Chapter 8. General Principles of Sensory Processing, Touch, and Pain
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Rose Eveleth Ranking pain isn’t a simple thing. The standard scale that goes from one to 10, often accompanied by smiley faces that become increasingly distressed, has been lampooned by many as being difficult to use. What does it mean to be a five? Or a three? What is that mildly sad frowny face saying? Do you have to be crying for it to really be a 10? And for some people, it’s even harder to put a number to a subjective experience. Patients with autism, for example, often struggle to express the pain they’re feeling. “We do see many members of our community who either experience altered pain perception, or who have difficulties communicating about and reporting pain,” Julia Bascom, the director of programs at the Autistic Self Advocacy Network, told me in an email. “So someone might experience acid reflux not as burning pain, but as pressure in their throat, and then struggle to interpret a numerical pain scale, or not realize they should bring the issue to the attention of those around them—or what words to use to be taken seriously.” Autism can also mean a difficulty interpreting facial expressions, so the happy and sad faces wouldn't be the most helpful visual cues. And some autistic patients aren’t verbal at all. In fact, for a long time, people thought that kids with autism didn’t feel pain at all, because they often didn’t show reactions to it the same way other people do. “They might not understand the words other people use to describe pain, even if they are feeling the exact same sensation, and their outward reactions might seem to indicate much more pain than they are actually feeling,” Bascom said. © 2015 by The Atlantic Monthly Group.
By Abby Phillip Your smartphone addiction is doing more than giving your thumbs a workout, it is also changing your brain. A new study suggests that using a smartphone -- touching the fingertips against the smooth surface of a screen -- can make the brain more sensitive to the thumb, index and middle finger tips being touched. The study, which was published in the journal Current Biology this week, found that the differences between people when it comes to how the brain responds to thumb stimulation is partly explained by how often they use their smartphones. "I was really surprised by the scale of the changes introduced by the use of smartphones," said Arko Ghosh, of the Institute of Neuroinformatics of the University of Zurich and one of the study's authors, in a news release. Other research has shown that musicians and expert video gamers show the same type of brain adaptations. Smartphone use isn't something most people would consider an "expertise," but frequent use of the devices might similarly lead to brain adaptations. Researchers used an electroencephalography (EEG) device to record the activity that occurred in the brain when people touched their thumbs, index and middle fingers to a mechanical object. They compared the brain recordings of smartphone users and regular cellphone users.
Keyword: Pain & Touch
Link ID: 20446 - Posted: 01.01.2015
By Maria Konnikova Last year, Dimitris Xygalatas, the head of the experimental anthropology lab at the University of Connecticut, decided to conduct a curious experiment in Mauritius, during the annual Thaipusam festival, a celebration of the Hindu god Murugan. For the ten days prior to the festival, devotees abstain from meat and sex. As the festival begins, they can choose to show their devotion in the form of several communal rituals. One is fairly mild. It involves communal prayer and singing beside the temple devoted to Murugan, on the top of a mountain. The other, however—the Kavadi—is one of the more painful modern religious rituals still in practice. Participants must pierce multiple parts of their bodies with needles and skewers and attach hooks to their backs, with which they then drag a cart for more than four hours. After that, they climb the mountain where Murugan’s temple is located. Immediately after each ritual was complete, the worshippers were asked if they would be willing to spend a few minutes answering some questions in a room near the temple. Xygalatas had them rate their experience, their attitude toward others, and their religiosity. Then he asked them a simple question: They would be paid two hundred rupees for their participation (about two days’ wages for an unskilled worker); did they want to anonymously donate any of those earnings to the temple? His goal was to figure out if the pain of the Kavadi led to increased affinity for the temple. For centuries, societies have used pain as a way of creating deep bonds. There are religious rites, such as self-flagellation, solitary pilgrimages, and physical mutilation.
