Chapter 5. The Sensorimotor System
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By Diana Kwon | In the human form of mad cow disease, called Creutzfeldt-Jakob, a person's brain deteriorates—literally developing holes that cause rapidly progressing dementia. The condition is fatal within one year in 90 percent of cases. The culprits behind the disease are prions—misfolded proteins that can induce normal proteins around them to also misfold and accumulate. Scientists have known that these self-propagating, pathological proteins cause some rare brain disorders, such as kuru in Papua New Guinea. But growing evidence suggests that prions are at play in many, if not all, neurodegenerative disorders, including Alzheimer's, Huntington's and Parkinson's, also marked by aggregations of malformed proteins. Until recently, there was no evidence that the abnormal proteins found in people who suffer from these well-known diseases could be transmitted directly from person to person. The tenor of that discussion suddenly changed this September when newly published research in the journal Nature provided the first hint such human-to-human transmission may be possible. (Scientific American is part of Springer Nature.) For the study, John Collinge, a neurologist at University College London, and his colleagues conducted autopsies on eight patients who died between the ages of 36 and 51 from Creutzfeldt-Jakob. All the subjects had acquired the disease after treatment with growth hormone later found to be contaminated with prions. The surprise came when the researchers discovered that six of the brains also bore telltale signs of Alzheimer's—in the form of clumps of beta-amyloid proteins, diagnostic for the disease—even though the patients should have been too young to exhibit such symptoms. © 2015 Scientific American,
by Helen Thompson Five, six, seven, eight! All together now, let's spread those jazz hands and get moving, because synchronized dancing improves our tolerance of pain and helps us bond as humans, researchers suggest October 28 in Biology Letters. A team of psychologists at the University of Oxford taught high school students varied dance routines — each requiring different levels of exertion and synchronized movement — and then tested their pain tolerance with the sharp squeeze of a blood pressure cuff. Statistically, routines with more coordinated choreography and full body movement produced higher pain thresholds and sunny attitudes toward others in the group. Coordinated dancing with a group and exerting more energy may independently promote the release of pain-blocking endorphins as well as increase social bonding, the team writes. |© Society for Science & the Public 2000 - 2015
Keyword: Pain & Touch
Link ID: 21575 - Posted: 10.28.2015
By Hanae Armitage CHICAGO, ILLINOIS—Huntingtons disease, a neurological condition caused by brain-destroying mutant proteins, starts with mood swings and twitching and ends in dementia and death. The condition, which afflicts about 30,000 Americans, has no cure. But now, a new gene-editing method that many believe will lead to a Nobel Prize has been shown to effectively halt production of the defective proteins in mice, leading to hope that a potent therapy for Huntingtons is on the distant horizon. That new method is CRISPR, which uses RNA-guided enzymes to snip out or add segments of DNA to a cell. In the first time it has been applied to Huntingtons disease, CRISPR’s results are “remarkably encouraging,” says neuroscientist Nicole Déglon of the University of Lausanne in Switzerland, who led the mouse study, results of which she and her co-researcher Nicolas Merienne shared yesterday at the Society for Neuroscience Conference in Chicago, Illinois. As neurological diseases go, Huntingtons is an ideal candidate for CRISPR therapy, because the disease is determined by a single gene, Déglon notes. A mutation in the gene, which codes for a normally helpful brain protein called huntingtin, consists of different numbers of “tandem repeats,” repeating segments of DNA that cause the protein to fold into a shape that is toxic to the brain. Déglon and her team wondered whether CRISPR could halt production of this dangerous molecule. Using a virus as a delivery vehicle, the researchers infected two separate groups of healthy adult mice with a mutant huntingtin gene, but only one group received the therapy: a CRISPR “cassette,” which includes DNA for the gene-editing enzyme Cas9 and the RNA to target the huntingtin gene. © 2015 American Association for the Advancement of Science
Link ID: 21538 - Posted: 10.21.2015
Alan Hoffman says nilotinib has changed his life. Just weeks after he started taking the drug in a clinical trial, he began to feel himself recovering from his Parkinson’s disease. The retired professor of social science first started to show the signs of Parkinson’s in 1997. Over the years, his symptoms worsened. “I couldn’t get out of bed without my wife,” Hoffman says. Once a prolific reader, devouring four or five books a week, Hoffman found himself unable to keep his attention on even a short magazine article. His body became increasingly rigid, and he started to lose his sense of balance. “I fell a lot,” he says. And it affected his social life. The disorder was such a struggle, Hoffman says he considered taking his own life. He tried a range of medications, which eased his symptoms to varying degrees. In 2008, he had surgery to implant an electrode into his brain. The deep brain stimulation that followed helped with the rigidity, he says. But deep brain stimulation doesn’t offer a cure – the brain cells continue to die. So Hoffman agreed to join a six-month clinical trial of nilotinib – a drug typically used to treat leukaemia. Nilotinib blocks a protein that interferes with lysosomes – cell structures that destroy harmful proteins. Researchers behind the trial think that nilotinib can free up lysosomes to do a better job of clearing out proteins associated with Parkinson’s disease. (For a full report on the effect of the drug see “People with Parkinson’s walk again after promising drug trial”.) © Copyright Reed Business Information Ltd.
