Posts Tagged Epilepsy

[WEB SITE] Neuroscientists unravel how two different types of brain plasticity work on synapses


The brain’s crucial function is to allow organisms to learn and adapt to their surroundings. It does this by literally changing the connections, or synapses, between neurons, strengthening meaningful patterns of neural activity in order to store information. The existence of this process – brain plasticity – has been known for some time.

But actually, there are two different types of brain plasticity at work on synapses. One is “Hebbian plasticity”; it is the one which effectively allows for the recording of information in the synapses, named after pioneering neuroscientist Donald Hebb. The other, more recently discovered, is “homeostatic synaptic plasticity” (HSP), and, like other “homeostatic” processes in the body such as maintaining a constant body temperature, its purpose is to keep things stable. In this case, HSP ensures that the brain doesn’t build up too much activity (as is the case in epilepsy) or become too quiet (as can happen when you lose synapses in Alzheimer’s Disease).

However, little is known about how these two types of plasticity actually interact in the brain. Now, a team of neuroscientists at the Champalimaud Centre for the Unknown, in Lisbon, Portugal, has begun to unravel the fundamental processes that happen in the synapse when the two mechanisms overlap. Their results were published in the journal iScience.

“In theory, the two types of plasticity act as opposing forces”, says Anna Hobbiss, first author of the new study, which was led by Inbal Israely. “Hebbian plasticity reacts to activity at the synapses by inciting them to get stronger while HSP reacts to it by making them weaker. We wanted to understand, on a cellular and molecular level, how the synapse deals with these two forces when they are present at the same time.”

In so doing, the authors have surprisingly shown that, contrary to what might be expected, HSP facilitates Hebbian plasticity, and thus influences memory formation and learning. This means that these two types of plasticity “may actually not be such distinct processes, but instead work together at the same synapses”, says Israely.

The team’s goal was to determine the changes in size of minute structures called dendritic spines, which are the “receiving end” of the synapse. The size of these spines changes to reflect the strength of the synaptic connection.

For this, they studied cells from the mouse hippocampus, a part of the brain which is crucial for learning. In their experiments, they blocked activity in the cells by introducing a potent neurotoxin called tetrodotoxin, thus simulating the loss of input to a certain part of the brain (“think about a person suddenly becoming blind, which leads to loss of input from the eyes to the brain”, says Hobbiss).

Forty eight hours later, they mimicked a small recovery of activity at only one synapse by releasing a few molecules of a neurotransmitter called glutamate on single spines of single neurons. This was possible thanks to a very high resolution, state-of-the-art laser technology, called two-photon microscopy, which allowed the scientists to very precisely visualize and target individual dendritic spines.

As this process evolved, the team closely watched what was happening to the spines – and they saw various anatomical changes. First, the silencing of all neural activity made the spines grow in size. “The spines are like little microphones, which, when there is silence, ramp up the ‘volume’ to try and catch even the faintest noise”, Hobbiss explains.

The scientists then activated individual spines with pulses of glutamate and watched them for two hours. One of the things they thought could happen was that the size of the spines would not grow further, since they had already turned up their ‘volume’ as far is it would go. But the opposite happened: the spines grew even more, with the smaller spines showing the biggest growth.

Finally, the authors also saw growth in neighboring spines, even though the experiment only targeted one spine. “We found that after a lack of activity, other spines in the vicinity also grew, further enhancing the cell’s sensitivity to restored neural transmission”, says Hobbiss. “The cells become more sensitive, more susceptible to encode information. It is as though the ‘gain’ has been turned up”, she adds.

“The fact that neighboring spines grew together with an active spine signifies that homeostatic plasticity changes one of the hallmark features of information storage, which is that plasticity is limited to the site of information entry”, Israely explains. “So, in this sense, the different plasticity mechanisms which are at work in the neuron can cooperate to change which and how many inputs respond to a stimulus. I think this is an exciting finding of our study.”

Taken together, these results show that homeostatic plasticity can actually rev up Hebbian plasticity, the type required for storing information. “Our work adds a piece to the puzzle of how the brain performs one of its fundamental tasks: being able to encode information while still keeping a stable level of activity”, concludes Hobbiss.

