What's Current?

The heart-brain connection: The link between LQTS and seizures

Science Daily - Fri, 07/29/2016 - 13:29
Patients carrying certain mutations that cause Long QT Syndrome, a rare cardiac rhythm disorder, have an increased risk for developing seizures and have more severe cardiac symptoms.
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A virtual brain helps decrypt epilepsy

Medical News Today - Fri, 07/29/2016 - 12:00
Researchers at CNRS, INSERM, Aix-Marseille University and AP-HM have just created a virtual brain that can reconstitute the brain of a person affected by epilepsy for the first time.
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Virtual brain helps decrypt epilepsy

Science Daily - Fri, 07/29/2016 - 09:30
A virtual brain has been created that can reconstitute the brain of a person affected by epilepsy for the first time. From this work we understand better how the disease works and can also better prepare for surgery, say scientists.
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News: Epilepsy Foundation new grant and award opportunities

Epilepsy and Behavior - Fri, 07/29/2016 - 03:10

Targeted Research Initiative for Research Related to Cannabinoid and Epilepsy (Applications due 9/12/16)

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Acute cognitive impact of antiseizure drugs in naive rodents and corneal-kindled mice

Epilepsia - Thu, 07/28/2016 - 02:06
Summary Objective

Some antiseizure drugs (ASDs) are associated with cognitive liability in patients with epilepsy, thus ASDs without this risk would be preferred. Little comparative pharmacology exists with ASDs in preclinical models of cognition. Few pharmacologic studies exist on the acute effects in rodents with chronic seizures. Predicting risk for cognitive impact with preclinical models may supply valuable ASD differentiation data.


ASDs (phenytoin [PHT]; carbamazepine [CBZ]; valproic acid [VPA]; lamotrigine [LTG]; phenobarbital [PB]; tiagabine [TGB]; retigabine [RTG]; topiramate [TPM]; and levetiracetam [LEV]) were administered equivalent to maximal electroshock median effective dose ([ED50]; mice, rats), or median dose necessary to elicit minimal motor impairment (median toxic dose [TD50]; rats). Cognition models with naive adult rodents were novel object/place recognition (NOPR) task with CF-1 mice, and Morris water maze (MWM) with Sprague-Dawley rats. Selected ASDs were also administered to rats prior to testing in an open field. The effect of chronic seizures and ASD administration on cognitive performance in NOPR was also determined with corneal-kindled mice. Mice that did not achieve kindling criterion (partially kindled) were included to examine the effect of electrical stimulation on cognitive performance. Sham-kindled and age-matched mice were also tested.


No ASD (ED50) affected latency to locate the MWM platform; TD50 of PB, RTG, TPM, and VPA reduced this latency. In naive mice, CBZ and VPA (ED50) reduced time with the novel object. Of interest, no ASD (ED50) affected performance of fully kindled mice in NOPR, whereas CBZ and LEV improved cognitive performance of partially kindled mice.


Standardized approaches to the preclinical evaluation of an ASD's potential cognitive impact are needed to inform drug development. This study demonstrated acute, dose- and model-dependent effects of therapeutically relevant doses of ASDs on cognitive performance of naive mice and rats, and corneal-kindled mice. This study highlights the challenge of predicting clinical adverse effects with preclinical models.

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New Guidance on Epilepsy care for people who are Homeless

Epilepsy Research - Wed, 07/27/2016 - 04:49

The Queen’s Nursing Institute (QNI), in London, has published guidance for community nurses to help them support homeless people who have epilepsy.

The guidance, entitled Working with Epilepsy and Homelessness: Guidance for Community Nurses, was produced by ten epilepsy specialist nurses in collaboration with ten specialist homeless health professionals.

In a press release, David Parker-Radford, Homeless Health Project Manager at the QNI said: “Epilepsy diagnosis and ongoing treatment can be complex and require multiple health appointments and tests. This means it is even more vital that epilepsy services find proactive ways to reach vulnerable high-risk people, including those who may not be registered with a GP.”

