as men age. “The market for testosterone gels evolved because there is an appetite among men and because there is advertising,” said Dr. Joel Finkelstein, an associate professor at Harvard Medical School who is studying male hormone changes with aging. “The problem is that no one has proved that it works and we don’t know the risks.” © 2013 The New York Times Company

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 18790 - Posted: 10.16.2013

by Alyssa Botelho A sense of touch lets you connect with loved ones, makes your limbs feel your own, and helps you to interact with your surroundings. But people who are paraplegics or have lost limbs have to navigate the world without this most fundamental of sensory inputs. Sliman Bensmaia at the University of Chicago, Illinois, is working to change that with a new model for transmitting a sense of touch to the brain that bypasses regular routes. He hopes it will be a blueprint for constructing prosthetics that convey touch in the same way that natural limbs do. To start, Bensmaia and his colleagues trained rhesus macaques to focus their gaze in different directions depending on whether their index finger or fourth finger were being prodded. Microelectrodes were then placed in an area of the brain called the primary somatosensory cortex. This area represents an entire map of the body, with each neuron responsible for sensing when a different part of the skin is touched. Microelectrodes record the activity pattern of neurons. They can also be used in reverse – to deliver electrical stimulation to make neurons fire. Fourth finger exercise Next, the team recorded what activity occurred and where it registered in the somatosensory cortex when a monkey had its index or fourth finger poked. Then they stimulated the brain using the same pattern of activity. The monkeys reacted as if they had been touched – fixing their gaze in the direction they been taught in response to a poke. © Copyright Reed Business Information Ltd.

Keyword: Pain & Touch; Robotics
Link ID: 18789 - Posted: 10.15.2013

By GINA KOLATA William Howard Taft, the only massively obese man ever to be president of the United States, struggled mightily to control his weight a century ago, worrying about his health and image, and endured humiliation from cartoonists who delighted in his corpulent figure. But new research has found that his weight-loss program was startlingly contemporary, and his difficulties keeping the pounds off would be familiar to many Americans today. On the advice of his doctor, a famed weight-loss guru and author of popular diet books, he went on a low-fat, low-calorie diet. He avoided snacks. He kept a careful diary of what he ate and weighed himself daily. He hired a personal trainer and rode a horse for exercise. And he wrote his doctor, Nathaniel E. Yorke-Davies, with updates on his progress, often twice a week. In a way, he was ahead of his time. Obesity became a medical issue by the middle of the 20th century, around the time the term “obesity” rather than “corpulence” came into vogue, said Abigail C. Saguy, a sociologist at the University of California, Los Angeles, who specializes in the study of obesity. Taft’s story shows that “at least in some cases, corpulence was already treated as a medical problem early in the century,” she added. Like many dieters today, Taft, 6 feet 2 inches tall, lost weight and regained it, fluctuating from more than 350 to 255 pounds. He was 48 when he first contacted Dr. Yorke-Davies, and spent the remaining 25 years of his life corresponding with the doctor and consulting other physicians in a quest to control his weight. Taft’s struggles are recounted by Deborah Levine, a medical historian at Providence College in Rhode Island. She discovered the extensive correspondence between Taft and the diet doctor, including Taft’s diet program, his food diary, and a log of his weight. Her findings were published Monday in The Annals of Internal Medicine. His story, Dr. Levine said, “sheds a lot of light on what we are going through now.” © 2013 The New York Times Company

Keyword: Obesity
Link ID: 18788 - Posted: 10.15.2013

By Sandra G. Boodman, Janet Ruddock was crushed: She had dreamed of greeting her first grandchild, and now that once-in-a-lifetime experience had been marred by the embarrassing problem that had derailed her life for nearly a decade. In June 2010, Ruddock, then 59, and her husband had flown to Vancouver, B.C., from Washington to meet their new grandson. But soon after they arrived, Ruddock’s in­trac­table sweating went into overdrive. As she sat in a rocking chair, perspiration drenched her head and upper body, soaking her shirt and dripping onto the 4-week-old infant. “I burst into tears,” Ruddock recalled. “All I can remember is the feeling that I’m wet, this poor baby’s wet and a moment you should always remember is ruined. You’re never going to get it back. “ For Ruddock, that event precipitated a suicidal depression. For the previous eight years she had undergone tests, taken drugs and endured the bafflement — and skepticism — of a parade of doctors she consulted about the extreme, unpredictable sweating that engulfed her head and upper body. After confiding her despair to a relative, she began seeing a psychiatrist. By chance, a few months later she learned about a woman whose experience mirrored her own and provided her a much-needed road map. “It’s a fascinoma,” said retired Washington internist Charles Abrams, using the medical slang for an unusual — or unusually interesting — case. “You usually hate for patients to come in and say, ‘I found this on the Internet,’ ” said Abrams, who treated Ruddock until his retirement last year. “But every once in a while, something is brought to your attention.” © 1996-2013 The Washington Post

Keyword: Miscellaneous
Link ID: 18787 - Posted: 10.15.2013

By SINDYA N. BHANOO Hungry babies instinctively open their mouths as their mother’s breast or a bottle draws near. Now, researchers from England and France report that this instinct — the anticipation of touch — is a skill fetuses teach themselves in the womb. Studying scans at monthly intervals between 24 and 36 weeks of pregnancy, the scientists found that the youngest fetuses were more likely to touch their heads and that as they matured, they began to touch their mouths more. And by 36 weeks, the fetuses began to open their mouths before they touched them. The anticipation of touch is a skill a baby uses during feeding, said Nadja Reissland, a psychologist at Durham University in England, who reports the findings along with colleagues in the journal Developmental Psychobiology. “We can’t say it’s a precursor to feeding, but it’s one element of feeding,” she said. “You actually need to open your mouth in order to feed.” Premature babies may not have fully grasped this skill, Dr. Reissland said. The study could provide more information about what premature babies can do and what special care they need. “The fetus might actually be learning the limits of its body, the texture of the body and what it feels like to be a person in the womb,” she said. © 2013 The New York Times Company

Keyword: Development of the Brain
Link ID: 18786 - Posted: 10.15.2013