Chapter 11. Motor Control and Plasticity

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By DENISE GRADY Dr. Lewis P. Rowland, a neurologist who made fundamental discoveries in nerve and muscle diseases and clashed with government investigators during the McCarthy era, died on March 16 in Manhattan. He was 91. The cause was a stroke, his son Steven said. Dr. Rowland, the chairman of Columbia University’s neurology department for 25 years, died at NewYork-Presbyterian/Columbia University Medical Center. Dr. Rowland was a prolific researcher and writer, with nearly 500 published scientific articles that focused on devastating neuromuscular diseases, including muscular dystrophy, myasthenia gravis and many rare syndromes. He took a special interest in amyotrophic lateral sclerosis, or A.L.S., also called Lou Gehrig’s disease, which causes degeneration of nerves in the brain and spinal cord, leading to weakness, paralysis and death. Dr. Rowland led research teams that delineated a number of uncommon diseases that had been poorly understood. They also found that in a subgroup of A.L.S. patients, the disease was linked to lymphoma, a cancer of the immune system. Other studies led to the discovery that a gene defect causes an unusual form of dementia in some patients with A.L.S. In myasthenia gravis, Dr. Rowland and his colleagues documented its high death rate and helped identify treatments that prolonged survival. In the 1970s, long before the tools existed to study DNA’s role in neurological diseases like A.L.S., Alzheimer’s and Parkinson’s, Dr. Rowland predicted correctly that genetics would be the key to understanding them. One of his accomplishments at Columbia was the expansion in 1982 of an intensive care unit that added beds for patients who were severely ill with neurological disorders. Before then, it was often difficult to find I.C.U. space for them. © 2017 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease ; Muscles
Link ID: 23399 - Posted: 03.24.2017

A study in Neurology suggests that analyzing levels of the protein p75ECD in urine samples from people with amyotrophic lateral sclerosis (ALS) may help monitor disease progression as well as determine the effectiveness of therapies. The study was supported by National Institute of Neurological Disorders and Stroke (NINDS) and National Center for Advancing Translational Sciences (NCATS), both part of the National Institutes of Health. Mary-Louise Rogers, Ph.D., senior research fellow at Flinders University in Adelaide, Australia, and Michael Benatar, M.D., Ph.D, professor of neurology at the University of Miami, and their teams, discovered that levels of urinary p75 ECD increased gradually in patients with ALS as their disease progressed over a 2-year study period. “It was encouraging to see changes in p75ECD over the course of the study, because it suggests an objective new method for tracking the progression of this aggressive disease,” said Amelie Gubitz, Ph.D., program director at NINDS. “In addition, it indicates the possibility of assessing whether levels of that protein decrease while patients try future treatments, to tell us whether the therapies are having any beneficial effects.” Further analysis of the samples from 54 patients revealed that those who began the study with lower levels of urinary p75ECD survived longer than did patients who had higher levels of the protein initially, suggesting that it could be a prognostic marker of the disease and may inform patients about their illness. Dr. Benatar and his team noted that this may be useful in selecting participants for clinical trials and in improving study design.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 23396 - Posted: 03.23.2017

By Timothy Revell A smartphone app that uses deep learning lets people with Parkinson’s disease test their symptoms at home in just 4 minutes. The app could help people monitor the disease’s progression more closely, and uncover how lifestyle factors may affect their symptoms. “There’s very little understanding as to how Parkinson’s arises, and patients say that every day the condition is different,” says George Roussos at Birkbeck, University of London. People report symptom changes related to everything from exercise to socialising to diet, but it’s not yet possible to build a solid picture of how these factors interact. “To understand these differences, we need to monitor the condition regularly, in a quick and easy way, over a long period of time,” says Roussos. People with Parkinson’s usually only see a specialist once or twice a year. This makes it hard to track the disease progression in an individual in detail, and means that side effects of medication such as deterioration of mood can go unnoticed. With their Android app, called CloudUPDRS, Roussos and his colleagues want to make it easier to track symptoms and flag potential problems earlier. Similar to how a clinician would conduct a Parkinson’s severity test, the app includes both self-assessment questions and physical tests using a smartphone’s sensors. © Copyright Reed Business Information Ltd.

