Category: Disorders and Syndromes

Post-sex blues is not a sexual behaviour commonly discussed, but a Queensland University of Technology (QUT) study of more than 200 young women has found one in three (32.9 per cent) had experienced the phenomenon at some point.

QUT Associate Professor Robert Schweitzer's research, published in the latest International Journal of Sexual Health, looked at the prevalence of postcoital dysphoria or the experience of negative feelings following otherwise satisfactory intercourse.

"While 32.9 per cent of women reported experiencing symptoms of postcoital dysphoria at least a little of the time in their life, what was even more surprising was that 10 per cent reported experiencing the symptoms some of the time or most of the time," said Professor Schweitzer from QUT's School of Psychology & Counselling.

"Under normal circumstances the resolution phase of sexual activity, or period just after sex, elicits sensations of well-being, along with psychological and physical relaxation.

"However, individuals who experience postcoital dysphoria may express their immediate feelings after sexual intercourse in terms of melancholy, tearfulness, anxiety, irritability or feeling of restlessness."

Professor Schweitzer said one woman described feeling "melancholy" after sex.

"I did not associate the feeling with an absence of love or affection for my sexual partner nor with an absence of love or affection from them towards me, because it seemed so unconnected with them," she said.

Professor Schweitzer said the cause of such negative feelings was virtually unknown.

"Research on the prevalence and causes of postcoital dysphroia has been virtually silent but internet searches reveal information on the subject is widely sought," he said.

"It has generally been thought that women who have experienced sexual abuse associate later sexual encounters with the trauma of the abuse along with sensations of shame, guilt, punishment and loss.

"This association is then purported to lead to sexual problems and the avoidance of sex."

But Professor Schweitzer said his study had instead found only limited correlation between sexual abuse and postcoital dysphoria.

"Psychological distress was also found to be only modestly associated with postcoital dysphoria," he said.

"This suggests other factors such as biological predisposition may be more important in understanding the phenomenon and identifying women at risk of experiencing postcoital dysphoria."

Professor Schweitzer's next stage of research will look at emotional characteristics of women who experience postcoital dysphoria.

"I want to look at how women view their 'sense of self'. Whether they are fragile or whether they are strong women, and investigate whether this leads to their postcoital dysphoria," he said.

Journal Reference:

1. Brian Bird, Robert Schweitzer, Donald Strassberg. The Prevalence and Correlates of Postcoital Dysphoria in Women. International Journal of Sexual Health, 2011; 23 (1): 14 DOI: 10.1080/19317611.2010.509689

The first two stereo-EEG explorations in Finland were carried out by neurosurgeons of the Epilepsy surgery team in Helsinki University Central Hospital this spring. The method reinforces other examination methods already in use and opens an excellent opportunity in the exploration of the electric activity of both the surface and the deep brain structures during epileptic seizures. The examination also enables exact localization of the functionally important areas of the brain and improves safety of epilepsy surgery at a later stage.

The stereo-EEG examination was developed already in the 1960's, but the recent modifications of the method in the last few years have made it safer and more feasible. The introduction of the method at HUCH benefits particularly patients with severe, drug resistant epilepsy

For the patient, the stereo-EEG is a considerably more pleasant experience than the earlier-used intracranial recording methods: no large craniotomy is required as thin recording electrodes are placed into the brain through small holes. The recording time can also be increased with the new method from one to as many as four weeks.

Epilepsy surgery in Finland has been centred in two university hospitals. In Helsinki University Central Hospital about 30 epilepsy surgery operations are performed each year, and the results are extremely good: more than half of the patients will be completely seizure-free thanks to the operation.

The new stereo-EEG method will be in active use.

"We have a large number of patients at the examination stage, and the ability to localize their epileptic foci through stereo-EEG is very beneficial. About a quarter of the presurgical patients will need an intracranial evaluation," neurosurgeon Atte Karppinen from HUCH Neurosurgery department informs.

