Chapter 11. Motor Control and Plasticity
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New findings reveal how a mutation, a change in the genetic code that causes neurodegeneration, alters the shape of DNA, making cells more vulnerable to stress and more likely to die. The particular mutation, in the C9orf72 gene, is the most common cause for amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease), and frontotemporal degeneration (FTD), the second most common type of dementia in people under 65. This research by Jiou Wang, Ph.D., and his colleagues at Johns Hopkins University (JHU) was published in Nature and was partially funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS). In ALS, the muscle-activating neurons in the spinal cord die, eventually causing paralysis. In FTD neurons in particular brain areas die leading to progressive loss of cognitive abilities. The mutation may also be associated with Alzheimer’s and Huntington’s diseases. DNA contains a person’s genetic code, which is made up of a unique string of bases, chemicals represented by letters. Portions of this code are divided into genes that provide instructions for making molecules (proteins) that control how cells function. The normal C9orf72 gene contains a section of repeating letters; in most people, this sequence is repeated two to 25 times. In contrast, the mutation associated with ALS and FTD can result in up to tens of thousands of repeats of this section.
By James Gallagher Health and science reporter, BBC News US doctors are warning of an emerging polio-like disease in California where up to 20 people have been infected. A meeting of the American Academy of Neurology heard that some patients had developed paralysis in all four limbs, which had not improved with treatment. The US is polio-free, but related viruses can also attack the nervous system leading to paralysis. Doctors say they do not expect an epidemic of the polio-like virus and that the infection remains rare. Polio is a dangerous and feared childhood infection. The virus rapidly invades the nervous system and causes paralysis in one in 200 cases. It can be fatal if it stops the lungs from working. There have been 20 suspected cases of the new infection, mostly in children, in the past 18 months, A detailed analysis of five cases showed enterovirus-68 - which is related to poliovirus - could be to blame. In those cases all the children had been vaccinated against polio. Symptoms have ranged from restricted movement in one limb to severe weakness in both legs and arms. Dr Emanuelle Waubant, a neurologist at the University of California, San Francisco, told the BBC: "There has been no obvious increase in the pace of new cases so we don't think we're about to experience an epidemic, that's the good news. BBC © 2014
Keyword: Movement Disorders
Link ID: 19283 - Posted: 02.24.2014
by Clare Wilson A monkey controlling the hand of its unconscious cage-mate with its thoughts may sound like animal voodoo, but it is a step towards returning movement to people with spinal cord injuries. The hope is that people who are paralysed could have electrodes implanted in their brains that pick up their intended movements. These electrical signals could then be sent to a prosthetic limb, or directly to the person's paralysed muscles, bypassing the injury in their spinal cord. Ziv Williams at Harvard Medical School in Boston wanted to see if sending these signals to nerves in the spinal cord would also work, as this might ultimately give a greater range of movement from each electrode. His team placed electrodes in a monkey's brain, connecting them via a computer to wires going into the spinal cord of an anaesthetised, unconscious monkey. The unconscious monkey's limbs served as the equivalent of paralysed limbs. A hand of the unconscious monkey was strapped to a joystick, controlling a cursor that the other monkey could see on a screen. Williams's team had previously had the conscious monkey practise the joystick task for itself and had recorded its brain activity to work out which signals corresponded to moving the joystick back and forth. Through trial and error, they deduced which nerves to stimulate in the spinal cord of the anaesthetised monkey to produce similar movements in that monkey's hand. When both parts were fed to the computer, the conscious monkey was able to move the "paralysed" monkey's hand to make the cursor hit a target. © Copyright Reed Business Information Ltd.
Link ID: 19266 - Posted: 02.19.2014
by Clare Wilson SOMETIMES you find out more about how something works by turning it off. That seems to be true for mirror neurons, the brain cells implicated in traits ranging from empathy and learning to language acquisition. Mirror neurons are said to help us interpret other people's behaviour, but this has yet to be shown convincingly in experiments. Now a study that briefly disabled these cells might give a better idea of what they do. Mirror neurons were discovered in the 1990s when an Italian team was measuring electrical activity in the brains of monkeys. In the region that controls movement, some of the neurons that fire to carry out a particular action – such as grasping an apple – also fired when the monkey saw another animal do the same thing. The tempting conclusion was that these neurons help interpret others' behaviour. Further work suggested that people also have this system, and some researchers claimed that conditions where empathy is lacking, such as autism or psychopathy, could arise from defective mirror neurons. Yet there has been little evidence to back this up and critics argued that mirror neuron activity could just be some sort of side effect of witnessing action. Powerful magnetic fields are known to temporarily disrupt brain cell activity, and a technique called transcranial magnetic stimulation (TMS) is increasingly used in the lab to dampen specific areas of the brain. © Copyright Reed Business Information Ltd.
