Chapter 5. The Sensorimotor System

Follow us on Facebook or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 3240

By Pam Belluck An experimental therapy for A.L.S., the paralyzing and fatal neurological disorder, has been approved in Canada, adding a new treatment option for a disease for which there are few effective therapies. The approval, the first in the world for the treatment — AMX0035, to be marketed in Canada as Albrioza — comes with the condition that the drug company later provide better evidence that the treatment works. It is likely to be of major interest to patients with A.L.S. (amyotrophic lateral sclerosis) in the United States, where the same therapy is being evaluated by the Food and Drug Administration, which has raised questions about the treatment’s effectiveness. An F.D.A. review earlier this year found the treatment to be safe, but said there was not enough evidence that it was effective either in helping patients live longer or slowing the rate at which they lose functions like muscle control, speaking or breathing without assistance. A committee of independent advisers to the F.D.A. voted by a narrow margin in March that the therapy was not ready for approval. The F.D.A. had been scheduled to issue a final decision this month, but recently extended the deadline to Sept. 29, saying it needed more time to review additional analyses of data submitted by the company. In the meantime, Calaneet Balas, president and chief executive of the A.L.S. Association, one of several patient advocacy organizations pressing for F.D.A. approval, said, “We expect that Americans living with A.L.S. will try to access Albrioza in Canada, just as we have heard reports of people trying to buy the ingredients on Amazon.” © 2022 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28369 - Posted: 06.14.2022

Sofia Quaglia When they are in the deep, dark ocean, seals use their whiskers to track down their prey, a study has confirmed after observing the sea mammals in their natural habitat. It’s hard for light to penetrate the gloom of the ocean’s depths, and animals have come up with a variety of adaptations in order to live and hunt there. Whales and dolphins, for example, use echolocation – the art of sending out clicky noises into the water and listening to their echo as they bounce off possible prey, to locate them. But deep-diving seals who don’t have those same acoustic projectors must have evolutionarily learned to deploy another sensory technique. Scientists have long hypothesised that the secret weapons are their long, cat-like whiskers, conducting over 20 years of experiments with artificial whiskers or captive seals blindfolded in a pool, given the difficulties of directly observing the hunters in the tenebrous depths of the ocean. Now a study may have confirmed the hypothesis, according to Taiki Adachi, assistant project scientist of University of California, Santa Cruz, and one of the lead authors of the study published in Proceedings of the National Academy of Science. Adachi and his team positioned small video cameras with infrared night-vision on the left cheek, lower jaw, back and head of five free-ranging northern elephant seals, the Mirounga angustirostris, in Año Nuevo state park in California. They recorded a total of approximately nine and a half hours of deep sea footage during their seasonal migration. By analysing the videos the scientists noted that diving seals held back their whiskers for the initial part of their dives and, and once they reached a depth suitable for foraging, they rhythmically whisked their whiskers back and forth, hoping to sense any vibration caused by the slightest water movements of swimming prey. © 2022 Guardian News & Media Limited o

Keyword: Pain & Touch
Link ID: 28368 - Posted: 06.14.2022

By Maria Temming The Terminator may be one step closer to reality. Researchers at the University of Tokyo have built a robotic finger that, much like Arnold Schwarzenegger’s titular cyborg assassin, is covered in living human skin. The goal is to someday build robots that look like real people — albeit for more altruistic applications. Super realistic-looking robots could more seamlessly interact with humans in medical care and service industries, say biohybrid engineer Shoji Takeuchi and his colleagues June 9 in Matter. (Whether cyborgs masked in living tissue would be more congenial or creepy is probably in the eye of the beholder.) To cover the finger in skin, Takeuchi and colleagues submerged the robotic digit in a blend of collagen and human skin cells called dermal fibroblasts. The mixture settled into a base layer of skin, or dermis, covering the finger. The team then poured a liquid containing human keratinocyte cells onto the finger, which formed an outer skin layer, or epidermis. After two weeks, skin covering the finger measured a few millimeters thick — comparable to the thickness of human skin. The lab-made skin was strong and stretchy enough to withstand the robotic finger bending. It could also heal itself: When researchers made a small cut on the robotic finger and covered it with a collagen bandage, the skin’s fibroblast cells merged the bandage with the rest of the skin within a week. Researchers at the University of Tokyo covered this robotic finger in living human skin to pave the way for ultrarealistic cyborgs. “This is very interesting work and an important step forward in the field,” says Ritu Raman, an MIT engineer who also builds machines with living components. “Biological materials are appealing because they can dynamically sense and adapt to their environments.” For instance, she’d like to see a future version of the living robot skin embedded with nerve cells to make robots more aware of their surroundings. © Society for Science & the Public 2000–2022.

