Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
Sam McDougle By now, perhaps you’ve seen the trailer for the new sci-fi thriller Lucy. It starts with a flurry of stylized special effects and Scarlett Johansson serving up a barrage of bad-guy beatings. Then comes Morgan Freeman, playing a professorial neuroscientist with the obligatory brown blazer, to deliver the film’s familiar premise to a full lecture hall: “It is estimated most human beings only use 10 percent of the brain’s capacity. Imagine if we could access 100 percent. Interesting things begin to happen.” Johansson as Lucy, who has been kidnapped and implanted with mysterious drugs, becomes a test case for those interesting things, which seem to include even more impressive beatings and apparently some kind of Matrix-esque time-warping skills. Of course, the idea that “you only use 10 percent of your brain” is, indeed, 100 hundred percent bogus. Why has this myth persisted for so long, and when is it finally going to die? Unfortunately, not any time soon. A survey last year by The Michael J. Fox Foundation for Parkinson's Research found that 65 percent of Americans believe the myth is true, 5 percent more than those who believe in evolution. Even Mythbusters, which declared the statistic a myth a few years ago, further muddied the waters: The show merely increased the erroneous 10 percent figure and implied, incorrectly, that people use 35 percent of their brains. The idea that swaths of the brain are stagnant pudding while one section does all the work is silly. Like most legends, the origin of this fiction is unclear, though there are some clues. © 2014 by The Atlantic Monthly Group
Keyword: Brain imaging
Link ID: 19848 - Posted: 07.17.2014
By Tanya Lewis and Live Science They say laughter is the best medicine. But what if laughter is the disease? For a 6-year-old girl in Bolivia who suffered from uncontrollable and inappropriate bouts of giggles, laughter was a symptom of a serious brain problem. But doctors initially diagnosed the child with “misbehavior.” “She was considered spoiled, crazy — even devil-possessed,” José Liders Burgos Zuleta of the Advanced Medical Image Centre in La Paz said in a statement. [ But Burgos Zuleta discovered that the true cause of the girl’s laughing seizures, medically called gelastic seizures, was a brain tumor. After the girl underwent a brain scan, the doctors discovered a hamartoma, a small, benign tumor that was pressing against her brain’s temporal lobe. Surgeons removed the tumor, the doctors said. She stopped having the uncontrollable attacks of laughter and now laughs only normally, they said. Gelastic seizures are a relatively rare form of epilepsy, said Solomon Moshé, a pediatric neurologist at Albert Einstein College of Medicine in New York. “It’s not necessarily ‘ha-ha-ha’ laughing,” Moshé said. “There’s no happiness in this. Some of the kids may be very scared,” he added. The seizures are most often caused by tumors in the hypothalamus, although they can also come from tumors in other parts of brain, Moshé said. Although laughter is the main symptom, patients may also have outbursts of crying.
In a new study, scientists at the National Institutes of Health took a molecular-level journey into microtubules, the hollow cylinders inside brain cells that act as skeletons and internal highways. They watched how a protein called tubulin acetyltransferase (TAT) labels the inside of microtubules. The results, published in Cell, answer long-standing questions about how TAT tagging works and offer clues as to why it is important for brain health. Microtubules are constantly tagged by proteins in the cell to designate them for specialized functions, in the same way that roads are labeled for fast or slow traffic or for maintenance. TAT coats specific locations inside the microtubules with a chemical called an acetyl group. How the various labels are added to the cellular microtubule network remains a mystery. Recent findings suggested that problems with tagging microtubules may lead to some forms of cancer and nervous system disorders, including Alzheimer’s disease, and have been linked to a rare blinding disorder and Joubert Syndrome, an uncommon brain development disorder. “This is the first time anyone has been able to peer inside microtubules and catch TAT in action,” said Antonina Roll-Mecak, Ph.D., an investigator at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), Bethesda, Maryland, and the leader of the study. Microtubules are found in all of the body’s cells. They are assembled like building blocks, using a protein called tubulin. Microtubules are constructed first by aligning tubulin building blocks into long strings. Then the strings align themselves side by side to form a sheet. Eventually the sheet grows wide enough that it closes up into a cylinder. TAT then bonds an acetyl group to alpha tubulin, a subunit of the tubulin protein.
