Chapter 5. The Sensorimotor System
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By D. T. Max When a spinal cord is damaged, location is destiny: the higher the injury, the more severe the effects. The spine has thirty-three vertebrae, which are divided into five regions—the coccygeal, the sacral, the lumbar, the thoracic, and the cervical. The nerve-rich cord traverses nearly the entire length of the spine. The nerves at the bottom of the cord are well buried, and sometimes you can walk away from damage to these areas. In between are insults to the long middle region of the spine, which begins at the shoulders and ends at the midriff. These are the thoracic injuries. Although they don’t affect the upper body, they can still take away the ability to walk or feel below the waist, including autonomic function (bowel, bladder, and sexual control). Injuries to the cord in the cervical area—what is called “breaking your neck”—can be lethal or leave you paralyzed and unable to breathe without a ventilator. Doctors who treat spinal-cord-injury patients use a letter-and-number combination to identify the site of the damage. They talk of C3s (the cord as it passes through the third cervical vertebra) or T8s (the eighth thoracic vertebra). These morbid bingo-like codes help doctors instantly gauge the severity of a patient’s injury. Darek Fidyka, who is forty-one years old, is a T9. He was born and raised in Pradzew, a small farming town in central Poland, not far from Lodz. ... Several of the wounds punctured his lungs, and one nearly cut his spinal cord in half. As Fidyka lay on the ground, he felt his body change. “I can remember very vividly losing feeling in my legs, bit by bit,” he says. “It started in the upper part of the spine and was moving down slowly while I lay waiting for the ambulance to arrive.”
Link ID: 22230 - Posted: 05.19.2016
A bionic body is closer than you think By Dwayne Godwin, Jorge Cham Dwayne Godwin is a neuroscientist at the Wake Forest University School of Medicine. Jorge Cham draws the comic strip Piled Higher and Deeper at www.phdcomics.com. © 2016 Scientific American
Link ID: 22222 - Posted: 05.17.2016
Dara Mohammadi As the small motorboat chugs to a halt, three travellers, wind-beaten from the three-hour journey along the Atrato river, step on to the muddy banks of Bellavista, an otherwise inaccessible town in the heart of the heavily forested north-west of Colombia. They swing their hessian bags – stuffed with bedsheets, dried beans and cuddly toys – to their shoulders and clamber up a dusty path. Tucked inside the bag of one of the travellers, neuropsychologist Sonia Moreno, is the reason they are here: a wad of unfinished, hand-drawn charts of family trees. The people whose names are circled on the charts have Huntington’s disease, an incurable genetic brain disorder that usually starts between the ages of 35 and 45 years. It begins with personality changes that can make them aggressive, violent, uninhibited, anxious and depressed. The disease progresses slowly, robbing them first of the control of their body, which jerks and twists seemingly of its own will, and then their ability to walk, talk and think until, about 20 years after the symptoms first begin, they die. Their children, each of whom has a 50% chance of inheriting the disease, watch and wait to see if it will happen to them. It is in this way that the disease strangles families. With Moreno is Ignacio Muñoz-Sanjuan, vice president of translational biology at CHDI Foundation, a US nonprofit research organisation that aims to find ways to prevent or slow down the progression of the disease. The foundation spent $140m–$150m (£97m-£104m) on research last year, but Muñoz-Sanjuan is not here on official business. He’s here for Factor-H, an initiative he founded four years ago to help with the other end of the problem – poor families with Huntington’s struggling in Latin America. © 2016 Guardian News and Media Limited o
Rae Ellen Bichell For Tim Goliver and Luther Glenn, the worst illness of their lives started in the same way — probably after having a stomach bug. Tim was 21 and a college student at the University of Michigan. He was majoring in English and biology and active in the Lutheran church. "I was a literature geek," says Tim. "I was really looking forward to my senior year and wherever life would take me." Luther was in his 50s. He'd spent most of his career as a U.S. military policeman and was working in security in Washington, D.C. He'd recently separated from his wife and had just moved into a new house with his two daughters, who were in their 20s. Both men recovered from their stomach bugs, but a few days later they started to feel sluggish. "Here we are trying to unpack, prepare ourselves for new life together and I'm flat out, dead tired," says Luther. He fell asleep in the car one morning and never made it out of the garage. Then he fell in the bathroom. For Tim, it started to feel like running a marathon just to lift a spoonful of soup. One morning, he tried to comb his hair and realized he couldn't lift his arm above his shoulder. "At that moment I started to freak out," he says. Both men got so weak that their families had to wheel them into the emergency room in wheelchairs. They got the same diagnosis: Guillain-Barre syndrome, a neurological disorder which can leave people paralyzed for weeks. © 2016 npr