He added: “All people living with epilepsy have the right to excellent care and treatment – not only those with stable support and housing.”

The 12-page long guidance comprises background information about the causes of epilepsy, the different types of seizures, and available treatments.

It also details the needs of homeless people, their particular risk factors and the practicalities of living with epilepsy if homeless.

Finally, it gives advice for nurses about first aid, supporting homeless people with epilepsy and coordinating their care.

The benefits of the guidance are two-fold. First, it offers knowledge to community nurses about epilepsy therefore allowing them to be more confident when supporting these people. Second, it allows epilepsy professionals to have a greater understanding of the risks and realities associated with homelessness.

The guidance was produced in response to evidence suggesting that homeless people are significantly more likely to have or develop epilepsy than the general population.

Author: Dr Özge Özkaya

Click here to read more stories about living with epilepsy.

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Investigating social cognition in epilepsy using a naturalistic task

Epilepsia - Wed, 07/27/2016 - 00:35
Summary Objective

The primary objective for this study was to assess social cognition in patients with focal epilepsy using a naturalistic task, which accurately models complex real-world social interaction.


We conducted an observational study of social cognition in 43 patients with focal epilepsy and in 22 controls. Patients and controls completed The Awareness of Social Inference Test, which measures both basic and advanced social cognition in a realistic video-based format. Patient and controls also completed standard measures of cognitive functioning and measures of depression.


Compared to controls, we found that patients with epilepsy (PWEs) had no difficulty identifying positively valenced emotional states (happiness) yet had difficulty identifying most negatively valenced emotional states (anger, fear, and disgust). In addition, PWEs were able to identify sincere exchanges correctly but could not identify sarcastic and insincere exchanges. We found that basic social cognition significantly correlated with standard generalized cognitive measures, whereas advanced social cognition did not. Finally, age at onset had significant impact on social cognition, whereas other epilepsy characteristics did not.


PWEs have deficits in social cognition when measured using a naturalistic video-based task. Advanced social cognition may be an independent cognitive domain in PWEs that is not adequately measured using standard psychometric instruments. Problems with social cognition may arise as a consequence of epilepsy during the periods of robust social development in childhood and adolescence.

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Investigation of mechanisms of vagus nerve stimulation for seizure using finite element modeling

Epilepsy Research Journal - Wed, 07/27/2016 - 00:00
Vagus Nerve Stimulation (VNS) was FDA approved nearly 20 years ago in 1997, implanted in over 65,000 patients and yet its mechanisms of action in treating epileptic seizures remain unclear. While responder rates are over 50% for the 30–40% of patients who are resistant to anti-seizure medications, most responders do not become seizure-free, but rather have the severity and frequency of seizures reduced by approximately 40–50% on average (Amar et al., 2009; Wu and Sharan, 2013).
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ERUK final report: A new technique to improve the diagnosis and treatment of epilepsy

Epilepsy Research - Tue, 07/26/2016 - 06:54


Electroencephalography (EEG) is widely used in the diagnosis of epilepsy, but it relies on a person having a seizure whilst being monitored. This can lead to delays in diagnosis and treatment, unnecessary anxiety and reduced quality of life.

To try and address this problem, Professor John Terry, at the University of Exeter, has been working alongside neurologists in London to develop computer models that can detect ‘hidden’ information within brain networks, in short resting EEG recordings (during which no seizure has taken place), and accurately identify whether or not a person has generalised epilepsy.

The study

In 2012, Professor Terry and his team were awarded £139,595 to refine their models and find out whether they could:

  1. differentiate more accurately between people with and without generalised epilepsy.
  2. distinguish, based on differences in brain network properties, between people with focal and generalised epilepsy.
  3. identify, based the activity of neuronal networks, people who have responded to antiepileptic drug (AED) treatment and those who have not.

