Links for Keyword: Epilepsy

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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

By David W. Loring, Ph.D. Epilepsy is a major public health concern, with prevalence estimated to be slightly less than 1% (Annegers, 1996). Each year, 25,000 to 40,000 children in the United States alone experience their first unprovoked seizure (Hirtz et al., 2003). Depending on the type of seizure (e.g., generalized versus focal) or specific epilepsy syndrome (e.g., juvenile myoclonic epilepsy, benign rolandic epilepsy), there are several recommended medications with demonstrated clinical efficacy from which to choose (Hirtz et al., 2003). Selection of a specific medication, however, is often based upon clinical experience due to the absence of adequate antiepileptic drug (AED) pediatric clinical trials. Antiepileptic drugs decrease membrane excitability, increase postsynaptic inhibition or alter synchronization of neural networks to decrease excessive neuronal excitability associated with seizure development. Common side effects of decreasing neuronal excitability, however, are slowed motor and psychomotor speed, poorer attention and mild memory impairment (Meador, 2005). Unlike adults, cognitive side effects in children occur against the backdrop of normal cognitive and psychosocial development, and treatment decisions made in childhood may have lifelong implications. Adults who developed epilepsy during their childhood tend to have less education, decreased rates of employment and employment at lower job levels, lower rates of marriage, poorer physical health, and increased incidence of psychiatric disorders (Jalava and Sillanpaa 1997a, 1997b; Jalava et al., 1997; Sillanpaa et al., 1998). Importantly, these long-term effects are also present in adults who are no longer taking medications. © 2005 Psychiatric Times.

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: 7992 - Posted: 06.24.2010

Bernadette Tansey, Chronicle Staff Writer The Food and Drug Administration has asked the makers of all epilepsy drugs to re-examine their clinical trial data in response to claims that one of the medicines, Pfizer's Neurontin, boosts the risk of suicide. Word of the FDA action came in response to a petition filed last May by personal injury attorney Andrew Finkelstein, who has been urging the agency to warn doctors that the commonly prescribed drug Neurontin can lead to severe depression and suicide. Neurontin, with $2.7 billion in sales last year, has been prescribed to more than 10 million people since it was put on the market in 1994. Although it was formally approved for patients suffering from epilepsy and later for pain related to a skin disorder, it has since been prescribed for illnesses ranging from psychiatric disorders to back pain. Finkelstein bases his claims on the FDA's own records as well as 318 suicides and about 2,000 suicide attempts among families he represents. The FDA's inquiry comes as it tries to repair its image as the guardian of drug safety after a series of controversies over its response to warnings about serious side effects linked to several other blockbuster medicines. ©2005 San Francisco Chronicle

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: 7238 - Posted: 06.24.2010

Helen Pearson A group of drugs already approved for humans can prolong the lifespan of worms. So, will these medicines be sought after by those seeking eternal youth? Researchers have long been trying to find drugs or elixirs that can stave off ageing. But they have met with little success, partly because it is laborious and time-consuming to show that a drug adds years to our lives. To get around this problem, Kerry Kornfeld of Washington University in St Louis, Missouri, and his team tested drugs on a tiny, short-lived worm called Caenorhabditis elegans. Researchers have shown before that tweaking certain genes can prolong this worm's life. The team split the worms into groups and doped their food with 19 prescription medicines, from steroids to diuretics to anti-inflammatory drugs. "We went through a pharmaceutical textbook and picked a drug from each class," Kornfeld says. Most of the drugs had no effect, or even killed the worms at high doses. But an anticonvulsant used to fight epilepsy, and two other similar compounds, lengthened the animals' lives by as much as 50%. Normal signs of ageing were also delayed in the animals. ©2005 Nature Publishing Group

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: 6695 - Posted: 06.24.2010

Sudden cardiac death from emotional stress may be triggered by uneven signals from the brain to the heart, according to a study by University College London (UCL) scientists published in the January issue of Brain . UCL researchers have discovered that a system which normally coordinates signalling from the brain to different parts of the heart may be disrupted in some people, making them vulnerable to potentially fatal abnormal heart rhythms during mentally taxing tasks or emotional events such as family gatherings. This is particularly true of people who already have heart disease, but it is the brain that may be most responsible. The new study suggests that uneven brain activity, in a region where nerves link directly to the heart, seems to result in an uneven distribution of signals across the heart, which stops the heart from contracting normally. Around a third of the 300,000 sudden cardiac deaths which occur each year in the US arise from a blood clot in a major artery, which leads to a fatal heart attack. Mental stress is thought to be responsible for a further 20 per cent of these deaths, but scientists have been baffled by the exact mechanisms by which stress can bring on a fatal short-circuiting of the heart. Copyright © 1999-2004 UCL

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: 6615 - Posted: 06.24.2010

By Laura Spinney Epilepsy often develops after the brain is damaged, and patients commonly must take anticonvulsant drugs for a lifetime despite unpleasant side effects. Such drugs target the seizures but not the underlying cause. Now, new theories promise to untangle the mechanisms of epileptogenesis and presage the possibility of a new generation of drugs that treat the initial brain damage and prevent epilepsy from developing. In roughly half of all patients with epilepsy, the condition develops later in life after the patient sustains a brain injury such as trauma or meningitis. The latency of onset can range from a few weeks to a decade after brain damage occurs. Researchers have been scrambling to uncover what happens during that delay. SIMPLE BALANCE A generally held theory suggests that something upsets the balance of excitatory and inhibitory signals in the brain, leading to overall hyperexcitability. This theory rests on observations that inhibitory cells become less active while excitatory pathways multiply, implying "a simple balance of inhibition and excitation," according to John Duncan of the Institute of Neurology in London. He says that this theory is probably wrong, or at least incomplete. "The reality is clearly more complicated, as neurons form intricate networks and interconnections." © 2004, The Scientist LLC,

