Links for Keyword: Epilepsy

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By DANA CANEDY MIAMI, — For Connie Standley, the final indignity came when the manager of a fast food restaurant asked why she was bringing her service dogs into his business in the Florida panhandle when she was obviously not blind. "He kept saying to me that these are not guide dogs," Ms. Standley, who has epilepsy, recalled of a trip home from the Grand Canyon last year. "I said, `No, they are seizure-alert dogs,' and he kept on saying he has never heard of that and `I don't want you in here.' " For the rest of the trip, she ate in her car. In the seven years since she bought her first service dog, Ms. Standley, who lives in Eustis, about 30 miles northwest of Orlando, has had to explain countless times that she relies on Alex, an 80-pound black Bouvier des Flandres, to keep her safe. Copyright 2002 The New York Times Company

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 1793 - Posted: 06.24.2010

Findings may provide novel insights into more common epilepsy New York, N.Y.— Columbia Health Sciences researchers have identified a gene implicated in a rare form of epilepsy, a finding that could provide insights into the cause of common epilepsy. Led by Dr. Ruth Ottman, Columbia investigators identified the gene, called LGI1, by extensively studying five families in which some members had an uncommon type of epilepsy characterized by auditory hallucinations and other symptoms. During a seizure, affected individuals often hear sounds that are not real. The findings will be published Jan. 28 in the online version of Nature Genetics and in the March issue of the journal. Dr. Ottman is professor of epidemiology in the Mailman School of Public Health and deputy director of research at the Gertrude H. Sergievsky Center. Researchers have not yet identified the genes associated with most forms of epilepsy, a chronic medical condition that affects at least 2.3 million Americans. People with epilepsy have repeated seizures, caused by that is due to temporary changes in the electrical function of the brain, that can causing seizures that can affect awareness, movement, and sensation. But scientists study rarer familial forms of the disease to get genetic clues about the more common cases.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 1475 - Posted: 06.24.2010

Stimulating brain region elicits illusion often attributed to the paranormal. HELEN PEARSON Activity in one region of the brain could explain out-of-body experiences. Researchers in Switzerland have triggered the phenomenon using electrodes1. People describe out-of-body experiences as feeling that their consciousness becomes detached from their body, often floating above it. Because these lucid states are popularly linked to the paranormal, "a lot of people are reluctant to talk about them", says neurologist Olaf Blanke of Geneva University Hospital in Switzerland. Blanke found that electrically stimulating one brain region — the right angular gyrus — repeatedly triggers out-of-body experiences. Blanke and his team were using electrodes to excite the brain of a woman being treated for epilepsy. © Nature News Service / Macmillan Magazines Ltd 2002

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 1: Biological Psychology: Scope and Outlook
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 1: An Introduction to Brain and Behavior
Link ID: 2667 - Posted: 06.24.2010

By STEPHANIE SAUL The drug maker Pfizer earlier this decade manipulated the publication of scientific studies to bolster the use of its epilepsy drug Neurontin for other disorders, while suppressing research that did not support those uses, according to experts who reviewed thousands of company documents for plaintiffs in a lawsuit against the company. Pfizer’s tactics included delaying the publication of studies that had found no evidence the drug worked for some other disorders, “spinning” negative data to place it in a more positive light, and bundling negative findings with positive studies to neutralize the results, according to written reports by the experts, who analyzed the documents at the request of the plaintiffs’ lawyers. One of the experts who reviewed the documents, Dr. Kay Dickersin of the Johns Hopkins Bloomberg School of Public Health, concluded that the Pfizer documents spell out “a publication strategy meant to convince physicians of Neurontin’s effectiveness and misrepresent or suppress negative findings.” Pfizer issued a statement Tuesday denying that it had manipulated Neurontin data, saying “study results are reported by Pfizer in an objective, accurate, balanced and complete manner, with a discussion of the strengths and limitations of the study, and are reported regardless of the outcome of the study or the country in which the study was conducted.” Copyright 2008 The New York Times Company

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 12111 - Posted: 06.24.2010

By ALIYAH BARUCHIN A formerly controversial high-fat diet has proved highly effective in reducing seizures in children whose epilepsy does not respond to medication, British researchers are reporting. As the first randomized trial of the diet, the new study lends legitimacy to a treatment that has been used since the 1920s but has until recently been dismissed by many doctors as a marginal alternative therapy. “This is the first time that we’ve really got Class 1 evidence that this diet works for treatment of epilepsy,” said Dr. J. Helen Cross, professor of pediatric neurology at University College London and Great Ormond Street Hospital. She is a principal investigator on the study, which will appear in the June issue of The Lancet Neurology. Though its exact mechanism is uncertain, the diet appears to work by throwing the body into ketosis, forcing it to burn fat rather than sugar for energy. Breakfast on the diet might consist of bacon, eggs with cheese, and a cup of heavy cream diluted with water; some children drink oil to obtain the fats that they need. Every gram of food is weighed, and carbohydrates are almost entirely restricted. Breaking the diet with so much as a few cookies can cause seizures to flare up. Copyright 2008 The New York Times Company