The misregulation of homeostatic plasticity – the stabilizing one – has started to be implicated in human health, specifically neurodevelopmental disorders such as Fragile X syndrome and Rett syndrome as well as neurodegenerative ones such as Alzheimer’s Disease. “Perhaps this balance is what allows us to be able to learn new information while retaining stability of that knowledge over a lifetime”, says Israely.


via Neuroscientists unravel how two different types of brain plasticity work on synapses

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[WEB SITE] Importance of Taking Medication on Schedule – Epilepsy Foundation

Taking Your Medication Regularly is Essential to Controlling Your Seizures

Taking seizure medications regularly, and as recommended by your doctor, is vitally important! It gives you the best chance to achieve the goals of epilepsy therapy: no seizures and no side effects. On the flip side, noncompliance with seizure medicines can have significant and possibly disastrous consequences.

Taking medicines regularly is easiest when you know about epilepsytreatment, and how to manage your seizures and medications. Managing medicines isn’t easy, but it certainly can be done! Think of it as a team approach involving your doctor, nurse, pharmacist, counselor, family and friends, and of course YOU. You are the captain of the team, because only you can decide if you are going to take the medicine. Only you can work together with the team to find ways to manage your meds best.

Here’s A Few Points About Why Adherence Is So Important.

  • You need to follow the doctor’s directions. If thos directions are confusing or complex, ask questions until you are sure you understand.
  • Seizure medicines must be taken each and every day as prescribed. If the right amount is not taken at the right time, the medicine may not be able to prevent seizures, or might cause unwanted side effects.
  • If the first medicine doesn’t work, others may be more successful.
  • Finding the right medicine at the right dose taken at the right time(s) of the day requires teamwork.
  • Any medication change recommended by the doctor is based on the assumption that the person has been taking the medicine the way it was intended. If this isn’t true, then the change may not work or may be the wrong thing to do!

Here are some thoughts by Joyce Cramer, a former president of the Epilepsy Therapy Project, that emphasizes the importance of medication compliance: The Titanic Impact of Medication Compliance on Epilepsy.

Learn More

via Importance of Taking Medication on Schedule | Epilepsy Foundation

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[REVIEW] Epilepsy and Cannabis: A Literature Review – Full Text PDF


Epilepsy is considered to be one of the most common non-communicable neurological diseases especially in low to middle-income countries. Approximately one-third of patients with epilepsy have seizures that are resistant to antiepileptic medications. Clinical trials for the treatment of medically refractory epilepsy have mostly focused on new drug treatments, and result in a significant portion of subjects whose seizures remain refractory to medication. The off-label use of cannabis sativa plant in treating seizures is known since ancient times. The active ingredients of this plant are delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD), the latter considered safer and more effective in treating seizures, and with less adverse psychotropic effects.

Clinical trials prior to two years ago have shown little to no significant effects of cannabis in reducing seizures. These trials seem to be underpowered, with a sample size less than 15. In contrast, more recent studies that have included over 100 participants showed that CBD use resulted in a significant reduction in seizure frequency. Adverse effects of CBD overall appear to be benign, while more concerning adverse effects (e.g., elevated liver enzymes) improve with continued CBD use or dose reduction.

In most of the trials, CBD is used in adjunct with epilepsy medication, therefore it remains to be determined whether CBD is itself antiepileptic or a potentiator of traditional antiepileptic medications. Future trials may evaluate the efficacy of CBD in treating seizures due to specific etiologies (e.g., post-traumatic, post-stroke, idiopathic).[…]

Full Text PDF

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[ARTICLE] Sleep Related Epilepsy and Pharmacotherapy: An Insight – Full Text

In the last several decades, sleep-related epilepsy has drawn considerable attention among epileptologists and neuroscientists in the interest of new paradigms of the disease etiology, pathogenesis and management. Sleep-related epilepsy is nocturnal seizures that manifest solely during the sleep state. Sleep comprises two distinct stages i.e., non-rapid eye movement (NREM) and rapid eye movement (REM) that alternate every 90 min with NREM preceding REM. Current findings indicate that the sleep-related epilepsy manifests predominantly during the synchronized stages of sleep; NREM over REM stage. Sleep related hypermotor epilepsy (SHE), benign partial epilepsy with centrotemporal spikes or benign rolandic epilepsy (BECTS), and Panayiotopoulos Syndrome (PS) are three of the most frequently implicated epilepsies occurring during the sleep state. Although some familial types are described, others are seemingly sporadic occurrences. In the present review, we aim to discuss the predominance of sleep-related epilepsy during NREM, established familial links to the pathogenesis of SHE, BECTS and PS, and highlight the present available pharmacotherapy options.


