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Cassie Martin Understanding sea anemones’ exceptional healing abilities may help scientists figure out how to restore hearing. Proteins that the marine invertebrates use to repair damaged cells can also repair mice’s sound-sensing cells, a new study shows. The findings provide insights into the mechanics of hearing and could lead to future treatments for traumatic hearing loss, researchers report in the Aug. 1 Journal of Experimental Biology. “This is a preliminary step, but it’s a very useful step in looking at restoring the structure and function of these damaged cells,” says Lavinia Sheets, a hearing researcher at Harvard Medical School who was not involved in the study. Tentacles of starlet sea anemones (Nematostella vectensis) are covered in tiny hairlike cells that sense vibrations in the water from prey swimming nearby.The cells are similar to sound-sensing cells found in the ears of humans and other mammals. When loud noises damage or kill these hair cells, the result can range from temporary to permanent hearing loss. Anemones’ repair proteins restore their damaged hairlike cells, but landlubbing creatures aren’t as lucky. Glen Watson, a biologist at the University of Louisiana at Lafayette, wondered if anemones’ proteins — which have previously been shown to mend similar cells in blind cave fish — might also work in mammals. |© Society for Science & the Public 2000 - 2016.
Tim Radford Eight paraplegics – some of them paralysed for more than a decade by severe spinal cord injury – have been able to move their legs and feel sensation, after help from an artificial exoskeleton, sessions using virtual reality (VR) technology and a non-invasive system that links the brain with a computer. In effect, after just 10 months of what their Brazilian medical team call “brain training” they have been able to make a conscious decision to move and then get a response from muscles that have not been used for a decade. Of the octet, one has been able to leave her house and drive a car. Another has conceived and delivered a child, feeling the contractions as she did so. The extent of the improvements was unexpected. The scientists had intended to exploit advanced computing and robotic technology to help paraplegics recover a sense of control in their lives. But their patients recovered some feeling and direct command as well. The implication is that even apparently complete spinal cord injury might leave some connected nerve tissue that could be reawakened after years of inaction. The patients responded unevenly, but all have reported partial restoration of muscle movement or skin sensation. Some have even recovered visceral function and are now able to tell when they need the lavatory. And although none of them can walk unaided, one woman has been able to make walking movements with her legs, while suspended in a harness, and generate enough force to make a robot exoskeleton move. © 2016 Guardian News and Media Limited
Rachel Ehrenberg Pulling consecutive all-nighters makes some brain areas groggier than others. Regions involved with problem solving and concentration become especially sluggish when sleep-deprived, a new study using brain scans reveals. Other areas keep ticking along, appearing to be less affected by a mounting sleep debt. The results might lead to a better understanding of the rhythmic nature of symptoms in certain psychiatric or neurodegenerative disorders, says study coauthor Derk-Jan Dijk. People with dementia, for instance, can be afflicted with “sundowning,” which worsens their symptoms at the end of the day. More broadly, the findings, published August 12 in Science, document the brain’s response to too little shut-eye. “We’ve shown what shift workers already know,” says Dijk, of the University of Surrey in England. “Being awake at 6 a.m. after a night of no sleep, it isn’t easy. But what wasn’t known was the remarkably different response of these brain areas.” The research reveals the differing effects of the two major factors that influence when you conk out: the body’s roughly 24-hour circadian clock, which helps keep you awake in the daytime and put you to sleep when it’s dark, and the body’s drive to sleep, which steadily increases the longer you’re awake. Dijk and collaborators at the University of Liege in Belgium assessed the cognitive function of 33 young adults who went without sleep for 42 hours. Over the course of this sleepless period, the participants performed some simple tasks testing reaction time and memory. The sleepy subjects also underwent 12 brain scans during their ordeal and another scan after 12 hours of recovery sleep. Throughout the study, the researchers also measured participants’ levels of the sleep hormone melatonin, which served as a way to track the hands on their master circadian clocks. |© Society for Science & the Public 2000 - 2016
Link ID: 22548 - Posted: 08.12.2016