Keyword: Parkinsons
Link ID: 23313 - Posted: 03.04.2017

By Matt Reynolds If you’re happy and you know it, clap someone else’s hands. A muscle stimulation system aims to evoke empathy by triggering involuntary hand gestures in one person in response to mood changes in another. “If you’re moving in the same way as another person you might understand that person better,” says Max Pfeiffer at the University of Hannover in Germany. Pfeiffer and his team wired up four people to an EEG machine that measured changes in the electrical activity in their brain as they watched film clips intended to provoke three emotional responses: amusement, anger and sadness. These people were the “emotion senders”. Each sender was paired with an “emotion recipient” who wore electrodes on their arms that stimulated their muscles and caused their arms and hands to move when the mood of their partner changed. The gestures they made were based on American Sign Language for amusement, anger and sadness. To express amusement, volunteers had their muscles stimulated to raise one arm, to express anger they raised an arm and made a claw gesture, and to express sadness they slowly slid an arm down their chest. These resemble natural movements associated with the feelings, so the team hypothesised that they would evoke the relevant emotion. Asked to rate how well the gestures corresponded to the emotions, the volunteers largely matched the gestures to the correct mood. © Copyright Reed Business Information Ltd.

Keyword: Brain imaging
Link ID: 23302 - Posted: 03.02.2017

By KATHRYN SHATTUCK After his short film screened at the Sundance Film Festival in 2008, a euphoric Simon Fitzmaurice was walking the snowy streets of Park City, Utah, when his foot began to hurt. Back home in Ireland that summer, by then dealing with a pronounced limp, he received a shattering diagnosis: motor neuron disease, or M.N.D. (more commonly known in the United States as A.L.S., or Lou Gehrig’s Disease), a neurological disorder that causes increasing muscle weakness and eventual paralysis and is, in most cases, fatal. The doctor gave Mr. Fitzmaurice, then 33, three or four years to live. That might have been the end of any normal existence. But Mr. Fitzmaurice, by his own measure a “bit of a stubborn bastard,” was determined to leave his wife, Ruth, and their two young sons — with a third on the way — a legacy other than self-pity. The result is Mr. Fitzmaurice’s first feature film, and perhaps his salvation — “My Name Is Emily.” The movie, which opened in limited release in the United States on Feb. 17, stars Evanna Lynch, the airy Luna Lovegood of “Harry Potter” fame, as a teenage outlier in both her Dublin foster home and high school who goes on the lam with her only friend (George Webster) to free her father (Michael Smiley) from a mental hospital. The film — with gorgeous scenes of Ms. Lynch plunged, nymphlike, into a cerulean sea or riding shotgun through the emerald countryside in a canary-yellow vintage Renault — won for best cinematography when it debuted at the Galway Film Fleadh in 2015. “I am not trying to prove anything,” Mr. Fitzmaurice wrote in an email, before quickly reconsidering. “Actually, I am trying to prove something. I remember thinking, ‘I must do this to show my children to never give up.’” Mr. Fitzmaurice was writing with his hands when he began the script for “My Name Is Emily.” By the time he was finished, he was writing with his eyes. © 2017 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 23275 - Posted: 02.24.2017

Laurel Hamers Clusters of a toxic bacterial protein have a surprising structure, differing from similar clumps associated with Alzheimer’s and Parkinson’s in humans, scientists report in the Feb. 24 Science. These clusters, called amyloids, are defined in part by their structure: straight regions of protein chains called beta strands, folded accordion-style into flat beta sheets, which then stack up to form a fiber. That definition might now need to be broadened. “All the amyloids that have been structurally looked at so far have certain characteristics,” says Matthew Chapman, a biologist at the University of Michigan in Ann Arbor who wasn’t part of the work. “This is the odd amyloid out right now.” In the human brain, misfolded proteins can form amyloids that trigger neurodegenerative diseases. But amyloids aren’t always a sign of something gone wrong — some bacteria make amyloids to help defend their turf. In Staphylococcus aureus, for example, the PSMα3 protein assembles into amyloids that help the bacteria kill other cells. Previous research suggested that PSMα3 clusters were like any other amyloid. But researchers using X-ray crystallography found that instead of straight beta strands, the PSMα3 fiber was made up of curly structures called alpha helices that resemble an old-fashioned phone cord. The helices still formed a familiar fiber shape just like the beta strands did, but the sheets making up that fiber were rippled instead of flat. |© Society for Science & the Public 2000 - 2017.

