Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
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Glioma, one of the most deadly and common types of brain tumor, is often associated with seizures, but the origins of these seizures and effective treatments for them have been elusive. Now a team funded by the National Institutes of Health has found that human gliomas implanted in mice release excess levels of the brain chemical glutamate, overstimulating neurons near the tumor and triggering seizures. The researchers also found that sulfasalazine, a drug on the market for treating certain inflammatory disorders, can reduce seizures in mice with glioma. About 80 percent of people with glioma will experience at least one seizure during their illness, often as the first symptom. About one-third of patients will develop recurring seizures, known as tumor-associated epilepsy. Sen. Ted Kennedy, D-Mass., whose death was caused by a malignant glioma in August 2009, was diagnosed after having a seizure 15 months earlier. "Seizures are a frequent symptom of glioma and are often poorly controlled by epilepsy medications," said Jane Fountain, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS). "Understanding why the seizures occur and how to counteract them could help us substantially improve the quality of life for people with glioma." "People have assumed that tumors cause seizures by irritating the brain, but that really isn't a scientific explanation. We have now shown that the seizures are caused by glutamate release from the tumor," said Harald Sontheimer, Ph.D., a professor of neurobiology and director of the Center for Glial Biology in Medicine at the University of Alabama Birmingham (UAB). Dr. Sontheimer and his team published their results in Nature Medicine.
Link ID: 15793 - Posted: 09.13.2011
By Lauren Ware In a clear Plexiglas laboratory cage, a mouse sleeps. A thin fiber optic cable projects upward from the top of its head and out through the cage’s lid. The cable lights with a pulse of blue light. The mouse continues to sleep; the light continues to pulse. After a few more pulses, the mouse wakes up. It rubs its face, stretches its legs and runs over to its food cup and begins to eat voraciously, as though it were starving. It keeps eating as the blue light pulses. The optical fiber that carries the blue light goes directly into the mouse’s brain. It targets a specific group of brain cells that have been modified to react to light. The experiment uses a technique called optogenetics, developed seven years ago, which can selectively activate or silence groups of nerve cells, or neurons, in real time. And it allows scientists to interact with the brain and begin to map how it works with a degree of detail that was previously unimaginable. That’s what Scott Sternson has done with the apparently starving mouse at Janelia Farm in Ashburn, Va., an interdisciplinary biomedical research center that is part of the Howard Hughes Medical Institute. In fact, this mouse was well fed and should not have been hungry. Sternson’s research group targeted a type of cell called the agouti-related peptide (AGRP) neuron. AGRP cells live in the hypothalamus and have been linked to feeding behavior in other studies. The scientists used a virus to insert the DNA of a light-sensitive protein from bacteria, channelrhodopsin-2, into the AGRP neurons. Some of the AGRP neurons take up the DNA and begin to produce the protein and send it to the cell membrane. When the blue light is flashed into the mouse’s brain via the optical fiber, the protein causes the neurons to move ions across the cell membrane, effectively stimulating them to fire an electrical signal, the action potential, which neurons use to communicate with each other. Sternson found that the more AGRP neurons are stimulated, the more the mouse eats. And as soon as the light stops, so does the feeding. Miller-McCune © 2011
Keyword: Genes & Behavior
Link ID: 15792 - Posted: 09.13.2011
By ALIYAH BARUCHIN FREETOWN, Sierra Leone — On a sweltering morning on a red-earth lane a few blocks from the largest mosque in this West African capital, Jeneba Kabba stands up. A tall, striking woman with a serious manner, Mrs. Kabba has been sitting under an awning in the outdoor classroom of a vocational training program for people with epilepsy. Every weekday, some 20 Sierra Leoneans, from teenagers to adults in middle age, gather here to learn skills like tailoring, weaving, tie-dyeing and soap-making, as well as reading — skills that, in this society, will give them a chance to earn a living. Mrs. Kabba, 30, a graduate of the program, is now a tutor. Her composure belies what she has survived. As a teenager she was taken to a traditional healer, who boiled herbs and made her inhale the fumes from a steam tent for hours. The treatment was supposed to drive out the demons thought to cause epilepsy; she nearly fainted and could have been burned. But worse was yet to come: She was forced to drink a two-liter bottle of kerosene. “Mi ches don cook,” she says in the Krio language, her voice faltering even now: “My chest started to boil.” Only a panicked trip to the hospital saved her life. Mrs. Kabba not only survived, but has been seizure-free for 10 years with the help of phenobarbital, one of the oldest anti-epileptic drugs and virtually the only one available here. And in a country where people with epilepsy are often considered uneducable, unemployable and unmarriageable, Mrs. Kabba teaches, is happily married and has a child. © 2011 The New York Times Company
Link ID: 15739 - Posted: 08.30.2011
