Chapter 5. The Sensorimotor System
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|By Lindsey Konkel For 28 years, Bill Gilmore lived in a New Hampshire beach town, where he surfed and kayaked. “I’ve been in water my whole life,” he said. “Before the ocean, it was lakes. I’ve been a water rat since I was four.” Now Gilmore can no longer swim, fish or surf, let alone button a shirt or lift a fork to his mouth. Earlier this year, he was diagnosed with amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease. In New England, medical researchers are now uncovering clues that appear to link some cases of the lethal neurological disease to people’s proximity to lakes and coastal waters. About five years ago, doctors at a New Hampshire hospital noticed a pattern in their ALS patients—many of them, like Gilmore, lived near water. Since then, researchers at Dartmouth-Hitchcock Medical Center have identified several ALS hot spots in lake and coastal communities in New England, and they suspect that toxic blooms of blue-green algae—which are becoming more common worldwide—may play a role. Now scientists are investigating whether breathing a neurotoxin produced by the algae may raise the risk of the disease. They have a long way to go, however: While the toxin does seem to kill nerve cells, no research, even in animals, has confirmed the link to ALS. As with all ALS patients, no one knows what caused Bill Gilmore’s disease. He was a big, strong guy—a carpenter by profession. One morning in 2011, his arms felt weak. “I couldn’t pick up my tools. I thought I had injured myself,” said Gilmore, 59, who lived half his life in Hampton and now lives in Rochester, N.H. © 2014 Scientific American
by Andy Coghlan To catch agile prey on the wing, dragonflies rely on the same predictive powers we use to catch a ball: that is, anticipating by sight where the ball will go and readying body and hand to snatch it from mid-air. Until now, dragonflies were thought to catch their prey without this predictive skill, instead blindly copying every steering movement made by their prey, which can include flies and bees. Now, sophisticated laboratory experiments have tracked the independent body and eye movements of dragonflies as they pursue prey, showing for the first time that dragonflies second guess where their prey will fly to next and then steer their flight accordingly. Throughout the pursuit, they lock on to their target visually while they orient their bodies and flight path for ultimate interception, rather than copying each little deviation in their prey's flight path in the hope of ultimately catching up with it. "The dragonfly lines up its body axis in the flight direction of the prey, but keeps the eyes in its head firmly fixed on the prey," says Anthony Leonardo of the Howard Hughes Medical Institute in Ashburn, Virginia. "It enables the dragonfly to catch the prey from beneath and behind, the prey's blind spot," he says. © Copyright Reed Business Information Ltd.
Link ID: 20412 - Posted: 12.13.2014
|By Claudia Wallis Touch a hot frying pan and the searing message of pain sprints up to your brain and back down to your hand so fast that the impulse to withdraw your fingers seems instantaneous. That rapid-fire signal begins in a heat-sensing molecule called a TRPV1 channel. This specialized protein is abundant on the surface of sensory nerve cells in our fingers and elsewhere and is a shape-shifter that can take an open or closed configuration. Heat opens a central pore in the molecule, so do certain spider toxins and capsaicin—the substance that gives chili peppers their burn. Once the pore is open, charged ions of sodium and calcium flow into the nerve cell, triggering the pain signal. Ouch! As neuroscientist-journalist Stephani Sutherland explains in “Pain that Won’t Quit,” in the December Scientific American, researchers have long been interested in finding ways to moderate the action of this channel—and other ion channels—in patients who suffer from chronic pain. Shutting down the TRPV1 channel completely, however, is not an option because it plays a vital role in regulating body temperature. In two papers published in Nature in December 2013 investigators at the University of California, San Francisco, gave pain researchers a big leg up in understanding TRPV1. They revealed, in exquisite atomic detail, the structure of the channel molecule (from a rat) using an electron cryomicroscope, an instrument designed to explore the 3-D structure of molecules at very low temperatures. One of those investigators, Yifan Cheng, also created this colorful animation, showing how the molecule looks when the channel is open. © 2014 Scientific American
Keyword: Pain & Touch
Link ID: 20411 - Posted: 12.13.2014