Link ID: 21537 - Posted: 10.21.2015
Mr Tickle can’t bamboozle a baby. Unlike grown-ups, young infants don’t let the positioning of their bodies confuse their sense of touch. If adults who can see are touched on each hand in quick succession while their hands are crossed, they can find it hard to name which hand was touched first. Adults who have been blind from birth don’t have this difficulty, but people who become blind later in life have the same trouble as those who can still see. “That suggests that early on in life, something to do with visual experience is crucial in setting up a typical way of perceiving touch,” says Andrew Bremner at Goldsmiths, University of London. To investigate how this develops in infancy, Bremner and his colleagues compared how babies reacted to having one foot tickled. With their legs crossed over, babies aged 6 months moved the foot being tickled half of the time. But 4-month-olds did better, moving the tickled foot 70 per cent of the time – as often as they did with their legs uncrossed. The team concludes that at 4 months, babies haven’t yet learned to relate what they touch to the physical space that their body occupies. For many adults, the concept might be difficult to envision. “It’s like imagining that you feel a touch on your body, but not really knowing how that’s related to what you’re looking at,” says Bremner. “It’s almost like you have multiple sensory worlds: a visual world, an auditory world and a tactile world, which are separate and not combined in space.” © Copyright Reed Business Information Ltd.
An expensive cancer drug may reverse late-stage Parkinson’s disease, enabling participants in a small clinical trial to speak and walk again for the first time in years. While there are several treatments for the symptoms of Parkinson’s, if confirmed this would be the first time a drug has worked on the causes of the disease. “We’ve seen patients at end stages of the disease coming back to life,” says Charbel Moussa of Georgetown University Medical Center in Washington DC, who led the trial. The drug, called nilotinib, works by boosting the brain’s own “garbage disposal system” to clear proteins that accumulate in the brains of people with Parkinson’s disease, says Moussa. These proteins are thought to trigger the death of brain cells that make molecules like dopamine that are needed for movement and other functions. Nilotinib is already approved to treat cancer – it blocks a protein that drives chronic myeloid leukaemia. It also blocks another protein that interferes with lysosomes – cell structures that destroy harmful proteins. Moussa thinks that nilotinib can free up lysosomes to do a better job of clearing out proteins associated with Parkinson’s disease. Tests in animals showed promise, so Moussa, his colleague Fernando Pagan and their team set up a small trial of 12 volunteers with Parkinson’s disease or a similar condition called dementia with Lewy bodies. The trial was designed to test only the safety of the oral drug, which was given as a daily dose for six months. © Copyright Reed Business Information Ltd.