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 11594 - Posted: 06.24.2010

Using a rodent model of epilepsy, researchers found one of the body’s own neurotransmitters released during seizures, glutamate, turns on a signaling pathway in the brain that increases production of a protein that could reduce medication entry into the brain. Researchers say this may explain why approximately 30 percent of patients with epilepsy do not respond to antiepileptic medications. The study, conducted by researchers at the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health, and the University of Minnesota College of Pharmacy and Medical School, in collaboration with Heidrun Potschka’s laboratory at Ludwig-Maximilians-University in Munich, Germany, is available online and will appear in the May 2008, issue of Molecular Pharmacology. "Our work identifies the mechanism by which seizures increase production of a drug transport protein in the blood brain barrier, known as P-glycoprotein, and suggests new therapeutic targets that could reduce resistance," said David Miller, Ph.D., a principal investigator in the NIEHS Laboratory of Pharmacology and co-author on the paper. The blood-brain barrier (BBB), which resides in brain capillaries, is a limiting factor in treatment of many central nervous system disorders. It is altered in epilepsy so that it no longer permits free passage of administered antiepileptic drugs into the brain. Miller explained that P-glycoprotein forms a functional barrier in the BBB that protects the brain by limiting access of foreign chemicals.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 11524 - Posted: 06.24.2010

By GARDINER HARRIS and BENEDICT CAREY Drugs for epilepsy, bipolar illness and mood problems double the risks of suicidal thoughts and behavior, and patients taking them should be watched for sudden behavioral changes, drug regulators have said. The increased risks, while double in relative terms, are small. The Food and Drug Administration undertook a combined analysis of 199 clinical trials with 43,892 patients and found 4 suicides and 105 reports of suicidal symptoms among the 27,863 patients who were given the drugs compared to no suicides and 35 reports of suicidal symptoms among the 16,029 patients treated with placebos. Taken together, the risk of suicidal thoughts and behavior was 0.43 percent for those on drug therapy and 0.22 percent for those given placebos. These medications are primarily used to help epileptics control seizures and to calm the surges in energy and mood that, along with bouts of depression, characterize bipolar disorder. The drugs, which include Depakote, Lamictal, Topamax, Keppra, Lyrica and Neurontin, are sometimes prescribed for chronic pain and headaches, as well. Doctors said Thursday that the increased risk did not outweigh the benefits of the drugs. “What’s really important to say is that bipolar disorder is very difficult to treat, the burden is enormous, and these medications help keep people free of mood and anxiety symptoms and allow them to function,” said Andrew A. Nierenberg, medical director of the bipolar clinic and research program at Massachusetts General Hospital. Copyright 2008 The New York Times Company

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 11267 - Posted: 06.24.2010

An anti-epilepsy drug first licensed in the UK in 1975 may cause long-term developmental problems in children born to pregnant women using it, suggest the results of a new study. Epilepsy experts already believe there is a strong link between using drugs containing sodium valproate during pregnancy and dysmorphic features - such as eyes set wider apart and a thinned upper lip - in children born subsequently. They have suspected that valproate use in pregnant mothers may also lead to longer term developmental problems in their children - but until now the evidence for this has been anecdotal. “The new research is saying something we’ve guessed for a long time,” says Tim Betts, a neuropsychiatrist at the University of Birmingham, UK. “Now they’ve measured it for the first time. It’s very important work.” The study, led by Naghme Adab from the Walton Centre for Neurology and Neurosurgery, Liverpool, UK, shows that children born to mothers who were on valproate when pregnant were eleven times more likely to have a verbal IQ score of 69 or below, compared with children born in the general population. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 13: Memory, Learning, and Development
Link ID: 6245 - Posted: 06.24.2010

By KATY J. VOPAL - Freeman Staff WEST ALLIS - When Karen Sebastian was born 37 years ago, her mother, Rose Sebastian, noticed something - a sizable purplish mark on her daughter’s forehead. The mark wasn’t a bruise, it wasn’t a birthmark. It was called a "port wine stain" and was linked to a rare condition called Sturge-Weber syndrome. But now, things are a little different for Rose. Karen died in August 2001 from acute lymphocytic leukemia, and her mother is speaking out about Sturge-Weber to raise awareness about the condition and campaign. The purpose of the campaign is to raise funds for much needed research about the unknown cause and the undiscovered cure of the syndrome. The Sturge-Weber National Day of Awareness is May 15. "Karen was diagnosed right away at birth," Rose said. "She didn’t start having convulsions until 18 months, and it was explained to us that since the stain was up on her forehead, it was linked to calcium deposits around her brain, and that’s what made her have the seizures."