Carl Zimmer For thousands of years, fishermen knew that certain fish could deliver a painful shock, even though they had no idea how it happened. Only in the late 1700s did naturalists contemplate a bizarre possibility: These fish might release jolts of electricity — the same mysterious substance as in lightning. That possibility led an Italian physicist named Alessandro Volta in 1800 to build an artificial electric fish. He observed that electric stingrays had dense stacks of muscles, and he wondered if they allowed the animals to store electric charges. To mimic the muscles, he built a stack of metal disks, alternating between copper and zinc. Volta found that his model could store a huge amount of electricity, which he could unleash as shocks and sparks. Today, much of society runs on updated versions of Volta’s artificial electric fish. We call them batteries. Now a new study suggests that electric fish have anticipated other kinds of technology. The research, by Kenneth C. Catania, a biologist at Vanderbilt University, reveals a remarkable sophistication in the way electric eels deploy their shocks. Dr. Catania, who published the study on Thursday in the journal Science, found that the eels use short shocks like a remote control on their victims, flushing their prey out of hiding. And then they can deliver longer shocks that paralyze their prey at a distance, in precisely the same way that a Taser stops a person cold. “It shows how finely adapted eels are to attack prey,” said Harold H. Zakon, a biologist at the University of Texas at Austin, who was not involved in the study. He considered Dr. Catania’s findings especially impressive since scientists have studied electric eels for more than 200 years. © 2014 The New York Times Company
Link ID: 20400 - Posted: 12.06.2014
Injections of a new drug may partially relieve paralyzing spinal cord injuries, based on indications from a study in rats, which was partly funded by the National Institutes of Health. The results demonstrate how fundamental laboratory research may lead to new therapies. “We’re very excited at the possibility that millions of people could, one day, regain movements lost during spinal cord injuries,” said Jerry Silver, Ph.D., professor of neurosciences, Case Western Reserve University School of Medicine, Cleveland, and a senior investigator of the study published in Nature. Every year, tens of thousands of people are paralyzed by spinal cord injuries. The injuries crush and sever the long axons of spinal cord nerve cells, blocking communication between the brain and the body and resulting in paralysis below the injury. On a hunch, Bradley Lang, Ph.D., the lead author of the study and a graduate student in Dr. Silver’s lab, came up with the idea of designing a drug that would help axons regenerate without having to touch the healing spinal cord, as current treatments may require. “Originally this was just a side project we brainstormed in the lab,” said Dr. Lang. After spinal cord injury, axons try to cross the injury site and reconnect with other cells but are stymied by scarring that forms after the injury. Previous studies suggested their movements are blocked when the protein tyrosine phosphatase sigma (PTP sigma), an enzyme found in axons, interacts with chondroitin sulfate proteoglycans, a class of sugary proteins that fill the scars.
Link ID: 20394 - Posted: 12.04.2014
By Beth Winegarner When Beth Wankel’s son, Bowie, was a baby, he seemed pretty typical. But his “terrible twos” were more than terrible: In preschool, he would hit and push his classmates to a degree that worried his parents and teachers. As Bowie got a little older, he was able tell his mom why he was so combative. “He would say things like, 'I thought they were going to step on me or push me,’” Wankel said. “He was overly uncomfortable going into smaller spaces; it was just too much for him.” Among other things, he refused to enter the school bathroom if another student was inside. When Bowie was 3, he was formally evaluated by his preschool teachers. They said he appeared to be having trouble processing sensory input, especially when it came to figuring out where his body is in relation to other people and objects. He’s also very sensitive to touch and to the textures of certain foods, said Wankel, who lives with her family in San Francisco. Bowie has a form of what’s known as sensory processing disorder. As the name suggests, children and adults with the disorder have trouble filtering sights, smells, sounds and more from the world around them. While so-called neurotypicals can usually ignore background noise, clothing tags or cluttered visual environments, people with SPD notice all of those and more — and quickly become overwhelmed by the effort. Rachel Schneider, a mental-health expert and a blogger for adults with SPD, describes it as a “neurological traffic jam” or “a soundboard, except the sound technician is terrible at his job.”
