Is this my finger? Sensory illusion study provides new insight for body representation brain disorders

People can be easily tricked into believing an artificial finger is their own, shows a study published today [23 September] in The Journal of Physiology. The results reveal that the brain does not require multiple signals to build a picture body ownership, as this is the first time the illusion has been created using sensory inputs from the muscle alone.

The discovery provides new insight into clinical conditions where body representation in the brain is disrupted due to changes in the central or peripheral nervous systems e.g. stroke, schizophrenia and phantom limb syndrome following amputation.

Professor Simon Gandevia, Deputy Director of Neuroscience Research Australia (NeuRA), says:

“It may seem silly to ask yourself whether your index finger is part of your body. However, our current findings demonstrate that this question has led to important insights into key brain functions.

“These findings could lead to new clinical interventions where the addition or the removal of specific sensory stimuli is used to change someone’s body image.”

In the experiment, subjects held an artificial finger with their left hand that was located 12 cm above their right index finger. Vision was eliminated and anaesthesia was used to numb the skin and remove feelings of joint movement. When the artificial finger and the right index finger were moved synchronously, subjects reported they were holding their own index finger: the brain incorrectly incorporated the artificial finger into its internal body representation.

The human brain uses sensory signals to maintain and update internal representation of the body, to plan and generate movements and interact with the world. The study gives new understanding as to how the brain decides what is part of our own body and where it is located. Contrary to previous theories which used multiple sensory inputs including touch and vision, these results demonstrate that messages coming from muscle receptors are enough to change the internal body representation.

The team additionally found a new type of sensory ‘grasp illusion’ in which perceived distances between index fingers decreases when subjects hold an artificial finger. This implies that the brain generates possible scenarios and tests them against available sensory information.

Professor Gandevia says:

“Grasping the artificial finger induces a sensation in some subjects that their hands are level with one another, despite being 12 cm apart. This illusion demonstrates that our brain is a thoughtful (yet at times gullible!) decision maker: it uses available sensory information and memories of past experiences to decide what scenario is most likely (i.e. ‘my hands are level’).”

Scientists create phantom sensations in non-amputees

The sensation of having a physical body is not as self-evident as one might think. Almost everyone who has had an arm or leg amputated experiences a phantom limb: a vivid sensation that the missing limb is still present. A new study by neuroscientists at the Karolinska Institutet in Sweden shows that it is possible to evoke the illusion of having a phantom hand in non-amputated individuals.

In an article in the scientific periodical Journal of Cognitive Neuroscience, the researchers describe a perceptual illusion in which healthy volunteers experience having an invisible hand. The experiment involves the participant sitting at a table with their right arm hidden from their view behind a screen. To evoke the illusion, the scientist touches the right hand of the participant with a small paintbrush while imitating the exact movements with another paintbrush in mid-air within full view of the participant.

"We discovered that most participants, within less than a minute, transfer the sensation of touch to the region of empty space where they see the paintbrush move, and experience an invisible hand in that position", says Arvid Guterstam, lead author of the study. "Previous research has shown that non-bodily objects, such as a block of wood, cannot be experienced as ones own hand, so we were extremely surprised to find that the brain can accept an invisible hand as part of the body."

The study comprises eleven experiments that explore in detail the illusory experience and include 234 volunteers. To demonstrate that the illusion actually worked, the researchers would make a stabbing motion with a knife towards the empty space ‘occupied’ by the invisible hand and measure the participant’s sweat response to the perceived threat. They found that the participants stress responses were elevated while experiencing the illusion but absent when the illusion was broken.

In another experiment, the volunteers were asked to close their eyes and quickly point with their left hand to their right hand (or to where they perceived it to be). After having experienced the illusion for a while, they would point to the location of the invisible hand rather than to their real hand.

The researchers also measured the brain activity of the participants using functional magnetic resonance imaging (fMRI). Perceiving the invisible hand illusion led to increased activity in the same parts of the brain that are normally active when individuals see their real hand being touched or when participants experience a prosthetic hand as their own.

"Taken together, our results show that the sight of a physical hand is remarkably unimportant to the brain for creating the experience of one’s physical self," says Arvid Guterstam.

The researchers hope that the results of their study will offer insight into future research on phantom pain in amputees.

"This illusion suggests that the experience of phantom limbs is not unique to amputated individuals, but can easily be created in non-amputees," says the principal investigator, Dr Henrik Ehrsson, Docent at the Department of Neuroscience. "These results add to our understanding of how phantom sensations are produced by the brain, which can contribute to future research on alleviating phantom pain in amputees."

Scientists Discover How Animals Taste, and Avoid, High Salt Concentrations

For consumers of the typical Western diet—laden with levels of salt detrimental to long-term health—it may be hard to believe that there is such a thing as an innate aversion to very high concentrations of salt.

But Charles Zuker, PhD, and colleagues at Columbia University Medical Center have discovered how the tongue detects high concentrations of salt (think seawater levels, not potato chips), the first step in a salt-avoiding behavior common to most mammals.

