Chapter 5. The Sensorimotor System
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By Kas Roussy, In a room at Sunnybrook Health Sciences Centre in Toronto, Brian Smith gives one last hug to his wife, Noreen. "You're doing really well, sweetheart," he says to her. Doctors have finished prepping the 76-year-old patient. She's clad in a blue hospital gown, her head has been shaved and metallic headgear is attached to her skull. Google's latest a spoon that steadies tremors New technology could help seniors stay independent longer She's ready to be wheeled into an MRI room, where she'll undergo a procedure that her doctors believe will revolutionize the way brain diseases are treated. Before that happens, Noreen leans into her husband for a kiss. "Best buddy," she whispers. Noreen Smith is among the three per cent of the Canadian population who suffer from a nervous system disorder called essential tremor. It causes uncontrollable shaking, most often in a person's hands. Smith noticed the first signs when she was 33. "It started developing in my dominant hand, which is my right hand," she said the day before her medical procedure from her home in Bobcaygeon, Ont. She went to a specialist who delivered the diagnosis: essential tremor. Media placeholder Smith ‘really, really excited’ about treatment’s potential0:48 Just as shocking was what he said next, alluding to a high-profile actor who had the condition. "This particular person wasn't terribly helpful because he said: 'Do you happen to know Katharine Hepburn? I'm going to give you some medication, and you can go home and get used to the idea that eventually you're going to end up looking like Katharine Hepburn.' I was devastated," says Smith. Medication helped for the first few years. But Smith's tremor was still severe and like others who suffer from this disorder, the shaking worsened with simple movements or everyday tasks like applying makeup or pouring a glass of water. ©2016 CBC/Radio-Canada.
Keyword: Movement Disorders
Link ID: 22603 - Posted: 08.25.2016
Neuroscience News Researchers have identified a brain mechanism that could be a drug target to help prevent tolerance and addiction to opioid pain medication, such as morphine, according to a study by Georgia State University and Emory University. The findings, published in the Nature journal Neuropsychopharmacology in August, show for the first time that morphine tolerance is due to an inflammatory response produced in the brain. This brain inflammation is caused by the release of cytokines, chemical messengers in the body that trigger an immune response, similar to a viral infection. Researchers’ results show blocking a particular cytokine eliminated morphine tolerance, and they were able to reduce the dose of morphine required to alleviate pain by half. “These results have important clinical implications for the treatment of pain and also addiction,” said Lori Eidson, lead author and a graduate student in the laboratory of Dr. Anne Murphy in the Neuroscience Institute of Georgia State. “Until now, the precise underlying mechanism for opioid tolerance and its prevention have remained unknown.” Over 67 percent of the United States population will experience chronic pain at some point in their lives. Morphine is the primary drug used to manage severe and chronic pain, with 3 to 4 percent of adults in the U.S. receiving long-term opioid therapy. However, tolerance to morphine, defined as a decrease in pain relief over time, significantly impedes treatment for about 60 percent of patients. Long-term treatment with opioids is associated with increased risk of abuse, dependence and fatal overdoses.
Laura Sanders For some people, fentanyl can be a life-saver, easing profound pain. But outside of a doctor’s office, the powerful opioid drug is also a covert killer. In the last several years, clandestine drugmakers have begun experimenting with this ingredient, baking it into drugs sold on the streets, most notably heroin. Fentanyl and closely related compounds have “literally invaded the entire heroin supply,” says medical toxicologist Lewis Nelson of New York University Langone Medical Center. Fentanyl is showing up in other drugs, too. In San Francisco’s Bay Area in March, high doses of fentanyl were laced into counterfeit versions of the pain pill Norco. In January, fentanyl was found in illegal pills sold as oxycodone in New Jersey. And in late 2015, fentanyl turned up in fake Xanax pills in California. This ubiquitous recipe-tinkering makes it impossible for users to know whether they’re about to take drugs mixed with fentanyl. And that uncertainty has proved deadly. Fentanyl-related deaths are rising sharply in multiple areas. National numbers are hard to come by, but in many regions around the United States, fentanyl-related fatalities have soared in recent years. Maryland is one of the hardest-hit states. From 2007 to 2012, the number of fentanyl-related deaths hovered around 30 per year. By 2015, that number had grown to 340. A similar rise is obvious in Connecticut, where in 2012, there were 14 fentanyl-related deaths. In 2015, that number was 188. |© Society for Science & the Public 2000 - 2016.