By Smitha Mundasad Health reporter, BBC News The precise part of the brain that gives people a sense of direction has been pinpointed by scientists. People with stronger nerve signals in their "internal compass" tended to be better navigators. The study, published in the journal Current Biology, suggested people get lost when their compass cannot keep up. The researchers in London hope the discovery will help explain why direction sense can deteriorate in conditions such as Alzheimer's disease. Scientists have long believed that such a signal existed within the brain, but until now it had been pure speculation. Volunteers were asked to navigate through a virtual environment Volunteers were asked to navigate towards certain objects placed in four corners of the virtual room They were then asked to navigate the area, from memory alone, while their brains were being scanned by an MRI machine. The scans revealed a part of the brain - known as the entorhinal region - fired up consistently during the tasks. The stronger the signal in the region, the better the volunteers were at finding their way around correctly. Dr Hugo Spiers, who led the study, said: "Studies on London cab drivers have shown that the first thing they do when they work out a route is calculate which direction they need to head in. "We now know the entorhinal cortex is responsible for such calculations and the quality of the signals from this region seem to determine how good someone's navigational skills will be." Dr Martin Chadwick, who was also involved in the study, explained: "Our results provide evidence to support the idea that your internal compass readjusts as you move through the environment. BBC © 2014
Keyword: Animal Migration
Link ID: 20431 - Posted: 12.20.2014
|By Claudia Wallis Touch a hot frying pan and the searing message of pain sprints up to your brain and back down to your hand so fast that the impulse to withdraw your fingers seems instantaneous. That rapid-fire signal begins in a heat-sensing molecule called a TRPV1 channel. This specialized protein is abundant on the surface of sensory nerve cells in our fingers and elsewhere and is a shape-shifter that can take an open or closed configuration. Heat opens a central pore in the molecule, so do certain spider toxins and capsaicin—the substance that gives chili peppers their burn. Once the pore is open, charged ions of sodium and calcium flow into the nerve cell, triggering the pain signal. Ouch! As neuroscientist-journalist Stephani Sutherland explains in “Pain that Won’t Quit,” in the December Scientific American, researchers have long been interested in finding ways to moderate the action of this channel—and other ion channels—in patients who suffer from chronic pain. Shutting down the TRPV1 channel completely, however, is not an option because it plays a vital role in regulating body temperature. In two papers published in Nature in December 2013 investigators at the University of California, San Francisco, gave pain researchers a big leg up in understanding TRPV1. They revealed, in exquisite atomic detail, the structure of the channel molecule (from a rat) using an electron cryomicroscope, an instrument designed to explore the 3-D structure of molecules at very low temperatures. One of those investigators, Yifan Cheng, also created this colorful animation, showing how the molecule looks when the channel is open. © 2014 Scientific American
Keyword: Pain & Touch
Link ID: 20411 - Posted: 12.13.2014
Carl Zimmer For thousands of years, fishermen knew that certain fish could deliver a painful shock, even though they had no idea how it happened. Only in the late 1700s did naturalists contemplate a bizarre possibility: These fish might release jolts of electricity — the same mysterious substance as in lightning. That possibility led an Italian physicist named Alessandro Volta in 1800 to build an artificial electric fish. He observed that electric stingrays had dense stacks of muscles, and he wondered if they allowed the animals to store electric charges. To mimic the muscles, he built a stack of metal disks, alternating between copper and zinc. Volta found that his model could store a huge amount of electricity, which he could unleash as shocks and sparks. Today, much of society runs on updated versions of Volta’s artificial electric fish. We call them batteries. Now a new study suggests that electric fish have anticipated other kinds of technology. The research, by Kenneth C. Catania, a biologist at Vanderbilt University, reveals a remarkable sophistication in the way electric eels deploy their shocks. Dr. Catania, who published the study on Thursday in the journal Science, found that the eels use short shocks like a remote control on their victims, flushing their prey out of hiding. And then they can deliver longer shocks that paralyze their prey at a distance, in precisely the same way that a Taser stops a person cold. “It shows how finely adapted eels are to attack prey,” said Harold H. Zakon, a biologist at the University of Texas at Austin, who was not involved in the study. He considered Dr. Catania’s findings especially impressive since scientists have studied electric eels for more than 200 years. © 2014 The New York Times Company