Epilepsy is characterized by frequent and unpredictable disruptions of brain functions resulting in “epileptic seizures.” Epilepsy has a great impact on the quality of life through increased incidence of injury and death, unemployment rates, lower monthly incomes, higher household costs and high absenteeism at work and schools (Jennum et al., 2017Trinka et al., 2018Wibecan et al., 2018). An epileptic seizure is considered as a transient episode of signs or symptoms, including transitory confusion, staring speech, irrepressible jerking movements, loss of consciousness, psychic symptoms such as fear and anxiety, due to the abnormal synchronous neuronal activity of the brain. The International League Against Epilepsy (ILAE) published a recent clinical definition of epilepsy in which a patient with any of the following conditions is considered to be an epileptic i.e., (i) two or more unprovoked seizures within more than 24 h apart; (ii) one unprovoked seizure and a probability of further seizures similar to the general recurrence risk, occurring over the next 10 years; (iii) definite diagnosis of an epilepsy syndrome (Fisher et al., 2014). Genesis of epilepsy is attributed to various predispositions that include neurological, perceptive, psychological, and social factors, which could either stimulate or worsen the syndrome. In early 2017, the point prevalence of active epilepsy was found to be 6.38/1,000 individuals, while the lifetime prevalence was 7.60/1,000 persons. Meanwhile, the annual cumulative incidence of epilepsy was 67.77/100,000 persons and the incidence rate was 61.44/100,000 person-years. The active annual prevalence, prevalence during lifetime and the incidence of epilepsy were found to be higher in the developing countries (Fiest et al., 2017).

A systematic review revealed that epilepsies of unknown etiology had the highest prevalence compared to the epilepsies of known origin (Fiest et al., 2017). These were due to known underlying factors that cause seizures such as brain damage (Sizemore et al., 2018), metabolic diseases (Tumiene et al., 2018), infections (Bartolini et al., 2018), hemorrhagic stroke (Zhao et al., 2018), and gene mutations (Leonardi et al., 2018). These precipitating factors tilt the balance between excitatory and inhibitory neurotransmissions which has been established in different types of epilepsy. Physical and psychological comorbidities are usually accompanied with epilepsy, such as depression (Jamal-Omidi et al., 2018), sleep disorders (Castro et al., 2018), and body injuries (Mahler et al., 2018). Advanced cases may suffer from memory loss (Reyes et al., 2018), behavioral disorders (Jalihal et al., 2018), and disturbance of autonomic functions (Fialho et al., 2018). The rate of sudden death in epileptic patients was reported to be three times higher than non-epileptic individuals (Kothare and Trevathan, 2018Pati et al., 2018).

Sleep deprivation is very common among the epileptic patients and lack of sleep could worsen the seizure expressions (Neto et al., 2016). In animal models, sleep deprivation was shown to heighten the propensity to seizures (McDermott et al., 2003). Sleep deprivation has been correlated with decline in various aspects of brain functional connectivity (Nilsonne et al., 2017). Generally, sleep deprivation is secondary to other factors such as illness, emotional or psychological stress, and alcohol use. Hence, lack of sleep alone may not be sufficient to cause seizures (Razavi and Fisher, 2017). A large body of literature on the effects of epilepsy on sleep and/or sleep-deprivation on the epileptic state has been collated (St Louis, 2011Unterberger et al., 2015).

