Chapter 5. The Sensorimotor System
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By Roni Caryn Rabin Sixty-five million Americans suffer from chronic lower back pain, and many feel they have tried it all: physical therapy, painkillers, shots. Now a new study reports many people may find relief with a form of meditation that harnesses the power of the mind to manage pain. The technique, called mindfulness-based stress reduction, involves a combination of meditation, body awareness and yoga, and focuses on increasing awareness and acceptance of one’s experiences, whether they involve physical discomfort or emotional pain. People with lower back pain who learned the meditation technique showed greater improvements in function compared to those who had cognitive behavioral therapy, which has been shown to help ease pain, or standard back care. Participants assigned to meditation or cognitive behavior therapy received eight weekly two-hour sessions of group training in the techniques. After six months, those learning meditation had an easier time doing things like getting up out of a chair, going up the stairs and putting on their socks, and were less irritable and less likely to stay at home or in bed because of pain. They were still doing better a year later. The findings come amid growing concerns about opioid painkillers and a surge of overdose deaths involving the drugs. At the beginning of the trial, 11 percent of the participants said they had used an opioid within the last week to treat their pain, and they were allowed to continue with their usual care throughout the trial. “This new study is exciting, because here’s a technique that doesn’t involve taking any pharmaceutical agents, and doesn’t involve the side effects of pharmaceutical agents,” said Dr. Madhav Goyal of Johns Hopkins University School of Medicine, who co-wrote an editorial accompanying the paper. © 2016 The New York Times Company
Results from a new study, funded in part by the National Center for Complementary and Integrative Health, demonstrate that mindfulness meditation works on a different pain pathway in the brain than opioid pain relievers. The researchers noted that because opioid and non-opioid mechanisms of pain relief interact synergistically, the results of this study suggest that combining mindfulness-based and pharmacologic/nonpharmacologic pain-relieving approaches that rely on opioid signaling may be particularly effective in treating pain. Previous research has shown that mindfulness meditation helps relieve pain, but researchers have been unclear about how the practice induces pain relief — specifically, if meditation is associated with the release of naturally occurring opiates. Researchers recorded pain reports in 78 healthy adults during meditation or a non-meditation control in response to painful heat stimuli and intravenous administration of the opioid antagonist naloxone (a drug that blocks the transmission of opioid activity) or placebo saline. Participants were randomized to one of four treatment groups: 1) meditation plus naloxone; 2) control plus naloxone; 3) meditation plus saline; or 4) control plus saline. People in the control groups were instructed to “close your eyes and relax until the end of the experiment.” The researchers found that participants who meditated during saline administration had significantly lower pain intensity and unpleasantness ratings compared to those who did not meditate while receiving saline. Importantly, data from the meditation plus naloxone group showed that naloxone did not block meditation’s pain-relieving effects. No significant differences in reductions of pain intensity or pain unpleasantness were seen between the meditation plus naloxone and the meditation plus saline groups. Participants who meditated during naloxone administration also had significantly greater reductions in pain intensity and unpleasantness than the control groups.
Keyword: Pain & Touch
Link ID: 22006 - Posted: 03.19.2016
BRAINS get data about the world through senses – sight, hearing, taste, smell and touch. In a lab in North Carolina, a group of rats is getting an extra one. Thanks to implants in their brains, they have learned to sense and react to infrared light. The rats show the brain’s ability to process unfamiliar data– an early step towards augmenting the human brain. Miguel Nicolelis of Duke University School of Medicine is leading the experiment. His team implanted four clusters of electrodes in the rats’ barrel cortex – the part of the brain that handles whisker sensation (doi.org/bdb6). Each cluster is connected to a sensor that converts infrared light into an electrical signal. Feeding stations placed at the four corners of the rats’ cage take turns emitting infrared signals that guide the rats to them, releasing a reward only when the rats press a button on the feeding station that is emiting the infrared signal. In an older, single sensor version of the experiment, it took the rats one month to adapt. With four sensors, it took them just three days. “This is a truly remarkable demonstration of the plasticity of the mammalian brain,” says Christopher James of the University of Warwick, UK. All the extra data that goes into making the rats’ new sense doesn’t appear to diminish their original senses. “The results show that nature has apparently designed the adult mammalian brain with the possibility of upgrades, and Nicolelis’ team is leading the way showing how to do it,” says Andrea Stocco of the University of Washington in Seattle. © Copyright Reed Business Information Ltd.