Link ID: 19729 - Posted: 06.14.2014
by Clare Wilson There is a new way to hack the brain. A technique that involves genetically engineering brain cells so that they fire in the presence of certain drugs has been used to treat an epilepsy-like condition in rats, and it could soon be trialled in humans. Chemogenetics builds on optogenetics, which involves engineering brain cells so they "fire" when lights are turned on. Selected neurons can then be activated with the flick of a switch. But this requires fibre optic cables to be implanted in the brain, which is impractical for treating human brain disorders. In chemogenetics, however, no cables are needed because neurons are altered to fire in the presence of a certain chemical rather than light. "It's got more potential in that you can give drugs to people more easily than you can get light into their brains," says Dimitri Kullmann of University College London. Stop the neurons Kullmann's team tested the approach by using a harmless virus to deliver a gene into the brains of rats. The gene encoded a protein that stops neurons from firing – but only in the presence of a chemical called clozapine N-oxide (CNO). Several weeks later, they injected the rats with chemicals that trigger brain seizures, to mimic epilepsy. If the rats were then given CNO, the severity of their seizures dropped within 10 minutes. This is the first time the technique has been used to treat a brain disorder, Kullmann says. "The system is neat," says Arnd Pralle of the University of Buffalo in New York state. But he points out that optogenetics allows faster control than this, because light can be turned on and off instantly. © Copyright Reed Business Information Ltd.
Link ID: 19668 - Posted: 05.28.2014
Sara Reardon The researchers' technique shows neurons throughout the body twinkling with activity. Researchers have for the first time imaged all of the neurons firing in a living organism, the nematode worm Caenorhabditis elegans. The achievement, reported today in Nature Methods1 shows how signals travel through the body in real time. Scientists mapped the connections among all 302 of the nematode's neurons in 19862 — a first that has not been repeated with any other organism. But this wiring diagram, or 'connectome', does not allow researchers to determine the neuronal pathways that lead to a particular action. Nor does it allow researchers to predict what the nematode will do at any point in time, says neuroscientist Alipasha Vaziri of the University of Vienna. By providing a means of displaying signaling activity between neurons in three dimensions and in real-time, the new technique should allow scientists to do both. Vaziri and his colleagues engineered C. elegans so that when a neuron fires and calcium ions pass through its cell membranes, the neuron lights up. To capture those signals, they imaged the whole worm using a technique called light-field deconvolution microscopy, which combines images from a set of tiny lenses and analyses them using an algorithm to give a high-resolution three-dimensional image. The researchers took as many as 50 images per second of the entire worm, enabling them to watch the neurons firing in the brain, ventral cord, and tail (see video). Next, the group applied the technique to the transparent larvae of the zebrafish (Danio rerio), imaging the entire brain as the fish responded to the odours of chemicals pumped into their water. They were able to capture the activity of about 5,000 neurons simultaneously (the zebrafish has about 100,000 total neurons). © 2014 Nature Publishing Group
Keyword: Brain imaging
Link ID: 19631 - Posted: 05.18.2014
By Pippa Stephens Health reporter, BBC News A key difference in the brains of male and female MS patients may explain why more women than men get the disease, a study suggests. Scientists at Washington University School of Medicine in the US found higher levels of protein S1PR2 in tests on the brains of female mice and dead women with MS than in male equivalents. Four times more women than men are currently diagnosed with MS. Experts said the finding was "really interesting". MS affects the nerves in the brain and spinal cord, which causes problems with muscle movement, balance and vision. It is a major cause of disability, and affects about 100,000 people in the UK. Abnormal immune cells attack nerve cells in the central nervous system in MS patients. There is currently no cure, although there are treatments that can help in the early stages of the disease. Researchers in Missouri looked at relapsing remitting MS, where people have distinct attacks of symptoms that then fade away either partially or completely. About 85% of people with MS are diagnosed with this type. Scientists studied the blood vessels and brains of healthy mice, mice with MS, and mice without the gene for S1PR2, a blood vessel receptor protein, to see how it affected MS severity. They also looked at the brain tissue samples of 20 people after they had died. They found high levels of S1PR2 in the areas of the brain typically damaged by MS in both mice and people. The activity of the gene coding for S1PR2 was positively correlated with the severity of the disease in mice, the study said. Scientists said S1PR2 could work by helping to make the blood-brain barrier, in charge of stopping potentially harmful substances from entering the brain and spinal fluid, more permeable. BBC © 2014
