Posts tagged chronic pain
Ache, agony, distress and pain draw more attention than non-pain related words when it comes to people who suffer from chronic pain, a York University research using state-of-the-art eye-tracking technology has found.
(Image credit)
“People suffering from chronic pain pay more frequent and longer attention to pain-related words than individuals who are pain-free,” says Samantha Fashler, a PhD candidate in the Faculty of Health and the lead author of the study. “Our eye movements — the things we look at — generally reflect what we attend to, and knowing how and what people pay attention to can be helpful in determining who develops chronic pain.”
Chronic pain currently affects about 20 per cent of the population in Canada.
The current study, “More than meets the eye: visual attention biases in individuals reporting chronic pain”, published in the Journal of Pain Research, incorporated an eye-tracker, which is a more sophisticated measuring tool to test reaction time than the previously used dot-probe task in similar studies.
“The use of an eye-tracker opens up a number of previously unavailable avenues for research to more directly tap what people with chronic pain attend to and how this attention may influence the presence of pain,” says Professor Joel Katz, Canada Research Chair in Health Psychology, the co-author of the study.
The researchers recorded both reaction time and eye movements of chronic pain (51) and pain-free (62) participants. Both groups viewed neutral and sensory pain-related words on a dot-probe task. They found reaction time did not indicate attention, but “the eye-tracking technology captured eye gaze patterns with millimetre precision,” according to Fashler. She points out that this helped researchers to determine how frequently and how long individuals looked at sensory pain words.
“We now know that people with and without chronic pain differ in terms of how, where and when they attend to pain-related words. This is a first step in identifying whether the attentional bias is involved in making pain more intense or more salient to the person in pain,” says Katz.
(Source: news.yorku.ca)
Filed under pain chronic pain eye-tracking technology attention psychology neuroscience science
New research shows that patients with fibromyalgia have hypersensitivity to non-painful events based on images of the patients’ brains, which show reduced activation in primary sensory regions and increased activation in sensory integration areas. Findings published in Arthritis & Rheumatology, a journal of the American College of Rheumatology (ACR), suggest that brain abnormalities in response to non-painful sensory stimulation may cause the increased unpleasantness that patients experience in response to daily visual, auditory and tactile stimulation.
Fibromyalgia is a chronic, musculoskeletal syndrome characterized by widespread pain, affecting roughly two percent of the world population, say experts. According to the ACR, five million people in the U.S. have fibromyalgia, which is more prevalent among women. In previous studies fibromyalgia patients report reduced tolerance to normal sensory (auditory, visual, olfactory, and tactile) stimulation in addition to greater sensitivity to pain.
For the present study, researchers used functional magnetic resonance imaging (fMRI) to assess brain response to sensory stimulation in 35 women with fibromyalgia and 25 healthy, age-matched controls. Patients had an average disease duration of 7 years and a mean age of 47.
According to the study, patients reported increased unpleasantness in response to multisensory stimulation in daily life activities. Furthermore, fMRI displayed reduced activation of both the primary and secondary visual and auditory areas of the brain, and increased activation in sensory integration regions. These brain abnormalities mediated the increased unpleasantness to visual, auditory and tactile stimulation that patients reported to experience in daily life.
Lead study author, Dr. Marina López-Solà from the Institute of Cognitive Science, University of Colorado Boulder said, “Our study provides new evidence that fibromyalgia patients display altered central processing in response to multisensory stimulation, which are linked to core fibromyalgia symptoms and may be part of the disease pathology. The finding of reduced cortical activation in the visual and auditory brain areas that were associated with patient pain complaints may offer novel targets for neurostimulation treatments in fibromyalgia patients.”
(Source: eu.wiley.com)
Filed under fibromyalgia chronic pain neuroimaging sensory sensitivity insular cortex neuroscience science
Researchers unlock new mechanism in pain management
It’s in the brain where we perceive the unpleasant sensations of pain, and researchers have long been examining how calcium channels in the brain and peripheral nervous system contribute to the development of chronic pain conditions.