Link ID: 21528 - Posted: 10.20.2015
Three teams of scientists supported by the National Institutes of Health showed that a genetic mutation linked to some forms of amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD) may destroy neurons by disrupting the movement of materials in and out of the cell’s nucleus, or command center where most of its DNA is stored. The results, published in the journals Nature and NatureNeuroscience, provide a possible strategy for treating the two diseases. “This research shines a spotlight on the role of nuclear transport in the health of neurons,” said Amelie Gubitz, Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). “The results provide new insights into how this mutation derails an essential process in neurons and opens new avenues for therapy development.” Both ALS and FTD are caused by the death of specific neurons. In ALS, this leads to movement difficulties and eventually paralysis, while in FTD, patients experience problems with language and decision making. Past research has connected a specific mutation in the C9orf72 gene to 40 percent of inherited ALS cases and 25 percent of inherited FTD cases, as well as nearly 10 percent of non-inherited cases of each disorder. The recent experiments, conducted in yeast, fruit flies, and neurons from patients, found that the mutation prevents proteins and genetic material called RNA from moving between the nucleus and the cytoplasm that surrounds it. “At the end of the day, this culminates in a defect in the flow of genetic information, which leads to problems expressing genes in the right place at the right time,” said J. Paul Taylor, M.D., Ph.D., a researcher at St. Jude’s Children’s Research Hospital in Memphis, Tennessee, and the senior author of one of the papers.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 21524 - Posted: 10.17.2015
By Robert F. Service Prosthetic limbs may work wonders for restoring lost function in some amputees, but one thing they can’t do is restore an accurate sense of touch. Now, researchers report that one day in the not too distant future, those artificial arms and legs may have a sense of touch closely resembling the real thing. Using a two-ply of flexible, thin plastic, scientists have created novel electronic sensors that send signals to the brain tissue of mice that closely mimic the nerve messages of touch sensors in human skin. Multiple research teams have long worked on restoring touch to people with prosthetic limbs. 2 years ago, for example, a group at Case Western Reserve University in Cleveland, Ohio, reported giving people with prosthetic hands a sense of touch by wiring pressure sensors on the hands to peripheral nerves in their arms. Yet although these advances have restored a rudimentary sense of touch, the sensors and signals are very different from those sent by mechanoreceptors, natural touch sensors in the skin. For starters, natural mechanoreceptors put out what amounts to a digital signal. When they sense pressure, they fire a stream of nerve impulses; the more pressure, the higher the frequency of pulses. But previous tactile sensors have been analogue devices, where more pressure produces a stronger electrical signal, rather than a more frequent stream of pulses. The electrical signals must then be sent to another processing chip that converts the strength of the signals to a digital stream of pulses that is only then sent on to peripheral nerves or brain tissue. © 2015 American Association for the Advancement of Science.
By Nicholas Bakalar Physical therapy may provide little relief for recent-onset low back pain, a small randomized trial has found. The study, published in JAMA, included 207 men and women, average age 37, with a score of 20 or higher on a widely used 100-point scale that quantifies disability from low back pain. The study included people with recent-onset pain who were assigned to one of two groups. The first received four sessions of exercise and manipulation under the guidance of a trained physical therapist. Those in the other group were told that low back pain usually gets better, and were advised to be as active as possible. There were no significant differences at any time in pain intensity, quality of life or the number of visits to health care providers. Compared with the usual care group, the physical therapy group did show significant improvement on the disability scale after three months. But after one year, there was no difference between the two groups in this measure either. “Most treatments that are effective have only modest effects,” said the lead author, Julie M. Fritz, a professor in the department of physical therapy at the University of Utah. “The pattern of low back pain is one of recurrence and remission, and changing that pattern is a real challenge. There are no magic answers.” © 2015 The New York Times Company
Keyword: Pain & Touch
Link ID: 21513 - Posted: 10.15.2015
By Gretchen Reynolds Can a shot of salt water make you a faster runner? The answer appears to be a resounding yes, if you believe that the salt water contains something that should make you a faster runner, according to a new study of the power of placebos in athletic performance. Anyone who exercises knows from experience that our minds and mental attitudes affect physical performance. Who hasn’t faced a moment when, tiring at the end of a strenuous workout or race, we are about to quit before suddenly being passed on the path or shown up in the gym by someone we know we should outperform, and somehow we find an extra, unexploited gear and spurt on? This phenomenon is familiar to physiologists, many of whom believe that our brains, in order to protect our bodies, send out signals telling those bodies to quit before every single resource in our muscles and other tissues is exhausted. We think we are at the outer limits of our endurance or strength, when, in reality, we may still have a physical reserve available to us, if we can find a way to tap it. Past studies have shown that lying to people is one way to exploit that reserve. Telling athletes that they are moving slower than in fact they are, for instance, often results in their speeding up past the pace that they thought they could maintain. Or give them a sugar pill that they think contains caffeine or steroids and they will run more swiftly or lift more weight than before. But none of these studies tested the effects of placebos and deception in relatively real-world competitive situations, which have their own effects on mental responses. People are almost always faster during competitive races than in training, studies show, even when they are trying to replicate race pace. © 2015 The New York Times Company