Researchers may have discovered a method of detecting changes in the eye which could identify Parkinson's disease before its symptoms develop. Scientists at University College London (UCL) say their early animal tests could lead to a cheap and non-invasive way to spot the disease. Parkinson's affects 1 in 500 people and is the second most common neurodegenerative disease worldwide. The charity Parkinson's UK welcomed the research as a "significant step". The researchers examined rats and found that changes could be seen at the back of their eyes before visible symptoms occurred. Professor Francesca Cordeiro who led the research said it was a "potentially revolutionary breakthrough in the early diagnosis and treatment of one of the world's most debilitating diseases". "These tests mean we might be able to intervene much earlier and more effectively treat people with this devastating condition." Symptoms of Parkinson's include tremors and muscle stiffness, slowness of movement and a reduced quality of life. These symptoms usually only emerge after brain cells have been damaged. But there is currently no brain scan, or blood test, that can definitively diagnose Parkinson's disease. Parkinson's does not directly cause people to die, but symptoms do get worse over time. © 2016 BBC
Link ID: 22577 - Posted: 08.20.2016
Dean Burnett A lot of people, when they travel by car, ship, plane or whatever, end up feeling sick. They’re fine before they get into the vehicle, they’re typically fine when they get out. But whilst in transit, they feel sick. Particularly, it seems, in self-driving cars. Why? One theory is that it’s due to a weird glitch that means your brain gets confused and thinks it’s being poisoned. This may seem surprising; not even the shoddiest low-budget airline would get away with pumping toxins into the passengers (airline food doesn’t count, and that joke is out of date). So where does the brain get this idea that it’s being poisoned? Despite being a very “mobile” species, humans have evolved for certain types of movement. Specifically, walking, or running. Walking has a specific set of neurological processes tied into it, so we’ve had millions of years to adapt to it. Think of all the things going on in your body when you’re walking, and how the brain would pick up on these. There’s the steady thud-thud-thud and pressure on your feet and lower legs. There’s all the signals from your muscles and the movement of your body, meaning the motor cortex (which controls conscious movement of muscles) and proprioception (the sense of the arrangement of your body in space, hence you can know, for example, where your arm is behind your back without looking at it directly) are all supplying particular signals. © 2016 Guardian News and Media Limited
Angus Chen Once people realized that opioid drugs could cause addiction and deadly overdoses, they tried to use newer forms of opioids to treat the addiction to its parent. Morphine, about 10 times the strength of opium, was used to curb opium cravings in the early 19th century. Codeine, too, was touted as a nonaddictive drug for pain relief, as was heroin. Those attempts were doomed to failure because all opioid drugs interact with the brain in the same way. They dock to a specific neural receptor, the mu-opioid receptor, which controls the effects of pleasure, pain relief and need. Now scientists are trying to create opioid painkillers that give relief from pain without triggering the euphoria, dependence and life-threatening respiratory suppression that causes deadly overdoses. That wasn't thought possible until 2000, when a scientist named Laura Bohn found out something about a protein called beta-arrestin, which sticks to the opioid receptor when something like morphine activates it. When she gave morphine to mice that couldn't make beta-arrestin, they were still numb to pain, but a lot of the negative side effects of the drug were missing. They didn't build tolerance to the drug. At certain dosages, they had less withdrawal. Their breathing was more regular, and they weren't as constipated as normal mice on morphine. Before that experiment, scientists thought the mu-opioid receptor was a simple switch that flicked all the effects of opioids on or off together. Now it seems they could be untied. © 2016 npr
