Category: Epilepsy

For years brain scientists have puzzled over the shadowy role played by the molecule putrescine, which always seems to be present in the brain following an epileptic seizure, but without a clear indication whether it was there to exacerbate brain damage that follows a seizure or protect the brain from it. A new Brown University study unmasks the molecule as squarely on the side of good: It seems to protect against seizures hours later.

Putrescine is one in a family of molecules called "polyamines" that are present throughout the body to mediate crucial functions such as cell division. Why they surge in the brain after seizures isn't understood. In a lengthy set of experiments, Brown neuroscientists meticulously traced their activity in the brains of seizure-laden tadpoles. What they found is that putrescine ultimately converts into the neurotransmitter GABA, which is known to calm brain activity. When they caused a seizure in the tadpoles, they found that the putrescine produced in a first wave of seizures helped tadpoles hold out longer against a second wave of induced seizures.

Carlos Aizenman, assistant professor of neuroscience and senior author of a study published in the journal Nature Neuroscience, said further research could ultimately produce a drug that targets the process, potentially helping young children with epilepsy. Tadpoles and toddlers aren't much alike, but this basic aspect of their brain chemistry is.

"Overall, the findings presented in this study may have important therapeutic implications," Aizenman and co-authors wrote. "We describe a novel role for polyamine metabolism that results in a protective effect on seizures induced in developing animals."

Detective work

The result that "priming" the tadpoles with a seizure led to them being 25 percent more resistant to a subsequent seizure four hours later was "puzzling," said Aizenman, who is affiliated with the Brown Institute for Brain Science. It took about a dozen more experiments before his team, led by graduate student Mark Bell, could solve the mystery.

First they hindered polyamine synthesis altogether and found that not only did the protection against seizures disappear, but it also left the tadpoles even more vulnerable to seizures. Then they interrupted the conversion of putrescine into other polyamines and found that this step enhanced the protection, indicating that putrescine was the beneficial member of the family.

Going with those results, they administered putrescine directly to the tadpoles and found that it took 65 percent longer to induce a seizure than in tadpoles that didn't get a dose of putrescine.

Further experiments showed that the protective effect occurs after putrescine is metabolized, with at least one intermediary step, into GABA, and GABA receptors are activated in brain cells.

"Potentially by manipulating this pathway we may be able to harness an ongoing protective effect against seizures," Aizenman said. "However I should caution that this is basic research and it is premature to predict how well this would translate into the clinic."

In the meantime, the research may also help explain a bit more about young brains in general, Aizenman said.

"Our findings may also tell us how normal brains, especially developing brains, may regulate their overall levels of activity and maybe keep a type of regulatory check on brain activity levels," he said.

In addition to Aizenman and Bell, the paper's other authors are undergraduates James Belarde and Hannah Johnson. The American Heart Association and the National Institutes of Health funded the study, while individual researchers were supported by the National Science Foundation, the Klingenstein Fund, and the Brain Science Siravo Awards for Epilepsy Research.

NewsPsychology (Feb. 28, 2011) — Whether on a battlefield, in a factory or at a rock concert, noise-induced hearing loss is one of the most common hazards people face.

Researchers at Washington University School of Medicine in St. Louis have identified a low-dose, two-drug cocktail that reduces hearing loss in mice when given before they are exposed to loud noise. The drugs, already FDA-approved for other conditions, also treat hearing loss after noise exposure.

While both drugs are known to protect hearing on their own, this is the first study to test the two in combination.

“We found they have synergy,” says Jianxin Bao, PhD, research associate professor of otolaryngology at the School of Medicine. “Two drugs at lower dosages can block more signaling pathways than one alone, improving results while reducing side effects. We got the idea from cancer and HIV studies that use multiple drugs at lower dosages.”

Bao presented the work Feb. 21 in Baltimore at a meeting of the Association for Research in Otolaryngology.

In earlier work, Bao’s group found that anticonvulsant drugs for treating epilepsy helped protect hearing in mice after exposure to loud noise. And other groups had determined that glucocorticoids, anti-inflammatory drugs often used to treat allergies and asthma, were also protective.

The reasons these drugs reduce noise-induced hearing loss are not well understood. But anticonvulsants are known to block calcium channels in nerve cells, and Bao’s group speculates that the drug helps protect neuronal connections between hair cells and auditory neurons.

For this work, Bao and colleagues chose two drugs from the anti-epilepsy family and two from the glucocorticoid family.

