Chapter 5. The Sensorimotor System
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Ewen Callaway Since August 2014, more than 100 children and young adults in the United States have developed a mysterious paralysis. Many of them had fevers before losing strength in one or more limbs, and the cases coincided with a wider epidemic of a little-known respiratory pathogen. That virus, enterovirus D68 (EV-D68), is the leading candidate for the cause of the paralysis, which few children have recovered from. Yet researchers have not definitively linked the two, or determined how the virus could cause the children’s symptoms. A study published on 28 January in The Lancet1 that describes a cluster of cases from Denver, Colorado, strengthens the link, but falls short of providing a 'smoking gun'. Here is what we know about the virus — and what scientists are trying to find out. It belongs to the enterovirus family, which includes poliovirus and the pathogens that cause common colds; it is most similar to the rhinoviruses that cause respiratory infections. Although EV-D68 was first isolated in the 1960s, it is relatively uncommon among enteroviruses circulating worldwide. However, since August 2014, the virus has been linked to more than 1,000 respiratory infections in the United States, some of them severe, and France has seen cases, too. John Watson, a medical epidemiologist at the US Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, says that last year, EV-D68 was the predominant type of enterovirus circulating in the country. “That’s a first,” he says. Genome sequencing2 of viruses recovered from respiratory cases in St Louis, Missouri, shows that the EV-D68 strain circulating in the United States is most closely related to viruses that caused a pneumonia-like illness in three children in Thailand in 20113. What is the evidence that links EV-D68 to the cases of paralysis? © 2015 Nature Publishing Group
Keyword: Movement Disorders
Link ID: 20533 - Posted: 01.29.2015
The presence of a romantic partner during painful medical procedures could make women feel worse rather than better, researchers say. A small study found this increase in pain was most pronounced in women who tended to avoid closeness in their relationships. The authors say bringing a loved one along for support may not be the best strategy for every patient. The work appears in the journal Social Cognitive and Affective Neuroscience. Researchers from University College London, King's College London and the University of Hertfordshire say there has been very little scientific research into the effects of a partner's presence on someone's perception of pain, despite this being common medical advice. They recruited 39 heterosexual couples and asked them a series of questions to measure how much they sought or avoided closeness and emotional intimacy in relationships. Each female volunteer was then subjected to a series of painful laser pulses while her partner was in and then out of the room. The women were asked to score their level of pain. They also had their brain activity measured using a medical test called an EEG. The researchers found that certain women were more likely to score high levels of pain while their partner was in the room. These were women who said they preferred to avoid closeness, trusted themselves more than their partners and felt uncomfortable in their relationships. © 2015 BBC
Keyword: Pain & Touch
Link ID: 20502 - Posted: 01.21.2015
by Jessica Hamzelou YOU'RE not imagining the pain. But your brain might be behind it, nonetheless. For the first time, it is possible to distinguish between brain activity associated with pain from a physical cause, such as an injury, and that associated with pain linked to your state of mind. A fifth of the world's population is thought to experience some kind of chronic pain – that which has lasted longer than three months. If the pain has no clear cause, people can find themselves fobbed off by doctors who they feel don't believe them, or given ineffective or addictive painkillers. But a study led by Tor Wager at the University of Colorado, Boulder, now reveals that there are two patterns of brain activity related to pain. One day, brain scans could be used to work out your relative components of each, helping to guide treatment. "Pain has always been a bit of a puzzle," says Ben Seymour, a neuroscientist at the University of Cambridge. Hearing or vision, for example, can be traced from sensory organs to distinct brain regions, but pain is more complex, and incorporates thoughts and emotions. For example, studies have linked depression and anxiety to the development of pain conditions, and volunteers put in bad moods have a lower tolerance for pain. So does this mean we can think our way into or out of pain? To find out, Wager and his colleagues used fMRI to look at the brain activity of 33 healthy adults while they were feeling pain. First, the team watched the changing activity as they applied increasing heat to the volunteers' arms. As the heat became painful, a range of brain structures lit up. The pattern was common to all the volunteers, so Wager's team called it the neurologic pain signature. © Copyright Reed Business Information Ltd.