|By Carl Erik Fisher After 22 years of failed treatments, including rehabilitation, psychotherapy and an array of psychiatric medications, a middle-aged Dutch man decided to take an extraordinary step to fight his heroin addiction. He underwent an experimental brain surgery called deep brain stimulation (DBS). At the University of Amsterdam, researchers bored small holes in his skull and guided two long, thin probes deep into his head. The ends of the probes were lined with small electrodes, which were positioned in his nucleus accumbens, a brain area near the base of the skull that is associated with addiction. The scientists ran the connecting wires under his scalp, behind his ear and down to a battery pack sewn under the skin of his chest. Once turned on, the electrodes began delivering constant electrical pulses, much like a pacemaker, with the goal of altering the brain circuits thought to be causing his drug cravings. At first the stimulation intensified his desire for heroin, and he almost doubled his drug intake. But after the researchers adjusted the pulses, the cravings diminished, and he drastically cut down his heroin use. Neurosurgeries are now being pursued for a variety of mental illnesses. Initially developed in the 1980s to treat movement disorders, including Parkinson's disease, DBS is today used to treat depression, dementia, obsessive-compulsive disorder, substance abuse and even obesity. Despite several success stories, many of these new ventures have attracted critics, and some skeptics have even called for an outright halt to this research. © 2014 Scientific American
By LAUREN BRADY When I was 18 I watched my father perform what would be his final surgery. It was the summer of 2007 and I had just returned to Colorado after surviving my freshman year of film school at New York University. One day my dad invited me to observe a vitrectomy. And while I hadn’t a clue what this would entail I immediately accepted, honored by the invitation and determined not to faint. My father’s 21 years as an ophthalmologist produced over 15,000 operations, a private practice spanning three offices, and very little vacation time. While I sensed from an early age that the long hours were taxing on him I never felt an absence. In fact, my childhood was picturesque: two loving parents, a rowdy little brother whom I pushed around until he was big enough to push back, family trips in the Jeep to the Rocky Mountains. He was the dad with the Handycam at every soccer game and school play. He worked as a surgeon, but he lived for his children. The morning of the vitrectomy we left extra early because of a limp in my dad’s right leg that had appeared a few months earlier and had gradually worsened. He suspected it was a pinched nerve and had been meaning to get it checked out. In the interim, he had started using a chair during surgery. Walking toward the hospital entrance we encountered a fellow doctor who greeted me with the familiarity of someone who’d been exposed to years of my father’s wallet photos. He asked how I liked Greenwich Village, whether I had directed any films yet and if I had tried a bialy. We walked and talked until I noticed at one point that my dad was no longer part of the conversation. Turning around I realized he was a half block back pushing himself up from the ground. © 2014 The New York Times Company
Keyword: ALS-Lou Gehrig's Disease
Link ID: 19192 - Posted: 02.01.2014
By JAMES GORMAN The question of how moles move all that dirt when they tunnel just under the surface of lawns has never attracted the extensive study that other forms of locomotion — like the flight of birds and insects, or even the jet-propulsion of jellyfish — have. But scientists at the University of Massachusetts and Brown University have recently been asking exactly how, and how hard, moles dig. Yi-Fen Lin, a graduate student at the University of Massachusetts, reported at a recent meeting of the Society for Integrative and Comparative Biology that moles seem to swim through the earth, and that the stroke they use allows them to pack a lot of power behind their shovel-like paws. Ms. Lin measured the power of hairy-tailed moles that she captured in Massachusetts and found they could exert a force up to 40 times their body weight. She also analyzed and presented X-ray videos taken of moles in a laboratory enclosure tunneling their way through a material chosen for its consistency and uniform particle size: cous cous. Angela M. Horner recorded the videos while studying the movement of Eastern moles in the lab of Thomas Roberts, a professor at Brown. One reason moles have not been studied as much as some other animals may be that they are not easy to capture or keep in a laboratory. “People said, ‘You won’t be able to catch them and you won’t be able to keep them alive,’ ” said Elizabeth R. Dumont, an evolutionary biologist who is Ms. Lin’s dissertation adviser. Ms. Lin solved the first problem by camping out in mole territory, on golf courses and farms, and marking their tunnels with sticks that she would watch for hours until movement indicated a mole on the move. © 2014 The New York Times Company
Link ID: 19179 - Posted: 01.29.2014