Link ID: 20400 - Posted: 12.06.2014
By Beth Winegarner When Beth Wankel’s son, Bowie, was a baby, he seemed pretty typical. But his “terrible twos” were more than terrible: In preschool, he would hit and push his classmates to a degree that worried his parents and teachers. As Bowie got a little older, he was able tell his mom why he was so combative. “He would say things like, 'I thought they were going to step on me or push me,’” Wankel said. “He was overly uncomfortable going into smaller spaces; it was just too much for him.” Among other things, he refused to enter the school bathroom if another student was inside. When Bowie was 3, he was formally evaluated by his preschool teachers. They said he appeared to be having trouble processing sensory input, especially when it came to figuring out where his body is in relation to other people and objects. He’s also very sensitive to touch and to the textures of certain foods, said Wankel, who lives with her family in San Francisco. Bowie has a form of what’s known as sensory processing disorder. As the name suggests, children and adults with the disorder have trouble filtering sights, smells, sounds and more from the world around them. While so-called neurotypicals can usually ignore background noise, clothing tags or cluttered visual environments, people with SPD notice all of those and more — and quickly become overwhelmed by the effort. Rachel Schneider, a mental-health expert and a blogger for adults with SPD, describes it as a “neurological traffic jam” or “a soundboard, except the sound technician is terrible at his job.”
Ewen Callaway Nerve cells that transmit pain, itch and other sensations to the brain have been made in the lab for the first time. Researchers say that the cells will be useful for developing new painkillers and anti-itch remedies, as well as understanding why some people experience unexplained extreme pain and itching. “The short take-home message would be ‘pain and itch in a dish’, and we think that’s very important,” says Kristin Baldwin, a stem-cell scientist at the Scripps Research Institute in La Jolla, California, whose team converted mouse and human cells called fibroblasts into neurons that detect sensations such as pain, itch or temperature1. In a second paper2, a separate team took a similar approach to making pain-sensing cells. Both efforts were published on 24 November in Nature Neuroscience. Peripheral sensory neurons, as these cells are called, produce specialized ‘receptor’ proteins that detect chemical and physical stimuli and convey them to the brain. The receptor that a cell makes determines its properties — some pain-sensing cells respond to chilli oil, for example, and others respond to different pain-causing chemicals. Mutations in the genes encoding these receptors can cause some people to experience chronic pain or, in rare cases, to become impervious to pain. To create these cells in the lab, independent teams led by Baldwin and by Clifford Woolf, a neuroscientist at Boston Children’s Hospital in Massachusetts, identified combinations of proteins that — when expressed in fibroblasts — transformed them into sensory neurons after several days. Baldwin's team identified neurons that make receptors that detect sensations including pain, itch, and temperature, whereas Woolf’s team looked only at pain-detecting cells. Both teams generated cells that resembled neurons in shape and fired in response to capsaicin, which gives chilli peppers their kick, and mustard oil. © 2014 Nature Publishing Group
Keyword: Pain & Touch
Link ID: 20362 - Posted: 11.26.2014
By RONI CARYN RABIN The Food and Drug Administration on Thursday approved a powerful long-acting opioid painkiller, alarming some addiction experts who fear that its widespread use may contribute to the rising tide of prescription drug overdoses. The new drug, Hysingla, and another drug approved earlier this year, Zohydro, contain pure hydrocodone, a narcotic, without the acetaminophen used in other opioids. But Hysingla is to be made available as an “abuse-deterrent” tablet that cannot easily be broken or crushed by addicts looking to snort or inject it. Nearly half of the nation’s overdose deaths involved painkillers like hydrocodone and oxycodone, according to a 2010 study by the Centers for Disease Control and Prevention. More than 12 million people used prescription painkillers for nonmedical reasons that year, according to the study. Prescription opioid abuse kills more adults annually than heroin and cocaine combined, and sends 420,000 Americans to emergency rooms every year, according to the C.D.C. Hysingla, however, will not be not abuse-proof, said officials at the F.D.A. and the drug’s manufacturer, Purdue Pharma. Its extended-release formulation, a pill to be taken once every 24 hours by patients requiring round-the-clock pain relief, will contain as much as 120 milligrams of hydrocodone. The F.D.A. warned that doses of 80 milligrams or more “should not be prescribed to people who have not previously taken an opioid medication,” but officials described the abuse-deterrent formulation as a step forward. © 2014 The New York Times Company