Ewen Callaway Nerve cells that transmit pain, itch and other sensations to the brain have been made in the lab for the first time. Researchers say that the cells will be useful for developing new painkillers and anti-itch remedies, as well as understanding why some people experience unexplained extreme pain and itching. “The short take-home message would be ‘pain and itch in a dish’, and we think that’s very important,” says Kristin Baldwin, a stem-cell scientist at the Scripps Research Institute in La Jolla, California, whose team converted mouse and human cells called fibroblasts into neurons that detect sensations such as pain, itch or temperature1. In a second paper2, a separate team took a similar approach to making pain-sensing cells. Both efforts were published on 24 November in Nature Neuroscience. Peripheral sensory neurons, as these cells are called, produce specialized ‘receptor’ proteins that detect chemical and physical stimuli and convey them to the brain. The receptor that a cell makes determines its properties — some pain-sensing cells respond to chilli oil, for example, and others respond to different pain-causing chemicals. Mutations in the genes encoding these receptors can cause some people to experience chronic pain or, in rare cases, to become impervious to pain. To create these cells in the lab, independent teams led by Baldwin and by Clifford Woolf, a neuroscientist at Boston Children’s Hospital in Massachusetts, identified combinations of proteins that — when expressed in fibroblasts — transformed them into sensory neurons after several days. Baldwin's team identified neurons that make receptors that detect sensations including pain, itch, and temperature, whereas Woolf’s team looked only at pain-detecting cells. Both teams generated cells that resembled neurons in shape and fired in response to capsaicin, which gives chilli peppers their kick, and mustard oil. © 2014 Nature Publishing Group
Keyword: Pain & Touch
Link ID: 20362 - Posted: 11.26.2014
By RONI CARYN RABIN The Food and Drug Administration on Thursday approved a powerful long-acting opioid painkiller, alarming some addiction experts who fear that its widespread use may contribute to the rising tide of prescription drug overdoses. The new drug, Hysingla, and another drug approved earlier this year, Zohydro, contain pure hydrocodone, a narcotic, without the acetaminophen used in other opioids. But Hysingla is to be made available as an “abuse-deterrent” tablet that cannot easily be broken or crushed by addicts looking to snort or inject it. Nearly half of the nation’s overdose deaths involved painkillers like hydrocodone and oxycodone, according to a 2010 study by the Centers for Disease Control and Prevention. More than 12 million people used prescription painkillers for nonmedical reasons that year, according to the study. Prescription opioid abuse kills more adults annually than heroin and cocaine combined, and sends 420,000 Americans to emergency rooms every year, according to the C.D.C. Hysingla, however, will not be not abuse-proof, said officials at the F.D.A. and the drug’s manufacturer, Purdue Pharma. Its extended-release formulation, a pill to be taken once every 24 hours by patients requiring round-the-clock pain relief, will contain as much as 120 milligrams of hydrocodone. The F.D.A. warned that doses of 80 milligrams or more “should not be prescribed to people who have not previously taken an opioid medication,” but officials described the abuse-deterrent formulation as a step forward. © 2014 The New York Times Company
By Emily Underwood WASHINGTON, D.C.—Rapid changes unfold in the brain after a person's hand is amputated. Within days—and possibly even hours—neurons that once processed sensations from the palm and fingers start to shift their allegiances, beginning to fire in response to sensations in other body parts, such as the face. But a hand transplant can bring these neurons back into the fold, restoring the sense of touch nearly back to normal, according to a study presented here this week at the annual conference of the Society for Neuroscience. To date, roughly 85 people worldwide have undergone hand replant or transplant surgery, an 8- to 10-hour procedure in which surgeons reattach the bones, muscles, nerves, blood vessels, and soft tissue between the patient's severed wrist and their own hand or one from a donor, often using a needle finer than a human hair. After surgery, studies have shown that it takes about 2 years for the peripheral nerves to regenerate, with sensation slowly creeping through the palm and into the fingertips at a rate of roughly 2 mm per day, says Scott Frey, a cognitive neuroscientist at the University of Missouri, Columbia. Even once the nerves have regrown, the surgically attached hand remains far less sensitive to touch than the original hand once was. One potential explanation is that the brain's sensory "map" of the body—a series of cortical ridges and folds devoted to processing touch in different body parts—loses its ability to respond to the missing hand in the absence of sensory input, Frey says. If that's true, the brain may need to reorganize that sensory map once again in order to fully restore sensation. © 2014 American Association for the Advancement of Science