The CDC recommends non-opioid therapy, including exercise and over-the-counter pain medications, as the preferred treatment for chronic pain. It says opioids should only be prescribed — at the lowest effective dosage possible — when the benefits from pain reduction and bodily function outweigh the risks. In 2014, American doctors wrote nearly 200 million prescriptions for opioid painkillers, while deaths linked to the drugs climbed to roughly 19,000 — the highest number on record. The number of Canadians who die every year from opioids is not readily known — the Canadian Centre on Substance Abuse does not track the statistics — but Toronto physician Nav Persaud told CBC News in 2014 that more than 1,000 Canadians die from painkillers every year. A 2012 study says one in eight deaths among young adults age 25 to 34 in Ontario and one out of every 170 deaths in the province as a whole are opioid overdoses. One in four people who entered a withdrawal management program at St. Joseph's Healthcare in Hamilton, Ont., were opioid patients in 2012, up from one in ten in 2002. Other studies have cast doubt on the effectiveness of opioids on chronic pain, raising questions on whether its limited long-term effects are worth the harmful risks. "The science is clear," CDC director Tom Frieden said Tuesday. "For the vast majority of patients, the known and often fatal risks [of opioids] far outweigh the proven and transient benefits." ©2016 CBC/Radio-Canada.
By Sandra G. Boodman Kim Pace was afraid he was dying. In six months he had lost more than 30 pounds because a terrible stabbing sensation on the left side of his face made eating or drinking too painful. Brushing his teeth was out of the question and even the slightest touch triggered waves of agony and a shocklike pain he imagined was comparable to electrocution. Painkillers, even morphine, brought little relief. Unable to work and on medical leave from his job as a financial consultant for a bank, Pace, then 59, had spent the first half of 2012 bouncing among specialists in his home state of Pennsylvania, searching for help from doctors who disagreed about the nature of his illness. Some thought his searing pain might be the side effect of a drug he was taking. Others suspected migraines, a dental problem, mental illness, or an attempt to obtain painkillers. Even after a junior doctor made what turned out to be the correct diagnosis, there was disagreement among specialists about its accuracy or how to treat Pace. His wife, Carol, a nurse, said she suspects that the couple’s persistence and propensity to ask questions led her husband to be branded “a difficult case” — the kind of patient whom some doctors avoid. And on top of that, a serious but entirely unrelated disorder further muddied the diagnostic picture. So on July 17, 2012, when Pace told his wife he thought he was dying, she fired off an emotional plea for help to the office of a prominent specialist in Baltimore. “I looked at Kim and it hit me: He was going to die,” she said. “He was losing weight and his color was ashen” and doctors were “blowing him off. I thought, ‘Okay, that’s it,’ and the nurse in me took over.”