By Robin Wylie Scientists have been searching for a genetic explanation for athletic ability for decades. So far their efforts have focused largely on genes related to physical attributes, such as muscular function and aerobic efficiency. But geneticists have also started to investigate the neurologicalbasis behind what makes someone excel in sports—and new findings implicate dopamine, a neurotransmitter responsible for the feelings of reward and pleasure. Dopamine is also involved in a host of other mental functions, including the ability to deal with stress and endure pain. Consequently, the new research supports the idea that the mental—not just the physical—is what sets elite athletes above the rest. In an effort to piece together what makes a great athlete great, researchers at the University of Parma in Italy collected DNA from 50 elite athletes (ones who had achieved top scores at an Olympic Games or other international competition) and 100 nonprofessional athletes (ones who played sports regularly, but below competitive level). They then compared four genes across the two groups that had previously been suggested as linked to athletic ability: one related to muscle development, one involved with transporting dopamine in the brain, another that regulates levels of cerebral serotonin and one involved in breaking down neurotransmitters. The researchers found a significant genetic difference between the two groups in only one of the genes: the one involved in transporting dopamine. Two particular variants of this gene (called the dopamine active transporter, or DAT) were significantly more common among the elite athletes than in the control group. One variant was almost five times more prevalent in the elite group (occurring in 24 percent of the elites versus 5 percent of the rest); the other variant was approximately 1.7 times more prevalent (51 percent versus 30 percent). The results were published in Journal of Biosciences. © 2016 Scientific American
Neuroscientists peered into the brains of patients with Parkinson’s disease and two similar conditions to see how their neural responses changed over time. The study, funded by the NIH’s Parkinson’s Disease Biomarkers Program and published in Neurology, may provide a new tool for testing experimental medications aimed at alleviating symptoms and slowing the rate at which the diseases damage the brain. “If you know that in Parkinson’s disease the activity in a specific brain region is decreasing over the course of a year, it opens the door to evaluating a therapeutic to see if it can slow that reduction,” said senior author David Vaillancourt, Ph.D., a professor in the University of Florida’s Department of Applied Physiology and Kinesiology. “It provides a marker for evaluating how treatments alter the chronic changes in brain physiology caused by Parkinson’s.” Parkinson’s disease is a neurodegenerative disorder that destroys neurons in the brain that are essential for controlling movement. While many medications exist that lessen the consequences of this neuronal loss, none can prevent the destruction of those cells. Clinical trials for Parkinson’s disease have long relied on observing whether a therapy improves patients’ symptoms, but such studies reveal little about how the treatment affects the underlying progressive neurodegeneration. As a result, while there are treatments that improve symptoms, they become less effective as the neurodegeneration advances. The new study could remedy this issue by providing researchers with measurable targets, called biomarkers, to assess whether a drug slows or even stops the progression of the disease in the brain. “For decades, the field has been searching for an effective biomarker for Parkinson’s disease,” said Debra Babcock, M.D., Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS).
