Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals

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By Daphne Merkin A trauma is a trauma is a trauma. Or is it? Over the past decade, the words “trauma” and “traumatic” have been used so profligately and have entered our cultural discourse to such an extent that they have almost lost their depth-charge, the reactive implosion of psychic damage to which they were originally meant to refer. Everyone in this era is traumatized by everything, from inappropriate sexual come-ons to the use of language in novels by such literary greats as Joseph Conrad and Mark Twain now considered inflammatory in its assumptions about class, race or privilege. (Hence: trigger warnings, safe spaces and microaggressions.) The late novelist and critic V. S. Naipaul saw himself in an epochal battle against the cloudy and clichéd thinking to which this kind of easy resort to the dichotomy of the abused versus the abusers is conducive, replete with right-thinking but ultimately wishful ideas about the ways in which power and human nature interact. And then along comes a book, like Kurt Eichenwald’s “A Mind Unraveled,” that makes you rethink not only the concept of trauma but its potential impact — the ways in which trauma can work not only to weaken but to strengthen the character of the person who has experienced it. His remarkable memoir reads, unaccountably, like the most hair-raising of psychological thrillers, despite the fact that the saga of Eichenwald’s life as an epileptic from his late teens up until the present, when he has become a Pulitzer Prize-winning journalist, would not seem to contain the potential for so much suspense. He grasps the gritty issues surrounding his own very real trauma and often horrific experiences — from enduring frequent convulsions and losses of consciousness to the threat of being thrown out of college to losing jobs — with so little self-pity and so much regard for the compensations the world has to offer even to those afflicted as he is. It’s a quality that sets this book vividly apart from other memoirs that deal with suffering. For anyone who wants to understand the complex dynamic between environmental battering and the sort of inner strength that often goes by the name of resilience, this is the book to turn to. “I have lived most of my life,” Eichenwald writes, “knowing I could be seconds away from falling to the ground, seizing, burning, freezing or worse. Am I too near that window? Am I too high up? Is the oven open? I ask these questions every day.” © 2018 The New York Times Company

Keyword: Epilepsy
Link ID: 25578 - Posted: 10.16.2018

By Mitch Leslie Our immune cells normally pounce on intruding bacteria and viruses. But in multiple sclerosis (MS), immune cells target the nervous system instead. Now, researchers may have pinpointed a long-sought molecule called a self-antigen that provokes these attacks, pointing a way toward potential new treatments. “The work is monumental, and it’s tantalizing,” says neuroimmunologist Hartmut Wekerle of the Max Planck Institute of Neurobiology in Munich, Germany, who wasn’t connected to the research. Researchers have long suspected that a self-antigen—a normal molecule in the body that the immune system mistakenly treats as a threat—can trigger MS. The prime suspects have been proteins in myelin, the nerve insulation that erodes in patients with the disease. But after years of searching, scientists haven’t been able to pinpoint the molecule. To uncover other candidates, immunologists Roland Martin and Mireia Sospedra of University Hospital of Zurich in Switzerland and their colleagues analyzed immune cells known as T cells that came from a patient who died from MS. T cells normally switch on when they encounter protein fragments containing just a few amino acids that belong to an invading microbe, but they also turn on in people who have MS. The researchers wanted to determine which protein shards stimulated the patients’ T cells, so they tested 200 fragment mixtures, each containing 300 billion varieties. The two fragments with the strongest effect turned out to be part of a human enzyme called guanosine diphosphate-L-fucose synthase, which helps cells remodel sugars that are involved in everything from laying down memories to determining our blood type. T cells from 12 of 31 patients who had who either had been diagnosed with MS or had shown early symptoms of the disease also reacted to the enzyme, the researchers report online today in Science Translational Medicine. What’s more, T cells from four of the eight patients tested responded to a bacterial version of the enzyme—lending credence to the recently proposed idea that intestinal bacteria may help spark the disease. © 2018 American Association for the Advancement of Science

