Chapter 8. General Principles of Sensory Processing, Touch, and Pain
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Angus Chen A common pain medication might make you go from "so cute!" to "so what?" when you look at a photo of an adorable kitten. And it might make you less sensitive to horrifying things too. It's acetaminophen, the active ingredient in Tylenol. Researchers say the drug might be taking the edge off emotions – not just pain. "It seems to take off the highs of your daily highs and the lows off your daily lows," says Baldwin Way, a psychologist at Ohio State University and the principal investigator on the study, "It kind of flattens out the vicissitudes of your life." The idea that over-the-counter pain pills might affect emotions has been circulating since 2010, when two psychologists, Naomi Eisenberger and Nathan DeWall, led a study showing that acetaminophen seemed to be having both a psychological and a neurological effect on people. They asked volunteers to play a rigged game that simulated social rejection. Not only did the acetaminophen appear to be deflecting social anxieties, it also seemed to be dimming activity in the insula, a region of the brain involved in processing emotional pain. A brain that can let other thoughts bubble up despite being in pain might help its owner benefit from meditation or other cognitive therapies. "But [the insula] is a portion of the brain that seems to be involved in a lot of things," Way says. In older studies, scientists saw that people with damage in their insula didn't react as strongly to either negative or positive images. So Way and one of his students, Geoffrey Durso, figured that if acetaminophen is doing something to the insula, then it might be having a wider effect, too. © 2015 NPR
by Penny Sarchet You've got a splitting migraine. If you were offered a sugar pill, would you bother taking it? What if you were told your genetic make-up means it is very likely to make you feel better? This is one of the questions raised by the burgeoning effort to understand which genes influence the placebo effect, and how these genes – collectively known as the placebome – determine a person's susceptibility to the phenomenon. There are tremendous differences in the placebo effect between individuals, says Kathryn Hall of Harvard Medical School. "It can vary from no measurable response to someone getting significantly better." Having drawn together all the studies carried out so far, Hall says there is reasonable evidence for at least 11 genes that influence a person's susceptibility. This is enough to warrant discussing the use of genetic screening to assess how likely a person is to respond to a placebo treatment, such as a sugar pill or saline injection. The idea is that this could lead to more personalised treatments for conditions like pain syndromes, migraines, depression, irritable bowel syndrome and even Parkinson's disease, symptoms of which seem to be relieved by placebo in some individuals. It could also lead to the design of more balanced clinical trials. Your personality can help you guess whether you're among the estimated third of the population who are placebo responders. Being agreeable, extroverted and open to new experiences all appear to be associated with placebo susceptibility. Although brain imaging techniques can also indicate a person's likely susceptibility, a genetic read-out would offer a convenient, easily applicable and clearly codified measure. © Copyright Reed Business Information Ltd
Keyword: Pain & Touch
Link ID: 20794 - Posted: 04.14.2015
|By Andrea Alfano To scratch an itch is to scratch many itches: placing nails to skin brings sweet yet short-lived relief because it often instigates another bout of itchiness. The unexpected culprit behind this vicious cycle, new research reveals, is serotonin, the so-called happiness hormone. Scientists thought itch was merely a mild form of pain until 2009, when Zhou-Feng Chen and his colleagues at the Center for the Study of Itch at Washington University in St. Louis discovered itch-specific neurons in mice. Though not identical, itch and pain are closely related; they share the same pathways in certain brain areas. Because of the doubling up, activating one suppresses the other, which is why scratching blocks the itch sensation momentarily. The act, however, also triggers the release of the chemical serotonin, which helps to alleviate pain. It is that burst that makes scratching feel good, but recent work by Chen's group showed that it exacerbates the itch-scratch cycle, too. Itch-sensing neurons have a set of receptors that facilitates pain relief and another that induces itch. Serotonin can bind only to the pain-related receptor, but because the two sets sit close to each other and physically interact, the chemical's arrival indirectly enhances the itch pathway. When Chen and his colleagues activated both receptors simultaneously in mice, the rodents scratched much more than if the itch-inducing receptor was turned on alone. In another experiment, mice lacking the cells that produce serotonin scratched less than normal mice when exposed to a skin irritant. The findings were published in the journal Neuron. © 2015 Scientific American