Keyword: Pain & Touch; Robotics
Link ID: 28365 - Posted: 06.11.2022

ByRobert F. Service An experimental drug is raising new hopes for those with Parkinson’s disease. So far, the compound has only been tested in animals and in an initial safety assessment in humans. But results show it inhibits a cellular pathway that gives rise to the disease, which researchers have been working to target for nearly 20 years. Investigators are now launching expanded clinical trials. “This is a very, very important step forward,” says Patrick Lewis, a neuroscientist who studies the mechanisms of Parkinson’s at the University of London’s Royal Veterinary College. If further tests prove the compound is effective in humans, says Lewis, who was not involved with the new study, it would likely be given to patients as soon as they exhibit the first signs of developing the progressive disorder. “The hope is that [the new drug] would slow down the progression of disease.” Parkinson’s affects as many as 10 million people worldwide. It results when cells in the brain that produce the neurotransmitter dopamine stop working or die. Over time this causes a widespread decline in brain function, leading to shaking and loss of muscle control. Current drugs can help replace lost dopamine and reduce symptoms, but no therapies slow or halt disease progression itself. The new study focuses on a gene called leucine-rich repeat kinase 2 (LRRK2). People with mutations in this gene are at high risk for developing Parkinson’s. Among other roles, LRRK2 modifies a suite of proteins called Rab guanosine triphosphates, which act like air traffic controllers, orchestrating the flow of proteins in and out of cells. The mutations kick Rab into overdrive and reduce the efficiency of cellular structures called lysosomes, which chew up and recycle unwanted proteins. This creates a buildup of toxic byproducts that can kill neurons and lead to Parkinson’s, says Carole Ho, chief medical officer of Denali Therapeutics, a biotech startup in California. © 2022 American Association for the Advancement of Science.

Keyword: Parkinsons
Link ID: 28362 - Posted: 06.09.2022

By Lisa Sanders, M.D. “You have to take your husband to the hospital right now,” the doctor urged over the phone. “His kidneys aren’t working at all, and we need to find out why.” The woman looked at her 82-year-old spouse. He was so thin and pale. She thanked the doctor and called 911. For the past couple of months, every meal was a struggle. Swallowing food was strangely difficult. Liquids were even worse. Whatever he drank seemed to go down the wrong pipe, and he coughed and sputtered after almost every sip. It was terrifying. He saw an ear, nose and throat specialist, who scoped his mouth and esophagus. There wasn’t anything blocking the way. The doctor recommended that he get some therapy to help him strengthen the muscles he used to swallow, and until he did that, he should thicken his liquids to make drinking easier. The patient tried that once, but it was so disgusting he gave up on it. His wife was worried as she watched him eat and drink less and less. She could see that he was getting weaker every day. He had a stroke four months earlier, and since then his right foot dragged a little. But now she had to help him get out of his recliner. And he wasn’t able to drive — she had to make the 45-minute trip with him each day to his office. Finally, he agreed to see Dr. Richard Kaufman, their primary-care doctor. Kaufman was shocked by the man’s appearance, how the skin on his face hung in folds as if air had been let out of his cheeks. He’d lost nearly 40 pounds. He struggled to walk the few steps to the exam table. His right side, which was weakened by his stroke, was now matched by weakness on his left side. His stroke hadn’t done this. There was something else going on. Kaufman ordered some preliminary blood tests to try to see where the problem might lie. Those were the results that sent the couple to the emergency room. © 2022 The New York Times Company