By Adam Gopnik On a bitter, soul-shivering, damp, biting gray February day in Cleveland—that is to say, on a February day in Cleveland—a handless man is handling a nonexistent ball. Igor Spetic lost his right hand when his forearm was pulped in an industrial accident six years ago and had to be amputated. In an operation four years ago, a team of surgeons implanted a set of small translucent “interfaces” into the neural circuits of his upper arm. This afternoon, in a basement lab at a Veterans Administration hospital, the wires are hooked up directly to a prosthetic hand—plastic, flesh-colored, five-fingered, and articulated—that is affixed to what remains of his arm. The hand has more than a dozen pressure sensors within it, and their signals can be transformed by a computer into electric waves like those natural to the nervous system. The sensors in the prosthetic hand feed information from the world into the wires in Spetic’s arm. Since, from the brain’s point of view, his hand is still there, it needs only to be recalled to life. Now it is. With the “stimulation” turned on—the electronic feed coursing from the sensors—Spetic feels nineteen distinct sensations in his artificial hand. Above all, he can feel pressure as he would with a living hand. “We don’t appreciate how much of our behavior is governed by our intense sensitivity to pressure,” Dustin Tyler, the fresh-faced principal investigator on the Cleveland project, says, observing Spetic closely. “We think of hot and cold, or of textures, silk and cotton. But some of the most important sensing we do with our fingers is to register incredibly minute differences in pressure, of the kinds that are necessary to perform tasks, which we grasp in a microsecond from the feel of the outer shell of the thing. We know instantly, just by touching, whether to gently squeeze the toothpaste or crush the can.”
Keyword: Pain & Touch
Link ID: 22215 - Posted: 05.14.2016
By Nicholas Bakalar Exposure to pesticides may increase the risk for amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease, a new study has found. The study, in JAMA Neurology, included 156 patients with A.L.S. and 128 controls. All participants completed questionnaires providing information on age, sex, ethnicity, education, marital status, residential history, occupational history, smoking and military service. The researchers used the information on residence and occupation to estimate long-term exposure to pesticides, and then took blood samples to determine serum levels of 122 persistent environmental pollutants. The scientists divided exposure into four time periods: ever exposed, exposed in the last 10 years, exposed 10 to 30 years ago, and exposed more than 30 years ago. Exposure to pesticides at any time was associated with a fivefold increased relative risk for A.L.S. compared to no exposure. Even exposure more than 30 years ago tripled the risk. Military service was associated with double the risk, confirming findings of previous studies. “This is an association, not causality,” cautioned the senior author, Dr. Eva L. Feldman, a professor of neurology at the University of Michigan. “We found that people with A.L.S. were five times more likely to have been exposed to pesticides, but we don’t want people to conclude that pesticides cause A.L.S.” © 2016 The New York Times Company
By Dan Kiefer I’m on the heavy bag, throwing left jabs, ignoring the relentless blare of Kanye’s “Drive Slow, Homie” played at a volume that would raise the dead. I punch to a one-two count: left jab, right cross. I’m working as hard as I’ve ever worked, and even in this unheated gym I sweat as if it’s a sauna. Finally, the bell rings. It feels as if I’ve been at it for an hour; actually, three minutes have passed. The ensuing one-minute break seems to last four seconds. Let’s be clear: Boxing, even when the opponent is only a heavy bag, is a brutal sport. But brutality is needed, even welcome, when you’re facing a progressive, incurable neurological disease. I have Parkinson’s disease, and it causes my body to just freeze up. Weirdly enough, boxing helps me get unstuck. All 12 of us in this class