By SAM ROBERTS When he was just 5 years old, Thomas Graboys declared that he intended to become a doctor. As a young physician, he visited a nephew serving in the Peace Corps in Mauritania and remained for two months, treating dozens of patients a day. He skied and played tennis and joined fellow cardiologists as the drummer in a rock band called the Dysrhythmics. In Boston, he was famous as a member of the team that diagnosed the Celtics star Reggie Lewis’s heart defect before he died abruptly on a basketball court. In short, “he was a medical version of one of Tom Wolfe’s masters of the universe,” one reviewer concluded after Dr. Graboys (pronounced GRAY-boys) published his autobiography. But barely 60, after experiencing horrific nightmares, frequently flailing in bed, losing his memory, suffering tremors and finally collapsing on his wedding day, he acknowledged that he was suffering from Parkinson’s disease and the onset of dementia. He informed his patients that he had no choice but to close his practice. “My face is often expressionless, though I still look younger than my 63 years,” he recalled in the autobiography, “Life in the Balance: A Physician’s Memoir of Life, Love, and Loss With Parkinson’s Disease and Dementia,” which was published in 2008. “I am stooped,” he continued. “I shuffle when I walk, and my body trembles. My train of thought regularly runs off the rails. There is no sugarcoating Parkinson’s. There is no silver lining here. There is anger, pain, and frustration at being victimized by a disease that can to some extent be managed but cannot be cured.” After managing for more than a decade, Dr. Graboys died on Jan. 5 at his home in Chestnut Hill, Mass., his daughter, Penelope Graboys Blair, said. The cause was complications of Lewy Body Dementia, which was diagnosed after his Parkinson’s. He was 70. © 2015 The New York Times Company
Link ID: 20485 - Posted: 01.15.2015
By Peter Holley "Lynchian," according to David Foster Wallace, "refers to a particular kind of irony where the very macabre and the very mundane combine in such a way as to reveal the former's perpetual containment within the latter." Perhaps no other word better describes the onetime fate of Martin Pistorius, a South African man who spent more than a decade trapped inside his own body involuntarily watching "Barney" reruns day after day. "I cannot even express to you how much I hated Barney," Martin told NPR during the first episode of a new program on human behavior, "Invisibilia." The rest of the world thought Pistorius was a vegetable, according to NPR. Doctors had told his family as much after he'd fallen into a mysterious coma as a healthy 12-year-old before emerging several years later completely paralyzed, unable to communicate with the outside world. The nightmarish condition, which can be caused by stroke or an overdose of medication, is known as "total locked-in syndrome," and it has no cure, according to the National Institute of Neurological Disorders and Stroke. In a first-person account for the Daily Mail, Pistorius described the period after he slipped into a coma: I was completely unresponsive. I was in a virtual coma but the doctors couldn’t diagnose what had caused it. When he finally did awaken in the early 1990s, around the age of 14 or 15, Pistorius emerged in a dreary fog as his mind gradually rebooted itself.
By Will Boggs MD NEW YORK (Reuters Health) - Patients with chronic pain show signs of glial activation in brain centers that modulate pain, according to results from a PET-MRI study. "Glia appears to be involved in the pathophysiology of chronic pain, and therefore we should consider developing therapeutic approaches targeting glia," Dr. Marco L. Loggia from Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, told Reuters Health by email. "Glial activation is accompanied by many cellular responses, which include the production and release of substances (such as so-called 'pro-inflammatory cytokines') that can sensitize the pain pathways in the central nervous system," he explained. "Thus, glial activation is not a mere reaction to a pain state but actively contributes to the establishment and/or maintenance of persistent pain." To test their hypothesis that patients with chronic pain demonstrate in vivo activation of brain glia, Dr. Loggia's team imaged the brains of 19 individuals diagnosed with chronic low back pain as well as 25 pain-free healthy volunteers using 11C-PBR28, a PET radioligand that binds to the translocator protein (TSPO), a protein upregulated in activated microglia and reactive astrocytes in animal models of pain. Each patient exhibited higher 11C-PBR28 uptakes than his/her age-, sex-, and TSPO genotype-matched control in the thalamus, and there were no brain regions for which the healthy controls showed statistically higher uptakes than the patients with chronic low back pain. © 2015 Scientific American
