Links for Keyword: Epilepsy

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By Karen Weintraub Paul Barney had his first seizure four days after his fourth birthday. By the time he was 10, his mom worried that if they didn’t get the seizures under control soon, he might lose IQ points along with his ready smile. When Brian Manning, 11, had a seizure on the school playground – instead of in his bed as usual – his parents knew it was time for drastic action. He’d already had brain surgery once, but doctors said he might need five or six more operations. Or he could have one, to completely remove the right half of his brain. Both boys have epilepsy and recently underwent surgery at Boston Children’s Hospital. And both represent the promise and frustration of epilepsy treatment today. Patients have more options, and there is more awareness, less stigma, and a better understanding of epilepsy than there has ever been. But available medications can’t control seizures in about one-third of patients, including Paul and Brian, and while surgery is safer, it still comes with high risks. It also remains unclear what causes the electrical disturbance in patients’ brains that triggers seizures. Roughly 1 in 26 Americans will develop epilepsy at some point in life – more than will have autism, AIDS, or Parkinson’s disease. Some patients do fine between seizures and can function normally. In others, their brains are constantly being disrupted, like a radio station filled with static, according to Dr. Blaise Bourgeois the director of the Division of Epilepsy and Clinical Neurophysiology at Boston Children’s. © 2012 NY Times Co.

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: 17156 - Posted: 08.13.2012

Duncan Graham-Rowe A skull implant that can detect an epileptic seizure and deliver therapeutic electrical impulses can reduce the length of these events by 60% in rats. The device, tested on nine rats with a ‘petit mal’ form of epilepsy, is described today in Science1. Most electrical stimulation devices, such as those that deliver deep-brain stimulation (DBS) to treat Parkinson’s disease and depression, operate continuously, delivering impulses regardless of the patient’s brain activity. But this can cause a range of undesirable side effects, such as headaches. Seizure-responsive versions of DBS devices are coming to market, such as the Responsive Neurostimulator System developed by NeuroPace, based in Mountain View, California. The system is awaiting approval by the US Food and Drug Administration and will be aimed at adults with certain types of partial-onset seizures, which tend to be localized to certain regions of the brain. But as the name implies, DBS uses electrodes that penetrate the brain, which can also carry certain risks, such as a worsening of epilepsy symptoms. In the latest study, György Buzsáki, a neuroscientist at the New York University School of Medicine, and his colleagues used a less invasive approach that involves transcranial electrical stimulation (TES) of neurons using electrodes implanted in the skull. This technique has been shown to be effective at modifying the brain's cortical (outermost) neurons, which become abnormally excited during epileptic seizures. To detect the onset of a seizure, recording electrodes that detect neural activity were implanted on the brain's surface. © 2012 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: 17148 - Posted: 08.11.2012

By Justin Moyer, On June 9, Commerce Secretary John Bryson was hospitalized after his reported involvement in three auto accidents. Although details were not disclosed, the White House confirmed that he had a seizure. On July 30, 2007, Chief Justice John Roberts collapsed on a boat dock at his Maine summer home. Although that seizure was Roberts’s second, he offered little explanation. When Time magazine asked “Does Justice Roberts Have Epilepsy?,” Roberts didn’t answer, and he hasn’t in five years. Reading these stories, I wish public figures such as Roberts and Bryson would talk publicly about their conditions. They should do this not because they are legally compelled to or because their health may affect their work. They should do it because hiding their problems makes it seem like their problems are worth hiding. I received a diagnosis of epilepsy in 2001, at age 24. My seizures are generalized, meaning they strike my whole brain and body. Without warning, I lose consciousness for several minutes and remain disoriented for a few hours. Later, I have no memory of the episode save muscle aches and a sore mouth from biting my tongue. My seizures are idiopathic: They have no known cause. They can be controlled with levetiracetam, a medication that regulates brain neurotransmitters. © 1996-2012 The Washington Post

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: 16930 - Posted: 06.19.2012