Sleep-related epilepsy represents nocturnal seizures that manifest solely during the sleep state (Tchopev et al., 2018). Approximately 12% epileptic patients are affected by sleep-related epilepsy with the majority suffering from focal epilepsy (Derry and Duncan, 2013Losurdo et al., 2014). In a recent case report, focal epilepsies were anatomically linked to epileptogenic origins at the right frontal lobe, using white matter tractography MRI (Tchopev et al., 2018). In a separate study, ambulatory electroencephalogram (EEG) measurement in outpatient setting reported frontal lobe seizures to manifest more readily between 12 a.m. and 12 p.m., particularly around 6:30 a.m., whereas temporal lobe seizures expressed more frequently between 12 p.m. and 12 a.m., specifically around 8:50 p.m. (Pavlova et al., 2012). In addition to seizure onset, few seizures seem to propagate more readily during sleep, based on anatomical locus. Medial temporal lobe regions were shown more likely to manifest spike production or propagation during NREM sleep stage compared to other brain regions (Lambert et al., 2018). Sleep-related epilepsy is often misdiagnosed as sleep disorders (Tinuper and Bisulli, 2017), especially in cases where the seizures manifest exclusively during sleep. Over the past decade, the discovery of numerous pre-disposing genes and availability of advanced diagnostic tools have shed more light in understanding the nature of sleep-related epilepsy.

In the present review, we discuss sleep-related epilepsy with particular emphasis on three of the most frequently implicated epilepsies during the sleep state which include sleep related hypermotor epilepsy (SHE), benign partial epilepsy with centrotemporal spikes (BECTS), and Panayiotopoulos Syndrome (PS).[…]


Continue —-> Frontiers | Sleep Related Epilepsy and Pharmacotherapy: An Insight | Pharmacology

Figure 1. Pathogenesis of sleep-related epilepsy. Mutations of genes associated with channelopathy and non-channelopathy origin of sleep related epilepsy could disrupt the balance between inhibitory and excitatory neurotransmissions in central nervous system, leading to manifestation of seizure. Various anti-epileptic drugs alleviate seizure by restoring chemical balance in brain. TPM, topiramate; VPA, valproic acid; CBZ, carbamazepine; OXC, oxcarbazepine; LTC, levetiracetam; LCS, lacosamide.

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[WEB SITE] Driving and Epilepsy: Issues to Discuss With Your Patients

epilepsy, driving

Dr Sanchez is Assistant Professor and Dr Krumholz is Professor Emeritus, Department of Neurology, University of Maryland School of Medicine, Baltimore, MD.

Worldwide there are more than 65 million individuals with epilepsy.1In the US because driving an automobile is such an important aspect of our culture, driving restriction is an enormous problem for many of these individuals and their families. Indeed, surveys find individuals with epilepsy report driving as a major concern.2 Physicians and other medical providers play an important role educating and counseling people with seizures and their families regarding driving. Here, we provide some background and guidance regarding this issue.

Individuals with seizures are restricted from driving because of concerns that a seizure while driving might result in loss of control of the vehicle and a crash, potentially injuring the driver or others, and damaging property. Tragically, such crashes cause fatalities.3 Therefore every state in the US restricts some individuals with epilepsy from driving. Driving restrictions vary by state and are ultimately determined by the Department of Motor Vehicles (DMV).4 Physicians and other medical providers are involved to varying degrees throughout this process of driving regulation and restriction. They serve as advisers to patients, with a duty to inform patients regarding rules and regulations as well as consultants to state regulatory authorities.

To properly counsel patents, it is important that physicians and other medical providers are familiar with the rules governing driving for patients with seizure disorders. Our recommended approach to counseling patients with seizures and epilepsy regarding driving is illustrated in some of the following examples and discussion.

Case example
A 23-year-old woman presents to your office with new-onset seizures. She generally feels well, has no other relevant history, and her examination is normal. Brain MRI with and without contrast and EEG were performed and were normal.

Question: As the medical provider, how would you counsel this patient regarding driving after her first unprovoked seizure (a seizure not related to an acute precipitating cause)?

Answer: She should be informed that a seizure while driving could be dangerous and result in a motor vehicle crash. Since she has had a seizure, she is at risk for further seizures. Regulations exist in an effort to prevent injury, death, or property damage that might result if a seizure were to occur while driving. She should be informed to stop driving and that patients are required by law to report their seizures to the DMV in their state. In some states, physicians and other medical providers are also required to report (Table 1) that a patient has had a seizure.4 The DMV will determine when she may resume driving.