Keyword: Neuroimmunology; Muscles
Link ID: 28339 - Posted: 05.28.2022

By Veronique Greenwood Lovebirds, small parrots with vibrant rainbow plumage and cheeky personalities, are popular pets. They swing from ropes, cuddle with companions and race for treats in a waddling gait with all the urgency of toddlers who spot a cookie. But, along with other parrots, they also do something strange: They use their faces to climb walls. Give these birds a vertical surface to clamber up, and they cycle between left foot, right foot and beak as if their mouths were another limb. In fact, a new analysis of the forces climbing lovebirds exert reveals that this is precisely what they are doing. Somehow, a team of scientists wrote in the journal Proceedings of the Royal Society B on Wednesday, the birds and perhaps other parrot species have repurposed the muscles in their necks and heads so they can walk on their beaks, using them the way rock climbers use their arms. Climbing with a beak as a third limb is peculiar because third limbs generally are not something life on Earth is capable of producing, said Michael Granatosky, an assistant professor of anatomy at the New York Institute of Technology and an author of the new paper. “There is this very deep, deep set aspect of our biology that everything is bilateral” in much of the animal kingdom, he said. The situation makes it developmentally unlikely to grow an odd numbers of limbs for walking. Some animals have developed workarounds. Kangaroos use their tails as a fifth limb when hopping slowly, pushing off from the ground with their posteriors the same way they push with their feet. To see if parrots were using their beaks in a similar way, Dr. Granatosky and a graduate student, Melody Young, as well as their colleagues brought six rosy-faced lovebirds from a pet store into the lab. They had the birds climb up a surface that was fitted with a sensor to keep track of how much force they were exerting and in what directions. The scientists found that the propulsive force the birds applied through their beaks was similar to what they provided with their legs. What had started as a way to eat had transformed into a way to walk, with beaks as powerful as their limbs. © 2022 The New York Times Company

Keyword: Evolution
Link ID: 28336 - Posted: 05.25.2022

Nicola Davis Science correspondent Mice with spinal cord injuries have shown remarkable recovery after being given a drug initially developed for people with lung disease, researchers have revealed, saying the treatment could soon be tested on humans. It is thought there are about 2,500 new spinal cord injuries in the UK every year, with some of those affected experiencing full loss of movement as a result. Despite a number of promising areas of research, at present damage to the spinal cord is not reversible. Now researchers at the University of Birmingham say a drug called AZD1236, initially developed to treat chronic obstructive pulmonary disease in humans, has shown promise in mice with spinal cord compression injuries, a type of injury often associated with motor accidents in humans, but which is also linked to conditions such as osteoarthritis. A similar drug, called AZD3342, showed comparable benefits in rats. The results, published in the journal Clinical and Translational Medicine, suggested the drugs block the action of enzymes known as MMP-9 and MMP-12 that rise after spinal cord injury. The upshot was that swelling of the spinal cord was reduced, levels of proteins linked to inflammation and pain were lowered, and breakdown of the blood-spinal cord barrier was limited. Scarring of connective tissue was also reduced. The team said that compared with injured mice not given AZD1236, those given the drug for three days showed 85% improvement in movement and sensation six weeks after the spinal injury, while their nerve function was 80% of that seen in uninjured mice. Furthermore, the benefits were similar whether the drug was given immediately after spinal injury or 24 hours later. © 2022 Guardian News & Media Limited

Keyword: Regeneration
Link ID: 28333 - Posted: 05.21.2022

By Eiman Azim, Sliman Bensmaia, Lee E. Miller, Chris Versteeg Imagine you are playing the guitar. You’re seated, supporting the instrument’s weight across your lap. One hand strums; the other presses strings against the guitar’s neck to play chords. Your vision tracks sheet music on a page, and your hearing lets you listen to the sound. In addition, two other senses make playing this instrument possible. One of them, touch, tells you about your interactions with the guitar. Another, proprioception, tells you about your arms’ and hands’ positions and movements as you play. Together, these two capacities combine into what scientists call somatosensation, or body perception. Our skin and muscles have millions of sensors that contribute to somatosensation. Yet our brain does not become overwhelmed by the barrage of these inputs—or from any of our other senses, for that matter. You’re not distracted by the pinch of your shoes or the tug of the guitar strap as you play; you focus only on the sensory inputs that matter. The brain expertly enhances some signals and filters out others so that we can ignore distractions and focus on the most important details. How does the brain accomplish these feats of focus? In recent research at Northwestern University, the University of Chicago and the Salk Institute for Biological Studies in La Jolla, Calif., we have illuminated a new answer to this question. Through several studies, we have discovered that a small, largely ignored structure at the very bottom of the brain stem plays a critical role in the brain’s selection of sensory signals. The area is called the cuneate nucleus, or CN. Our research on the CN not only changes the scientific understanding of sensory processing, but it might also lay the groundwork for medical interventions to restore sensation in patients with injury or disease. © 2022 Scientific American