By ALASTAIR GEE In November 2008, when he was just 6, William Moller had his first epileptic seizure, during a reading class at school. For about 20 seconds, he simply froze in place, as if someone had pressed a pause button. He could not respond to his teacher. This is known as an absence seizure, and over the next year William, now 10, who lives with his family in Brooklyn, went from having one or two a day to suffering constant seizures. Not all were absence seizures; others were frightening tonic-clonics, also known as grand mals, during which he lost consciousness and convulsed. The seizures often came while he was eating. As his body went rigid, William dropped his food and his eyes rolled back into their sockets. If he seized while standing, he suddenly crashed to the ground — in a corridor, in the driveway, on the stairs. “It’s the scariest thing for any mother to hear that thump, and each time he would hit his head, so it only made things worse and worse,” said his mother, Elisa Moller, a pediatric nurse. William is among the one-third of epilepsy sufferers who do not respond, or respond only poorly, to anti-epileptic medications. Now he and others with refractory epilepsy are benefiting from treatment that targets inflammation, the result of new research into how epilepsy damages the brain. “Many of us theorize that the two are tied — inflammation causes seizures, and seizures cause inflammation,” said Orrin Devinsky, director of the Comprehensive Epilepsy Center at the New York University Langone Medical Center and William’s doctor. “Over time, both of them may feed off each other.” © 2012 The New York Times Company

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 16873 - Posted: 06.05.2012

By NICHOLAS BAKALAR Surgery for epilepsy is usually seen as a last resort for patients when medications do not work, and it is often delayed for many years after the failure of drug treatment. Now a randomized, controlled trial suggests that surgery as soon as possible after the failure of two antiepileptic drugs is a significantly better approach than continued medical care. Previous studies have shown that patients referred for surgery have had epilepsy for an average of 22 years, and are referred on average more than 10 years after the use of two drugs has failed to stop the seizures. People with continued seizures are at increased risk for drowning and other accidents, depression, progressive loss of memory, and, in younger people, a failure to develop vocational and social skills. Their risk of death is 10 times as high as that of the general population. Researchers studied a group of 38 epilepsy patients, randomly assigning 15 to brain surgery and 23 to continued medical treatment. The surgery involves the removal of a piece of tissue about the size of a walnut from the temporal lobe, the part of the brain just above the ear. The surgery has been performed for many years, but the institution of high-resolution M.R.I. and microsurgical techniques have greatly improved its safety and efficacy. The patients in both groups were similar in age, duration of epilepsy, the number of antiepileptic drugs used and the number of seizures they had had. All had been taking drugs for one to two years without relief. The participants were seen at the study site every three months for two years after the start of the study. A group of specialists who did not know which patients had had surgery evaluated them for seizure type and severity as recorded in patient diaries. The study appears in the March 7 issue of The Journal of the American Medical Association. © 2012 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: 16507 - Posted: 03.13.2012

By Sandra G. Boodman, “Men in Black” was flickering on the screen, and Laura Cossolotto and her husband were enjoying a rare night at the movies in their home town of Centerville, Iowa, when her brother-in-law rushed into the darkened theater. The couple’s third child, 6-month-old Michaela, had just suffered a serious seizure and was at a nearby hospital. As Cossolotto raced to be with the baby, she immediately remembered that Michaela had been running a fever after receiving a vaccine against diphtheria, pertussis and tetanus (DPT) three days earlier. “I thought the shot must have something to do with it,” Cossolotto recalled. “I had three kids, and nothing like this had ever happened, so what else could it have been?” At the hospital, doctors reassured her that Michaela had suffered a febrile seizure, a frightening and usually harmless event they said was unlikely to recur. As a precaution, the baby was admitted for observation. Hours later, after doctors had trouble controlling a second, more severe seizure, the infant was whisked by helicopter to a larger hospital in Des Moines, 100 miles north. That night in July 1997 marked the beginning of a 101 / 2-year ordeal, as more than a dozen specialists in four states tried without success to find an underlying cause for Michaela’s frequent, in­trac­table seizures — and a treatment that would control them before they caused irreparable brain damage or death. © 1996-2012 The Washington Post

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: 16327 - Posted: 01.31.2012

By Brian Alexander “Laughing seizures” have long been one of the mysteries surrounding epilepsy. During an event, an epileptic suffering a laughing seizure can guffaw, sometimes hysterically, but certainly not because he or she finds anything funny. Now a new study published in the journal Brain, from a team led by Josef Parvizi of Stanford University, has helped clear up some of the mystery. Earlier research traced these events, more formally called gelastic seizures, to abnormal clumps of neurons in the hypothalamus called hamartomas. “The hamartomas start firing on their own and cause the seizures,” Parvizi explained. But exactly where in the hypothalamus are gelastic seizure-related hamartomas located? That answer’s important because the hypothalamus has several regions, or nuclei, that manage input and create output related to a variety of body functions like temperature regulation, sexual behavior and hormone release. Parvizi likens it to a college campus. “Just like a campus, you have different buildings and every department has its own students and own connections,” he said. In looking at 100 cases of children with gelastic seizures who’ve had their brains imaged, Parvizi and his colleagues were able to show that in every case the hamartoma lesions were located in a region known as the mammillary bodies. (They don’t have anything to do with breasts. They just sort of look like breasts and the neuroscientists who first described them were men, so there you go.) © 2011 msnbc.com

