1. Study suggests noise sens­it­iv­ity is vis­ible in brain struc­tures

    December 26, 2017 by Ashley

    From the University of Helsinki press release:

    Recent functional studies conducted at the University of Helsinki and Aarhus University suggest that noise sensitivity, a trait describing attitudes towards noise and predicting noise annoyance, is associated with altered processing in the central auditory system. Now, the researchers have found that noise sensitivity is associated with the grey matter volume in selected brain structures previously linked to auditory perceptual, emotional and interoceptive processing.

    Having an increased amount of grey matter in these areas may mean that noise sensitivity requires more neural resources to be involved in dealing with sound.

    “We found greater grey matter volume in people with high noise sensitivity in the brain temporal regions, as well as the hippocampus and the right insula. These cortical and subcortical areas are parts of brain networks supporting listening experience,” says researcher Marina Kliuchko, the first author of the research article published in NeuroImage journal.

    The research included brain images of 80 subjects from which grey matter volume, cortical thickness, and other anatomical parameters were measured and correlated with noise sensitivity. The work brings new insight into the physiological mechanisms of noise sensitivity.

    Noise sensitivity may be related to self-awareness in noise-sensitive individuals about the sensations that noise induces in them. That is suggested from the increased volume of the anterior part of the right insular cortex, which is known to be important for matching external sensory information with internal state of the body and bringing it to one’s conscious awareness,” Kliuchko says.


  2. Researchers construct whole-brain map of electrical connections key to forming memories

    December 19, 2017 by Ashley

    From the University of Pennsylvania press release:

    A team of neuroscientists at the University of Pennsylvania has constructed the first whole-brain map of electrical connectivity in the brain based on data from nearly 300 neurosurgical patients with electrodes implanted directly on the brain. The researchers found that low-frequency rhythms of brain activity, when brain waves move up and down slowly, primarily drive communication between the frontal, temporal and medial temporal lobes, key brain regions that engage during memory processing.

    The research, part of the Restoring Active Memory project, was conducted by Michael Kahana, Penn professor of psychology and principal investigator of the Defense Advanced Research Projects Agency’s RAM program; Ethan Solomon, an M.D./Ph.D. student in the Department of Bioengineering; and Daniel Rizzuto, director of cognitive neuromodulation at Penn. They published their findings in Nature Communications.

    This work elucidates the way different regions of the brain communicate during cognitive processes like memory formation. Though many studies have examined brain networks using non-invasive tools like functional MRI, observations of large-scale networks using direct human-brain recordings have been difficult to secure because these data can only come from neurosurgical patients.

    For several years, the Penn team gathered this information from multiple hospitals across the country, allowing the researchers to observe such electrical networks for the first time. Patients undergoing clinical monitoring for seizures performed a free-recall memory task that asked them to view a series of words on a screen, then repeat back as many as they could remember.

    At the same time, the researchers examined brain activity occurring on slow and fast time scales, also called low- and high-frequency neural activity. They discovered that when a person is effectively creating new memories — in this case, remembering one of the presented words — alignment between brain regions tends to strengthen with slow waves of activity but weaken at higher frequencies.

    “We found,” said Solomon, the paper’s lead author, “that the low-frequency connectivity of a brain region was associated with increased neural activity at that site. This suggests that, for someone to form new memories, two functions must happen simultaneously: brain regions must individually process a stimulus, and then those regions must communicate with each other at low frequencies.”

    Areas of the brain identified in this paper — the frontal, temporal and medial temporal lobes — have long intrigued neuroscientists because of their crucial role in such memory functions.

    This work supports the RAM project goal of using brain stimulation to enhance memory.

    “Better understanding the brain networks that activate during memory processing,” Kahana said, “gives us a better ability to fine-tune electrical stimulation that might improve it. We’re now prepared to ask whether we can use measures of functional connectivity to guide our choice of which brain region to target with electrical stimulation. Ultimately, given the size of this dataset, these discoveries would not be possible without years of effort on the part of our participants, clinical teams and research scientists.”

    Earlier this month, the RAM team publicly released its extensive intracranial brain recording and stimulation dataset that included thousands of hours of data from 250 patients performing memory tasks. Previous research showed for the first time that electrical stimulation delivered when memory was predicted to fail could improve memory function in the human brain. That same stimulation generally became disruptive when electrical pulses arrived during periods of effective memory function.