By Emily Underwood WASHINGTON, D.C.—Rapid changes unfold in the brain after a person's hand is amputated. Within days—and possibly even hours—neurons that once processed sensations from the palm and fingers start to shift their allegiances, beginning to fire in response to sensations in other body parts, such as the face. But a hand transplant can bring these neurons back into the fold, restoring the sense of touch nearly back to normal, according to a study presented here this week at the annual conference of the Society for Neuroscience. To date, roughly 85 people worldwide have undergone hand replant or transplant surgery, an 8- to 10-hour procedure in which surgeons reattach the bones, muscles, nerves, blood vessels, and soft tissue between the patient's severed wrist and their own hand or one from a donor, often using a needle finer than a human hair. After surgery, studies have shown that it takes about 2 years for the peripheral nerves to regenerate, with sensation slowly creeping through the palm and into the fingertips at a rate of roughly 2 mm per day, says Scott Frey, a cognitive neuroscientist at the University of Missouri, Columbia. Even once the nerves have regrown, the surgically attached hand remains far less sensitive to touch than the original hand once was. One potential explanation is that the brain's sensory "map" of the body—a series of cortical ridges and folds devoted to processing touch in different body parts—loses its ability to respond to the missing hand in the absence of sensory input, Frey says. If that's true, the brain may need to reorganize that sensory map once again in order to fully restore sensation. © 2014 American Association for the Advancement of Science
By Kate Baggaley WASHINGTON — Being stroked in the right place at the right speed activates specialized nerve fibers. The caresses that people rate most pleasant line up with the probable locations of the fibers on the skin, new research suggests. “Touch is important in terms of our physical health and our psychological well-being,” said Susannah Walker, who presented the research November 17 at the annual meeting of the Society for Neuroscience. “But very little attention has been paid to the neurological basis of that effect.” Sensors in the skin known as C-tactile afferents respond strongly to being stroked at between three and 10 centimeters per second. The sensors send signals to the brain that make touch rewarding, says Walker, a neuroscientist at Liverpool John Moores University in England. Walker and a colleague played videos for 93 participants, showing a hand caressing a person’s palm, back, shoulder or forearm, either at 5 cm/s or 30 cm/s. Participants rated the 5 cm/s stroking — the best speed to get the skin’s sensors firing — as the most pleasant, except on the palm, where there are no stroking sensors. The back got the highest pleasantness ratings, forearms lowest. The spots where people like to be touched may not line up with the areas traditionally considered most sensitive. Though less finely attuned to texture or temperature than the hands or face, the back and shoulders are sensitive to a different, social sort of touch. © Society for Science & the Public 2000 - 2014.
By Elahe Izadi Putting very little babies through numerous medical procedures is especially challenging for physicians, in part because reducing the pain they experience is so difficult. Typically for patients, "the preferred method of reducing pain is opiates. Obviously you don't want to give opiates to babies," says neurologist Regina Sullivan of NYU Langone Medical Center. "Also, it's difficult to know when a baby is in pain and not in pain." In recent years, research has shown environmental factors, like a mother or caregiver having contact with a baby during a painful procedure, appears to reduce the amount of pain felt by the baby, at least as indicated by the child's behavior, Sullivan said. But she and Gordon Barr of the University of Pennsylvania, an expert in pain, were interested in whether a mother's presence actually changed the brain functioning of a baby in pain. So Sullivan and Barr turned to rats. Specifically mama and baby rats who were in pain. And they found that hundreds of genes in baby rats' brains were more or less active, depending on whether the mothers were present. Sullivan and Barr presented their committee peer-reviewed research before the Society for Neuroscience annual meeting Tuesday. They gave mild electric shocks to infant rats, some of which had their mothers around and others who didn't. The researchers analyzed a specific portion of the infants' brains, the amygdala region of neurons, which is where emotions like fear are processed.
