Chapter 11. Motor Control and Plasticity
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By SAM ROBERTS When he was just 5 years old, Thomas Graboys declared that he intended to become a doctor. As a young physician, he visited a nephew serving in the Peace Corps in Mauritania and remained for two months, treating dozens of patients a day. He skied and played tennis and joined fellow cardiologists as the drummer in a rock band called the Dysrhythmics. In Boston, he was famous as a member of the team that diagnosed the Celtics star Reggie Lewis’s heart defect before he died abruptly on a basketball court. In short, “he was a medical version of one of Tom Wolfe’s masters of the universe,” one reviewer concluded after Dr. Graboys (pronounced GRAY-boys) published his autobiography. But barely 60, after experiencing horrific nightmares, frequently flailing in bed, losing his memory, suffering tremors and finally collapsing on his wedding day, he acknowledged that he was suffering from Parkinson’s disease and the onset of dementia. He informed his patients that he had no choice but to close his practice. “My face is often expressionless, though I still look younger than my 63 years,” he recalled in the autobiography, “Life in the Balance: A Physician’s Memoir of Life, Love, and Loss With Parkinson’s Disease and Dementia,” which was published in 2008. “I am stooped,” he continued. “I shuffle when I walk, and my body trembles. My train of thought regularly runs off the rails. There is no sugarcoating Parkinson’s. There is no silver lining here. There is anger, pain, and frustration at being victimized by a disease that can to some extent be managed but cannot be cured.” After managing for more than a decade, Dr. Graboys died on Jan. 5 at his home in Chestnut Hill, Mass., his daughter, Penelope Graboys Blair, said. The cause was complications of Lewy Body Dementia, which was diagnosed after his Parkinson’s. He was 70. © 2015 The New York Times Company
Link ID: 20485 - Posted: 01.15.2015
By Peter Holley "Lynchian," according to David Foster Wallace, "refers to a particular kind of irony where the very macabre and the very mundane combine in such a way as to reveal the former's perpetual containment within the latter." Perhaps no other word better describes the onetime fate of Martin Pistorius, a South African man who spent more than a decade trapped inside his own body involuntarily watching "Barney" reruns day after day. "I cannot even express to you how much I hated Barney," Martin told NPR during the first episode of a new program on human behavior, "Invisibilia." The rest of the world thought Pistorius was a vegetable, according to NPR. Doctors had told his family as much after he'd fallen into a mysterious coma as a healthy 12-year-old before emerging several years later completely paralyzed, unable to communicate with the outside world. The nightmarish condition, which can be caused by stroke or an overdose of medication, is known as "total locked-in syndrome," and it has no cure, according to the National Institute of Neurological Disorders and Stroke. In a first-person account for the Daily Mail, Pistorius described the period after he slipped into a coma: I was completely unresponsive. I was in a virtual coma but the doctors couldn’t diagnose what had caused it. When he finally did awaken in the early 1990s, around the age of 14 or 15, Pistorius emerged in a dreary fog as his mind gradually rebooted itself.