If successful, the models would have real potential  to enhance the diagnosis of epilepsy, and perhaps even allow neurologists to predict a) whether or not a person would respond to an AED, and b) what the best AED treatment for a person might be, thus reducing the time to optimal therapy.

This grant has now come to an end and the final report has been submitted.


With regards to aims one and two above, the findings are extremely encouraging. The researchers now have a model that can distinguish with considerable accuracy, from resting EEG recordings, groups of people with generalised epilepsy from healthy controls (who do not have epilepsy). Professor Terry reports that in a test of 30 people with epilepsy and 38 without epilepsy, the model had a misdiagnosis rate of less than 5%. This is highly significant, and the team has already been exploring how they might incorporate the model into a clinical device. On the advice of feedback from commercial companies, they intend to develop a working prototype in the near future.

In terms of differentiating between people with focal and generalised epilepsy, the preliminary data obtained through this grant suggest that this should indeed be possible using computer network modelling. Professor Terry was awarded another ERUK project grant in 2015 to progress these findings and we look forward to hearing the outcome.

For a number of reasons, mainly an unexpected lack of viable resting EEG data from before and after AED treatment, it wasn’t possible to make a lot of progress on aim three. However, there has been significant follow-on funding generated from this grant, particularly from EPSRC, which will enable the team to carry out this research.


This grant has further highlighted the potential of computer models as clinical tools for the diagnosis and management of epilepsy. There is a lot more work to be done to establish their full potential, but the funding is in place and the preliminary evidence is encouraging. We are very excited about this work, as it stands to make a real difference to people’s treatment journeys and quality of life.

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A new genetic link to Temporal Lobe Epilepsy

Epilepsy Research - Tue, 07/26/2016 - 02:20

There may be an association between natural differences (known as polymorphisms) in a gene called ADAM10 and temporal lobe epilepsy, according to new research led by Dr Keshen Li from Jinan University in China.

The study, published in the scientific journal Frontiers in Neurology, is the first that shows such an association and suggests that by analysing these natural differences early on, it could be possible to predict someone’s risk of temporal lobe epilepsy.

The team of researchers examined the regulatory region of the ADAM10 gene in 496 people with temporal lobe epilepsy and in 528 healthy volunteers. They saw that in people with temporal lobe epilepsy the frequency of ‘component‘ A in the DNA was consistently increased compared to healthy controls, who had a higher frequency of component C at the same position on the DNA.

Further analyses suggested that the presence of A on both chromosomes at that location could be a factor that makes people more susceptible to temporal lobe epilepsy, whilst having one A and one C could be protective against generalised tonic-clonic seizures and drug resistant temporal lobe epilepsy.

It is important to note that all of the people recruited to this study were of Han Chinese decent and that the genetic polymorphisms might be different in other ethnic groups. The authors write: “Caution should be exercised before generalizing these findings to other ethnic populations.” However, at the very least these findings will guide future research that could ultimately lead to new diagnostic techniques and better treatments for temporal lobe epilepsy.

It is known that there are as many as 6,771 polymorphisms in the ADAM10 gene, which encodes for a cell-surface protein crucial in Alzheimer’s disease. Two of these differences, found in the regulatory region of the gene, are particularly important because they have been shown to decrease or ‘downregulate’ the expression* of the ADAM10 gene and give rise to epileptic seizures in Alzheimer’s disease.

Experiments in rodents have also shown that downregulating ADAM10 results in repetitive seizures, which may well mean that low levels of ADAM10 can also cause seizures in people. A ‘reverse’ experiment showed that in mice where ADAM10 was mildly overexpressed, induced seizures were less severe and recovery times were shorter, again suggesting that ADAM10 may be protective against seizures.

* The term ‘gene expression’ refers to the process by which information from a gene is used to create a functioning gene product, very often a protein.

Author: Dr Özge Özkaya

Click here for more articles about brain science including genetics.