In a global study of myasthenia gravis, an autoimmune disease that causes muscle weakness and fatigue, researchers found that surgical removal of an organ called the thymus reduced patients’ weakness, and their need for immunosuppressive drugs. The study, published in the New England Journal of Medicine, was partially funded by the National Institutes of Health. “Our results support the idea that thymectomy is a valid treatment option for a major form of myasthenia gravis,” said Gil Wolfe, M.D., Professor and Irvin and Rosemary Smith Chair of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, New York, and a leader of the study. The Thymectomy Trial in Non-Thymomatous Myasthenia Gravis Patients Receiving Prednisone (MGTX) was a randomized, controlled study conducted on 126 patients aged 18-65 between 2006 and 2012. The researchers compared the combination of surgery and immunosuppression with the drug prednisone with prednisone treatment alone. They performed extended transternal thymectomies on 57 patients. This major surgical procedure aims to remove most of the thymus, which requires opening of a patient’s chest. On average the researchers found that the combination of surgery and prednisone treatment reduced overall muscle weakness more than prednisone treatment alone. After 36 months of prednisone treatment, both groups of patients had better QMG scores, a measure of muscle strength. Scores for the patients who had thymectomies and prednisone were 2.84 points better than patients who were on prednisone alone.
By Sharon Begley, The Massachusetts Institute of Technology brain sciences department and, separately, a group of some 200 neuroscientists from around the world have written letters to The New York Times claiming that a book excerpt in the newspaper’s Sunday magazine this week contains important errors, misinterpretations of scientific disputes, and unfair characterizations of an MIT neuroscientist who did groundbreaking research on human memory. In particular, the excerpt contains a 36-volley verbatim exchange between author Luke Dittrich and MIT’s Suzanne Corkin in which she says that key documents from historic experiments were “shredded.” “Most of it has gone, is in the trash, was shredded,” Corkin is quoted as telling Dittrich before she died in May, explaining, “there’s no place to preserve it.” Destroying files related to historic scientific research would raise eyebrows, but Corkin’s colleagues say it never happened. “We believe that no records were destroyed and, to the contrary, that professor Corkin worked in her final days to organize and preserve all records,” said the letter that Dr. James DiCarlo, head of the MIT Department of Brain and Cognitive Sciences, sent to the Times late Tuesday. Even as Corkin fought advanced liver cancer, he wrote, “she instructed her assistant to continue to organize, label, and maintain all records” related to the research, and “the records currently remain within our department.” © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 22546 - Posted: 08.11.2016
Mo Costandi The human brain is often said to be the most complex object in the known universe, and there’s good reason to believe that it is. That lump of jelly inside your head contains at least 80 billion nerve cells, or neurons, and even more of the non-neuronal cells called glia. Between them, they form hundreds of trillions of precise synaptic connections; but they all have moveable parts, and these connections can change. Neurons can extend and retract their delicate fibres; some types of glial cells can crawl through the brain; and neurons and glia routinely work together to create new connections and eliminate old ones. These processes begin before we are born, and occur until we die, making the brain a highly dynamic organ that undergoes continuous change throughout life. At any given moment, many millions of them are being modified in one way or another, to reshape the brain’s circuitry in response to our daily experiences. Researchers at Yale University have now developed an imaging technique that enables them to visualise the density of synapses in the living human brain, and offers a promising new way of studying how the organ develops and functions, and also how it deteriorates in various neurological and psychiatric conditions. The new method, developed in Richard Carson’s lab at Yale’s School of Engineering and Applied Sciences, is based on positron emission tomography (PET), which detects the radiation emitted by radioactive ‘tracers’ that bind to specific proteins or other molecules after being injected into the body. Until now, the density of synapses in the human brain could only be determined by autopsy, using antibodies that bind to and stain specific synaptic proteins, or electron microscopy to examine the fine structure of the tissue. © 2016 Guardian News and Media Limited
Keyword: Brain imaging
Link ID: 22545 - Posted: 08.11.2016
By Andy Coghlan The switching-off of genes in the human brain has been watched live for the first time. By comparing this activity in different people’s brains, researchers are now on the hunt for abnormalities underlying disorders such as Alzheimer’s disease and schizophrenia. To see where genes are most and least active in the brain, Jacob Hooker at Harvard Medical School and his team developed a radioactive tracer chemical that binds to a type of enzyme called an HDAC. This enzyme deactivates genes inside our cells, stopping them from making the proteins they code for. When injected into people, brain scans can detect where this tracer has bound to an enzyme, and thus where the enzyme is switching off genes. Live epigenetics The switching-off of genes by HDACs is a form of epigenetics – physical changes to the structure of DNA that modify how active genes are without altering their code. Until now, the only way to examine such activity in the brain has been by looking at post-mortem brain tissue. In the image above from the study, genes are least active in the red regions, such as the bulb-shaped cerebellum area towards the bottom right. The black and blue areas show the highest levels of gene activity – where barely any HDACs are present – and the yellow and green areas fall in between. © Copyright Reed Business Information Ltd.