The findings, which were published online in the journal Nature, could serve as a springboard for the development of taste modulators to help control the appetite for a high-salt diet and reduce the ill effects of too much sodium.

The sensation of saltiness is unique among the five basic tastes. Whereas mammals are always attracted to the tastes of sweet and umami, and repelled by sour and bitter, their behavioral response to salt dramatically changes with concentration.

“Salt taste in mammals can trigger two opposing behaviors,” said Dr. Zuker, professor in the Departments of Biochemistry & Molecular Biophysics and of Neuroscience at Columbia University College of Physicians & Surgeons. “Mammals are attracted to low concentrations of salt; they will choose a salty solution over a salt-free one. But they will reject highly concentrated salt solutions, even when salt-deprived.”

Over the past 15 years, the receptors and other cells on the tongue responsible for detecting sweet, sour, bitter, and umami tastes—as well as low concentrations of salt—have been uncovered largely through the efforts of Dr. Zuker and his collaborator Nicholas Ryba from the National Institute of Dental and Craniofacial Research.

“But we didn’t understand what was behind the aversion to high concentrations of salt,” said Yuki Oka, a postdoctoral fellow in Dr. Zuker’s laboratory and the lead author of the study.

The researchers expected high-salt receptors to reside in cells committed only to detecting high salt. “Over the years our studies have shown that each taste quality—sweet, bitter, sour, umami, and low-salt—is mediated by different cells,” Dr. Ryba said. “So we thought there must be different taste receptor cells for high-salt. But unexpectedly, Dr. Oka found high salt is mediated by cells we already knew.”

Itchy Wool Sweaters Explained

Johns Hopkins researchers have uncovered strong evidence that mice have a specific set of nerve cells that signal itch but not pain, a finding that may settle a decades-long debate about these sensations, and, if confirmed in humans, help in developing treatments for chronic itch, including itch caused by life-saving medications.

At the heart of their discovery is a type of sensory nerve cell whose endings receive information from the skin and relay it to other nerves in the spinal cord, which then coordinates a response to the stimulus. Published online Dec. 23 in Nature Neuroscience, a report on the research suggests that even when the itch-specific nerve cells receive stimuli that are normally pain-inducing, the message they send isn’t “That hurts!” but rather “That itches!”

Pain and itch are both important sensations that help organisms survive. And pain is arguably more important because it tells us to withdraw the pained body part in order to prevent tissue damage. But itch also warns us of the presence of irritants, as in an allergic reaction. However, “when either of these sensations continues for weeks or months, they are no longer helpful. We even see patients stop taking life-saving medications because they cause such horrible itchiness all over,” says Xinzhong Dong, Ph.D., a Howard Hughes early career scientist and associate professor of neuroscience at the Institute for Basic Biomedical Sciences at the Johns Hopkins University School of Medicine. “And sometimes when we try to suppress chronic pain, with morphine for example, we end up causing chronic itchiness. So the two sensations are somehow related, and this study has begun to untangle them,” he says.

Because nerve cells send their messages as electrical currents that flow through them just as they would through wires, scientists can plug tiny monitors into individual nerve cells to detect the moment of stimulation. The scientific controversy over pain and itch centers around a group of nerve cells known to respond electrically to painful stimuli such as molecules of capsaicin, the fiery ingredient in chili peppers. A small subset of these nerve cells also responds electrically to itchy stimuli because they have on their surfaces receptors for molecules like histamine. One of these itchy receptors, called MrgA3, binds the anti-malaria drug chloroquine, causing serious itchiness in many patients.

Sensory nerve scientists have not known whether the nerves with itchy receptors and pain receptors were actually sending both types of messages to the brain, or just itch messages. What the current study found is that, in nerves with the itchy receptor MrgA3, electrical signals sent in response to both painful and itchy stimuli are interpreted by the brain as itch.

To reach this conclusion, the researchers first used a genetic trick to label the MrgA3 cells in mice with a glowing protein that allowed them to see the cells under the microscope. Aided by the glow, they were able to plug in those tiny electricity monitors and watch nerve cell responses to different stimuli. The cells transmitted electrical signals when the mice were exposed to itch-inducing chloroquine and histamine, as well as pain-inducing capsaicin and heat. Based on this result, the researchers tentatively concluded that the cells could send both pain and itch signals.

In the next experiment, the researchers monitored the behavioral responses of mice to the different stimuli. As expected, when the tails of normal mice were placed in hot water, they quickly pulled them out; when normal mice were given a bit of chloroquine or histamine, they scratched vigorously with their hind legs.