By CATHERINE SAINT LOUIS A nationwide outbreak of a respiratory virus last fall sent droves of children to emergency departments. The infections have now subsided, as researchers knew they would, but they have left behind a frightening mystery. Since August, 103 children in 34 states have had an unexplained, poliolike paralysis of an arm or leg. Each week, roughly three new cases of so-called acute flaccid myelitis are still reported to the Centers for Disease Control and Prevention. Is the virus, called enterovirus 68, really the culprit? Experts aren’t certain: Unexplained cases of paralysis in children happen every year, but they are usually scattered and unrelated. After unusual clusters of A.F.M. appeared this fall, enterovirus 68 became the leading suspect, and now teams of researchers are racing to figure out how it could have led to such damage. “It’s unsatisfying to have an illness and not know what caused it,” said Dr. Samuel Dominguez, an epidemiologist and an infectious disease specialist at Children’s Hospital Colorado, which has had the largest cluster of patients. For many families, the onset of persistent limb paralysis has been a bewildering experience. Roughly two thirds of the children with A.F.M. have reported some improvement, according to the C.D.C. About a third show none. Only one child has fully recovered. In August, Jack Wernick, a first grader in Kingsport, Tenn., developed a “crummy little cold,” said his father, Dan Wernick, who works for a paper company. It seemed ordinary, until Jack complained that his right arm was heavy, his face began drooping and pain started shooting down his right leg. © 2015 The New York Times Company
Keyword: Movement Disorders
Link ID: 20477 - Posted: 01.13.2015
By James Gallagher Health editor, BBC News website An elastic implant that moves with the spinal cord can restore the ability to walk in paralysed rats, say scientists. Implants are an exciting field of research in spinal cord injury, but rigid designs damage surrounding tissue and ultimately fail. A team at Ecole Polytechnique Federale de Lausanne (EPFL) has developed flexible implants that work for months. It was described by experts as a "groundbreaking achievement of technology". The spinal cord is like a motorway with electrical signals rushing up and down it instead of cars. Injury to the spinal cord leads to paralysis when the electrical signals are stuck in a jam and can no longer get from the brain to the legs. The same group of researchers showed that chemically and electrically stimulating the spinal cord after injury meant rats could "sprint over ground, climb stairs and even pass obstacles". Rat walks up stairs Previous work by the same researchers But that required wired electrodes going directly to the spinal cord and was not a long-term option. Implants are the next step, but if they are inflexible they will rub, causing inflammation, and will not work properly. The latest innovation, described in the journal Science, is an implant that moves with the body and provides both chemical and electrical stimulation. When it was tested on paralysed rats, they moved again. One of the scientists, Prof Stephanie Lacour, told the BBC: "The implant is soft but also fully elastic to accommodate the movement of the nervous system. "The brain pulsates with blood so it moves a lot, the spinal cord expands and retracts many times a day, think about bending over to tie your shoelaces. "In terms of using the implant in people, it's not going to be tomorrow, we've developed dedicated materials which need approval, which will take time. © 2015 BBC.
Link ID: 20465 - Posted: 01.10.2015
|William Mullen, Tribune reporter Researchers at Northwestern University say they have discovered a common cause behind the mysterious and deadly affliction of amyotrophic lateral sclerosis, or Lou Gehrig's disease, that could open the door to an effective treatment. Dr. Teepu Siddique, a neuroscientist with Northwestern's Feinberg School of Medicine whose pioneering work on ALS over more than a quarter-century fueled the research team's work, said the key to the breakthrough is the discovery of an underlying disease process for all types of ALS. The discovery provides an opening to finding treatments for ALS and could also pay dividends by showing the way to treatments for other, more common neurodegenerative diseases such as Alzheimer's, dementia and Parkinson's, Siddique said. The Northwestern team identified the breakdown of cellular recycling systems in the neurons of the spinal cord and brain of ALS patients that results in the nervous system slowly losing its ability to carry brain signals to the body's muscular system. Without those signals, patients gradually are deprived of the ability to move, talk, swallow and breathe. "This is the first time we could connect (ALS) to a clear-cut biomedical mechanism," Siddique said. "It has really made the direction we have to take very clear and sharp. We can now test for drugs that would regulate this protein pathway or optimize it, so it functions as it should in a normal state."