By Helen Thomson Take a walk while I look inside your brain. Scientists have developed the first wearable PET scanner – allowing them to capture the inner workings of the brain while a person is on the move. The team plans to use it to investigate the exceptional talents of savants, such as perfect memory or exceptional mathematical skill. All available techniques for scanning the deeper regions of our brains require a person to be perfectly still. This limits the kinds of activities we can observe the brain doing, but the new scanner will enable researchers to study brain behaviour in normal life, as well providing a better understanding of the tremors of Parkinson’s disease, and the effectiveness of treatments for stroke. Positron emission tomography scanners track radioactive tracers, injected into the blood, that typically bind to glucose, the molecule that our cells use for energy. In this way, the scanners build 3D images of our bodies, enabling us to see which brain areas are particularly active, or where tumours are guzzling glucose in the body. To adapt this technique for people who are moving around, Stan Majewski at West Virginia University in Morgantown and his colleagues have constructed a ring of 12 radiation detectors that can be placed around a person’s head. This scanner is attached to the ceiling by a bungee-cord contraption, so that the wearer doesn’t feel the extra weight of the scanner. © Copyright Reed Business Information Ltd
Keyword: Brain imaging
Link ID: 22557 - Posted: 08.13.2016
David R. Jacobs, We all know that exercise improves our physical fitness, but staying in shape can also boost our brainpower. We are not entirely sure how, but evidence points to several explanations. First, to maintain normal cognitive function, the brain requires a constant supply of oxygen and other chemicals, delivered via its abundant blood vessels. Physical exercise—and even just simple activities such as washing dishes or vacuuming—helps to circulate nutrient-rich blood efficiently throughout the body and keeps the blood vessels healthy. Exercise increases the creation of mitochondria—the cellular structures that generate and maintain our energy—both in our muscles and in our brain, which may explain the mental edge we often experience after a workout. Studies also show that getting the heart rate up enhances neurogenesis—the ability to grow new brain cells—in adults. Regardless of the mechanism, mounting evidence is revealing a robust relation between physical fitness and cognitive function. In our 2014 study, published in Neurology, we found that physical activity has an extensive, long-lasting influence on cognitive performance. We followed 2,747 healthy people between the ages of 18 and 30 for 25 years. In 1985 we evaluated their physical fitness using a treadmill test: the participants walked up an incline that became increasingly steep every two minutes. On average, they walked for about 10 minutes, reaching 3.4 miles per hour at an 18 percent incline (a fairly steep hill). Low performers lasted for only seven minutes and high performers for about 13 minutes. A second treadmill test in 2005 revealed that our participants' fitness levels had declined with age, as would be expected, but those who were in better shape in 1985 were also more likely to be fit 20 years later. © 2016 Scientific American
Link ID: 22555 - Posted: 08.13.2016
Tim Radford Eight paraplegics – some of them paralysed for more than a decade by severe spinal cord injury – have been able to move their legs and feel sensation, after help from an artificial exoskeleton, sessions using virtual reality (VR) technology and a non-invasive system that links the brain with a computer. In effect, after just 10 months of what their Brazilian medical team call “brain training” they have been able to make a conscious decision to move and then get a response from muscles that have not been used for a decade. Of the octet, one has been able to leave her house and drive a car. Another has conceived and delivered a child, feeling the contractions as she did so. The extent of the improvements was unexpected. The scientists had intended to exploit advanced computing and robotic technology to help paraplegics recover a sense of control in their lives. But their patients recovered some feeling and direct command as well. The implication is that even apparently complete spinal cord injury might leave some connected nerve tissue that could be reawakened after years of inaction. The patients responded unevenly, but all have reported partial restoration of muscle movement or skin sensation. Some have even recovered visceral function and are now able to tell when they need the lavatory. And although none of them can walk unaided, one woman has been able to make walking movements with her legs, while suspended in a harness, and generate enough force to make a robot exoskeleton move. © 2016 Guardian News and Media Limited
In a global study of myasthenia gravis, an autoimmune disease that causes muscle weakness and fatigue, researchers found that surgical removal of an organ called the thymus reduced patients’ weakness, and their need for immunosuppressive drugs. The study, published in the New England Journal of Medicine, was partially funded by the National Institutes of Health. “Our results support the idea that thymectomy is a valid treatment option for a major form of myasthenia gravis,” said Gil Wolfe, M.D., Professor and Irvin and Rosemary Smith Chair of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, New York, and a leader of the study. The Thymectomy Trial in Non-Thymomatous Myasthenia Gravis Patients Receiving Prednisone (MGTX) was a randomized, controlled study conducted on 126 patients aged 18-65 between 2006 and 2012. The researchers compared the combination of surgery and immunosuppression with the drug prednisone with prednisone treatment alone. They performed extended transternal thymectomies on 57 patients. This major surgical procedure aims to remove most of the thymus, which requires opening of a patient’s chest. On average the researchers found that the combination of surgery and prednisone treatment reduced overall muscle weakness more than prednisone treatment alone. After 36 months of prednisone treatment, both groups of patients had better QMG scores, a measure of muscle strength. Scores for the patients who had thymectomies and prednisone were 2.84 points better than patients who were on prednisone alone.