“We picked drugs that have fewer side effects and that can be chronically used,” says Bao, also associate professor of audiology and communication sciences.

To test each drug’s ability to prevent hearing loss, they gave various doses to mice two hours before exposing them to noise. To test treatment, they administered the drugs to different groups of mice 24 hours after noise exposure.

Three of the four drugs showed increasing protection with higher doses. And two of the drugs in combination, the anticonvulsant zonisamide and the glucocorticoid methylprednisolone, showed comparable hearing protection at much lower doses than when administered alone.

While the drugs do not prevent all hearing loss following sustained exposure to noise at 110 decibels, or about the sound of a chain saw, they can significantly reduce the loss by about 10 to 30 decibels.

In other words, a mouse with normal hearing might be able to hear a sound at 30 decibels. After exposure to loud noise, that mouse might only hear sounds that reach 50 decibels. But if that mouse were treated, it might be able to hear sounds at 40 decibels. In humans, protecting 5 or 10 decibels makes a difference in being able to hear everyday speech.

Bao says their next step is to test the drugs in animals that model human hearing more closely.

Bao et al. “Development of a combination therapy for noise-induced hearing loss.” Presented Feb. 21, 2011 at a meeting of the Association for Research in Otolaryngology.

This work was supported by the National Institute on Deafness and Other Communication Disorders.

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The above story is reprinted (with editorial adaptations by newsPsychology staff) from materials provided by Washington University School of Medicine. The original article was written by Julia Evangelou Strait.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of NewsPsychology ( or its staff.

NewsPsychology (Feb. 22, 2011) — A newly published report reveals patients with epilepsy and low socioeconomic status (SES) are more likely to have uncontrolled seizures, drug-related side effects, and a lower overall quality of life. The study also indicates that low SES patients used the hospital emergency room more often and had more visits to a general practitioner than epileptic patients at higher socioeconomic levels.

Full findings are now available in Epilepsia, a journal published by Wiley-Blackwell on behalf of the International League Against Epilepsy.

The Centers for Disease Control and Prevention (CDC) estimates that two million Americans have epilepsy and roughly 140,000 new cases are diagnosed each year. Prior studies in epilepsy literature provide evidence of disparities in healthcare use between individuals of different SES. One study found that epileptic patients with incomes below the poverty level in California were 50% less likely than those with higher income (not in poverty) to report taking epilepsy medication (Elliott et al., 2009).

“Current medical evidence is based on point-in-time comparisons across population and suggests that disparities in healthcare may be due to access difficulties,” explains lead study author Dr. Charles E. Begley, Professor of Management & Health Sciences at the University of Texas Health Science Center in Houston. “Our study investigates disparities in healthcare over time, examining the impact of SES in patients with epilepsy who have access to regular care.”

Researchers enrolled 566 adult patients with epilepsy from three clinics in Houston and New York City serving a low-SES population, and one in Houston serving high-SES patients. Participants were interviewed at baseline regarding healthcare use, seizure frequency and type, anti-epileptic drug (AED) side effects, and outcomes during the prior three-month and one-year periods. The survey was repeated several times during the year-long study period.

Indicators of SES — income, education, employment, and insurance coverage — were significantly lower for patients at low-SES sites compared to the higher-SES site. Patients at the low-SES sites had consistently higher emergency room use and visits to the general practitioner. Throughout the one-year study period low-SES patients had significantly higher likelihoods of poor outcomes — 2.2 to 3.9 times more likely to have uncontrolled seizures and 4.9 to 16.3 times more likely to have AED side effects — compared with higher-SES patients.

The authors determined that significant disparities in patterns of care and outcomes of low and high-SES patients receiving regular care for epilepsy were persistent over the one-year study period. “Future research needs to examine specific site-related factors that may be associated with these disparities in care for individuals with epilepsy,” concluded Dr. Begley.

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The above story is reprinted (with editorial adaptations by newsPsychology staff) from materials provided by Wiley – Blackwell, via AlphaGalileo.

Journal Reference:

1. Charles Begley, Rituparna Basu, David Lairson, Thomas Reynolds, Stephanie Dubinsky, Michael Newmark, Forbes Barnwell, Allen Hauser, Dale Hesdorffer. Socioeconomic status, health care use, and outcomes: Persistence of disparities over time. Epilepsia, 2011; DOI: 10.1111/j.1528-1167.2010.02968.x

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of NewsPsychology ( or its staff.

