Chapter 11. Motor Control and Plasticity
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By Smitha Mundasad Health reporter A type of diabetes drug may offer a glimmer of hope in the fight against Parkinson's disease, research in the journal Plos Medicine suggests. Scientists found people taking glitazone pills were less likely to develop Parkinson's than patients on other diabetes drugs. But they caution the drugs can have serious side-effects and should not be given to healthy people. Instead, they suggest the findings should prompt further research. 'Unintended benefits' There are an estimated 127,000 people in the UK with Parkinson's disease, which can lead to tremor, slow movement and stiff muscles. And charities say with no drugs yet proven to treat the condition, much more work is needed in this area. The latest study focuses solely on people with diabetes who did not have Parkinson's disease at the beginning of the project. Researchers scoured UK electronic health records to compare 44,597 people prescribed glitazone pills with 120,373 people using other anti-diabetic treatment. They matched participants to ensure their age and stage of diabetes treatment were similar. Scientists found fewer people developed Parkinson's in the glitazone group - but the drug did not have a long-lasting benefit. Any potential protection disappeared once patients switched to another type of pill. Dr Ian Douglas, lead researcher at the London School of Hygiene and Tropical Medicine, said: "We often hear about negative side-effects associated with medications, but sometimes there can also be unintended beneficial effects. "Our findings provide unique evidence that we hope will drive further investigation into potential drug treatments for Parkinson's disease." © 2015 BBC
Link ID: 21199 - Posted: 07.22.2015
Results from tests of the drug, announced this week, show that it breaks up plaques in mice affected with Alzheimer’s disease or Parkinson’s disease, and improves the memories and cognitive abilities of the animals. Other promising results in rats and monkeys mean that the drug developers, NeuroPhage Pharmaceuticals, are poised to apply for permission to start testing it in people, with trials starting perhaps as early as next year. The drug is the first that seems to target and destroy the multiple types of plaque implicated in human brain disease. Plaques are clumps of misfolded proteins that gradually accumulate into sticky, brain-clogging gunk that kills neurons and robs people of their memories and other mental faculties. Different kinds of misfolded proteins are implicated in different brain diseases, and some can be seen within the same condition (see “Proteins gone rogue”, below). One thing they share, however, is a structural kink known as a canonical amyloid fold, and it is this on which the new drug acts (Journal of Molecular Biology, DOI: 10.1016/j.jmb.2014.04.015). Animal tests show that the drug reduces levels of amyloid beta plaques and tau protein deposits implicated in Alzheimer’s disease, and the alpha-synuclein protein deposits thought to play a role in Parkinson’s disease. Tests on lab-made samples show that the drug also targets misfolded transthyretin, clumps of which can clog up the heart and kidney, and prion aggregates, the cause of CJD, another neurodegenerative condition. Because correctly folded proteins do not have the distinct “kink”, the drug has no effect on them. © Copyright Reed Business Information Ltd.
Carl Zimmer A single neuron can’t do much on its own, but link billions of them together into a network and you’ve got a brain. But why stop there? In recent years, scientists have wondered what brains could do if they were linked together into even bigger networks. Miguel A. Nicolelis, director of the Center for Neuroengineering at Duke University, and his colleagues have now made the idea a bit more tangible by linking together animal brains with electrodes. In a pair of studies published on Thursday in the journal Scientific Reports, the researchers report that rats and monkeys can coordinate their brains to carry out such tasks as moving a simulated arm or recognizing simple patterns. In many of the trials, the networked animals performed better than individuals. “At least some times, more brains are better than one,” said Karen S. Rommelfanger, director of the Neuroethics Program at the Center for Ethics at Emory University, who was not involved in the study. Brain-networking research might someday allow people to join together in useful ways, Dr. Rommelfanger noted. Police officers might be able to make collective decisions on search-and-rescue missions. Surgeons might collectively operate on a single patient. But she also warned that brain networks could create a host of exotic ethical quandaries involving privacy and legal responsibility. If a brain network were to commit a crime, for example, who exactly would be guilty? © 2015 The New York Times Company
Link ID: 21160 - Posted: 07.11.2015