By ABBY GOODNOUGH TUSCALOOSA, Ala. — Roslyn Lewis was at work at a dollar store here in Tuscaloosa, pushing a heavy cart of dog food, when something popped in her back: an explosion of pain. At the emergency room the next day, doctors gave her Motrin and sent her home. Her employer paid for a nerve block that helped temporarily, numbing her lower back, but she could not afford more injections or physical therapy. A decade later, the pain radiates to her right knee and remains largely unaddressed, so deep and searing that on a recent day she sat stiffly on her couch, her curtains drawn, for hours. The experience of African-Americans, like Ms. Lewis, and other minorities illustrates a problem as persistent as it is complex: Minorities tend to receive less treatment for pain than whites, and suffer more disability as a result. While an epidemic of prescription opioid abuse has swept across the United States, African-Americans and Hispanics have been affected at much lower rates than whites. Researchers say minority patients use fewer opioids, and they offer a thicket of possible explanations, including a lack of insurance coverage and a greater reluctance among members of minority groups to take opioid painkillers even if they are prescribed. But the researchers have also found evidence of racial bias and stereotyping in recognizing and treating pain among minorities, particularly black patients. “We’ve done a good job documenting that these disparities exist,” said Salimah Meghani, a pain researcher at the University of Pennsylvania. “We have not done a good job doing something about them.” Dr. Meghani’s 2012 analysis of 20 years of published research found that blacks were 34 percent less likely than whites to be prescribed opioids for conditions such as backaches, abdominal pain and migraines, and 14 percent less likely to receive opioids for pain from traumatic injuries or surgery. © 2016 The New York Times Company
Meghan Rosen Exercise may not erase old memories, as some studies in animals have previously suggested. Running on an exercise wheel doesn’t make rats forgetprevious trips through an underwater maze, Ashok Shetty and colleagues report August 2 in the Journal of Neuroscience. Exercise or not, four weeks after learning how to find a hidden platform, rats seem to remember the location just fine, the team found. The results conflict with two earlier papers that show that running triggers memory loss in some rodents by boosting the birth of new brain cells. Making new brain cells rejiggers memory circuits, and that can make it hard for animals to remember what they’ve learned, says Paul Frankland, a neuroscientist at the Hospital for Sick Children in Toronto. He has reported this phenomenon in mice, guinea pigs and degus (SN: 6/14/14, p. 7). Maybe rats are the exception, he says, “but I’m not convinced.” In 2014, Frankland and colleagues reported that brain cell genesis clears out fearful memories in three different kinds of rodents. Two years later, Frankland’s team found similar results with spatial memories. After exercising, mice had trouble remembering the location of a hidden platform in a water maze, the team reported in February in Nature Communications. Again, Frankland and colleagues pinned the memory wipeout on brain cell creation — like a chalkboard eraser that brushes away old information. The wipe seemed to clear the way for new memories to form. Shetty, a neuroscientist at Texas A&M Health Science Center in Temple, wondered if the results held true in rats, too. “Rats are quite different from mice,” he says. “Their biology is similar to humans.” |© Society for Science & the Public 2000 - 2016. All rights reserved.