Keyword: Pain & Touch
Link ID: 20793 - Posted: 04.14.2015
Jon Hamilton Researchers have discovered the exact structure of the receptor that makes our sensory nerves tingle when we eat sushi garnished with wasabi. And because the "wasabi receptor" is also involved in pain perception, knowing its shape should help pharmaceutical companies develop new drugs to fight pain. The receptor, which scientists call TRPA1, is "an important molecule in the pain pathway," says David Julius, a professor of physiology at the University of California, San Francisco and an author of a paper published in this week's Nature. "A dream of mine is that some of the work we do will translate into medicines people can take for chronic pain." Julius led a team that discovered the receptor about a decade ago. Since then, researchers have shown that TRPA1 receptors begin sending distress signals to the brain whenever they encounter pungent chemical irritants, including not only wasabi but tear gas and air pollution from cars or wood fires. The receptors also become activated in response to chemicals released by the body itself when tissue becomes inflamed from an injury or a disease like rheumatoid arthritis. © 2015 NPR
Keyword: Pain & Touch
Link ID: 20780 - Posted: 04.10.2015
by Andy Coghlan Who needs sight to get around when you've got a digital compass in your head? A neuroprosthesis that feeds geomagnetic signals into the brains of blind rats has enabled them to navigate around a maze. The results demonstrate that the rats could rapidly learn to deploy a completely unnatural "sense". It raises the possibility that humans could do the same, potentially opening up new ways to treat blindness, or even to provide healthy people with extra senses. "I'm dreaming that humans can expand their senses through artificial sensors for geomagnetism, ultraviolet, radio waves, ultrasonic waves and so on," says Yuji Ikegaya of the University of Tokyo in Japan, head of the team that installed and tested the 2.5-gram implant. "Ultrasonic and radio-wave sensors may enable the next generation of human-to-human communicationMovie Camera," he says. The neuroprosthesis consists of a geomagnetic compass – a version of the microchip found in smartphones – and two electrodes that fit into the animals' visual cortices, the areas of the brain that process visual information. Whenever the rat positioned its head within 20 degrees either side of north, the electrodes sent pulses of electricity into its right visual cortex. When the rat aligned its head in a southerly direction, the left visual cortex was stimulated. The stimulation allowed blind rats to build up a mental map of their surroundings without any visual cues. During training, blind rats equipped with digital compasses improved at finding food rewards in a five-pronged maze, despite being released from one of three different arms of the maze at random each time. © Copyright Reed Business Information Ltd
By Catherine Saint Louis Joni Mitchell, 71, was taken to a hospital in Los Angeles on Tuesday after she was found unconscious at her Los Angeles home. In recent years, the singer has complained of a number of health problems, including one particularly unusual ailment: Morgellons disease. People who believe they have the condition report lesions that don’t heal, “fibers” extruding from their skin and uncomfortable sensations like pins-and-needles tingling or stinging. Sufferers may also report fatigue and problems with short-term memory and concentration. But Morgellons is not a medically accepted diagnosis. Scientists have struggled for nearly a decade to find a cause and have come up mostly empty-handed. Researchers at the Centers for Disease Control and Prevention studied 115 people who said they had the condition. In a report published in 2012, they said they were unable to identify an infectious source for the patients’ “unexplained dermopathy.” There was no evidence of an environmental link, and the “fibers” from patients resembled those from clothing that had gotten trapped in a scab or crusty skin. The investigators cast doubt on Morgellons as a distinct condition and said that it might be something doctors were already familiar with: delusional infestation, a psychiatric condition characterized by an unshakable but erroneous belief that one’s skin is infested with bugs or parasites. Drug use can contribute to such delusions, and the investigators noted evidence of drug use — prescription or illicit — in half of the people they examined. Of the 36 participants who completed neuropsychological testing, 11 percent had high scores for depression, and 63 percent, unsurprisingly, were preoccupied with health issues. © 2015 The New York Times Company