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 2028 - Posted: 06.24.2010

Heidi Ledford A drug used to treat epilepsy could also ease cravings in alcoholics, say researchers who have investigated the effect in rats. The drug, called gabapentin, is approved for the treatment of epileptic seizures and for some conditions that cause chronic pain. And now, researchers led by Marisa Roberto, of the Scripps Research Institute in La Jolla, California, have shown that alcohol-dependent rats given gabapentin drink less alcohol and are less anxious than those not given the drug1. Preliminary small clinical trials have suggested that gabapentin could also be useful in the treatment of drug addiction, and trials are now under way to determine whether the drug can ease alcoholism in people. The current results are promising, says Robert Swift, a researcher at the Center for Alcohol and Addiction Studies at Brown University in Rhode Island. “This paper really suggests that gabapentin may be efficacious in reducing drinking [in alcoholics],” he says. Gabapentin is structurally similar to a neurotransmitter called -aminobutyric acid, or GABA, which can slow communication between neurons in the brain. Although the drug does not function in precisely the same way as GABA, it can prevent the chaotic electrical activity in the brain that triggers a seizure. © 2008 Nature Publishing Group

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 11672 - Posted: 06.24.2010

Sleeping woes may explain why children with epilepsy are often so hyperactive, say researchers with the University of Florida's Evelyn F. and William L. McKnight Brain Institute. Characterized at its extreme by physical convulsions, epilepsy has long been thought to cause excitability and contrariness in children. But UF researchers writing in the journal Epilepsy & Behavior believe the real reason some of these children cannot sit still or pay attention is because they don't get enough shut-eye. “When we treated kids with sleep disturbances, not only did their epilepsy get better, their daytime behavior, concentration and capacity to learn increased,” said Paul Carney, M.D., chief of pediatric neurology at UF's College of Medicine and a professor at the B.J. and Eve Wilder Center for Excellence in Epilepsy Research . “Many kids with epilepsy aren't being adequately assessed for underlying sleep disorders. We can significantly have an impact over their cognition, learning and maybe even improve their epilepsy by improving their sleep.” Epilepsy describes a group of disorders that occur when electrical activity in the brain goes haywire, resulting in bursts of frenetic activity that cause seizures. It strikes more than 2 million people in the United States, according to the National Institute of Neurological Diseases and Stroke. Copyright © 2004 | University of Florida

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 10: Biological Rhythms and Sleep
Link ID: 7114 - Posted: 06.24.2010

Physicians at UC Davis Medical Center have identified a promising new treatment for epilepsy that reduces the number of seizures while helping patients lead more productive lives. The study is the first to show that Levetiracetam (LEV), an antiepileptic drug typically used in combination with other drugs, might be successful as a single drug. The results were published in the October issue of Epilepsy and Behavior and will be presented at the American Epilepsy Association conference in Seattle this December. “We found that LEV can be effective as a single drug, or monotherapy, in patients with newly diagnosed epilepsy, as well as in patients with difficult-to-control seizures,” said Taoufik M. Alsaadi, assistant professor of neurology and co-director of the UC Davis Comprehensive Epilepsy Program. “In addition, it is very well tolerated, with only a small number of patients discontinuing the drug due to side effects.”

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 2892 - Posted: 06.24.2010

By Sam Kean Two medical problems caused by misfiring electrical signals, epilepsy and heart arrhythmia, probably have a common molecular cause, scientists report. The research points to treatments that could lower the chances of young people dying of seizures. The scientists, at Baylor College of Medicine in Houston, Texas, were studying mice that had a mutation in the KCNQ gene, which builds potassium ion channels that set up an action potential across a cell membrane. These channels help the heart beat by resetting the potential after cardiac muscle cells contract. The mutation--also found in humans--produces a faulty protein that delays restoration of the potential, causing erratic beating and sometimes death. The ion channel was long thought to operate only in heart muscle, but recent work implied that it functions in other tissues. Now Alica Goldman, a neurologist and co-author of the paper, has discovered the first definitive evidence that the channel was working in mouse neurons. It was especially active in regions of the brain susceptible to seizures, the researchers report online this week in Science Translational Medicine. The team also monitored the mutant mice with EEG and ECG machines and determined that seizures often accompanied abnormal heart rhythm. "This is exciting because it provides the first molecular clue" that potassium ion channels underlie epilepsy and arrhythmia, says Jeffrey Noebels, a neurologist and lead author of the paper. © 2009 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 13367 - Posted: 06.24.2010