Keyword: Alzheimers
Link ID: 23274 - Posted: 02.24.2017

Daqing Li and Ying Li In 1969 Geoffrey Raisman, who has died aged 77, introduced the term “plasticity” to describe the ability of damaged nerve tissue to form new synaptic connections. He discovered that damaged nerves in the central nervous system (CNS) could be repaired and developed the theory that white matter (nerve fibres and supporting cells) is like a pathway – when it is disrupted by injury, such as spinal cord injury, growth of the regenerating fibres is blocked. In 1985 he described how olfactory ensheathing cells (OECs) “open doors” for newly formed nerve fibres in the nose to enter the CNS. Believing that reconstruction of the damaged pathway is essential to repair of the injured CNS and using the unique door-opening capability of OECs, in 1997, together with colleagues, Geoffrey showed that transplantation of OECs into the damaged spinal cord in experimental models repairs the damaged pathway and results in the regeneration of severed nerve fibres and the restoration of lost functions. The study led to a joint clinical trial with Pawel Tabakow and his team at Wroclaw Medical University, Poland. In 2014 the first patient with a complete severance of the thoracic spinal cord received transplantation of his own OECs. The operation enabled the patient, Darek Fidyka, to gain significant neurological recovery of sensation and voluntary movement. He can now get out of his wheelchair and ride a tricycle. The wider application of OECs has also been investigated. In 2012, with his team at University College London, collaborating with the UCL Institute of Ophthalmology and Southwest hospital, at the Third Military Medical University in Chongqing, China, Geoffrey described the protective effect of OECs in an experimental glaucoma model. The discovery has led to a plan to translate this research to clinical application which, it is hoped, will help many sufferers regain sight.

Keyword: Regeneration; Glia
Link ID: 23266 - Posted: 02.22.2017

By Jessica Hamzelou Three people with paralysis have learned to type by thought alone using a brain implant – at the fastest speeds recorded using such a system. Two have motor neurone disease, also known as ALS – a degenerative disorder that destroys neurons associated with movement – while the other has a spinal cord injury. All three have weakness or paralysis in all of their limbs. There is a chance that those with ALS will eventually lose the ability to speak, too, says Jaimie Henderson, a neurosurgeon at Stanford University Medical Center in California. People who have lost the ability to talk may be offered devices that allow them to select letters on a screen using head, cheek or eye movements. This is how Stephen Hawking communicates, for example. But brain-machine interfaces are also being developed in the hope that they may one day be a more intuitive way of communicating. These involve reading brain activity, either externally or via an implant embedded in the brain, and turning it into a signal that can be used to direct something in the environment. At the moment, these devices are a little slow. Henderson and his colleagues wanted to make a device that was quicker and easier to use than those currently in trials. © Copyright Reed Business Information Ltd.

Keyword: ALS-Lou Gehrig's Disease ; Robotics
Link ID: 23264 - Posted: 02.22.2017

Many people think of fish and seafood as being healthy. However, new research suggests eating certain species that tend to have high levels of mercury may be linked to a greater risk of developing amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease. Questions remain about the possible impact of mercury in fish, according to a preliminary study released Monday that will be presented at the American Academy of Neurology's 69th annual meeting in Boston in April. Fish and seafood consumption as a regular part of the diet was not associated with ALS, the study said. "For most people, eating fish is part of a healthy diet," said study author Elijah Stommel of Dartmouth College in Hanover, N.H., and a fellow of the academy. In addition, the authors said their study does not negate the fact that eating fish provides many health benefits. Instead, it suggests people may want to choose species that are known to have a lower mercury content, and avoid consuming fish caught in waters where there is mercury contamination. The researchers stressed that more research is needed before fish consumption guidelines for neurodegenerative illness can be made. While the exact cause of ALS is not known, some previous studies have suggested the neurotoxic metal to be a risk factor for ALS, a progressive neurological disease. ©2017 CBC/Radio-Canada.