By Kate Baggaley WASHINGTON — Being stroked in the right place at the right speed activates specialized nerve fibers. The caresses that people rate most pleasant line up with the probable locations of the fibers on the skin, new research suggests. “Touch is important in terms of our physical health and our psychological well-being,” said Susannah Walker, who presented the research November 17 at the annual meeting of the Society for Neuroscience. “But very little attention has been paid to the neurological basis of that effect.” Sensors in the skin known as C-tactile afferents respond strongly to being stroked at between three and 10 centimeters per second. The sensors send signals to the brain that make touch rewarding, says Walker, a neuroscientist at Liverpool John Moores University in England. Walker and a colleague played videos for 93 participants, showing a hand caressing a person’s palm, back, shoulder or forearm, either at 5 cm/s or 30 cm/s. Participants rated the 5 cm/s stroking — the best speed to get the skin’s sensors firing — as the most pleasant, except on the palm, where there are no stroking sensors. The back got the highest pleasantness ratings, forearms lowest. The spots where people like to be touched may not line up with the areas traditionally considered most sensitive. Though less finely attuned to texture or temperature than the hands or face, the back and shoulders are sensitive to a different, social sort of touch. © Society for Science & the Public 2000 - 2014.
By Elahe Izadi Putting very little babies through numerous medical procedures is especially challenging for physicians, in part because reducing the pain they experience is so difficult. Typically for patients, "the preferred method of reducing pain is opiates. Obviously you don't want to give opiates to babies," says neurologist Regina Sullivan of NYU Langone Medical Center. "Also, it's difficult to know when a baby is in pain and not in pain." In recent years, research has shown environmental factors, like a mother or caregiver having contact with a baby during a painful procedure, appears to reduce the amount of pain felt by the baby, at least as indicated by the child's behavior, Sullivan said. But she and Gordon Barr of the University of Pennsylvania, an expert in pain, were interested in whether a mother's presence actually changed the brain functioning of a baby in pain. So Sullivan and Barr turned to rats. Specifically mama and baby rats who were in pain. And they found that hundreds of genes in baby rats' brains were more or less active, depending on whether the mothers were present. Sullivan and Barr presented their committee peer-reviewed research before the Society for Neuroscience annual meeting Tuesday. They gave mild electric shocks to infant rats, some of which had their mothers around and others who didn't. The researchers analyzed a specific portion of the infants' brains, the amygdala region of neurons, which is where emotions like fear are processed.
By Tanya Lewis WASHINGTON — From the stroke of a mother's hand to the embrace of a lover, sensations of gentle touch activate a specialized set of nerves in humans. The brain is widely believed to contain a "map" of the body for sensing touch. But humans may also have an emotional body map that corresponds to feelings of gentle touch, according to new research presented here Sunday (Nov. 16) at the 44th annual meeting of the Society for Neuroscience. For humans and all social species, touch plays a fundamental role in the formation and maintenance of social bonds, study researcher Susannah Walker, a behavioral neuroscientist at Liverpool John Moores University in the United KIngdom, said in a news conference. [Top 10 Things That Make Humans Special] "Indeed, a lack of touch can have a detrimental effect on both our physical health and our psychological well-being," Walker said. In a clinical setting, physical contact with premature infants has been shown to boost growth, decrease stress and aid brain development. But not much research has focused on the basis of these effects in the nervous system, Walker said. The human body has a number of different kinds of nerves for perceiving touch. Thicker nerves surrounded by a fatty layer of insulation (called myelin) identify touch and temperature and rapidly send those signals to the brain, whereas thinner nerves that lack this insulation send sensory information more slowly.
