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

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Bret Stetka As the story goes, nearly 80 years ago on the Faroe Islands - a stark North Atlantic archipelago 200 miles off the coast of Scotland — a neurologic epidemic may have washed, or rather convoyed, ashore. Before 1940 the incidence of multiple sclerosis on the Faroes was near, if not, zero, according to the tantalizing lore I recall from medical school. Yet in the years following British occupation of the islands during World War II, the rate of MS rose dramatically, leading many researchers to assume the outbreak was caused by some unknown germ transmitted by the foreign soldiers. We now know that MS is not infectious in the true sense of the word. It is not contagious in the way, say, the flu is. But infection does likely play a role in MS. As may be the case in Alzheimer's disease, it's looking more and more like MS strikes when infectious, genetic and immune factors gang up to eventually impair the function of neurons in the brain and spinal cord. Researchers are hoping to better understand this network of influences to develop more effective ways to treat MS, and perhaps prevent it in the first place. In the MS-free brain, electrical impulses zip down nerve fibers called axons causing the release of neurotransmitters. The wiring allows neurons to communicate with each other and generate biologic wonders like thought, sensation and movement. In many regions of the brain those axons are encased in an insulating jacket of protein and fat called myelin, which increases the speed that electrical nerve impulses travel. © 2019 npr

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 25893 - Posted: 01.22.2019

Laura Sanders Using laser light, ballooning tissue and innovative genetic tricks, scientists are starting to force brains to give up their secrets. By mixing and matching powerful advances in microscopy and cell biology, researchers have imaged intricate details of individual nerve cells in fruit flies and mice, and even controlled small groups of nerve cells in living mice. The techniques, published in two new studies, represent big steps forward for understanding how the brain operates, says molecular neuroscientist Hongkui Zeng of the Allen Institute for Brain Science in Seattle. “Without this kind of technology, we were only able to look at the soup level,” in which diverse nerve cells, or neurons, are grouped and analyzed together, she says. But the new studies show that nerve cells can be studied individually. That zoomed-in approach will begin to uncover the tremendous diversity that’s known to exist among cells, says Zeng, who was not involved in the research. “That is where the field is going. It’s very exciting to see that technologies are now enabling us to do that,” she says. These novel abilities came from multiple tools. At Howard Hughes Medical Institute’s Janelia Research Campus in Ashburn, Va., physicist Eric Betzig and his colleagues had developed a powerful microscope that can quickly peer deep into layers of brain tissue. Called a lattice light sheet microscope, the rig sweeps a thin sheet of laser light down through the brain, revealing cells’ structures. But like any microscope, it hits a wall when structures get really small, unable to resolve the most minute aspects of the scene. |© Society for Science & the Public 2000 - 2019.

Keyword: Brain imaging
Link ID: 25878 - Posted: 01.18.2019

By Kelly Servick In multiple sclerosis (MS), a disease that strips away the sheaths that insulate nerve cells, the body’s immune cells come to see the nervous system as an enemy. Some drugs try to slow the disease by keeping immune cells in check, or by keeping them away from the brain. But for decades, some researchers have been exploring an alternative: wiping out those immune cells and starting over. The approach, called hematopoietic stem cell transplantation (HSCT), has long been part of certain cancer treatments. A round of chemotherapy knocks out the immune system and an infusion of stem cells—either from a patient’s own blood or, in some cases, that of a donor—rebuilds it. The procedure is already in use for MS and other autoimmune diseases at several clinical centers around the world, but it has serious risks and is far from routine. Now, new results from a randomized clinical trial suggest it can be more effective than some currently approved MS drugs. “A side-by-side comparison of this magnitude had never been done,” says Paolo Muraro, a neurologist at Imperial College London who has also studied HSCT for MS. “It illustrates really the power of this treatment—the level of efficacy—in a way that’s very eloquent.” Nearly 30 years ago, when hematologist Richard Burt saw how HSCT worked in patients with leukemia and lymphoma, he was struck by a curious effect: After those patients rebuilt their immune systems, their childhood vaccines no longer protected them, recalls Burt, now at Northwestern University’s Feinberg School of Medicine in Evanston, Illinois. Without a new vaccination, the new immune cells wouldn’t recognize viruses such as measles and mumps and launch a prompt counterattack. That suggested that in the case of an autoimmune disease, reseeding the immune system might help the body “forget” that its own cells were the enemy. © 2018 American Association for the Advancement of Science