Nicola Davis Scientists say that they have discovered a possible explanation for how Alzheimer’s disease spreads in the brain. Alzheimer’s is linked to a buildup of protein plaques and tangles that spread across particular tissues in the brain as the disease progresses. But while the pattern of this spread is well-known, the reason behind the pattern is not. Now scientists say they have uncovered a potential explanation as to why certain tissues of the brain are more vulnerable to Alzheimer’s disease. The vulnerability appears to be linked to variations in the levels of proteins in the brain that protect against the clumping of other proteins - variations that are present decades before the onset of the disease. Hope for Alzheimer's treatment as researchers find licensed drugs halt brain degeneration Read more “Our results indicate that within healthy brains a tell-tale pattern of protein levels predicts the progression of Alzheimer’s disease through the brain [in those that are affected by the disease],” said Rosie Freer, a PhD student at the University of Cambridge and first author of the study. The results could open up the possibility of identifying individuals who are at risk of developing Alzheimer’s long before symptoms appear, as well as offering new insights to those attempting to tackle the disease. Charbel Moussa, director of the Laboratory for Dementia and Parkinsonism at Georgetown University Medical Center said that he agreed with the conclusions of the study. “It is probably true that in cases of diseases like Alzheimer’s and Parkinson’s we may have deficiencies in quality control mechanisms like cleaning out bad proteins that collect in the brain cells,” he said, although he warned that using such findings to predict those more at risk of such disease is likely to be difficult. © 2016 Guardian News and Media Limited
By Effy Redman “There is no one who has not smiled at least once,” writes Marianne LaFrance, a Yale University psychology professor, in her 2011 book “Lip Service: Smiles in Life, Death, Trust, Lies, Work, Memory, Sex and Politics.” Her book explores how smiling unifies us. Like breath, the smile is universal. We smile to connect, to forgive, to love. A smile is beauty, human. But I have never smiled. Not once. I was born with Moebius syndrome — a rare form of facial paralysis that results from damage in the womb to the sixth and seventh cranial nerves, which control the muscles of the face. I was born in Britain, on the same day in 1982 the country’s first test-tube twins were born. But while science has created medical miracles like test-tube babies, there’s little that doctors can do for someone with Moebius syndrome. Decades later, I still cannot smile. Or frown. Or do any of the infinite subtle and not-so-subtle things with my face that I see others in the world around me doing every day. Doctors describe people with Moebius as having a “mask-like expression.” And that is what strangers must see. A frozen face, eyes unblinking. My mouth always open, motionless, the left corner of my lips slightly lower than the right. Walking down the street, I can feel the touch of casual observers’ eyes. A child’s very first “social smile” usually occurs six to eight weeks after birth, eagerly awaited by new parents. Because, as an infant, my face remained so expressionless, when I began laughing it took my mother a while to realize that the sound I was making was laughter. At what point, I wonder, did I begin to compensate for the absence of my smile. © 2016 The New York Times Company