Keyword: ALS-Lou Gehrig's Disease ; Neurotoxins
Link ID: 23257 - Posted: 02.21.2017

By Timothy Revell It can be difficult to communicate when you can only move your eyes, as is often the case for people with ALS (also known as motor neurone disease). Microsoft researchers have developed an app to make talking with your eyes easier, called GazeSpeak. GazeSpeak runs on a smartphone and uses artificial intelligence to convert eye movements into speech, so a conversation partner can understand what is being said in real time. The app runs on the listener’s device. They point their smartphone at the speaker as if they are taking a photo. A sticker on the back of the phone, visible to the speaker, shows a grid with letters grouped into four boxes corresponding to looking left, right, up and down. As the speaker gives different eye signals, GazeSpeak registers them as letters. “For example, to say the word ‘task’ they first look down to select the group containing ‘t’, then up to select the group containing ‘a’, and so on,” says Xiaoyi Zhang, who developed GazeSpeak whilst he was an intern at Microsoft. GazeSpeak selects the appropriate letter from each group by predicting the word the speaker wants to say based on the most common English words, similar to predictive text messaging. The speaker indicates they have finished a word by winking or looking straight ahead for two seconds. The system also takes into account added lists of words, like names or places that the speaker is likely to use. The top four word predictions are shown onscreen, and the top one is read aloud. © Copyright Reed Business Information Ltd.

Keyword: ALS-Lou Gehrig's Disease ; Robotics
Link ID: 23248 - Posted: 02.18.2017

Sarah Jane Tribble In response to outrage from patients and lawmakers, Marathon Pharmaceuticals has delayed the launch of an $89,000 drug for Duchenne muscular dystrophy. The company had announced the annual list price for Emflaza, which is a steroid, after the Food and Drug Administration approved the drug Thursday. Emflaza is approved as an orphan drug, which means it is intended to treat a rare disease. Duchenne is an inherited disorder that causes muscles to become weak. There is no cure for the condition, which mainly affects boys, but some drugs, including Emflaza, are used to lessen symptoms. For years, many American patients have imported deflazacort, the generic version of Emflaza, for about $1,200 a year. But because the medicine wasn't approved in the U.S., the cost of the medicine wasn't typically covered by insurers. That contrast in price between became a flash point Monday as Sen. Bernie Sanders, I-Vt., and Rep. Elijah Cummings, D-Md., sent a letter to Marathon on Monday morning demanding answers about the $89,000 price for a drug that isn't new. It has been used routinely by Duchenne patients in the U.S. since at least 2005. "We believe Marathon is abusing our nation's 'orphan drug' program, which grants companies seven years of market exclusivity to encourage research into new treatments for rare diseases — not to provide companies like Marathon with lucrative market exclusivity rights for drugs that have been available for decades," Sanders and Cummings wrote. Marathon said FDA approval would help more patients get the drug. © 2017 npr

Keyword: Movement Disorders
Link ID: 23234 - Posted: 02.15.2017

Katherine Bourzac Kristopher Boesen, who broke his neck in a car accident, regained the ability to move his arms and hands after his spinal cord was injected with stem cells. Two years after having a stroke at 31, Sonia Olea Coontz remained partially paralysed on her right side. She could barely move her arm, had slurred speech and needed a wheelchair to get around. In 2013, Coontz enrolled in a small clinical trial. The day after a doctor injected stem cells around the site of her stroke, she was able to lift her arm up over her head and speak clearly. Now she no longer uses a wheelchair and, at 36, is pregnant with her first child. Coontz is one of stem-cell therapy's “miracle patients”, says Gary Steinberg, chair of neurosurgery at Stanford School of Medicine in California, and Coontz's doctor. Conventional wisdom said that her response was impossible: the neural circuits damaged by the stroke were dead. Most neuroscientists believed that the window for functional recovery extends to only six months after the injury. Stem-cell therapies have shown great promise in the repair of brain and spinal injuries in animals. But animal models often behave differently from humans — nervous-system injuries in rats, for example, heal more readily than they do in people. Clinical trial results have been mixed. Interesting signals from small trials have faded away in larger ones. There are plenty of unknowns: which stem cells are the right ones to use, what the cells are doing when they work and how soon after an injury they can be used. © 2016 Macmillan Publishers Limited,