Neuroscientist Gerald Zamponi, PhD, and his team at the University of Calgary’s Hotchkiss Brain Institute have discovered a new mechanism that can reverse chronic pain. Using an animal model, their research has found that pain signals in nerve cells can be shut off by interfering with the communication of a specific enzyme with calcium channels, a group of important proteins that control nerve impulses.
Their Canadian Institutes of Health Research-funded study was published in the September issue of Neuron — one of the most influential journals in the field of neuroscience.
Zamponi is now applying his research and partnering with the Centre for Drug Research and Development (CDRD) in Vancouver to develop a drug that could one day improve the lives of those with inflammatory pain such as arthritis, irritable bowel disease or neuropathic pain. Their approach may be able to reduce the pain associated with these conditions.
Opening the door to new treatments
“Chronic pain can be a debilitating condition that affects many people and is often poorly controlled by currently available treatments. Therefore, new treatment avenues are needed. Our discovery opens the door towards new treatments, and based on the data that we have so far, it is a viable strategy,” says Zamponi, the lead author of the study and senior associate dean of research at the Cumming School of Medicine.
With CDRD, Zamponi and his team are screening more than 100,000 molecules in hopes of finding one that would stop the enzyme from communicating with the calcium channel. If they can isolate the right molecule, they can potentially turn it into a drug. So far, they have already found two viable molecules that have been validated by his group as painkillers in animals.
Promising innovation from basic research
Commercialization of the project Zamponi and his team are working on is one of six funded through the competition of the Alberta/Pfizer Translational Research Fund Opportunity. “AIHS is delighted that the strong partnership created with Pfizer, Western Economic Diversification, and Alberta Innovation and Advanced Education is helping to develop promising innovations from basic research into technologies, drugs, and tools to improve health,” says Dr. Cy Frank, president and CEO of Alberta Innovates – Health Solutions.
The Alberta/Pfizer Translational Research Fund Opportunity is a partnership between Pfizer Canada Inc., Alberta Innovates – Health Solutions, Alberta’s Ministry of Innovation and Advanced Education, and Western Economic Diversification Canada. This partnership will provide opportunities to focus on the development and commercialization of innovations in health. More than $3.25 million has been committed to identify and support promising health-care innovations with market potential.
Filed under pain chronic pain USP5 calcium channel neuroscience science
Chronic pain is among the most abundant of all medical afflictions in the developed world. It differs from a short-term episode of pain not only in its duration, but also in triggering in its sufferers a psychic exhaustion best described by the question, “Why bother?”
A new study in mice, conducted by investigators at the Stanford University School of Medicine, has identified a set of changes in key parts of the brain that may explain chronic pain’s capacity to stifle motivation. The discovery could lead to entirely new classes of treatment for this damaging psychological consequence of chronic pain.
Many tens of millions of people in the United States suffer persistent pain due to diverse problems including migraines, arthritis, lower back pain, sports injuries, irritable bowel syndrome and shingles. For many of these conditions, there are no good treatments, and a crippling loss of mojo can result.
“With chronic pain, your whole life changes in a way that doesn’t happen with acute pain,” said Robert Malenka, MD, PhD, the Nancy Friend Pritzker Professor in Psychiatry and Behavioral Sciences and the study’s senior author. “Yet this absence of motivation caused by chronic pain, which can continue even when the pain is transiently relieved, has been largely ignored by medical science.”
A series of experiments in mice by Malenka and his colleagues, described in a study published Aug. 1 in Science, showed that persistent pain causes changes in a set of nerve cells in a deep-brain structure known to be important in reward-seeking behavior: the pursuit of goals likely to yield pleasurable results. Malenka’s lab has been studying this brain structure, the nucleus accumbens, for two decades.
“We showed that those brain changes don’t go away when you transiently relieve the mice’s pain,” Malenka said. The experiments also indicated that the mice’s diminished motivation to perform reward-generating tasks didn’t stem from their pain’s rendering them incapable of experiencing pleasure or from any accompanying physical impairment, he said.