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 25560 - Posted: 10.11.2018

By JoAnna Klein Plants have no eyes, no ears, no mouth and no hands. They do not have a brain or a nervous system. Muscles? Forget them. They’re stuck where they started, soaking up the sun and sucking up nutrients from the soil. And yet, when something comes around to eat them, they sense it. And they fight back. How is this possible? “You’ve got to think like a vegetable now,” says Simon Gilroy, a botanist who studies how plants sense and respond to their environments at the University of Wisconsin-Madison. “Plants are not green animals,” Dr. Gilroy says. “Plants are different, but sometimes they’re remarkably similar to how animals operate.” To reveal the secret workings of a plant’s threat communication system for a study published Thursday in Science, Masatsugu Toyota (now a professor at Saitama University in Japan) and other researchers in Dr. Gilroy’s lab sent in munching caterpillars like in the video above. They also slashed leaves with scissors. They applied glutamate, an important neurotransmitter that helps neurons communicate in animals. In these and about a dozen other videos, they used a glowing, green protein to trace calcium and accompanying chemical and electrical messages in the plant. And they watched beneath a microscope as warnings transited through the leafy green appendages, revealing that plants aren’t as passive as they seem. The messages start at the point of attack, where glutamate initiates a wave of calcium that propagates through the plant’s veins, or plumbing system. The deluge turns on stress hormones and genetic switches that open plant arsenals and prepare the plant to ward off attackers — with no thought or movement. © 2018 The New York Times Company

Keyword: Evolution
Link ID: 25450 - Posted: 09.14.2018

Results from a clinical trial of more than 250 participants with progressive multiple sclerosis (MS) revealed that ibudilast was better than a placebo in slowing down brain shrinkage. The study also showed that the main side effects of ibudilast were gastrointestinal and headaches. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, and published in the New England Journal of Medicine. “These findings provide a glimmer of hope for people with a form of multiple sclerosis that causes long-term disability but does not have many treatment options,” said Walter J. Koroshetz, M.D., director of the NINDS. Robert J. Fox, M.D., a neurologist at Cleveland Clinic in Ohio, led a team of researchers across 28 clinical sites in a brain imaging study to investigate whether ibudilast was better than placebo in reducing the progression of brain atrophy, or shrinkage, in patients with progressive multiple sclerosis. In the study, 255 patients were randomized to take up to 10 capsules of ibudilast or placebo per day for 96 weeks. Every six months, the participants underwent MRI brain scans. Dr. Fox’s team applied a variety of analysis techniques on the MRI images to assess differences in brain changes between the two groups. The study showed that ibudilast slowed down the rate of brain atrophy compared to placebo. Dr. Fox and his colleagues discovered that there was a difference in brain shrinkage of 0.0009 units of atrophy per year between the two groups, which translates to approximately 2.5 milliliters of brain tissue. In other words, although both groups experienced atrophy, the brains of the patients in the placebo group shrank on average 2.5 milliliters more over two years compared to the ibudilast group. The whole adult human brain has a volume of approximately 1,350 milliliters. However, it is unknown whether that difference had an effect on symptoms or loss of function.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 25400 - Posted: 08.31.2018

By Jake Buehler Whether it’s avoiding the slap of a flyswatter or shooting a tongue out at just the right moment to capture prey, fast reflexes can mean the difference between life and death in the animal kingdom. But a new study finds that not all reflexes are created equal: Larger animals are slower on the draw than smaller ones and because of that, they can’t move nearly as fast as they should be able to. When it comes to reflexes, there’s no doubt that bigger animals are a little slower. Big animals have longer neurons, and that means more time for a signal to travel from the spine to a leg muscle, for example. But nerve speed isn’t the only thing that slows down reflexes. So in the new study, researchers decided to look at myriad factors, like how fast muscles can generate force. They combed through data from other studies on electrically stimulated nerves and muscles in animals as small as shrews to as large as elephants. They also looked at the gaits of these mammals to calculate how long their stride and foot-down positions were in relation to their body size, which allowed researchers to look at how relatively quick their reflexes are. As size scales up, so does the total time it takes for muscles to respond, the team reported yesterday in the Proceedings of the Royal Society B. Large mammals experience a delay between nerve firing and muscle movement that is more than 15 times longer than small mammals. But, relative to the speed of their body movements, that delay is only twice as long—which means to compensate for slow signals, they’re moving more slowly. If this didn’t happen, a running 250-kilogram elk would be a cartoonish blur of legs, taking steps far faster than its reflexes could ever respond to. Call it a biological speed limit. © 2018 American Association for the Advancement of Science