by Andy Coghlan A pregnancy hormone could prove a simple way to treat multiple sclerosis, after showing promise in a trial of 158 women with MS. MS is a neurological condition that results from damage to the brain and nerves inflicted by the body's own immune system. It affects 2.3 million people worldwide. Symptoms include extreme tiredness, blurred vision, muscle weakness and problems with balance and movement. The symptoms of women with MS tend to ease when they are pregnant, but worsen again after giving birth. This could be because of a hormone called oestriol, which is only produced in significant amounts during pregnancy. The hormone is thought to help suppress the mother's immune system to prevent it attacking the fetus. Fewer relapses Rhonda Voskuhl of the University of California, Los Angeles, and her colleagues wondered whether giving oestriol to people with MS who aren't pregnant might also help with symptoms. They gave 8 milligrams of oestriol daily to 86 women with MS, along with their medication, Copaxone (glatiramer acetate). The women had the most common form of MS, called relapsing-remitting MS, which results in periodic flare-ups of symptoms followed by recovery. After one year, they had 47 per cent fewer relapses than a control group that took Copaxone and a placebo. After two years, the relapse rate was 32 per cent lower than the control group in the group given the hormone, suggesting the effects had plateaued. "We think the oestriol group had bottomed out, and there was nothing left to improve," Voskuhl said, as she presented the preliminary results at the annual meeting of the American Academy of Neurology in Philadelphia last week. © Copyright Reed Business Information Ltd.
Combining the estrogen hormone estriol with Copaxone, a drug indicated for the treatment of patients with relapsing forms of multiple sclerosis (MS), may improve symptoms in patients with the disorder, according to preliminary results from a clinical study of 158 patients with relapsing remitting multiple sclerosis (RRMS). The findings were presented today by Rhonda Voskuhl, M.D., from the University of California, Los Angeles, at the American Academy of Neurology Annual Meeting in Philadelphia. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health; and the National Multiple Sclerosis Society. “While these results are encouraging, the results of this Phase II study should be considered preliminary as a larger study would be needed to know whether benefits outweigh the risks for persons affected by MS. At present, we cannot recommend estrogen as part of standard therapy for MS. We encourage patients to talk with their doctors before making any changes to their treatment plans,” said Walter Koroshetz, M.D., deputy director of NINDS. MS is an autoimmune disorder in which immune cells break down myelin, a protective covering that wraps around nerve cells. Loss of myelin results in pain, movement and balance problems as well as changes in cognitive ability. RRMS is the most common form of the disorder. Patients with RRMS experience relapses, or flare-ups, of neurological symptoms, followed by recovery periods during which the symptoms improve.
Scientists have bioengineered, in neurons cultured from rats, an enhancement to a cutting edge technology that provides instant control over brain circuit activity with a flash of light. The research funded by the National Institutes of Health adds the same level of control over turning neurons off that, until now, had been limited to turning them on. “What had been working through a weak pump can now work through a highly responsive channel with many orders of magnitude more impact on cell function,” explained Karl Deisseroth, M.D., Ph.D., It is like going from a squirt to a gushing hose. Deisseroth and colleagues report on what is being hailed as a marvel of genetic engineering in the April 25, 2014 issue of the journal Science. Deisseroth’s team had pioneered the use of light pulses to control brain circuitry in animals genetically engineered to be light-responsive — optogenetics. Genes that allow the sun to control light-sensitive primitive organisms like algae, melded with genes that make fluorescent marker proteins, are fused with a deactivated virus that delivers them to specific types of neurons which they become part of — allowing pulses of light to similarly commandeer brain cells.