Getting ready for Deep Brain Stimulation

HUCH neurosurgery clinic is also getting ready to introduce the so-called deep brain stimulation therapy. The equipment and methods used in the DBS and in the stereo-EEG follow the same basic principles. In HUCH they have several decades' experience and expertise in DBS surgery regarding other illnesses, such as Parkinson's disease.

"Starting DBS therapy in the treatment of epilepsy is well-founded at the stage when we have sufficient, reliable research-based information on the results of the method in the treatment of epilepsy," Dr Karppinen says.

"The methods we use complement each other, and our team's technical research facilities, expertise and results achieved by surgery represent the cutting edge in the whole world. We have all the knowhow and capacity for DBS surgery, but we proceed with patience."

 When an aggressive form of breast cancer strikes a young woman, what kind of stress, anxiety and other psychological and social challenges does she face?

That question hasn't been answered in the published psychological cancer literature, but a new pilot study just launched is gathering data to change that, according to psychologist Georita M. Frierson at SMU.

The two-year study will survey up to 60 women recently diagnosed with an aggressive form of breast cancer that typically strikes younger women under 40, mostly African-American or Hispanic, or those who test positive for a mutation of the human gene that suppresses tumors, BRCA1.

Known as Triple Negative Breast Cancer, this unconventional subtype categorized as "nonhormonal" strikes 10 to 20 percent of women diagnosed with breast cancer.

The study is probing patients' stress, anxiety and concerns about the psychological and social hurdles they face, said Frierson, principal investigator. SMU is collaborating on the Triple Negative study with the University of Texas Southwestern Simmons Cancer Center, a National Cancer Institute-designated cancer center.

"We don't know anything about this population psychologically," said Frierson, an expert in behavioral health psychology and an assistant professor in the SMU Department of Psychology. "But based on this study, for any of their concerns we could tailor a psychological intervention to help other women like the women in my pilot. These women will be our pioneers in the psychological area to help their sisters that may have Triple Negative in the future."

For younger, minority women: Different cancer, different challenges

Triple Negative patients face far different challenges than women with traditional hormonal-type breast cancer, whose psychological and social challenges have been widely examined in the published psychological cancer literature, Frierson said. Traditional hormonal-type patients are typically over age 50, in a later career phase, raising their families, and probably have peers who may be struggling with a chronic illness.

In contrast, a Triple Negative patient is young, maybe mid-career, may not have started a family, and her peers are largely healthy and active. Because Triple Negative is a very aggressive cancer, Triple Negative patients can have lower survival rates and higher recurrence rates, and the medical treatment is different from hormonal-type cancer, Frierson said. For example, while chemotherapy can be an effective treatment for the Triple Negative patient, it can lead to short-term menopause, which may or may not be reversible, she said.

Breast cancer is the second leading cause of cancer death among women after lung cancer. In 2010, there were more than 192,300 new breast cancer cases in the United States, with more than 40,000 deaths.

The subtype is called Triple Negative because it tests negative for all three of the hormone receptors that fuel many types of breast cancer: estrogen, progesterone and human epidermal receptor 2. Some traditional breast cancer hormonal treatment therapy drugs, such as Tamoxifen, aren't effective against Triple Negative Breast Cancer.

Results will establish protocol to develop interventions

Health care providers, social workers and others can use the study data to develop programs to reduce and manage stressors in the lives of Triple Negative patients, Frierson said.

"We want to fill a gap that needs to be addressed," she said. "The information from this pilot can help us develop programs and support groups to ease the burden on Triple Negative survivors. When we talk about breast cancer, many people think about the woman in her 50s. But these are young cancer survivors. Really understanding those differences is important."

Health providers who have agreed to refer patients with medical approval by their physicians include: U.T. Southwestern and Parkland Hospital in Dallas; and Moncrief Cancer Institute in Fort Worth. As a partner in the study, The Cooper Institute in Dallas will provide participants with fitness testing. The survey is also online, so a woman outside the Dallas-Fort Worth area can answer a one-time questionnaire and participate in the study.