Then, to examine the role of MrgA3 cells in pain and itch, the scientists selectively killed MrgA3 nerve cells in adult mice and retested their responses. Presumably, the researchers noted, because MrgA3 cells are only a small fraction of all pain-sensing nerve cells, the mice had normal withdrawal responses to painful stimuli like hot water. However, when exposed to itchy stimuli, their scratching responses were reduced to varying degrees depending on the stimulus, most significantly in response to chloroquine. The fact that some stimuli still caused scratching suggested to the scientists that MrgA3 cells are not the only ones in the body that respond to itch. “We were convinced that MrgA3 cells are responsible for much of the sensation of itch, but it wasn’t yet clear whether MrgA3 cells could also relay painful information,” says Dong.

In their final experiments, the scientists used genetic techniques to create mice in which the MrgA3 cells were the only cells in the body capable of responding to capsaicin, that peppery pain-inducing substance. When injected into the cheeks of mice, normal mice massage the area with their forepaws to relieve the hot sensation. When injected into the experimental mice, they vigorously scratched their cheeks with their hind legs, suggesting that this normally painful stimulus had been communicated to the brain—by MrgA3 cells—as itchiness.

"Now that we have disentangled these itchy sensations from painful ones, we should be able to design drugs that target itch-specific nerve cells to combat chronic itchiness," says Dong. "We hope that this will not only provide relief, but also increase people’s faithfulness to their drug plans, particularly for deadly diseases like malaria and cancer."

Experimental prosthetic leg lets amputees ‘feel’ each step

Human prosthetics have come a long way in recent decades. We’ve gone from simple plastic molds that vaguely resemble the original limb, to high-tech articulating devices that return most of a person’s mobility. Through all this progress, one nagging issue has continued to plague doctors — there’s still no way for a patient to feel a prosthetic. A new project out of UCLA might be on the path to changing that.

Having something that acts like a leg turns out to be only part of the puzzle, says UCLA grad student Zachary McKinney. When you take a step with your flesh-and-blood leg, the limb is constantly sending sensory signals back to the brain that inform you when it touches the ground, how much weight is on it, and how that weight is distributed among other things. Lacking that kind of feedback in a prosthetic causes long-term problems like uneven gait or strain on the remaining limb.

The UCLA project is not seeking to exactly replicate the sensation of having a real leg, but to provide a system that can relay the same information. The system currently consists of four sensors in the shoe of the prosthetic leg. As the subject takes a step, the system register how much pressure is on each sensor and sends that data to a small computer strapped to the user’s midsection.

The computer will analyze the data, and control the inflation of a series of small balloons on the thigh cuff. These 12 dime-sized silicon balloons are split into four sets of three, each one corresponding to one of the shoe sensors. The more pressure detected, the larger the balloons inflate. Current lag time is roughly 0.1 seconds, which is only a little slower than nerve impulses. For the patient, it is functionally instantaneous.

Results have been encouraging in initial testing. Nine subjects who had lost a leg were asked to walk across a 30-foot wide space with a normal prosthetic. After being given time to acclimate to the pressure-sensitive system, the test was run again. According to the researchers, seven distinct measurements of gait improved with the test rig.

Stanford’s touch-sensitive plastic skin heals itself

Nobody knows the remarkable properties of human skin like the researchers struggling to emulate it. Not only is our skin sensitive – sending the brain precise information about pressure and temperature – but it also heals efficiently to preserve a protective barrier against the world. Combining these two features in a single synthetic material presented an exciting challenge for Stanford chemical engineering Professor Zhenan Bao and her team.

Now, they have succeeded in making the first material that can both sense subtle pressure and heal itself when torn or cut. Their findings will be published Nov. 11 in the journal Nature Nanotechnology.

In the last decade, there have been major advances in synthetic skin, said Bao, the study’s principal investigator, but even the most effective self-healing materials had major drawbacks. Some had to be exposed to high temperatures, making them impractical for day-to-day use. Others could heal at room temperature, but repairing a cut changed their mechanical or chemical structure, so they could heal themselves only once. Most important, no self-healing material was a good bulk conductor of electricity, a crucial property.

"To interface this kind of material with the digital world, ideally you want it to be conductive," said Benjamin Chee-Keong Tee, a researcher on the project.

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Scientists have claimed to have solved the mystery of why coffee never tastes as good as it smells.

Apparently, the act of swallowing the drink sends a burst of aroma up the back of the nose from inside the mouth, activating a “second sense of smell” in the brain that is less receptive to the flavour, causing a completely different and less satisfying sensation.

“We have got two senses of smell. One sense is when you inhale things from the environment into you, and the other is when the air comes out of you up the nasal passage and is breathed out through the nose,” the Telegraph quoted Prof Barry Smith, of the University of London, as saying at the British Science Festival in Aberdeen.

The phenomenon is down to the fact that, although we have sensors on our tongue, 80 percent of what we think of as taste actually reaches us through smell receptors in our nose, the paper said. The receptors, which relay messages to our brain, react to odours differently depending on which direction they are moving in, it added.

In the case of coffee, the taste is also hampered by the fact that 300 of the 631 chemicals that combine to form its complex aroma are wiped out by saliva, causing the flavour to change before we swallow it, Prof Smith added.