Skinny jeans can seriously damage muscles and nerves, doctors have said. A 35-year-old woman had to be cut out of a pair after her calves ballooned in size, the medics said in the Journal of Neurology, Neurosurgery and Psychiatry. She had spent hours squatting to empty cupboards for a house move in Australia. By evening, her feet were numb and she found it hard to walk. Doctors believe the woman developed a condition called compartment syndrome, made worse by her skinny jeans. Compartment syndrome is a painful and potentially serious condition caused by bleeding or swelling within an enclosed bundle of muscles - in this case, the calves. The condition caused the woman to trip and fall and, unable to get up, she then spent several hours lying on the ground. On examination at the Royal Adelaide Hospital, her lower legs were severely swollen. Although her feet were warm and had enough blood supplying them, her muscles were weak and she had lost some feeling. As the pressure had built in her lower legs, her muscles and nerves became damaged. She was put on an intravenous drip and after four days was able to walk unaided. Other medics have reported a number of cases where patients have developed tingly, numb thighs from wearing the figure-hugging low-cut denim trousers - although the chance of it happening is still slim for most people. Priya Dasoju, professional adviser at the Chartered Society of Physiotherapy, said: "As with many of these warnings, the very unfortunate case highlighted is an extreme one. © 2015 BBC
Keyword: Movement Disorders
Link ID: 21084 - Posted: 06.23.2015
by Laura Sanders The motor homunculus is a funny-looking fellow with a hulking thumb, delicate toes and a tongue that wags below his head. His body parts and proportions stem from decades-old experiments that mapped brain areas to the body parts they control. Now, a new study suggests that the motor homunculus’ neck was in the wrong place. Hyder Jinnah of Emory University in Atlanta and colleagues used fMRI to scan the brains of volunteers as they activated their head-turning neck muscles. (Pads held participants’ heads still, so the muscles fired but heads didn’t move.) This head turn was accompanied by activity in part of the brain that controls movement. The exact spot seems to be between the brain areas that control the shoulder and the trunk — not between the areas responsible for moving the thumb and the top of the head as earlier motor homunculi had suggested, the team reports in the June 17 Journal of Neuroscience. © Society for Science & the Public 2000 - 2015.
Keyword: Pain & Touch
Link ID: 21060 - Posted: 06.17.2015
by Penny Sarchet Simon Sponberg of Georgia Institute of Technology in Atlanta and his team have figured out the secret to the moths' night vision by testing them with robotic artificial flowers (see above). By varying the speed of a fake flower's horizontal motion and changing brightness levels, the team tested moths' abilities under different conditions. It has been theorised that the moth brain slows down, allowing their visual system to collect light for longer, a bit like lengthening a camera's exposure. But the strategy might also introduce blur, making it hard to detect fast movement. If the moths were using this brain-slowing tactic, they would be expected to react to fast flower movements more slowly in darker conditions. The team found that there was indeed a lag. It helped them see motion in the dark while still allowing them to keep up with flowers swaying at normal speeds. The size of the lags matched the expected behaviour of a slowed nervous system, providing evidence that moths could be slowing down the action of neurons in their visual system. Previously, placing hawkmoths in a virtual obstacle courseMovie Camera revealed that they vary their navigation strategies depending on visibility conditions. Journal reference: Science, DOI: 10.1126/science.aaa3042 © Copyright Reed Business Information Ltd
Link ID: 21041 - Posted: 06.13.2015
By Sandra G. Boodman The test had become something of an annual ritual. Every year beginning when he turned 45, Thomas Clark Semmes, an IT consultant for the federal government, would visit his internist for a physical. In a standard test of the sensory system that is often part of a physical, the Baltimore doctor would prick the soles of Semmes’s feet with a pin. “He’d look at me and say, ‘Tell me when you feel it,’ and I’d say ‘I will when I can,’ ” Semmes, now 56, recalled of the pinprick test. Because he never felt anything, he said nothing. “It never really concerned me very much,” he recalled. His doctor would then dutifully jot something in his chart, never exploring it further. But in 2013, nearly a decade after that first test, a quick evaluation by a podiatrist revealed the reason for his unfeeling feet and provided an explanation for an anatomical oddity in one of Semmes’s close relatives. In retrospect, Semmes wishes he had asked his internist about the lack of sensation, but he assumed it wasn’t important — otherwise, the doctor would have said something. And as Semmes would later learn, not knowing what was wrong had cost him valuable time. “I definitely wish I’d been diagnosed sooner,” he said. “There are things that could have been done to lessen the impact.” Before 2013, Semmes never had much reason to think about his feet. He knew he had hammertoes — toes that bend downward at the middle joint as a result of heredity or trauma — as well as extremely high arches, but neither condition was painful or limiting. At least, he thought, he did not have bird legs like his father, whose limbs were so storklike that they were a running family joke. “I had big, muscular legs,” Semmes said.