How pain and reward interact
“This study is important — to my knowledge, the first to explain how pain and reward interact. It begins to get to an understanding of why it’s such a struggle for people undergoing chronic pain to get through the day,” said Howard Fields, MD, PhD, a professor of neurology at the University of California-San Francisco and founder of that school’s pain management center.
Fields, who did not participate in the Malenka group’s study but wrote an accompanying perspective piece published simultaneously in Science, described the psychological effect of chronic pain as “the clouding of the future. There’s no escape from it. You want it to end, but it doesn’t.” As a result, people become pessimistic and irritable, he said. “People come to expect the next day is going to wind up being painful. It just takes the edge off of life’s little pleasures — and big pleasures, for that matter.”
The experiments were spearheaded by the study’s first author, Neil Schwartz, PhD, a postdoctoral scholar in Malenka’s lab. “You can’t just ask a hungry mouse how motivated it is to pursue its heart’s desire,” Malenka said. “But there are ways of asking that mouse, ‘How hard are you willing to work for food?’”
Schwartz, Malenka and their associates looked at lab mice enduring chronic paw pain due either to persistent inflammation or to nerve damage. The mice also happened to be hungry. The scientists trained the mice to poke their noses into a hole to get a food pellet. At first, a single nose poke earned a pellet. But over time, the number of nose pokes required for a reward was increased. In essence, the researchers were asking these mice: How hard are you willing to work for food? Will you poke your nose into that hole once to satisfy your hunger? Ten times? Even 150 times?
Fading motivation
Within a week after the onset of chronic pain, the animals grew increasingly less likely to work hard for food than pain-free control animals were. The researchers next explored three possible explanations: Were the mice unable to work because their pain was too severe? Did something about being in pain cause them to not value the food reward as much? Or was their failure to seek food due simply to a lack of motivation? Additional tests showed that the mice had no movement problems. “Like other research groups, we found that they can scamper around just fine,” said Malenka. Also, when the mice were given free access to food, they ate just as much as the animals who weren’t in pain — so they still valued the food. But they were less willing to put in an effort to obtain food than mice who’d suffered no pain.
Moreover, the difference didn’t disappear even when the scientists relieved the mice’s pain with analgesics. “They were in demonstrably less pain, but they were still less willing to work,” Malenka said.
The Stanford scientists then focused on the nucleus accumbens, a brain structure known to be involved in computing the behavioral strategies that prompt us to seek or avoid things that can affect our survival. They found that chronic pain permanently changed certain connections to the nucleus accumbens, causing an enduring downshift in the excitation transmitted by them. Importantly, Malenka’s group showed that a particular brain chemical called galanin plays a critical role in this enduring suppression of nucleus accumbens excitability.
Galanin is a short signaling-protein snippet secreted by certain cells in various places in the brain. While its presence in the brain has been known for a good 60 years or so, galanin’s role is not well-defined and probably differs widely in different brain structures. There have been hints, though, that galanin activity might play a role in pain. For example, it’s been previously shown in animal models that galanin levels in the brain increase with the persistence of pain.
Possible therapies?
Schwartz, Malenka and their peers identified receptors for galanin on a set of nerve cells in the nucleus accumbens and demonstrated that disabling galanin’s signaling via this receptor prevented the long-term suppression of motivation seen in mice — and people — with chronic pain. This suggests that therapeutic compounds with similar effects could someday be developed, although they would have to be carefully targeted so as to not disrupt galanin signaling in other important brain circuits.
“There’s no reason to think this finding won’t generalize to people,” said Fields of UCSF. “Our brains have galanin, and a nucleus accumbens, just as mouse brains do. However, before jumping from mice to humans it would be wise to test other animal species. If the same things happen in a non-rodent species that happen in mice, then it’s probable they happen in humans, too.”