Keyword: Multiple Sclerosis
Link ID: 25870 - Posted: 01.16.2019

Abby Olena In the never-ending search for ways to help people eat healthy, scientists have been looking into brain stimulation, specifically, sending a weak electrical current to the brain through two scalp electrodes—a technique called transcranial direct current stimulation. It has previously shown promise in limiting both food cravings and consumption in people, but in a study published yesterday (January 9) in Royal Society Open Science, researchers didn’t find any effects of tDCS on food-related behavior, indicating that the technique’s use needs another look. “The good things about the study are the large sample size and the fact that it’s fairly rigorous,” says Mark George, a psychiatrist and neurologist at the Medical University of South Carolina who did not participate in the study. “The problem [is] interpreting studies where there’s a failure to find. All you can say is that it didn’t work . . . with this group.” During tDCS, one to two milliamps of electricity—enough to feel tingles or pins and needles, but far less than the 800 or so milliamps used for electroconvulsive therapy—are delivered to the brain. Over the last two decades, scientists have reported targeting the technique to the dorsolateral prefrontal cortex, a brain area that’s been shown to be involved in food-related behavior. They’ve found it has helped people crave less and, to a lesser extent, eat fewer sweets and other tempting foods. Yet these experiments have generally included groups of 20 or fewer people, and other studies have failed to replicate their effects. © 1986 - 2019 The Scientist.

Keyword: Obesity
Link ID: 25861 - Posted: 01.14.2019

By Kara Manke A new neurostimulator developed by engineers at UC Berkeley can listen to and stimulate electric current in the brain at the same time, potentially delivering fine-tuned treatments to patients with diseases like epilepsy and Parkinson’s. The device, named the WAND, works like a “pacemaker for the brain,” monitoring the brain’s electrical activity and delivering electrical stimulation if it detects something amiss. These devices can be extremely effective at preventing debilitating tremors or seizures in patients with a variety of neurological conditions. But the electrical signatures that precede a seizure or tremor can be extremely subtle, and the frequency and strength of electrical stimulation required to prevent them is equally touchy. It can take years of small adjustments by doctors before the devices provide optimal treatment. WAND, which stands for wireless artifact-free neuromodulation device, is both wireless and autonomous, meaning that once it learns to recognize the signs of tremor or seizure, it can adjust the stimulation parameters on its own to prevent the unwanted movements. And because it is closed-loop — meaning it can stimulate and record simultaneously — it can adjust these parameters in real-time. © 2019 UC Regents;

Keyword: Epilepsy
Link ID: 25830 - Posted: 01.01.2019

By Kimon de Greef CAPE TOWN — A musician from South Africa had a tumor in his brain, so doctors opened a hole in his skull to remove it. But they had a crucial request: He must play his acoustic guitar during the surgery. The musician, Musa Manzini, a jazz bassist, was awake when the doctors performed the surgery last week, and video footage from the local media site News24 shows him strumming an acoustic guitar slowly as they operated. The technique, known as “awake craniotomy,” allows doctors to operate on delicate areas of the brain — like the right frontal lobe, the site of Mr. Manzini’s tumor — without causing damage. Presumably, had he hit a wrong note, it would have been an immediate signal for the surgeons to probe elsewhere. “It can be very difficult to tell the difference between the tumor and normal brain tissue,” said Dr. Basil Enicker, a specialist neurosurgeon who led the operation at Inkosi Albert Luthuli Central Hospital, in the coastal city of Durban. “Once you’re near a critical area, you can pick it up early, because he will tell you.” The surgery is not unusual. The first craniotomies date to prehistoric times, with fossil records showing that patients had holes drilled in their skulls — and survived — as early as 8,000 years ago. In the 1930s, the Canadian-American neurosurgeon Wilder Penfield pioneered modern craniotomies, which he used to treat epilepsy. The procedure has become fairly common globally since then, posing no greater technical challenge than regular brain surgery, Dr. Enicker said. But choosing patients is very important: People who cough, for example, or who cannot lie still for extended periods, are far more dangerous to operate on. © 2018 The New York Times Company

Keyword: Brain imaging; Epilepsy
Link ID: 25815 - Posted: 12.22.2018

It started when Andi Dreher was only three years old. Her head slumped over, her face went blank. It was the first of many epileptic seizures that the Ontario child would endure. At the beginning, Andi would have a couple of seizures a year, but the condition slowly progressed. By the time she turned seven, she was having up to 150 seizures a day. Her family has come to call them "glitches." "The other day at school, she had 27 glitches in less than an hour," said her mom, Lori Dreher. The seizures make it difficult for Andi to do even the simplest tasks, such as walking, talking and eating. "She knows she used to play soccer and she used to do cheerleading — that she used to do these things and now she can't. That's hard." her mom said. 'We're guinea pigs': Canada's oversight process for implanted medical devices stuns suffering patients Among serious neurological conditions in children, epilepsy is the most common. For most, the condition can be controlled by medications. "But about one-third of children who have epilepsy don't respond to medication. A subset of them can potentially be helped by a variety of surgical treatment," said Dr. George Ibrahim, the pediatric neurosurgeon at the Hospital for Sick Children who operated on Andi. Dr. George Ibrahim, pediatric neurosurgeon at the Hospital for Sick Children, examines an image of Andi's brain. (Kelda Yuen/ CBC) When Andi and her family came from Kitchener to meet him last year, Ibrahim said he was struck by the severity of her case. "Her brain is developed in a very unique way," he said. ©2018 CBC/Radio-Canada