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20459 - Posted: 01.08.2015
|By Lindsey Konkel For 28 years, Bill Gilmore lived in a New Hampshire beach town, where he surfed and kayaked. “I’ve been in water my whole life,” he said. “Before the ocean, it was lakes. I’ve been a water rat since I was four.” Now Gilmore can no longer swim, fish or surf, let alone button a shirt or lift a fork to his mouth. Earlier this year, he was diagnosed with amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease. In New England, medical researchers are now uncovering clues that appear to link some cases of the lethal neurological disease to people’s proximity to lakes and coastal waters. About five years ago, doctors at a New Hampshire hospital noticed a pattern in their ALS patients—many of them, like Gilmore, lived near water. Since then, researchers at Dartmouth-Hitchcock Medical Center have identified several ALS hot spots in lake and coastal communities in New England, and they suspect that toxic blooms of blue-green algae—which are becoming more common worldwide—may play a role. Now scientists are investigating whether breathing a neurotoxin produced by the algae may raise the risk of the disease. They have a long way to go, however: While the toxin does seem to kill nerve cells, no research, even in animals, has confirmed the link to ALS. As with all ALS patients, no one knows what caused Bill Gilmore’s disease. He was a big, strong guy—a carpenter by profession. One morning in 2011, his arms felt weak. “I couldn’t pick up my tools. I thought I had injured myself,” said Gilmore, 59, who lived half his life in Hampton and now lives in Rochester, N.H. © 2014 Scientific American
by Andy Coghlan To catch agile prey on the wing, dragonflies rely on the same predictive powers we use to catch a ball: that is, anticipating by sight where the ball will go and readying body and hand to snatch it from mid-air. Until now, dragonflies were thought to catch their prey without this predictive skill, instead blindly copying every steering movement made by their prey, which can include flies and bees. Now, sophisticated laboratory experiments have tracked the independent body and eye movements of dragonflies as they pursue prey, showing for the first time that dragonflies second guess where their prey will fly to next and then steer their flight accordingly. Throughout the pursuit, they lock on to their target visually while they orient their bodies and flight path for ultimate interception, rather than copying each little deviation in their prey's flight path in the hope of ultimately catching up with it. "The dragonfly lines up its body axis in the flight direction of the prey, but keeps the eyes in its head firmly fixed on the prey," says Anthony Leonardo of the Howard Hughes Medical Institute in Ashburn, Virginia. "It enables the dragonfly to catch the prey from beneath and behind, the prey's blind spot," he says. © Copyright Reed Business Information Ltd.
Link ID: 20412 - Posted: 12.13.2014
Injections of a new drug may partially relieve paralyzing spinal cord injuries, based on indications from a study in rats, which was partly funded by the National Institutes of Health. The results demonstrate how fundamental laboratory research may lead to new therapies. “We’re very excited at the possibility that millions of people could, one day, regain movements lost during spinal cord injuries,” said Jerry Silver, Ph.D., professor of neurosciences, Case Western Reserve University School of Medicine, Cleveland, and a senior investigator of the study published in Nature. Every year, tens of thousands of people are paralyzed by spinal cord injuries. The injuries crush and sever the long axons of spinal cord nerve cells, blocking communication between the brain and the body and resulting in paralysis below the injury. On a hunch, Bradley Lang, Ph.D., the lead author of the study and a graduate student in Dr. Silver’s lab, came up with the idea of designing a drug that would help axons regenerate without having to touch the healing spinal cord, as current treatments may require. “Originally this was just a side project we brainstormed in the lab,” said Dr. Lang. After spinal cord injury, axons try to cross the injury site and reconnect with other cells but are stymied by scarring that forms after the injury. Previous studies suggested their movements are blocked when the protein tyrosine phosphatase sigma (PTP sigma), an enzyme found in axons, interacts with chondroitin sulfate proteoglycans, a class of sugary proteins that fill the scars.