Keyword: Attention
Link ID: 28330 - Posted: 05.18.2022

By Gina Kolata The very treatments often used to soothe pain in the lower back, which the Centers for Disease Control and Prevention says is the most common type of pain, might cause it to last longer, according to a new study. Managing pain with steroids and nonsteroidal anti-inflammatory drugs, like ibuprofen, can actually turn a wrenched back into a chronic condition, the study found. Some medical experts urged caution in interpreting the results too broadly. The study did not use the gold standard for medical research, which would be a clinical trial in which people with back pain would be randomly assigned to take a nonsteroidal anti-inflammatory drug or a placebo and followed to see who developed chronic pain. Instead, it involved observations of patients, an animal study and an analysis of patients in a large database. “It’s intriguing but requires further study,” said Dr. Steven J. Atlas, director of primary care practice-based research and quality improvement at Massachusetts General Hospital. Dr. Bruce M. Vrooman, a pain specialist at Dartmouth Hitchcock Medical Center in New Hampshire, agreed, but also called the study “impressive in its scope” and said that if the results hold up in a clinical trial, it could “force reconsideration of how we treat acute pain.” Dr. Thomas Buchheit, director of the regenerative pain therapies program at Duke, had a different view. “People overuse the term ‘paradigm shift’, but this is absolutely a paradigm shift,” Dr. Buchheit said. “There is this unspoken rule: If it hurts, take an anti-inflammatory, and if it still hurts, put a steroid on it,” he added. “But,” he said, the study shows that “we have to think of healing and not suppression of inflammation.” Guidelines from professional medical societies already say that people with back pain should start with nondrug treatments like exercise, physical therapy, heat or massage. Those measures turn out to be as effective as pain-suppressing drugs, without the same side effects. © 2022 The New York Times Company

Keyword: Pain & Touch
Link ID: 28328 - Posted: 05.18.2022

By Ferris Jabr To hear more audio stories from publications like The New York Times, download Audm for iPhone or Android. On the evening of Oct. 10, 2006, Dennis DeGray’s mind was nearly severed from his body. After a day of fishing, he returned to his home in Pacific Grove, Calif., and realized he had not yet taken out the trash or recycling. It was raining fairly hard, so he decided to sprint from his doorstep to the garbage cans outside with a bag in each hand. As he was running, he slipped on a patch of black mold beneath some oak trees, landed hard on his chin, and snapped his neck between his second and third vertebrae. While recovering, DeGray, who was 53 at the time, learned from his doctors that he was permanently paralyzed from the collarbones down. With the exception of vestigial twitches, he cannot move his torso or limbs. “I’m about as hurt as you can get and not be on a ventilator,” he told me. For several years after his accident, he “simply laid there, watching the History Channel” as he struggled to accept the reality of his injury. Some time later, while at a fund-raising event for stem-cell research, he met Jaimie Henderson, a professor of neurosurgery at Stanford University. The pair got to talking about robots, a subject that had long interested DeGray, who grew up around his family’s machine shop. As DeGray remembers it, Henderson captivated him with a single question: Do you want to fly a drone? Henderson explained that he and his colleagues had been developing a brain-computer interface: an experimental connection between someone’s brain and an external device, like a computer, robotic limb or drone, which the person could control simply by thinking. DeGray was eager to participate, eventually moving to Menlo Park to be closer to Stanford as he waited for an opening in the study and the necessary permissions. In the summer of 2016, Henderson opened DeGray’s skull and exposed his cortex — the thin, wrinkled, outermost layer of the brain — into which he implanted two 4-millimeter-by-4-millimeter electrode arrays resembling miniature beds of nails. Each array had 100 tiny metal spikes that, collectively, recorded electric impulses surging along a couple of hundred neurons or so in the motor cortex, a brain region involved in voluntary movement. © 2022 The New York Times Company