Keyword: Learning & Memory
Link ID: 22510 - Posted: 08.03.2016
By Libby Copeland Don’t get him wrong: Dean Burnett loves the brain as much as the next neuroscientist. But if he’s being honest, it’s “really quite rubbish in a lot of ways,” he says. In his new book, Idiot Brain, Burnett aims to take our most prized organ down a peg or two. Burnett is most fascinated by the brain’s tendency to trip us up when it’s just trying to help. His book explores many of these quirks: How we edit our own memories to make ourselves look better without knowing it; how anger persuades us we can take on a bully twice our size; and what may cause us to feel like we’re falling and jerk awake just as we’re falling asleep. (It could have something to do with our ancestors sleeping in trees.) We caught up with Burnett, who is also a science blogger for The Guardian and a stand-up comic, to ask him some of our everyday questions and frustrations with neuroscience. Why is it that we get motion sickness when we’re traveling in a plane or a car? We haven’t evolved, obviously, to ride in vehicles; that’s a very new thing in evolutionary terms. So the main theory as to why we get motion sickness is that it’s essentially a conflict in the senses that are being relayed to the subcortical part of the brain where the senses are integrated together. The body and the muscles are saying we are still. Your eyes are saying the environment is still. The balance sense in the ears are detecting movement. The brain is getting conflicting messages from the fundamental senses, and in evolutionary terms there’s only one thing that can cause that, which is a neurotoxin. And as a result the brain thinks it’s been poisoned and what do you do when you’ve been poisoned? Throw up.
Link ID: 22508 - Posted: 08.03.2016
Nisha Gaind Most people in the United States are more worried than enthusiastic about the prospect of scientific advances such as gene editing and brain-chip implants, a survey of thousands suggests. The Pew Research Center in Washington DC asked 4,726 US people about the potential uses of three biomedical technologies that it classified as ‘potential human enhancement’: gene editing to reduce disease risk in babies; brain implants to enhance concentration and brain processes, and transfusions of synthetic blood to improve strength and stamina. (None of these procedures are a reality, but the underlying technologies are being researched.) Those who took the survey were overwhelmingly wary about all of the ideas. In each case, more than 60% said that they would be worried about the technologies, and fewer than half expressed enthusiasm about them — with the prospect of brain implants prompting the most concern and least excitement. More than 70% thought that the procedures would become available before they were well understood or officially deemed safe. Around one-third thought the technologies were morally unacceptable, and about 70% were concerned that such enhancements would widen social divides — for instance, because initially only wealthy people would be able to afford them. © 2016 Macmillan Publishers Limited
Link ID: 22505 - Posted: 08.02.2016
Ian Sample and Nicky Woolf When Bill Gates pulled on a red and white-striped cord to upturn a bucket of iced water positioned delicately over his head, the most immediate thought for many was not, perhaps, of motor neurone disease. But the ice bucket challenge, the charity campaign that went viral in the summer of 2014 and left scores of notable persons from Gates and Mark Zuckerberg to George W. Bush and Anna Wintour shivering and drenched, has paid off in the most spectacular way. Dismissed by some at the time as “slacktivism” - an exercise that appears to do good while achieving very little - the ice bucket challenge raised more than $115m (£88m) for motor neurone disease in a single month. Now, scientists funded with the proceeds have discovered a gene variant associated with the condition. In the near term the NEK1 gene variant, described in the journal Nature Genetics this week, will help scientists understand how the incurable disorder, known also as Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrig’s disease, takes hold. Once the mechanisms are more clearly elucidated, it may steer researchers on a path towards much-needed treatments. The work may never have happened were it not for the curious appeal of the frozen water drenchings. The research grants that scientists are awarded do not get close to the €4m the study required. Instead, Project MinE, which aims to unravel the genetic basis of the disease and ultimately find a cure, was funded by the ALS Association through ice bucket challenge donations. © 2016 Guardian News and Media Limited