bear the unmistakable signs of Parkinson’s disease. I spot a dapper, cheerful white-haired fellow shaking like a leaf (tremor). Next, a balding, heavyset guy stumbling forward awkwardly on his toes (dystonia, or muscle cramping). Then I see myself in a mirror: a man in a white T-shirt, khaki shorts and Nike running shoes, standing still, seemingly paralyzed. I’m in the midst of a Parkinson’s freeze (an extreme form of bradykinesia, or slow movement). Although Parkinson’s is generally thought of as an old-person’s disease, I was diagnosed with a young-onset version 18 years ago, at age 35. Since then, I’ve taken every sort of medication known to science. I’ve had brain surgery — two tiny electrodes were implanted deep in my brain to stimulate an area affected by Parkinson’s — which unquestionably have helped treat some of my symptoms. But medicine and surgery have not cured my freezing and falling, my gait and balance issues that worsen as my disease progresses: When walking across a busy street, I may suddenly, inexplicably come to a full stop as the light is about to change. Even the slightest downhill slope of a path causes me to fall forward.
Link ID: 22198 - Posted: 05.10.2016
By JAN HOFFMAN The pop superstar Prince may have lived an outsize life, but emerging details about his long struggle with pain and reliance on opioids will resonate with thousands of patients who have stumbled down that well-trod path. It is a remarkably common narrative in the unfolding story of the nation’s opioid epidemic. Many details have yet to be confirmed about Prince’s case, but a typical trajectory can go something like this. A patient undergoes a procedure to address a medical issue — extracted wisdom teeth for example, or, as Prince did, orthopedic surgery. To help the patient get through recovery, a dentist or surgeon writes a prescription for opioid painkillers, like Percocet or Vicodin. Procedure over, problem addressed. But that prescription may not be written judiciously. “Opioids may be required after a procedure for a few days, but sometimes, physicians practice sloppy prescribing habits and they give patients much more than they need,” said Dr. Patrick G. O’Connor, a professor of medicine at Yale School of Medicine and a past president of the American Board of Addiction Medicine. “And the more patients take, the more likely they are to become dependent.” After a follow-up visit or two, the specialist who did the procedure has no reason to continue seeing the patient. (That doctor could also be an emergency room physician who treated kidney stones, sciatica or any number of other conditions involving stabbing pain.) Yet the patient’s pain may persist, demanding to be tamed. The patient, who now knows just how effective these drugs are, wants to refill the prescription. “The default approach is you go to your primary care provider, and they’ll take care of it,” said Dr. Jonathan H. Chen, an instructor at the Stanford University School of Medicine, who has researched the distribution of opioid prescriptions. As he spoke during a break in his shift in a same-day urgent care clinic, he had just attended to a patient who had recently had shoulder surgery but said she was still in pain. © 2016 The New York Times Company
By Jocelyn Kaiser Gene therapy is living up to its promise of halting a rare, deadly brain disease in young boys. In a new study presented in Washington, D.C., yesterday at the annual meeting of the American Society of Gene and Cell Therapy, all but one of 17 boys with adrenoleukodystrophy (ALD) remained relatively healthy for up to 2 years after having an engineered virus deliver into their cells a gene to replenish a missing protein needed by the brain. The results, which expand on an earlier pilot study, bring this ALD therapy one step closer to the clinic. About one in 21,000 boys are born with ALD, which is caused by a flaw in a gene on the X chromosome that prevents cells from making a protein that the cells need to process certain fats—females have a backup copy of the gene on their second X chromosome. Without that protein, the fats build up and gradually destroy myelin sheaths that protect nerves in the brain. In the cerebral form of ALD, which begins in childhood, patients quickly lose vision and mobility, usually dying by age 12. The disease achieved some degree of fame with the 1992 film Lorenzo’s Oil, inspired by a family’s struggle to prolong their son’s life with a homemade remedy. The only currently approved treatment for ALD is a bone marrow transplant -- white blood cells in the marrow go to the brain and turn into glial cells that produce normal ALD proteins. But bone marrow transplants carry many risks, including immune rejection, and matching donors can’t always be found. As an alternative, in the late 2000s, French researchers treated the bone cells of two boys with a modified virus carrying the ALD gene. They reported in Science in 2009 that this halted progression of the disease. © 2016 American Association for the Advancement of Science