Link ID: 20394 - Posted: 12.04.2014
Stem cells can be used to heal the damage in the brain caused by Parkinson's disease, according to scientists in Sweden. They said their study on rats heralded a "huge breakthrough" towards developing effective treatments. There is no cure for the disease, but medication and brain stimulation can alleviate symptoms. Parkinson's UK said there were many questions still to be answered before human trials could proceed. The disease is caused by the loss of nerve cells in the brain that produce the chemical dopamine ,which helps to control mood and movement. To simulate Parkinson's, Lund University researchers killed dopamine-producing neurons on one side of the rats' brains. They then converted human embryonic stem cells into neurons that produced dopamine. Parkinson's Disease Parkinson's is one of the commonest neurodegenerative diseases These were injected into the rats' brains, and the researchers found evidence that the damage was reversed. There have been no human clinical trials of stem-cell-derived neurons, but the researchers said they could be ready for testing by 2017. Malin Parmar, associate professor of developmental and regenerative neurobiology, said: "It's a huge breakthrough in the field [and] a stepping stone towards clinical trials." A similar method has been tried in a limited number of patients. It involved taking brain tissue from multiple aborted foetuses to heal the brain. Clinical trials were abandoned after mixed results, but about a third of the patients had foetal brain cells that functioned for 25 years. BBC © 2014
Link ID: 20292 - Posted: 11.08.2014
By Kelly Servick Using data from old clinical trials, two groups of researchers have found a better way to predict how amyotrophic lateral sclerosis (ALS) progresses in different patients. The winning algorithms—designed by non-ALS experts—outperformed the judgments of a group of ALS clinicians given the same data. The advances could make it easier to test whether new drugs can slow the fatal neurodegenerative disease. The new work was inspired by the so-called ALS Prediction Prize, a joint effort by the ALS-focused nonprofit Prize4Life and Dialogue for Reverse Engineering Assessments and Methods, a computational biology project whose sponsors include IBM, Columbia University, and the New York Academy of Sciences. Announced in 2012, the $50,000 award was designed to bring in experts from outside the ALS field to tackle the notoriously unpredictable illness. Liuxia Wang, a data analyst at the marketing company Sentrana in Washington, D.C., was used to helping companies make business decisions based on big data sets, such as information about consumer choices, but says she “didn’t know too much about this life science thing” until she got an unusual query from a client. One of the senior managers she worked with revealed that her son had just been diagnosed with ALS and wondered if Sentrana’s analytics could apply to patient data, too. When Wang set out to investigate, she found the ALS Prediction Prize. The next step, she said, was to learn something about ALS. The disease destroys the neurons that control muscle movement, causing gradual paralysis and eventually killing about half of patients within 3 years of diagnosis. But the speed of its progression varies widely. About 10% of patients live a decade or more after being diagnosed. That makes it hard for doctors to answer patients’ questions about the future, and it’s a big problem for testing new ALS treatments. © 2014 American Association for the Advancement of Science.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20278 - Posted: 11.04.2014
|By Sandra Upson Jan Scheuermann is not your average experimental subject. Diagnosed with spinocerebellar degeneration, she is only able to move her head and neck. The paralysis, which began creeping over her muscles in 1996, has been devastating in many ways. Yet two years ago she seized an opportunity to turn her personal liability into an extraordinary asset for neuroscience. In 2012 Scheuermann elected to undergo brain surgery to implant two arrays of electrodes on her motor cortex, a band of tissue on the surface of the brain. She did so as a volunteer in a multi-year study at the University of Pittsburgh to develop a better brain-computer interface. When she visits the lab, researchers hook up her brain to a robotic arm and hand, which she practices moving using her thoughts alone. The goal is to eventually allow other paralyzed individuals to regain function by wiring up their brains directly to a computer or prosthetic limb. The electrodes in her head record the firing patterns of about 150 of her neurons. Specific patterns of neuronal activity encode her desire to perform different movements, such as swinging the arm to the left or clasping the fingers around a cup. Two thick cables relay the data from her neurons to a computer, where software can identify Scheuermann’s intentions. The computer can then issue appropriate commands to move the robotic limb. On a typical workday, Jan Scheuermann arrives at the university around 9:15 am. Using her chin, she maneuvers her electric wheelchair into a research lab headed by neuroscientist Andrew Schwartz and settles in for a day of work. Scientific American Mind spoke to Scheuermann to learn more about her experience as a self-proclaimed “guinea pig extraordinaire.” © 2014 Scientific American,