Keyword: Robotics
Link ID: 28326 - Posted: 05.14.2022

By Laura Sanders Deep in the human brain, a very specific kind of cell dies during Parkinson’s disease. For the first time, researchers have sorted large numbers of human brain cells in the substantia nigra into 10 distinct types. Just one is especially vulnerable in Parkinson’s disease, the team reports May 5 in Nature Neuroscience. The result could lead to a clearer view of how Parkinson’s takes hold, and perhaps even ways to stop it. The new research “goes right to the core of the matter,” says neuroscientist Raj Awatramani of Northwestern University Feinberg School of Medicine in Chicago. Pinpointing the brain cells that seem to be especially susceptible to the devastating disease is “the strength of this paper,” says Awatramani, who was not involved in the study. Parkinson’s disease steals people’s ability to move smoothly, leaving balance problems, tremors and rigidity. In the United States, nearly 1 million people are estimated to have Parkinson’s. Scientists have known for decades that these symptoms come with the death of nerve cells in the substantia nigra. Neurons there churn out dopamine, a chemical signal involved in movement, among other jobs (SN: 9/7/17). But those dopamine-making neurons are not all equally vulnerable in Parkinson’s, it turns out. “This seemed like an opportunity to … really clarify which kinds of cells are actually dying in Parkinson’s disease,” says Evan Macosko, a psychiatrist and neuroscientist at Massachusetts General Hospital in Boston and the Broad Institute of MIT and Harvard. © Society for Science & the Public 2000–2022.

Keyword: Parkinsons
Link ID: 28320 - Posted: 05.07.2022

Perspective by Susan Berger As I faced a prophylactic double mastectomy in hopes of averting cancer, I had many questions for my surgeons — one of which was about pain. I was stunned when both my breast surgeon and plastic surgeon said that a nerve block would leave me pain-free for about three days, after which the worst of the pain would be over. Pectoralis nerve (PECS) blocks were developed to provide analgesia or pain relief for chest surgeries, including breast surgery. That is what happened. I went through the mastectomy Dec. 1 after learning I had the PALB2 gene mutation that carried a sharply elevated risk of breast cancer as well as a higher risk of ovarian and pancreatic cancers. I also had my fallopian tubes and ovaries removed in July. I had learned about the gene mutation in April 2021, when one of my daughters found out she was a carrier. As a 24-year breast cancer survivor and longtime health reporter, I was astonished that I had heard nothing about this mutation. I researched it and wrote “This Breast Cancer Gene Is Less Well Known, but Nearly as Dangerous” in August. After the double mastectomy, I also wrote about it for The Washington Post. Just as my surgeons at NorthShore University HealthSystem predicted, I was released from the hospital the same day as my surgery and remarkably pain-free. I took one Tramadol (a step down from stronger medications containing codeine) when I got home — only because it was suggested I take one pill. As I recovered, I only took Advil and Tylenol. The opioid epidemic is a major public health issue in the United States and nerve blocks could be a solution. According to a study published in the Journal of Clinical Medicine in 2021, 1 in 20 surgical patients will continue to use opioids beyond 90 days. “There is no association with magnitude of surgery, major versus minor, and the strongest predictor of continued use is surgical exposure,” the study states. © 1996-2022 The Washington Post

Keyword: Pain & Touch; Drug Abuse
Link ID: 28316 - Posted: 05.07.2022

By Jim Robbins TUCSON, Ariz. — In a small room in a building at the Arizona-Sonora Desert Museum, the invertebrate keeper, Emma Califf, lifts up a rock in a plastic box. “This is one of our desert hairies,” she said, exposing a three-inch-long scorpion, its tail arced over its back. “The largest scorpion in North America.” This captive hairy, along with a swarm of inch-long bark scorpions in another box, and two dozen rattlesnakes of varying species and sub- species across the hall, are kept here for the coin of the realm: their venom. Efforts to tease apart the vast swarm of proteins in venom — a field called venomics — have burgeoned in recent years, and the growing catalog of compounds has led to a number of drug discoveries. As the components of these natural toxins continue to be assayed by evolving technologies, the number of promising molecules is also growing. “A century ago we thought venom had three or four components, and now we know just one type of venom can have thousands,” said Leslie V. Boyer, a professor emeritus of pathology at the University of Arizona. “Things are accelerating because a small number of very good laboratories have been pumping out information that everyone else can now use to make discoveries.” She added, “There’s a pharmacopoeia out there waiting to be explored.” It is a striking case of modern-day scientific alchemy: The most highly evolved of natural poisons on the planet are creating a number of effective medicines with the potential for many more. One of the most promising venom-derived drugs to date comes from the deadly Fraser Island funnel web spider of Australia, which halts cell death after a heart attack. Blood flow to the heart is reduced after a heart attack, which makes the cell environment more acidic and leads to cell death. The drug, a protein called Hi1A, is scheduled for clinical trials next year. In the lab, it was tested on the cells of beating human hearts. It was found to block their ability to sense acid, “so the death message is blocked, cell death is reduced, and we see improved heart cell survival,” said Nathan Palpant, a researcher at the University of Queensland in Australia who helped make the discovery. © 2022 The New York Times Company