Stem cells can be used to heal the damage in the brain caused by Parkinson's disease, according to scientists in Sweden. They said their study on rats heralded a "huge breakthrough" towards developing effective treatments. There is no cure for the disease, but medication and brain stimulation can alleviate symptoms. Parkinson's UK said there were many questions still to be answered before human trials could proceed. The disease is caused by the loss of nerve cells in the brain that produce the chemical dopamine ,which helps to control mood and movement. To simulate Parkinson's, Lund University researchers killed dopamine-producing neurons on one side of the rats' brains. They then converted human embryonic stem cells into neurons that produced dopamine. Parkinson's Disease Parkinson's is one of the commonest neurodegenerative diseases These were injected into the rats' brains, and the researchers found evidence that the damage was reversed. There have been no human clinical trials of stem-cell-derived neurons, but the researchers said they could be ready for testing by 2017. Malin Parmar, associate professor of developmental and regenerative neurobiology, said: "It's a huge breakthrough in the field [and] a stepping stone towards clinical trials." A similar method has been tried in a limited number of patients. It involved taking brain tissue from multiple aborted foetuses to heal the brain. Clinical trials were abandoned after mixed results, but about a third of the patients had foetal brain cells that functioned for 25 years. BBC © 2014
Link ID: 20292 - Posted: 11.08.2014
By Kelly Servick Using data from old clinical trials, two groups of researchers have found a better way to predict how amyotrophic lateral sclerosis (ALS) progresses in different patients. The winning algorithms—designed by non-ALS experts—outperformed the judgments of a group of ALS clinicians given the same data. The advances could make it easier to test whether new drugs can slow the fatal neurodegenerative disease. The new work was inspired by the so-called ALS Prediction Prize, a joint effort by the ALS-focused nonprofit Prize4Life and Dialogue for Reverse Engineering Assessments and Methods, a computational biology project whose sponsors include IBM, Columbia University, and the New York Academy of Sciences. Announced in 2012, the $50,000 award was designed to bring in experts from outside the ALS field to tackle the notoriously unpredictable illness. Liuxia Wang, a data analyst at the marketing company Sentrana in Washington, D.C., was used to helping companies make business decisions based on big data sets, such as information about consumer choices, but says she “didn’t know too much about this life science thing” until she got an unusual query from a client. One of the senior managers she worked with revealed that her son had just been diagnosed with ALS and wondered if Sentrana’s analytics could apply to patient data, too. When Wang set out to investigate, she found the ALS Prediction Prize. The next step, she said, was to learn something about ALS. The disease destroys the neurons that control muscle movement, causing gradual paralysis and eventually killing about half of patients within 3 years of diagnosis. But the speed of its progression varies widely. About 10% of patients live a decade or more after being diagnosed. That makes it hard for doctors to answer patients’ questions about the future, and it’s a big problem for testing new ALS treatments. © 2014 American Association for the Advancement of Science.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20278 - Posted: 11.04.2014
|By Sandra Upson Jan Scheuermann is not your average experimental subject. Diagnosed with spinocerebellar degeneration, she is only able to move her head and neck. The paralysis, which began creeping over her muscles in 1996, has been devastating in many ways. Yet two years ago she seized an opportunity to turn her personal liability into an extraordinary asset for neuroscience. In 2012 Scheuermann elected to undergo brain surgery to implant two arrays of electrodes on her motor cortex, a band of tissue on the surface of the brain. She did so as a volunteer in a multi-year study at the University of Pittsburgh to develop a better brain-computer interface. When she visits the lab, researchers hook up her brain to a robotic arm and hand, which she practices moving using her thoughts alone. The goal is to eventually allow other paralyzed individuals to regain function by wiring up their brains directly to a computer or prosthetic limb. The electrodes in her head record the firing