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 16111 - Posted: 12.06.2011

Glioma, one of the most deadly and common types of brain tumor, is often associated with seizures, but the origins of these seizures and effective treatments for them have been elusive. Now a team funded by the National Institutes of Health has found that human gliomas implanted in mice release excess levels of the brain chemical glutamate, overstimulating neurons near the tumor and triggering seizures. The researchers also found that sulfasalazine, a drug on the market for treating certain inflammatory disorders, can reduce seizures in mice with glioma. About 80 percent of people with glioma will experience at least one seizure during their illness, often as the first symptom. About one-third of patients will develop recurring seizures, known as tumor-associated epilepsy. Sen. Ted Kennedy, D-Mass., whose death was caused by a malignant glioma in August 2009, was diagnosed after having a seizure 15 months earlier. "Seizures are a frequent symptom of glioma and are often poorly controlled by epilepsy medications," said Jane Fountain, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS). "Understanding why the seizures occur and how to counteract them could help us substantially improve the quality of life for people with glioma." "People have assumed that tumors cause seizures by irritating the brain, but that really isn't a scientific explanation. We have now shown that the seizures are caused by glutamate release from the tumor," said Harald Sontheimer, Ph.D., a professor of neurobiology and director of the Center for Glial Biology in Medicine at the University of Alabama Birmingham (UAB). Dr. Sontheimer and his team published their results in Nature Medicine.

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: 15793 - Posted: 09.13.2011

By ALIYAH BARUCHIN FREETOWN, Sierra Leone — On a sweltering morning on a red-earth lane a few blocks from the largest mosque in this West African capital, Jeneba Kabba stands up. A tall, striking woman with a serious manner, Mrs. Kabba has been sitting under an awning in the outdoor classroom of a vocational training program for people with epilepsy. Every weekday, some 20 Sierra Leoneans, from teenagers to adults in middle age, gather here to learn skills like tailoring, weaving, tie-dyeing and soap-making, as well as reading — skills that, in this society, will give them a chance to earn a living. Mrs. Kabba, 30, a graduate of the program, is now a tutor. Her composure belies what she has survived. As a teenager she was taken to a traditional healer, who boiled herbs and made her inhale the fumes from a steam tent for hours. The treatment was supposed to drive out the demons thought to cause epilepsy; she nearly fainted and could have been burned. But worse was yet to come: She was forced to drink a two-liter bottle of kerosene. “Mi ches don cook,” she says in the Krio language, her voice faltering even now: “My chest started to boil.” Only a panicked trip to the hospital saved her life. Mrs. Kabba not only survived, but has been seizure-free for 10 years with the help of phenobarbital, one of the oldest anti-epileptic drugs and virtually the only one available here. And in a country where people with epilepsy are often considered uneducable, unemployable and unmarriageable, Mrs. Kabba teaches, is happily married and has a child. © 2011 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: 15739 - Posted: 08.30.2011

Analysis by Marianne English Gene expression plays a larger role than thought in the development of temporal lobe epilepsy, a common form of epilepsy, finds an international team of scientists. The study was published in the journal Annals of Neurology by scientists from France's biomedical institution Inserm, the University of Marseille in France and the University of California-Irvine. Previously, experts thought neurons, or nerve cells, in the brain began acting abnormally after they were damaged by head trauma or previous illnesses that caused high fevers. Healthy neurons normally transmit messages to one another by moving ions -- or charged particles -- back and forth in channels between cells. These coordinated efforts allow humans and animals to do a variety of things, ranging from eating to reading science news articles on the Internet. But for people living with epilepsy, neurons in the brain can behave abnormally, sometimes firing uncontrollably and causing seizures. Though epilepsy can be caused by many things, the majority of cases cannot be traced back to a particular cause. Looking beyond neurons, the research team found that a "master switch" gene called NRSF controls the expression of some 1,800 genes suppressed in patients with epilepsy. Researchers think brain trauma still activates the gene, but there's evidence that keeping its proteins from influencing other genes can prevent brain tissue from becoming epileptic. So what does this mean for the 50 million people worldwide living with epilepsy? © 2011 Discovery Communications, LLC.