(Source: med.stanford.edu)
Filed under pain chronic pain motivation reward nucleus accumbens neuroscience science
Discovery of new means to erase pain
A study published in the scientific journal Nature Neuroscience by Yves De Koninck and Robert Bonin, two researchers at Université Laval, reveals that it is possible to relieve pain hypersensitivity using a new method that involves rekindling pain so that it can subsequently be erased. This discovery could lead to novel means to alleviate chronic pain.
The researchers from the Faculty of Medicine at Université Laval and Institut universitaire en santé mentale de Québec (IUSMQ) were inspired by previous work on memory conducted some fifteen years ago. These studies had revealed that when a memory is reactivated during recall, its neurochemical encoding is temporarily unlocked. Simultaneous administration of a drug that blocks neurochemical reconsolidation of the memory results in its erasure.
The investigators wanted to see whether a similar mechanism was at play during neurochemical encoding of pain sensitization. To this end, they injected capsaicin in the foot of mice. Capsaicin, the pungent chemical in chili pepper, triggers a burning sensation. The procedure, which causes no physical damage, triggers pain hypersensitivity through a process of protein synthesis in the spinal cord. After capsaicin injections, the mechanical pressure at which mice would flinch was about a third of that in the normal situation.
Three hours later, the researchers administered a second dose of capsaicin and, at the same time, a drug that blocks protein synthesis. The hypersensitivity then vanished rapidly. Within less than 2 hours, the pressure tolerated by the mice was back to 70% of normal.
Yves De Koninck explains that “when the protein synthesis inhibitor is administered alone, the hypersensitivity remains. The second injection of capsaicin is necessary to render the sensitivity to pain unstable and be able to interfere with its neurochemical reconsolidation. The challenge now will be to find protein synthesis inhibitors that are nontoxic and cause minimal side effects in humans”.
Filed under hyperalgesia capsaicin chronic pain memory reconsolidation memory neuroscience science
Researchers find new target for chronic pain treatment
Researchers at the UNC School of Medicine have found a new target for treating chronic pain: an enzyme called PIP5K1C. In a paper published today in the journal Neuron, a team of researchers led by Mark Zylka, PhD, Associate Professor of Cell Biology and Physiology, shows that PIP5K1C controls the activity of cellular receptors that signal pain.
By reducing the level of the enzyme, researchers showed that the levels of a crucial lipid called PIP2 in pain-sensing neurons is also lessened, thus decreasing pain.
They also found a compound that could dampen the activity of PIP5K1C. This compound, currently named UNC3230, could lead to a new kind of pain reliever for the more than 100 million people who suffer from chronic pain in the United States alone.
In particular, the researchers showed that the compound might be able to significantly reduce inflammatory pain, such as arthritis, as well as neuropathic pain – damage to nerve fibers. The latter is common in conditions such as shingles, back pain, or when bodily extremities become numb due to side effects of chemotherapy or diseases such as diabetes.
The creation of such bodily pain might seem simple, but at the cellular level it’s quite complex. When we’re injured, a diverse mixture of chemicals is released, and these chemicals cause pain by acting on an equally diverse group of receptors on the surface of pain-sensing neurons.
“A big problem in our field is that it is impractical to block each of these receptors with a mixture of drugs,” said Zylka, the senior author of the Neuron article and member of the UNC Neuroscience Center. “So we looked for commonalities – things that each of these receptors need in order to send a signal.” Zylka’s team found that the lipid PIP2 (phosphatidylinositol 4,5-bisphosphate) was one of these commonalities.
“So the question became: how do we alter PIP2 levels in the neurons that sense pain?” Zylka said. “If we could lower the level of PIP2, we could get these receptors to signal less effectively. Then, in theory, we could reduce pain.”
Many different kinases can generate PIP2 in the body. Brittany Wright, a graduate student in Zylka’s lab, found that the PIP5K1C kinase was expressed at the highest level in sensory neurons compared to other related kinases. Then the researchers used a mouse model to show that PIP5K1C was responsible for generating at least half of all PIP2 in these neurons.