patterns of about 150 of her neurons. Specific patterns of neuronal activity encode her desire to perform different movements, such as swinging the arm to the left or clasping the fingers around a cup. Two thick cables relay the data from her neurons to a computer, where software can identify Scheuermann’s intentions. The computer can then issue appropriate commands to move the robotic limb. On a typical workday, Jan Scheuermann arrives at the university around 9:15 am. Using her chin, she maneuvers her electric wheelchair into a research lab headed by neuroscientist Andrew Schwartz and settles in for a day of work. Scientific American Mind spoke to Scheuermann to learn more about her experience as a self-proclaimed “guinea pig extraordinaire.” © 2014 Scientific American,
Link ID: 20276 - Posted: 11.04.2014
Colin Barras It's the sweetest relief… until it's not. Scratching an itch only gives temporary respite before making it worse – we now know why. Millions of people experience chronic itching at some point, as a result of conditions ranging from eczema to kidney failure to cancer. The condition can have a serious impact on quality of life. On the face of it, the body appears to have a coping mechanism: scratching an itch until it hurts can bring instant relief. But when the pain wears off the itch is often more unbearable than before – which means we scratch even harder, sometimes to the point of causing painful skin damage. "People keep scratching even though they might end up bleeding," says Zhou-Feng Chen at the Washington University School of Medicine in St Louis, Missouri, who has now worked out why this happens. His team's work in mice suggests it comes down to an unfortunate bit of neural crosstalk. We know that the neurotransmitter serotonin helps control pain, and that pain – from the heavy scratching – helps soothe an itch, so Chen's team set out to explore whether serotonin is also involved in the itching process. They began by genetically engineering mice to produce no serotonin. Normally, mice injected with a chemical that irritates their skin will scratch up a storm, but the engineered mice seemed to have almost no urge to scratch. Genetically normal mice given a treatment to prevent serotonin leaving the brain also avoided scratching after being injected with the chemical, indicating that the urge to scratch begins when serotonin from the brain reaches the irritated spot. © Copyright Reed Business Information Ltd.
Keyword: Pain & Touch
Link ID: 20270 - Posted: 11.03.2014
BY Laura Sanders The first time Nathan Whitmore zapped his brain, he had a college friend standing by, ready to pull the cord in case he had a seizure. That didn’t happen. Instead, Whitmore started experimenting with the surges of electricity, and he liked the effects. Since that first cautious attempt, he’s become a frequent user of, and advocate for, homemade brain stimulators. Depending on where he puts the electrodes, Whitmore says, he has expanded his memory, improved his math skills and solved previously intractable problems. The 22-year-old, a researcher in a National Institute on Aging neuroscience lab in Baltimore, writes computer programs in his spare time. When he attaches an electrode to a spot on his forehead, his brain goes into a “flow state,” he says, where tricky coding solutions appear effortlessly. “It’s like the computer is programming itself.” Whitmore no longer asks a friend to keep him company while he plugs in, but he is far from alone. The movement to use electricity to change the brain, while still relatively fringe, appears to be growing, as evidenced by a steady increase in active participants in an online brain-hacking message board that Whitmore moderates. This do-it-yourself community, some of whom make their own devices, includes people who want to get better test scores or crush the competition in video games as well as people struggling with depression and chronic pain, Whitmore says. As reckless as it sounds to juice a brain at home with a 9-volt battery and 40 dollars’ worth of spare parts, this technology’s buzz is based on legit science. Small laboratory studies suggest that carefully controlled brain stimulation can boost a person’s memory and math abilities, hone attention and fast-track learning. The U. S. military is interested and is funding studies to test brain stimulation as a way to boost soldiers’ alertness and vigilance. The technique may even be a viable treatment for pernicious mental disorders such as major depression, according to other laboratory-based studies. © Society for Science & the Public 2000 - 2014.