The survey, which takes 45 minutes to an hour to answer, asks questions about physical activity, diet, nutrition, compliance with doctor appointments, stress levels, body image, quality of life, relationships, friendships, fertility, depression, anxiety, sleep and fatigue.

The research is funded with a two-year, $50,000 grant from The Discovery Foundation, Dallas.

When we suddenly get the answer to a riddle or understand the solution to a problem, we can practically feel the light bulb click on in our head. But what happens after the "Aha!" moment? Why do the things we learn through sudden insight tend to stick in our memory?

"Much of memory research involves repetitive, rote learning," says Kelly Ludmer, a research student in the group of Prof. Yadin Dudai of the Institute's Neurobiology Department, "but in fact, we regularly absorb large blocks of information in the blink of an eye and remember things quite well from single events. Insight is an example of a one-time event that is often well-preserved in memory."

To investigate how lessons we gain from insight get embedded in our long-term memory, Ludmer, Dudai and Prof. Nava Rubin of New York University designed a test with "camouflage images" — photographs that had been systematically degraded until they resembled inkblots. When volunteers first viewed the images, they were hard pressed to identify them. But after the camouflage was switched with the original, undoctored picture for a second, the subjects experienced an 'Aha!' moment — the image now popped out clearly even in the degraded image. Their perceptions, says Ludmer, underwent a sudden change — just as a flash of insight instantly shifts our world view. To tax their memory of the insightful moment, participants were asked to repeat the exercise with dozens of different images and, in a later repeat session, they were given only the camouflaged images (together with some they hadn't seen before) to identify.

The team found that some of the memories disappeared over time, but the ones that made it past a week were likely to remain. All in all, about half of all the learned "insights" seemed to be consolidated in the subjects' memories.

To reveal what occurs in the brain at the moment of insight, the initial viewing session was conducted in a functional MRI (fMRI) scanner. When the scientists looked at the fMRI results, they were surprised to find that among the areas that lit up in the scans — those known to be involved in object recognition, for instance — was the amygdala. The amygdala is more famously known as the seat of emotion in the brain. Though it has recently been found to play a role in the consolidation of certain memories, studies have implied that it does so by attaching special weight to emotion-laden events. But the images used in the experiment — hot-air balloons, dogs, people looking through binoculars, etc. — were hardly the sort to elicit an emotional response. Yet, not only was the amygdala lighting up in the fMRI, the team found that its activity was actually predictive of the subject's ability to identify the degraded image long after that moment of induced insight in which it was first recognized.

"Our results demonstrate, for the first time, that the amygdala is important for creating long-term memories — not only when the information learned is explicitly emotional, but also when there is a sudden reorganization of information in our brain, for example, involving a sudden shift in perception," says Ludmer. "It might somehow evaluate the event, 'deciding' whether it is significant and therefore worthy of preservation."

Children suffering from extreme social anxiety are trapped in a nightmare of misinterpreted facial expressions: They confuse angry faces with sad ones, a new study shows.

"If you misread facial expressions, you're in social trouble, no matter what other social skills you have," says Emory psychologist Steve Nowicki, a clinical researcher who developed the tests used in the study. "It can make life very difficult, because other people's faces are like a prism through which we look at the world."

It's easy to assume that a socially anxious child would be especially sensitive to anger. "It turns out that they never learn to pick up on anger and often make the error of seeing it as sadness," Nowicki says. "It sets up a very problematic interaction." Some socially anxious children long to interact with others, he says, and may try to comfort someone they think is sad, but who is actually angry. "They want to help, because they're good kids," Nowicki says. "I've seen these kids trying to make a friend, and keep trying, but they keep getting rebuffed and are never aware of the reason why."

The study was co-authored by Amy Walker, a former undergraduate student at Emory, now at Yeshiva University, and will be published in the Journal of Genetic Psychology.

It is unclear whether misreading the facial expression is linked to the cause of the anxiety, or merely contributing to it.

By identifying the patterns of errors in nonverbal communication, Nowicki hopes to create better diagnostic tools and interventions for those affected with behavioral disorders.