Laura Sanders Iron, says aging expert Naftali Raz, is like the Force. It can be good or bad, depending on the context. When that context is the human brain, though, scientists wrangle over whether iron is a dark force for evil or a bright source of support. Some iron is absolutely essential for the brain. On that, scientists agree. But recent studies suggest to some researchers that too much iron, and the chemical reactions that ensue, can be dangerous or deadly, especially to nerve cells in the vulnerable brain area that deteriorates with Parkinson’s disease. Yet other work raises the possibility that those cells die because of lack of iron, rather than too much. “There are a lot of surprises in this field,” says iron biologist Nancy Andrews of Duke University. The idea that too much iron is dangerous captivates many researchers, including analytical neurochemist Dominic Hare of the University of Technology Sydney. “All of life is a chemical reaction,” he says, “so the start of disease is a chemical reaction as well.” And as Raz points out, reactions involving iron are both life-sustaining and dangerous. “Iron is absolutely necessary for conducting the very fundamental business in every cell,” says Raz, of Wayne State University in Detroit. It helps produce energy-storing ATP molecules. And that’s a dirty job, throwing off dangerous free radicals that can cause cellular mayhem as energy is made. But those free radicals are not the most worrisome aspect of iron, Hare believes. “The reaction that is much more dangerous is the reaction you get when iron and dopamine come together,” he says. © Society for Science & the Public 2000 - 2016.
Link ID: 22173 - Posted: 05.03.2016
Nicola Davis People with a larger circle of friends are better able to tolerate pain, according to research into the pain thresholds and social networks of volunteers. The link is thought to be down a system in the brain that involves endorphins: potent pain-killing chemicals produced by the body that also trigger a sense of wellbeing. “At an equivalent dose, endorphins have been shown to be stronger than morphine,” said Katerina Johnson, a doctoral student at the University of Oxford, who co-authored the research. Writing in the journal Scientific Reports, Johnson and Robin Dunbar, professor of evolutionary psychology at the University of Oxford, sought to probe the theory that the brain’s endorphin system might have evolved to not only handle our response to physical discomfort, but influence our experience of pleasure from social interactions too. “Social behaviour and being attached to other individuals is really important for our survival - whether that is staying close to our parents, or our offspring or cooperating with others to find food or to help defend ourselves,” said Johnson. To test the link, the authors examined both the social networks and pain thresholds of 101 adults aged between 18 and 34. Each participant was asked to complete a questionnaire, designed to quiz them on friends they contacted once a week and those they got in touch with once a month. The personality of each participant was probed, looking at traits such as “agreeableness”; they were also asked to rate their fitness and stress levels. © 2016 Guardian News and Media Limited
Keyword: Pain & Touch
Link ID: 22156 - Posted: 04.28.2016
By ANDREW POLLACK In a confrontation between the hopes of desperate patients and clinical trial data, advisers to the Food and Drug Administration voted on Monday not to recommend approval of what would become the first drug for Duchenne muscular dystrophy. The negative votes came despite impassioned pleas from patients, parents and doctors who insisted that the drug, called eteplirsen, was prolonging the ability of boys with the disease to walk well beyond when they would normally be in wheelchairs. The problem was that the drug’s manufacturer, Sarepta Therapeutics, was trying to win approval based on a study involving only 12 patients without an adequate placebo control. The advisory panel voted 7 to 3, with three abstentions, that the clinical data did not meet the F.D.A. requirements for well controlled studies necessary for approval. However, some of the panel members had trouble reconciling the often compelling patient testimony with the F.D.A. legal requirements. “I was just basically torn between my mind and my heart,” said Richard P. Hoffmann, a pharmacist who was the consumer representative on the committee and who abstained. Dr. Bruce I. Ovbiagele, chairman of neurology at the Medical University of South Carolina, voted against approval but said, “Based on all I heard, the drug definitely works, but the question was framed differently.” On another question of whether the drug could qualify for so-called accelerated approval, a lower hurdle, the panel voted 7 to 6 against the drug. The F.D.A., which does not have to follow the advice of its advisory panels, is scheduled to decide whether to approve eteplirsen by May 26. © 2016 The New York Times Company