Fergus Walsh Medical correspondent Scientists in Austria have created an artificial leg which allows the amputee to feel lifelike sensations from their foot. The recipient, Wolfang Rangger, who lost his right leg in 2007, said: "It feels like I have a foot again. It's like a second lease of life." Prof Hubert Egger of the University of Linz, said sensors fitted to the sole of the artificial foot, stimulated nerves at the base of the stump. He added it was the first time that a leg amputee had been fitted with a sensory-enhanced prosthesis. How it works Surgeons first rewired nerve endings in the patient's stump to place them close to the skin surface. Six sensors were fitted to the base of the foot, to measure the pressure of heel, toe and foot movement. These signals were relayed to a micro-controller which relayed them to stimulators inside the shaft where it touched the base of the stump. These vibrated, stimulating the nerve endings under the skin, which relayed the signals to the brain. Prof Egger said: "The sensors tell the brain there is a foot and the wearer has the impression that it rolls off the ground when he walks." Wolfgang Ranger, a former teacher, who lost his leg after a blood clot caused by a stroke, has been testing the device for six months, both in the lab and at home. He says it has given him a new lease of life He said: "I no longer slip on ice and I can tell whether I walk on gravel, concrete, grass or sand. I can even feel small stones." © 2015 BBC.
by Helen Thomson Imagine a world where you think of something and it happens. For instance, what if the moment you realise you want a cup of tea, the kettle starts boiling? That reality is on the cards, now that a brain implant has been developed that can decode a person's intentions. It has already allowed a man paralysed from the neck down to control a robotic arm with unprecedented fluidity. But the implications go far beyond prosthetics. By placing an implant in the area of the brain responsible for intentions, scientists are investigating whether brain activity can give away future decisions – before a person is even aware of making them. Such a result may even alter our understanding of free will. Fluid movement "These are exciting times," says Pedro Lopes, who works at the human-computer interaction lab at Hasso Plattner Institute in Potsdam, Germany. "These developments give us a glimpse of an exciting future where devices will understand our intentions as a means of adapting to our plans." The implant was designed for Erik Sorto, who was left unable to move his limbs after a spinal cord injury 12 years ago. The idea was to give him the ability to move a stand-alone robotic arm by recording the activity in his posterior parietal cortex – a part of the brain used in planning movements. "We thought this would allow us to decode brain activity associated with the overall goal of a movement – for example, 'I want to pick up that cup'," Richard Andersen at the California Institute of Technology in Pasadena told delegates at the NeuroGaming Conference in San Francisco earlier this month. © Copyright Reed Business Information Ltd
by Andy Coghlan A man in his mid-50s with Parkinson's disease had fetal brain cells injected into his brain last week. He is the first person in nearly 20 years to be treated this way – and could recover full control of his movements in roughly five years. "It seemed to go fine," says Roger Barker of the University of Cambridge, who is leading the international team that is reviving the procedure. The treatment was pioneered 28 years ago in Sweden, but two trials in the US reported no significant benefit within the first two years following the injections, and the procedure was abandoned in favour of deep brain stimulation treatments. What these trials overlooked is that it takes several years for fetal cells to "bed in" and connect properly to the recipient's brain. Many Swedish and North American recipients improved dramatically, around three years or more after the implants – long after the trials had finished. "In the best cases, patients who had the treatment pretty much went back to normal," says Barker. After the fetal cells were wired up properly in their brains, they started producing the brain signalling chemical dopamine – low levels of this cause the classic Parkinson's symptom of uncontrolled movements. In fact, the cells produced so much dopamine that many patients could stop taking their Parkinson's drugs. "The prospect of not having to take medications for Parkinson's is fantastic," says James Beck of the Parkinson's Disease Foundation in the US. © Copyright Reed Business Information Ltd
by Helen Thomson A brain implant that can decode what someone wants to do has allowed a man paralysed from the neck down to control a robotic arm with unprecedented fluidity – and enjoy a beer at his own pace. Erik Sorto was left unable to move any of his limbs after an accident severed his spinal cord 12 years ago. People with similar injuries have previously controlled prosthetic limbs using implants placed in their motor cortex – an area of the brain responsible for the mechanics of movement. This is far from ideal because it results in delayed, jerky motions as the person thinks about all the individual aspects of the movement. When reaching for a drink, for example, they would have to think about moving their arm forward, then left, then opening their hand, then closing their hand around the cup and so on. Richard Andersen at the California Institute of Technology in Pasadena and his colleagues hoped they could achieve a more fluid movement by placing an implant in the posterior parietal cortex – a part of the brain involved in planning motor movements. "We thought this would allow us to decode brain activity associated with the overall goal of a movement – for example, 'I want to pick up that cup', rather than the individual components," said Anderson at the NeuroGaming Conference in San Francisco, California, where he presented the work this month. © Copyright Reed Business Information Ltd.