Link ID: 22542 - Posted: 08.11.2016
By MIKE SACKS You’ve seen me. I know you have. I’m the guy wearing gloves on the subway in October. Or even into April. Perhaps I’m wearing just one glove, allowing my naked hand to turn the pages of a book. No big deal. Just another one-gloved commuter, heading home. If it’s crowded, you may have noticed me doing my best to “surf,” sans contact, until the car comes to a stop, in which case I may knock into a fellow passenger. Aboveground you may have seen me acting the gentleman, opening doors for others with a special paper towel I carry in my front left pocket for just such a momentous occasion. No? How about that guy walking quickly ahead of you, the one impishly avoiding sidewalk cracks? Or perhaps you’ve noticed a stranger who turns and makes eye contact with you for seemingly no reason. You may have asked, “You got a problem?” Oh, I definitely have a problem. But it has nothing to do with you, sir or madam. (And, yes, even in my thoughts I refer to you as “sir” and “madam.”) The problem here is what multiple doctors have diagnosed as obsessive-compulsive disorder. You may refer to it by its kicky abbreviation, O.C.D. I prefer to call it Da Beast. Da Beast is a creature I have lived with since I was 11, a typical age for O.C.D. to snarl into one’s life without invitation or warning. According to the International O.C.D. Foundation, roughly one in 100 adults suffers from the disorder. Each of us has his or her own obsessive thoughts and fears to contend with. My particular beast of burden is a fear of germs and sickness. It’s a popular one, perhaps the most common. © 2016 The New York Times Company
Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 22541 - Posted: 08.11.2016
By Robert Lavine Just the briefest eye contact can heighten empathetic feelings, giving people a sense of being drawn together. But patients who suffer from autism, even in its most high-functioning forms, often have trouble establishing this sort of a social connection with other people. Researchers are delving into what’s going on behind the eyes when these magical moments occur, and the hormones and neural substrates involved may offer hope of helping people with autism. University of Cambridge neuroscientist Bonnie Auyeung and colleagues gave oxytocin—a compound commonly referred to as the “love hormone,” as it’s been found to play roles in maternal and romantic bonding—to both normal men and those with a high-functioning form of autism also called Asperger’s syndrome. The scientists then tracked the eye movements of the study subjects and found that, compared with controls, those who received oxytocin via nasal spray showed increases in the number of fixations—pauses of about 300 milliseconds—on the eye region of an interviewer’s face and in the fraction of time spent looking at this region during a brief interview (Translational Psychiatry, doi:10.1038/tp.2014.146, 2015). Oxytocin, a neuropeptide hormone secreted by the pituitary gland, has long been known to activate receptors in the uterus and mammary glands, facilitating labor and milk letdown. But research on the neural effects of oxytocin has been accelerated by the availability of a nasal spray formulation of the hormone, which can deliver it more directly to the brain, also rich with oxytocin receptors. Auyeung adds that her study used a unique experimental setup. “Other studies have shown that [oxytocin] increases looking at the eye region when presented with a picture of a face,” Auyeung says. “The new part is that we are using a live interaction.”