Keyword: Pain & Touch; Neurotoxins
Link ID: 28315 - Posted: 05.04.2022

Ellen Phiddian Tricyclic antidepressants have long been known to have more than one purpose: among other things, they can alleviate pain – particularly nerve pain. Recent research has finally established why these tricyclic antidepressants (TCAs) can help with nerve pain. The discovery could lead to the rapid development of pain relief medications that don’t include the side effects of TCAs. Nerve pain comes from a variety of sources – including cancer, diabetes, trauma, multiple sclerosis, and infections. These treatments could address a range of different types of nerve pain. It turns out the drugs inhibit a key protein in our nerves, called an N-type calcium channel. These N-type calcium channels are shaped like tiny gates, allowing positively charged calcium ions, or Ca2+, through them. This helps with the transmission of pain signals in the body. Researchers have long been keen to find things that “close” the gate of these calcium channels because that’s likely to have analgesic effects. Adjunct Professor Peter Duggan, a researcher with the CSIRO and senior collaborator on the project, says that he and his colleagues initially stumbled across TCAs from a very different direction: they were investigating the toxins of venomous marine cone snails. “A few of the components in that toxin are actually painkillers and they block these calcium ion channels very, very effectively,” says Duggan. The cone snail toxin has the potential to be very dangerous to people, as well as needing to be administered in an impractical way, so the researchers started looking at similar compounds that might have some of the same properties.

Keyword: Pain & Touch; Depression
Link ID: 28312 - Posted: 05.04.2022

By Helen Ouyang After an hour-and-a-half bus ride last November, Julia Monterroso arrived at a white Art Deco building in West Hollywood, just opposite a Chanel store and the Ivy, a restaurant famous for its celebrity sightings. Monterroso was there to see Brennan Spiegel, a gastroenterologist and researcher at Cedars-Sinai who runs one of the largest academic medical initiatives studying virtual reality as a health therapy. He started the program in 2015 after the hospital received a million-dollar donation from an investment banker on its board. Spiegel saw Monterroso in his clinic the week before and thought he might be able to help alleviate her symptoms. Monterroso is 55 and petite, with youthful bangs and hair clipped back by tiny jeweled barrettes. Eighteen months earlier, pain seized her lower abdomen and never went away. After undergoing back surgery in September to treat a herniated disc — and after the constant ache in her abdomen worsened — she had to stop working as a housecleaner. Eventually, following a series of tests that failed to reveal any clear cause, she landed in Spiegel’s office. She rated her pain an 8 on a 10-point scale, with 10 being the most severe. Chronic pain is generally defined as pain that has lasted three months or longer. It is one of the leading causes of long-term disability in the world. By some measures, 50 million Americans live with chronic pain, in part because the power of medicine to relieve pain remains woefully inadequate. As Daniel Clauw, who runs the Chronic Pain and Fatigue Research Center at the University of Michigan, put it in a 2019 lecture, there isn’t “any drug in any chronic-pain state that works in better than one out of three people.” He went on to say that nonpharmacological therapy should instead be “front and center in managing chronic pain — rather than opioids, or for that matter, any of our drugs.” Virtual reality is emerging as an unlikely tool for solving this intractable problem. The V.R. segment in health care alone, which according to some estimates is already valued at billions of dollars, is expected to grow by multiples of that in the next few years, with researchers seeing potential for it to help with everything from anxiety and depression to rehabilitation after strokes to surgeons strategizing where they will cut and stitch. In November, the Food and Drug Administration gave authorization for the first V.R. product to be marketed for the treatment of chronic pain. © 2022 The New York Times Company

