Parenting after the death of a child a difficult balancing act

One of the tough challenges a parent faces when a child dies is to learn how to parent the surviving children, and the task begins immediately, according to York University psychology professor Stephen Fleming.

From the moment their child dies, parents are faced with the two extremes of loss and life — the suffocating loss of a child and the ongoing, daily demands from their surviving children, says Fleming, co-author of the recently-published book, Parenting After the Death of a Child: A Practitioner's Guide.

"The challenge that parents face is this: In the midst of grief, how do you stop parenting the deceased child while you are simultaneously struggling to meet the parenting needs of the children who remain?"

Fleming, a psychology professor in the Faculty of Health at York University, and co-author Jennifer Buckle, now a professor at Memorial University, did the research for the book when Buckle was a graduate student at York. Their research is based on in-depth interviews with parents who had lost a child and had one or more surviving children.

They found bereaved parents do not "recover" from the loss. Instead, bereaved parenting is an act of regeneration — picking up the pieces in the face of the devastation, and regenerating both a sense of self, and a sense of the family.

"Dads tend to be instrumental grievers. They go back to work, commit to working for the family, and they tend to overcome the fear of putting their children out into an unsafe world, sooner than moms do," says Fleming. "Moms tend to be more intuitive grievers, more focused on internal feelings, and they have an almost paralyzing fear that if one child can die, another could die as well. So, often, moms are dragged back into parenting, by the surviving children."

Parenting After the Death of a Child fills a gap in the research about the impact of a child's death, because it focuses not only the grief experienced, but on the balancing act of grieving and parenting at the same time. A clinical psychologist, Fleming said he hopes the guide will educate counsellors about the importance of looking for psychological complications in mourning the loss of a child − for example, depression, generalized anxiety disorder, and posttraumatic stress disorder. Too often, parents are not assessed for these reactions, and they may be traumatized by images of their child's death, or illness, and reliving it, he says.

The qualitative research and excerpts from the parents who were interviewed are also intended to help bereaved parents deal with the expectations they put on themselves, and those imposed by the outside world. The research reassures parents, for example, that it is healthy to honour the role of the deceased child in the family by continuing to talk about the child with the surviving siblings. It may also offer comfort by busting myths — for example, the myth that losing a child increases the likelihood that parents will divorce, and that surviving family members will be split up. Roles change, and parents often struggle to be consistently present physically and emotionally for their children, Fleming says, but bereaved parents rebuild their lives because their children need it.

Neural mechanisms linked with vulnerability to anxiety

NewsPsychology (Feb. 10, 2011) — New research examines the anxious brain during a fear conditioning task and provides insight into why some individuals may be more or less prone to anxiety disorders. The study, published by Cell Press in the Feb. 10 issue of the journal Neuron, reveals neural mechanisms that may contribute to resilience against pathological fear and anxiety. The findings may help to direct therapeutic strategies for individuals who suffer from chronic anxiety as well as strategies that could help “at risk” individuals avoid developing anxiety disorders.

Previous studies have implicated a brain structure called the amygdala in the acquisition and expression of conditioned fear, this occurring when a stimulus (the conditioned stimulus, CS) becomes associated with an aversive object or event (the unconditioned stimulus, UCS). Another brain region, the ventromedial prefrontal cortex (vmPFC), has been shown in both animals and humans to help inhibit conditioned fear after extinction training, during which the CS is repeatedly presented without the UCS. However, it is not clear how certain personality characteristics, like a tendency or vulnerability towards anxiety, influence these mechanisms.

“We were interested in examining why it is that some of us can overcome the discrete fears and nonspecific anxiety that we experience in our lives more easily than others,” explains senior study author, Dr. Sonia J. Bishop from the University of California, Berkeley. “Or, in other words, what differences in brain function might confer increased vulnerability for chronic fear and anxiety disorders?”