Keyword: Pain & Touch
Link ID: 20749 - Posted: 04.02.2015
The commonly-prescribed drug acetaminophen or paracetamol does nothing to help low back pain, and may affect the liver when used regularly, a large new international study has confirmed. Reporting in today's issue of the British Medical Journal researchers also say the benefits of the drug are unlikely to be worth the risks when it comes to treating osteoarthritis in the hip or knee. "Paracetamol has been widely recommended as being a safe medication, but what we are saying now is that paracetamol doesn't bring any benefit for patients with back pain, and it brings only trivial benefits to those with osteoarthritis," Gustavo Machado of The George Institute for Global Health and the University of Sydney, tells the Australian Broadcasting Corporation. "In addition to that it might bring harm to those patients." Most international clinical guidelines recommend acetaminophen as the "first choice" of treatment for low back pain and osteoarthritis of the hip and knee. However, despite a trial last year questioning the use of acetaminophen to treat low back pain, there has never been a systematic review of the evidence for this. Machado and colleagues analyzed three clinical trials and confirmed that acetaminophen is no better than placebo at treating low back pain. An analysis of 10 other clinical trials by the researchers quantified for the first time the effect acetaminophen has on reducing pain from osteoarthritis in the knee and hip. "We concluded that it is too small to be clinically worthwhile," says Machado. He says the effects of acetaminophen on the human body are not well understood and just because it can stop headaches, it doesn't mean the drug will work in all circumstances. ©2015 CBC/Radio-Canada.
Keyword: Pain & Touch
Link ID: 20748 - Posted: 04.02.2015
By Virginia Morell Rats and mice in pain make facial expressions similar to those in humans—so similar, in fact, that a few years ago researchers developed rodent “grimace scales,” which help them assess an animal’s level of pain simply by looking at its face. But scientists have questioned whether these expressions convey anything to other rodents, or if they are simply physiological reactions devoid of meaning. Now, researchers report that other rats do pay attention to the emotional expressions of their fellows, leaving an area when they see a rat that’s suffering. “It’s a finding we thought might be true, and are glad that someone figured out how to do an experiment that shows it,” says Jeffrey Mogil, a neuroscientist at McGill University in Montreal, Canada. Mogil’s lab developed pain grimace scales for rats and mice in 2006, and it discovered that mice experience pain when they see a familiar mouse suffering—a psychological phenomenon known as emotional contagion. According to Mogil, a rodent in pain expresses its anguish through narrowed eyes, flattened ears, and a swollen nose and cheeks. Because people can read these visual cues and gauge the intensity of the animal’s pain, Mogil has long thought that other rats could do so as well. In Japan, Satoshi Nakashima, a social cognition psychologist at NTT Communication Science Laboratories in Kanagawa, thought the same thing. And, knowing that other scientists had recently shown that mice can tell the difference between paintings by Picasso and Renoir, he decided to see if rodents could also discriminate between photographs of their fellows’ expressions. He designed the current experiments as part of his doctoral research. © 2015 American Association for the Advancement of Science