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: 6454 - Posted: 06.24.2010

Researchers at the University of Alabama have found a way to mimic epileptic seizures in the tiny roundworm C. elegans. The finding could make the worm a powerful model for unraveling the molecular regulation of epilepsy, a condition that affects two percent of the population. Guy A. Caldwell, coordinator of the Howard Hughes Medical Institute's (HHMI) Undergraduate Research Intern Program and assistant professor of biological sciences at the University of Alabama, led a research team that included Kim A. Caldwell, assistant professor of biological sciences and director of the university's HHMI-sponsored Rural Science Scholars Program; Shelli N. Williams, a Ph.D. student; and two HHMI undergraduate research interns, Cody J. Locke and Andrea L. Braden. They studied worms with a mutation in the LIS1 gene. In its human form, the gene has been linked to a rare birth defect called lissencephaly, which affects one out of every 30,000 children born. In children with lissencephaly, the normally wrinkled surface of the brain's cortex is smooth. They also have mental retardation and severe epilepsy, the causes of which are not well understood. The team traced the mutation's effect on specific neurons in the simple nervous system of the 1-millimeter roundworm and published their findings in the September 15, 2004 issue of the journal Human Molecular Genetics, published online August 31. © 2004 Howard Hughes Medical Institute.

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: 6056 - Posted: 06.24.2010

By JANET McCONNAUGHEY NEW ORLEANS -- Japanese children who had seizures during a "Pokemon" cartoon in 1997 have generally not had another one unless they already had epilepsy, researchers say. The TV show sent at least 685 Japanese viewers, mostly children, to emergency rooms with symptoms ranging from nausea and hyperventilation to convulsions. They were apparently made sick by a scene with extremely rapid flashes of red and blue. To find out whether the incident had any lasting effects, Dr. Akihisa Okumura and colleagues in Nagoya sent questionnaires to doctors who had treated 103 "Pokemon" patients in the prefecture, or state, of Aichi. They got back results for 91 patients. Twenty-five had had at least one more convulsion in the five years since the "Pokemon" episode. They were divided almost evenly between those diagnosed with epilepsy and those who weren't. However, electroencephalograms revealed that 10 of the 13 who had not been diagnosed with epilepsy did, in fact, have the disease. Copyright © 2004, The Associated Press

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: 5866 - Posted: 06.24.2010

Some dogs can predict when a child will have an epileptic seizure, a new study has revealed. These dogs not only protect their charges from injuries, such as falling, but also seem to help kids deal with the daily struggle of epilepsy. Nine of the 60 dogs in the study (15 per cent) were able to predict a seizure by licking, whimpering, or standing next to the child. These dogs were remarkably accurate - they predicted 80 per cent of seizures, with no false reports. However, those interested in owning a dog with these skills cannot yet just order one. The dogs were not trained, but instead began predicting seizures spontaneously within a month of moving in with their owners. "No one is reliably training such dogs yet," says Adam Kirton, a neurologist at Alberta Children's Hospital in Canada and lead author of the study. His group is looking into setting up a training program. However, some epilepsy patients do have already dogs that have been trained to protect them during a seizure. © Copyright Reed Business Information Ltd

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: 5688 - Posted: 06.24.2010

Flexible brain-wiring could guard against epilepsy. TANGUY CHOUARD The nervous system is not hard-wired, according to research on spinal cord cells in tadpole embryos. Nerve cells can change their function as they develop, responding to their own electrical activity rather than playing a role that is preordained by genetics, say US biologists. Scientists thought that the precise nature of each nerve cell was determined by an irreversible programme of development, initiated by the cell's genetic code. But Nick Spitzer and his fellow neurobiologists from the University of California, San Diego, challenge that fatalistic view in this week's Nature1,2. The team finds that certain patterns of electrical activity in a young nerve cell can override its basic genetic instructions, changing the way that the cell will communicate with its peers. Nerve cells use neurotransmitter chemicals to talk to each other, and different chemicals will either excite or inhibit activity in neighbouring cells. © Nature News Service / Macmillan Magazines Ltd 2003

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 5577 - Posted: 06.24.2010

A scathing report has led to the sudden removal of a well-known British epilepsy researcher as the director of the National Neuroscience Institute (NNI) in Singapore. Simon Shorvon, 54, was fired from the institute on 4 April after an investigation found he had compromised patients' safety and well-being during a clinical trial involving patients with Parkinson's disease. "This shows that people can't get away with shortcuts in Singapore," says Lim Pin, a member of the investigative panel and chair of Singapore's Bioethics Advisory Committee. "We're very protective and jealous about our reputation." Shorvon, while acknowledging he made mistakes, says the panel used some extraordinary tactics, such as locking him out of his office and going through years of e-mails, and that its overall conclusion was too harsh. The $5.6 million study was funded by the Singaporean government and aimed at elucidating the genetic basis of Parkinson's disease and two other disorders. When recruitment for the trial was lagging, the panel says, Shorvon and his colleague, Ramachandran Viswanathan, obtained lists of Parkinson's patients from two hospitals and started contacting patients directly. That was a breach of confidentiality, the panel concluded. Equally serious was Shorvon's failure to inform the ethical oversight committee and the patients themselves that participation would require them not only to donate blood but also to briefly halt their medication and undergo extensive tests. Neither step was mentioned in the consent forms signed by patients. Although the procedures weren't life-threatening, the panel says, the assessment caused severe discomfort in some patients and put them at risk of complications. The 127 patients involved "were treated like experimental subjects, without any rights," the panel concludes. Copyright © 2003 by the American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 5: The Sensorimotor System
Link ID: 3668 - Posted: 06.24.2010