Dr. Bishop and colleagues performed a neuroimaging study to examine fear conditioning in human subjects who had been classified as having varying levels of “trait anxiety,” a tendency to experience anxiety across a range of everyday situations. The researchers observed that subjects who had a high level of trait anxiety were more likely to have an enhanced amygdala response to CS fear cues and to show faster acquisition of learned “fear” of these cues. Individual differences in amygdala reactivity were independent of the second dimension of risk, this involving the vmPFC. Recruitment of this region during conditioned fear expression prior to extinction was linked with greater reduction in fear responses and was more pronounced in fear-resilient individuals.

The findings suggest that individual differences in amygdala and vmPFC function are independently associated with vulnerability to anxiety, with the amygdala potentially influencing the development of cue-specific fears (or phobias) and the vmPFC impacting the ability to downregulate both phasic fears and generalized anxiety. “An understanding of the neurocognitive mechanisms by which trait vulnerability to pathological anxiety is conferred may aid not only in explaining the variability in symptoms, but also in informing choice intervention and prediction of treatment response,” concludes Dr. Bishop.

Earlier this month, Dr. Bishop attended an awards ceremony at NIH in recognition of her receipt of one of twelve prestigious Biobehavioral Research Awards for Innovative New Scientists given to enable her further pursuit of this important line of research.

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

Journal Reference:

  1. Iole Indovina, Trevor W. Robbins, Anwar O. Núñez-Elizalde, Barnaby D. Dunn, Sonia J. Bishop. Fear-Conditioning Mechanisms Associated with Trait Vulnerability to Anxiety in Humans. Neuron, 2011; 69 (3): 563-571 DOI: 10.1016/j.neuron.2010.12.034

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.

Stress management program helps prevent heart events in patients with heart disease

A cognitive behavioral therapy program focusing on stress management appears to decrease the risk of recurrent heart attacks and other cardiovascular events in patients with heart disease, according to a report in the January 24 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.

Psychosocial factors account for an estimated 30 percent of heart attack risk, according to background information in the article. "Psychosocial factors that may promote atherosclerosis and cardiovascular disease belong to two general categories: chronic stressors, including low socioeconomic status, low social support, marital distress and work distress; and emotional factors, including major depression, hostility, anger and anxiety," the authors write. These issues are believed to contribute to the risk of heart disease even after adjusting for the effects of traditional risk factors.

Mats Gulliksson, M.D., Ph.D., and colleagues at Uppsala University Hospital, Uppsala, Sweden, conducted a randomized controlled clinical trial of cognitive behavioral therapy (CBT) among 362 men and women discharged from the hospital after a coronary heart disease event within the previous 12 months. A group of 192 patients were randomly assigned to participate in CBT. "The program has five key components with specific goals — education, self-monitoring, skills training, cognitive restructuring and spiritual development — and is focused on stress management, coping with stress and reducing experience of daily stress, time urgency and hostility," the authors write. Therapy was delivered in 20 two-hour sessions during one year, in small groups separated by sex. The other 170 patients received traditional care.

During an average 94 months of follow-up, 23 participants in the CBT group died, 69 (35.9 percent) had a non-fatal cardiovascular event and 41 (21.4 percent) had a non-fatal heart attack. This compares to 25 deaths, 77 non-fatal cardiovascular events (45.3 percent) and 51 non-fatal heart attacks (30 percent) in the traditional care group. Patients in the CBT group had a 41 percent lower rate of both fatal and non-fatal heart events, 45 percent fewer recurrent heart attacks and a non-significantly lower rate of death (28 percent) than patients in the traditional care group. Attending a higher proportion of the therapy sessions was associated with a further reduction in risk.

"These results imply that, to affect cardiovascular disease or coronary heart disease end points, the interventions need to be long-term (possibly six to 12 months), be conducted in groups and include specific techniques for altering behavior," the authors write. "A possible mechanism is decreased behavioral and emotional reactivity, which would lead to less psychophysiologic burden on the cardiovascular system."