Researchers at the University of Calgary have documented serious health complications in multiple sclerosis patients who travelled outside of Canada to undergo a controversial treatment for their disease. Many MS patients have travelled overseas to find clinics willing to provide the treatment invented by Italian physician Paolo Zamboni, which uses balloon angioplasty to open up blocked veins in the necks of those who suffer from the disease. The new study followed five patients who had the vein opening therapy and were treated in Calgary hospitals in October and November last year after complications from their surgeries. The lead author of the paper, Dr. Jodie Burton, admits that it is difficult to draw conclusions since there were only five patients involved and it's not known how many Canadians went to locations like the United States, Mexico, India, and Poland to have the procedure done. But she says the seriousness of the complications should serve as a — quote — "cautionary tale" to anyone considering having the procedure done. Burton says patients shouldn't be afraid to let their doctors know they had the treatment and physicians need to know what to watch for as a result. In June, the federal government announced it will hold early-stage clinical trials into the treatment. © The Canadian Press, 2011 © CBC 2011
Keyword: Multiple Sclerosis
Link ID: 15722 - Posted: 08.25.2011
Researchers at the National Institutes of Health have discovered in mice a molecular trigger that initiates myelination, the process by which brain cell networks are reinforced with an insulating material called myelin that speeds their ability to transmit messages. The myelination process is an essential part of brain development. Myelin formation is necessary for brain cells to communicate and it may contribute to development of skills and learning. The researchers showed that an electrical signal passing through a brain cell (neuron) results in the brain cell releasing the molecule glutamate. Glutamate, in turn, triggers another type of brain cell, called an oligodendrocyte, to form a point of contact with the neuron. Signals transmitted through this contact point stimulate the oligodendrocyte to make myelin protein and begin the process of myelination. In this process, the oligodendrocyte wraps myelin around axons— the long, cable-like projections that extend from each neuron. The myelination process is analogous to wrapping electrical tape around bare wires. Myelin formation Electrical signals transmitted from one neuron to the next are a basic form of communication in the brain. The myelin layers that oligodendrocytes wrap around neurons boost these signals so that they travel 50 times faster than before. The study was conducted by Hiroaki Wake, Philip R. Lee, and R. Douglas Fields.
Link ID: 15667 - Posted: 08.11.2011
By Steve Connor, Science Editor One of the biggest studies ever undertaken into multiple sclerosis has identified 29 new genetic factors that are implicated in the development of the disease. The nature of the genes that have been linked with MS has demonstrated with a high degree of certainty that the root causes of the illness can be traced to the faulty functioning of the body's immune system, scientists said. Nearly 10,000 individuals with multiple sclerosis took part in the study and their genomes were scanned to find the genetic differences with the DNA of over 17,000 healthy people. The total number of genetic faults linked with the disease now amounts to 57. Alastair Compston, of the University of Cambridge, one of the lead authors of the study published in Nature, said there have been rival theories about what are the important factors implicated in triggering the disease, one of the most common neurological conditions affecting young adults. "Our research settles a long-standing debate on what happens first in the complex sequences of events that leads to disability in multiple sclerosis," he said. "This has important implications for future treatment strategies. It puts immunology right at the front end of the disease, absolutely." The study involved a relatively new technique called genome-wide scanning, which involves analysing the entire length of a patient's DNA for anomalies that appear not to exist in healthy people and could therefore be linked with the disease. Previous research had established that multiple sclerosis has a strong genetic component. ©independent.co.uk
NIH-funded scientists have developed a strain of mice with a built-in off switch that can selectively shut down the animals’ serotonin-producing cells, which make up a brain network controlling breathing, temperature regulation, and mood. The switch controls only the serotonin-producing cells, and does not affect any other cells in the animal’s brains or bodies. When the researchers powered down the animals’ serotonin cells, the animals failed to sufficiently step up their breathing to compensate for an increase of carbon dioxide in the air, and their body temperatures dropped to match the surrounding temperature. The finding has implications for understanding sudden infant death syndrome, or SIDS, which has been linked to low serotonin levels, and is thought to involve breathing abnormalities and problems with temperature control. The finding may also provide insight into depressive disorders, which also involve serotonin metabolism. The study results appear in the current issue of the journal Science. SIDS is the death of an infant before his or her first birthday that cannot be explained after a complete autopsy, an investigation of the scene and circumstances of the death, and a review of the medical history of the infant and of his or her family. According to the National Center for Health Statistics, SIDS is the third leading cause of infant death. To conduct the study, the researchers developed mice with a unique molecule, or receptor, on the surface of their serotonin-producing brain cells, or neurons. Typically, cells communicate via chemicals that bind to receptors on their surfaces, with the molecules binding to their receptors in much the same way a key fits into a lock.