Mo Costandi During the 1960s, neuroscientists Ronald Melzack and Patrick Wall proposed an influential new theory of pain. At the time, researchers were struggling to explain the phenomenon. Some believed that specific nerve fibres carry pain signals up into the brain, while others argued that the pain signals are transmitted by intense firing of non-specific fibres. Neither idea was entirely satisfactory, because they could not explain why spinal surgery often fails to abolish pain, why gentle touch and other innocuous stimuli can sometimes cause excruciating pain, or why intensely painful stimuli are not always experienced as such. Melzack and Wall’s Gate Control Theory stated that inhibitory neurons in the spinal cord control the relay of pain signals into the brain. Despite having some holes in it, the theory provided a revolutionary new framework for understanding the neural basis of pain, and ushered in the modern era of pain research. Now, almost exactly 50 years after the publication of Melzack and Wall’s theory, European researchers provide direct evidence of gatekeeper cells that control the flow of pain and itch signals from the spinal cord to the brain. The experience that we call “pain” is an extremely complex one that often involves emotional aspects. Researchers therefore distinguish it from nociception, the process by which the nervous system detects noxious stimuli. Nociception is mediated by primary sensory neurons, whose cell bodies are clumped together in the dorsal root ganglia that run alongside the spinal cord. Each has a single fibre that splits in two not far from the cell body, sending one branch out to the skin surface and the other into the spinal cord. © 2015 Guardian News and Media Limited
Claudia Dreifus Twenty-three states and the District of Columbia have legalized medical marijuana, but scientific research into its appropriate uses has lagged. Dr. Mark Ware would like to change that. Dr. Ware, 50, is the director of the Canadian Consortium for the Investigation of Cannabinoids and the director of clinical research of the Alan Edwards Pain Management Unit of McGill University Health Center. Medical marijuana has been legal in Canada for 16 years, and Dr. Ware, a practicing physician, studies how his patients take the drug and under what conditions it is effective. We spoke for two hours at the recent meeting of the American Association for the Advancement of Science and later by telephone. Our interviews have been condensed and edited for space. Q. How did you become interested in the medical possibilities of cannabis? A. In the late 1990s, I was working in Kingston, Jamaica, at a clinic treating people with sickle cell anemia. My British father and Guyanese mother had raised me in Jamaica, and I’d attended medical school there. One day, an elderly Rastafarian came for his annual checkup. I asked him, “What are your choices of medicines?” He leaned over the table and said, “You must study the herb.” That night, I went back to my office and looked up “cannabis and pain.” What I found were countless anecdotes from patients who’d obtained marijuana either legally or not and who claimed good effect with a variety of pain-related conditions. There were also the eye-opening studies showing that the nervous system had specific receptors for cannabinoids and that these receptors were located in areas related to pain. Everything ended with, “More studies are needed.” So I thought, “This is what I should be doing; let’s go!” © 2015 The New York Times Company
by Emiko Jozuka Touch, says David J. Linden, is something we take for granted. "It's very hard to imagine it gone," he tells WIRED.co.uk. "You can imagine what it's like to be blind or deaf, or have no sense of smell, but there's no way to turn off touch". Touch might not be an obvious starting point for Linden, who is a professor of neuroscience at the John Hopkins University, studying learning and memory. But according to the professor, "the story of the neuroscience underlying touch has yet to be told". Pointing to the advances made in touch research over the last 20 years, Linden tells us that his own interest in the topic was sparked over lunch by colleagues working in the School of Medicine. Making the complex links between the brain and our sense of touch accessible to a wider audience is no easy feat. Yet in his recent book entitled, Touch: The Science of Hand, Heart, and Mind, Linden offers anecdotal and factual ways in to exploring different aspects of touch, whether that be in the form of pain, itches, hot and cold sensations or caresses. "We think of touch as being a one sense modality, but it's many different sensors in the skin acting in parallel," says Linden. He explains how the information in the form of, for example, an itch, pain or caress relays to the brain, dividing them into either discriminative or emotional forms of touch. The discriminative touch allows a person to understand where the body is being touched, or to understand if an object is textured, smooth or 3D. While emotional touch is what makes pain feel emotionally negative, or an orgasm feel positive, says Linden.