Keyword: Pain & Touch
Link ID: 21509 - Posted: 10.14.2015
By Christopher Intagliata If you're lost, you need a map and a compass. The map pinpoints where you are, and the compass orients you in the right direction. Migratory birds, on the other hand, can traverse entire hemispheres and end up just a couple miles from where they bred last year, using their senses alone. Their compass is the Sun, the stars and the Earth's magnetic field. But their map is a little more mysterious. One theory goes that they use olfactory cues—how a place smells. Another is that they rely on their sense of magnetism. Researchers in Russia investigated the map issue in a past study by capturing Eurasian reed warblers on the Baltic Sea as they flew northeast towards their breeding grounds near Saint Petersburg. They moved the birds 600 miles east, near Moscow. And the birds just reoriented themselves to the northwest—correctly determining their new position. Now the same scientists have repeated that experiment—only this time, they didn't move the birds at all. They just put them in cages that simulated the magnetic field of Moscow, while still allowing the birds to experience the sun, stars and smells of the Baltic. Once again, the birds re-oriented themselves to the northwest—suggesting that the magnetic field alone—regardless of smells or other cues, is enough to alter the birds' mental map. The study is in the journal Current Biology. [Dmitry Kishkinev et al, Eurasian reed warblers compensate for virtual magnetic displacement] And if you're envious of that sixth sense—keep in mind that since the Earth's magnetic field fluctuates, the researchers say magnetic route-finding is best for crude navigation. Meaning for door-to-door directions—you’re still better off with your GPS. © 2015 Scientific American,
Keyword: Animal Migration
Link ID: 21508 - Posted: 10.14.2015
By Nancy Szokan Sensory deprivation is Sushma Subramanian’s topic in the October issue of Women’s Health magazine, and she offers a couple of extreme examples. Julie Malloy, 33, from York, Pa., describes living without the sense of touch: “I was born with a rare sensory illness that leaves me unable to feel pain, temperature, deep pressure, or vibrations in my arms, legs, and the majority of my chest and back. I use vision to compensate as much as I can. . . . “I always wash my face with cold water; I once burned myself without realizing it. . . . When I drive, I can’t really tell how hard I’m pushing on the pedals. I watch others really enjoy it when someone kisses their arm or get tingly when someone hugs them, but I can’t even feel anything during sex.” Erin Napoleone, 31, from Havre de Grace, Md., describes losing her sense of smell: “As a teen, I was in a car accident. A few days later, I watched my father make homemade tomato sauce — but I didn’t smell a thing. Then I couldn’t detect my mom’s familiar perfume. A head CT scan confirmed my sense of smell was gone for good.” The magazine points out that some senses naturally deteriorate with age and that taking care of your skin — say, by keeping it moisturized and protecting it from damage — can help preserve the sense of touch. But olfactory nerves facing “prolonged exposure to rank odors (think freeway fumes or curbside trash)” can be permanently damaged.
It can start with flashing lights, a tingling sensation and a feeling of unease, followed by excruciating pain. Migraines can be triggered by lack of food or too much stress but their underlying cause has remained a mystery. Now researchers have found that a migraine may be triggered by a protein deep in the brain that stimulates the neurons controlling facial sensations. The discovery creates a potential new target for safer migraine medicines and adds weight to the theory that neurons, not blood vessels, are responsible for migraine attacks. “Where a migraine starts is a key question,” says Debbie Hay at the University of Auckland in New Zealand. “There has been a great deal of debate around the mechanisms of migraine. If we can pin this down, we may have better chances of preventing it.” To investigate, Simon Akerman at New York University and Peter Goadsby at Kings College London, UK, studied two neuropeptides released by neurons thought to play a role in the pain associated with migraine. These protein-like molecules, called VIP and PACAP, first raised suspicion after they were found to be elevated in blood drained from the brains of people having a migraine attack. When researchers administered these peptides to volunteers, they found that they could cause a headache or migraine about two hours later. Both peptides widen blood vessels, which was thought to be significant in migraine. In fact, the only drugs specifically developed for migraine that are in use today – triptans – were designed to shrink blood vessels in the brain. As a result, they cannot be used by people with cardiovascular disorders. © Copyright Reed Business Information Ltd.