Keyword: Regeneration; Stem Cells
Link ID: 23210 - Posted: 02.10.2017

Swedish researchers say a simple blood test is effective at differentiating symptoms of Parkinson's disease from similar disorders, but it isn't ready for clinical use. In its early stages, neurologists say Parkinson's is difficult to distinguish from rarer disorders, called atypical parkinsonian disorders. They have overlapping symptoms that tend to worsen more quickly and are more likely to lead to death. Researchers are on the hunt for biomarkers to help diagnosis these disorders. One potential biomarker, a nerve protein that can be detected when nerve cells die, is found in higher concentrations in spinal fluid collected by lumbar puncture. Now medical scientists have also found the protein in less invasive blood tests. For the study published in Wednesday's online issue of the journal Neurology, Dr. Oskar Hansson of Sweden's Lund University and his team examined 504 people in three groups. Two of the groups, in England and Sweden, included healthy people and those who had been living with one of the disorders for an average of four to six years. The third group of 109 patients had the diseases for three years or less. "The results of the present study strongly indicate that NfL when measured in blood can be used to distinguish between patients with Parkinson's disease and patients with progressive supranuclear palsy multiple system atrophy and corticobasal degeneration with high diagnostic accuracy," the study's authors said. ©2017 CBC/Radio-Canada.

Keyword: Parkinsons
Link ID: 23206 - Posted: 02.09.2017

Rae Ellen Bichell By the time Kay Schwister got her diagnosis last summer, she couldn't talk anymore. But she could still scowl, and scowl she did. After weeks of decline and no clue what was causing it, doctors had told Schwister — a 53-year-old vocational rehab counselor and mother of two from Chicago — that she had an incurable disease called Creutzfeldt-Jakob disease, or CJD. The disease was shrinking Kay's brain, and riddling it with holes. She would likely only live a few more weeks, the doctors said. It was a diagnosis that no one could ever want. But the fact that Schwister was able to get a firm diagnosis while still alive is a relatively new development that represents a step forward in understanding a group of devastating neurological disorders. And, some biochemists say, it could lead to better ways of diagnosing brain diseases that are much more common, including Parkinson's and Alzheimer's. For Kay Schwister it all started in the spring of 2016, when she started getting headaches and feeling dizzy all the time. Aging, she told herself, just didn't feel very good. Over the next few weeks, she got steadily worse. "She got to the point where she was so nauseous and so dizzy that she stopped driving and actually stopped working," says her husband, Tim Schwister. By the time Kay entered the emergency room last June her speech had changed. She was enunciating things in a strange way, and finishing each sentence on a really high note. Doctors drew blood and spinal fluid and tested it for things like multiple sclerosis and mercury poisoning. Those tests came back negative. Soon, Kay couldn't talk or walk. © 2017 npr

Keyword: Prions
Link ID: 23191 - Posted: 02.06.2017

Sara Constantino Certain multisensory conditions can alter the experience of bodily ownership. For instance, in the rubber hand illusion, simultaneous visual and haptic inputs lead to the adoption of sensations applied to an artificial limb as one's own. Understanding body ownership, and its malleability, has implications for the development of prosthetics. In a recent paper, Kelly Collins and colleagues at the University of Washington and Karolinska Institute elicited the illusion of ownership of an artificial hand in two epilepsy patients with embedded electrodes through the direct electrical stimulation of the hand area in somatosensory cortex (SI) applied in synchrony with visible touches to a rubber hand. When stimulation was asynchronous or administered to a different SI area, feelings of ownership were no longer induced, stressing the importance of temporal and spatial congruence. They also found that the details of the visual signal (for example, type of touch) affected the sensation. This method extends previous studies by eliciting ownership without stimulation of the peripheral nervous system, which is damaged in patients with spinal cord or nerve lesions. Human–technology mixtures have a long history, with the first known prosthesis, a wooden toe, dating as far back as 950 bc. Today, recent materials, electronics and neuroscience advances are enabling the development of prosthetic limbs that both look and feel real. © 2017 Macmillan Publishers Limited,