    Next, the Penn researchers plan to examine the interaction between brain stimulation and the functional connections the latest study uncovered.

    “There’s still significant work to do,” Rizzuto said, “before we can use these connectivity maps to guide therapeutic brain stimulation for patients with memory disorders such as traumatic brain injury or Alzheimer’s disease, but we’re working toward that goal.”


  3. First brain training exercise positively linked to dementia prevention identified

    by Ashley

    From the Indiana University press release:

    Aging research specialists have identified, for the first time, a form of mental exercise that can reduce the risk of dementia.

    The cognitive training, called speed of processing, showed benefits up to 10 years after study participants underwent the mental exercise program, said Frederick W. Unverzagt, PhD, professor of psychiatry at Indiana University School of Medicine.

    The proportion of participants who underwent the training and later developed dementia was significantly smaller than among those who received no cognitive training, the researchers said.

    There were measurable benefits even though the amount of training was small and spread out over time: 10 one-hour sessions over six weeks initially and up to eight booster sessions after that.

    “We would consider this a relatively small dose of training, a low intensity intervention. The persistence — the durability of the effect was impressive,” said Dr. Unverzagt, who explains more in a Q&A blog post.

    Results from the Advanced Cognitive Training in Vital Elderly — ACTIVE — study of 2,802 older adults were recently reported in Alzheimer & Dementia Translational Research and Clinical Interventions, a peer-reviewed journal of the Alzheimer’s Association.

    The researchers, from IU, the University of South Florida, Pennsylvania State University and Moderna Therapeutics, examined healthy adults aged 65 years and older from multiple sites and who were randomly assigned to one of four treatment groups:

    • Participants who received instructions and practice in strategies to improve memory of life events and activities.
    • Participants who received instruction and practice in strategies to help with problem solving and related issues.
    • Participants who received computer-based speed of processing exercises — exercises designed to increase the amount and complexity of information they could process quickly.
    • A control group whose members did not participate in any cognitive training program.

    Initial training consisted of 10 sessions lasting about an hour, over a period of five to six weeks. A subset of participants who completed least 80 percent of the first round of training sessions were eligible to receive booster training, which consisted of four 60 to 75-minute sessions 11 months and 35 months following the initial training. Participants were assessed immediately after training and at one, two, three, five and 10 years after training.

    After attrition due to death and other factors, 1,220 participants completed the 10-year follow-up assessment. During that time, 260 participants developed dementia. The risk of developing dementia was 29 percent lower for participants in speed of processing training than for those who were in the control group, a statistically significant difference. Moreover, the benefits of the training were stronger for those who underwent booster training. While the memory and reasoning training also showed benefits for reducing dementia risk, the results were not statistically significant.

    Dr. Unverzagt noted that the speed of processing training used computerized “adaptive training” software with touch screens. Participants were asked to identify objects in the center of the screen, while also identifying the location of briefly appearing objects in the periphery. The software would adjust the speed and difficulty of the exercises based on how well participants performed.

    In contrast the memory and reasoning programs used more traditional instruction and practice techniques as might occur in a classroom setting.

    Earlier studies had shown that ACTIVE cognitive training improved participants’ cognitive abilities and the ease of engaging in activities of daily living five and 10 years after the initial training. However, an examination of the role of ACTIVE cognitive training on dementia incidence was not significant after five years of follow-up.


  4. Study looks at why we can’t always stop what we’ve started

    by Ashley

    From the Johns Hopkins University press release:

    When we try to stop a body movement at the last second, perhaps to keep ourselves from stepping on what we just realized was ice, we can’t always do it — and Johns Hopkins University neuroscientists have figured out why.

    Stopping a planned behavior requires extremely fast choreography between several distinct areas of the brain, the researchers found. If we change our mind about taking that step even a few milliseconds after the original “go” message has been sent to our muscles, we simply can’t stop our feet.

    “We have to process all of these pieces of information quickly,” said senior author Susan Courtney, a professor of psychological and brain sciences. “The question is: When we do succeed, how do we do that? What needs to happen in order for us to stop in time?”

    These findings, which will appear Dec. 20 in the journal Neuron, map the neural basis for inhibiting movement. They help explain what’s going wrong in the brain when people fall more as they age and when addicts can’t stop binge behavior.