Keyword: Evolution
Link ID: 25398 - Posted: 08.31.2018

Lesley Mcclurg The first prescription medication extracted from the marijuana plant is poised to land on pharmacists' shelves this fall. Epidiolex, made from purified cannabidiol, or CBD, a compound found in the cannabis plant, is approved for two rare types of epilepsy. Its journey to market was driven forward by one family's quest to find a treatment for their son's epilepsy. Scientific and public interest in CBD had been percolating for several years before the Food and Drug Administration finally approved Epidiolex in June. But CBD — which doesn't cause the mind-altering high that comes from THC, the primary psychoactive component of marijuana — was hard to study, because of tight restrictions on using cannabis in research. Sam Vogelstein's family and his doctors found ways to work around those restrictions in their fight to control his seizures. Sam's seizures started in 2005 when he was four years old. It's a moment his mother, Evelyn Nussenbaum, will never forget. The family was saying goodbye to a dinner guest when Sam's face suddenly slackened and he fell forward at the waist. Article continues after sponsorship "He did something that looked like a judo bow after a match," says Nussenbaum. Two months passed before Sam had another seizure, but then he started having them every week. Eventually he was suffering through 100 seizures a day. © 2018 npr

Keyword: Epilepsy; Drug Abuse
Link ID: 25296 - Posted: 08.06.2018

by Lindsey Bever It was a solution no parent wants to hear: To get rid of a brain tumor and stop their young son's seizures, surgeons would need to cut out one-sixth of his brain. But for Tanner Collins, it was the best option. A slow-growing tumor was causing sometimes-daily seizures, and medications commonly used to treat them did not seem to be working, his father said. But removing a portion of his brain was no doubt risky. That region — the right occipital and posterior temporal lobes — is important for facial recognition, and, without it, Tanner's parents wondered if he would recognize them. Tanner, who was 6 at the time, underwent surgery at the University of Pittsburgh Medical Center's Children's Hospital. Although his brain has had to work to adapt since then, he's had no major problems. Other than some visual impairment, Tanner, now 12, said he's “perfectly fine.” “As far as I’m concerned, I’m a perfectly normal 12-year-old boy,” Tanner said. Tanner's case was published Tuesday in the scientific journal Cell Reports, explaining how the 12-year-old's brain learned to adapt after a part largely responsible for visual processing was taken out. Marlene Behrmann, a cognitive neuroscientist and lead author of the paper, said Tanner was one of the first pediatric patients studied over the past several years in her laboratory at Carnegie Mellon University to determine the extent to which a child's brain can reorganize itself after certain sections are surgically removed. In Tanner's case, she said, surgeons took out his right occipital and posterior temporal lobes, which made up about one-third of the right hemisphere of his brain. © 1996-2018 The Washington Post

Keyword: Development of the Brain; Epilepsy
Link ID: 25287 - Posted: 08.03.2018

Jessica Wright When Abigail was 19 months old, she took a ferry with her mother Gillian across the English Channel during a move from Germany to England. On board, she played with a Belgian toddler whose mother, a doctor, took notice of Abigail’s tight muscles and lack of language. (Gillian asked that we omit their last names to protect their privacy.) “What syndrome does she have?” the doctor asked Gillian. Gillian didn’t know. In the coming years, Abigail would receive diagnoses of autism and intellectual disability; she also has recurrent seizures. But it took 20 years to get an answer to the Belgian doctor’s question. In 2013, Abigail’s doctor, Meena Balasubramanian, enrolled Abigail in Deciphering Developmental Disorders (DDD), a study in which researchers sequence an individual’s genes to find the cause of undiagnosed genetic conditions. In Abigail, they found a de novo, or spontaneous, mutation in a known epilepsy gene called HNRNPU. Gillian learned of the result just last year. Over the past year, this gene has emerged as a new autism candidate associated with a neurodevelopmental syndrome. Finding the genetic cause for Abigail’s condition sparked Balasubramanian’s interest in the gene. She has since collected clinical information from six other people with these mutations, five of whom were identified through DDD. These participants share Abigail’s learning difficulties and seizures. © 1986 - 2018 The Scientist.