By Tanya Lewis WASHINGTON — From the stroke of a mother's hand to the embrace of a lover, sensations of gentle touch activate a specialized set of nerves in humans. The brain is widely believed to contain a "map" of the body for sensing touch. But humans may also have an emotional body map that corresponds to feelings of gentle touch, according to new research presented here Sunday (Nov. 16) at the 44th annual meeting of the Society for Neuroscience. For humans and all social species, touch plays a fundamental role in the formation and maintenance of social bonds, study researcher Susannah Walker, a behavioral neuroscientist at Liverpool John Moores University in the United KIngdom, said in a news conference. [Top 10 Things That Make Humans Special] "Indeed, a lack of touch can have a detrimental effect on both our physical health and our psychological well-being," Walker said. In a clinical setting, physical contact with premature infants has been shown to boost growth, decrease stress and aid brain development. But not much research has focused on the basis of these effects in the nervous system, Walker said. The human body has a number of different kinds of nerves for perceiving touch. Thicker nerves surrounded by a fatty layer of insulation (called myelin) identify touch and temperature and rapidly send those signals to the brain, whereas thinner nerves that lack this insulation send sensory information more slowly.
Colin Barras It's the sweetest relief… until it's not. Scratching an itch only gives temporary respite before making it worse – we now know why. Millions of people experience chronic itching at some point, as a result of conditions ranging from eczema to kidney failure to cancer. The condition can have a serious impact on quality of life. On the face of it, the body appears to have a coping mechanism: scratching an itch until it hurts can bring instant relief. But when the pain wears off the itch is often more unbearable than before – which means we scratch even harder, sometimes to the point of causing painful skin damage. "People keep scratching even though they might end up bleeding," says Zhou-Feng Chen at the Washington University School of Medicine in St Louis, Missouri, who has now worked out why this happens. His team's work in mice suggests it comes down to an unfortunate bit of neural crosstalk. We know that the neurotransmitter serotonin helps control pain, and that pain – from the heavy scratching – helps soothe an itch, so Chen's team set out to explore whether serotonin is also involved in the itching process. They began by genetically engineering mice to produce no serotonin. Normally, mice injected with a chemical that irritates their skin will scratch up a storm, but the engineered mice seemed to have almost no urge to scratch. Genetically normal mice given a treatment to prevent serotonin leaving the brain also avoided scratching after being injected with the chemical, indicating that the urge to scratch begins when serotonin from the brain reaches the irritated spot. © Copyright Reed Business Information Ltd.