Keyword: Pain & Touch
Link ID: 21489 - Posted: 10.08.2015
Jo Marchant Most new painkiller drugs fail in clinical trials — but a growing placebo response may be to blame. Drug companies have a problem: they are finding it ever harder to get painkillers through clinical trials. But this isn't necessarily because the drugs are getting worse. An extensive analysis of trial data1 has found that responses to sham treatments have become stronger over time, making it harder to prove a drug’s advantage over placebo. The change in reponse to placebo treatments for pain, discovered by researchers in Canada, holds true only for US clinical trials. “We were absolutely floored when we found out,” says Jeffrey Mogil, who directs the pain-genetics lab at McGill University in Montreal and led the analysis. Simply being in a US trial and receiving sham treatment now seems to relieve pain almost as effectively as many promising new drugs. Mogil thinks that as US trials get longer, larger and more expensive, they may be enhancing participants’ expectations of their effectiveness. Stronger placebo responses have already been reported for trials of antidepressants and antipsychotics2, 3, triggering debate over whether growing placebo effects are seen in pain trials too. To find out, Mogil and his colleagues examined 84 clinical trials of drugs for the treatment of chronic neuropathic pain (pain which affects the nervous system) published between 1990 and 2013. © 2015 Nature Publishing Group,
Keyword: Pain & Touch
Link ID: 21484 - Posted: 10.07.2015
Laura Sanders Scribes usually have pretty good handwriting. That’s not the case for one prolific 13th century writer known to scholars only as the Tremulous Hand of Worcester. Now scientists suggest the writer suffered from a neurological condition called essential tremor. Neurologist Jane Alty and historical handwriting researcher Deborah Thorpe, both of the University of York in England, made the retrospective diagnosis August 31 in Brain after studying the spidery wiggles that pervade the scribe’s writing. Essential tremor can cause shaking of the hands, head and voice and is distinct from other tremor-causing conditions such as Parkinson’s disease. Here, the anonymous writer’s peculiar script is evident (lighter portion of text) in an early Middle English version of the Nicene Creed, a summary of the Christian faith. Buried in the manuscript are clues that helped the researchers conclude that essential tremor plagued the Tremulous Hand. The Tremulous Hand of Worcester’s writing appeared in more than 20 books, including the Nicene Creed, a summary of the Christian faith. The writer’s distinctive script is the lighter portion of the text, about a third of the way down the page. Several clues led researchers to diagnose the scribe with essential tremor (see following images). © Society for Science & the Public 2000 - 2015.
Keyword: Movement Disorders
Link ID: 21482 - Posted: 10.07.2015
By Jon Cohen A virus that long ago spliced itself into the human genome may play a role in amyotrophic lateral sclerosis (ALS), the deadly muscle degenerative disease that crippled baseball great Lou Gehrig and ultimately took his life. That’s the controversial conclusion of a new study, which finds elevated levels of human endogenous retrovirus K (HERV-K) in the brains of 11 people who died from the disease. “This certainly is interesting and provocative work,” says Raymond Roos, a neurologist at the University of Chicago in Illinois who treats and studies ALS but who was not involved with the finding. Still, even the scientists behind the work caution that more research is needed to confirm the link. “I’m very careful to say HERV-K doesn’t cause the disease but may play a role in the pathophysiology,” says study leader Avindra Nath, a neuroimmunologist at the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland. “The darn thing is in the chromosomes to begin with. It’s going to be very hard to prove causation.” It was another retrovirus, HIV, that led Nath to first suspect a connection between viruses and ALS. In 2006, he was helping a patient control his HIV infection with antiretroviral drugs when he noticed that the man’s ALS also improved. “That intrigued me, and I looked in the ALS literature and saw that people had reported they could see reverse transcriptase in the blood.” Reverse transcriptase, an enzyme that converts RNA to DNA, is a hallmark of retroviruses, which use it to insert copies of their genes into chromosomes of their hosts. © 2015 American Association for the Advancement of Science
James Hamblin Mental exercises to build (or rebuild) attention span have shown promise recently as adjuncts or alternatives to amphetamines in addressing symptoms common to Attention Deficit Hyperactivity Disorder (ADHD). Building cognitive control, to be better able to focus on just one thing, or single-task, might involve regular practice with a specialized video game that reinforces "top-down" cognitive modulation, as was the case in a popular paper in Nature last year. Cool but still notional. More insipid but also more clearly critical to addressing what's being called the ADHD epidemic is plain old physical activity. This morning the medical journal Pediatrics published research that found kids who took part in a regular physical activity program showed important enhancement of cognitive performance and brain function. The findings, according to University of Illinois professor Charles Hillman and colleagues, "demonstrate a causal effect of a physical program on executive control, and provide support for physical activity for improving childhood cognition and brain health." If it seems odd that this is something that still needs support, that's because it is odd, yes. Physical activity is clearly a high, high-yield investment for all kids, but especially those attentive or hyperactive. This brand of research is still published and written about as though it were a novel finding, in part because exercise programs for kids remain underfunded and underprioritized in many school curricula, even though exercise is clearly integral to maximizing the utility of time spent in class.