“That told us that a 50 percent reduction in the levels of PIP5K1C was sufficient to reduce PIP2 levels in the tissue we were interested in – where pain-sensing neurons are located” Zylka said. “That’s what we wanted to do – block signaling at this first relay in the pain pathway.”
Once Zylka and colleagues realized that they could reduce PIP2 in sensory neurons by targeting PIP5K1C, they teamed up with Stephen Frye, PhD, the Director of the Center for Integrative Chemical Biology and Drug Discovery at the UNC Eshelman School of Pharmacy.
They screened about 5,000 small molecules to identify compounds that might block PIP5K1C. There were a number of hits, but UNC3230 was the strongest. It turned out that Zylka, Frye, and their team members had come upon a drug candidate. They realized that the chemical structure of UNC3230 could be manipulated to potentially turn it into an even better inhibitor of PIP5K1C. Experiments to do so are now underway at UNC.
Filed under chronic pain pain PIP5K1C dorsal root ganglia spinal cord neurons neuroscience science
Pain’s Benefit to Squid May Hold Clues to Chronic Human Pain
For the longfin inshore squid, pain can mean the difference between life and death, according to a new study. That’s because pain prompts injured squid to behave in ways that help it survive encounters with a fish predator, researchers said.
That finding may also provide hints as to why other animals, including humans, experience long-lasting or chronic pain, behavior experts say.
It’s long been thought that pain causes an animal to act self-protectively, says Robert Elwood, an animal behavior researcher at Queen’s University Belfast who was not involved in the study. Pain teaches an organism to avoid situations that will bring it on. It seems obvious, but it hasn’t really been tested until now, Elwood said in an email interview.
In a study published today in Current Biology, researchers report that the sensitivity with which injured squid reacted to aggressive moves from a predator, in this case a black sea bass, gave the squid better odds of surviving an attack.
Read more
Filed under pain chronic pain nociception predation animal behavior neuroscience science
Pain curbs sex drive in female mice, but not in males
“Not tonight, dear, I have a headache.” Generally speaking, that line is attributed to the wife in a couple, implying that women’s sexual desire is more affected by pain than men’s.
Now, researchers from McGill University and Concordia University in Montreal have investigated, possibly for the first time in any species, the direct impact of pain on sexual behaviour in mice. Their study, published in the April 23 issue of The Journal of Neuroscience, found that pain from inflammation greatly reduced sexual motivation in female mice in heat — but had no such effect on male mice.
“We know from other studies that women’s sexual desire is far more dependent on context than men’s – but whether this is due to biological or social/cultural factors, such as upbringing and media influence, isn’t known,” says Jeffrey Mogil, a psychology professor at McGill and corresponding author of the new study. “Our finding that female mice, too, show pain-inhibited sexual desire suggests there may be an evolutionary biology explanation for these effects in humans – and not simply a sociocultural one.”
To conduct the study, the researchers placed mice in a mating chamber divided by a barrier with openings too small for male mice to squeeze through. This enabled the females to decide whether, and for how long, to spend time with a male partner. Female mice in pain spent less time on the “male side” of the testing chamber, and as a result less sexual behaviour occurred. The researchers found that the sexual motivation of the female mice could be revived, however with a pain-relieving drug (pregabalin) or with either of two known desire-enhancing drugs.
Male mice, for their part, were tested in an undivided chamber in which they had free access to a female partner in heat. Their sexual behaviour was entirely unaffected by the same inflammatory pain. There were no differences in pain perception between the sexes, the researchers determined.
“Chronic pain is very often accompanied by sexual problems in humans,” says Prof. Yitzchak Binik, a professor of psychology at McGill and Director of the Sex and Couple Therapy Service at the McGill University Health Center. “This research provides an animal model of pain-inhibited sexual desire that will help scientists study this important symptom of chronic pain.”
Melissa Farmer, now a postdoctoral fellow at Northwestern University, led the study as a doctoral student at McGill under the supervision of Prof. Mogil, a pain researcher, and Prof. Binik, a human sexual-disorder researcher.