By Katherine Harmon Courage Unless you’ve eaten sannakji, the Korean specialty of semi-live octopus, you might never have had a squirming octopus arm in your mouth. But you’ve most likely had a very similar experience. In fact, you’re probably having one right now. Octopus arms might seem strange and mysterious, but they are remarkably similar to the human tongue. Known as muscular hydrostats, both of these appendages can easily bend, extend and change shape (remember that time you had to stretch out your tongue to lick that last bit of chocolate pudding from the bottom of the cup?). Researchers are hoping a new interdisciplinary project to look at movement in the octopus arm and the human tongue will shed light on how both of these complex structures are activated. This, in turn, could help scientists understand neurological diseases that affect speech, such as Parkinson’s. “The human tongue is a very different muscular system than the rest of the human body,” Khalil Iskarous, an assistant professor of linguistics at the University of Southern California who is helping to lead the research, said in a prepared statement. “Our bodies are vertebrate mechanisms that operate by muscle working on bone to move. The tongue is in a different muscular family, much like an invertebrate. It’s entirely muscle—it’s muscle moving muscle.” Both move by compressing fluid in one section of a muscle, creating movement in another part. But we know little about exactly how that movement is initiated and so finely controlled. © 2014 Scientific American
Keyword: Movement Disorders
Link ID: 19117 - Posted: 01.11.2014
Just in time for all those New Year’s resolutions to exercise more, scientists have a better idea of how the body turns pain into gain. Exertion stimulates muscles to release a molecule that modifies fat cells, turning them into calorie-burning machines, a research team has found. Exercise works the muscles but affects cells throughout the body, even in the brain. An important player in this process is a protein called PGC-1α. In exercising muscles, it activates genes that ramp up energy use. But its impact extends beyond these tissues. The protein somehow indirectly prompts, for example, white fat—the energy-storing variety that pads our hips and stomachs—to switch on genes that are characteristic of brown fat, a form that burns calories. PGC-1α doesn’t travel outside muscle cells, so researchers aren’t sure how its influence spreads, however. By sifting through the secretions of PGC-1α-making muscle cells, Robert Gerszten of Harvard Medical School in Boston and colleagues have nabbed one molecule that might be doing the protein’s bidding: β-aminoisobutyric acid (BAIBA). They found that BAIBA induces white fat cells to become more like brown fat cells, altering their gene activity patterns. And it stimulates other cell types, stoking fat metabolism in the liver, the team also reveals today in Cell Metabolism. These effects may translate into a healthier metabolism. When mice lapped up water laced with the molecule, the rodents lost weight and were better at absorbing glucose. © 2014 American Association for the Advancement of Science
Don’t worry about watching all those cat videos on the Internet. You’re not wasting time when you are at your computer—you’re honing your fine-motor skills. A study of people’s ability to translate training that involves clicking and twiddling a computer mouse reveals that the brain can apply that expertise to other fine-motor tasks requiring the hands. We know that computers are altering the way that people think. For example, using the Internet changes the way that you remember information. But what about use of the computer itself? You probably got to this story by using a computer mouse, for example, and that is a bizarre task compared with the activities that we’ve encountered in our evolutionary history. You made tiny movements of your hand in a horizontal plane to cause tiny movements of a cursor in a completely disconnected vertical plane. But with daily practice—the average computer user makes more than 1000 mouse clicks per day—you have become such an expert that you don’t even think about this amazing feat of dexterity. Scientists would love to know if that practice affects other aspects of your brain’s control of your body. The problem is finding people with no computer experience. So Konrad Kording, a psychologist at Northwestern University’s Rehabilitation Institute of Chicago in Illinois, and his former postdoc Kunlin Wei, now at Peking University in Beijing, turned to migrant Chinese workers. The country’s vast population covers the whole socioeconomic spectrum, from elite computer hackers to agricultural laborers whose lifestyles have changed little over the past century. The country’s economic boom is bringing people in waves from the countryside to cities in search of employment. © 2013 American Association for the Advancement of Science
Keyword: Learning & Memory
Link ID: 19060 - Posted: 12.21.2013
by Ashley Yeager With a little help from implanted electrodes, Parkinson's patients make fewer driving errors, at least on a computer. When steering a simulator, patients with active brain stimulators averaged 3.8 driving errors, compared with 7.5 for healthy people and 11.4 for those with Parkinson's disease who did not have implants. The Parkinson’s patients’ driving skills were also more accurate when receiving deep brain stimulation than when taking levodopa, a common treatment for the disease, researchers report December 18 in Neurology. © Society for Science & the Public 2000 - 2013