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: 15506 - Posted: 06.30.2011

By PAULINE W. CHEN, M.D. One day during medical school, my classmates and I learned that one of the most well-liked doctors-in-training in the hospital had had a seizure while leading morning work rounds. The sight of him writhing had caused the other doctors and nurses on the ward to panic. Some stood mute, frozen with fear. An intern, believing that the seizure arose from low blood sugar levels, took his half-eaten jelly doughnut and held it against the mouth of his seizing colleague. Others yelled to the ward secretary to “call a code,” and continued to do so even after another dozen doctors and nurses had already arrived on the floor. The young doctor eventually recovered. But for many of the medical students and doctors who heard about the episode or were on the wards that day, the dread of that morning would linger long beyond our years of training. Epilepsy was, and remains, a frightening and mysterious malady. For the last 20 years, Dr. Brien J. Smith has tried to change how doctors and patients view epilepsy. Earlier this year, Dr. Smith, chief of neurology at Spectrum Health in Michigan, became chairman of the Epilepsy Foundation. Being elected head of a national organization does not seem unusual for a doctor who is a well-recognized authority and advocate in his or her field. What is extraordinary is that Dr. Smith knows firsthand about the disease and what his patients experience: He learned he had epilepsy when he was in high school. © 2011 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: 15502 - Posted: 06.28.2011

by Ferris Jabr Talk about intelligent design: a new polymer-covered electrode has the potential to monitor and deliver drugs to out-of-sync brain cells. If trials in animals are successful, it could one day help people to control epilepsy. Neuroscientists implant microelectrode arrays in brains to eavesdrop on – and sometimes influence – the electrical activity of neurons. Why not chemically influence the brain alongside this electrical manipulation, thought Xinyan Tracy Cui at the University of Pittsburgh, Pennsylvania, and her colleagues. So the team coated microelectrodes with an electrically conductive polypyrrole film. Then they loaded pockets within the film with different drugs and neurotransmitters such as glutamate, GABA and dopamine, and attached the arrays to samples of rat brain tissue. Applying an electrical current to the polymer caused it to change shape and release its drug cargo, which then acted on surrounding cells. Cui is currently working on replicating this demonstration in living rodents. Hits the spot Polypyrrole-coated microelectrode arrays, like ordinary arrays, could not only monitor neurons for unusual electrical activity but also deliver electrical impulses to keep neurons firing at the right tempo, like the brain pacemakers sometimes used to treat epilepsy. With the polypyrrole coating, however, microelectrode arrays could release drugs when they detect unusual activity – such as the haphazard electrical firing that characterises a seizure. Because electrodes reach into specific regions of the brain, the drugs would affect only neighbouring neurons. © 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: 15411 - Posted: 06.09.2011

By Sandra G. Boodman, During the 11 years Sonja MacDonald and her family lived with her spells, they had planned what to do when she sensed — or they observed — one coming on. If she was driving, MacDonald was to pull over to the side of the road; her husband had taught their young children how to take the wheel if she was unable to steer, something that luckily never happened. When she took a shower, someone was always in the bathroom, in case she suddenly passed out. And if it happened in the nursing home where she worked, MacDonald gambled on being able to make it to an empty bed. Over the years doctors had given the Milton, Pa., resident various diagnoses for the episodes, which she said began with an aura — an odd feeling of disorientation sometimes tinged with fear. She would stare blankly, sometimes grasping at unseen objects or briefly losing consciousness. These incidents, which lasted two minutes at most, occurred without warning, leaving her feeling tired and cold but with no memory of what had just happened. Most specialists agreed that the spells were seizures that sometimes follow a migraine headache. But how, MacDonald wondered, could she have migraine seizures when the occasional headaches she had were not severe? Doctors brushed that question aside, and MacDonald resigned herself to living with whatever was wrong. “I told my husband, ‘I will not go back to another doctor. I guess when I drop over someone will believe me,’ ” said MacDonald, now 39. In 2009, a new neurologist took a fresh look at her case and in short order figured out what was wrong. The answer, this doctor subsequently learned, had been buried in MacDonald’s records for years.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 5: The Sensorimotor System
Link ID: 15263 - Posted: 04.26.2011