Wisconsin researchers have released a free software tool that could help web surfers susceptible to certain seizures. An estimated one in 4,000 people has photosensitive epilepsy and could suffer a seizure when exposed to bright colours and rapidly flashing images. The condition gained prominence in 1997 when more than 800 Japanese children were hospitalized after viewing a cartoon. Since then, television directors, video-game makers and others have tested their content to make sure it doesn't reach seizure-inducing thresholds. Web developers, though, didn't have simple ways to run such tests. Researchers at the University of Wisconsin-Madison set out to change that. "On the web you really never know what's going to pop up on the screen until it does, and one second later you could be having a seizure," said Gregg Vanderheiden, the centre's director. Web developers can use the Photosensitive Epilepsy Analysis Tool, or PEAT, to determine how fast an image blinks, for example, and let developers know whether it poses a seizure risk. Content that doesn't pass the test isn't always risky. Researchers say flashy content that doesn't fill at least 10 per cent of a screen isn't a danger. © CBC 2009

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 13138 - Posted: 06.24.2010

By Sandra G. Boodman Although he had never seen a case like it in his career, cardiologist David Lomnitz felt certain he knew why his new patient kept blacking out when she ate. At the time of her first appointment in September 2004, Martha Bryce, then a 36-year-old health-care consultant, was feeling desperate. Four years earlier she had been given a diagnosis of epilepsy, and had taken medication to prevent seizures. But doctors had been unable to explain the frequent swooning episodes that occurred when she started to eat, forcing her to put her head down on the table in an intermittently successful attempt to avoid passing out. Doctors seemed unconcerned and told her the episodes might be a symptom of her seizure disorder. Bryce, a registered nurse, wasn't so sure. But after a frightening incident drove home the potential danger of the baffling condition, she made an appointment with Lomnitz, now assistant chief of cardiology at Norwalk Hospital in Norwalk, Conn. "Her story rang a bell for me," he said. His hunch about her condition, triggered by cases he heard about during his training years earlier, would upend her diagnosis and radically alter her treatment. The first sign something was wrong was dramatic. While on a business trip to Las Vegas in January 2000, Bryce, who lives in Ridgefield, Conn., decided to visit the Hoover Dam before catching a red-eye flight home. Standing at an overlook preparing to photograph the concrete behemoth, Bryce recalled, "all of a sudden I felt a way I'd never felt before." She fainted and, after regaining consciousness, learned she had suffered a grand mal seizure during which she had bitten her tongue. © 2009 The Washington Post Company

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 13122 - Posted: 06.24.2010

By Nikhil Swaminathan Stacey Gayle used to love music. Listening to it and performing it was a big part of her life. She had stacks of CDs in her car, went to concerts of artists like Sean Paul, and would go to parties where hot songs would blare. She was also an active member of the choir at her church: Solid Rock Church of the Nazarene. Then she started having seizures. The first one happened while she slept in her bedroom in Rosedale, Queens in New York City on the night of March 3, 2005. She had just turned 22. Her mother rushed her to the emergency room, where doctors stabilized her. Several brain scans and blood tests gave no clue as to why she seized. Soon after, she had another, this time at a friend's barbecue. She blacked out, fell down and started to shake like crazy as her brain cells went out of whack, firing electrical signals without pause. At first, the seizures seemed to occur randomly. In the spring of 2006, however, she noticed a pattern. At the time, Sean Paul's "Temperature" was sitting at the top of the Billboard Hot 100 singles chart, continually being played on urban radio stations. It was playing at nearly every barbecue and party she went to. That was a problem: "Every time it would go on, I would pass out and go into a seizure," she recalls. © 1996-2008 Scientific American Inc.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 11699 - Posted: 06.24.2010