By CATHERINE SAINT LOUIS A nationwide outbreak of a respiratory virus last fall sent droves of children to emergency departments. The infections have now subsided, as researchers knew they would, but they have left behind a frightening mystery. Since August, 103 children in 34 states have had an unexplained, poliolike paralysis of an arm or leg. Each week, roughly three new cases of so-called acute flaccid myelitis are still reported to the Centers for Disease Control and Prevention. Is the virus, called enterovirus 68, really the culprit? Experts aren’t certain: Unexplained cases of paralysis in children happen every year, but they are usually scattered and unrelated. After unusual clusters of A.F.M. appeared this fall, enterovirus 68 became the leading suspect, and now teams of researchers are racing to figure out how it could have led to such damage. “It’s unsatisfying to have an illness and not know what caused it,” said Dr. Samuel Dominguez, an epidemiologist and an infectious disease specialist at Children’s Hospital Colorado, which has had the largest cluster of patients. For many families, the onset of persistent limb paralysis has been a bewildering experience. Roughly two thirds of the children with A.F.M. have reported some improvement, according to the C.D.C. About a third show none. Only one child has fully recovered. In August, Jack Wernick, a first grader in Kingsport, Tenn., developed a “crummy little cold,” said his father, Dan Wernick, who works for a paper company. It seemed ordinary, until Jack complained that his right arm was heavy, his face began drooping and pain started shooting down his right leg. © 2015 The New York Times Company
Keyword: Movement Disorders
Link ID: 20477 - Posted: 01.13.2015
By James Gallagher Health editor, BBC News website An elastic implant that moves with the spinal cord can restore the ability to walk in paralysed rats, say scientists. Implants are an exciting field of research in spinal cord injury, but rigid designs damage surrounding tissue and ultimately fail. A team at Ecole Polytechnique Federale de Lausanne (EPFL) has developed flexible implants that work for months. It was described by experts as a "groundbreaking achievement of technology". The spinal cord is like a motorway with electrical signals rushing up and down it instead of cars. Injury to the spinal cord leads to paralysis when the electrical signals are stuck in a jam and can no longer get from the brain to the legs. The same group of researchers showed that chemically and electrically stimulating the spinal cord after injury meant rats could "sprint over ground, climb stairs and even pass obstacles". Rat walks up stairs Previous work by the same researchers But that required wired electrodes going directly to the spinal cord and was not a long-term option. Implants are the next step, but if they are inflexible they will rub, causing inflammation, and will not work properly. The latest innovation, described in the journal Science, is an implant that moves with the body and provides both chemical and electrical stimulation. When it was tested on paralysed rats, they moved again. One of the scientists, Prof Stephanie Lacour, told the BBC: "The implant is soft but also fully elastic to accommodate the movement of the nervous system. "The brain pulsates with blood so it moves a lot, the spinal cord expands and retracts many times a day, think about bending over to tie your shoelaces. "In terms of using the implant in people, it's not going to be tomorrow, we've developed dedicated materials which need approval, which will take time. © 2015 BBC.
Link ID: 20465 - Posted: 01.10.2015
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.
|William Mullen, Tribune reporter Researchers at Northwestern University say they have discovered a common cause behind the mysterious and deadly affliction of amyotrophic lateral sclerosis, or Lou Gehrig's disease, that could open the door to an effective treatment. Dr. Teepu Siddique, a neuroscientist with Northwestern's Feinberg School of Medicine whose pioneering work on ALS over more than a quarter-century fueled the research team's work, said the key to the breakthrough is the discovery of an underlying disease process for all types of ALS. The discovery provides an opening to finding treatments for ALS and could also pay dividends by showing the way to treatments for other, more common neurodegenerative diseases such as Alzheimer's, dementia and Parkinson's, Siddique said. The Northwestern team identified the breakdown of cellular recycling systems in the neurons of the spinal cord and brain of ALS patients that results in the nervous system slowly losing its ability to carry brain signals to the body's muscular system. Without those signals, patients gradually are deprived of the ability to move, talk, swallow and breathe. "This is the first time we could connect (ALS) to a clear-cut biomedical mechanism," Siddique said. "It has really made the direction we have to take very clear and sharp. We can now test for drugs that would regulate this protein pathway or optimize it, so it functions as it should in a normal state."