By Rachel Feltman Sometimes the process of scientific discovery can be a real headache. In a recent Danish study, scientists were thrilled to give painful migraines to 86 percent of their study subjects. Migraines are a particularly painful mystery for researchers to solve: More than 10 percent of people worldwide are affected by these intense headaches, but no one has been able to pinpoint a specific cause. What makes these headaches, which can cause incapacitating pain and nausea, different from all other headaches? That's why scientists had to make their patients suffer -- researchers keep trying to trigger migraines using different mechanisms. The more successful they are, the more likely it is that the mechanism being tested is actually a common cause of migraines. And once we know what the common causes are, we can try to develop better treatments that target them. In this case the 86 percent "success" rate, which the researchers say is much higher than results with other triggers, was owed to increases of a naturally occurring substance called cyclic AMP, or cAMP. Our bodies use cAMP to dilate blood vessels, so an increase of it can increase the flow of blood. To see if cAMP might cause migraines, the researchers dosed their subjects with cilostazol, a drug that increases cAMP concentrations in the body.
Keyword: Pain & Touch
Link ID: 20264 - Posted: 11.01.2014
By CATHERINE SAINT LOUIS More than 50 children in 23 states have had mysterious episodes of paralysis to their arms or legs, according to data gathered by the Centers for Disease Control and Prevention. The cause is not known, although some doctors suspect the cases may be linked to infection with enterovirus 68, a respiratory virus that has sickened thousands of children in recent months. Concerned by a cluster of cases in Colorado, the C.D.C. last month asked doctors and state health officials nationwide to begin compiling detailed reports about cases of unusual limb weakness in children. Experts convened by the agency plan next week to release interim guidelines on managing the condition. That so many children have had full or partial paralysis in a short period is unusual, but officials said that the cases seemed to be extremely rare. “At the moment, it looks like whatever the chances are of getting this syndrome are less than one in a million,” said Mark A. Pallansch, the director of the division of viral diseases at the C.D.C. Some of the affected children have lost the use of a leg or an arm, and are having physical therapy to keep their muscles conditioned. Others have sustained more extensive damage and require help breathing. Marie, who asked to be identified by her middle name to protect her family’s privacy, said her 4-year-old son used to climb jungle gyms. But in late September, after the whole family had been sick with a respiratory illness, he started having trouble climbing onto the couch. He walked into Boston Children’s Hospital the day he was admitted. But soon his neck grew so weak, it “flopped completely back like he was a newborn,” Marie said. Typically, the time from when weakness begins until it reaches its worst is one to three days. But for her son, eight mornings in a row, he awoke with a "brand new deficit" until he had some degree of weakness in each limb and had trouble breathing. He was eventually transferred to a Spaulding rehabilitation center, where he is now. © 2014 The New York Times Company
by Bethany Brookshire In many scientific fields, the study of the body is the study of boys. In neuroscience, for example, studies in male rats, mice, monkeys and other mammals outnumber studies in females 5.5 to 1. When scientists are hunting for clues, treatments or cures for a human population that is around 50 percent female, this boys-only club may miss important questions about how the other half lives. So in an effort to reduce this sex bias in biomedical studies, National Institutes of Health director Francis Collins and Office of Research on Women’s Health director Janine Clayton announced in May a new policy that will roll out practices promoting sex parity in research, beginning with a requirement that scientists state whether males, females or both were used in experiments, and moving on to mandate that both males and females are included in all future funded research. The end goal will be to make sure that NIH-funded scientists “balance male and female cells and animals in preclinical studies in all future [grant] applications” to the NIH. In 1993, the NIH Revitalization Act mandated the inclusion of women and minorities in clinical trials. This latest move extends that inclusion to cells and animals in preclinical research. Because NIH funds the work of morethan 300,000 researchers in the United States and other countries, many of whom work on preclinical and basic biomedical science, the new policy has broad implications for the biomedical research community. And while some scientists are pleased with the effort, others are worried that the mandate is ill-conceived and underfunded. In the end, whether it succeeds or fails comes down to interpretation and future implementation. © Society for Science & the Public 2000 - 2014