    Scientists had believed only one brain region was active when people changed plans. But the findings of Courtney’s team suggest it takes a lightning-fast interaction between two areas in the prefrontal cortex and another in the pre-motor cortex to stop, reverse or otherwise change a plan already in progress.

    There is even another brain area, Courtney says, that continues to process what we should have done if we are unable to stop. She jokingly calls it the “oops” area.

    In addition to all three areas of the brain communicating successfully, the key to being able to stop, the researchers found, is timing.

    Suppose you’re driving and approaching an intersection when the light turns yellow. You decide to accelerate and speed though. But just after you send that decision to the part of the brain that will move your foot to hit the gas, you notice a police car and change your mind.

    “Which plan is going to win?” said first author Kitty Z. Xu, a former Johns Hopkins graduate student who is now a researcher at Pinterest. “The sooner you see the police car after deciding to go through the light, the better your chance of being able to move your foot to the break instead.”

    And by soon, Xu means milliseconds.

    If you attempt to change your mind after 100 milliseconds or less, you most likely can. If it takes you 200 milliseconds or more — that’s less than a quarter of a second — you’re still going through with the original plan. That’s because the original signal is already on its way to the muscles by then — past the point of no return.

    “If you’re already executing the plan when you see the police car,” Xu said, “you’re going to go through the light.”

    The team devised a near-identical computer task for human and non-human subjects. While having their brain activity monitored, both the people and one monkey saw one of two shapes on the screen — one shape meant that blue means stop and yellow means go, the other shape meant the opposite. A black circle would then appear and participants would try to move their eyes to look at it quickly. But then a blue or yellow dot might appear, after varying lengths of time, and subjects would have to stop or continue their planned eye movement.

    The researchers were able to observe what happened across the full brain with the human fMRI results, while electrodes implanted in the monkey’s brain measured single cells. Having strong, converging results at both the macro and micro levels provided a more holistic view of how the prefrontal cortex and the pre-motor cortex communicate with each other to stop, Xu said.

    When these brain areas don’t properly communicate, or don’t interact fast enough, that’s when we run into trouble, Courtney says.

    “We know people with damage to these parts of the brain have trouble changing plans or inhibiting actions,” she said. “We know as we age, our brain slows down and it takes us longer to find words or to try to make these split-second plan changes. It could be part of the reason why old people fall.”

    Knowing more about how the brain can stop an intended activity could also be revealing for those dealing with addictions, Courtney said.

    “We think there are similar processes in ‘should I do this’ and ‘can I turn off that thought about the drink,'” Courtney said. “The sooner I can turn off the plan to drink, the less likely I’ll carry out the plan. It’s very relevant.”

    Co-authors included Brian Anderson, a former Johns Hopkins graduate student and postdoctoral researcher who is now an assistant professor at Texas A&M University; Erik Emeric, a research technologist at Johns Hopkins’ Zanvyl Krieger Mind/Brain Institute; Anthony W. Sali, a former Johns Hopkins graduate student who is now a postdoctoral researcher at Duke University; Veit Stuphorn, an associate professor of psychological and brain sciences at Johns Hopkins; and Steven Yantis, a professor of psychological and brain sciences at Johns Hopkins who died in 2014.

    This project was supported by the National Institute in Drug Abuse R01-DA013165 and RO1DA040990, and the National Institute of Neurological Disorders and Stroke, R01NS086104.


  5. Researchers link post-right stroke delirium and spatial neglect to common brain mechanism

    by Ashley

    From the Kessler Foundation press release:

    Stroke researchers at Kessler Foundation have proposed a theory for the high incidence of delirium and spatial neglect after right-brain stroke. Their findings are detailed in “Disruption of the ascending arousal system and cortical attention network in post-stroke delirium and spatial neglect,” which was published online ahead of print on September 27, 2017 by Neuroscience & Biobehavioral Reviews. The authors are Olga Boukrina, PhD, research scientist, and A.M. Barrett, MD, director of Stroke Rehabilitation Research at Kessler Foundation.

    Delirium and spatial neglect affect approximately half of individuals with right brain stroke, increasing their risk for prolonged stays and rehospitalization. Identifying the factors associated with these often disabling conditions is the initial step toward minimizing their impact on recovery and rehabilitation. Stroke survivors with spatial neglect are more likely to develop delirium, an acute disorder of attention and cognition, suggesting that these conditions may share a common brain mechanism.