A seizure-free interval is typically necessary for the DMV to approve a person to drive after a first seizure, this too varies by state. The typically required seizure-free interval may be as short as three months to as long as one year.4 There may be positive or negative modifiers that shorten or lengthen the seizure-free interval (Table 2).5 Antiseizure medication (ASM) is not always prescribed after a first seizure; this is a variable that may be considered on a case by case basis.6

After reporting her seizures to the DMV, the patient and the medical provider are required to complete paperwork regarding the condition. A medical advisory board or similar type of state review will consider the case and make recommendations. Then a final decision regarding any driving restrictions will be made by the DMV. Decisions may be appealed by the patient.


via Driving and Epilepsy: Issues to Discuss With Your Patients | Neurology Times

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[WEB SITE] New technique looks inside the brain to understand more about epilepsy

Created:7 September 2018


Dr Simona Balestrini is about to begin a three year project using a pioneering technique to look at the activity of the brain in people with epilepsy. Here she explains what she hopes to achieve in her work with Transcranial Magnetic Stimulation (TMS) used in conjunction with electroencephalography (EEG).

We are at a very exciting time in our research into epilepsy. Genetic sequencing is beginning to generate large amounts of information with the potential to help us understand more about the causes of epilepsy and how we can best treat the condition.

When we sequence a person’s DNA, we look at the three billion letters that are packaged within almost every cell of the body. This can help to clarify whether that person’s epilepsy has a genetic contribution. But to make sense of that information, we also need to use other tools to interpret that information.

Genomics toolkit

TMS is a sophisticated tool that is part of our genomics toolkit. It is a means of looking inside a person’s brain without using needles or electrodes and can be used to interpret information gained through genetic sequencing.

TMS uses a strong magnet, similar to the one used in the MRI scanner, to induce very brief electric currents in the brain. We can measure the response of cortical circuits in the brain  to TMS and generate a direct profile of brain activity and function.

Put simply, TMS can establish a link between brain activity and different types of sensory, motor and cognitive functions. We can then establish whether a specific genetic change is impacting on the function of the brain.

How our muscles react

For some time we have been looking at the brain using TMS together with electromyogram (EMG). This allows us to measure electrical activity of muscles and their reaction time. But this technique has only allowed us to look at the motor cortex in the brain.

Now with TMS-EEG ( we are able to look at brain activity across the whole of the cortical part of the brain. It can extend the area of the brain that is being investigated, guiding and monitoring potential treatment options.

By repeating the test over a period of time, TMS can be used to show the course of epilepsy in the brain and whether different medications lead to an improvement or a decline in the condition.

Individual drug response

It is hoped that in the future TMS will be used to predict the way a person will respond to individual anti-epileptic medications. We also hope that it may help us to predict outcome in epilepsy, including the risk of SUDEP (Sudden Unexpected Death in Epilepsy).

I am really excited about this project. I feel it will help us to gain a greater understanding of the causes of epilepsy and translate clinical research into clinical care. I really hope to make a difference to the lives of the people I see in clinic every day. If we can improve seizure control for people, we can improve their quality of life.

Epilepsy Society is the best example of transformational research being translated into care for people with epilepsy.

Find out more

TMS used to measure motor cortex excitability in alternating hemiplegia.

Long-interval intracortical inhibition as biomarker for epilepsy: A transcranial magnetic stimulation study


Author: Nicola Swanborough

via New technique looks inside the brain to understand more about epilepsy

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[REVIEW] Summary of Antiepileptic Drugs Available in the United States of America – AMERICAN EPILEPSY SOCIETY

The current review summarizes the
main antiepileptic drugs available for
prescription in the United States as of
July 2018. One condensed, and one
expanded, table of the major properties
of 28 AEDs are presented both
to assist clinicians in providing care to
persons with epilepsy and to facilitate
the training of those in health care
educational programs.

This table is not intended to constitute
recommendations, only to provide an
easy reference listing of products on
the market.

Download Table (PDF)

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[WEB SITE] Electronic device implanted in the brain could stop seizures – University of Cambridge

Green arrow points to the implant in the hippocampus of a mouse brain
Credit: Christopher Proctor

Researchers have successfully demonstrated how an electronic device implanted directly into the brain can detect, stop and even prevent epileptic seizures.