Researchers from the Department of Neurology at NYU Langone Medical Center identified potential benefits of a new computer application that automatically detects subtle brain lesions in MRI scans in patients with epilepsy. In a study published in the February 2011 issue of PLoS ONE, the authors discuss the software's potential to assist radiologists in better identifying and locating visually undetectable, operable lesions.

"Our method automatically identified abnormal areas in MRI scans in 92 percent of the patients sampled, which were previously identified by expert radiologists reviewing multiple images," said first-author Thomas Thesen, PhD, assistant professor, Department of Neurology, NYU Langone Medical Center. "Based on these findings, we will focus on the ability of our application to detect the more subtle epileptic malformations that are not easily detectable by the human eye. We believe this could lead to new tools to greatly help radiologists provide more accurate and faster results with objective measures for standardizing readings."

The proof-of-concept study, entitled "Detection of epileptogenic cortical malformations with surface-based MRI morphometry," demonstrates that non-invasive and automated detection of known epileptogenic structural abnormalities in cortex is possible, and supports its potential use as a tool for diagnosis and planning of epilepsy surgery.

The researchers are encouraged by the initial results and have already started evaluating the applications ability to determine undetected lesions in previously negative MRI scans, with findings to be published later this year.

The study's other authors include Chad Carlson, Brian T. Quinn, Orrin Devinsky, Jonathan DuBois, Jacqueline French, Olga Felsovalyi, Xiuyuan Wang and Ruben Kuzniecky from NYU Langone Medical Center; Carrie R. McDonald and Eric Halgren from the University of California, San Diego and Richard Leventer from the Royal Children's Hospital, Murdoch Children's Research Institute, University of Melbourne, Australia.

Journal Reference:

1. Thomas Thesen, Brian T. Quinn, Chad Carlson, Orrin Devinsky, Jonathan DuBois, Carrie R. McDonald, Jacqueline French, Richard Leventer, Olga Felsovalyi, Xiuyuan Wang, Eric Halgren, Ruben Kuzniecky. Detection of Epileptogenic Cortical Malformations with Surface-Based MRI Morphometry. PLoS ONE, 2011; 6 (2): e16430 DOI: 10.1371/journal.pone.0016430

The composer Frédéric Chopin, who regularly hallucinated, probably had temporal lobe epilepsy throughout his short life, reveals research published online in Medical Humanities. Hallucinations typically feature in seizure disorders, the study's authors say.

Chopin was renowned, among other things, for his frailty and sensitivity, which turned him into the epitome of the romantic artist.

While his well documented bouts of melancholy have been attributed to bipolar disorder or clinical depression, the hallucinatory episodes to which he was also prone have tended to be overlooked, suggest the authors.

They draw on the composer's own descriptions of these hallucinatory episodes, and accounts of his life, given by friends and pupils.

Chopin, who was plagued by poor health throughout his life, died at the age of 39 as a result of chronic lung disease in 1849, which has recently been attributed to cystic fibrosis, based on the composer's family history.

During a performance of his Sonata in B flat minor, in England in 1848 at a private salon, Chopin suddenly stopped playing and left the stage — an event recorded by the Manchester Guardian's music critic.

In a letter written to the daughter of George Sand in September that year, Chopin describes the moment during the performance when he saw creatures emerging from the piano, which forced him to leave the room to recover himself.

In her memoirs, George Sand recalled a trip she and the composer took to Spain in 1838. She describes the monastery where they stayed as being "full of terrors and ghosts for him," and various incidents in which Chopin appeared pale, or with wild eyes, and his hair on end. She also recounts the vivid descriptions he gave her of the visions he had had.

There are other accounts, both by George Sand, and by one of Chopin's pupils Madame Streicher, of similar incidents, and the composer's own description of a "cohort of phantoms" in 1844.

Hallucinations are a hallmark of several psychiatric disorders, such as schizophrenia and dissociative states, say the authors, but usually take the form of voices.

Migraine can also produce hallucinations, but these can last up to half an hour, while Chopin's were often brief; and migraine auras without headache mostly mainly occur in patients over the age of 50, say the authors. Charles Bonnet syndrome is also discounted as Chopin had no eye disorders.

Chopin did take laudanum to quell his various physical symptoms, but the type of visual hallucinations associated with this do not correspond to Chopin's and the composer also began experiencing them before taking this medication, say the authors.

Rather, they think that temporal lobe epilepsy is a more likely explanation as it can produce complex visual hallucinations, which are usually brief, fragmentary, and stereotyped, just like those Chopin said he experienced.