The findings represent not only statistical significance but also clinical importance, the authors note. "This demonstrates the potential efficacy of adding CBT to secondary preventive programs after acute myocardial infarction [heart attack] for better patient adherence to treatment and better outcome," they conclude.


Journal Reference:

  1. M. Gulliksson, G. Burell, B. Vessby, L. Lundin, H. Toss, K. Svardsudd. Randomized Controlled Trial of Cognitive Behavioral Therapy vs Standard Treatment to Prevent Recurrent Cardiovascular Events in Patients With Coronary Heart Disease: Secondary Prevention in Uppsala Primary Health Care Project (SUPRIM). Archives of Internal Medicine, 2011; 171 (2): 134 DOI: 10.1001/archinternmed.2010.510

Risks, consequences of video game addiction identified in new study

Parents may have good reason to be concerned about how much time their kids have been spending playing their new video games since the holidays. A new study by an international research team — including an Iowa State University psychologist — found further evidence that video game "addiction" exists globally and that greater amounts of gaming, lower social competence and greater impulsivity were risk factors for becoming pathological gamers.

The two-year longitudinal study of 3,034 third through eighth grade students in Singapore found approximately nine percent of gamers to be pathological players according to standards similar to those established by the American Psychiatric Association for diagnosing gambling addiction. And some serious problems — including depression, anxiety, social phobias and lower school performance — seemed to be outcomes of their pathological play.

Douglas Gentile, an Iowa State associate professor of psychology, and five researchers from Singapore and Hong Kong collaborated on the study, which will be published in the February 2011 issue of Pediatrics — the journal of the American Academy of Pediatrics. The study was jointly funded by Singapore's Ministry of Education and media Development Authority in a grant given to professors from the National Institute of Education.

One in 10 gaming youths addicted

The researchers report that the percentage of pathological youth gamers in Singapore is similar to other recent video game addiction studies in other countries, including the United States (8.5 percent), China (10.3 percent), Australia (8.0 percent), Germany (11.9 percent) and Taiwan (7.5 percent).

"We're starting to see a number of studies from different cultures — in Europe, the U.S. and Asia — and they're all showing that somewhere around 7 to 11 percent of gamers seem to be having real problems to the point that they're considered pathological gamers," said Gentile, who published the first national American study on pathological video game addiction in youths in the May 2009 issue of the journal Psychological Science. "And we define that as damage to actual functioning — their school, social, family, occupational, psychological functioning, etc. To be considered pathological, gamers must be damaging multiple areas of their lives."

"This study is important because we didn't know until this research whether some types of children are at greater risk, how long the problem lasts, or whether pathological gaming was a separate problem or simply a symptom of some other problem — such as depression," said Angeline Khoo, associate professor of psychological studies at the National Institute of Education in Singapore and principal investigator of the overall project.

The researchers gathered data from students attending 12 Singapore schools, including five boys' schools. The subjects were surveyed annually on their video game play and behavior between 2007 and 2009. Surveys were conducted in classrooms by teachers who had been trained by the research team. The study had a 99 percent response rate.

Using the American Psychiatric Association's "Diagnostic and Statistical Manual of Mental Disorders" as a guide to define the addictive condition, the researchers found between 7.6 and 9.9 percent of the student sample could be defined as pathological gamers over the two-year period. Eighty-four percent of those subjects who were first classified as pathological gamers were found to still be classified that way two years later. Yet in that same two-year window, only one percent of the sample became new pathological gamers.

A serious behavioral problem

Through their analyses, the researchers conclude that video game addiction is a serious behavioral problem that is separate from other afflictions.

"Once they become addicted, pathological gamers were more likely to become depressed, have increased social phobias, and increased anxiety. And they received poorer grades in school," Gentile said. "Therefore, it looks like pathological gaming is not simply a symptom of depression, social phobia or anxiety. In fact, those problems seem to increase as children become more addicted. In addition, when children stopped being addicted, depression, anxiety and social phobias decreased as well."