For more than two decades, in association with Emory psychologist Marshall Duke, Nowicki has produced a groundbreaking body of work on how non-verbal communication impacts a child's development. They have found that in a range of children with behavioral disorders, including high-functioning autism, direct teaching can improve their non-verbal communication.

"When I first started this work, people asked me, why are you doing this? Everybody can recognize emotions in faces," Nowicki recalls. Nonverbal communication was not taken that seriously, and relegated to popular magazine articles like, "Seven ways to improve your body language."

In his clinical practice, however, Nowicki noticed that some children who had trouble socializing appeared to misinterpret nonverbal clues. He sought ways to measure the deficits and remediate them.

"My heart went out to these kids," he says. "I had the idea that nonverbal communication could be taught. It's a skill, not something mysterious."

Nowicki and Duke termed the coin "dyssemia," meaning the inability to process signs. They also developed the Diagnostic Analysis of Nonverbal Accuracy (DANVA) to assess subtle cues to emotional expressions, including visual signals and tone and cadence of voice. DANVA is now widely used by researchers in studies of everything from emotionally disturbed children to the relationships between doctors and their patients.

Roughly 15% of children suffer from migraines, and approximately one-third of these affected children have migraines with aura, a collection of symptoms that can include weakness, blind spots, and even hallucinations. Although the causes of migraines are unclear, a new study in The Journal of Pediatrics suggests a connection between migraine headaches in children and a heart defect called patent foramen ovale, which affects 25% of people in the U.S.

Dr. Rachel McCandless and colleagues from the Primary Children's Medical Center and the University of Utah studied children 6-18 years old who were diagnosed with migraines between 2008 and 2009. The 109 children enrolled in the study were treated at the Primary Children's Medical Center, which serves kids from Utah, Idaho, Montana, Nevada, Colorado, and parts of Wyoming.

The researchers took two-dimensional echocardiograms of each child's heart, looking for a patent foramen ovale (PFO), a common defect in the wall between the two upper chambers of the heart. Although a PFO is not necessarily dangerous, it can allow unfiltered blood to bypass the lungs and circulate throughout the body. As Dr. McCandless explains, "Some adult studies have suggested a link between having a PFO and migraine headaches."

Of the studied children who had migraines with aura, 50% also had a PFO; this is nearly double the PFO rate of the general population. However, only 25% of children who had migraines without aura had a PFO. Dr. McCandless and colleagues hypothesize that if a causal relationship can be established, closure of a PFO with a catheter device may help in the treatment of certain kinds of migraines, specifically migraines with aura. It is her hope that "our study will help guide future research about this difficult problem."

Journal Reference:

1. Rachel T. McCandless, Cammon B. Arrington, Douglas C. Nielsen, James F. Bale, L.LuAnn Minich. Patent Foramen Ovale in Children with Migraine Headaches. The Journal of Pediatrics, 2011; DOI: 10.1016/j.jpeds.2011.01.062

Everyone would like MDs to have the best education — and to absorb what they are taught. The lead article in the April 4 issue of the journal Academic Medicine* connects research on how the brain learns to how to incorporate this understanding into real world education, particularly the education of doctors.

"Repetition, reward, and visualization are tried and true teaching strategies. Now, knowing what is happening in the brain will enhance teaching and learning," said Michael J. Friedlander, executive director of the Virginia Tech Carilion Research Institute and professor of biological sciences and of biomedical engineering and science at Virginia Tech. He is the lead author on the article, "What can medical education learn from the neurobiology of learning?"

Friedlander collaborated on the article with Dr. Linda Andrews, senior associate dean for medical education, Baylor College of Medicine; Elizabeth G. Armstrong, director of Harvard Macy Institute, Harvard Medical School; Dr. Carol Aschenbrenner, executive vice president of the Association of American Medical Colleges; Dr. Joseph S. Kass, chief of neurology and director of the Stroke Center at Ben Taub Hospital and assistant professor of neurology, Center for Ethics and Health Policy, Baylor College of Medicine; Dr. Paul Ogden, associate dean for educational program development, Texas A&M Health Sciences Center and College of Medicine; Dr. Richard Schwartzstein, director of the Harvard Medical School Academy; and Dr. Tom Viggiano, the associate dean for faculty affairs, professor of medical education and medicine, and the Barbara Woodward Lips professor at Mayo Medical School.

