Links for Keyword: Epilepsy

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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: The Biology 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

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