Keyword: Pain & Touch
Link ID: 20708 - Posted: 03.21.2015
Loss of sensation in the eye that gradually leads to blindness has been prevented with an innovative technique, Canadian surgeons say. Abby Messner, 18, of Stouffville, Ont., lost feeling in her left eye after a brain tumour was removed, along with a nerve wrapped around it, when she was 11. Messner said she didn’t notice the loss of feeling until she scratched the eye. Messner wasn’t able to feel pain in the eye, a condition called corneal anaesthesia. Despite her meticulous care, the eye wouldn’t blink to protect itself when confronted by dust. A scar formed on her cornea, burrowed through, and formed a scar doctors feared would eventually obliterate her vision. "Everyone was like, 'Wow, she had a brain tumour and she’s fine," Messner recalled. "You don't really think that everything that is holding me back is my eye." Messner had to give up competitive swimming because of irritation from the chlorine, playing hockey, spending time outdoors where wind was a hazard or inside dry shopping malls. Over time, ophthalmology surgeon Dr. Asam Ali at SickKids introduced the idea of a nerve graft to restore feeling in the eye. "She started getting feeling back at about the two, three-month mark and that was a real surprise to her and we were very happy at that point because that was a lot faster than anything that had been reported before," Ali said. ©2015 CBC/Radio-Canada.
Sara Reardon Annie is lying down when she answers the phone; she is trying to recover from a rare trip out of the house. Moving around for an extended period leaves the 56-year-old exhausted and with excruciating pain shooting up her back to her shoulders. “It's really awful,” she says. “You never get comfortable.” In 2011, Annie, whose name has been changed at the request of her lawyer, slipped and fell on a wet floor in a restaurant, injuring her back and head. The pain has never eased, and forced her to leave her job in retail. Annie sued the restaurant, which has denied liability, for several hundred thousand dollars to cover medical bills and lost income. To bolster her case that she is in pain and not just malingering, Annie's lawyer suggested that she enlist the services of Millennium Magnetic Technologies (MMT), a Connecticut-based neuroimaging company that has a centre in Birmingham, Alabama, where Annie lives. MMT says that it can detect pain's signature using functional magnetic resonance imaging (fMRI), which measures and maps blood flow in the brain as a proxy for neural activity. The scan is not cheap — about US$4,500 — but Steven Levy, MMT's chief executive, says that it is a worthwhile investment: the company has had ten or so customers since it began offering the service in 2013, and all have settled out of court, he says. If the scans are admitted to Annie's trial, which is expected to take place early this year, it could establish a legal precedent in Alabama. Most personal-injury cases settle out of court, so it is impossible to document how often brain scans for pain are being used in civil law. But the practice seems to be getting more common, at least in the United States, where health care is not covered by the government and personal-injury cases are frequent. Several companies have cropped up, and at least one university has offered the service. © 2015 Nature Publishing Group
By Emily Underwood SAN JOSE, CALIFORNIA—If you've ever had a migraine, you know it's no ordinary headache: In addition to throbbing waves of excruciating pain, symptoms often include nausea, visual disturbances, and acute sensitivity to sounds, smells, and light. Although there's no cure for the debilitating headaches, which affect roughly 10% of people worldwide, researchers are starting to untangle their cause and find more effective treatments. Here today at the annual meeting of AAAS (which publishes Science), Science sat down with Teshamae Monteith, a clinical neurologist at the University of Miami Health System in Florida, today to discuss the latest advances in the field. Q: How is our understanding of migraine evolving? A: It's more complicated than we thought. In the past, researchers thought of migraine as a blood vessel disorder, in part because some patients can feel a temple pulsation during a migraine attack. Now, migraine is considered a sensory perceptual disorder, because so many of the sensory systems—light, sound, smell, hearing—are altered. During an attack, patients have concentration impairments, appetite changes, mood changes, and sleeping is off. What fascinates me is that patients are often bothered by manifestations of migraine, such as increased sensitivity to light, in between attacks, suggesting that they may be wired differently, or their neurobiology may be altered. About two-thirds of patients with acute migraine attacks have allodynia, a condition that makes people so sensitive to certain stimuli that even steam from a shower can be incredibly painful. One way to view it is that migraineurs at baseline are at a different threshold for sensory stimuli. © 2015 American Association for the Advancement of Science.