Keyword: Brain imaging
Link ID: 19537 - Posted: 04.26.2014
By JAMES GORMAN SAN DIEGO — Dr. Karl Deisseroth is having a very early breakfast before the day gets going at the annual meeting of the Society for Neuroscience. Thirty thousand people who study the brain are here at the Convention Center, a small city’s worth of badge-wearing, networking, lecture-attending scientists. For Dr. Deisseroth, though, this crowd is a bit like the gang at Cheers — everybody knows his name. He is a Stanford psychiatrist and a neuroscientist, and one of the people most responsible for the development of optogenetics, a technique that allows researchers to turn brain cells on and off with a combination of genetic manipulation and pulses of light. He is also one of the developers of a new way to turn brains transparent, though he was away when some new twists on the technique were presented by his lab a day or two earlier. “I had to fly home to take care of the kids,” he explained. He went home to Palo Alto to be with his four children, while his wife, Michelle Monje, a neurologist at Stanford, flew to the conference for a presentation from her lab. Now she was home and, here he was, back at the conference, looking a bit weary, eating eggs, sunny side up, and talking about the development of new technologies in science. A year ago, President Obama announced an initiative to invest in new research to map brain activity, allocating $100 million for the first year. The money is a drop in the bucket compared with the $4.5 billion the National Institutes of Health spends annually on neuroscience, but it is intended to push the development of new techniques to investigate the brain and map its pathways, starting with the brains of small creatures like flies. Cori Bargmann of Rockefeller University, who is a leader of a committee at the National Institutes of Health setting priorities for its piece of the brain initiative, said optogenetics was a great example of how technology could foster scientific progress. © 2014 The New York Times Company
Keyword: Brain imaging
Link ID: 19520 - Posted: 04.22.2014
by Ashley Yeager A nerve cell's long, slender tentacle isn’t evenly coated with an insulating sheath as scientists had thought. Instead, many nerve cells in the brains of mice have stretches of these tentacles, called axons, that are naked, researchers report April 18 in Science. The unsheathed feeler can be as long as 80 micrometers. Nerve cells can also have specific patterns in the gaps of the insulating layer, called myelin. The differences in the thickness of that coating may control how fast signals travel between nerve cells, the scientists suggest. The finding could have implications for understanding nerve-based diseases, such as multiple sclerosis, and improve scientists’ understanding of how signals are transmitted in the brain. © Society for Science & the Public 2000 - 2013.
Everything we do — all of our movements, thoughts and feelings – are the result of neurons talking with one another, and recent studies have suggested that some of the conversations might not be all that private. Brain cells known as astrocytes may be listening in on, or even participating in, some of those discussions. But a new mouse study suggests that astrocytes might only be tuning in part of the time — specifically, when the neurons get really excited about something. This research, published in Neuron, was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. For a long time, researchers thought that the star-shaped astrocytes (the name comes from the Greek word for star) were simply support cells for the neurons. It turns out that these cells have a number of important jobs, including providing nutrients and signaling molecules to neurons, regulating blood flow, and removing brain chemicals called neurotransmitters from the synapse. The synapse is the point of information transfer between two neurons. At this connection point, neurotransmitters are released from one neuron to affect the electrical properties of the other. Long arms of astrocytes are located next to synapses, where they can keep tabs on the conversations going on between neurons. In recent years, it has been shown that astrocytes may also play a role in neuronal communication. When neurons release neurotransmitters, levels of calcium change within astrocytes. Calcium is critical for many processes, including release of molecules from the cell, and activation of a host of proteins within the cell. The role of this astrocytic calcium signaling for brain function remains a mystery.