    “The brain networks for spatial attention and arousal may underlie the impairments in delirium and spatial neglect,” noted Dr. Boukrina. “These networks comprise ascending projections from the midbrain nuclei and integrate dorsal and ventral cortical and limbic components. We propose that right-brain stroke disproportionately impairs these cortical and limbic components, causing the lateralized deficits that characterize spatial neglect,” she explained. “Spatial neglect may lower the threshold for delirium, which could account for the higher incidence of both post-stroke complications.”

    Further research is needed in order to identify individuals at risk soon after stroke, and develop an effective protocol for reducing the risk of these complications and their contributions to mortality and morbidity.


  6. Electrical stimulation in brain bypasses senses, instructs movement

    by Ashley

    From the University of Rochester Medical Center press release:

    The brain’s complex network of neurons enables us to interpret and effortlessly navigate and interact with the world around us. But when these links are damaged due to injury or stroke, critical tasks like perception and movement can be disrupted. New research is helping scientists figure out how to harness the brain’s plasticity to rewire these lost connections, an advance that could accelerate the development of neuro-prosthetics.

    A new study authored by Marc Schieber, M.D., Ph.D., and Kevin Mazurek, Ph.D. with the University of Rochester Medical Center Department of Neurology and the Del Monte Institute for Neuroscience, which appears in the journal Neuron, shows that very low levels of electrical stimulation delivered directly to an area of the brain responsible for motor function can instruct an appropriate response or action, essentially replacing the signals we would normally receive from the parts of the brain that process what we hear, see, and feel.

    “The analogy is what happens when we approach a red light,” said Schieber. “The light itself does not cause us to step on the brake, rather our brain has been trained to process this visual cue and send signals to another parts of the brain that control movement. In this study, what we describe is akin to replacing the red light with an electrical stimulation which the brain has learned to associate with the need to take an action that stops the car.”

    The findings could have significant implications for the development of brain-computer interfaces and neuro-prosthetics, which would allow a person to control a prosthetic device by tapping into the electrical activity of their brain.

    To be effective, these technologies must not only receive output from the brain but also deliver input. For example, can a mechanical arm tell the user that the object they are holding is hot or cold? However, delivering this information to the part of the brain responsible for processing sensory inputs does not work if this part of the brain is injured or the connections between it and the motor cortex are lost. In these instances, some form of input needs to be generated that replaces the signals that combine sensory perception with motor control and the brain needs to “learn” what these new signals mean.

    “Researchers have been interested primarily in stimulating the primary sensory cortices to input information into the brain,” said Schieber. “What we have shown in this study is that you don’t have to be in a sensory-receiving area in order for the subject to have an experience they can identify.”

    A similar approach is employed with cochlear implants for hearing loss which translate sounds into electrical stimulation of the inner ear and, over time, the brain learns to interpret these inputs as sound.

    In the new study, the researchers detail a set of experiments in which monkeys were trained to perform a task when presented with a visual cue, either turning, pushing, or pulling specific objects when prompted by different lights. While this occurred, the animals simultaneously received a very mild electrical stimulus called a micro-stimulation in different areas of the premotor cortex — the part of the brain that initiates movement — depending upon the task and light combination.

    The researchers then replicated the experiments, but this time omitted the visual cue of the lights and instead only delivered the micro-stimulation. The animals were able to successfully identify and perform the tasks they had learned to associate with the different electrical inputs. When the pairing of micro-stimulation with a particular action was reshuffled, the animals were able to adjust, indicating that the association between stimulation and a specific movement was learned and not fixed.

    “Most work on the development of inputs to the brain for use with brain-computer interfaces has focused primarily on the sensory areas of the brain,” said Mazurek. “In this study, we show you can expand the neural real estate that can be targeted for therapies. This could be very important for people who have lost function in areas of their brain due to stroke, injury, or other diseases. We can potentially bypass the damaged part of the brain where connections have been lost and deliver information to an intact part of the brain.”


  7. Study links canola oil to worsened memory and learning ability in Alzheimer’s

    December 17, 2017 by Ashley

    From the Temple University Health System press release:

    Canola oil is one of the most widely consumed vegetable oils in the world, yet surprisingly little is known about its effects on health. Now, a new study published online December 7 in the journal Scientific Reports by researchers at the Lewis Katz School of Medicine at Temple University (LKSOM) associates the consumption of canola oil in the diet with worsened memory, worsened learning ability and weight gain in mice which model Alzheimer’s disease. The study is the first to suggest that canola oil is more harmful than healthful for the brain.