The authors acknowledge that without the aid of modern day tests, it is difficult to make a definitive diagnosis, but comment: "A condition such as that described in this article could easily have been overlooked by Chopin's doctors," adding that there was limited understanding of epilepsy at that time.

"We doubt that another diagnosis added to the already numerous list will help us understand the artistic world of Frédéric Chopin. But we do believe that knowing he had this condition could help to separate romanticised legend from reality and shed new light in order to better understand the man and his life."

Journal Reference:

1. Manuel Vázquez Caruncho, Franciso Brañas Fernández. The hallucinations of Frédéric Chopin. Medical Humanities, 2011; DOI: 10.1136/jmh.2010.005405

The Institute of Tropical Medicine Antwerp is intensifying its fight in Congo against the pork tapeworm, which in spite of its name is also a human parasite, causing epilepsy. ITM scientists have worked for years on the tapeworm infection. That work now receives an important boost, thanks to a grant of the Gates Foundation, one of the most important health charities in the world. The Gates Foundations invests 1.5 million dollars in an international project to improve control of the tapeworm.

Humans are infected by the pork tapeworm, Taenia solium, by eating undercooked pork meat, containing larvae. The larva grows into a tapeworm and installs itself in your gut, where it normally causes little harm. It produces eggs that leave your body with your excrements. Where pigs have access to human faeces, as is the case in poor developing countries, the eggs produce larvae that settle in the pig, and the cycle is maintained. Problems develop when a human ingests the eggs, through contaminated water or food. In humans, these eggs grow into cysts in the tissues, including the brain, where they can cause severe neurological problems such as epilepsy.

The incidence of epilepsy has increased in sub-Saharan Africa as pig keeping and pork consumption have become more widespread in the past decade. A recent study in Tanzania shows that 14 per cent of all epilepsy may be caused by this parasite. Last year, ITM scientists found the pork tapeworm in four Congolese pigs out of ten, a worrying number.

Also last year, researchers at ITM have shown that pigs can be vaccinated against the tapeworm, so for the first time breaking the cycle. The vaccine is not yet on the market.

The ITM is one of the partners in a project of the Schistosomiasis Control Initiative (SCI), that will investigate if efforts to combat the pork tapeworm with drugs, can be integrated into existing disease prevention programmes. This program now receives a grant from the Gates Foundation.The project is coordinated by Imperial College London; the ITM researchers are responsible for the Congolese part. The WHO and other international aid workers are increasingly focussing on targeting many diseases at once. Instead of sending in a separate team for each disease, such a program treats up to seven diseases at once. Until now, diseases that jump from animals to humans did not get much attention. Yet the pork tapeworm is an evident candidate, as infected humans can be treated with praziquantel, a low-cost drug that already is part of the combination package, against the Schistosoma worm (albeit in a different dose).

In Congo, the ITM scientists will investigate if repeated administrations of high doses of praziquantel against Schistosoma, lower the number of tapeworms in humans and larvae in pigs. These numbers also will help refine the models for disease transmission in a population. The Institute of Tropical Medicine is one of the few institutions with the right expertise for combined research on humans and pigs, because it disposes of a Unit of Medical Helminthology and a Unit of Veterinary Helminthology.

The researchers not only will document the impact of integrated approaches on the burden of disease; they also will assess the cost-effectiveness of these interventions. Indeed, also the pigs profit from controlling the tapeworm in humans. To poor farmers a healthy pig is a considerable financial asset; the money in turn supports their general quality of life, including their health.

— Most anti-epileptic drugs are associated with an increased risk of non-traumatic fracture in individuals 50 years of age and older, according to a report in the January issue of Archives of Neurology, one of the JAMA/Archives journals.

Anti-epileptic drugs are considered a secondary risk factor for osteoporosis, according to background information in the article, because epilepsy is highly prevalent in older adults, a population already at risk for osteoporosis. Additionally, anti-epileptic drugs are associated with greater bone density reduction in post-menopausal women with epilepsy.

While there have been studies that examined the link between anti-epileptic drugs and bone density loss in adults older than 65, little evidence exists for the association of individual anti-epileptic drugs with bone loss. Nathalie Jetté, M.D., M.Sc., of the University of Calgary, Foothills Hospital, Alberta, Canada, and colleagues studied medical records of 15,792 individuals who experienced non-traumatic fractures between April 1996 and March 2004. Each person was matched with up to three controls, persons without a history of fracture, for a total of 47,289 controls.