Keyword: Pain & Touch
Link ID: 20270 - Posted: 11.03.2014
BY Laura Sanders The first time Nathan Whitmore zapped his brain, he had a college friend standing by, ready to pull the cord in case he had a seizure. That didn’t happen. Instead, Whitmore started experimenting with the surges of electricity, and he liked the effects. Since that first cautious attempt, he’s become a frequent user of, and advocate for, homemade brain stimulators. Depending on where he puts the electrodes, Whitmore says, he has expanded his memory, improved his math skills and solved previously intractable problems. The 22-year-old, a researcher in a National Institute on Aging neuroscience lab in Baltimore, writes computer programs in his spare time. When he attaches an electrode to a spot on his forehead, his brain goes into a “flow state,” he says, where tricky coding solutions appear effortlessly. “It’s like the computer is programming itself.” Whitmore no longer asks a friend to keep him company while he plugs in, but he is far from alone. The movement to use electricity to change the brain, while still relatively fringe, appears to be growing, as evidenced by a steady increase in active participants in an online brain-hacking message board that Whitmore moderates. This do-it-yourself community, some of whom make their own devices, includes people who want to get better test scores or crush the competition in video games as well as people struggling with depression and chronic pain, Whitmore says. As reckless as it sounds to juice a brain at home with a 9-volt battery and 40 dollars’ worth of spare parts, this technology’s buzz is based on legit science. Small laboratory studies suggest that carefully controlled brain stimulation can boost a person’s memory and math abilities, hone attention and fast-track learning. The U. S. military is interested and is funding studies to test brain stimulation as a way to boost soldiers’ alertness and vigilance. The technique may even be a viable treatment for pernicious mental disorders such as major depression, according to other laboratory-based studies. © Society for Science & the Public 2000 - 2014.
By Rachel Feltman Sometimes the process of scientific discovery can be a real headache. In a recent Danish study, scientists were thrilled to give painful migraines to 86 percent of their study subjects. Migraines are a particularly painful mystery for researchers to solve: More than 10 percent of people worldwide are affected by these intense headaches, but no one has been able to pinpoint a specific cause. What makes these headaches, which can cause incapacitating pain and nausea, different from all other headaches? That's why scientists had to make their patients suffer -- researchers keep trying to trigger migraines using different mechanisms. The more successful they are, the more likely it is that the mechanism being tested is actually a common cause of migraines. And once we know what the common causes are, we can try to develop better treatments that target them. In this case the 86 percent "success" rate, which the researchers say is much higher than results with other triggers, was owed to increases of a naturally occurring substance called cyclic AMP, or cAMP. Our bodies use cAMP to dilate blood vessels, so an increase of it can increase the flow of blood. To see if cAMP might cause migraines, the researchers dosed their subjects with cilostazol, a drug that increases cAMP concentrations in the body.
Keyword: Pain & Touch
Link ID: 20264 - Posted: 11.01.2014
by Bethany Brookshire In many scientific fields, the study of the body is the study of boys. In neuroscience, for example, studies in male rats, mice, monkeys and other mammals outnumber studies in females 5.5 to 1. When scientists are hunting for clues, treatments or cures for a human population that is around 50 percent female, this boys-only club may miss important questions about how the other half lives. So in an effort to reduce this sex bias in biomedical studies, National Institutes of Health director Francis Collins and Office of Research on Women’s Health director Janine Clayton announced in May a new policy that will roll out practices promoting sex parity in research, beginning with a requirement that scientists state whether males, females or both were used in experiments, and moving on to mandate that both males and females are included in all future funded research. The end goal will be to make sure that NIH-funded scientists “balance male and female cells and animals in preclinical studies in all future [grant] applications” to the NIH. In 1993, the NIH Revitalization Act mandated the inclusion of women and minorities in clinical trials. This latest move extends that inclusion to cells and animals in preclinical research. Because NIH funds the work of morethan 300,000 researchers in the United States and other countries, many of whom work on preclinical and basic biomedical science, the new policy has broad implications for the biomedical research community. And while some scientists are pleased with the effort, others are worried that the mandate is ill-conceived and underfunded. In the end, whether it succeeds or fails comes down to interpretation and future implementation. © Society for Science & the Public 2000 - 2014
By Elizabeth Pennisi Four years ago, Igor Spetic lost his right arm in an industrial accident. Doctors outfitted him with a prosthetic arm that restored some function, but they couldn't restore his sense of touch. Without it, simple tasks like picking up a glass or shaking hands became hit-or-miss propositions. The lack of touch also robs Spetic of basic pleasures. “I would love to feel my wife’s hand,” he says. In time, he may regain that pleasure: Two independent research teams have now equipped artificial hands with sensors that send signals to the wearer’s nerves to recreate this missing sense. The sensing technologies work only in the lab, but they have proved durable, and amputees who have tried them, including Spetic, say that they are effective. One technology advances the range of touch sensations available, while the other promises to enable touch through a better way to attach the prosthesis. “All of these results are very positive,” says Mandayam Srinivasan, a neuroengineer at the Massachusetts Institute of Technology in Cambridge, who was not involved in either project. “Each of them fills a piece of the puzzle in terms of [prosthesis] development.” Almost 40 years ago, researchers tried to provide sensory feedback by adding pressure sensors to prostheses that relayed the sensation through electrodes attached to nerves. But for the most part, they just made it seem like the hand was tingling. And durability has been an issue in such efforts, too. In February, Silvestro Micera, a neuroengineer at the Sant'Anna School of Advanced Studies in Pisa, Italy, and the Swiss Federal Institute of Technology in Lausanne and his team showed that it was possible for sensor-equipped prosthetic arms to gently or powerfully grab objects and even to distinguish a round from a square object. But the study lasted just 4 weeks, in part because of the delicate interface with the body. © 2014 American Association for the Advancement of Science.