Link ID: 19054 - Posted: 12.19.2013
People with dementia who exercise improve their thinking abilities and everyday life, a body of medical research concludes. The Cochrane Collaboration carried out a systematic review of eight exercise trials involving more than 300 patients living at home or in care. Exercise did little for patients' moods, the research concluded. But it did help them carry out daily activities such as rising from a chair, and boosted their cognitive skills. Whether these benefits improve quality of life is still unclear, but the study authors say the findings are reason for optimism. Dementia affects some 800,000 people in the UK. And the number of people with the condition is steadily increasing because people are living longer. It is estimated that by 2021, the number of people with dementia in the UK will have increased to around one million. With no cure, ways to improve the lives of those living with the condition are vital. Researcher Dorothy Forbes, of the University of Alberta, and colleagues who carried out the Cochrane review, said: "Clearly, further research is needed to be able to develop best practice guidelines to enable healthcare providers to advise people with dementia living at home or in institutions. "We also need to understand what level and intensity of exercise is beneficial for someone with dementia." BBC © 2013
Link ID: 18999 - Posted: 12.05.2013
At the Society for Neuroscience meeting earlier this month in San Diego, California, Science sat down with Geoffrey Ling, deputy director of the Defense Sciences Office at the Defense Advanced Research Projects Agency (DARPA), to discuss the agency’s plans for the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, a neuroscience research effort put forth by President Barack Obama earlier this year. So far, DARPA has released two calls for grant applications, with at least one more likely: The first, called SUBNETS (Systems-Based Neurotechnology for Emerging Therapies), asks researchers to develop novel, wireless devices, such as deep brain stimulators, that can cure neurological disorders such as posttraumatic stress (PTS), major depression, and chronic pain. The second, RAM (Restoring Active Memory), calls for a separate wireless device that repairs brain damage and restores memory loss. Below is an extended version of a Q&A that appears in the 29 November issue of Science. Q: Why did DARPA get involved in the BRAIN project? G.L.: It’s really focused on our injured warfighters, but it has a use for civilians who have stress disorders and civilians who also have memory disorders from dementia and the like. But at the end of the day, it is still meeting [President Obama’s] directive. Of all the things he could have chosen—global warming, alternative fuels—he chose this, so in my mind the neuroscience community should be as excited as all get-up. Q: Why does SUBNETS focus on deep brain stimulation (DBS)? G.L.: We’ve opened the possibility of using DBS but we haven’t exclusively said that. We’re challenging people to go after neuropsychiatric disorders like PTS [and] depression. We’re challenging the community to come up with something in 5 years that’s clinically feasible. DBS is an area that has really been traditionally underfunded, so we thought what the heck, let’s give it a go—in this new BRAIN Initiative the whole idea is to go after the things that there aren’t 400 R01 grants for—and let’s be bold, and boy, if it works, fabulous. © 2013 American Association for the Advancement of Science
Scientists at the National Institutes of Health have used RNA interference (RNAi) technology to reveal dozens of genes which may represent new therapeutic targets for treating Parkinson’s disease. The findings also may be relevant to several diseases caused by damage to mitochondria, the biological power plants found in cells throughout the body. “We discovered a network of genes that may regulate the disposal of dysfunctional mitochondria, opening the door to new drug targets for Parkinson’s disease and other disorders,” said Richard Youle, Ph.D., an investigator at the National Institute of Neurological Disorders and Stroke (NINDS) and a leader of the study. The findings were published online in Nature. Dr. Youle collaborated with researchers from the National Center for Advancing Translational Sciences (NCATS). Mitochondria are tubular structures with rounded ends that use oxygen to convert many chemical fuels into adenosine triphosphate, the main energy source that powers cells. Multiple neurological disorders are linked to genes that help regulate the health of mitochondria, including Parkinson’s, and movement diseases such as Charcot-Marie Tooth Syndrome and the ataxias. Some cases of Parkinson’s disease have been linked to mutations in the gene that codes for parkin, a protein that normally roams inside cells, and tags damaged mitochondria as waste. The damaged mitochondria are then degraded by cells’ lysosomes, which serve as a biological trash disposal system. Known mutations in parkin prevent tagging, resulting in accumulation of unhealthy mitochondria in the body.