Among this sample, pathological gamers started with an average of 31 hours of play per week, compared with 19 hours per week for those who never became pathological gamers. But Gentile says those thresholds don't necessarily translate across all cultures, particularly in American children.

"In general, Singaporean children spend more time playing video games than American children," he said. "In the U.S., we didn't follow the kids across time, so we don't know where that threshold is across each culture or if there is a certain amount that is too much. We do know, however, that playing a lot is not the same as being a pathological gamer — the gaming must be causing problems for it to be considered pathological."

Gentile is visiting Singapore to meet with his research colleagues and present their findings during the final two weeks of January.


Journal Reference:

  1. D. A. Gentile, H. Choo, A. Liau, T. Sim, D. Li, D. Fung, A. Khoo. Pathological Video Game Use Among Youths: A Two-Year Longitudinal Study. Pediatrics, 2011; DOI: 10.1542/peds.2010-1353

Women with false-positive mammograms report high anxiety and reduced quality of life

Doctors are calling for women to receive more information about the pitfalls of breast cancer screening, as well as the benefits, after some women who received false-positive results faced serious anxiety and reduced quality of life for at least a year.

A study published online by BJS, the British Journal of Surgery, shows that patients with false-positive results — where the mammogram is abnormal but no cancer is present — had to undergo more diagnostic procedures than women with breast cancer before they were given the all clear.

Researchers from The Netherlands spoke to 385 women with abnormal mammogram results — 152 were subsequently diagnosed with breast cancer, but the other 233 had false-positive results and did not have cancer.

"Common sense tells us that early detection of breast cancer is good and most screening programmes have been successful in reducing breast cancer deaths" says lead author Dr Lideke van der Steeg from the Department of Surgery, St Elisabeth Hospital, Tilburg, and the Centre of Research and Psychology in Somatic Diseases, Tilburg University.

"However, while some women truly benefit from early detection, others experience harm and unnecessary anxiety. The women who received false-positives in our study experienced a significant reduction in their quality of life, especially if they were prone to anxiety, and the effects of this lasted at least a year.

"In fact, women who had a tendency to be anxious fared much worse if they received a false-positive — which is estimated to happen in 60 per cent of abnormal mammograms — than if they were actually diagnosed with breast cancer."

Women with abnormal mammograms attending three hospitals over a five-year period were invited to participate. Their quality of life (QoL) was assessed using the World Health Organization's Quality of Life instrument 100, which assesses QoL in six domains — physical health, psychological health, level of independence, social relationships, environment and spirituality.

Clinical data were obtained from the women's medical records and they were also asked to complete questionnaires providing demographic information such as age, marital status, education and socioeconomic status.

Women in the breast cancer (BC) group were significantly older than the women in the false-positive (FP) group — 60.2 years versus 57.3 years. They also had larger tumours than the FP group — 17.4mm versus 9.9mm.

The key factors influencing QoL scores differed between the two groups:

  • Trait anxiety (a tendency to experience anxiety) accounted for up to 55 per cent of the variance in the QoL score in the FP group. It reached this peak at three months, but was similar at months one and 12 (43 per cent and 40 per cent respectively).
  • State anxiety (temporary anxiety due to a specific situation) accounted for up to 46 per cent of the variance in the BC group. It peaked at six months, but was similar in months one and 12 (32 per cent and 34 per cent).
  • State anxiety levels did not significantly influence QoL in the FP group and trait anxiety levels did not influence QoL in the BC group.

Significantly more diagnostic procedures, including biopsies, were needed in the FP group to reach a final diagnosis. Only 14 per cent of the BC group required four procedures — the other 86 per cent required three — while 32 per cent of the FP group required more than three. Fifty-five per cent of the FP group returned to the outpatient clinic in the first year, some as many as eight times.

The authors believe that the anxiety and lower QoL experienced by women in the FP group were soley due to the recall after screening and the subsequent diagnostic procedures.

"The decision to participate in a screening programme requires balanced information about the potential benefits and dangers" says Dr van der Steeg.