Keyword: Pain & Touch; Vision
Link ID: 28304 - Posted: 04.27.2022

By Brittany Shammas and Timothy Bella William Husel, an Ohio doctor who was accused of killing 14 patients with what prosecutors described as “wildly excessive” doses of fentanyl between 2015 and 2018, was acquitted on all counts of murder Wednesday, concluding one of the most significant murder cases of its kind against a health-care professional. Husel, a onetime physician of the year trained at the Cleveland Clinic, faced one count of murder for each of the 14 critically ill patients he was accused of killing. The jury deliberated for seven days before finding him not guilty on all 14 counts in what was one of the largest murder trials in Ohio history. He had been charged with causing or hastening their deaths amid a period of lax oversight of fentanyl at Mount Carmel West, a Catholic hospital in Columbus. Husel would have faced life in prison with just one guilty verdict. While the synthetic opioid is significantly more powerful than morphine and has wreaked havoc on American streets, it can provide pain relief in medical settings that is crucial to end-of-life care. The alleged victims in the Ohio case suffered critical medical conditions including overdoses, cancer, strokes and internal bleeding. Prosecutors acknowledged that all were being kept alive on ventilators and that many of them were dying. “In truth, William Husel was an innocent man, and thank goodness the justice system prevailed,” Jose Baez, one of Husel’s defense attorneys, told reporters. The 46-year-old’s acquittal came after a two-month trial that triggered a debate on end-of-life medical care. Husel and Baez argued in the trial that the doctor offered comfort care for dying patients and was not trying to kill them. They pointed out that the doctor’s actions did not occur in secret — nurses were the ones to administer the doses — and alleged that hospital officials made Husel the villain after realizing the systemic failures at play. The fallout over the allegations at Mount Carmel West had repercussions: the firing of 23 employees; the resignation of the hospital’s chief executive, chief clinical officer and chief pharmacy officer; and Medicare and Medicaid funding for the institution was put in jeopardy. © 1996-2022 The Washington Post

Keyword: Pain & Touch; Drug Abuse
Link ID: 28297 - Posted: 04.23.2022

Liam Drew James Johnson hopes to drive a car again one day. If he does, he will do it using only his thoughts. In March 2017, Johnson broke his neck in a go-carting accident, leaving him almost completely paralysed below the shoulders. He understood his new reality better than most. For decades, he had been a carer for people with paralysis. “There was a deep depression,” he says. “I thought that when this happened to me there was nothing — nothing that I could do or give.” But then Johnson’s rehabilitation team introduced him to researchers from the nearby California Institute of Technology (Caltech) in Pasadena, who invited him to join a clinical trial of a brain–computer interface (BCI). This would first entail neurosurgery to implant two grids of electrodes into his cortex. These electrodes would record neurons in his brain as they fire, and the researchers would use algorithms to decode his thoughts and intentions. The system would then use Johnson’s brain activity to operate computer applications or to move a prosthetic device. All told, it would take years and require hundreds of intensive training sessions. “I really didn’t hesitate,” says Johnson. The first time he used his BCI, implanted in November 2018, Johnson moved a cursor around a computer screen. “It felt like The Matrix,” he says. “We hooked up to the computer, and lo and behold I was able to move the cursor just by thinking.” Johnson has since used the BCI to control a robotic arm, use Photoshop software, play ‘shoot-’em-up’ video games, and now to drive a simulated car through a virtual environment, changing speed, steering and reacting to hazards. “I am always stunned at what we are able to do,” he says, “and it’s frigging awesome.” © 2022 Springer Nature Limited

Keyword: Brain imaging; Robotics
Link ID: 28292 - Posted: 04.20.2022

ByKelly Servick An experimental pain drug that may offer an alternative to opioids has shown promise in two small clinical trials for acute pain, its developer announced today. Vertex Pharmaceuticals’s compound, called VX-548, outperformed a placebo in phase 2 trials for two types of postsurgical pain, the company said in a press release. The results pave the way for larger trials that could lead to regulatory approval. “This is a major advance in the effort to supersede opioids,” says John Wood, a neurobiologist at University College London who has studied the cellular channel that VX-548 targets. “These results are terrific, and the side effect profile is very good.” Opioids are powerful pain relievers, but they can cause side effects including slowed breathing, and they come with the potential for addiction. An epidemic of overdose deaths has prompted a hunt for safer alternatives. The new trials grew out of research into sodium channels on the surface of pain-sensing neurons, which let them fire electrical signals. One such channel, called Nav1.8, is crucial to relaying pain signals to the spinal cord from nerves throughout the body. People with genetic mutations that make Nav1.8 hyperactive can suffer pain even in the absence of injury. But relieving pain by blocking either Nav1.8 or another channel, Nav1.7, has proved difficult. One issue is their structure closely resembles those of other sodium channels, which regulate vital functions in the heart, muscles, and brain. To be safe, a compound needs to target the channel of interest and not accidentally target these other, critical channels. Vertex has spent years developing highly specific Nav1.8-blocking drugs, but it has abandoned previous candidates before they reached pivotal phase 3 trials. One drug, known as VX-150, succeeded in three phase 2 clinical studies but never advanced to larger ones, in part because its high dose might be impractical for clinical use. “We wanted to have higher potency,” explains Vertex Chief Scientific Officer David Altshuler. © 2022 American Association for the Advancement of Science.