The individual anti-epileptic drugs studied included carbamazepine, clonazepam, ethosuximide, gabapentin, phenobarbital, phenytoin and valproic acid. Additional anti-epileptic drugs with fewer numbers of users were included together under "other anti-epileptic drugs."

The likelihood of fractures was highest for persons taking phenytoin followed by carbamazepine, other, phenobarbital, gabapentin and clonazepam. The only anti-epileptic drug not associated with an increased likelihood of fracture was valproic acid.

Similar results were found when testing for the use of anti-epileptic drugs in monotherapy (individuals taking only one anti-epileptic drug) and in polytherapy (individuals taking more than one anti-epileptic drug). All anti-epileptic drugs used in monotherapy were associated with a significantly increased risk of fracture except for valproic acid, phenobarbital and "other anti-epileptic drugs." The greatest risk of fracture was found in individuals in the polytherapy subgroups.

"In conclusion, our study showed that most anti-epileptic drugs except for valproic acid are associated with an increased likelihood of non-traumatic fracture in individuals aged 50 years or older," the authors write. "Future prospective studies of anti-epileptic drugs in newly treated drug-naïve patients are needed to better examine the individual effects of anti-epileptic drugs on bone health."

Editor's Note: This study was supported in part by an operating grant and New Investigator Awards from the Canadian Institutes of Health research and a research salary award from the Alberta Innovates Health Solutions.

Journal Reference:

1. N. Jette, L. M. Lix, C. J. Metge, H. J. Prior, J. McChesney, W. D. Leslie. Association of Antiepileptic Drugs With Nontraumatic Fractures: A Population-Based Analysis. Archives of Neurology, 2011; 68 (1): 107 DOI: 10.1001/archneurol.2010.341

 In the Old West, camps sent smoke signals across distances to share key developments or strategy. Likewise, two important signaling molecules communicate across nerve cells to regulate electrical and chemical activity, neuroscientists from the UT Health Science Center San Antonio have reported.

The findings in rodent models have implications for potential future treatment of epilepsy, stroke and other problems, the researchers said.

"We now have novel targets for therapeutic intervention for a range of neurological and cardiovascular diseases, including stroke, epilepsy, dementia, hypertension, mental illness and others," said senior author Mark S. Shapiro, Ph.D., professor of physiology at the Health Science Center. "This study should guide clinicians and pharmaceutical companies in developing new therapies against mental, neurological, cardiovascular or cerebrovascular diseases that afflict many millions of people."

By isolating nerve cells from rats, the San Antonio team found a relationship between signaling enzymes called phosphoinositide kinases and calcium ions. Calcium transport and levels of calcium concentrations inside nerve cells are extremely important for proper neurobiological function, Dr. Shapiro said.

In epilepsy, for example, it is thought that the hyper-excitability in the brain causes abnormal elevations of intracellular calcium ions, which is extremely toxic. Thus, epileptic seizures often predispose people to additional seizures, as the normal regulation of brain activity increasingly breaks down.

The study is in the Jan. 7 issue of the Journal of Biological Chemistry.

Journal Reference:

1. O. Zaika, J. Zhang, M. S. Shapiro. Combined Phosphoinositide and Ca2 Signals Mediating Receptor Specificity toward Neuronal Ca2 Channels. Journal of Biological Chemistry, 2010; 286 (1): 830 DOI: 10.1074/jbc.M110.166033

NewsPsychology (Jan. 4, 2011) — Sudden, catastrophic childhood epilepsy is a parent’s worst nightmare, especially in the case of fever-induced refractory epileptic encephalopathy in school-age children (FIRES). While not much is known about the condition, new research published in the January issue of The Journal of Nuclear Medicine shows that positron emission tomography (PET) scans can offer an evaluation of cognitive dysfunction of FIRES, its evolution and further prognosis.

FIRES, a recently named condition, occurs in previously healthy children who, after a brief fever, experience acute seizures that are resistant to medication and last for several weeks. After the seizures stop, children are left with severe cognitive dysfunction, mainly involving language, memory and behavior.

The study, “18F-FDG PET Reveals Frontotemporal Dysfunction in Children with Fever-Induced Refractory Epileptic Encephalopathy,” was conducted with eight patients diagnosed with FIRES. The patients were given a neuropsychologic evaluation, a brain MRI and an 18F-FDG PET scan. Severe cognitive dysfunction was noted, and while the MRI tests showed no abnormalities for the patients, the PET scans reported significant cognitive impairment.