Link ID: 20276 - Posted: 11.04.2014
By CATHERINE SAINT LOUIS More than 50 children in 23 states have had mysterious episodes of paralysis to their arms or legs, according to data gathered by the Centers for Disease Control and Prevention. The cause is not known, although some doctors suspect the cases may be linked to infection with enterovirus 68, a respiratory virus that has sickened thousands of children in recent months. Concerned by a cluster of cases in Colorado, the C.D.C. last month asked doctors and state health officials nationwide to begin compiling detailed reports about cases of unusual limb weakness in children. Experts convened by the agency plan next week to release interim guidelines on managing the condition. That so many children have had full or partial paralysis in a short period is unusual, but officials said that the cases seemed to be extremely rare. “At the moment, it looks like whatever the chances are of getting this syndrome are less than one in a million,” said Mark A. Pallansch, the director of the division of viral diseases at the C.D.C. Some of the affected children have lost the use of a leg or an arm, and are having physical therapy to keep their muscles conditioned. Others have sustained more extensive damage and require help breathing. Marie, who asked to be identified by her middle name to protect her family’s privacy, said her 4-year-old son used to climb jungle gyms. But in late September, after the whole family had been sick with a respiratory illness, he started having trouble climbing onto the couch. He walked into Boston Children’s Hospital the day he was admitted. But soon his neck grew so weak, it “flopped completely back like he was a newborn,” Marie said. Typically, the time from when weakness begins until it reaches its worst is one to three days. But for her son, eight mornings in a row, he awoke with a "brand new deficit" until he had some degree of weakness in each limb and had trouble breathing. He was eventually transferred to a Spaulding rehabilitation center, where he is now. © 2014 The New York Times Company
By BENEDICT CAREY A Polish man who was paralyzed from the chest down after a knife attack several years ago is now able to get around using a walker and has recovered some sensation in his legs after receiving a novel nerve-regeneration treatment, according to a new report that has generated both hope and controversy. The case, first reported widely by the BBC and other British news outlets, has stirred as much excitement on the Internet as it has extreme caution among many experts. “It is premature at best, and at worst inappropriate, to draw any conclusions from a single patient,” said Dr. Mark H. Tuszynski, director of the translational neuroscience unit at the medical school of the University of California, San Diego. That patient — identified as Darek Fidyka, 40 — is the first to recover feeling and mobility after getting the novel therapy, which involves injections of cultured cells at the site of the injury and tissue grafts, the report said. The techniques have shown some promise in animal studies. But the medical team, led by Polish and English doctors, also emphasized that the results would “have to be confirmed in a larger group of patients sustaining similar types of spinal injury” before the treatment could be considered truly effective. The case report was published in the journal Cell Transplantation. The history of spinal injury treatment is studded with false hope and miracle recoveries that could never be replicated, experts said. In previous studies, scientists experimented with some of the same methods used on Mr. Fidyka, with disappointing results. © 2014 The New York Times Company
By Fergus Walsh Medical correspondent A paralysed man has been able to walk again after a pioneering therapy that involved transplanting cells from his nasal cavity into his spinal cord. Darek Fidyka, who was paralysed from the chest down in a knife attack in 2010, can now walk using a frame. The treatment, a world first, was carried out by surgeons in Poland in collaboration with scientists in London. Prof Wagih El Masri Consultant spinal injuries surgeon Details of the research are published in the journal Cell Transplantation. BBC One's Panorama programme had unique access to the project and spent a year charting the patient's rehabilitation. Darek Fidyka, 40, from Poland, was paralysed after being stabbed repeatedly in the back in the 2010 attack. He said walking again - with the support of a frame - was "an incredible feeling", adding: "When you can't feel almost half your body, you are helpless, but when it starts coming back it's like you were