"Women often overestimate their risk of breast cancer and the material provided by healthcare professionals and government agencies often focus on the positive aspects of screening and are not always objective.

"Women deserve more balanced information to help them to chose whether or not to accept a breast screening invitation. This should not only cover the supposed benefits, but explain the potential side-effects of a false-positive, such as the increased feelings of anxiety and reduced QoL found by our study."


Journal Reference:

  1. A. F. W. van der Steeg, C. M. G. Keyzer-Dekker, J. De Vries, J. A. Roukema. Effect of abnormal screening mammogram on quality of life. British Journal of Surgery, 2010; DOI: 10.1002/bjs.7371

Possible off-switch for anxiety discovered

Scientists from the Agency of Science, Technology and Research/Duke-NUS Neuroscience Research Partnership (A*STAR/Duke-NUS NRP), A*STAR's Institute of Molecular and Cell Biology, and the National University of Singapore have made a breakthrough concerning how anxiety is regulated in the vertebrate brain. Their work, published in the journal Current Biology, sheds light on how the brain normally shuts off anxiety and also establishes the relevance of zebrafish as a model for human psychiatric disorders.

The team of scientists, led by Dr Suresh Jesuthasan from the A*STAR/Duke-NUS NRP, showed that disrupting a specific set of neurons in the habenula[1] prevents normal response to stressful situations. In their experiments, Dr Jesuthasan's team trained larval zebrafish to swim away from a light in order to avoid a mild electric shock. While normal fish easily learned this task, fish that had a specific set of neurons in the habenula damaged displayed signs of "helplessness."

Although they initially tried to avoid the shock, they soon gave up. What's more, these fish showed indications that they were more anxious than normal fish, such as being startled easily by non-harmful stimuli. Because of the similarity of the zebrafish[2] brain to the mammalian brain, the study suggests that malfunction of the habenula is a possible cause of certain anxiety disorders in humans. This means that it may be possible to use direct stimulation of the habenula as a way of treating some types of anxiety disorders in humans. The zebrafish model which the scientists developed in the course of their work may also be used in future drug discovery efforts for psychiatric medicines.

Dr Jesuthasan said, "Our work deals with fundamental aspects of human experience — stress and anxiety. We think that the habenula of the brain is associated with the assessment of whether a stress has been overcome. Our study provides one possible explanation as to why the need to control the environment is such a critical component of human behavior — the feeling of control enables organisms to deal with stress."

Notes:

[1] The habenula has been shown to be involved in many functions of the brain, such as pain processing, reproductive behavior, and learning. It also seems to be involved in reward processing, particularly with respect to negative/adverse feedback.

[2] The habenula is difficult to study in humans and in other mammals because it is located deep in the brain. However, the habenula in the zebrafish is located located near the surface of its brain, and is thus easily accessible for study.

Body dysmorphic disorder patients who loathe appearance often get better, but it could take years

In the longest-term study so far to track people with body dysmorphic disorder, a severe mental illness in which sufferers obsess over nonexistent or slight defects in their physical appearance, researchers at Brown University and Rhode Island Hospital found high rates of recovery, although recovery can take more than five years.

The results, based on following 15 sufferers of the disease over an eight-year span, appear in the current issue of the Journal of Nervous and Mental Disease.

"Compared to what we expected based on a prior longitudinal study of BDD, there was a surprisingly high recovery rate and a low recurrence rate in the present study," said Andri Bjornsson, first author of the paper and a postdoctoral research fellow in the Department of Psychiatry and Human Behavior at the Warren Alpert Medical School of Brown University. He works in the BDD program at Rhode Island Hospital, run by co-author Katharine Phillips, professor of psychiatry and human behavior.

After statistical adjustments, the recovery rate for sufferers in the study over eight years was 76 percent and the recurrence rate was 14 percent. While a few sufferers recovered within two years, only about half had recovered after five years.