Researchers compared the FIRES patients with a pseudo-control group of epilepsy patients with normal MRI and PET scan results. Using statistical parametric mapping, an objective approach to analyzing brain activity, the study exposed that the brain dysfunction was related to the epilepsy in the FIRES patients.

“The fact that the dysfunctional network is superimposed over the epileptic network is a strong argument that FIRES is the cause of cognitive deterioration in these previously normal children. Moreover, localizing such a dysfunction may help to specify the re-adaptation more accurately,”said Catherine Chiron, M.D., Ph.D., pediatric epileptologist and head of the Research Program on Epilepsy at Hospital Necker — Enfants Malades in Paris and one of the authors of the study.

She continued, “These findings may open the way for using 18F-FDG PET more extensively and more accurately in pediatric imaging, as this methodology allows us to investigate not only unilateral but also bilateral diseases, and to interpret PET images in an objective and sensitive manner.”

Much remains unknown about FIRES; however, with the further understanding of the condition achieved through this research, physicians can recommend better intervention, ultimately leading to improved patient outcomes.

Authors of the scientific article include: Michel Mazzuca, Olivier Dulac and Catherine Chiron, Inserm, U663 — University Paris Descartes, and APHP, Neuropediatric Department, Hospital Necker — Enfants Malades, Paris, France; Isabelle Jambaque, Lucie Hertz-Pannier, Viviane Bouilleret, Frederique Archambaud and Sebastian Rodrigo, Inserm, U663 — University Paris Descartes, Paris, France and Verne Caviness, Department of Neurology, Massachusetts General Hospital, Boston, Mass.

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The above story is reprinted (with editorial adaptations by newsPsychology staff) from materials provided by Society of Nuclear Medicine, via EurekAlert!, a service of AAAS.

Journal Reference:

1. M. Mazzuca, I. Jambaque, L. Hertz-Pannier, V. Bouilleret, F. Archambaud, V. Caviness, S. Rodrigo, O. Dulac, C. Chiron. 18F-FDG PET Reveals Frontotemporal Dysfunction in Children with Fever-Induced Refractory Epileptic Encephalopathy. Journal of Nuclear Medicine, 2010; 52 (1): 40 DOI: 10.2967/jnumed.110.077214

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of NewsPsychology or its staff.

NewsPsychology (Dec. 27, 2010) — Epilepsy, a common and serious neurologic disorder that affects millions of people, is not getting the public attention and funding for research it deserves, according to an editorial on a study published in the January 4, 2011, print issue of Neurology®, the medical journal of the American Academy of Neurology.

“We have almost nonexistent epilepsy surveillance, or ongoing collection of data on newly diagnosed epilepsy, in the United States,” said Edwin Trevathan, MD, MPH, Dean of the St. Louis University School of Public Health in St. Louis and a member of the Neurology® Editorial Board. “As a result, we do not have good data to inform decisions made by our health leaders, and some of our best researchers are analyzing data that are 30 to 50 years old.”

Trevathan points to narrowly focused funding lines from Congress to the Centers for Disease Control and Prevention (CDC) as one cause of inadequate epilepsy data. For example, these narrow funding lines result in funding for public awareness campaigns instead of essential public health infrastructure, such as public health surveillance for epilepsy. Major federal agencies such as the CDC also have other priorities that receive the limited, optional funding.

“Epilepsy has a major impact on public health. A national approach to monitoring epilepsy trends is desperately needed in order to monitor the impact of improvements in epilepsy care, to identify problems with epilepsy care that need to be corrected, and to provide up-to-date data for researchers,” said Trevathan.

In the corresponding study, scientists aimed to discover the lifetime risk of developing epilepsy. They analyzed data on 412 people from Rochester, Minn., diagnosed with epilepsy between 1960 and 1979. The study found that at least one in 26 people will develop epilepsy in their lifetime. The risk was higher in the elderly, with a risk of 1.6 percent in people under age 50 and a 3.0 percent risk for people up to age 80.

“Our results highlight the need for more research using epilepsy surveillance data, especially given the aging population in the United States. Such surveillance will also provide useful information for health care planners as they address the service needs of people with epilepsy,” said study author Dale C. Hesdorffer, PhD, associate professor of clinical epidemiology in the Sergievsky Center at Columbia University Medical Center.

The study was supported by the National Institute for Neurologic Disorders and Stroke and the National Institutes of Health.

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The above story is reprinted (with editorial adaptations by newsPsychology staff) from materials provided by American Academy of Neurology.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of NewsPsychology or its staff.