Keyword: Pain & Touch
Link ID: 23168 - Posted: 01.31.2017

By GRETCHEN REYNOLDS When people get up and move, even a little, they tend to be happier than when they are still, according to an interesting new study that used cellphone data to track activities and moods. In general, the researchers found, people who move are more content than people who sit. There already is considerable evidence that physical activity is linked to psychological health. Epidemiological studies have found, for example, that people who exercise or otherwise are active typically are less prone to depression and anxiety than sedentary people. But many of these studies focused only on negative moods. They often also relied on people recalling how they had felt and how much they had moved or sat in the previous week or month, with little objective data to support these recollections. For the new study, which was published this month in PLoS One, researchers at the University of Cambridge in England decided to try a different approach. They would look, they decided, at correlations between movement and happiness, that most positive of emotions. In addition, they would look at what people reported about their activity and compare it with objective measures of movement. To accomplish these goals, they first developed a special app for Android phones. Available free on the Google app store and ultimately downloaded by more than 10,000 men and women, it was advertised as helping people to understand how lifestyle choices, such as physical activity, might affect people’s moods. (The app, which is no longer available for download, opened with a permission form explaining to people that the data they entered would be used for academic research.) The app randomly sent requests to people throughout the day, asking them to enter an estimation of their current mood by answering questions and also using grids in which they would place a dot showing whether they felt more stressed or relaxed, depressed or excited, and so on. © 2017 The New York Times Company

Keyword: Depression; Obesity
Link ID: 23147 - Posted: 01.26.2017

By JANE E. BRODY Susan Sills, a Brooklyn artist who until recently made life-size cutouts on plywood using a power saw, long suspected she might be at risk for developing Parkinson’s disease. Both her mother and grandfather had this neurological movement disorder, and she knew that it sometimes runs in families. So she was not surprised when at age 72 she first noticed hand tremors and a neurologist confirmed that she had the disease. But to watch her in action three years later, it would be hard for a layperson to tell. She stands straight, walks briskly, speaks in clarion tones and maintains a schedule that could tire someone half her age. Having wisely put the power saw aside, Ms. Sills now makes intricately designed art jewelry. She is also a docent at the Brooklyn Museum, participates in a cooperative art gallery and assists her husband’s business by entertaining customers. Ms. Sills attributes her energy and well-being partly to the medication she takes but primarily to the hours she spends working out with a physical therapist and personal trainer, who have helped her develop an exercise regimen that, while not a cure, can alleviate Parkinson’s symptoms and slow progression of the disease. “The exercises opened me up,” said Ms. Sills, allowing such symptoms as small steps, slow movements and tiny, cramped handwriting to subside. “The earlier people begin exercising after a Parkinson’s diagnosis, and the higher the intensity of exercise they achieve, the better they are,” Marilyn Moffat, a physical therapist on the faculty of New York University, said. “Many different activities have been shown to be beneficial, including cycling, boxing, dancing and walking forward and backward on a treadmill. If someone doesn’t like one activity, there are others that can have equally good results.” © 2017 The New York Times Company

Keyword: Parkinsons
Link ID: 23132 - Posted: 01.23.2017

Charles Q. Choi Prions, the infectious agents best known for causing degenerative brain disorders such as ‘mad cow’ disease, may have been spotted in bacteria. A section of a protein in Clostridium botulinum, the microbe that causes botulism, can behave like a prion when it is inserted into yeast and Escherichia coli bacteria, researchers report in the 13 January issue of Science1. Prions are formed by proteins that can fold in a number of structurally distinct ways. A prion version of a protein can perpetuate itself in an infectious manner by converting normal forms of that protein into the prion version. Scientists first discovered prions in the 1980s as the agents behind fatal brain disorders known as transmissible spongiform encephalopathies. Since then, researchers have found the misfolded proteins in mammals, insects, worms, plants and fungi2, and learned that not all prions harm their hosts. But until now, prions were only seen in the cells of eukaryotic organisms, a group that includes animals, plants and fungi. In the latest study, researchers analysed roughly 60,000 bacterial genomes using software trained to recognize prion-forming proteins in yeast. They focused on a section of the bacterial protein Rho. In many bacteria, such as C. botulinum and E. coli, Rho is a global regulator of gene expression, meaning that it can control the activity of many genes. © 2017 Macmillan Publishers Limited,