The research

In the past 50 years, behavioral approaches combined with functional brain imaging and computational neuroscience have revealed strategies employed by mammals' brains to acquire, store, and retrieve information. In addition to molecular and cellular approaches to describe the workings of the underlying hardware changes that occur in the brain during learning and the formation of memories, there has also been progress in higher-order, human-based studies of cognition, including learning and memory. Scientists have used functional magnetic resonance imaging (fMRI) of the living brain combined with computational modeling to elucidate the strategies employed and the underlying biological processes.

The research has shown how learning leads to functional and structural changes in the cellular networks including the chemical communication points or synapses between neurons at a variety of sites throughout the central nervous system. The functional changes in the effectiveness of communication between individual neurons and within networks of neurons are accompanied by substantial changes in the structural circuitry of the brain, once thought to be hard-wired in adults.

"One of the most exciting advances, as a result of optical imaging of the living brain, is the demonstration that there is growth, retraction, and modifying connectivity between neurons," said Friedlander. "We have also seen that the mature brain can generate new neurons, although, this research is so new that the functional implications of these new neurons and their potential contribution to learning and memory formation remain to be determined," he said.

The recommendations

The most effective delivery of the best possible care requires identifying and assigning levels of importance to the biological components of learning. Here are 10 key aspects of learning based on decades of research by many scientists that the article's authors believe can be incorporated into effective teaching.

Repetition: Medical curricula often employ compressed coverage over limited time frames of a great amount of material. Learning theory and the neurobiology of learning and memory suggest that going deeper is more likely to result in better retention and depth of understanding. With repetition, many components of the neural processes become more efficient, requiring less energy and leaving higher-order pathways available for additional cognitive processing. However, repetitions must be appropriately spaced.

Reward and reinforcement: Reward is a key component of learning at all stages of life. "The brain's intrinsic reward system — self-congratulations with the realization of success — plays a major role in reinforcement of learned behaviors," Friedlander said. "An important factor is the realization that accomplishing an immediate goal and a successful step toward a future goal can be equally rewarding."

In the case of medical students, there are considerable rewards ahead of them in addition to the more immediate rewards of the satisfaction of understanding medicine. The students who derive joy from learning as they proceed through their medical education may have a greater chance of using the brain's capacity to provide reward signals on an ongoing basis, facilitating their learning process.

Visualization: Visualization and mental rehearsal are real biological processes with associated patterned activation of neural circuitry in sensory, motor, executive, and decision-making pathways in the brain. Internally generated activity in the brain from thoughts, visualization, memories, and emotions should be able to contribute to the learning process.

Active engagement: There is considerable neurobiological evidence that functional changes in neural circuitry that are associated with learning occur best when the learner is actively engaged.. Learners' having multiple opportunities to assume the role of teacher also invoke neural motivation and reward pathways — and another major biological component of the learning process: stress.

Stress: Although the consequences of stress are generally considered undesirable, there is evidence that the molecular signals associated with stress can enhance synaptic activity involved in the formation of memory. However, particularly high levels of stress can have opposite effects. The small, interactive teaching format may be judiciously employed to moderately engage the stress system.

Fatigue: Patterns of neuronal activity during sleep reinforce the day's events. Research suggests that it is important to have appropriate downtime between intense problem-solving sessions. Downtime permits consolidation away from the formal teaching process.

Multitasking: Multitasking is a distraction from learning, unless all of the tasks are relevant to the material being taught. The challenge is to integrate information from multiple sources, such as a lecture and a hand-held device.

Individual learning styles: Neural responses of different individuals vary, which is the rationale for embracing multiple learning styles to provide opportunities for all learners to be most effectively reached.

Active involvement: Doing is learning. And success at doing and learning builds confidence.