Link ID: 20972 - Posted: 05.23.2015
Scientists at Mayo Clinic, Jacksonville, Florida created a novel mouse that exhibits the symptoms and neurodegeneration associated with the most common genetic forms of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS, Lou Gehrig’s disease), both of which are caused by a mutation in the a gene called C9ORF72. The study was partially funded by the National Institutes of Health and published in the journal Science. More than 30,000 Americans live with ALS, which destroys nerves that control essential movements, including speaking, walking, breathing and swallowing. After Alzheimer’s disease, FTD is the most common form of early onset dementia. It is characterized by changes in personality, behavior and language due to loss of neurons in the brain’s frontal and temporal lobes. Patients with mutations in the chromosome 9 open reading frame 72 (C9ORF72) gene have all or some symptoms associated with both disorders. “Our mouse model exhibits the pathologies and symptoms of ALS and FTD seen in patients with theC9ORF72 mutation,” said the study’s lead author, Leonard Petrucelli, Ph.D., chair and Ralph and Ruth Abrams Professor of the Department of Neuroscience at Mayo Clinic, and a senior author of the study. “These mice could greatly improve our understanding of ALS and FTD and hasten the development of effective treatments.” To create the model, Ms. Jeannie Chew, a Mayo Graduate School student and member of Dr. Petrucelli’s team, injected the brains of newborn mice with a disease-causing version of the C9ORF72 gene. As the mice aged, they became hyperactive, anxious, and antisocial, in addition to having problems with movement that mirrored patient symptoms.
By Lisa Sanders, M.D On Thursday we challenged Well readers to solve the difficult case of twin sisters who, in the prime of youth, developed a weakness that forced them to use their arms to rise from a chair. Nearly 300 of you wrote in with thoughts on this difficult case. Many of you recognized that this was likely to be a genetic disorder, though I greatly admired the “House”-ian thinking that led to a host of possible reasons why two sisters, living in different states, might develop the same symptoms independent of their shared DNA. It took this patient, Katie Buryk, four years to get her answer, which was: Late onset Tay-Sachs disease Although several of you made this difficult diagnosis, the first to do so was George Bonadurer, a second year medical student at Mayo Medical School in Rochester, Minn. He says he recently read about this disease in a book of unusual cases that had come to the Mayo clinic for help. This is actually Mr. Bonadurer’s second win of this contest. Strong work! Tay-Sachs disease was first identified by two physicians, independently, in the 1880s. Dr. Warren Tay was an ophthalmologist in London. Dr. Bernard Sachs was a neurologist in New York City. Each described a disease in infants that caused profound weakness, blindness and, usually by age 4, death. Careful consideration of cases over the following decades showed that the disease was inherited and often seen in children of Ashkenazi descent. Studying the patterns of inheritance, it became clear that both parents had to have the abnormal gene and that each of their children would have a one in four chance of being born with the disease. The terrible manifestations of the disease derive from an inherited inability to make an essential protein in the brain. This protein acts to break down discarded components of the cells. Without this protein, these discarded cell parts accumulate, interrupting normal nerve and brain cell functioning. This mechanism and the missing protein was identified in 1969, allowing for the development of a test for carriers. Since the development of this test, the incidence of Tay-Sachs in the United States has dropped by 90 percent. © 2015 The New York Times Company
Andrew Griffin Companies are taking out a huge amount of patents related to reading brainwaves, according to analysis, with a range of different applications. Fewer than 400 neuro-technology related patents were filed between 2000-2009. But in 2010 alone that reached 800, and last year 1,600 were filed, according to research company SharpBrains. The patents are for a range of uses, not just for the healthcare technology that might be expected. The company with the most patents is market research firm Nielsen, which has 100. Microsoft also has 89 related patents. Other uses of the technology that have been patented include devices that can change the thoughts of feelings of those that they are used on. But there are still medical uses — some of those patents awarded include technology to measure brain lesions and improve vision. The volume and diversity of the patents shows that we are at the beginning of “the pervasive neurotechnology age”, the company’s CEO Alvaro Fernandez said. "Neurotech has gone well beyond medicine, with non-medical corporations, often under the radar, developing neurotechnologies to enhance work and life," said Fernandez.