Keyword: Epilepsy
Link ID: 25784 - Posted: 12.13.2018

Ashley P. Taylor Electrically stimulating the lateral orbitofrontal cortex, a brain area behind the eyes, improves the moods of people with depression, according to a study published yesterday (November 29) in Current Biology. The technique used by the researchers, led by Edward Chang of the University of California, San Francisco, is called deep brain stimulation (DBS), in which surgically implanted electrodes send electrical pulses to particular areas of the brain. The approach is already in use as a treatment for movement disorders such as Parkinson’s disease and tremors. But results on its ability to treat depression have been mixed, as NPR reports. The researchers worked with 25 epilepsy patients who already had electrodes implanted into their brains as part of their treatments. Many of the study participants also had signs of depression as evaluated by mood tests the researchers administered, Science News reports. The investigators tried stimulating many areas of the brain, and they found that jolts to the lateral orbitofrontal cortex made patients with signs of depression—but not others who didn’t have symptoms—feel better right away. “Wow, I feel a lot better. . . . What did you guys do?” study coauthor Kristin Sellers recalls a patient exclaiming after receiving the stimulation, she tells NPR. “Only the people who had symptoms [of depression] to start with improved their mood, which suggests that perhaps the effect of what we’re doing is to normalize activity that starts off abnormal,” adds another coauthor, Vikram Rao.

Keyword: Depression
Link ID: 25742 - Posted: 12.03.2018

Jon Hamilton There's new evidence that mild pulses of electricity can relieve depression — if they reach the right target in the brain. A study of 25 people with epilepsy found that those who had symptoms of depression felt better almost immediately when doctors electrically stimulated an area of the brain just above the eyes, a team reported Thursday in the journal Current Biology. These people were in the hospital awaiting surgery and had wires inserted into their brains to help doctors locate the source of their seizures. Several of the patients talked about the change they felt when the stimulation of the lateral orbitofrontal cortex began, says Kristin Sellers, an author of the paper and a postdoctoral researcher at the University of California, San Francisco. One person's response was: "Wow, I feel a lot better. ... What did you guys do?" The stimulation only lasted a few minutes. After it stopped, the effect on mood quickly faded. To be sure that the effect was real, the researchers also pretended to stimulate the lateral OFC in the same patients without actually running current through the tiny wires implanted in their brains. In those sham treatments, there was no discernible change. DBS is an approved treatment for tremors, including those associated with Parkinson's disease. But results with depression have been less consistent, and DBS isn't approved for this purpose by the Food and Drug Administration. © 2018 npr

Keyword: Depression
Link ID: 25735 - Posted: 11.30.2018

By R. Douglas Fields SAN DIEGO—In the textbook explanation for how information is encoded in the brain, neurons fire a rapid burst of electrical signals in response to inputs from the senses or other stimulation. The brain responds to a light turning on in a dark room with the short bursts of nerve impulses, called spikes. Each close grouping of spikes can be compared to a digital bit, the binary off-or-on code used by computers. Neuroscientists have long known, though, about other forms of electrical activity present in the brain. In particular, rhythmic voltage fluctuations in and around neurons—oscillations that occur at the same 60-cycle-per-second frequency as AC current in the U.S.—have caught the field’s attention. These gamma waves encode information by changing a signal’s amplitude, frequency or phase (relative position of one wave to another)—and the rhythmic voltage surges influence the timing of spikes. Heated debate has arisen in recent years as to whether these analog signals, akin to the ones used to broadcast AM or FM radio, may play a role in sorting, filtering and organizing the information flows required for cognitive processes. They may be instrumental in perceiving sensory inputs, focusing attention, making and recalling memories and coupling various cognitive processes into one coherent scene. It is thought that populations of neurons that oscillate at gamma frequencies may unite the neural activity in the same way the violin section of an orchestra is coupled together in time and rhythm with the percussion section to create symphonic music. When gamma waves oscillate in resonance, “you get very rich repertoires of behaviors,” says Wolf Singer, a neuroscientist at the Ernst Strüngmann Institute in Frankfurt, Germany, who researches gamma waves. Just as your car’s dashboard will vibrate in sync with the motor vibrating at a resonant frequency, so too can separate populations of neurons couple in resonance. © 2018 Scientific American