Link ID: 19505 - Posted: 04.17.2014
By CATHERINE SAINT LOUIS ALEXANDRIA, N.H. — For most of his life, Kevin Ramsey has lived with epileptic seizures that drugs cannot control. At least once a month, he would collapse, unconscious and shaking violently, sometimes injuring himself. Nighttime seizures left him exhausted at dawn, his tongue a bloody mess. After episodes at work, he struggled to stay employed. Driving became too risky. At 28, he sold his truck and moved into his mother’s spare bedroom. Cases of intractable epilepsy rarely have happy endings, but today Mr. Ramsey is seizure-free. A novel battery-powered device implanted in his skull, its wires threaded into his brain, tracks its electrical activity and quells impending seizures. At night, he holds a sort of wand to his head and downloads brain data from the device to a laptop for his doctors to review. “I’m still having seizures on the inside, but my stimulator is stopping all of them,” said Mr. Ramsey, 36, whose hands shake because of one of the three anti-seizure drugs he still must take. “I can do things on my own I couldn’t do before. I can go to the store on my own, and get my groceries. Before, I wouldn’t have been able to drive.” Just approved by the Food and Drug Administration, the long-awaited device, called the RNS System, aims to reduce seizures and to improve the lives of an estimated 400,000 Americans whose epilepsy cannot be treated with drugs or brain surgery. “This is the first in what I believe is a new generation of therapy for epilepsy,” said Dr. Dileep R. Nair, head of adult epilepsy at the Cleveland Clinic and an investigator in the pivotal trial for NeuroPace’s RNS. “It’s delivering local therapy. It’s not taking tissue out; the brain is left intact. And it’s unlike a drug, which is a shotgun approach.” © 2014 The New York Times Company
Link ID: 19407 - Posted: 03.25.2014
By Maggie Fox Medical marijuana pills or an oral spray made from cannabis may help ease some of the painful spasms caused by multiple sclerosis that make day-to-day life hard for patients, according to new guidelines from the American Academy of Neurology. But the synthetic formulations of marijuana don’t change the course of the disease and might cause unpleasant side-effects, the experts at the academy caution. There is not enough evidence to make any recommendation on smoking marijuana for MS patients, stresses Dr. Vijayshree Yadav of Oregon Health & Science University, who led the team writing the guidelines. Synthetic marijuana in pill form, including the Marinol brand, is legal for use in treating nausea and loss of appetite in cancer. An oral spray called Sativex is approved for treating MS symptoms in Britain but not in the U.S. MS patients often seek alternative and complementary therapies because they have so few options for the chronic and incurable condition, caused when the immune system mistakenly attacks the nerves. A review of those therapies found there's no evidence most of them work. The review found that the herb Ginkgo biloba might help fatigue, but not thinking and memory problems. There’s also some evidence that magnetic therapy may help fatigue.