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20459 - Posted: 01.08.2015
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 Lindsey Konkel For 28 years, Bill Gilmore lived in a New Hampshire beach town, where he surfed and kayaked. “I’ve been in water my whole life,” he said. “Before the ocean, it was lakes. I’ve been a water rat since I was four.” Now Gilmore can no longer swim, fish or surf, let alone button a shirt or lift a fork to his mouth. Earlier this year, he was diagnosed with amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease. In New England, medical researchers are now uncovering clues that appear to link some cases of the lethal neurological disease to people’s proximity to lakes and coastal waters. About five years ago, doctors at a New Hampshire hospital noticed a pattern in their ALS patients—many of them, like Gilmore, lived near water. Since then, researchers at Dartmouth-Hitchcock Medical Center have identified several ALS hot spots in lake and coastal communities in New England, and they suspect that toxic blooms of blue-green algae—which are becoming more common worldwide—may play a role. Now scientists are investigating whether breathing a neurotoxin produced by the algae may raise the risk of the disease. They have a long way to go, however: While the toxin does seem to kill nerve cells, no research, even in animals, has confirmed the link to ALS. As with all ALS patients, no one knows what caused Bill Gilmore’s disease. He was a big, strong guy—a carpenter by profession. One morning in 2011, his arms felt weak. “I couldn’t pick up my tools. I thought I had injured myself,” said Gilmore, 59, who lived half his life in Hampton and now lives in Rochester, N.H. © 2014 Scientific American
by Andy Coghlan To catch agile prey on the wing, dragonflies rely on the same predictive powers we use to catch a ball: that is, anticipating by sight where the ball will go and readying body and hand to snatch it from mid-air. Until now, dragonflies were thought to catch their prey without this predictive skill, instead blindly copying every steering movement made by their prey, which can include flies and bees. Now, sophisticated laboratory experiments have tracked the independent body and eye movements of dragonflies as they pursue prey, showing for the first time that dragonflies second guess where their prey will fly to next and then steer their flight accordingly. Throughout the pursuit, they lock on to their target visually while they orient their bodies and flight path for ultimate interception, rather than copying each little deviation in their prey's flight path in the hope of ultimately catching up with it. "The dragonfly lines up its body axis in the flight direction of the prey, but keeps the eyes in its head firmly fixed on the prey," says Anthony Leonardo of the Howard Hughes Medical Institute in Ashburn, Virginia. "It enables the dragonfly to catch the prey from beneath and behind, the prey's blind spot," he says. © Copyright Reed Business Information Ltd.
Link ID: 20412 - Posted: 12.13.2014
|By Claudia Wallis Touch a hot frying pan and the searing message of pain sprints up to your brain and back down to your hand so fast that the impulse to withdraw your fingers seems instantaneous. That rapid-fire signal begins in a heat-sensing molecule called a TRPV1 channel. This specialized protein is abundant on the surface of sensory nerve cells in our fingers and elsewhere and is a shape-shifter that can take an open or closed configuration. Heat opens a central pore in the molecule, so do certain spider toxins and capsaicin—the substance that gives chili peppers their burn. Once the pore is open, charged ions of sodium and calcium flow into the nerve cell, triggering the pain signal. Ouch! As neuroscientist-journalist Stephani Sutherland explains in “Pain that Won’t Quit,” in the December Scientific American, researchers have long been interested in finding ways to moderate the action of this channel—and other ion channels—in patients who suffer from chronic pain. Shutting down the TRPV1 channel completely, however, is not an option because it plays a vital role in regulating body temperature. In two papers published in Nature in December 2013 investigators at the University of California, San Francisco, gave pain researchers a big leg up in understanding TRPV1. They revealed, in exquisite atomic detail, the structure of the channel molecule (from a rat) using an electron cryomicroscope, an instrument designed to explore the 3-D structure of molecules at very low temperatures. One of those investigators, Yifan Cheng, also created this colorful animation, showing how the molecule looks when the channel is open. © 2014 Scientific American
Keyword: Pain & Touch
Link ID: 20411 - Posted: 12.13.2014
Carl Zimmer For thousands of years, fishermen knew that certain fish could deliver a painful shock, even though they had no idea how it happened. Only in the late 1700s did naturalists contemplate a bizarre possibility: These fish might release jolts of electricity — the same mysterious substance as in lightning. That possibility led an Italian physicist named Alessandro Volta in 1800 to build an artificial electric fish. He observed that electric stingrays had dense stacks of muscles, and he wondered if they allowed the animals to store electric charges. To mimic the muscles, he built a stack of metal disks, alternating between copper and zinc. Volta found that his model could store a huge amount of electricity, which he could unleash as shocks and sparks. Today, much of society runs on updated versions of Volta’s artificial electric fish. We call them batteries. Now a new study suggests that electric fish have anticipated other kinds of technology. The research, by Kenneth C. Catania, a biologist at Vanderbilt University, reveals a remarkable sophistication in the way electric eels deploy their shocks. Dr. Catania, who published the study on Thursday in the journal Science, found that the eels use short shocks like a remote control on their victims, flushing their prey out of hiding. And then they can deliver longer shocks that paralyze their prey at a distance, in precisely the same way that a Taser stops a person cold. “It shows how finely adapted eels are to attack prey,” said Harold H. Zakon, a biologist at the University of Texas at Austin, who was not involved in the study. He considered Dr. Catania’s findings especially impressive since scientists have studied electric eels for more than 200 years. © 2014 The New York Times Company