born again." He said what had been achieved was "more impressive than man walking on the moon". UK research team leader Prof Geoff Raisman: Paralysis treatment "has vast potential" The treatment used olfactory ensheathing cells (OECs) - specialist cells that form part of the sense of smell. OECs act as pathway cells that enable nerve fibres in the olfactory system to be continually renewed. In the first of two operations, surgeons removed one of the patient's olfactory bulbs and grew the cells in culture. Two weeks later they transplanted the OECs into the spinal cord, which had been cut through in the knife attack apart from a thin strip of scar tissue on the right. They had just a drop of material to work with - about 500,000 cells. About 100 micro-injections of OECs were made above and below the injury. BBC © 2014
BY Tina Hesman Saey SAN DIEGO — A Golden retriever that inherited a genetic defect that causes muscular dystrophy doesn’t have the disease, giving scientists clues to new therapies for treating muscle-wasting diseases. The dog, Ringo, was bred to have a mutation that causes Duchenne muscular dystrophy in both animals and people. His weak littermates that inherited the same mutation could barely suckle at birth. But Ringo was healthy, with muscles that function normally. One of Ringo’s sons also has the mutation but doesn’t have the disease, said geneticist Natassia Vieira of Boston Children’s Hospital and Harvard University October 19 at the annual meeting of the American Society of Human Genetics. The dogs without the disease had a second genetic variant that caused their muscles to make more of a protein called Jagged 1, Vieira and her colleagues discovered. That protein allows muscles to repair themselves. Making more of Jagged 1 appears to compensate for the wasting effect of the muscular dystrophy mutation, although the researchers don’t yet know the exact mechanism. The finding suggests that researchers may one day be able to devise treatments for people with muscular dystrophies by boosting production of Jagged 1 or other muscle repair proteins. N. M. Vieira. The muscular dystrophies: Revealing the genetic and phenotypic variability. American Society of Human Genetics Annual Meeting, San Diego, October 19, 2014. © Society for Science & the Public 2000 - 2014
by Flora Graham This glowing blue web of neurons is usually what researchers examine when searching for a cure for Parkinson's. But a new study, part-funded by Parkinson's UK, hones in on the tiny yellow dots. These are the connections between brain cells known as synapses, has discovered a killer that targets these links, potentially paving the way for new treatments. Soledad Galli at University College London and her colleagues have found that the death of synapses in mice may be due to malfunctioning proteins called Wnt proteins. "If we confirm that Wnt is involved in the early stages of Parkinson's, this throws up exciting possibilities, not just for new treatment targets, but also for new ways to identify people with Parkinson's early on in their condition," says Galli. Most patients currently depend on the drug levodopa, which is over 50 years old and can have severe side-effects, in addition to becoming less effective over time. Moreover, it only masks the symptoms: there is no cure for Parkinson's and no way to stop its progression. Journal reference: Nature Communications, DOI: 10.1038/ncomms5992 © Copyright Reed Business Information Ltd
|By Amy Yee Pouring a bucket of ice water over one’s head may seem like a distant summer memory. But although the “ice bucket challenge” craze has died down, public awareness of amyotrophic lateral sclerosis (ALS), commonly known as Lou Gehrig’s disease, has never been stronger. The viral video campaign raised $115 million from more than 3 million donors for the ALS Association. In one month, from July 29 to August 29, donors raised $100.9 million, compared with $2.8 million during the same period the previous year. In early October, the ALS Association began spending that money. It approved $21.7 million of funding for six programs and initiatives by groups that include the academic-industry partnership ALS Accelerated Therapeutics, the New York Genome Center, three California labs that form the Neuro Collaborative, and Project MinE, which will map the genomes of 15,000 people with ALS (about 10 percent of ALS patients have a family member with the disease). The grants focus on developing gene therapies for common ALS genes and exploring approaches to counter two major contributors to the disease, the inflammation of nervous tissue and misfolded proteins in brain cells that control movement. These efforts may not only someday lead to new treatments, but may also point to the cause of ALS. At the level of basic research, scientists do not have a dominant theory from which to work, notes Tom Jessell, a neuroscientist and co-director of Columbia University’s new Zuckerman Mind Brain Behavior Institute. Jessell is also the chair of the research advisory board of Project ALS, a nonprofit that identifies and funds ALS research. © 2014 Scientific American