Scientists say they have discovered a "maintenance" protein that helps keep nerve fibres that transmit messages in the brain operating smoothly. The University of Edinburgh team says the finding could improve understanding of disorders such as epilepsy, dementia, MS and stroke. In such neurodegenerative disorders, electrical impulses from the brain are disrupted. This leads to an inability to control movement, and muscles wasting away. The brain works like an electrical circuit, sending impulses along nerve fibres in the same way that current is sent through wires. These fibres can measure up to a metre, but the area covered by the segment of nerve that controls transmission of messages is no bigger than the width of a human hair. Signal failure The scientists discovered that the protein Nfasc186 is crucial for maintaining the health and function of the segment of nerve fibres - called the axon initial segment (AIS) - that controls transmission of messages within the brain. They found that the AIS and the protein within it are important in ensuring the nerve impulse has the right properties to convey the message as it should. Professor Peter Brophy, director of the University of Edinburgh's Centre for Neuroregeneration, said: "Knowing more about how signals in the brain work will help us better understand neurodegenerative disorders and why, when these illnesses strike, the brain can no longer send signals to parts of the body." BBC © MMXI

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: 15098 - Posted: 03.14.2011

ANN CURRY, co-host: It sounds almost too incredible to imagine, doctors removing half of a person's brain so that they could live a better life . Well, that's exactly what they did to this two-year-old girl from Washington state to help her deal with a rare disorder. In a moment we're going to meet her and her parents, but first, NBC 's Miguel Almaguer has their story. MIGUEL ALMAGUER reporting: For two-year-old Katie Verdecchia , simple steps have meant great strides in her recovery. Katie was a beautiful baby and appeared to be healthy, but just a month after her parents, Maryalicia and Brian , brought their little girl home, they noticed something was wrong. Katie had a twitch in her arm, a shake in her leg. She was having seizures. Mr. BRIAN VERDECCHIA: She was seizing 25, 30 percent of the time, at -- any time she was awake. Ms. MARYALICIA VERDECCHIA: Sometimes as much as 10 minutes, you know, in length, each episode. ALMAGUER: The diagnosis, Aicardi syndrome , a rare disorder where the right and left sides of the brain don't connect. The seizures meant Katie 's brain couldn't develop. Ms. VERDECCHIA: When you're told that your child's going to be going downhill and possibly having, you know, a shorter life than eight years, you're going to do what you have to do for your child. © 2011 MSNBC Interactive

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Language and Our Divided Brain
Link ID: 14940 - Posted: 02.01.2011

By Emily Sohn Frédéric Chopin's music was moving and expressive. But the Polish composer and pianist was a frail and sickly man who died young; his life ended just 39 years after it began. Over the years, experts have proposed a variety of diagnoses for Chopin's health woes, ranging from bipolar disorder to pulmonary tuberculosis. A new analysis adds another theory. Regular hallucinations, bouts of melancholy and other symptoms point to epilepsy, the researchers say. Their findings may offer new insight into a gifted man and his brief life. "The hallucinations of Chopin were considered the manifestation of a sensitive soul, a romantic cliché," said Manuel Várquez Caruncho, a radiologist at the Xeral-Calde Hospital Complex in Lugo, Spain. "We think that to split the romanticized view from reality could help to better understand the man." The results of Chopin's autopsy have long been lost, but plenty of scientists and historians have written about the composer's health. Born in 1810, Chopin suffered throughout his life from breathing troubles and fevers. He was emaciated, coughed often and had frequent lung infections. He had diarrhea as a teen and severe headaches in adulthood. Melancholy plagued him. © 2011 Discovery Communications, 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: 14917 - Posted: 01.25.2011

NEW YORK (Reuters Health) - Older adults on certain epilepsy drugs have an increased risk of breaking their wrist, hip or spine, according to a new Canadian study. The drugs have been suspected of weakening bones for years, researchers say, but whether individual medications are different hadn't been clear. The Canadian team found patients on all but one of 15 common epilepsy drugs studied had higher odds of breaking a bone, with increases ranging from 25 percent to nearly 200 percent higher than people not taking the drugs. While the study didn't give absolute risks, in general about a third of women and a fifth of men over 50 suffer fractures related to bone thinning, or osteoporosis, according to the International Osteoporosis Foundation. Lead researcher Dr. Nathalie Jette, of the University of Calgary in Alberta, advised that older adults on epilepsy medicine try to boost their bone health. For instance, she said, they could stop smoking, cut back on drinking, exercise more and take calcium and vitamin D supplements. Still, the researchers caution that they can't be sure exactly why people taking the drugs have weaker bones. SOURCE: http://bit.ly/fxSI93 Archives of Neurology, January 2011. Copyright 2011 Thomson Reuters.