Link ID: 15627 - Posted: 07.30.2011
By Laura Sanders Almost a minute after a rat’s head is severed from its body, an eerie shudder of activity ripples through the animal’s brain. Some researchers think this post-decapitation wave marks the border between life and death. But the phenomenon can be explained by electrical changes that, in some cases, are reversible, researchers report online July 13 in PLoS ONE. Whether a similar kind of brain wave happens in humans, and if so, whether it is inextricably tied to death could have important implications. An unambiguous marker could help doctors better decide when to diagnose brain death, knowledge that could give clarity to loved ones and boost earlier organ donation. In a PLoS ONE paper published in January, neuroscientist Anton Coenen and colleagues at the Radboud University Nijmegen in the Netherlands described this wave of electrical activity in the rat brain occurring 50 seconds after decapitation. The Nijmegen team, which was exploring whether decapitation is a humane way to sacrifice lab animals, wrote that this brain activity seemed to be the ultimate border between life and death. They dubbed the phenomenon the “wave of death.” But neurologist Michel van Putten of the University of Twente in Enschede, the Netherlands, wasn’t convinced. “We have no doubt the observation is real,” he says. “But the interpretation is completely speculative.” © Society for Science & the Public 2000 - 2011
Keyword: Animal Rights
Link ID: 15596 - Posted: 07.25.2011
By Tia Ghose Blocking a death receptor causes damaged myelin, the protective coating surrounding nerve cells, to repair itself, according to a study published Sunday (July 3) in Nature Medicine. The finding suggests that drugs targeting the receptor could help treat multiple sclerosis by reversing the myelin damage characteristic of the disease. “Showing remyelination, as they do in vivo and in vitro, is a pretty cool result,” said Richard Ransohoff, a Cleveland Clinic neuroscientist who was not involved in the work. The new receptor is a novel first step in potentially repairing damaged nerves of multiple sclerosis patients, he said. Current multiple sclerosis drugs slow the disease’s progression by quieting the inflammatory response of the immune system, which attacks the myelin surrounding nerve cells and kills oligodendrocytes, brain cells that make and repair myelin. Without their myelin, nerve cells gradually lose their ability to send electrical signals. But because they suppress the immune response, these drugs make patients more susceptible to rare infections such as viral brain inflammation and diseases such as leukemia. They also cannot undo existing damage, leading scientists to seek out approaches that stimulate the growth of new myelin or the restoration of existing myelin. Though research has identified several candidate molecules that promote myelin survival, none have yet proven to do so successfully in patients. © 1986-2011 The Scientist
Analysis by Marianne English Gene expression plays a larger role than thought in the development of temporal lobe epilepsy, a common form of epilepsy, finds an international team of scientists. The study was published in the journal Annals of Neurology by scientists from France's biomedical institution Inserm, the University of Marseille in France and the University of California-Irvine. Previously, experts thought neurons, or nerve cells, in the brain began acting abnormally after they were damaged by head trauma or previous illnesses that caused high fevers. Healthy neurons normally transmit messages to one another by moving ions -- or charged particles -- back and forth in channels between cells. These coordinated efforts allow humans and animals to do a variety of things, ranging from eating to reading science news articles on the Internet. But for people living with epilepsy, neurons in the brain can behave abnormally, sometimes firing uncontrollably and causing seizures. Though epilepsy can be caused by many things, the majority of cases cannot be traced back to a particular cause. Looking beyond neurons, the research team found that a "master switch" gene called NRSF controls the expression of some 1,800 genes suppressed in patients with epilepsy. Researchers think brain trauma still activates the gene, but there's evidence that keeping its proteins from influencing other genes can prevent brain tissue from becoming epileptic. So what does this mean for the 50 million people worldwide living with epilepsy? © 2011 Discovery Communications, LLC.