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20213 - Posted: 10.18.2014
By Carl T. Hall Even Clayton Kershaw, the Los Angeles Dodgers’ pitching ace, makes mistakes now and then. And although very few of his mistakes seemed to do Giants hitters much good this season, a team of San Francisco scientists found a way to take full advantage. A new study by UCSF researchers revealed a tendency of the brain’s motion-control system to run off track in a predictable way when we try to perform the same practiced movement over and over. The scientists found the phenomenon first in macaque monkeys, then documented exactly the same thing in Kershaw’s game video. Although he struggled in a playoff appearance last week, the left-hander’s pitching performance during the regular season was among the best on record. It included a minuscule 1.77 earned run average, a nearly flawless no-hitter in June, 239 strikeouts and only 31 walks. He led the major leagues with 10.85 strikeouts per nine innings pitched. In what turned out to be an early warm-up to the playoffs, UCSF scientists Kris Chaisanguanthum, Helen Shen and Philip Sabes delved into the motor-control system of the primate brain. Their study, published in the Journal of Neuroscience, could help design better prosthetic limbs — or make robots that move less like robots and more like Kershaw. Unlike most machines, our brains seem to never stop trying to adapt to new information, making subtle adjustments each time we repeat a particular movement no matter how practiced. This trial-by-trial form of learning has obvious advantages in a fast-changing world, but also seems prone to drift away from spot-on accuracy as those small adjustments go too far.
Keyword: Learning & Memory
Link ID: 20193 - Posted: 10.11.2014
by Andy Coghlan Ten years after the death of everyone's favourite Superman, Christopher Reeve, his son Matthew Reeve is pushing ahead with a spine-tingling clinical trial You're planning a large study of a paralysis treatment that has already helped four young men. What will it entail? This study will include 36 people with spinal cord injuries who will be treated with epidural stimulation – a technique in which a device is used to apply electrical current to the spinal cord. If we see the same results as we did in the first four, this therapy could have a profound impact on thousands of people living with paralysis. It has the potential to become as commonplace as the pacemaker is for cardiac patients. How well has the treatment worked for the four men who have already received it? Prior to epidural stimulation, they had all suffered chronic injuries caused by completely severed spinal cords. All four have seen dramatic improvements, including the ability to voluntarily move their toes, feet, ankles and legs, and even stand at times, when the device is on. One unexpected bonus has been the return of autonomic function, such as bladder and bowel control and sexual function. From a quality-of-life point of view, this is the biggest improvement. Also unexpectedly, these autonomic functions continue in all four men even when the device is switched off, although they still need it to stand, move their legs and do exercises. © Copyright Reed Business Information Ltd.
Posted by Rachel Dolhun, MD, The ability to quit smoking, especially “cold turkey” or on the first attempt, has been heralded as a marker of strong willpower and determination. But could the ease with which one eschews cigarettes also serve as an early sign of Parkinson’s disease (PD)? This is the conclusion drawn by Beate Ritz, MD, PhD, and colleagues from the University of California, Los Angeles in a recent study published in Neurology. Researchers compared lifelong tobacco use, use of nicotine substitutes, and individual’s rating of their difficulty in trying to quit tobacco among 1,808 Danish people with PD and 1,876 control volunteers. They found that those with PD were less inclined to ever pick up the smoking habit, but, even if they did, they were less likely to need nicotine replacement therapies and able to more effortlessly stop smoking cigarettes. Therefore, ease of quitting smoking may be a sign of early PD. This joins a short list of other symptoms — smell loss, constipation and REM sleep behavior disorder — that usually predate diagnosis and are strongly associated with PD. Physicians rely heavily on such information to help confirm the diagnosis of Parkinson’s, given that biomarkers, objective measurements of disease, are currently lacking. Research led by The Michael J. Fox Foundation is ongoing to identify biological markers of PD, which could help diagnose and treat people earlier. In the meantime, doctors must look for symptoms and behaviors to help identify Parkinson’s. Researchers have long known that tobacco use was linked to a lower risk of PD. An ongoing Foundation-funded study is investigating whether nicotine might guard against or slow the progression of PD.