By Gretchen Reynolds Learning requires more than the acquisition of unfamiliar knowledge; that new information or know-how, if it’s to be more than ephemeral, must be consolidated and securely stored in long-term memory. Mental repetition is one way to do that, of course. But mounting scientific evidence suggests that what we do physically also plays an important role in this process. Sleep, for instance, reinforces memory. And recent experiments show that when mice and rats jog on running wheels after acquiring a new skill, they learn much better than sedentary rodents do. Exercise seems to increase the production of biochemicals in the body and brain related to mental function. Researchers at the Donders Institute for Brain, Cognition and Behavior at Radboud University in the Netherlands and the University of Edinburgh have begun to explore this connection. For a study published this month in Current Biology, 72 healthy adult men and women spent about 40 minutes undergoing a standard test of visual and spatial learning. They observed pictures on a computer screen and then were asked to remember their locations. Afterward, the subjects all watched nature documentaries. Two-thirds of them also exercised: Half were first put through interval training on exercise bicycles for 35 minutes immediately after completing the test; the others did the same workout four hours after the test. Two days later, everyone returned to the lab and repeated the original computerized test while an M.R.I. machine scanned their brain activity. Those who exercised four hours after the test recognized and recreated the picture locations most accurately. Their brain activity was subtly different, too, showing a more consistent pattern of neural activity. The study’s authors suggest that their brains might have been functioning more efficiently because they had learned the patterns so fully. But why delaying exercise for four hours was more effective than an immediate workout remains mysterious. By contrast, rodents do better in many experiments if they work out right after learning. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22486 - Posted: 07.28.2016
By KATHARINE Q. SEELYE PORTLAND, Me. — A woman in her 30s was sitting in a car in a parking lot here last month, shooting up heroin, when she overdosed. Even after the men she was with injected her with naloxone, the drug that reverses opioid overdoses, she remained unconscious. They called 911. Firefighters arrived and administered oxygen to improve her breathing, but her skin had grown gray and her lips had turned blue. As she lay on the asphalt, the paramedics slipped a needle into her arm and injected another dose of naloxone. In a moment, her eyes popped open. Her pupils were pinpricks. She was woozy and disoriented, but eventually got her bearings as paramedics put her on a stretcher and whisked her to a hospital. Every day across the country, hundreds, if not thousands, of people who overdose on opioids are being brought back to life with naloxone. Hailed as a miracle drug by many, it carries no health risk; it cannot be abused and, if given mistakenly to someone who has not overdosed on opioids, does no harm. More likely, it saves a life. As a virulent opioid epidemic continues to ravage the country, with 78 people in the United States dying of overdoses every day, naloxone’s use has increasingly moved out of medical settings, where it has been available since the 1970s, and into the homes and hands of the general public. But naloxone, also known by the brand name Narcan, has also had unintended consequences. Critics say that it gives drug users a safety net, allowing them to take more risks as they seek higher highs. Indeed, many users overdose more than once, some multiple times, and each time, naloxone brings them back. © 2016 The New York Times Company
By Maia Szalavitz When a family member, spouse or other loved one develops an opioid addiction — whether to pain relievers like Vicodin or to heroin — few people know what to do. Faced with someone who appears to be driving heedlessly into the abyss, families often fight, freeze or flee, unable to figure out how to help. Families are sometimes overwhelmed with conflicting advice about what should come next. Much of the advice given by treatment groups and programs ignores what the data says in a similar way that anti-vaccination or climate skeptic websites ignore science. The addictions field is neither adequately regulated nor effectively overseen. There are no federal standards for counseling practices or rehab programs. In many states, becoming an addiction counselor doesn’t require a high school degree or any standardized training. “There’s nothing professional about it, and it’s not evidence-based,” said Dr. Mark Willenbring, the former director of treatment research at the National Institute on Alcohol Abuse and Alcoholism, who now runs a clinic that treats addictions. Consequently, families are often given guidance that bears no resemblance to what the research evidence shows — and patients are commonly subjected to treatment that is known to do harm. People who are treated as experts firmly proclaim that they know what they are doing, but often turn out to base their care entirely on their own personal and clinical experience, not data. “Celebrity Rehab with Dr. Drew,” which many people see as an example of the best care available, for instance, used an approach that is not known to be effective for opioid addiction. More than 13 percent of its participants died after treatment,1 mainly of overdoses that could potentially have been prevented with evidence-based care. Unethical practices such as taking kickbacks for patient referrals are also rampant.