These thin, organic films do minimal damage in the brain, and their electrical properties are well-suited for these types of applications.

George Malliaras

The researchers, from the University of Cambridge, the École Nationale Supérieure des Mines and INSERM in France, implanted the device into the brains of mice, and when the first signals of a seizure were detected, delivered a native brain chemical which stopped the seizure from progressing. The results, reported in the journal Science Advances, could also be applied to other conditions including brain tumours and Parkinson’s disease.

The work represents another advance in the development of soft, flexible electronics that interface well with human tissue. “These thin, organic films do minimal damage in the brain, and their electrical properties are well-suited for these types of applications,” said Professor George Malliaras, the Prince Philip Professor of Technology in Cambridge’s Department of Engineering, who led the research.

While there are many different types of seizures, in most patients with epilepsy, neurons in the brain start firing and signal to neighbouring neurons to fire as well, in a snowball effect that can affect consciousness or motor control. Epilepsy is most commonly treated with anti-epileptic drugs, but these drugs often have serious side effects and they do not prevent seizures in three out of 10 patients.

In the current work, the researchers used a neurotransmitter which acts as the ‘brake’ at the source of the seizure, essentially signalling to the neurons to stop firing and end the seizure. The drug is delivered to the affected region of the brain by a neural probe incorporating a tiny ion pump and electrodes to monitor neural activity.

When the neural signal of a seizure is detected by the electrodes, the ion pump is activated, creating an electric field that moves the drug across an ion exchange membrane and out of the device, a process known as electrophoresis. The amount of drug can be controlled by tuning the strength of the electric field.

“In addition to being able to control exactly when and how much drug is delivered, what is special about this approach is that the drugs come out of the device without any solvent,” said lead author Dr Christopher Proctor, a postdoctoral researcher in the Department of Engineering. “This prevents damage to the surrounding tissue and allows the drugs to interact with the cells immediately outside the device.”

The researchers found that seizures could be prevented with relatively small doses of drug representing less than 1% of the total amount of drug loaded into the device. This means the device should be able to operate for extended periods without needing to be refilled. They also found evidence that the delivered drug, which was in fact a neurotransmitter that is native to the body, was taken up by natural processes in the brain within minutes which, the researchers say, should help reduce side effects from the treatment.

Although early results are promising, the potential treatment would not be available for humans for several years. The researchers next plan to study the longer-term effects of the device in mice.

Malliaras is establishing a new facility at Cambridge which will be able to prototype these specialised devices, which could be used for a range of conditions. Although the device was tested in an animal model of epilepsy, the same technology could potentially be used for other neurological conditions, including the treatment of brain tumours and Parkinson’s disease.

The research was funded by the European Union.

Christopher M. Proctor et al. ‘Electrophoretic drug delivery for seizure control.’ Science Advances (2018). DOI: 10.1126/sciadv.aau1291


Researcher profile: Dr Christopher Proctor

Dr Christopher Proctor is one of the first nine recipients of the Borysiewicz Biomedical Sciences Fellowship programme.

My research sets out to develop medical devices to treat and diagnose various health problems that have been difficult to address with conventional approaches such as epilepsy, Parkinson’s disease and brain tumours. As an engineer with expertise in electronics and materials, I work closely with biologists and clinicians in all stages of device development from early stage designing to late-stage testing.

The most exciting day I’ve had in research so far was when a concept that I took from a drawing on paper to a real device that I could hold in my hand, prevented a seizure for the third time. I say the third time because I am forever a sceptic, so I was hesitant to believe our initial results until we repeated it a couple times. Having seen that it was a repeatable result was very exciting because that is when you know you may really be on to something special.

I hope my research will ultimately lead to a better quality of life for people with health problems. I believe we are only scraping the surface of what is possible when we pair electronic devices with biology. It is difficult to project where early-stage research will go, but I suspect the way we address some of the most difficult to treat diseases may be radically different in the coming decades.

Cambridge is a great place to research and develop medical devices because this type of work is truly a team effort that requires expertise in everything from engineering to chemistry to medicine up to government regulations, finance and marketing. There is an ecosystem in and around the University of Cambridge that can bring all these experts together and that is exactly what is needed to take an early stage technology all the way to the patients that we are trying to help.


via Electronic device implanted in the brain could stop seizures | University of Cambridge

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[Abstract] Dead in the water: Epilepsy‐related drowning or sudden unexpected death in epilepsy?