By CATHERINE SAINT LOUIS and MATT APUZZO The Obama administration is planning to remove a major roadblock to marijuana research, officials said Wednesday, potentially spurring broad scientific study of a drug that is being used to treat dozens of diseases in states across the nation despite little rigorous evidence of its effectiveness. The new policy is expected to sharply increase the supply of marijuana available to researchers. And in taking this step, the Obama administration is further relaxing the nation’s stance on marijuana. President Obama has said he views it as no more dangerous than alcohol, and the Justice Department has not stood in the way of states that have legalized the drug. For years, the University of Mississippi has been the only institution authorized to grow the drug for use in medical studies. This restriction has so limited the supply of marijuana federally approved for research purposes that scientists said it could often take years to obtain it and in some cases it was impossible to get. But soon the Drug Enforcement Administration will allow other universities to apply to grow marijuana, three government officials said. While 25 states have approved the medical use of marijuana for a growing list of conditions, including Parkinson’s, Crohn’s disease, Tourette’s syndrome, Alzheimer’s, lupus and rheumatoid arthritis, the research to back up many of those treatments is thin. The new policy could begin to change that. “It will create a supply of research-grade marijuana that is diverse, but more importantly, it will be competitive and you will have growers motivated to meet the demand of researchers,” said John Hudak, a senior fellow at the Brookings Institution. The new policy will be published as soon as Thursday in the federal register, according to the three officials, who have seen the policy but spoke on condition of anonymity because they were not authorized to discuss it. © 2016 The New York Times Company
Keyword: Drug Abuse
Link ID: 22539 - Posted: 08.11.2016
By Virginia Morell Fourteen years ago, a bird named Betty stunned scientists with her humanlike ability to invent and use tools. Captured from the wild and shown a tiny basket of meat trapped in a plastic tube, the New Caledonian crow bent a straight piece of wire into a hook and retrieved the food. Researchers hailed the observation as evidence that these crows could invent new tools on the fly—a sign of complex, abstract thought that became regarded as one of the best demonstrations of this ability in an animal other than a human. But a new study casts doubt on at least some of Betty’s supposed intuition. Scientists have long agreed that New Caledonian crows (Corvus moneduloides), which are found only on the South Pacific island of the same name, are accomplished toolmakers. At the time of Betty’s feat, researchers knew that in the wild these crows could shape either stiff or flexible twigs into tools with a tiny, barblike hook at one end, which they used to lever grubs from rotting logs. They also make rakelike tools from the leaves of the screw pine (Pandanus) tree. But Betty appeared to take things to the next level. Not only did she fashion a hook from a material she’d never previously encountered—a behavior not observed in the wild—she seemed to know she needed this specific shape to solve her particular puzzle. © 2016 American Association for the Advancement of Science. A
Laura Sanders A busy protein known for its role in aging may also have a hand in depression, a study on mice hints. Under certain circumstances, the aging-related SIRT1 protein seems to make mice despondent, scientists report August 10 in the Journal of Neuroscience. The results are preliminary, but they might ultimately help find new depression treatments. Today’s treatments aren’t always effective, and new approaches are sorely needed. “This is one potential new avenue,” says study coauthor Deveroux Ferguson of the University of Arizona College of Medicine in Phoenix. Ferguson and colleagues subjected mice to 10 days of stressful encounters with other mice. After their demoralizing ordeal, the mice showed signs of depression, such as eschewing sugar water and giving up attempts to swim. Along with these signs of rodent despair, the mice had more SIRT1 gene activity in the nucleus accumbens, a brain area that has been linked to motivation and depression. Resveratrol, a compound found in red grapes, supercharges the SIRT1 protein, making it more efficient at its job. When Ferguson and colleagues delivered resveratrol directly to the nucleus accumbens, mice displayed more signs of depression and anxiety. When the researchers used a different compound to hinder SIRT1 activity, the mice showed the opposite effect, appearing bolder in some tests than mice that didn’t receive the compound. |© Society for Science & the Public 2000 - 2016.