By PAULINE W. CHEN, M.D. One day during medical school, my classmates and I learned that one of the most well-liked doctors-in-training in the hospital had had a seizure while leading morning work rounds. The sight of him writhing had caused the other doctors and nurses on the ward to panic. Some stood mute, frozen with fear. An intern, believing that the seizure arose from low blood sugar levels, took his half-eaten jelly doughnut and held it against the mouth of his seizing colleague. Others yelled to the ward secretary to “call a code,” and continued to do so even after another dozen doctors and nurses had already arrived on the floor. The young doctor eventually recovered. But for many of the medical students and doctors who heard about the episode or were on the wards that day, the dread of that morning would linger long beyond our years of training. Epilepsy was, and remains, a frightening and mysterious malady. For the last 20 years, Dr. Brien J. Smith has tried to change how doctors and patients view epilepsy. Earlier this year, Dr. Smith, chief of neurology at Spectrum Health in Michigan, became chairman of the Epilepsy Foundation. Being elected head of a national organization does not seem unusual for a doctor who is a well-recognized authority and advocate in his or her field. What is extraordinary is that Dr. Smith knows firsthand about the disease and what his patients experience: He learned he had epilepsy when he was in high school. © 2011 The New York Times Company
Link ID: 15502 - Posted: 06.28.2011
Ferris Jabr, reporter Toddlers with autism are more likely to have brain regions that are out of sync. The discovery could help doctors to diagnose the disorder at an earlier age. Coordination of brainwaves is thought to help different areas of the brain communicate effectively with one another. To see whether abnormal synchronisation may occur in autism, Ilan Dinstein at the Weizmann Institute of Science in Rehovot in Israel, and colleagues, analysed the brain activity of 72 toddlers as they slept inside functional MRI scanners. The toddlers, who were aged between 1 and 3-and-a-half years old, were classed as either "normally developing", or diagnosed as having delayed language skills or autism. Dinstein's team aggregated data from several different scanning sessions, zeroing in on brain regions that previous studies have shown are synchronised in typically developing children such as the inferior frontal gyrus (IFG) - linked with language comprehension and attention - and the superior temporal gyrus (STG) - involved in auditory processing. Such regions remain synchronised even in the complete absence of external stimuli during rest or sleep. Abnormal synchronisation appeared in significantly more autistic children than the other two groups. Using this data, the researchers were then able to reverse engineer the results to try to predict whether a child has autism based solely on synchronised brain activity. © Copyright Reed Business Information Ltd.
Link ID: 15490 - Posted: 06.25.2011
by Ferris Jabr Talk about intelligent design: a new polymer-covered electrode has the potential to monitor and deliver drugs to out-of-sync brain cells. If trials in animals are successful, it could one day help people to control epilepsy. Neuroscientists implant microelectrode arrays in brains to eavesdrop on – and sometimes influence – the electrical activity of neurons. Why not chemically influence the brain alongside this electrical manipulation, thought Xinyan Tracy Cui at the University of Pittsburgh, Pennsylvania, and her colleagues. So the team coated microelectrodes with an electrically conductive polypyrrole film. Then they loaded pockets within the film with different drugs and neurotransmitters such as glutamate, GABA and dopamine, and attached the arrays to samples of rat brain tissue. Applying an electrical current to the polymer caused it to change shape and release its drug cargo, which then acted on surrounding cells. Cui is currently working on replicating this demonstration in living rodents. Hits the spot Polypyrrole-coated microelectrode arrays, like ordinary arrays, could not only monitor neurons for unusual electrical activity but also deliver electrical impulses to keep neurons firing at the right tempo, like the brain pacemakers sometimes used to treat epilepsy. With the polypyrrole coating, however, microelectrode arrays could release drugs when they detect unusual activity – such as the haphazard electrical firing that characterises a seizure. Because electrodes reach into specific regions of the brain, the drugs would affect only neighbouring neurons. © Copyright Reed Business Information Ltd.