Keyword: Pain & Touch
Link ID: 28265 - Posted: 04.02.2022

By Lisa Sanders, M.D. The 51-year-old man sat at his desk preparing for his next online meeting when he suddenly became aware of a familiar stiffness and exhaustion. Had he slept badly? Or was this the beginning of one of his strange episodes? As the symptoms worsened, he had his answer. He knew that when he started to feel this way, the only recourse was to get into bed before he got any weaker. As he made his way slowly down the hall, his legs felt heavy, as if he were wearing ankle weights. Just lifting them was real work. He passed his wife’s home office without a word. She knew just from looking at him that he would probably have to spend the rest of the day in bed. For much of their 30-year marriage, he had these strange spells; he would suddenly feel exhausted and weak and have to lie down. He couldn’t work. He was a software engineer, and any mental exertion was too much for him. Once the fatigue fully set in — maybe after the first hour or so — he couldn’t walk, couldn’t stand, couldn’t even sit up. It was as if his body was totally out of gas, worse than how it felt when he ran a marathon. He would lie in a dark room, too weak to even hold up a book and too tired to think. But by the next morning, he would usually be fine, brimming with energy and enthusiasm, like normal. It was so strange. After more than 20 years, they both had come to expect these episodes. For most of that time, the spells were infrequent, maybe once a month. But recently they became more frequent. The monthly episodes became weekly, then a couple of times a week. They often came, as they did that morning, out of nowhere. Just before leaving his office, he sent an email to the woman he was to meet online. Sorry, he wrote, I’m not feeling well. Could we reschedule? Seeing a Psychiatrist Over the years the man saw many doctors. They had their theories, but so far none panned out. A few were convinced that he had periodic paralysis, a disorder sometimes linked to thyroid disease, where patients become temporarily paralyzed by too much or too little potassium in the bloodstream. But his potassium was always normal, even during these episodes. © 2022 The New York Times Company

Keyword: Pain & Touch
Link ID: 28263 - Posted: 04.02.2022

Allison Whitten Every time you reach for your coffee mug, a neuroscientific mystery takes shape. Moments before you voluntarily extend your arm, thousands of neurons in the motor regions of your brain erupt in a pattern of electrical activity that travels to the spinal cord and then to the muscles that power the reach. But just prior to this massively synchronized activity, the motor regions in your brain are relatively quiet. For self-driven movements like reaching for your coffee, the “go” signal that tells the neurons precisely when to act — instead of the moment just before or after — has yet to be found. In a recent paper in eLife, a group of neuroscientists led by John Assad at Harvard Medical School finally reveals a key piece of the signal. It comes in the form of the brain chemical known as dopamine, whose slow ramping up in a region lodged deep below the cortex closely predicted the moment that mice would begin a movement — seconds into the future. Dopamine is commonly known as one of the brain’s neurotransmitters, the fast-acting chemical messengers that are shuttled between neurons. But in the new work, dopamine is acting as a neuromodulator. It’s a term for chemical messengers that slightly alter neurons to cause longer-lasting effects, including making a neuron more or less likely to electrically communicate with other neurons. This neuromodulatory tuning mechanism is perfect for helping to coordinate the activity of large populations of neurons, as dopamine is likely doing to help the motor system decide precisely when to make a movement. The new paper is one of the latest results to expand our knowledge of the crucial and varied roles that neuromodulators play in the brain. With recent advances in technology, neuroscientists can now view neuromodulators at work in networks that traverse the entire brain. The new findings are overturning some long-held views about these modulators adrift in the brain, and they’re revealing exactly how these molecules allow the brain to flexibly change its internal state amid ever-changing environments. All Rights Reserved © 2022

Keyword: Movement Disorders; Drug Abuse
Link ID: 28251 - Posted: 03.23.2022