Keyword: Epilepsy; Autism
Link ID: 25250 - Posted: 07.26.2018

Catherine Offord Researchers at Caltech have designed a noninvasive method to control specific neural circuits in the mouse brain. The technique, published earlier this week (July 9) in Nature Biomedical Engineering, combines ultrasound waves with genetic engineering and the administration of designer compounds to selectively activate or inhibit neurons. Although currently only tested in mice, the approach could offer a novel way to administer therapy to regions of the human brain that are difficult to access using surgery. “By using sound waves and known genetic techniques, we can, for the first time, noninvasively control specific brain regions and cell types as well as the timing of when neurons are switched on or off,” study coauthor Mikhail Shapiro says in a statement. While several emerging methods in neuroscience allow researchers to manipulate brain circuits, most “require invasive techniques such as stereotaxic surgery, which can damage tissue and initiate a long-lasting immune response,” note neuroscientists Caroline Menard and Scott Russo of Quebec City’s Université Laval and the Icahn School of Medicine at Mount Sinai, respectively, in an accompanying News and Views article. “Also, conventional pharmacological approaches lack the spatial, temporal and cell-type specificity required to treat the brain, and can lead to deleterious side effects.” © 1986 - 2018 The Scientist.

Keyword: Brain imaging
Link ID: 25218 - Posted: 07.17.2018

Amy Maxmen Legal hurdles to exploring marijuana’s medicinal properties might soon fall in the wake of the US Food and Drug Administration’s (FDA) first approval of a cannabis-derived drug. On 25 June, the FDA announced its approval of Epidiolex — a treatment for epileptic seizures that is based on a cannabis compound called cannabidiol (CBD). The US Drug Enforcement Administration (DEA) has until 24 September to re-classify Epidiolex so that it’s legal for doctors across the country to prescribe it. Many researchers hope that the agency will re-classify CBD itself, instead of just Epidiolex, so that they can more easily study this non-psychedelic component of marijuana. Now that the FDA has approved Epidiolex, “we have a clear recognition that this plant has more potential than people credited it for, and that has reverberations that are scientific as well as legal”, says Daniele Piomelli, director of a new centre for cannabis research at the University of California, Irvine. At the very least, he says, the DEA ought to grant researchers an exemption permitting them to study CBD — especially now that people consume it and other cannabis compounds, known as cannabinoids, in states where marijuana is legal. At this point, the limits on research seem irrational, he adds. Lessening restrictions on the study of CBD would also be good news for biotech startups that have been producing cannabinoids through genetic engineering. These products could be purer and more affordable than those obtained through older methods of extraction from marijuana plants or chemical synthesis. © 2018 Springer Nature Limited.

Keyword: Drug Abuse; Epilepsy
Link ID: 25194 - Posted: 07.11.2018

By Simon Makin The electrical oscillations we call brain waves have intrigued scientists and the public for more than a century. But their function—and even whether they have one, rather than just reflecting brain activity like an engine’s hum—is still debated. Many neuroscientists have assumed that if brain waves do anything, it is by oscillating in synchrony in different locations. Yet a growing body of research suggests many brain waves are actually “traveling waves” that physically move through the brain like waves on the sea. Now a new study from a team at Columbia University led by neuroscientist Joshua Jacobs suggests traveling waves are widespread in the human cortex—the seat of higher cognitive functions—and that they become more organized depending on how well the brain is performing a task. This shows the waves are relevant to behavior, bolstering previous research suggesting they are an important but overlooked brain mechanism that contributes to memory, perception, attention and even consciousness. Brain waves were first discovered using electroencephalogram (EEG) techniques, which involve placing electrodes on the scalp. Researchers have noted activity over a range of different frequencies, from delta (0.5 to 4 hertz) through to gamma (25 to 140 Hz) waves. The slowest occur during deep sleep, with increasing frequency associated with increasing levels of consciousness and concentration. Interpreting EEG data is difficult due to its poor ability to pinpoint the location of activity, and the fact that passage through the head blurs the signals. The new study, published earlier this month in Neuron, used a more recent technique called electrocorticography (ECoG). This involves placing electrode arrays directly on the brain’s surface, minimizing distortions and vastly improving spatial resolution. © 2018 Scientific American