Prof. James Pfaus of Concordia University’s Centre for Studies in Behavioral Neurobiology, an expert on rodent sexual behaviour, also co-authored the study. “The sex differences in pain reactivity open new doors to understanding how sexual responses are organized in the brain,” Prof. Pfaus said. “In fact, the growing trend towards personalized medicine requires us to understand how particular ailments, along with their treatments, might impact the sexual lives of women and men.“
Filed under sexual behavior mating sex differences pain chronic pain neuroscience science
Setting the stage for possible advances in pain treatment, researchers at The Johns Hopkins University and the University of Maryland report they have pinpointed two molecules involved in perpetuating chronic pain in mice. The molecules, they say, also appear to have a role in the phenomenon that causes uninjured areas of the body to be more sensitive to pain when an area nearby has been hurt. A summary of the research will be published on Jan. 23 in the journal Neuron.
Image caption: Nerves in mouse skin that are actively responding to the painful stimulus capsaicin have been genetically engineered to glow green. Hairs appear in yellow. Credit: David Rini
"With the identification of these molecules, we have some additional targets that we can try to block to decrease chronic pain," says Xinzhong Dong, Ph.D., associate professor of neuroscience at the Johns Hopkins University School of Medicine and an early career scientist at Howard Hughes Medical Institute. "We found that persistent pain doesn’t always originate in the brain, as some had believed, which is important information for designing less addictive drugs to fight it."
Chronic pain that persists for weeks, months or years after an underlying injury or condition is resolved afflicts an estimated 20 to 25 percent of the population worldwide and about 116 million people in the U.S., costing Americans a total of $600 billion in medical interventions and lost productivity. It can be caused by everything from nerve injuries and osteoarthritis to cancer and stress.
In their new research, the scientists focused on a system of pain-sensing nerves within the faces of mice, known collectively as the trigeminal nerve. The trigeminal nerve is a large bundle of tens of thousands of nerve cells. Each cell is a long “wire” with a hub at its center; the hubs are grouped together into a larger hub. On one side of this hub, three smaller bundles of wires — V1, V2 and V3 — branch off. Each bundle contains individual pain-sensing wires that split off to cover a specific territory of the face. Signals are sent through the wires to the hubs of the cells and then travel to the spinal cord through a separate set of bundles. From the spinal cord, the signals are relayed to the brain, which interprets them as pain.
When the researchers pinched the V2 branch of the trigeminal nerve for a prolonged period of time, they found that the V2 and V3 territories were extra sensitive to additional pain. This spreading of pain to uninjured areas is typical of those experiencing chronic pain, but it can also be experienced during acute injuries, as when a thumb is hit with a hammer and the whole hand throbs with pain.
To figure out why, the researchers studied pain-sensing nerves in the skin of mouse ears. The smaller branches of the trigeminal V3 reach up into the skin of the lower ear. But an entirely different set of nerves is responsible for the skin of the upper ear. This distinction allowed the researchers to compare the responses of two unrelated groups of nerves that are in close proximity to each other.
To overcome the difficulty of monitoring nerve responses, Dong’s team inserted a gene into the DNA of mice so that the primary sensory nerve cells would glow green when activated. The pain-sensing nerves of the face are a subset of these.
When skin patches were then bathed in a dose of capsaicin — the active ingredient in hot peppers — the pain-sensing nerves lit up in both regions of the ear. But the V3 nerves in the lower ear were much brighter than those of the upper ear. The researchers concluded that pinching the connected-but-separate V2 branch of the trigeminal nerve had somehow sensitized the V3 nerves to “overreact” to the same amount of stimulus. (Watch nerves light up in this video.)
Applying capsaicin again to different areas, the researchers found that more nerve branches coming from a pinched V2 nerve lit up than those coming from an uninjured one. This suggests that nerves that don’t normally respond to pain can modify themselves during prolonged injury, adding to the pain signals being sent to the brain.