Roger Dobson Tapping your fingers on the table is usually a sign of boredom or irritation. But not all tappers are equal, it seems. Men drum their digits slightly faster than women and people in their twenties tap substantially faster than people twice their age. The results of the first study into finger-tapping speeds also found that smokers tap a little faster than non-smokers and fit people tap faster than those who avoid exercise. The research, carried out by scientists at two universities in Istanbul – Bogazici University and Fatih University – examined the tapping rates and “finger load capacities” of 148 people aged between 18 and 85. Each participant was asked to perform a one-minute tapping exercise on a keyboard at “maximum volitional tempo”. Researchers found that the index finger on the right hand of both men and women was the fastest digit, achieving a tapping rate of up to five beats a second among those in their twenties. The middle finger was almost as nifty as the index finger, but the little finger – the slowest digit in the bunch – was capable only of a sluggish 3.8 taps a second among people in the same age group. At first glance, the study might appear to be rather frivolous. But a deeper understanding of finger tapping could aid the design of computer keyboards and musical instruments. It may also aid researchers who use finger-tapping tests for medical assessment of neurological conditions such as Parkinson’s disease, schizophrenia and Alzheimer’s.
Scientists have raised hopes that they may be able to create a vaccine to block the progress of Parkinson’s disease. They believe new research provides evidence that an abnormal protein may trigger the condition. If the theory is correct, researchers say it might be possible to prime a person’s immune system – using a special vaccine – so it is ready to attack the rogue protein as it passes through the body. In this way, the protein would be prevented from destroying a person’s dopamine-manufacturing cells, where the disease inflicts its greatest damage. This new vision of Parkinson’s has been arousing excitement among researchers. “It has transformed the way we see Parkinson’s,” said Roger Barker, professor of clinical neurosciences at Cambridge University. Parkinson’s does not usually affect people until they are over 50. However, researchers have uncovered recent evidence that suggests it may be caused by an event occurring 10 to 20 years before its main symptoms – tremors, rigidity and slowness of movement – manifest themselves. “If you ask Parkinson’s patients if, in the past, they have experienced loss of sense of smell or suffer from disturbed sleep or have problems with their bowels, very often they reply they have,” said Barker, whose work is backed by the charity Parkinson’s UK, whose Parkinson Awareness week ends on Sunday. “Frequently these patients manifest symptoms several years before it becomes apparent they have the disease. We now believe there is a link.” © 2015 Guardian News and Media Limited
Link ID: 20855 - Posted: 04.28.2015
By Emily Dwass In the frightening world of brain tumors, “benign” is a good word to hear. But even a nonmalignant tumor can be dangerous — especially if, as in my case, it goes undetected, becoming a stealth invader. “Anecdotally, we often hear about women who were originally misdiagnosed — sometimes for years,” said Tom Halkin, a spokesman for the patient advocacy nonprofit National Brain Tumor Society. When I developed tingling in my limbs 12 years ago, two Los Angeles neurologists diagnosed Guillain-Barré syndrome, a disorder in which the immune system attacks the nervous system. The symptoms of numbness and weakness ebbed and flowed for three years. Then one day, I couldn’t slide my right foot into a flip-flop. This got me a ride in a magnetic resonance imaging machine, which revealed a brain mass the size of a tennis ball. It was a benign meningioma, a tumor that grows in the membranes surrounding the brain and spinal cord. After the diagnosis, I consulted with Los Angeles surgeons. “We’re going to cut your head open like a pumpkin,” one told me. I chose someone else, who had a stellar reputation, who was compassionate, and who did not compare my skull to a squash. “You’re cured,” he said as I awoke in the operating room. Recovery took about six weeks and went smoothly, except for my right foot, which remains partly numb. I relearned to walk and to drive with my left foot, using adaptive equipment. Had my tumor been diagnosed earlier, I might have avoided a large craniotomy and permanent foot issues. “It’s critical to find these tumors when they are small, when radiosurgery is an option, rather than when they are very big or produce a lot of symptoms, at which point it’s not optimal to treat them without doing open surgery,” said Dr. Susan Pannullo, the director of neuro-oncology and neurosurgical radiosurgery at NewYork-Presbyterian Hospital and Weill Cornell Medical College. © 2015 The New York Times Company
Keyword: Movement Disorders
Link ID: 20854 - Posted: 04.28.2015