By Ann Griswold, Autism shares genetic roots with obsessive-compulsive disorder (OCD) andattention deficit hyperactivity disorder (ADHD). The three conditions have features in common, such as impulsivity. New findings suggest that they also share a brain signature. The first comparison of brain architecture across these conditions has found that all are associated with disruptions in the structure of the corpus callosum. The corpus callosum is a bundle of nerve fibers that links the brain’s left and right hemispheres. The results appeared July 1 in the American Journal of Psychiatry. Clinicians may find it difficult to distinguish autism from ADHD based on symptoms alone. But if the conditions are marked by similar structural problems in the brain, the same interventions might be useful no matter what the diagnosis is, says lead researcher Stephanie Ameis, assistant professor of psychiatry at the University of Toronto. The unique aspects of each condition might arise from other brain attributes, such as differences in the connections between neurons, says Thomas Frazier, director of research at the Cleveland Clinic Foundation. “A reasonable conclusion is that autism and ADHD don’t differ dramatically in a structural way, but could differ in connectivity,” says Frazier, who was not involved in the study. Ameis’ team examined the brains of 71 children with autism, 31 with ADHD, 36 with OCD and 62 typical children using diffusion tensor imaging. This method provides a picture of the brain’s white matter, the long fibers that connect nerve cells, by measuring the diffusion of water across these fibers. © 2016 Scientific American
Amy McDermott You’ve got to see it to be it. A heightened sense of red color vision arose in ancient reptiles before bright red skin, scales and feathers, a new study suggests. The finding bolsters evidence that dinosaurs probably saw red and perhaps displayed red color. The new finding, published in the Aug. 17 Proceedings of the Royal Society B, rests on the discovery that birds and turtles share a gene used both for red vision and red coloration. More bird and turtle species use the gene, called CYP2J19, for vision than for coloration, however, suggesting that its first job was in sight. “We have this single gene that has two very different functions,” says evolutionary biologist Nicholas Mundy of the University of Cambridge. Mundy’s team wondered which function came first: the red vision or the ornamentation. In evolution, what an animal can see is often linked with what others can display, says paleontologist Martin Sander of the University of Bonn in Germany, who did not work on the new study. “We’re always getting at color from these two sides,” he says, because the point of seeing a strong color is often reading visual signals. Scientists already knew that birds use CYP2J19 for vision and color. In bird eyes, the gene contains instructions for making bright red oil droplets that filter red light. Other forms of red color vision evolved earlier in other animals, but this form allows birds to see more shades of red than humans can. Elsewhere in the body, the same gene can code for pigments that stain feathers red. Turtles are the only other land vertebrates with bright red oil droplets in their eyes. But scientists weren’t sure if the same gene was responsible, Mundy says. |© Society for Science & the Public 2000 - 2016
By BENEDICT CAREY HOLYOKE, Mass. — Some of the voices inside Caroline White’s head have been a lifelong comfort, as protective as a favorite aunt. It was the others — “you’re nothing, they’re out to get you, to kill you” — that led her down a rabbit hole of failed treatments and over a decade of hospitalizations, therapy and medications, all aimed at silencing those internal threats. At a support group here for so-called voice-hearers, however, she tried something radically different. She allowed other members of the group to address the voice, directly: What is it you want? “After I thought about it, I realized that the voice valued my safety, wanted me to be respected and better supported by others,” said Ms. White, 34, who, since that session in late 2014, has become a leader in a growing alliance of such groups, called the Hearing Voices Network, or HVN. At a time when Congress is debating measures to extend the reach of mainstream psychiatry — particularly to the severely psychotic, who often end up in prison or homeless — an alternative kind of mental health care is taking root that is very much anti-mainstream. It is largely nonmedical, focused on holistic recovery rather than symptom treatment, and increasingly accessible through an assortment of in-home services, residential centers and groups like the voices network Ms. White turned to, in which members help one another understand each voice, as a metaphor, rather than try to extinguish it. For the first time in this country, experts say, psychiatry’s critics are mounting a sustained, broadly based effort to provide people with practical options, rather than solely alleging abuses like overmedication and involuntary restraint. “The reason these programs are proliferating now is society’s shameful neglect of the severely ill, which creates a vacuum of great need,” said Dr. Allen Frances, a professor emeritus of psychiatry at Duke University. © 2016 The New York Times Company
Link ID: 22534 - Posted: 08.09.2016