Keyword: Attention
Link ID: 25159 - Posted: 06.29.2018

Shawna Williams The US Food and Drug Administration today (June 25) approved for the first time a marijuana-derived drug, Epidiolex, for the treatment of two rare forms of epilepsy. The drug contains cannabidiol, or CBD, and does not make users high while reducing the rate of seizures in patients with Dravet or Lennox-Gastaut syndromes, clinical trials show. “In my practice, I often see patients with these highly treatment-resistant epilepsies who have tried and failed existing therapies and are asking about CBD,” says Orrin Devinsky of NYU Langone Health, a lead investigator in the trials, in a statement released by the company that makes Epidiolex. “I am delighted that my physician colleagues and I will now have the option of a prescription cannabidiol that has undergone the rigor of controlled trials and been approved by the FDA to treat both children and adults.” Both Dravet and Lennox-Gastaut are relatively severe forms of epilepsy that can be fatal, STAT News notes. While there are other drugs approved to treat Lennox-Gastaut, there had previously been none for Dravet. Some parents have used unapproved CBD oils to treat their children. In a statement released today, FDA notes that it “has taken recent actions against companies distributing unapproved CBD products. . . . We’ll continue to take action when we see the illegal marketing of CBD-containing products with unproven medical claims.” © 1986 - 2018 The Scientist Magazine®

Keyword: Epilepsy; Drug Abuse
Link ID: 25148 - Posted: 06.27.2018

By Amanda Svachula Marcos Gardiana, a self-proclaimed Disney fanatic with five tattoos of Disney characters on his body to prove it, was excited to see the company’s latest blockbuster, “Incredibles 2,” on Sunday, and took his girlfriend along with him. He never got to see the end of it. Mr. Gardiana, 27, who has epilepsy as a result of a brain injury from a 2011 car accident, said he started getting lightheaded and dizzy in the theater. He had a “small” seizure at first, he said, and then a “blackout seizure, a full-on shaking seizure.” His girlfriend, Courtney Anderson, 21, led him to a bench outside. “He sat down for a minute, pale as a ghost,” she said. “He had a second, full-on seizure, eyes rolled back. And he lost consciousness.” Mr. Gardiana had apparently suffered seizures triggered by flashing lights during the movie, an unusual but also a well-established peril for some people with epilepsy. It was unclear whether the Walt Disney Company, which did not respond to requests for comment on Monday, had warned theaters about the danger. But beginning on Friday, the first full day of showings for “Incredibles 2,” signs began appearing in movie houses warning that a “sequence of flashing lights” may affect people who are susceptible to “photosensitive epilepsy or other photosensitivities.” But it appears that some epileptic viewers did not get the memo. Mr. Gardiana said he saw no warning signs in the Las Vegas theater he went to. The manager of the theater said that a sign had been posted on Friday but that she could not comment further. In Times Square, where the movie was showing at the Regal Cinemas, a sign did not go up on Monday until this reporter asked where it was; that theater’s manager declined to comment. © 2018 The New York Times Company

Keyword: Epilepsy
Link ID: 25103 - Posted: 06.19.2018

The Home Office has rejected a County Tyrone mother's plea to legalise cannabis oil for her epileptic son. Charlotte Caldwell accused Home Office minister Nick Hurd of having "likely signed my son's death warrant". Ms Caldwell brought cannabis oil from Canada for her son Billy, but it was confiscated at Heathrow on Monday. In 2017, the 12-year-old became the first person in the UK to be prescribed cannabis oil, but last month his GP was told he could no longer do so. Ms Caldwell, from Castlederg, said she was "absolutely devastated" to have the supply confiscated after she declared it to border officials. Ms Caldwell later met Mr Hurd at the Home Office to plead with him "parent to parent" to get the oil back. "It's Billy's anti-epileptic medication that Nick Hurd has taken away, it's not some sort of joint full of recreational cannabis," she said. "We had an honest and genuine conversation. I have asked him to give Billy back his medicines, but he said no." She also warned of the dangers of Billy missing his first dose of cannabis oil in 19 months. "The reason they don't do it is that it can cause really bad side-effects - they wean them down slowly," she said. "So what Nick Hurd has just done is most likely signed my son's death warrant." A Home Office spokeswoman said it was "sympathetic to the rare situation that Billy and his family are faced with". © 2018 BBC.