Sara Reardon Elite ski jumpers rely on extreme balance and power to descend the steep slopes that allow them to reach up to 100 kilometres per hour. But the US Ski and Snowboard Association (USSA) is seeking to give its elite athletes an edge by training a different muscle: the mind. Working with Halo Neuroscience in San Francisco, California, the sports group is testing whether stimulating the brain with electricity can improve the performance of ski jumpers by making it easier for them to hone their skills. Other research suggests that targeted brain stimulation can reduce an athlete’s ability to perceive fatigue1. Such technologies could aid recovery from injury or let athletes try 'brain doping' to gain a competitive advantage. Yet many scientists question whether brain stimulation is as effective as its proponents claim, pointing out that studies have looked at only small groups of people. “They’re cool findings, but who knows what they mean,” says cognitive psychologist Jared Horvath at the University of Melbourne in Australia. The USSA is working with Halo to judge the efficacy of a device that delivers electricity to the motor cortex, an area of the brain that controls physical skills. The company claims that the stimulation helps the brain build new connections as it learns a skill. It tested its device in an unpublished study of seven elite Nordic ski jumpers, including Olympic athletes. © 2016 Nature Publishing Group,
Keyword: Movement Disorders
Link ID: 21979 - Posted: 03.12.2016
By Amy Ellis Nutt Surgeons snaked the electrodes under the 65-year-old woman’s scalp. Thirty years of Parkinson’s disease had almost frozen her limbs. The wires, connected to a kind of pacemaker under the skin, were aimed at decreasing the woman’s rigidity and allowing for more fluid movement. But five seconds after the first electrical pulse was fired into her brain, something else happened. Although awake and fully alert, she seemed to plunge into sadness, bowing her head and sobbing. One of the doctors asked what was wrong. “I no longer wish to live, to see anything, to hear anything, feel anything,” she said. Was she in some kind of pain? “No, I’m fed up with life. I’ve had enough,” she replied. “Everything is useless.” The operating team turned off the current. Less than 90 seconds later, the woman was smiling and joking, even acting slightly manic. Another five minutes more, and her normal mood returned. The patient had no history of depression. Yet in those few minutes after the electrical pulse was fired, the despair she expressed met nine of the 11 criteria for severe major depressive disorder in the Diagnostic and Statistical Manual of Mental Disorders. Fascinated by the anomaly, the French physicians wrote up the episode for the New England Journal of Medicine. The year was 1999, and hers was one of the first documented cases of an electrically induced, instantaneous, yet reversible depression. © 1996-2016 The Washington Post
Laura Sanders For some adults, Zika virus is a rashy, flulike nuisance. But in a handful of people, the virus may trigger a severe neurological disease. About one in 4,000 people infected by Zika in French Polynesia in 2013 and 2014 got a rare autoimmune disease called Guillain-Barré syndrome, researchers estimate in a study published online February 29 in the Lancet. Of 42 people diagnosed with Guillain-Barré in that outbreak, all had antibodies that signaled a Zika infection. Most also had recent symptoms of the infection. In a control group of hospital patients who did not have Guillain-Barré, researchers saw signs of Zika less frequently: Just 54 out of 98 patients tested showed signs of the virus. The message from this earlier Zika outbreak is that countries in the throes of Zika today “need to be prepared to have adequate intensive care beds capacity to manage patients with Guillain-Barré syndrome,” writes study coauthor Arnaud Fontanet of the Pasteur Institute in Paris and colleagues, some of whom are from French Polynesia. The study, says public health researcher Ernesto Marques of the University of Pittsburgh, “tells us what I think a lot of people already thought: that Zika can cause Guillain-Barré syndrome.” As with Zika and the birth defect microcephaly (SN: 2/20/16, p. 16), though, more work needs to be done to definitively prove the link. Several countries currently hard-hit by Zika have reported upticks in Guillain-Barré syndrome. Colombia, for instance, usually sees about 220 cases of the syndrome a year. But in just five weeks between mid-December 2015 to late January 2016, doctors diagnosed 86 cases, the World Health Organization reports. Other Zika-affected countries, including Brazil, El Salvador and Venezuela, have also reported unusually high numbers of cases. © Society for Science & the Public 2000 - 2016. All rights reserved.