by Erika Engelhaupt If you had to have a prosthetic hand, would you want it to look like a real hand? Or would you prefer a gleaming metallic number, something that doesn’t even try to look human? A new study looks at one of the issues that prosthetic designers and wearers face in making this decision: the creepy factor. People tend to get creeped out by robots or prosthetic devices that look almost, but not quite, human. So Ellen Poliakoff and colleagues at the University of Manchester in England had people rate the eeriness of various prosthetic hands. Forty-three volunteers looked at photographs of prosthetic and real hands. They rated both how humanlike (realistic) the hands were and how eerie they were, defined as “mysterious, strange, or unexpected as to send a chill up the spine.” Real human hands were rated both the most humanlike and the least eerie (a good thing for humans). Metal hands that were clearly mechanical were rated the least humanlike, but less eerie overall than prosthetic hands made to look like real hands, the team reports in the latest issue of Perception. The realistic prosthetics, like the rubber hand shown above, fell into what's known as the uncanny valley. That term, invented by roboticist Matsuhiro Mori in 1970, describes how robots become unnerving as they come to look more humanlike. The superrealistic Geminoid DK robot and the animated characters in the movie The Polar Express suffer from this problem. They look almost human, but not quite, and this mismatch between expectation and reality is one of the proposed explanations for the uncanny valley. In particular, if something looks like a human but doesn’t quite move like one, it’s often considered eerie. © Society for Science & the Public 2000 - 2013
Helen Shen To researchers who study how living things move, the octopus is an eight-legged marvel, managing its array of undulating appendages by means of a relatively simple nervous system. Some studies have suggested that each of the octopus’s tentacles has a 'mind' of its own, without rigid central coordination by the animal’s brain1. Now neuroscientist Guy Levy and his colleagues at the Hebrew University in Jerusalem report that the animals can rotate their bodies independently of their direction of movement, reorienting them while continuing to crawl in a straight line. And, unlike species that use their limbs to move forward or sideways relative to their body's orientation, octopuses tend to slither around in all directions. The team presented its findings on 10 November at the annual meeting of the Society for Neuroscience in San Diego, California. The new description of octopus movement is “not how one would imagine that would happen, but it seems to give a lot of control to the animal", says Gal Haspel, a neuroscientist at the New Jersey Institute of Technology in Newark. Haspel studies worm locomotion, and he was also surprised by the researchers’ report that the octopus pushes itself with worm-like contractions of its tentacles. Different combinations flex together to produce movement in different directions. Levy, who began the research as part of a project to design and control flexible, octopus-like robots, says that the work could also help to uncover basic biological principles of locomotion. Levy’s team deconstructed octopus movement using a transparent tank rigged with a system of mirrors and video cameras, in which they tested nine adult common octopuses (Octopus vulgaris). © 2013 Nature Publishing Group
by Jessica Griggs, San Diego No practice required. Wouldn't it be great if you could get better at playing sport or hone your piano skills simply by thinking about it? A small pilot study suggests that it might be possible. In the last few years, brain training using computer games that provide neurofeedback – a real-time representation of your brain activity – has become a popular, if controversial, method of enhancing cognitive abilities such as spatial memory, planning and multitasking. It has even been used to help actors get into character. Most of the games aim to enhance activation in a single part of the brain. But motor skills are known to involve two main areas – the premotor cortex and the supplementary motor cortex. Both are involved when people make movements or imagine moving. Brain activity between these regions is known to be less synchronised in people who are poor at motor tasks than in those who excel at them. So to see if brain training could target both areas and improve motor performance, Sook-Lei Liew and her colleagues from the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland, recruited eight young adults. The researchers and asked the participants to watch a white circle on a screen while an fMRI machine scanned their brain. When the circle turned into a red triangle, the volunteers were told to move their fingers. This movement caused activation in their premotor cortex and supplementary motor cortex, which in turn moved a bar on the screen. The higher the synchronisation of activity between the two brain areas, the higher the bar went. © Copyright Reed Business Information Ltd.