Keyword: Drug Abuse; Epilepsy
Link ID: 25079 - Posted: 06.12.2018

By Abby Olena The gut-brain axis is line of communication between the two organs, involved in everything from brain development to the progression of neurological diseases, with gut microbiota often pitching in to the conversation. In a study published today (May 16) in Nature, researchers present evidence that multiple sclerosis (MS) may also be influenced by commensal microbes in the gut acting upon cells in the brain. They show in a mouse model of the disease that metabolites from gut bacteria alter the behavior of microglia—immune cells that reside in the brain—which in turn regulate the activity of astrocytes to promote or prevent inflammation. The authors also found evidence in vitro and in patient samples that a similar gut-brain connection exists in people with MS, suggesting that microbes and the cells that receive their signals could be targets for disease treatment. “The beauty of this paper is that it provides a very detailed mechanistic understanding of how things work,” Jonathan Kipnis, a neuroscientist at the University of Virginia who did not participate in the study, tells The Scientist. Previous research linked the microbiome and the development of MS in mice, he says, but “we never understood how the gut communicates with the brain.” In work published in Nature Medicine in 2016, Francisco Quintana of Brigham and Women’s Hospital in Boston and colleagues found part of the answer to the question of gut-brain communication. In that study, they showed that mouse and human astrocytes—star-shape glial cells—respond to molecules generated by microbes from the intestine. And because prior work from other groups had demonstrated that microglia can regulate astrocyte behavior, Quintana says, “one of the biggest unanswered questions we had is: what mediates the crosstalk between microglia and astrocytes?” © 1986-2018 The Scientist

Keyword: Multiple Sclerosis; Glia
Link ID: 24992 - Posted: 05.18.2018

By Shawna Williams Even as patients with Parkinson’s disease, obsessive-compulsive disorder, and other conditions turn to deep brain stimulation (DBS) to keep their symptoms in check, it’s been unclear to scientists why the therapy works. Now, researchers in Texas report that in mice, the treatment dials the activity of hundreds of genes up or down in brain cells. Their results, published in eLife March 23, hint that DBS’s use could be expanded to include improving learning and memory in people with intellectual disabilities. “The paper is very well done. . . . It’s really a rigorous study,” says Zhaolan “Joe” Zhou, a neuroscientist at the University of Pennsylvania’s Perelman School of Medicine who reviewed the paper for eLife. Now that the genes and pathways DBS affects are known, researchers can home in on ways to improve the treatment, or perhaps combine the therapy with pharmacological approaches to boost its effect, he says. In DBS, two electrodes are surgically implanted in a patient’s brain (the area depends on the disorder being treated), and connected to generators that are placed in the chest. Gentle pulses of electricity are then passed continuously through the electrodes. The treatment reduces motor symptoms in many people with Parkinson’s, and allows some patients to reduce their use of medications, but it does not eliminate symptoms or slow the disease’s progression. In addition to its use in movement disorders, DBS is being explored as a potential therapy for a range of other brain-related disorders. For instance, as a way to boost learning and memory in people with Alzheimer’s disease, researchers are looking into stimulating the fimbria-fornix, a brain region thought to regulate the activity of the memory-storing hippocampus. © 1986-2018 The Scientist

Keyword: Parkinsons; Epigenetics
Link ID: 24982 - Posted: 05.16.2018

By PAM BELLUCK PORTLAND, Ore. — By the time her mother received the doctor’s email, Yuna Lee was already 2 years old, a child with a frightening medical mystery. Plagued with body-rattling seizures and inconsolable crying, she could not speak, walk or stand. “Why is she suffering so much?” her mother, Soo-Kyung Lee, anguished. Brain scans, genetic tests and neurological exams yielded no answers. But when an email popped up suggesting that Yuna might have a mutation on a gene called FOXG1, Soo-Kyung froze. “I knew,” she said, “what that gene was.” Almost no one else in the world would have had any idea. But Soo-Kyung is a specialist in the genetics of the brain—“a star,” said Robert Riddle, a program director in neurogenetics at the National Institute of Neurological Disorders and Stroke. For years, Soo-Kyung, a developmental biologist at Oregon Health and Science University, had worked with the FOX family of genes. “I knew how critical FOXG1 is for brain development,” she said. She also knew harmful FOXG1 mutations are exceedingly rare and usually not inherited — the gene mutates spontaneously during pregnancy. Only about 300 people worldwide are known to have FOXG1 syndrome, a condition designated a separate disorder relatively recently. The odds her own daughter would have it were infinitesimal. “It is an astounding story,” Dr. Riddle said. “A basic researcher working on something that might help humanity, and it turns out it directly affects her child.” Suddenly, Soo-Kyung, 42, and her husband Jae Lee, 57, another genetics specialist at O.H.S.U., had to transform from dispassionate scientists into parents of a patient, desperate for answers. © 2018 The New York Times Company