Cathleen O'Grady When we speak, listen, read, or write, almost all of the language processing that happens in our brains goes on below the level of conscious awareness. We might be aware of grasping for a particular forgotten word, but we don’t actively think about linguistic concepts like morphemes (the building blocks of words, like the past tense morpheme “-ed”). Psycholinguists try to delve under the surface to figure out what’s actually going on in the brain, and how well this matches up with our theoretical ideas of how languages fit together. For instance, linguists talk about morphemes like “-ed”, but do our brains actually work with morphemes when we’re producing or interpreting language? That is, do theoretical linguistic concepts have any psychological reality? An upcoming paper in the journal Cognition suggests an unusual way to investigate this: by testing synaesthetes. Synaesthesia comes in many forms. Some synaesthetes associate musical tones or notes with particular colours; others attach personalities to letters or numbers. A huge number of synaesthetes have associations that are in some way linguistic, and one of the most common forms of all is grapheme-colour (GC) synaesthesia, which is the association of colours with particular letters or numbers. For instance, a GC synaesthete might have a consistent perception of the letter “A” being red. This association often extends to a whole word, so “ant” might be red, too. © 2016 Guardian News and Media Limited
Link ID: 21937 - Posted: 02.27.2016
Mo Costandi People who are prone to falling and injuring and injuring themselves in middle age are at significantly increased risk of developing Parkinson’s Disease decades later, according to a new study by researchers in Sweden. The findings, published earlier this month in the open access journal PLoS Medicine, suggest that frailty – and especially an increased risk of falling and fracturing one’s hip – could be a marker for degenerative brain changes, which may occur decades before disease symptoms appear, and possibly aid in early diagnosis. Parkinson’s Disease is a progressive neurodegenerative disease characterised by the death of dopamine-producing neurons in a region of the midbrain called the substantia nigra. This causes the three main symptoms of tremor, muscle rigidity, and slow movements, which typically appear at around 60 years of age, and progress at varying rates. Although widely considered to be a movement disorder, Parkinson’s is also associated with cognitive impairments, which in severe cases can develop into full-blown dementia. Last year, Peter Nordström of Umeå University and his colleagues published the results of a large population study, in which they examined the medical records of all the approximately 1.35 million Swedish men conscripted at age 18 for compulsory military service between the years of 1969 and 1996. Looking specifically at measures of muscle strength, they found that those who scored lowest on handgrip and elbow flexion strength at the time of conscription were significantly more likely to develop Parkinson’s 30 years later. © 2016 Guardian News and Media Limited
Link ID: 21919 - Posted: 02.20.2016
By Gretchen Reynolds Some forms of exercise may be much more effective than others at bulking up the brain, according to a remarkable new study in rats. For the first time, scientists compared head-to-head the neurological impacts of different types of exercise: running, weight training and high-intensity interval training. The surprising results suggest that going hard may not be the best option for long-term brain health. As I have often written, exercise changes the structure and function of the brain. Studies in animals and people have shown that physical activity generally increases brain volume and can reduce the number and size of age-related holes in the brain’s white and gray matter. Exercise also, and perhaps most resonantly, augments adult neurogenesis, which is the creation of new brain cells in an already mature brain. In studies with animals, exercise, in the form of running wheels or treadmills, has been found to double or even triple the number of new neurons that appear afterward in the animals’ hippocampus, a key area of the brain for learning and memory, compared to the brains of animals that remain sedentary. Scientists believe that exercise has similar impacts on the human hippocampus. These past studies of exercise and neurogenesis understandably have focused on distance running. Lab rodents know how to run. But whether other forms of exercise likewise prompt increases in neurogenesis has been unknown and is an issue of increasing interest, given the growing popularity of workouts such as weight training and high-intensity intervals. So for the new study, which was published this month in the Journal of Physiology, researchers at the University of Jyvaskyla in Finland and other institutions gathered a large group of adult male rats. The researchers injected the rats with a substance that marks new brain cells and then set groups of them to an array of different workouts, with one group remaining sedentary to serve as controls. © 2016 The New York Times Company
Link ID: 21902 - Posted: 02.17.2016
By Sheena Goodyear, A brain implant the size of a paper-clip might one day help paralyzed people regain the ability to use their arms and legs via a wireless connection that will transmit their thoughts to an exoskeleton. It's not the first technology to allow paralyzed people to operate mechanical limbs with signals from their brain, but it has the potential to revolutionize the field because it's minimally invasive and totally wireless. It's made possible because of a matchstick-sized implant called a stentrode, crafted from nitinol, an alloy that is commonly used in brassiere underwires and eyeglass frames, according to a study published in the journal Nature Biotechnology. "It's really a new method for getting brain data out of the brain without performing brain surgery," Thomas Oxley, a neurologist at the University of Melbourne who designed the device, told CBC News. "Part of the reason that brain-machine interfaces have not been successful to this point is because they get rejected by the body, and the reason they get rejected is because they all require direct implantation into the brain. And to do that you have to take off the skull — you have to perform a craniotomy." ©2016 CBC/Radio-Canada.