Knowing from previous studies that the protein TRPV1 is needed to activate pain-sensing nerve cells, the researchers next looked at its activity in the trigeminal nerve. They showed it was hyperactive in injured V2 nerve branches and in uninjured V3 branches, as well as in the branches that extended beyond the hub of the trigeminal nerve cell and into the spinal cord.
Next, University of Maryland experts in the neurological signaling molecule serotonin, aware that serotonin is involved in chronic pain, investigated its role in the TRPV1 activation study. The team, led by Feng Wei, M.D., Ph.D., blocked the production of serotonin, which is released from the brain stem into the spinal cord, and found that TRPV1 hyperactivity nearly disappeared.
Says Dong: “Chronic pain seems to cause serotonin to be released by the brain into the spinal cord. There, it acts on the trigeminal nerve at large, making TRPV1 hyperactive throughout its branches, even causing some non-pain-sensing nerve cells to start responding to pain. Hyperactive TRPV1 causes the nerves to fire more frequently, sending additional pain signals to the brain.”
Filed under chronic pain trigeminal nerve nerve cells capsaicin serotonin neuroscience science
TAU researchers study the long-term effects of torture on the human pain system
Israeli soldiers captured during the 1973 Yom Kippur War were subjected to brutal torture in Egypt and Syria. Held alone in tiny, filthy spaces for weeks or months, sometimes handcuffed and blindfolded, they suffered severe beatings, burns, electric shocks, starvation, and worse. And rather than receiving treatment, additional torture was inflicted on existing wounds.
Forty years later, research by Prof. Ruth Defrin of the Department of Physical Therapy in the Sackler Faculty of Medicine at Tel Aviv University shows that the ex-prisoners of war (POWs), continue to suffer from dysfunctional pain perception and regulation, likely as a result of their torture. The study — conducted in collaboration with Prof. Zahava Solomon and Prof. Karni Ginzburg of TAU’s Bob Shapell School of Social Work and Prof. Mario Mikulincer of the School of Psychology at the Interdisciplinary Center, Herzliya — was published in the European Journal of Pain.
"The human body’s pain system can either inhibit or excite pain. It’s two sides of the same coin," says Prof. Defrin. "Usually, when it does more of one, it does less of the other. But in Israeli ex-POWs, torture appears to have caused dysfunction in both directions. Our findings emphasize that tissue damage can have long-term systemic effects and needs to be treated immediately."
A painful legacy
The study focused on 104 combat veterans of the Yom Kippur War. Sixty of the men were taken prisoner during the war, and 44 of them were not. In the study, all were put through a battery of psychophysical pain tests — applying a heating device to one arm, submerging the other arm in a hot water bath, and pressing a nylon fiber into a middle finger. They also filled out psychological questionnaires.
The ex-POWs exhibited diminished pain inhibition (the degree to which the body eases one pain in response to another) and heightened pain excitation (the degree to which repeated exposure to the same sensation heightens the resulting pain). Based on these novel findings, the researchers conclude that the torture survivors’ bodies now regulate pain in a dysfunctional way.
It is not entirely clear whether the dysfunction is the result of years of chronic pain or of the original torture itself. But the ex-POWs exhibited worse pain regulation than the non-POW chronic pain sufferers in the study. And a statistical analysis of the test data also suggested that being tortured had a direct effect on their ability to regulate pain.
Head games
The researchers say non-physical torture may have also contributed to the ex-POWs’ chronic pain. Among other forms of oppression and humiliation, the ex-POWs were not allowed to use the toilet, cursed at and threatened, told demoralizing misinformation about their loved ones, and exposed to mock executions. In the later stages of captivity, most of the POWs were transferred to a group cell, where social isolation was replaced by intense friction, crowding, and loss of privacy.
"We think psychological torture also affects the physiological pain system," says Prof. Defrin. "We still have to fully analyze the data, but preliminary analysis suggests there is a connection."
(Source: aftau.org)
Filed under torture chronic pain pain psychology neuroscience science