The subjects were a small group diagnosed with the disorder out of hundreds of people participating in the Harvard/Brown Anxiety Research Project (HARP). Study co-author Martin Keller, professor of psychiatry and human behavior and principal investigator of the HARP research program which has been ongoing for more than 20 years, said that because the BDD sufferers were identified through this broader anxiety study, rather than being recruited specifically because they had been diagnosed with BDD, they generally had more subtle cases of the disorder than people in other BDD studies. In comparing the HARP study with the prior longitudinal study of BDD, it is possible that the high recovery rate in the HARP study is due to participants having less severe BDD on average.

In fact, despite the sometimes-debilitating nature of the disorder, a third of those in this study were working full-time.

Acknowledging that many doctors are unfamiliar with BDD or may even be skeptical about the disorder, Keller said doctors should consider the light that these findings shed on the clinical progress of the illness.

"We want to make people aware of BDD — aware that it exists and that it's a real mental illness," said Keller. "These people should be assessed very carefully and steered toward treatment very quickly."

In addition to Bjornsson, Phillips and Keller, other authors include Ingrid Dyck, Ethan Moitra, Robert L. Stout, and Risa B. Weisberg.

The study was funded by the National Institutes of Health.


Journal Reference:

  1. Andri S. Bjornsson, Ingrid Dyck, Ethan Moitra, Robert L. Stout, Risa B. Weisberg, Martin B. Keller, Katharine A. Phillips. The Clinical Course of Body Dysmorphic Disorder in the Harvard/Brown Anxiety Research Project (HARP). The Journal of Nervous and Mental Disease, 2011; 199 (1): 55 DOI: 10.1097/NMD.0b013e31820448f7

'Long-shot' discovery may lead to advances in treating anxiety, memory disorders

An unexpected discovery by UCLA life scientists holds promise for the future development of treatments for post-traumatic stress disorder and other anxiety disorders, and potentially for Alzheimer's disease and other memory-impairment diseases.

The researchers, led by UCLA professor of psychology Michael Fanselow, have discovered what may be a completely unexplored drug target for the treatment of anxiety disorders. The research is published Jan. 7 in the journal Science.

Normally, when people or animals experience a frightening event, they learn to fear the place of the event and any signals that were present at the time. This occurs because the nerve cells in certain brain regions increase their ability to excite or stimulate one another, said Fanselow, a member of UCLA's Brain Research Institute.

Most neuroscience research has emphasized how this phenomenon occurs through chemical communication among neurotransmitters flowing across synapses — the space between neurons. However, there are also small, inhibitory neurons in these regions as well, which have direct electrical contact with one another through connecting channels known as "gap junctions," Fanselow said. Gap junctions are very common in invertebrates but rare in mammals, where they are found on only certain inhibitory interneurons.

"Because of this, no one has looked at the importance of these gap junctions for learning, memory and emotion," Fanselow said. "We hypothesized that these gap junctions may be very important. Because the gap junctions cause the inhibitory neurons to fire together, they may cause these inhibitory neurons to act as a pacemaker for the excitatory neurons, making them fire at the same time so they are better able to make fear memories."

Fanselow's research team used several drugs in rats that block the gap junctions and found that they disrupted critical rhythms in the dorsal hippocampus — the brain region most involved in cognition — and prevented fear memories for places from forming. The drugs could block the formation of fear of places when given after the frightening experience.

Neuronal gap junctions may be an unexplored drug target for the treatment of anxiety disorders such as PTSD; they hold promise because giving a regular injection of drugs in a cavity near the abdomen worked as effectively as an injection directly into the brain. In addition, the injections worked when given right after the frightening experience.

"Because we don't know when a person will experience trauma, treatments that can work after the experience hold more promise," Fanselow said.

"The brain has many processes we have not yet explored," he added. "Understanding them and how they normally work can open up new approaches that may help in very prevalent and debilitating diseases, such as anxiety disorders and memory disorders."