Link ID: 21886 - Posted: 02.11.2016
Jo Marchant The brain cells of people with Parkinson’s disease can be trained to reliably respond to placebo drugs, Italian neuroscientists report. The training wears off after 24 hours but the effect shows it may be possible to reduce the medication needed to treat Parkinson’s by interspersing real drugs with inert injections or pills, says placebo researcher Fabrizio Benedetti at the University of Turin, Italy, who led the work. A few people with Parkinson’s disease do respond dramatically to placebos, but most do not1. People with the condition suffer characteristic tremors and stiff muscles because their dopamine-producing brain cells are gradually dying off. They alleviate their symptoms by taking drugs such as apomorphine, which activate receptors for dopamine. For some conditions — such as pain and immune disorders — trials have shown2 that it is possible to train people to respond to placebos, although this practice hasn’t made its way into clinical care. Benedetti and his colleagues wondered whether the same effect might be possible for neurological disorders. They studied 42 people with advanced Parkinson’s disease who were having electrodes implanted into their brains for a therapy called deep brain stimulation, which eases symptoms by stimulating affected brain areas directly. That surgery gave Benedetti’s team a rare opportunity to measure the activity of individual neurons in the thalamus, a brain region known to be inhibited by lack of dopamine in people with Parkinson's. © 2016 Nature Publishing Grou
Link ID: 21884 - Posted: 02.10.2016
Colombia says three people have died after contracting the Zika virus and developing a rare nerve disorder. Health Minister Alejandro Gaviria said there was a "causal connection" between Zika, the Guillain-Barre disorder and the three deaths. Earlier, Brazilian scientists said they had detected for the first time active samples of Zika in urine and saliva. However, it is not clear whether the virus can be transmitted through bodily fluids. Zika, a mosquito-borne disease, has been linked to cases of babies born in Brazil with microcephaly - underdeveloped brains. "We have confirmed and attributed three deaths to Zika," said the head of Colombia's National Health Institute, Martha Lucia Ospina. "In this case, the three deaths were preceded by Guillain-Barre syndrome." Guillain-Barre is a rare disorder in which the body's immune system attacks part of the nervous system. It isn't normally fatal. Ms Ospina said another six deaths were being investigated for possible links to Zika. "Other cases (of deaths linked to Zika) are going to emerge," she said. "The world is realising that Zika can be deadly. The mortality rate is not very high, but it can be deadly." Mr Gaviria said one of the fatalities took place in San Andres and the other two in Turbo, in Antioquia department. UK virologist Prof Jonathan Ball, of the University of Nottingham, told the BBC: "We have been saying Zika has been associated with Guillain-Barre. One of the complications of that could be respiratory failure. But it is still probably a very rare event." Although Zika usually causes mild, flu-like symptoms, it has been linked to thousands of suspected birth defects. However, it has not yet been proved that Zika causes either microcephaly or Guillain-Barre. © 2016 BBC
Rare ‘allergy’ to vibrations tied to faulty gene By Kelly Servick If you have the rare condition known as vibratory urticaria, you may be wary of handling lawnmowers and electric mixers. Rubbing or vibration against your skin—even from drying off with a towel—can cause you to break out in hives, make your face flush, give you headaches, or produce the sensation of a metallic taste. The condition, which runs in families, is so rare that the researchers who work on it have only tracked down a few cases over years of searching. But a genetic study on three such unique families has revealed a potential mechanism for the strange symptoms. Research published online today in the New England Journal of Medicine describes a mutation in a gene called ADGRE2, found in 22 people with vibratory urticaria, but not in 14 of their unaffected relatives. The gene codes for a receptor protein that was found on the surface of mast cells—immune cells in the skin that dump out inflammatory molecules such as histamines that increase blood flow to an area and can cause hives. The researchers observed that shaking mast cells in a dish breaks apart two subunits of this receptor protein, which prompts histamine release. In people with the newly discovered mutation, the receptor is more prone to breakage, which causes this protective immune response at the site of physical trauma to run amok. © 2016 American Association for the Advancement of Science.