By Sarah C. P. Williams Looking at photos of starving refugees or earthquake victims can trigger a visceral sense of empathy. But how, exactly, do we feel others’ agony as our own? A new study suggests that seeing others in pain engages some of the same neural pathways as when we ourselves are in pain. Moreover, both pain and empathy can be reduced by a placebo effect that acts on the same pathways as opioid painkillers, the researchers found. “This study provides one of the most direct demonstrations to date that first-hand pain and pain empathy are functionally related,” says neurobiologist Bernadette Fitzgibbon of Monash University in Melbourne, Australia, who was not involved in the new research. “It’s very exciting.” Previous studies have used functional magnetic resonance imaging (fMRI) scans to show that similar areas of the brain are activated when someone is in pain and when they see another person in pain. But overlaps on a brain scan don’t necessarily mean the two function through identical pathways—the shared brain areas could relate to attention or emotional arousal, among other things, rather than pain itself. Social neuroscientist Claus Lamm and colleagues at the University of Vienna took a different approach to test whether pain and empathy are driven by the same pathways. The researchers first divided about 100 people into control or placebo groups. They gave the placebo group a pill they claimed to be an expensive, over-the-counter painkiller, when in fact it was inactive. This well-established placebo protocol is known to function similarly to opioid painkillers, while avoiding the drugs’ side effects. © 2015 American Association for the Advancement of Science.
By Jane E. Brody Mark Hammel’s hearing was damaged in his 20s by machine gun fire when he served in the Israeli Army. But not until decades later, at 57, did he receive his first hearing aids. “It was very joyful, but also very sad, when I contemplated how much I had missed all those years,” Dr. Hammel, a psychologist in Kingston, N.Y., said in an interview. “I could hear well enough sitting face to face with someone in a quiet room, but in public, with background noise, I knew people were talking, but I had no idea what they were saying. I just stood there nodding my head and smiling. “Eventually, I stopped going to social gatherings. Even driving, I couldn’t hear what my daughter was saying in the back seat. I live in the country, and I couldn’t hear the birds singing. “People with hearing loss often don’t realize what they’re missing,” he said. “So much of what makes us human is social contact, interaction with other human beings. When that’s cut off, it comes with a very high cost.” And the price people pay is much more than social. As Dr. Hammel now realizes, “the capacity to hear is so essential to overall health.” Hearing loss is one of the most common conditions affecting adults, and the most common among older adults. An estimated 30 million to 48 million Americans have hearing loss that significantly diminishes the quality of their lives — academically, professionally and medically as well as socially. One person in three older than 60 has life-diminishing hearing loss, but most older adults wait five to 15 years before they seek help, according to a 2012 report in Healthy Hearing magazine. And the longer the delay, the more one misses of life and the harder it can be to adjust to hearing aids. © 2015 The New York Times Company
By Simon Makin Most people associate the term “subliminal conditioning” with dystopian sci-fi tales, but a recent study has used the technique to alter responses to pain. The findings suggest that information that does not register consciously teaches our brain more than scientists previously suspected. The results also offer a novel way to think about the placebo effect. Our perception of pain can depend on expectations, which explains placebo pain relief—and placebo's evil twin, the nocebo effect (if we think something will really hurt, it can hurt more than it should). Researchers have studied these expectation effects using conditioning techniques: they train people to associate specific stimuli, such as certain images, with different levels of pain. The subjects' perception of pain can then be reduced or increased by seeing the images during something painful. Most researchers assumed these pain-modifying effects required conscious expectations, but the new study, from a team at Harvard Medical School and the Karolinska Institute in Stockholm, led by Karin Jensen, shows that even subliminal input can modify pain—a more cognitively complex process than most that have previously been discovered to be susceptible to subliminal effects (timeline below). The scientists conditioned 47 people to associate two faces with either high or low pain levels from heat applied to their forearm. Some participants saw the faces normally, whereas others were exposed subliminally—the images were flashed so briefly, the participants were not aware of seeing them, as verified by recognition tests. © 2015 Scientific American