    “Canola oil is appealing because it is less expensive than other vegetable oils, and it is advertised as being healthy,” explained Domenico Praticò, MD, Professor in the Departments of Pharmacology and Microbiology and Director of the Alzheimer’s Center at LKSOM, as well as senior investigator on the study. “Very few studies, however, have examined that claim, especially in terms of the brain.”

    Curious about how canola oil affects brain function, Dr. Praticò and Elisabetta Lauretti, a graduate student in Dr. Pratico’s laboratory at LKSOM and co-author on the new study, focused their work on memory impairment and the formation of amyloid plaques and neurofibrillary tangles in an Alzheimer’s disease mouse model. Amyloid plaques and phosphorylated tau, which is responsible for the formation of tau neurofibrillary tangles, contribute to neuronal dysfunction and degeneration and memory loss in Alzheimer’s disease. The animal model was designed to recapitulate Alzheimer’s in humans, progressing from an asymptomatic phase in early life to full-blown disease in aged animals.

    Dr. Praticò and Lauretti had previously used the same mouse model in an investigation of olive oil, the results of which were published earlier in 2017. In that study, they found that Alzheimer mice fed a diet enriched with extra-virgin olive oil had reduced levels of amyloid plaques and phosphorylated tau and experienced memory improvement. For their latest work, they wanted to determine whether canola oil is similarly beneficial for the brain.

    The researchers started by dividing the mice into two groups at six months of age, before the animals developed signs of Alzheimer’s disease. One group was fed a normal diet, while the other was fed a diet supplemented with the equivalent of about two tablespoons of canola oil daily.

    The researchers then assessed the animals at 12 months. One of the first differences observed was in body weight — animals on the canola oil-enriched diet weighed significantly more than mice on the regular diet. Maze tests to assess working memory, short-term memory, and learning ability uncovered additional differences. Most significantly, mice that had consumed canola oil over a period of six months suffered impairments in working memory.

    Examination of brain tissue from the two groups of mice revealed that canola oil-treated animals had greatly reduced levels of amyloid beta 1-40. Amyloid beta 1-40 is the more soluble form of the amyloid beta proteins. It generally is considered to serve a beneficial role in the brain and acts as a buffer for the more harmful insoluble form, amyloid beta 1-42.

    As a result of decreased amyloid beta 1-40, animals on the canola oil diet further showed increased formation of amyloid plaques in the brain, with neurons engulfed in amyloid beta 1-42. The damage was accompanied by a significant decrease in the number of contacts between neurons, indicative of extensive synapse injury. Synapses, the areas where neurons come into contact with one another, play a central role in memory formation and retrieval.


  8. PET tracer gauges effectiveness of promising Alzheimer’s treatment

    by Ashley

    From the Society of Nuclear Medicine and Molecular Imaging press release:

    In the December featured basic science article in The Journal of Nuclear Medicine, Belgian researchers report on the first large-scale longitudinal imaging study to evaluate BACE1 inhibition with micro-PET in mouse models of Alzheimer’s disease. PET imaging has been established as an excellent identifier of the amyloid plaque and tau tangles that characterize Alzheimer’s disease. Now it is proving to be an effective way to gauge treatment effectiveness.

    The tracer makes it possible to image the effects of chronic administration of an inhibitor for an enzyme, called beta (?)-site amyloid precursor protein-cleaving enzyme 1 (BACE1), which cuts off protein fragments that can lead to amyloid-? development and is more prevalent in brains affected by Alzheimer’s. It does this by binding to BACE1.

    The study compared control mice with those genetically-altered to have Alzheimer’s, and tested 18F-florbetapir (18F-AV45) along with two other tracers, 18F-FDG PET and 18F-PBR111. The mice received the BACE inhibitor at 7 weeks, then brain metabolism, neuroinflammation and amyloid-? pathology were measured using a micro-PET (?PET) scanner and each of the tracers. Baseline scans were done at 6-7 weeks and follow-up scans at 4,7 and 12 months. 18F-AV45 uptake was measured at 8 and 13 months of age. After the final scans, microscopic studies were performed.

    While all three tracers detected pathological differences between the genetically modified mice and the controls, only 18F-AV45 showed the effects of inhibitor treatment by identifying reduced amyloid-? pathology in the genetically modified mice. This was confirmed in the microscopic studies.