Neuronal gap junctions form where inhibitory neurons touch one another. They are like an opening between nerve cells, a gap in the membranes separating the cells from one another; they let the electrical activity in one neuron affect the neuron it touches.

"Our research shows a way that neurons can coordinate their activity, and this coordination is critical for memory formation," Fanselow said. "Perhaps if we had a way of enhancing gap junction function, we may improve memory formation by facilitating gap junctions when memory is impaired by diseases such as Alzheimer's. However, we have not shown this yet."

"I was completely surprised by this discovery," he said. "I really thought we were taking a long shot and was surprised that gap junctions were not only playing a role but that their importance was so great.

"The formation of fear memories is the major cause of anxiety disorders. These disorders are very common and can be very debilitating. Gap junctions appear to be key in coordinating the activity of the network of neurons that produce fear memories, specifically, and probably other memories, generally, as well."

The lead author on the Science paper is Stephanie Bissiere, an assistant researcher in Fanselow's laboratory, who last week was selected as a recipient of a Young Investigator Award from the National Alliance for Research on Schizophrenia and Depression.

Other co-authors are Moriel Zelikowsky, a graduate student in Fanselow's laboratory; Ravikumar Ponnusamy, an assistant researcher in Fanselow's laboratory; Nate Jacobs, a former UCLA undergraduate who is currently a graduate student at UC Irvine; and Hugh Tad Blair, a UCLA associate professor of psychology.

The research was funded by the National Institute of Mental Health and the Swiss National Science Foundation.


Journal Reference:

  1. Stephanie Bissiere, Moriel Zelikowsky, Ravikumar Ponnusamy, Nathan S. Jacobs, Hugh T. Blair, Michael S. Fanselow. Electrical Synapses Control Hippocampal Contributions to Fear Learning and Memory. Science, 2011; 331 (6013): 87-91 DOI: 10.1126/science.1193785

Maternal depression adversely affects quality of life in children with epilepsy

A study by Canadian researchers examined the prevalence of maternal depression and its impact on children newly diagnosed with epilepsy. Prevalence of depression in mothers ranged from 30%-38% within the first 24 months following a child's epilepsy diagnosis. The mother's depressive symptoms negatively impacted the child's health-related quality of life, but the effects were moderated by the amount of family resources and mediated by how well the family functions and the extent of family demands.

Details of this novel study appear online in Epilepsia, a journal published by Wiley-Blackwell on behalf of the International League Against Epilepsy.

A report from the World Health Organization (WHO) estimates that depression affects 121 million people worldwide. One significant source of stress for parents is caring for a child with a chronic illness, such as epilepsy. Prior studies have shown that families of a child with epilepsy experience significantly more stress, anxiety, and restrictions in family life. Mothers, in particular, are at greatest risk for psychological distress or depression in response to their child's epilepsy, as they are often the primary caregivers for their children.

"Risk for clinical depression is common among mothers of children with new-onset epilepsy," said Mr. Mark Ferro, a PhD candidate in the Department of Epidemiology and Biostatistics from The University of Western Ontario and lead study author. To determine the prevalence of maternal depression, researchers surveyed 339 mothers whose children were part of the Health-related Quality of Life of Children with Epilepsy Study (HERQULES). The Center for Epidemiological Studies Depression Scale was used to assess the maternal risk of clinical depression; at baseline, 38% of mothers were at risk, 30% at 6 months, 32% at 12 months, and 30% at 24 months.

In further analysis of the same 339 mother-child pairs from the HERQULES cohort, the researchers assessed the mothers' depressive symptoms, the children's health-related quality of life [reported by the mother using the Quality of Life in Childhood Epilepsy (QOLCE) questionnaire], and severity of epilepsy [reported by the neurologist using the Global Assessment of Severity of Epilepsy (GASE) scale]. Children had a mean age of seizure onset of 7 years and mean health-related quality of life score of 70, indicating relatively good health-related quality of life. Approximately 60% of the pediatric participants had "a little severe" or "somewhat severe" epilepsy.