Keyword: Brain imaging
Link ID: 25731 - Posted: 11.29.2018

Jef Akst After publishing a 2014 study showing that noninvasive magnetic stimulation of the brain boosted people’s ability to remember an association between two items, Northwestern University neuroscientist Joel Voss began fielding a lot of questions from patients and their families. “We’re of course guarded in the publication talking about what we found—small but reliable increases in memory ability,” he says (Science, 345:1054–57). But some of the news coverage of that paper alluded to the procedure’s potential to treat Alzheimer’s disease and other memory-related disorders. “I got calls—at least two a day for quite a long period of time—and emails: ‘My loved one is suffering from X, Y, or Z; thank God now you can cure it. How do we get to your lab?’” Voss says. He would have to explain to them that this was a scientific study, not an approved treatment. “There are a million steps between here and there, and maybe it would never work—we don’t really know.” But Voss’s team continues to connect those dots, in hopes that one day the technique—the use of magnetic fields to influence activity in neurons close to the brain’s surface—could help patients with any number of brain disorders, and perhaps cognitively healthy people as well. In August, the researchers reported that transcranial magnetic stimulation (TMS) could moderately improve episodic memory—the ability to remember people, events, and other things you’ve encountered in your life (as opposed to, say, how to do something)—when targeted at the correct part of the brain. Voss and his colleagues were interested in activating the hippocampus, a structure near the brain’s center that serves as a hub of memory production and storage. Because the hippocampus itself is inaccessible by TMS—the magnetic field falls off precipitously with depth, explains Voss—the researchers instead targeted areas of the brain where activity correlated with activity in the hippocampus, to try to activate the networks that link more-superficial regions with the deep-brain structure. © 1986 - 2018 The Scientist

Keyword: Learning & Memory
Link ID: 25722 - Posted: 11.27.2018

At 35, Sharon Jakab knew something was wrong when she started hallucinating. "I saw my grandmother on the wall in the room. She was talking to me. I wasn't sleeping, and I was a mess," she says from her home in Burlington, Ont. Jakab had been suffering from postpartum depression following the birth of her daughter. About a year and a half later, Jakab had another episode of postpartum depression following an ectopic pregnancy. It became so bad, she was suicidal. "There was a gun in the house and there were cartridges. I was all set to kill myself." She had to suicide-proof her home by taking away all dangerous objects, even skates, which have sharp blades. Now 61, Jakab has been in and out of hospitals, dealing with what she calls "waves of depression" that have lasted most of her adult life. She's tried about a dozen medications, including the antipsychotic drug clozapine. "Clozapine really helped me a lot, but I still suffered from depression, psychosis and mania." Because standard treatment like medication and therapy weren't effective, Jakab was diagnosed with treatment-resistant depression, a severe form of depression that close to a million Canadians experience. Electroconvulsive therapy or ECT, better known as shock treatment, is still considered the go-to treatment but comes with the common side effect of memory loss. So doctors are now exploring less invasive experimental approaches like brain stimulation that rewires the brain's circuits. ©2018 CBC/Radio-Canada

Keyword: Depression
Link ID: 25718 - Posted: 11.26.2018

Sara Reardon ‘Mini brains’ grown in a dish have spontaneously produced human-like brain waves for the first time — and the electrical patterns look similar to those seen in premature babies. The advancement could help scientists to study early brain development. Research in this area has been slow, partly because it is difficult to obtain fetal-tissue samples for analysis and nearly impossible to examine a fetus in utero. Many researchers are excited about the promise of these ‘organoids’, which, when grown as 3D cultures, can develop some of the complex structures seen in brains. But the technology also raises questions about the ethics of creating miniature organs that could develop consciousness. A team of researchers led by neuroscientist Alysson Muotri of the University of California, San Diego, coaxed human stem cells to form tissue from the cortex — a brain region that controls cognition and interprets sensory information. They grew hundreds of brain organoids in culture for 10 months, and tested individual cells to confirm that they expressed the same collection of genes seen in typical developing human brains1. The group presented the work at the Society for Neuroscience meeting in San Diego this month. Muotri and his colleagues continuously recorded electrical patterns, or electroencephalogram (EEG) activity, across the surface of the mini brains. By six months, the organoids were firing at a higher rate than other brain organoids previously created, which surprised the team. © 2018 Springer Nature Limited.

Keyword: Development of the Brain; Epilepsy
Link ID: 25694 - Posted: 11.16.2018

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