    The team of the Molecular Imaging Center Antwerp, Belgium, however warns, “This study clearly showed that accurate quantification of amyloid-beta tracers is critically important and that the non-specific uptake in the brain of subjects might be underestimated for some existing Alzheimer’s tracers that have fast metabolization profiles. The aim of this translational research is advancing results discovered at the bench so that they can be applied to patients at the bedside.”

    The statistics on Alzheimer’s are sobering. Approximately 10 percent of people 65 and older have Alzheimer’s dementia, according to the Alzheimer’s Association. More than 5 million Americans are living with the disease, and that number could rise to 16 million by 2050.


  9. New method helps identify causal mechanisms in depression

    by Ashley

    From the Elsevier press release:

    People with major depressive disorder have alterations in the activity and connectivity of brain systems underlying reward and memory, according to a new study in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging. The findings provide clues as to which regions of the brain could be at the root of symptoms, such as reduced happiness and pleasure, in depression.

    As the first of its kind, the new study by Prof. Edmund Rolls, Prof. Jianfeng Feng, Dr. Wei Cheng, and colleagues at the University of Warwick, UK uses a new approach to measure the influence of one brain region on another, referred to as effective connectivity, in depression. The approach goes beyond the limitations of previous brain imaging studies, which show if — but not how — activity of different brain regions is related. “The new method allows the effect of one brain region on another to be measured in depression, in order to discover more about which brain systems make causal contributions to depression,” said Prof. Rolls.

    “This represents an exciting new methodological advance in the development of diagnostic biomarkers and the identification of critical brain circuitry for targeted interventions for major depression,” said Dr. Cameron Carter, Editor of Biological Psychiatry: Cognitive Neuroscience and Neuroimaging.

    Rolls and colleagues compared 336 people with major depressive disorder to 350 healthy controls. Brain regions involved in reward and subjective pleasure received less drive (or reduced effective connectivity) in patients, which may contribute to the decreased feeling of happiness in depression.

    In addition, brain regions involved in punishment and responses when a reward is not received had decreased effective connectivity and increased activity, providing evidence for the source of sadness that occurs in the disorder.

    Memory-related areas of the brain had increased activity and connectivity in people with depression, which the authors suggest may be related to heightened memory processing, possibly of unpleasant memories, in depression.

    “These findings are part of a concerted approach to better understand the brain mechanisms related to depression, and thereby to lead to new ways of understanding and treating depression,” said Prof. Rolls.


  10. Seizure study sheds light on lasting brain effects in children

    December 16, 2017 by Ashley

    From the University of Edinburgh press release:

    Prolonged convulsive seizures in childhood could be linked to the development of other brain conditions, a study suggests.

    Lasting effects are more pronounced in children who had other neurological problems before their seizure, researchers say.

    The study — the first of its kind worldwide — provides insight into the long-term health impact of convulsive status epilepticus (CSE), in which a single seizure, or series of seizures, lasts for at least 30 minutes.

    Its findings will be important for doctors as they try to predict what the lasting outcomes might be for families, and how to monitor and treat children who had CSE.

    CSE is the most common medical emergency in young children, affecting 1 in 5000 people per year in the developed world. Long-term consequences of CSE are not well established.

    Researchers based at the University of Edinburgh and UCL (University College London) followed the health of more than 100 children for nine years after they had CSE.

    Lasting neurological conditions, including epilepsy, learning disabilities and movement problems were more common than expected for children from the general population, the study found.

    Children who had existing neurological or developmental issues at the time of a CSE were more likely to have a neurological problem at follow up, researchers say.

    Children without an existing neurological or developmental issue tended to have more positive outcomes.

    The findings offer fresh insights into the biological cause of long-term brain conditions in children after CSE and could help doctors decide on treatment for patients.

    The study is published in the journal The Lancet Child and Adolescent Health.

    Richard Chin, Director of the University of Edinburgh’s Muir Maxwell Epilepsy Centre, who led the study, said: “Our study indicates that children with pre-existing neurological conditions are far more likely to experience chronic neurological and cognitive problems following convulsive status epilepticus. This is a very important finding for planning long-term treatment for children whose brains may be more vulnerable to the effects of a prolonged seizure.

    “The findings also give hope to families whose children did not have neurological problems before, as the long-term effects of their child’s prolonged seizure may not be as marked as might be expected.”