By Elsa Youngsteadt Sometimes seizures become a nightmare without end. Roughly 15% of epileptics will, at some point, experience status epilepticus, a medical emergency in which convulsions can only be stopped with strong anesthetics. Now researchers have found a piece of cellular machinery--an acid-activated ion channel-- that helps bring seizures under control. They hope the discovery will lead to new drugs that could stop these deadly events. For decades, researchers have suspected a link between brain acidity and seizures. In 1929, doctors noted that patients breathing CO2 had shorter seizures; the gas boosts the acidity of blood reaching the brain. Even without intervention, brain pH can drop during a seizure due to changes in breathing and metabolism. John Wemmie, a psychiatrist at the University of Iowa in Iowa City and colleagues wondered if an ion channel called ASIC1a might play a role, as it is known to activate neurons by pumping calcium and sodium across the cell membrane when the brain becomes acidic. Wemmie's team compared normal mice with those that were genetically engineered to lack the channel. When they injected these knockouts and controls with chemicals that cause epilepsy-like seizures, the normal mice fared much better than the ones without ASIC1a. A compound called kainate produced serious whole-body convulsions in all seven knockout mice, whereas the six normal mice had only minor seizures in their heads and fore-limbs. A second group of knockouts injected with a different drug, PTZ, had longer seizures than control mice--and those seizures were several times more likely to become deadly tonic-clonic whole-brain seizures (formerly known as "grand mal" seizures). In contrast, mice genetically engineered to have double the normal number of ASIC1a channels had shorter and less severe seizures than wild-type mice, the team reports online this week in Nature Neuroscience. © 2008 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 11697 - Posted: 06.24.2010

Frank Eltman, -- Now that surgeons have operated on Stacey Gayle's brain, her favorite musician no longer makes her ill. Four years after being diagnosed with epilepsy, Gayle recently underwent brain surgery at Long Island Jewish Medical Center to cure a rare condition known as musicogenic epilepsy. Gayle, a 25-year-old customer service employee at a bank in Alberta, Canada, was suffering as many as 10 grand mal seizures a day, despite being treated with medications designed to control them. The condition became so bad she eventually had to quit her job and leave the church choir where she sang. Eighteen months ago, she began to suspect that music by reggae and hip-hop artist Sean Paul was triggering some of her seizures. She recalled being at a barbecue and collapsing when the Jamaican rapper's music started playing, and then remembered having a previous seizure when she heard his music. Her suspicions were confirmed on a visit to the Long Island medical center last February, when she played Paul's hit "Temperature" on her iPod for doctors. Soon after, she suffered three seizures. © 2008 Discovery Communications, LLC

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 11224 - Posted: 06.24.2010

By Prashant Nair Scientists have found a way to suppress epileptic seizures in rats by inhibiting the animals' ability to break down sugars. If the approach works in humans, it could herald a novel class of antiepileptic drugs. Epilepsy arises when brain neurons fire in an uncontrolled frenzy, causing seizures. Most current treatments are aimed at decreasing neuronal activity, but these approaches have side-effects, such as drowsiness and cognitive difficulties. Neurobiologists Thomas Sutula and Avtar Roopra at the University of Wisconsin, Madison, decided to tackle epileptic seizures from a different angle. Scientists have long known that seizures can sometimes be kept at bay when people with epilepsy steer clear of sugars and other carbohydrates--the so-called ketogenic diet. In addition, removing glucose from slices of the hippocampus--the brain region activated in epilepsy--leads to a dip in neuronal firing in animal studies. Sutula and Roopra focused on an inhibitor of sugar breakdown--or glycolysis--known as 2DG. When rats predisposed to epileptic seizures were given 2DG, the amount of electric current needed to set off a seizure in these animals was significantly higher than that in animals not given the drug. Furthermore, treated rats required twice as many electric discharges than untreated ones to produce seizures. An analysis of the hippocampus of treated rats revealed that 2DG was blocking the action of a protein complex that drives the expression of seizure-related genes. The activity of this complex is dependent on the end products of glycolysis, the team reports in the October issue of Nature Neuroscience. © 2006 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 9494 - Posted: 06.24.2010

Roxanne Khamsi Experiments on immature rats' brains suggest that treating epileptic children with benzodiazepine drugs could do more harm than good, scientists in France have claimed. They have found that the neurotransmitters unlocked by these drugs cause changes in brain chemistry that actually promote epileptic activity. Anticonvulsant benzodiazepines are a last-ditch treatment used to stop seizures in both infants and adults. Some medical experts think that the electrical activity associated with seizures can change brain networks, making them more susceptible to future epileptic activity. So understanding the chemistry of seizures might lead to drugs that can counteract epilepsy's development, says Yehezkel Ben-Ari, a neuroscientist at the Mediterranean Institute of Neurobiology in Marseille. His team studied the electrical and chemical activity of brains removed from baby rats. They were particularly interested in the hippocampus, a part of the brain important in epileptic seizures. The researchers found that the neurotransmitter gamma-aminobutyric acid (GABA) triggers rapid electrical signalling in the immature hippocampus - a hallmark of epileptic seizures. Benzodiazepine drugs enhance the action of this neurotransmitter. ©2005 Nature Publishing Group

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 8279 - Posted: 06.24.2010