Revisiting information and concepts using multimedia: Addressing the same information using different sensory processes, such as seeing and hearing, enhances the learning process, potentially bringing more neural hardware to bear to process and store information.

The researchers recommend that medical students be taught the underlying neurobiological principles that shape their learning experiences. "By appealing not only to students' capacity to derive pleasure from learning about medicine but also to their intellectual capacity for understanding the rationale for the educational process selected … real motivation can be engendered. … They become more effective communicators and enhance their patients' success at learning the information they need for managing their own health and treatments as well."

Journal Reference:

1. Michael J. Friedlander et al. What Can Medical Education Learn From the Neurobiology of Learning?Academic Medicine, Vol. 86, No. 4 / April 2011

NewsPsychology (Mar. 29, 2011) — Protein aggregation, generally associated with Alzheimer’s and mad cow disease, turns out to play a significant role in cancer. In a paper published in Nature Chemical Biology, Frederic Rousseau and Joost Schymkowitz of VIB, K.U.Leuven and Vrije Universiteit Brussel describe that certain mutations of p53, an important tumor suppressor, cause the protein to misfold in a way that the proteins start to aggregate. This not only disrupts the protective function of normal p53, but of other related proteins as well.

p53 plays a central role in protection against cancer

In the study, the focus was on the p53 protein which plays a key role in protecting the body against cancer. If p53 works normally, it controls cell division. If p53 control ceases — e.g. when there is a mutation in the protein — the cells start to divide in an uncontrolled manner and this may result in a tumor. Mutations in p53 are observed in about half of cancer cases, making the protein an important target in the development of new cancer therapies.

Mutated p53 aggregates

“We have revealed a new mechanism for the action of mutant p53,” Joost Schymkowitz and Frederic Rousseau of VIB, Vrije Universiteit Brussel and K.U. Leuven say. “Mutations in p53 cause the protein to lose its protective function. The proteins change in shape, hook into each other and begin to aggregate. The active p53 disappears from the cell and can no longer carry out its control function properly.” The mechanism has been encountered in about one third of p53 mutations.

Complete switch of character

Moreover, the mutations cause p53 to assume a completely different character. From being a protective factor, the mutated p53 changes into a substance which in fact speeds up tumor growth. It seems to form aggregates with control substances (p63 and p73) in the cell, causing them to lose their function as well.

Other proteins underlying cancer and Alzheimer

Even though the underlying principle — protein aggregation — occurs similarly in particular cancers, Alzheimer and systemic amyloidosis, the diseases are otherwise totally unconnected with each other. In cancer, the clustering of p53 protein leads to uncontrolled cell growth. In Alzheimer, clustering of the beta-amyloid protein causes brain cells to die off.

Email or share this story:

Story Source:

The above story is reprinted (with editorial adaptations by newsPsychology staff) from materials provided by VIB.

Journal Reference:

1. Jie Xu, Joke Reumers, José R Couceiro, Frederik De Smet, Rodrigo Gallardo, Stanislav Rudyak, Ann Cornelis, Jef Rozenski, Aleksandra Zwolinska, Jean-Christophe Marine, Diether Lambrechts, Young-Ah Suh, Frederic Rousseau, Joost Schymkowitz. Gain of function of mutant p53 by coaggregation with multiple tumor suppressors. Nature Chemical Biology, 2011; DOI: 10.1038/nchembio.546

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.

Conventional antipsychotics, antidepressants and benzodiazepines often administered to nursing home residents are no safer than atypical antipsychotics and may carry increased risks, according to an article in CMAJ (Canadian Medical Association Journal).

Psychotropic medications are often used to manage behavioral symptoms in seniors, particularly people with dementing illnesses, with up to two-thirds of dementia patients in nursing homes prescribed these medications. However, the effectiveness of these drugs in this indication is unclear and important safety concerns exist, especially related to antipsychotics.