Medical research and new drugs to treat human illness usually start with studies on mice and rats. But that type of research has been traditionally sexist — using far more male than female rodents. Scientists warn that has already led to drugs and treatments that are potentially dangerous for women and say the approach slows down the development of treatments and drugs that are safe and effective for everyone. Cara Tannenbaum, scientific director of the Institute of Gender and Health at the Canadian Institutes of Health Research, cited a couple of examples on CBC's The Current of cases where drug side-effects turned out to be far more harmful in women: A stomach drug called cisapride that was sold in the 1990s under the name Prepulsid was withdrawn by Health Canada in 2000 because it sometimes caused irregular heartbeat and sudden death "in women only," Tannenbaum said. Among the victims was the 15-year-old daughter of former Ontario MP Terence Young. "It's not clear that the drug was ever tested in female animals or minors," Tannenbaum added. Health Canada has issued a warning about sleeping pills containing the drug zolpiclone, also known as Ambien, Tannenbaum said. Women are recommended to take half the dose that is prescribed to men. "It was recently discovered that the level of the drug was 45 per cent higher in women the next day, which can lead to car accidents," Tannenbaum said. Jeffrey Mogil, a neuroscientist and pain specialist at McGill University, said there are lots of reasons to suspect men and women respond differently to many different kinds of drugs, but very little actual data. "We actually don't know the scope of the problem," he told The Current. ©2016 CBC/Radio-Canada.
Melissa Davey Researchers have developed the world’s first blood test that can detect the abnormal metabolism of blood cells in people with Parkinson’s disease, which means the blood test could be used to diagnose the disorder. At present the only way to diagnose Parkinson’s disease, a degenerative neurological condition, is through ordering a range of tests and scans to rule out other disorders, combined with examining symptoms. Patients are often diagnosed only after they have developed symptoms and brain cells have already been destroyed. While there is no cure for Parkinson’s, early detection allows treatment with medication and physiotherapy to begin, which may slow the deterioration of motor functions in patients. Because diagnosing the disease is a process of elimination, and the symptoms mimic those of other neurological disorders, patients are also at risk being diagnosed and treated for the wrong disease. The group of Australian researchers from La Trobe University believe their blood test will enable doctors to detect Parkinson’s disease with unprecedented reliability and lead to earlier treatment. Their findings are under review by an international medical journal. © 2016 Guardian News and Media Limited
Link ID: 22120 - Posted: 04.20.2016
By BENEDICT CAREY Five years ago, a college freshman named Ian Burkhart dived into a wave at a beach off the Outer Banks in North Carolina and, in a freakish accident, broke his neck on the sandy floor, permanently losing the feeling in his hands and legs. On Wednesday, doctors reported that Mr. Burkhart, 24, had regained control over his right hand and fingers, using technology that transmits his thoughts directly to his hand muscles and bypasses his spinal injury. The doctors’ study, published by the journal Nature, is the first account of limb reanimation, as it is known, in a person with quadriplegia. Doctors implanted a chip in Mr. Burkhart’s brain two years ago. Seated in a lab with the implant connected through a computer to a sleeve on his arm, he was able to learn by repetition and arduous practice to focus his thoughts to make his hand pour from a bottle, and to pick up a straw and stir. He was even able to play a guitar video game. “It’s crazy because I had lost sensation in my hands, and I had to watch my hand to know whether I was squeezing or extending the fingers,” Mr. Burkhart, a business student who lives in Dublin, Ohio, said in an interview. His injury had left him paralyzed from the chest down; he still has some movement in his shoulders and biceps. The