Both drowning and sudden unexpected death in epilepsy (SUDEP) are diagnoses of exclusion with predominantly nonspecific autopsy findings. We hypothesized that people with epilepsy found dead in water with no clear sign of submersion could be misdiagnosed as SUDEP.


All reported seizure‐related deaths undergoing medicolegal investigation in three medical examiner’s offices (New York City, Maryland, San Diego County) over different time periods were reviewed to identify epilepsy‐related drownings and SUDEPs. Drowning cases that fulfilled inclusion criteria were divided into two groups according to the circumstances of death: definite drowning and possible drowning. The SUDEP group included two sex‐ and age (±2 years)‐matched definite SUDEP/definite SUDEP plus cases for each drowning case.


Of 1346 deaths reviewed, we identified 36 definite (76.6%) and 11 possible drowning deaths (23.4%), most of which occurred in a bathtub (72.3%). There were drowning‐related findings, including fluid within the sphenoid sinuses, foam in the airways, clear fluid in the stomach content, and lung hyperinflation in 58.3% (21/36) of the definite drowning group, 45.5% (5/11) of the possible drowning group, and 4.3% of the SUDEP group (4/92). There was no difference in the presence of pulmonary edema/congestion between the definite drowning group, possible drowning group, and SUDEP group. The definite drowning group had a higher mean combined lung weight than the SUDEP group, but there was no difference in mean lung weights between the possible drowning and SUDEP groups or between the possible drowning and definite drowning groups.


No distinguishable autopsy finding could be found between SUDEPs and epilepsy‐related drownings when there were no drowning‐related signs and no clear evidence of submersion. SUDEP could be the cause of death in such possible drowning cases. As most drowning cases occurred in the bathtub, supervision and specific bathing precautions could be effective prevention strategies.


via Dead in the water: Epilepsy‐related drowning or sudden unexpected death in epilepsy? – Cihan – – Epilepsia – Wiley Online Library



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[Abstract] The use of antidepressant drugs in pregnant women with epilepsy: A study from the Australian Pregnancy Register



To study interactions between first‐trimester exposure to antidepressant drugs (ADDs) and antiepileptic drugs (AEDs), and a history of clinical depression and/or anxiety, on pregnancy outcomes and seizure control in pregnant women with epilepsy (WWE).


We examined data from the Australian Pregnancy Register of Antiepileptic Drugs in Pregnancy, collected from 1999 to 2016. The register is an observational, prospective database, from which this study retrospectively analyzed a cohort. Among the AED‐exposed outcomes, comparisons were made among 3 exposure groups: (1) pregnancy outcomes with first‐trimester exposure to ADDs; (2) outcomes with mothers diagnosed with depression and/or anxiety but who were not medicated with an ADD; and (3) those with mothers who were not diagnosed with depression and/or anxiety and were not medicating with ADD. Prevalence data was analyzed using Fisher’s exact test.


A total of 2124 pregnancy outcomes were included in the analysis; 1954 outcomes were exposed to AEDs in utero, whereas 170 were unexposed. Within the group of WWE taking AEDs, there was no significant difference in the prevalence of malformations in infants who were additionally exposed to ADDs (10.2%, 95% confidence interval [CI] 3.9‐16.6), compared to individuals in the non–ADD‐medicated depression and/or anxiety group (7.7%, 95% CI 1.2‐14.2), or those without depression or anxiety (6.9%, 95% CI 5.7‐8.1; = 0.45). The malformation rates in pregnancy outcomes unexposed to AEDs were also similar in the above groups (= 0.27). In WWE medicated with AEDs and ADDs, the frequency of convulsive seizures (= 0.78), or nonconvulsive seizures (= 0.45) throughout pregnancy, did not differ across comparative groups.


Co‐medicating with ADDs in WWE taking AEDs does not appear to confer a significant added teratogenic risk, and it does not affect seizure control.


via The use of antidepressant drugs in pregnant women with epilepsy: A study from the Australian Pregnancy Register – Sivathamboo – – Epilepsia – Wiley Online Library

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