Keyword: Multiple Sclerosis
Link ID: 19402 - Posted: 03.25.2014
By Michelle Roberts Health editor, BBC News online Statins may be useful in treating advanced multiple sclerosis (MS), say UK researchers. Early trial results in The Lancet show the cholesterol-lowering pills slow brain shrinkage in people with MS. The University College London (UCL) scientists say large trials can now begin. These will check whether statins benefit MS patients by slowing progression of the disease and easing their symptoms. MS is a major cause of disability, affecting nerves in the brain and spinal cord, which causes problems with muscle movement, balance and vision. Currently there is no cure, although there are treatments that can help in the early stages of the disease. Usually, after around 10 years, around half of people with MS will go on to develop more advanced disease - known as secondary progressive MS. It is this later stage disease that Dr Jeremy Chataway and colleagues at UCL hope to treat with low cost statins. To date, no licensed drugs have shown a convincing impact on this later stage of the disease. For their phase two trial, which is published in the Lancet, Dr Chataway's team randomly assigned 140 people with secondary progressive MS to receive either 80mg of a statin called simvastatin or a placebo for two years. The high, daily dose of simvastatin was well tolerated and slowed brain shrinkage by 43% over two years compared with the placebo. Dr Chataway said: "Caution should be taken regarding over-interpretation of our brain imaging findings, because these might not necessarily translate into clinical benefit. However, our promising results warrant further investigation in larger phase three disability-driven trials." BBC © 2014
Keyword: Multiple Sclerosis
Link ID: 19383 - Posted: 03.19.2014
By Klint Finley Today’s neuroscientists need expertise in more than just the human brain. They must also be accomplished hardware engineers, capable of building new tools for analyzing the brain and collecting data from it. There are many off-the-shelf commercial instruments that help you do such things, but they’re usually expensive and hard to customize, says Josh Siegle, a doctoral student at the Wilson Lab at MIT. “Neuroscience tends to have a pretty hacker-oriented culture,” he says. “A lot of people have a very specific idea of how an experiment needs to be done, so they build their own tools.” The problem, Siegle says, is that few neuroscientists share the tools they build. And because they’re so focused on creating tools for their specific experiments, he says, researchers don’t often consider design principles like modularity, which would allow them to reuse tools in other experiments. That can mean too much redundant work as researchers spend time solving problems others already have solved, and building things from scratch instead of repurposing old tools. ‘We just want to build awareness of how open source eliminates redundancy, reduces costs, and increases productivity’ That’s why Siegle and Jakob Voigts of the Moore Lab at Brown University founded Open Ephys, a project for sharing open source neuroscience hardware designs. They started by posting designs for the tools they use to record electrical signals in the brain. They hope to kick start an open source movement within neuroscience by making their designs public, and encouraging others to do the same. “We don’t necessarily want people to use our tools specifically,” Siegle says. “We just want to build awareness of how open source eliminates redundancy, reduces costs, and increase productivity.” © 2014 Condé Nast.
Link ID: 19353 - Posted: 03.12.2014
by Nathan Seppa MS patients who harbor low levels of vitamin D early in their disease fare worse over the next several years than patients with higher levels. Multiple sclerosis is marked by damage to the fatty sheaths coating nerve fibers in the brain. The result can be an off-and-on series of symptoms including loss of muscle control, numbness and problems thinking. Vitamin D, which the body makes from sun exposure, has shown promise in fighting a variety of diseases and may limit this MS onslaught (SN: 7/16/11, p. 22). In 2002, researchers studying the effect of the drug beta-interferon-1b against MS set aside blood samples from 465 patients. When researchers recently analyzed those samples, they found that patients who had blood levels of vitamin D exceeding 20 nanograms per milliliter at six and 12 months after the onset of MS had fewer symptom flare-ups during the rest of the five-year study than those with lower readings did. Some scientists think 20 nanograms per milliliter is a healthy level; others see 30 as a healthier minimum. MRI scans revealed that, after five years, those who had started out with low vitamin D levels had four times as much myelin damage as those who had higher levels. The results appear in the March JAMA Neurology. A. Ascherio et al. Vitamin D as an early predictor of multiple sclerosis activity and progression. JAMA Neurology. Vol. 71, March 2014, p. 306. doi:10.1001/jamaneurol.2013.5993. © Society for Science & the Public 2000 - 2013