new technology is not a cure for paralysis. Mr. Burkhart could use his hand only when connected to computers in the lab, and the researchers said there was much work to do before the system could provide significant mobile independence. But the field of neural engineering is advancing quickly. Using brain implants, scientists can decode brain signals and match them to specific movements. Previously, people have learned to guide a cursor on a screen with their thoughts, monkeys have learned to skillfully use a robotic arm through neural signals and scientists have taught monkeys who were partly paralyzed to use an arm with a bypass system. This new study demonstrates that the bypass approach can restore critical skills to limbs no longer directly connected to the brain. © 2016 The New York Times Company
Link ID: 22106 - Posted: 04.14.2016
Dr. Perri Klass First of all, nobody takes a small child on an airplane for the fun of it. I have been there and I know. Don’t get me wrong, I’m no airplane saint; you won’t generally catch me offering to hold someone else’s kid, or making friends around the seatback. I don’t usually admit to being a pediatrician, for fear of hearing a medical saga. But I have put in my time on airplanes with my own infants and toddlers and small children, and I certainly know how it feels. Probably the best thing that can be said for traveling with young children is that it teaches you to appreciate traveling without them, however puzzling the inflight announcements, however long the delays, however tightly spaced the seats. I did enough economy-class traveling with children while my own were young that my reflexive reaction to all flight cancellations, turbulence or the moment when the person in front of me reclines the seat very suddenly, knocking my laptop closed, is now: At least I don’t have a small child with me – thank heavens. Babies do not cry on airplanes for the fun of it either. Nor do they cry, by and large, to let you know that their parents are neglectful or callous. They cry for infant versions of the same reasons that adults snap at one another about reclining seats, or elbow each other with quiet savagery over the armrest. They cry because their ears hurt and they’re being made to stay in a certain position when they don’t want to or the air smells strange and the noises are loud, or their stomachs feel upset or the day has been too long and they still aren’t there yet or they’re just plain cranky. As are we all. Crying is an evolutionary strategy to summon adult aid; over millennia, crying has probably evolved to be hard to ignore. I don’t know if it’s any comfort, but when you’re the parent with the crying baby, it doesn’t particularly help to be an expert. “I remember one flight where my daughter screamed the whole way and kept trying to get out of her seatbelt,” said my old friend, Dr. Elizabeth Barnett, a professor of pediatrics at Boston University and a travel medicine specialist. “As a parent, you feel two things — you’re in distress because you’re trying to comfort your child and not succeeding, so you feel bad for your child, and you also feel guilty because you know your child is disturbing everybody else.” © 2016 The New York Times Company
For decades, it was thought that scar-forming cells called astrocytes were responsible for blocking neuronal regrowth across the level of spinal cord injury, but recent findings challenge this idea. According to a new mouse study, astrocyte scars may actually be required for repair and regrowth following spinal cord injury. The research was funded by the National Institutes of Health, and published in Nature. “At first, we were completely surprised when our early studies revealed that blocking scar formation after injury resulted in worse outcomes. Once we began looking specifically at regrowth, though, we became convinced that scars may actually be beneficial,” said Michael V. Sofroniew, M.D., Ph.D., professor of neurobiology at the University of California, Los Angeles, and senior author of the study. “Our results suggest that scars may be a bridge and not a barrier towards developing better treatments for paralyzing spinal cord injuries.” Neurons communicate with one another by sending messages down long extensions called axons. When axons in the brain or spinal cord are severed, they do not grow back automatically. For example, damaged axons in the spinal cord can result in paralysis. When an injury occurs, astrocytes become activated and go to the injury site, along with cells from the immune system and form a scar. Scars have immediate benefits by decreasing inflammation at the injury site and preventing spread of tissue damage. However, long-term effects of the scars were thought to interfere with axon regrowth.