By Simon Makin A technology with the potential to blur the boundaries between biology and electronics has just leaped a major hurdle in the race to demonstrate its feasibility. A team at the University of California, Berkeley, led by neuroscientist Jose Carmena and electrical and computer engineer Michel Maharbiz, has provided the first demonstration of what the researchers call “ultrasonic neural dust” to monitor neural activity in a live animal. They recorded activity in the sciatic nerve and a leg muscle of an anesthetized rat in response to electrical stimulation applied to its foot. “My lab has always worked on the boundary between biology and man-made things,” Maharbiz says. “We build tiny gadgets to interface synthetic stuff with biological stuff.” The work was published last week in the journal Neuron. The system uses ultrasound for both wireless communication and the device’s power source, eliminating both wires and batteries. It consists of an external transceiver and what the team calls a “dust mote” about 0.8x1x3 mm size, which is implanted inside the body. The transceiver sends ultrasonic pulses to a piezoelectric crystal in the implant, which converts them into electricity to provide power. The implant records electrical signals in the rat via electrodes, and uses this signal to alter the vibration of the crystal. These vibrations are reflected back to the transceiver, allowing the signal to be recorded—a technique known as backscatter. “This is the first time someone has used ultrasound as a method of powering and communicating with extremely small implantable systems,” says one of the paper’s authors, Dongjin Seo. “This opens up a host of applications in terms of embodied telemetry: being able to put something super-tiny, super-deep in the body, which you can park next to a nerve, organ, muscle or gastrointestinal tract, and read data out wirelessly.” © 2016 Scientific American
Keyword: Brain imaging
Link ID: 22533 - Posted: 08.09.2016
By ABBY GOODNOUGH TUSCALOOSA, Ala. — Roslyn Lewis was at work at a dollar store here in Tuscaloosa, pushing a heavy cart of dog food, when something popped in her back: an explosion of pain. At the emergency room the next day, doctors gave her Motrin and sent her home. Her employer paid for a nerve block that helped temporarily, numbing her lower back, but she could not afford more injections or physical therapy. A decade later, the pain radiates to her right knee and remains largely unaddressed, so deep and searing that on a recent day she sat stiffly on her couch, her curtains drawn, for hours. The experience of African-Americans, like Ms. Lewis, and other minorities illustrates a problem as persistent as it is complex: Minorities tend to receive less treatment for pain than whites, and suffer more disability as a result. While an epidemic of prescription opioid abuse has swept across the United States, African-Americans and Hispanics have been affected at much lower rates than whites. Researchers say minority patients use fewer opioids, and they offer a thicket of possible explanations, including a lack of insurance coverage and a greater reluctance among members of minority groups to take opioid painkillers even if they are prescribed. But the researchers have also found evidence of racial bias and stereotyping in recognizing and treating pain among minorities, particularly black patients. “We’ve done a good job documenting that these disparities exist,” said Salimah Meghani, a pain researcher at the University of Pennsylvania. “We have not done a good job doing something about them.” Dr. Meghani’s 2012 analysis of 20 years of published research found that blacks were 34 percent less likely than whites to be prescribed opioids for conditions such as backaches, abdominal pain and migraines, and 14 percent less likely to receive opioids for pain from traumatic injuries or surgery. © 2016 The New York Times Company
BENEDICT CAREY As a boy growing up in Massachusetts, Luke Dittrich revered his grandfather, a brain surgeon whose home was full of exotic instruments. Later, he learned that he was not only a prominent doctor but had played a significant role in modern medical history. In 1953, at Hartford Hospital, Dr. William Scoville had removed two slivers of tissue from the brain of a 27-year-old man with severe epilepsy. The operation relieved his seizures but left the patient — Henry Molaison, a motor repairman — unable to form new memories. Known as H. M. to protect his privacy, Mr. Molaison went on to become the most famous patient in the history of neuroscience, participating in hundreds of experiments that have helped researchers understand how the brain registers and stores new experiences. By the time Mr. Dittrich was out of college — and after a year and a half in Egypt, teaching English — he had become fascinated with H. M., brain science and his grandfather’s work. He set out to write a book about the famous case but discovered something unexpected along the way. His grandfather was one of a cadre of top surgeons who had performed lobotomies and other “psycho-surgeries” on thousands of people with mental problems. This was not a story about a single operation that went wrong; it was far larger. The resulting book — “Patient H. M.: A Story of Memory, Madness, and Family Secrets,” to be published Tuesday — describes a dark era of American medicine through a historical, and deeply personal, lens. Why should scientists and the public know this particular story in more detail? The textbook story of Patient H. M. — the story I grew up with — presents the operation my grandfather performed on Henry as a sort of one-off mistake. It was not. Instead, it was the culmination of a long period of human experimentation that my grandfather and other leading doctors and researchers had been conducting in hospitals and asylums around the country. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22531 - Posted: 08.09.2016