Link ID: 15411 - Posted: 06.09.2011
by Kai Kupferschmidt The source of a deadly outbreak of Escherichia coli bacteria in Germany remains elusive as German officials today announced that the first tests of samples from a sprouts farm implicated in the outbreak were negative. The German farm had been shut down yesterday by authorities and the region's health minister had advised people not to eat the vegetables. The confusing turn of events comes less than a week after German officials suggested Spanish cucumbers were the source, only to later backtrack. Researchers are now analyzing the genome of the bacterium to understand its evolutionary history and possibly identify its source. Closer analysis of the genome might also offer some clues to how the Shiga toxin made by the bacterium is attacking the brain. This toxin normally targets the kidney, triggering the often fatal development of hemolytic-uremic syndrome (HUS). Usually neurological symptoms are seen in only a few percent of HUS cases, but in the current outbreak "about half the patients with HUS are developing neurological symptoms," Christian Gerloff, head of the neurology department at the University Medical Center Hamburg-Eppendorf, told ScienceInsider today. Alarm bells started going off when some patients showed problems finding words or giving the date, Gerloff recalls. It quickly became clear that a lot of patients were developing problems reading or doing simple calculations. "Patients were mixing up words and were disoriented. Later they developed muscle twitching and then progressing to epileptic fits," Gerloff says. © 2010 American Association for the Advancement of Science.
By CARL E. SCHOONOVER and ABBY RABINOWITZ Treating anxiety no longer requires years of pills or psychotherapy. At least, not for a certain set of bioengineered mice. In a study recently published in the journal Nature, a team of neuroscientists turned these high-strung prey into bold explorers with the flip of a switch. The group, led by Dr. Karl Deisseroth, a psychiatrist and researcher at Stanford, employed an emerging technology called optogenetics to control electrical activity in a few carefully selected neurons. First they engineered these neurons to be sensitive to light. Then, using implanted optical fibers, they flashed blue light on a specific neural pathway in the amygdala, a brain region involved in processing emotions. And the mice, which had been keeping to the sides of their enclosure, scampered freely across an open space. While such tools are very far from being used or even tested in humans, scientists say optogenetics research is exciting because it gives them extraordinary control over specific brain circuits — and with it, new insights into an array of disorders, among them anxiety and Parkinson’s disease. Mice are very different from humans, as Dr. Deisseroth (pronounced DICE-er-roth) acknowledged. But he added that because “the mammalian brain has striking commonalities across species,” the findings might lead to a better understanding of the neural mechanisms of human anxiety. © 2011 The New York Times Company
Link ID: 15337 - Posted: 05.17.2011
By Sandra G. Boodman, During the 11 years Sonja MacDonald and her family lived with her spells, they had planned what to do when she sensed — or they observed — one coming on. If she was driving, MacDonald was to pull over to the side of the road; her husband had taught their young children how to take the wheel if she was unable to steer, something that luckily never happened. When she took a shower, someone was always in the bathroom, in case she suddenly passed out. And if it happened in the nursing home where she worked, MacDonald gambled on being able to make it to an empty bed. Over the years doctors had given the Milton, Pa., resident various diagnoses for the episodes, which she said began with an aura — an odd feeling of disorientation sometimes tinged with fear. She would stare blankly, sometimes grasping at unseen objects or briefly losing consciousness. These incidents, which lasted two minutes at most, occurred without warning, leaving her feeling tired and cold but with no memory of what had just happened. Most specialists agreed that the spells were seizures that sometimes follow a migraine headache. But how, MacDonald wondered, could she have migraine seizures when the occasional headaches she had were not severe? Doctors brushed that question aside, and MacDonald resigned herself to living with whatever was wrong. “I told my husband, ‘I will not go back to another doctor. I guess when I drop over someone will believe me,’ ” said MacDonald, now 39. In 2009, a new neurologist took a fresh look at her case and in short order figured out what was wrong. The answer, this doctor subsequently learned, had been buried in MacDonald’s records for years.