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New findings could help scientists prevent the Development of Epilepsy

Epilepsy Research - Mon, 07/25/2016 - 14:14

Scientists at Louisiana State University, and at Spain’s University of Alcala, have developed compounds that can prevent seizures in a rodent model of epilepsy. They believe that so-called ‘neuroprotective’ compounds like these may also prevent epilepsy in humans in the future.

In earlier work, the team screened a range of compounds that block a specific inflammatory molecule in neurons, and discovered that one in particular, LAU-0901, stopped seizures in epilepsy models. In the current study they focused on LAU-0901, and a more refined version of it known as LAU-09021, to try and find out exactly how they work.

They found that the compounds’ actions preserved dendritic spines, which are vital to communication between neurons. Dendritic spines are damaged during seizures and other ‘insults’, causing a chain of events that make neurons hyperexcitable, which promotes the development of epilepsy. The team discovered that the animals were still protected from seizures up to 100 days after treatment with LAU-09021, suggesting that the process of epilepsy development had been arrested.

These findings, published in the journal Scientific Reports, indicate that, in the future, new therapies that preserve dendritic spines could potentially stop seizures and prevent the development of epilepsy.

Senior Author Dr Nicolas Bazan, at the Louisiana State University Health Sciences Center, said: “Most of the anti-epileptic drugs currently available treat the symptom – seizures – not the disease itself. Understanding the potential therapeutic usefulness of compounds that may interrupt the development process may pave the way for disease-modifying treatments for patients at risk for epilepsy.”

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Novel compounds arrested epilepsy development in mice

Medical News Today - Mon, 07/25/2016 - 03:00
A team led by Nicolas Bazan, MD, PhD, Boyd Professor and Director of LSU Health New Orleans' Neuroscience Center of Excellence, has developed neuroprotective compounds that may prevent the...
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US suicide rate for people with Epilepsy exceeds levels in general population

Medical News Today - Mon, 07/25/2016 - 03:00
Researchers at Columbia University's Mailman School of Public Health and the Centers for Disease Control studied the prevalence of suicide among people with epilepsy compared to the population...
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New Method to look at Synapses in the Living Human Brain

Epilepsy Research - Sat, 07/23/2016 - 15:44

Researchers at Yale University have developed a new, non-invasive method to examine synapses – the points of communication between neurons. The work is published in the leading journal Science Translational Medicine.

In the future, this novel technique could improve the diagnosis and treatment of epilepsy, and of other neurological conditions.

In a press release, Dr Richard Carson, Professor of Radiology and Biomedical Imaging and Senior Author of the study, said: “This is the first time we have synaptic density measurement in live human beings. Up to now any measurement of synaptic density was post-mortem (after death).”

The researchers developed a radioactive tracer that binds to a protein called SV2A, found at synapses. They injected the tracer into the body and, using a type of imaging called positron emission tomography (PET), were able to visualise synapses in the brain of animals, healthy people and people with epilepsy. They then used mathematical tools to calculate synaptic density, the number of functional synapses per volume of brain tissue, to assess how much and how well the subjects’ neurons were communicating. They discovered that in the brains of people with temporal epilepsy, synaptic density measurements reflected damage to certain regions.

The scientists hope that this method can eventually be used routinely, to monitor the course of various neurological conditions, including epilepsy, and assess how well certain drugs are working. Its non-invasive nature will help make assessment a more comfortable and less daunting experience for patients, which is so important.

There are trillions of synapses in the brain, which transmit signals from one neuron to another. Changes in the density of synapses are associated with a number of neurological disorders, including epilepsy.

Author: Dr Özge Özkaya

Click here for more articles about brain science including genetics.

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Novel compounds arrested epilepsy development in mice

Science Daily - Fri, 07/22/2016 - 09:29
Neuroprotective compounds have been developed by scientists that may prevent the development of epilepsy. The researchers explained that the compounds prevented seizures and their damaging effects on dendritic spines, specialized structures that allow brain cells to communicate. In epilepsy, these structures are damaged and rewire incorrectly, creating brain circuits that are hyper-connected and prone to seizures, an important example of pathological plasticity.
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