Aaron E. Carroll For a drug to be approved by the Food and Drug Administration, it must prove itself better than a placebo, or fake drug. This is because of the “placebo effect,” in which patients often improve just because they think they are being treated with something. If we can’t compare a new drug with a placebo, we can’t be sure that the benefit seen from it is anything more than wishful thinking. But when it comes to medical devices and surgery, the requirements aren’t the same. Placebos aren’t required. That is probably a mistake. At the turn of this century, arthroscopic surgery for osteoarthritis of the knee was common. Basically, surgeons would clean out the knee using arthroscopic devices. Another common procedure was lavage, in which a needle would inject saline into the knee to irrigate it. The thought was that these procedures would remove fragments of cartilage and calcium phosphate crystals that were causing inflammation. A number of studies had shown that people who had these procedures improved more than people who did not. However, a growing number of people were concerned that this was really no more than a placebo effect. And in 2002, a study was published that proved it. A total of 180 patients who had osteoarthritis of the knee were randomly assigned (with their consent) to one of three groups. The first had a standard arthroscopic procedure, and the second had lavage. The third, however, had sham surgery. They had an incision, and a procedure was faked so that they didn’t know that they actually had nothing done. Then the incision was closed. The results were stunning. Those who had the actual procedures did no better than those who had the sham surgery. They all improved the same amount. The results were all in people’s heads. © 2014 The New York Times Company
Keyword: Pain & Touch
Link ID: 20167 - Posted: 10.07.2014
By Lisa Sanders, M.D. On Thursday, we challenged Well readers to solve the mystery of a 62-year-old man with severe neck pain that spread down his arm, a facial droop, and numbness on his torso. Nearly 200 of you wrote in, and 20 of you correctly diagnosed the patient. The correct diagnosis is… Lyme disease. And more precisely, the early disseminated form of Lyme disease with neurological involvement The first person with the correct answer was Dr. Arielle Hay, a pediatric rheumatologist in Miami, who nailed it just half an hour after the case was posted. Dr. Hay said that the biggest clue was the UConn letterhead. When combined with the odd neurological symptoms, this reminder of where the case took place brought Lyme disease to mind. Lyme disease is one of those diseases that hardly needs an explanation. It was first described in 1977, in a case series of 51 children and parents who had mysterious episodes of joint pain and swelling. The children were initially diagnosed with juvenile rheumatoid arthritis, but the clustering of cases eventually led the investigators, Dr. Allen Steere and Dr. Stephen Malawista, to consider an infectious disease. The illness was named after the Connecticut town where most of the initial cases were located. The disease is caused by a spirochete, a spiral shaped bacterium carried by the Ixodes tick, and usually presents first with a distinctive, expanding red rash (called erythema migrans) that appears at the site of the bite in the early, localized stage of the disease. It is thought that the rash appears in up to 80 percent of Lyme infections. © 2014 The New York Times Company