By Anne Pycha Future doctors may ask us to say more than “Ahhh.” Several groups of neuroscientists, psychiatrists and computer scientists are now investigating the extent to which patients' language use can provide diagnostic clues—before a single laboratory test is run. Increased computing power and new methods to measure the relation between behavior and brain activity have advanced such efforts. And although tests based on the spoken word may not be as accurate as gene sequencing or MRI scans, for diseases lacking clear biological indicators, language mining could help fill the gap. Psychiatrists at Columbia University interviewed 34 young adults at risk for psychosis, a common sign of schizophrenia that includes delusions and hallucinations. Two and a half years later five of the subjects had developed psychosis, and the remaining 29 remained free of the disorder. A specially designed algorithm combed the initial interviews collectively to look for language features that distinguished the two groups and found that psychosis correlated with shorter sentences, loss of flow in meaning from one sentence to the next and less frequent use of the words “that,” “what” and “which.” When later tested on each individual interview, the computer program predicted who did and who did not develop psychosis with 100 percent accuracy. The results were recently published in Schizophrenia, and a second round of testing with another group of at-risk subjects is now under way. Parkinson's Disease Twenty-seven subjects in a study at Favaloro University in Argentina listened to recorded sentences containing verbs associated with specific hand shapes (such as “applaud” or “punch”). As soon as they understood the sentence, participants pressed a button while keeping both hands in either a flat or clenched-fist position. © 2016 Scientific American
Videos just discovered show the first people ever to be treated for the symptoms of Parkinson’s disease. The footage, hidden for half a century, shows Chilean miners with severe movement problems improving on daily doses of L-dopa. The videos were filmed by George Cotzias at Brookhaven National Laboratory in Upton, New York. In 1963, while studying the toxic effects of manganese in human tissues, Cotzias learned of four workers in the Corral del Quemado mine in Andacollo, Chile, who had developed a syndrome called manganism – which resembled Parkinson’s – through inhaling manganese dust. Cotzias travelled to Chile to include the miners in a trial of leva-dopa, a chemical building block that the body converts into dopamine, low levels of which cause uncontrolled movements in people with Parkinson’s. L-dopa was being tested in Parkinson’s patients around the same time but with little success – even small amounts caused adverse side-effects that prevented a high enough dose reaching the brain. The footage clearly shows the severe problems with walking and turning miners had before treatment. After several months of receiving a daily dose of L-dopa, they were able to feed themselves, shave, tie their shoelaces, and run. “It’s a very important part of the history of neurology,” says Marcelo Miranda, a researcher at Clinica Las Condes in Santiago, Chile, who found the footage, some of which was shown at a conference in the 1960s, but hasn’t been seen since. “It’s the only available document of that period that shows the first patients with Parkinson’s symptoms treated with L-dopa and their extraordinary response.” © Copyright Reed Business Information Ltd.