Psychotropic or psychoactive medications act upon the central nervous system and are prescribed for the management of mental and emotional disorders. They include, amongst others, first and second generation antipsychotics (also known as conventional and atypical antipsychotics), antidepressants, benzodiazepines and other sedatives. Despite their widespread use, none of these treatments has been approved by the FDA or Health Canada for the management of behavioral symptoms associated with dementia.

A team of researchers from Brigham and Women's Hospital in Boston, Massachusetts, undertook the study to evaluate the comparative safety of various psychotropic medication classes, focusing on patients in nursing homes because of the extensive use of these drugs in this setting and the complexity of these patients' illnesses. The study cohort included all BC residents admitted to a nursing home between Jan. 1, 1996 and March 31, 2006 and who received a psychotropic drug within 90 days of admission.

Of the 10 900 patients in the study, 1942 received an atypical antipsychotic, 1902 a conventional antipsychotic, 2169 an antidepressant and 4887 a benzodiazepine. Rigorous methodological approaches were applied to ensure this non-randomized study was not affected by the selective prescribing that tends to occur in routine care.

"In 10 900 older adults newly admitted to nursing homes in BC who began taking psychotropic medications, we observed risks of death that were higher among those who initiated conventional antipsychotics, antidepressants and benzodiazepines. We also observed risks of femur fracture that were higher with conventional antipsychotics, antidepressants and benzodiazepines used for anxiety, all compared with atypical antipsychotics. No clinically meaningful differences were observed for risk of pneumonia or heart failure, except possibly a lower risk of pneumonia and a higher risk of heart failure with benzodiazepines," state the authors.

They conclude that a large randomized trial is required to confirm their findings but that clinicians should weigh the increased risks against potential benefits when considering prescribing these medications for their patients in nursing homes.

Journal Reference:

1. Krista F. Huybrechts, Kenneth J. Rothman, Rebecca A. Silliman, Alan Brookhart and Sebastian Schneeweiss. Risk of death and hospital admission for major medical events after initiation of psychotropic medications in older adults admitted to nursing homes. CMAJ, 101406; 2011 DOI: 10.1503/cmaj.101406

 If common anticonvulsant drugs fail to manage epileptic seizures, then perhaps the anti-inflammatory route is the way to go. That's according to Mattia Maroso and colleagues from the Mario Negri Institute for Pharmacological Research in Milan, Italy, who found that giving mice repeated doses of a specific enzyme inhibitor significantly reduced both chronic epileptic activity and acute seizures.

Their findings, published online in the Springer journal Neurotherapeutics, open up the possibility of a new target system for anticonvulsant drug intervention, to control epileptic activity that does not respond to certain anticonvulsant treatments.

An enzyme known as ICE/Caspase-1 is involved in epileptic seizures; it induces inflammatory processes by producing IL-1beta, a pro-inflammatory molecule, in brain regions where epileptic activity originates and spreads. Mattia Maroso and colleagues looked at the elective inhibitor for this enzyme, in a mouse model of acute seizures and in mice with chronic epilepsy showing spontaneous recurrent epileptic activity.

The researchers artificially induced chronic epileptic seizures in 21 adult male mice and acute seizures in 46 mice. They then injected them with the enzyme inhibitor (VX-765) and recorded the resulting epileptic activity in brains of the mice.

They found that the enzyme inhibitor had powerful anticonvulsant effects. Repeated systemic administration reduced chronic epileptic activity in mice in a dose-dependent manner, and the effect was reversible after four days of treatment when the drug regime was discontinued. The same dose regimen also reduced acute seizures in the mice.

The authors conclude: "Our results support a new target system for anticonvulsant drug intervention. Our findings open new perspectives for the clinical use of this anti-inflammatory strategy for treating established drug-resistant epileptic conditions."

Journal Reference:

1. Mattia Maroso, Silvia Balosso, Teresa Ravizza, Valentina Iori, Christopher Ian Wright, Jacqueline French, Annamaria Vezzani. Interleukin-1β Biosynthesis Inhibition Reduces Acute Seizures and Drug Resistant Chronic Epileptic Activity in Mice. Neurotherapeutics, 2011; DOI: 10.1007/s13311-011-0039-z