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: 14868 - Posted: 01.13.2011

by Allison Bohac Most people know how hard it can be to stick to a diet. But for children with epilepsy, maintaining a restrictive high-fat, low-carbohydrate regimen known as the ketogenic diet is far more difficult than any weight-loss plan. Someday, however, they may be able to control seizures with a simple supplement instead, if a new finding in mice holds up in humans. Almost a third of epilepsy patients, many of them children, don't respond to antiseizure drugs. For reasons that are not well understood, the ketogenic diet can prevent seizures for some of these children. But it's by no means an easy fix. Patients need to eat 80% to 90% of their daily calories as fat, usually in the form of vegetable oil or butter. Only some versions of the diet allow any carbohydrates at all, and sugary desserts are off-limits. "Eating a cookie can break the effect of the diet, resulting in a seizure," explains Karin Borges, a neurobiologist at the University of Queensland, Brisbane, in Australia. Hoping to design a more palatable alternative to the ketogenic diet, Borges and her colleagues began experimenting with a synthetic oil often found in antiwrinkle creams and other cosmetics. The compound, called triheptanoin, is already used to treat certain metabolic disorders; researchers believe it works because it replenishes specific molecules needed to produce the energy-carrying molecule adenosine triphosphate (ATP). Borges reasoned that these metabolites, which are also the building blocks for certain chemical messengers in the brain, might be depleted by the flurry of brain activity that occurs during a seizure. Lower ATP levels in the brain can destabilize neurons, triggering more seizures. Borges hoped that a diet supplemented with triheptanoin would replenish the brain's supply of metabolites and boost ATP production, helping to control epileptic bursts. © 2010 American Association for the Advancement of Science.

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: 14818 - Posted: 12.27.2010

By Nathan Seppa Epilepsy that strikes in childhood and lingers into adulthood triples an individual’s risk of dying, researchers find. But children who “outgrow” epilepsy and see their seizures fade as adults don’t have this added mortality risk, researchers report in the Dec. 23 New England Journal of Medicine. The findings, from a 40-year study in Finland, provide a long-term look that doctors can use as they puzzle over whether to recommend surgery for patients or continue with medication, says neurologist David Ficker of the University of Cincinnati, who wasn’t involved in the study. “We probably should be treating epilepsy aggressively in people who aren’t seizure-free,” he says. Doctors tracked the fate of 245 children diagnosed with epilepsy in the early 1960s. Half of the patients had epilepsy stemming from no clear cause and were neurologically normal, apart from having seizures. The other half had a clear epilepsy trigger, such as severe head trauma, brain injury from meningitis or encephalitis, or other brain damage that was identifiable on scans such as magnetic resonance imaging. All the patients got checkups every five years until 2002. By then, 60 had died, a rate three times the average for people in Finland of comparable age, ranging up to 54 years. Of those 60 deaths, 51 occurred in the 107 patients who were still having seizures. Only five occurred in the 35 who had been in remission for five years or more with the help of medication, and four deaths occurred in the 103 people whose seizures had been in remission for that long without medication. Overall, 33 deaths were tied to epilepsy. The other deaths were mainly due to pneumonia and heart disease. © Society for Science & the Public 2000 - 2010

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: 14817 - Posted: 12.27.2010

By Sandra G. Boodman As the all-too-familiar number flashed on his cellphone shortly before 9 p.m., Dan Landri-gan reflexively braced himself for bad news. The caller was one of the doctors treating his wife, Donna, who had been in a coma for four months. "She sounded pretty choked up," Landrigan recalled. "I think we've found out what's making your wife sick," the specialist at the University of Rochester's Strong Memorial Hospital told him, as a wave of relief flooded his body. "I was completely shocked," said the telecommunications executive, now 37. "My hope for so long was that this was the phone call I was going to get." Doctors at three Upstate New York hospitals had been stymied by Donna Landrigan, whose case was unlike any they had seen. The previously healthy 35-year-old mother of three had initially become so psychotic she had to be tied to her hospital bed to keep her from hurting herself or attacking others. A few weeks later she had been placed in a medically induced coma to protect her from the continuous seizures wracking her brain, spasms that could have killed her. Every promising lead had seemed to turn into a dead end, and the dangers of prolonged coma, including severe brain damage, were mounting. Things looked so hopeless that doctors had begun discussing whether to suggest terminating life support. © 2010 The Washington Post Company

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 8: Hormones and Sex
Link ID: 14749 - Posted: 12.07.2010