By JOANNA KLEIN Misconception: Migraines are psychological manifestations of women’s inability to manage stress and emotions Actually: Neurologists are very clear that migraines are a real, debilitating medical condition related to temporary abnormal brain activity. The fact that they may be more common for some women during “that time of the month” has nothing to do with emotions. For centuries, doctors explained migraines as a woman’s problem caused by emotional disturbances like hysteria, depression or stress. “Bizarrely, the recommended cure was marriage!” said Dr. Anne MacGregor, the lead author of the British Association for the Study of Headache’s guidelines for diagnosing and managing migraines. While that prescription may be far behind us, the misconception that migraines are fueled by a woman’s inability to cope persists. “It was considered psychological, or that I was a nervous overachiever, so I would never tell people that I have them,” said Lorie Novak, an artist in her sixties who has suffered from migraines since she was 8. After reading Joan Didion’s 1968 essay “In Bed,” about the writer’s struggle with migraines, Ms. Novak decided to tackle the representation of these debilitating headaches. Starting in 2009, Ms. Novak photographed herself every time she got a migraine. Under the hashtag #notjustaheadache, hundreds of others on Twitter and Instagram have demonstrated their own frustration with a widespread lack of understanding of the reality of migraines. © 2016 The New York Times Company
By Sandhya Somashekhar African Americans are routinely under-treated for their pain compared with whites, according to research. A study released Monday sheds some disturbing light on why that might be the case. Researchers at the University of Virginia quizzed white medical students and residents to see how many believed inaccurate and at times "fantastical" differences about the two races -- for example, that blacks have less sensitive nerve endings than whites or that black people's blood coagulates more quickly. They found that fully half thought at least one of the false statements presented was possibly, probably or definitely true. Moreover, those who held false beliefs often rated black patients' pain as lower than that of white patients and made less appropriate recommendations about how they should be treated. The study, published in the Proceedings of the National Academy of Sciences, could help illuminate one of the most vexing problems in pain treatment today: That whites are more likely than blacks to be prescribed strong pain medications for equivalent ailments. A 2000 study out of Emory University found that at a hospital emergency department in Atlanta, 74 percent of white patients with bone fractures received painkillers compared with 50 percent of black patients. Similarly, a paper last year found that black children with appendicitis were less likely to receive pain medication than their white counterparts. And a 2007 study found that physicians were more likely to underestimate the pain of black patients compared with other patients.
By C. CLAIBORNE RAY Q. Why do we become desensitized to a perfume we are wearing while others can still smell it? A. Ceasing to smell one’s perfume after continuous exposure while casual passers-by can still smell it is just one example of a phenomenon called olfactory adaptation or odor fatigue. After some time without exposure, sensitivity is usually restored. A similar weakening of odor signals with continued exposure also takes place in animals other than humans, and researchers often rely on animal studies to try to understand the cellular and molecular bases for the condition. It has been suggested that odor fatigue is useful because it enables animals to sort out the signals of a new odor from the background noise of continuous odors. It may also enable them to sense when an odor grows stronger. Studies published in the journal Science in 2002 pinpointed a chemical that seems to act as a gatekeeper for neurons involved in smell, opening and closing their electric signal channels. Genetically engineered mice that did not produce the substance, a protein called CNGA4, had profoundly impaired olfactory adaptation. A separate test-tube study found similar changes on a cellular level, with the signal channels remaining open when CNGA4 was absent. firstname.lastname@example.org © 2016 The New York Times Company
Keyword: Chemical Senses (Smell & Taste)
Link ID: 22042 - Posted: 03.29.2016