Link ID: 20400 - Posted: 12.06.2014
Injections of a new drug may partially relieve paralyzing spinal cord injuries, based on indications from a study in rats, which was partly funded by the National Institutes of Health. The results demonstrate how fundamental laboratory research may lead to new therapies. “We’re very excited at the possibility that millions of people could, one day, regain movements lost during spinal cord injuries,” said Jerry Silver, Ph.D., professor of neurosciences, Case Western Reserve University School of Medicine, Cleveland, and a senior investigator of the study published in Nature. Every year, tens of thousands of people are paralyzed by spinal cord injuries. The injuries crush and sever the long axons of spinal cord nerve cells, blocking communication between the brain and the body and resulting in paralysis below the injury. On a hunch, Bradley Lang, Ph.D., the lead author of the study and a graduate student in Dr. Silver’s lab, came up with the idea of designing a drug that would help axons regenerate without having to touch the healing spinal cord, as current treatments may require. “Originally this was just a side project we brainstormed in the lab,” said Dr. Lang. After spinal cord injury, axons try to cross the injury site and reconnect with other cells but are stymied by scarring that forms after the injury. Previous studies suggested their movements are blocked when the protein tyrosine phosphatase sigma (PTP sigma), an enzyme found in axons, interacts with chondroitin sulfate proteoglycans, a class of sugary proteins that fill the scars.
Link ID: 20394 - Posted: 12.04.2014
By Beth Winegarner When Beth Wankel’s son, Bowie, was a baby, he seemed pretty typical. But his “terrible twos” were more than terrible: In preschool, he would hit and push his classmates to a degree that worried his parents and teachers. As Bowie got a little older, he was able tell his mom why he was so combative. “He would say things like, 'I thought they were going to step on me or push me,’” Wankel said. “He was overly uncomfortable going into smaller spaces; it was just too much for him.” Among other things, he refused to enter the school bathroom if another student was inside. When Bowie was 3, he was formally evaluated by his preschool teachers. They said he appeared to be having trouble processing sensory input, especially when it came to figuring out where his body is in relation to other people and objects. He’s also very sensitive to touch and to the textures of certain foods, said Wankel, who lives with her family in San Francisco. Bowie has a form of what’s known as sensory processing disorder. As the name suggests, children and adults with the disorder have trouble filtering sights, smells, sounds and more from the world around them. While so-called neurotypicals can usually ignore background noise, clothing tags or cluttered visual environments, people with SPD notice all of those and more — and quickly become overwhelmed by the effort. Rachel Schneider, a mental-health expert and a blogger for adults with SPD, describes it as a “neurological traffic jam” or “a soundboard, except the sound technician is terrible at his job.”
Ewen Callaway Nerve cells that transmit pain, itch and other sensations to the brain have been made in the lab for the first time. Researchers say that the cells will be useful for developing new painkillers and anti-itch remedies, as well as understanding why some people experience unexplained extreme pain and itching. “The short take-home message would be ‘pain and itch in a dish’, and we think that’s very important,” says Kristin Baldwin, a stem-cell scientist at the Scripps Research Institute in La Jolla, California, whose team converted mouse and human cells called fibroblasts into neurons that detect sensations such as pain, itch or temperature1. In a second paper2, a separate team took a similar approach to making pain-sensing cells. Both efforts were published on 24 November in Nature Neuroscience. Peripheral sensory neurons, as these cells are called, produce specialized ‘receptor’ proteins that detect chemical and physical stimuli and convey them to the brain. The receptor that a cell makes determines its properties — some pain-sensing cells respond to chilli oil, for example, and others respond to different pain-causing chemicals. Mutations in the genes encoding these receptors can cause some people to experience chronic pain or, in rare cases, to become impervious to pain. To create these cells in the lab, independent teams led by Baldwin and by Clifford Woolf, a neuroscientist at Boston Children’s Hospital in Massachusetts, identified combinations of proteins that — when expressed in fibroblasts — transformed them into sensory neurons after several days. Baldwin's team identified neurons that make receptors that detect sensations including pain, itch, and temperature, whereas Woolf’s team looked only at pain-detecting cells. Both teams generated cells that resembled neurons in shape and fired in response to capsaicin, which gives chilli peppers their kick, and mustard oil. © 2014 Nature Publishing Group
Keyword: Pain & Touch
Link ID: 20362 - Posted: 11.26.2014