Link ID: 21811 - Posted: 01.23.2016
A map for other people’s faces has been discovered in the brain. It could help explain why some of us are better at recognising faces than others. Every part of your body that you can move or feel is represented in the outer layer of your brain. These “maps”, found in the motor and sensory cortices (see diagram, below), tend to preserve the basic spatial layout of the body – neurons that represent our fingers are closer to neurons that represent our arms than our feet, for example. The same goes for other people’s faces, says Linda Henriksson at Aalto University in Helsinki, Finland. Her team scanned 12 people’s brains while they looked at hundreds of images of noses, eyes, mouths and other facial features and recorded which bits of the brain became active. This revealed a region in the occipital face area in which features that are next to each other on a real face are organised together in the brain’s representation of that face. The team have called this map the “faciotopy”. The occipital face area is a region of the brain known to be involved in general facial processing. “Facial recognition is so fundamental to human behaviour that it makes sense that there would be a specialised area of the brain that maps features of the face,” she says. © Copyright Reed Business Information Ltd.
The Chamorro people of the Pacific island of Guam know it as lytigo-bodig. For decades, they have been struck down by a mysterious illness that resembles the muscle-wasting disease amyotrophic lateral sclerosis (ALS), Parkinson’s disease and Alzheimer’s-like dementia. It now looks like we have a clue that could point to a way of slowing its development. Lytigo-bodig is a progressive disease. ALS symptoms arrive when people are in their mid-40s and early 50s. By the time they reach their 60s, they also have the shaking and lack of coordination that characterises Parkinson’s, before the cognitive problems associated with dementia also set in. “Initially they stumble a bit, but as their muscles wither, they need help with eating and going to the toilet, as well as having difficulty swallowing and breathing,” says Paul Cox of the Institute for Ethnomedicine in Wyoming. For a long time, a chemical called BMAA, found in the cycad seeds that the Chamorro grind up to make flour, has been suspected as the cause of the disease. The toxin builds up in the cyanobacteria that grow in the roots of cycad plants. It also accumulates in the tissue of seed-eating flying foxes, which the Chamorro hunt and eat. To see if they could confirm BMAA as the culprit, Cox fed fruit spiked with the toxin to vervet monkeys for 140 days. They estimated this was equivalent to the dose a typical islander might get over a lifetime. Although they didn’t show cognitive problems, the animals did develop brain abnormalities called tau tangles and deposits of amyloid plaque. The density and placement of these abnormalities were similar to those seen in the islanders. “The structure of the pathology is almost identical,” says Cox. “We were stunned.” © Copyright Reed Business Information Ltd.
By Ralph G. Neas In mid-February of 1979, I started experiencing tingling sensations in my feet and fingers. I told myself I was only feeling some residual effects from a bout with the flu several weeks before, and I caught the afternoon plane to Minneapolis to join my new boss, U.S. Sen. David Durenberger (R-Minn.), for several days of political meetings. That was on Sunday. On Tuesday, midway through a presentation, I began slurring my words and I found it hard to swallow. A local doctor, on hearing I’d had the flu, told me to go to my hotel room, take a couple of aspirin and call him in the morning. I spent the night moving from the bed to the couch to the chair to the floor, seeking relief from pain that was affecting more and more of my body. Just before dawn, I noticed that the right side of my face was paralyzed. On my way to the ER, the left side became paralyzed. I wasn’t having a recurrence of the flu. A spinal tap confirmed doctors’ suspicions that I’d come down with Guillain-Barré syndrome, or GBS, a rare neurological disorder that can cause total paralysis. Within 10 days I was so weakened by the spreading paralysis in my legs and arms that I could not get out of my bed at St. Mary’s, the Minneapolis hospital where I was being treated. Within three weeks, doctors performed a tracheostomy — connecting a mechanical respirator to my windpipe — because my ability to breathe was getting so poor.