Link ID: 18928 - Posted: 11.14.2013
Helen Shen Long used to treat movement disorders, deep-brain stimulation (DBS) is rapidly emerging as an experimental therapy for neuropsychiatric conditions including depression, Tourette’s syndrome, obsessive–compulsive disorder and even Alzheimer’s disease. But despite some encouraging results in patients, it remains largely unknown how the electrical pulses delivered by implants deep within the brain affect neural circuits and change behaviour. Now there is a prototype DBS device that could provide some answers, researchers reported on 10 November at the Society for Neuroscience’s annual meeting in San Diego, California. Called Harmoni, the device is the first DBS implant to monitor electrical and chemical responses in the brain while delivering electrical stimulation. “That’s new data that we haven’t really had access to in humans before,” says Cameron McIntyre, a biomedical engineer at Case Western Reserve University in Cleveland, Ohio, who is not involved in the work. Researchers hope that the device will identify the electrical and chemical signals in the brain that correlate in real time with the presence and severity of symptoms, including the tremors experienced by people with Parkinson’s disease. This information could help to uncover where and how DBS exerts its therapeutic effects on the brain, and why it sometimes fails, says Kendall Lee, a neurosurgeon at the Mayo Clinic in Rochester, Minnesota, who is leading the project. The results come at a time of great excitement in the DBS field. Last month, the US government's Defense Advanced Research Projects Agency (DARPA) announced a 5-year, US$70-million initiative to support development of the next generation of therapeutic brain-stimulating technologies. © 2013 Nature Publishing Group,
Link ID: 18922 - Posted: 11.13.2013
Sedentary adults may improve their memory as soon as six weeks after taking up aerobic exercise, a small brain imaging study suggests. Cardiovascular fitness and cognitive performance such as attention seem to improve after six months or more of aerobic exercise in previous aging studies. Now researchers in Texas have found signs of increased regional blood flow in the brain of 37 sedentary adults with an average age of 64 who were randomized to physical training or a control group who had the training after a waiting period. They found a higher resting cerebral blood flow in the brain's anterior cingulate region in the physical training group compared with controls. The anterior cingulate region is associated with better memory functions. The size of this brain region was also larger in another study of "successful cognitive agers" over the age of 80 compared to middle-aged or elderly controls. "A relatively rapid health benefit across brain, memory and fitness in sedentary adults soon after starting to exercise, some gains starting as early as six weeks, could motivate adults to start exercising regularly," the study's lead author, Sandra Bond Champman of the Center for BrainHealth in Dallas and her co-authors concluded in Monday's issue of the journal Frontiers in Aging Neuroscience. "The current findings shed new light on ways exercise promotes cognitive/brain health in aging." The participants all had a physical exam and screening for dementia, early cognitive impairment, depression and IQ before the study began. A noninvasive type of MRI was used to measure brain blood flow before, half way through the 6-week training sessions and at 12 weeks. © CBC 2013
Keyword: Learning & Memory
Link ID: 18920 - Posted: 11.13.2013
Babies born to women who exercised during pregnancy have enhanced brain development compared with babies born to moms who didn’t exercise while they were pregnant, a new Canadian study suggests. The babies of 10 women who did as little as 20 minutes of moderate exercise three times a week during pregnancy showed more advanced brain activity when they were tested at eight to 12 days old than the babies of eight women who did not exercise during pregnancy, reported University of Montreal researcher David Ellemberg and his colleagues at the Neuroscience 2013 conference in San Diego on Sunday. “We are optimistic that this will encourage women to change their health habits, given that the simple act of exercising during pregnancy could make a difference for their child's future,” Ellemberg said in a statement. The women in the study were randomly assigned to an exercise group or a sedentary group at the beginning of their second trimester. Those in the exercise group had to spend at least 20 minutes three times a week doing exercise intense enough to lead to at least a slight shortness of breath. After their babies were born, the researchers tested them by placing a cap of electrodes on the babies' heads and then playing novel sounds while they slept. They measured the electrical response of the babies' brains to see how well they could distinguish between different sounds. The researchers found that the babies in the exercise group produced signals associated with more mature brains. The researchers said they plan to test the children’s cognitive, motor and language development at age one to see if there are lasting effects. © CBC 2013
Keyword: Development of the Brain
Link ID: 18916 - Posted: 11.12.2013