By Jerry Adler Smithsonian Magazine | In London, Benjamin Franklin once opened a bottle of fortified wine from Virginia and poured out, along with the refreshment, three drowned flies, two of which revived after a few hours and flew away. Ever the visionary, he wondered about the possibility of incarcerating himself in a wine barrel for future resurrection, “to see and observe the state of America a hundred years hence.” Alas, he wrote to a friend in 1773, “we live in an age too early . . . to see such an art brought in our time to its perfection.” If Franklin were alive today he would find a kindred spirit in Ken Hayworth, a neuroscientist who also wants to be around in 100 years but recognizes that, at 43, he’s not likely to make it on his own. Nor does he expect to get there preserved in alcohol or a freezer; despite the claims made by advocates of cryonics, he says, the ability to revivify a frozen body “isn’t really on the horizon.” So Hayworth is hoping for what he considers the next best thing. He wishes to upload his mind—his memories, skills and personality—to a computer that can be programmed to emulate the processes of his brain, making him, or a simulacrum, effectively immortal (as long as someone keeps the power on). Hayworth’s dream, which he is pursuing as president of the Brain Preservation Foundation, is one version of the “technological singularity.” It envisions a future of “substrate-independent minds,” in which human and machine consciousness will merge, transcending biological limits of time, space and memory. “This new substrate won’t be dependent on an oxygen atmosphere,” says Randal Koene, who works on the same problem at his organization, Carboncopies.org. “It can go on a journey of 1,000 years, it can process more information at a higher speed, it can see in the X-ray spectrum if we build it that way.”
By Brady Dennis In recent months, Pasadena-based Genervon has galvanized many patients with ALS by repeatedly touting the results of 12-week, 12-person trial involving the company's drug, GM604. The company asserted its early results were “statistically significant,” “very robust” and “dramatic.” It also has said it "submitted an accelerated approval application" to the FDA which, if approved, "would allow immediate access" to patients with ALS, also known as Lou Gehrig's disease. But the Wall Street Journal reported Monday that Genervon said in an email that it is “at the point of communicating with FDA about whether [the agency] would accept our formal application” for accelerated approval. In other words, the company has not yet submitted a New Drug Application, a step needed to officially set the FDA approval process in motion. The company's acknowledgement that it has not filed an NDA appears to contradict earlier press releases and statements made by the firm's owners, Winston and Dorothy Ko -- or at least to have sown confusion about the actual status of GM604. In one February press release, for example, the company said that in a meeting with the FDA, "three times during the one-hour meeting we requested that the FDA grant GM604 accelerated approval." Asking, however, is not the same as filing the necessary paperwork and the accompanying data required for the FDA to accept it as sufficient. The difference might seem to be a matter of semantics. But the real-world consequence is that, if Genervon has no application pending at the FDA, there is no imminent decision for the FDA to make about approving GM604.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20833 - Posted: 04.22.2015
Carl Zimmer In 1998, Dr. Philip A. Starr started putting electrodes in people’s brains. A neurosurgeon at the University of California, San Francisco, Dr. Starr was treating people with Parkinson’s disease, which slowly destroys essential bits of brain tissue, robbing people of control of their bodies. At first, drugs had given his patients some relief, but now they needed more help. After the surgery, Dr. Starr closed up his patients’ skulls and switched on the electrodes, releasing a steady buzz of electric pulses in their brains. For many patients, the effect was immediate. “We have people who, when they’re not taking their meds, can be frozen,” said Dr. Starr. “When we turn on the stimulator, they start walking.” First developed in the early 1990s, deep brain stimulation, or D.B.S., was approved by the Food and Drug Administration for treating Parkinson’s disease in 2002. Since its invention, about 100,000 people have received implants. While D.B.S. doesn’t halt Parkinson’s, it can turn back the clock a few years for many patients. Yet despite its clear effectiveness, scientists like Dr. Starr have struggled to understand what D.B.S. actually does to the brain. “We do D.B.S. because it works,” said Dr. Starr, “but we don’t really know how.” In a recent experiment, Dr. Starr and his colleagues believe they found a clue. D.B.S. may counter Parkinson’s disease by liberating the brain from a devastating electrical lock-step. The new research, published on Monday in Nature Neuroscience, may help scientists develop better treatments for Parkinson’s disease. It may also help researchers adapt D.B.S. for treatment of such brain disorders as depression and obsessive compulsive disorder. © 2015 The New York Times Company
Link ID: 20817 - Posted: 04.18.2015