Keyword: Pain & Touch
Link ID: 20585 - Posted: 02.16.2015
By Siri Carpenter “I don’t look like I have a disability, do I?” Jonas Moore asks me. I shake my head. No, I say — he does not. Bundled up in a puffy green coat in a drafty Starbucks, Moore, 35 and sandy-haired, doesn’t stand out in the crowd seeking refuge from the Wisconsin cold. His handshake is firm and his blue eyes meet mine as we talk. He comes across as intelligent and thoughtful, if perhaps a bit reserved. His disability — autism — is invisible. That’s part of the problem, says Moore. Like most people with autism spectrum disorders, he finds relationships challenging. In the past, he has been quick to anger and has had what he calls “meltdowns.” Those who don’t know he has autism can easily misinterpret his actions. “People think that when I do misbehave I’m somehow intentionally trying to be a jerk,” Moore says. “That’s just not the case.” His difficulty managing emotions has gotten him into some trouble, and he’s had a hard time holding onto jobs — an outcome he might have avoided, he says, if his coworkers and bosses had better understood his intentions. Over time, things have gotten better. Moore has held the same job for five years, vacuuming commercial buildings on a night cleaning crew. He attributes his success to getting the right amount of medication and therapy, to time maturing him and to the fact that he now works mostly alone. Moore is fortunate. His parents help support him financially. He has access to good mental health care. And with the help of the state’s division of vocational rehabilitation, he has found a job that suits him. Many adults with autism are not so lucky. © Society for Science & the Public 2000 - 2015.
Link ID: 20574 - Posted: 02.13.2015
|By Stephani Sutherland More than half a billion people carry a genetic mutation that incapacitates the enzyme responsible for clearing alcohol from the body. The deficiency is responsible for an alcohol flush reaction, colloquially known as the “Asian glow” because the vast majority of carriers are descendants of the Han Chinese. Now research published last September in Science Translational Medicine suggests that the mutation might also compromise carriers' pain tolerance. The finding points to a new target for pharmaceutical pain relief and implies that drinking alcohol might exacerbate inflammatory conditions such as arthritis. When people consume alcohol, the body breaks it down into several by-products, including chemicals called aldehydes. These compounds are noxious if they remain in the system too long, causing flushing, nausea, dizziness and other symptoms of the alcohol flush reaction. In most people, aldehydes are immediately broken down by the enzyme aldehyde dehydrogenase (ALDH2), but in those with the genetic mutation, the enzyme is incapacitated. Researchers led by Daria Mochly-Rosen of Stanford University genetically modified some mice to carry the mutation seen in humans that disables ALDH2. When they injected those mice and normal mice in the paw with an inflammatory compound that turned it red and swollen, mice carrying the mutation showed increased sensitivity to a poke compared with those with functioning ALDH2. When the researchers treated all the rodents with a novel drug called Alda-1 that boosts ALDH2 activity, the pain symptoms were reduced regardless of whether they carried the gene mutation. © 2015 Scientific American
By Lenny Bernstein Parkinson's Disease patients secretly treated with a placebo instead of their regular medication performed better when told they were receiving a more expensive version of the "drug," researchers reported Wednesday in an unprecedented study that involved real patients. The research shows that the well-documented "placebo effect" -- actual symptom relief brought about by a sham treatment or medication -- can be enhanced by adding information about cost, according to the lead author of the study. It is the first time that concept has been demonstrated using people with a real illness, in this case Parkinson's, a progressive neurological disease that has no cure, according to an expert not involved in the study. "The potentially large benefit of placebo, with or without price manipulations, is waiting to be untapped for patients with [Parkinson's Disease], as well as those with other neurologic and medical diseases," the authors wrote in a study published online Wednesday in the journal Neurology. But deceiving actual patients in a research study raised ethical questions about violating the trust involved in a doctor-patient relationship. Most studies in which researchers conceal their true aims or other information from subjects are conducted with healthy volunteers. This one was subjected to a lengthy review before it was allowed to proceed, and, in an editorial that accompanied the article, two other physicians wrote that "the authors do not mention whether there was any possible effect (reduction) on trust in doctors or on willingness to engage in future clinical research."
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 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