Keyword: Development of the Brain; Genes & Behavior
Link ID: 24897 - Posted: 04.24.2018

An epilepsy drug that can damage unborn babies must no longer be prescribed to girls and women of childbearing age in the UK unless they sign a form to say that they understand the risks. Drug regulator the MHRA says the new measures it's introducing will keep future generations of children safe. Those already on valproate medication should see their GP to have their treatment reviewed. No woman or girl should stop taking it without medical advice though. It is thought about 20,000 children in the UK have been left with disabilities caused by valproate since the drug was introduced in the 1970s. Affected families have called for a public inquiry and compensation. Epilepsy charities say one in five women on sodium valproate are unaware that taking it during pregnancy can harm the development and physical health of an unborn baby. Image caption This warning has been on the outside of valproate pill packets since 2016 in Britain And more than one in four have not been given information about risks for their unborn child. The MHRA has changed the licence for valproate, which means any doctor prescribing it will have to ensure female patients are put on a Pregnancy Prevention Programme, © 2018 BBC

Keyword: Development of the Brain; Epilepsy
Link ID: 24894 - Posted: 04.24.2018

By SHEILA KAPLAN WASHINGTON — A Food and Drug Administration advisory panel on Thursday unanimously recommended approval of an epilepsy medication made with an ingredient found in marijuana. If the agency follows the recommendation, as is expected, the drug would be the first cannabis-derived prescription medicine available in the United States. The drug, called Epidiolex, is made by GW Pharmaceuticals, a British company. Its active ingredient, cannabidiol, also called CBD, is one of the chemical compounds found in the cannabis plant, but it does not contain the properties that make people high. That makes it different from the “medical marijuana” allowed by a growing number of states. In those cases, certain patients are legally authorized to smoke or ingest marijuana to treat severe pain, nausea and other ailments. There are already several drugs on the market that are derived from synthetic versions of THC and other chemicals of the cannabis plant, generally used to ease nausea in cancer patients, and to help AIDS patients avoid weight loss. Advocates for development of marijuana-based treatments, and those pushing for better treatments of epilepsy, were pleased with the panel’s recommendation. “This is a very good development, and it basically underscores that there are medicinal properties to some of the cannabinoids,” said Dr. Igor Grant, director of the Center for Medicinal Cannabis Research at the University of California San Diego. “I think there could well be other cannabinoids that are of therapeutic use, but there is just not enough research on them to say.” © 2018 The New York Times Company

Keyword: Epilepsy; Drug Abuse
Link ID: 24889 - Posted: 04.21.2018

Nicky Phillips Before playing a guitar, musicians tune the strings to particular frequencies to get the pitch they want. Starting this week, a team of neuroscientists in Australia will apply a similar tuning process to human brains as part of a study to recalibrate abnormal neural patterns to a healthy state. The group, at Monash University in Melbourne, is conducting one of the first trials to use electrodes on people’s scalps, both to monitor their brain activity and to provide customized electrical stimulation. By tuning groups of neurons to specific frequencies, the team will attempt to alleviate people’s depression and other mood disorders. The Monash team is one of several around the world experimenting with such ‘closed loop’ systems — where stimulation is directed by the patient’s brain activity, which is in turn altered by the stimulation. “They’re doing something right at the cutting edge,” says Charlotte Stagg, a neurophysiologist at the University of Oxford, UK. “It’ll be pretty cool if they can get it to work.” Researchers hope such techniques will offer a better way than current stimulation techniques to correct abnormal brain patterns. Although at an early stage, the approach is a fundamental shift in the field and seeks to offer more personalization than is possible with brain-stimulation treatments routinely used in the clinic. Other teams, in the United States and Europe, have trialled closed-loop brain stimulation to treat Parkinson’s disease and for cognitive training, but the Melbourne team is among the first to use this approach for mood disorders. © 2018 Macmillan Publishers Limited,

Keyword: Depression
Link ID: 24829 - Posted: 04.06.2018