People with multiple sclerosis may show blocked neck veins as a result of the disease rather than as a cause, a large study published Wednesday suggests. The findings cast doubt on the theory that blocked or narrowed veins are a main cause of MS, study author Dr. Robert Zivadinov of the University of Buffalo said. The findings published in the journal Neurology were consistent with thinking that the condition — also known as chronic cerebrospinal venous insufficiency, or CCSVI — is more common in patients with multiple sclerosis but not to the degree first reported by the Italian doctor Paolo Zamboni. "These findings indicate that CCSVI does not have a primary role in causing MS," said Zivadinov, who has worked with Zamboni. Zamboni proposed that multiple sclerosis may be linked with vascular problems, and that using angioplasty, or ballooning, to open blocked neck veins can help treat MS symptoms by changing blood flow patterns. Patients eager for surgery For more than a year, Canadians with MS have been leaving the country to get the surgery, despite reluctance from neurologists at home. An ultrasound technician, who did not know which group the subjects were in, did the test. The team found 56 per cent of people in the MS group met the criteria for CCSVI, as did 23 per cent of the healthy controls and 46 per cent of people with other neurological diseases. © CBC 2011
Keyword: Multiple Sclerosis
Link ID: 15213 - Posted: 04.14.2011
By Rachel Ehrenberg Nerve cell tendrils readily thread their way through tiny semiconductor tubes, researchers find, forming a crisscrossed network like vines twining towards the sun. The discovery that offshoots from nascent mouse nerve cells explore the specially designed tubes could lead to tricks for studying nervous system diseases or testing the effects of potential drugs. Such a system may even bring researchers closer to brain-computer interfaces that seamlessly integrate artificial limbs or other prosthetic devices. “This is quite innovative and interesting,” says nanomaterials expert Nicholas Kotov of the University of Michigan in Ann Arbor. “There is a great need for interfaces between electronic and neuronal tissues.” To lay the groundwork for a nerve-electronic hybrid, graduate student Minrui Yu of the University of Wisconsin–Madison and his colleagues created tubes of layered silicon and germanium, materials that could insulate electric signals sent by a nerve cell. The tubes were various sizes and shapes and big enough for a nerve cell’s extensions to crawl through but too small for the cell’s main body to get inside. When the team seeded areas outside the tubes with mouse nerve cells the cells went exploring, sending their threadlike projections into the tubes and even following the curves of helical tunnels, the researchers report in an upcoming ACS Nano. © Society for Science & the Public 2000 - 2011
Link ID: 15115 - Posted: 03.19.2011
Scientists say they have discovered a "maintenance" protein that helps keep nerve fibres that transmit messages in the brain operating smoothly. The University of Edinburgh team says the finding could improve understanding of disorders such as epilepsy, dementia, MS and stroke. In such neurodegenerative disorders, electrical impulses from the brain are disrupted. This leads to an inability to control movement, and muscles wasting away. The brain works like an electrical circuit, sending impulses along nerve fibres in the same way that current is sent through wires. These fibres can measure up to a metre, but the area covered by the segment of nerve that controls transmission of messages is no bigger than the width of a human hair. Signal failure The scientists discovered that the protein Nfasc186 is crucial for maintaining the health and function of the segment of nerve fibres - called the axon initial segment (AIS) - that controls transmission of messages within the brain. They found that the AIS and the protein within it are important in ensuring the nerve impulse has the right properties to convey the message as it should. Professor Peter Brophy, director of the University of Edinburgh's Centre for Neuroregeneration, said: "Knowing more about how signals in the brain work will help us better understand neurodegenerative disorders and why, when these illnesses strike, the brain can no longer send signals to parts of the body." BBC © MMXI
An oral drug for multiple sclerosis has been approved for some MS patients in Canada. Until Thursday's announcement, drug treatment options for MS patients in this country were limited to medications taken regularly by injection or infusion. Gilenya, also called fingolimod, is a capsule taken once a day for people with the relapsing-remitting form of MS. These patients have relapses that continue to worsen in severity, disability level, or who are unable to tolerate injections. "It's a very long awaited type of medication for our patients," said Dr. Heather MacLean, a neurologist at the Ottawa Hospital who specializes in MS. Needle injections under the skin are painful and are associated with itching and lumpy skin reactions, and the weekly intramuscular medication can also cause muscle pain, noted MacLean, who has treated patients with the new drug as part of early clinical trials. From her experience, MacLean estimated that 10 to 20 per cent of relapsing-remitting MS patients currently on treatment stand to benefit from Gilenya. "It always surprises me how patients really require different modalities of treatment based on their own personal disease course and their own treatment goals. To have another available option for them, I think they'll be thrilled." Gilenya's manufacturer, Novartis, submitted clinical trial data to Health Canada to get the approval. © CBC 2011
Keyword: Multiple Sclerosis
Link ID: 15097 - Posted: 03.11.2011