By Debra Weiner An active lifestyle improves brain health, scientists have long believed. The studies bear this out: physical, intellectual and social activity—or “environmental enrichment,” in the parlance—enhances learning and memory and protects against aging and neurological disease. Recent research suggests one benefit of environmental enrichment at the cellular level: it repairs brain myelin, the protective insulation surrounding axons, or nerve fibers, which can be lost because of aging, injury or diseases such as multiple sclerosis. But how does an enriched environment trigger myelin repair in the first place? The answer appears to involve naturally occurring membrane-wrapped packets called exosomes. A number of different cell types release these little sacs of proteins and genetic material into the body's fluids. Loaded with signaling molecules, exosomes spread through the body “like messages in a bottle,” says R. Douglas Fields, a neurobiologist at the National Institutes of Health. They target particular cells and change their behavior. In animal studies, exosomes secreted by immune cells during environmental enrichment caused cells in the brain to start myelin repair. Researchers think exosomes might find use as biomarkers for diagnosing diseases or as vehicles to deliver cancer drugs or other therapeutic agents. The exosomes produced during environmental enrichment carry microRNAs—small pieces of genetic material—which appear to instruct immature cells in the brain to develop into myelin-making cells called oligodendrocytes. When researchers at the University of Chicago withdrew exosomes from the blood of rats and administered them to aging animals, the older rats' myelin levels rose by 62 percent, the team reported in February in Glia. © 2014 Scientific American
By Ariana Eunjung Cha, Standing in a Wisconsin State Capitol hearing room surrounded by parents hugging their seriously ill children, Sally Schaeffer began to cry as she talked about her daughter. Born with a rare chromosomal disorder, 6-year-old Lydia suffers from life-threatening seizures that doctors haven’t been able to control despite countless medications. The family’s last hope: medical marijuana. Schaeffer, 39, didn’t just ask lawmakers to legalize the drug. She begged. “If it was your child and you didn’t have options, what would you do?” she said during her testimony in Madison on Feb. 12. The representatives were so moved that they introduced a bipartisan bill to allow parents in situations similar to Schaeffer’s to use the drug on their children. Emboldened by stories circulated through Facebook, Twitter and the news media about children with seizure disorders who have been successfully treated with a special oil extract made from cannabis plants, mothers have become the new face of the medical marijuana movement. Similar scenes have been playing out in recent weeks in other states where medical marijuana remains illegal: Oklahoma, Florida, Georgia, Utah, New York, North Carolina, Alabama, Kentucky. The “mommy lobby” has been successful at opening the doors to legalizing marijuana — if only a crack, in some places — where others have failed. In the 1970s and ’80s, mothers were on the other side of the issue, successfully fending off efforts to decriminalize marijuana with heartbreaking stories about how their teenage children’s lives unraveled when they began to use the drug. © 1996-2014 The Washington Post
By NICHOLAS RICCARDI, Associated Press COLORADO SPRINGS, Colo. (AP) — The doctors were out of ideas to help 5-year-old Charlotte Figi. Suffering from a rare genetic disorder, she had as many as 300 grand mal seizures a week, used a wheelchair, went into repeated cardiac arrest and could barely speak. As a last resort, her mother began calling medical marijuana shops. Two years later, Charlotte is largely seizure-free and able to walk, talk and feed herself after taking oil infused with a special pot strain. Her recovery has inspired both a name for the strain of marijuana she takes that is bred not to make users high — Charlotte's Web — and an influx of families with seizure-stricken children to Colorado from states that ban the drug. "She can walk, talk; she ate chili in the car," her mother, Paige Figi, said as her dark-haired daughter strolled through a cavernous greenhouse full of marijuana plants that will later be broken down into their anti-seizure components and mixed with olive oil so patients can consume them. "So I'll fight for whomever wants this." Doctors warn there is no proof that Charlotte's Web is effective, or even safe. In the frenzy to find the drug, there have been reports of non-authorized suppliers offering bogus strains of Charlotte's Web. In one case, a doctor said, parents were told they could replicate the strain by cooking marijuana in butter. Their child went into heavy seizures. "We don't have any peer-reviewed, published literature to support it," Dr. Larry Wolk, the state health department's chief medical officer, said of Charlotte's Web. Still, more than 100 families have relocated since Charlotte's story first began spreading last summer, according to Figi and her husband. The relocated families have formed a close-knit group in Colorado Springs, the law-and-order town where the dispensary selling the drug is located. They meet for lunch, support sessions and hikes. © 2014 Hearst Communications, Inc.