Keyword: Prions
Link ID: 23104 - Posted: 01.14.2017

Parkinson’s disease, a chronic, progressive movement disorder characterized by tremors and stiffness, is not considered a fatal disease in and of itself, though it may reduce life expectancy by a modest amount. It is often said that people die “with” Parkinson’s rather than “of” the disease. “People who are healthy when diagnosed will generally live about as long as other people in their age cohort,” said James Beck, the vice president for scientific affairs at the Parkinson’s Disease Foundation, which is involved in research, education and advocacy. “It is not a death sentence.” Since Parkinson’s generally affects people later in life — patients are typically given a diagnosis in their 60s — patients often die of unrelated age-related diseases like cancer, heart disease or stroke. But the most common cause of death in those with Parkinson’s is pneumonia, because the disease impairs patients’ ability to swallow, putting them at risk for inhaling or aspirating food or liquids into their lungs, leading to aspiration pneumonia. Since Parkinson’s also impairs mobility and balance, those with the disease are also at high risk for falls and accidents, which can trigger a cascade of medical problems, including being bedridden and developing pneumonia, Dr. Beck said. In its advanced stages, the disease can make walking and talking difficult and cause other problems not related to movement, including cognitive impairment. Patients often cannot care for themselves and need assistance carrying out simple activities of daily living. One long-term study followed a group of 142 Parkinson’s patients after they were given their diagnosis; their mean age at diagnosis was around 70. The researchers found that 23 percent were generally doing well 10 years later, meaning they could maintain their balance and did not have dementia. But over half of the patients in the original group had died, with the most common cause related to Parkinson’s being pneumonia. © 2017 The New York Times Company

Keyword: Parkinsons
Link ID: 23094 - Posted: 01.13.2017

Valerie Piro The alarm goes off at 4:30 a.m. Groggy, I turn on the lamp on my night stand and try to sit up. I put my right hand on the wall next to my bed to steady myself, and push my left into the bed. Right away, my abs and back seize up and my legs spasm and kick out straight, forcing me back down onto the bed. Clearly my body thinks it is too early to get up, but I don’t have time to argue with it. I have to get physical therapy out of the way so I can be on time for my medieval history class. After I sit up, I place my hands under my right knee and clasp them together as I bring my knee up and closer to my chest. I reach out to my right foot and cross its heel over my left thigh so that I can plant my heel on the bed. I hug my right leg against my torso and chest and feel a stretch in my lower back and butt. I repeat this on my other side and then proceed to stretch each ankle. Paralysis requires maintenance. I then hop toward the foot of my bed, where my commode chair sits. I set both feet on the footrests as best I can, grab the armrest on the far side of the chair with my left hand, and, using my right hand to drive down into my bed, lift myself onto the commode wheelchair, and wheel to the bathroom. I emerge at 5:35 a.m. I transfer now into a wheelchair whose dimensions are friendly toward my Functional Electrical Stimulation (F.E.S.) cycle — something like a gym exercise bike, without the seat. I pull some milk out of the mini-fridge and pour it over a bowl of cereal. I eat while checking and answering email. At 6:30 it’s time to start cycling. I put two small rectangular electrodes on my left shin muscles, and then two on my right, connect them to the cycle, then strap in my legs and feet. Then two more electrodes then two more, and so on, until most of my lower body is tapped and wired. After I turn on the tablet that’s attached to the cycle, I choose from one of several preset programs to start my workout. Within a couple of minutes, electrical shocks are pulsing into my legs, causing them to contract into pedaling. Imagine pedaling a bicycle uphill for an hour; this is my workout. © 2017 The New York Times Company

Keyword: Movement Disorders
Link ID: 23081 - Posted: 01.11.2017