Results showed that children of mothers with elevated levels of depressive symptoms have poorer health-related quality of life than children of mothers with low levels of depression. Furthermore, children of mothers who are depressed are unlikely to experience a significantly positive change in health-related quality of life during the first 24 months after diagnosis. Conversely, children of mothers with lower levels of depressive symptoms display improved health-related quality of life scores over time. The team found that the accumulation of supportive resources for both the mother and the child with epilepsy resulted in improvement to children's health-related quality of life over time, moderating the effect of maternal depression. Family function and demands partially mediated the impact of maternal depression.

"It is important for clinicians to be aware of how a child's epilepsy diagnosis can impact the mother's mental health and family environment," concluded Mr. Ferro. "Adopting a family-centered approach will enable healthcare professionals to intervene at the maternal or family level, which in turn may help to promote more positive outcomes for children living with epilepsy."


Journal Reference:

  1. Mark A. Ferro, William R. Avison, M. Karen Campbell, Kathy N. Speechley. The impact of maternal depressive symptoms on health-related quality of life in children with epilepsy: A prospective study of family environment as mediators and moderators. Epilepsia, 2010; DOI: 10.1111/j.1528-1167.2010.02769.x

Stress can enhance ordinary, unrelated memories

Stress can enhance ordinary, unrelated memories, a team of neuroscientists has found in a study of laboratory rats. Their results, which appear in the journal PLoS Biology, may bolster our understanding of post-traumatic stress disorder (PTSD) and could offer a pathway for addressing PTSD and related afflictions.

The study was conducted by researchers at the Czech Republic's Academy of Sciences, the State University of New York (SUNY) Downstate Medical Center, and Rockefeller University.

"Our results show that stress can activate memory, even if that memory is unrelated to the stressful experience," explained André Fenton, the study's lead author and a professor at New York University's Center for Neural Science.

"Additional investigations into the effects of stress on memories could shed light on PTSD and other stress-related mood disorders," added Fenton, who directed the studies while he was a Research Scientist in the Czech Republic and an associate professor of physiology and pharmacology at SUNY Downstate.

The study's other authors are: Karel Ježek of the Czech Republic's Academy of Sciences; Benjamin Lee and Eduard Kelemen of SUNY Downstate; and Katharine McCarthy and Bruce McEwen of Rockefeller University.

A common feature of PTSD and various mood and anxiety disorders is the formation of negative associations from otherwise innocuous stimuli or the recall of negative memories stimulated by unrelated, neutral circumstances. What's less clear is how stress influences these phenomena.

To explore the impact of stress on these disorders, the researchers conducted several experiments using laboratory rats.

In these experiments, rats learned to make distinctions between left and right in a T-shaped maze. One day later, the researchers induced stress in the rats through a commonly practiced technique — placing them in a bucket of water in which they had to swim. Other rats were placed in shallow water, where swimming was not necessary. Subsequent to this procedure, the rats were again tasked with navigating the maze. Their results showed that the rats who had undergone the stressful swim showed better memory for which way to turn in the T-maze than those placed in shallow water.

To test the validity of their findings — that the memory for navigating the maze was enhanced by the stressful swim and not other forces — the researchers conducted a series of additional experiments. These procedures ruled out that learning the maze itself was a source of stress and showed a clear link between the stress induced by the swim and changes in the memories of navigating the maze, even though the changed memories were unrelated to the stressful experience.

These results show that stress can reactivate unrelated memories, leading the authors to hypothesize that, in humans, traumatic stress might reactivate non-traumatic memories and link them to the traumatic memory, thereby facilitating the pathological effects seen in post-traumatic stress disorder and other conditions.


Journal Reference:

  1. Karel Ježek, Benjamin B Lee, Eduard Kelemen, Katharine M McCarthy, Bruce S McEwen, André A Fenton. Stress-Induced Out-of-Context Activation of Memory. PLoS Biology, 2010; 8 (12): e1000570 DOI: 10.1371/journal.pbio.1000570