CURE Epilepsy Update June 2023

Greetings Epilepsy Community,

Summer is here and brings many things to appreciate and enjoy. The weather is warmer, students are completing their school year, graduation ceremonies are taking place, and many CURE Epilepsy Champions hold their events. These Champions are working on events across the United States, rallying their professional networks, friends, family members, and local businesses to help increase epilepsy awareness and raise money for critical epilepsy research. In honor of CURE Epilepsy’s 25th anniversary, we have created the 2023 Champion Challenge, where we are challenging our existing and new Champions to raise a total of $425,000 this year. We are currently at just over $270,000 (well over halfway to our goal)!

I am honored to lead an organization that has so many dedicated community members who are focused on making our goal of a world without epilepsy a reality. We’ve already seen some creative CURE Epilepsy Champion events this year including a 40-mile bike tour, partnering with a local Massachusetts brewery for a month, the second annual Mansfield Walk to CURE Epilepsy (focused on SUDEP awareness), EpiPalooza (a multi-concert performance focused on epilepsy awareness), and the 10th annual 5K Strides for Epilepsy in Maryland (the longest running CURE Epilepsy Champion event)! Coming up this summer we still have plenty of Champion events including the annual Ella’s Race in Illinois, an EpiPalooza concert in North Carolina, and more. If you are interested in hosting a Champion event of your own, you can learn more about how to do so here.

With a commitment to inspire hope and deliver impact.

In this CURE Epilepsy Update, please find information on:

Watch the Recording of Our Webinar: Mental Health and Childhood Epilepsy

Watch the recording or access the transcript for our latest webinar, Mental Health and Childhood Epilepsy. Epilepsy is not a mental health disorder, but epilepsy or epilepsy medications can impact an individual’s mental health. It is important for medical professionals and caregivers to address these concerns quickly. This webinar with Dr. Clemente Vega covers the prevalence of mental health conditions in children with epilepsy, risk factors, resources, and more.




Epilepsy Awareness Night at Chicago White Sox Game

Join the CURE Epilepsy community for a very special night at the ballpark: Epilepsy Awareness Night with the Chicago White Sox on Saturday, September 2! Come celebrate CURE Epilepsy’s 25th Anniversary with a specially discounted ticket offer, plus, $5 of each ticket purchased for our selected sections will go towards epilepsy research. See the White Sox in a matchup against the Detroit Tigers, sit with other community members, and raise money for epilepsy!




New Epilepsy Surgery Resource

Surgery may help cure or significantly reduce the incidence of seizures. To help individuals learn about surgical options and what epilepsies they work for best, CURE Epilepsy has created the Epilepsy Surgery section of our Understanding Epilepsy resource.


Explore Resource



CURE Epilepsy CARES Comes to Seattle

CURE Epilepsy CARES (Conversations About Research in Epilepsy & Seizures) is a free, educational event for patients, families, medical professionals, researchers, and all those touched by or interested in learning more about epilepsy. Join us in Seattle on Saturday, June 10 as clinicians answer your questions about cutting-edge research and epilepsy treatments.




Join Team CURE Epilepsy for the Marine Corps Marathon (MCM)

Join us on October 29 in Washington DC for the 2023 Marine Corps Marathon (MCM). CURE Epilepsy is proud to be a new partner of this annual marathon. You can join fellow Team CURE Epilepsy runners in our nation’s capital as we raise critical funds and awareness in our efforts to find a cure for epilepsy, by promoting and funding patient-focused research.




CURE Epilepsy Discovery: Strides Made in the Understanding of Acquired Epilepsies by CURE Epilepsy Grantees


An acquired epilepsy can occur as a result of brain infection, tumor, or injury leading to spontaneous seizures. CURE Epilepsy grantees, Dr. Annamaria Vezzani and Dr. Teresa Ravizza, study neuroinflammation and the underlying mechanisms that may contribute to epileptogenesis. Their work is instrumental not only to understanding why and how the brain generates and sustains seizures, but also to discovering biomarkers that could predict if someone will have seizures. The ultimate hope is that the work of Drs. Vezzani and Ravizza will lead to the ability to prevent or cure acquired epilepsies.

Explore Discovery


What’s New from the Seizing Life® Podcast

A Daughter’s Diagnosis Inspires Concerts for Epilepsy


Matt Perrone shares his epilepsy onset and treatment journey, the impacts of seizures and medication on his mental health, and how his daughter’s diagnosis at the age of four spurred him to create EpiPalooza, a multi-band concert aimed at raising awareness and funds for epilepsy research.

Watch or Listen



Epilepsy Researcher Compounds Lab Work with Fundraising


Dr. Patrice Jackson-Ayotunde, an organic chemist and Associate Professor of Pharmaceutical Sciences at the University of Maryland Eastern Shore (UMES), explains why bringing new epilepsy drugs to market can take 15 to 20 years and tells us about the UMES 5K Strides for Epilepsy fundraiser that she and her students have been running for the past 10 years.

Watch or Listen


Watch these and all of our upcoming Seizing Life episodes here.

The CURE Epilepsy Store


Start summer off right with apparel or accessories to spread epilepsy awareness and help support funding research to find a cure!




Please mark your calendar for the following key dates in the epilepsy community:

  • January 1 – December 31, 2023 – CURE Epilepsy’s 25th Anniversary
  • October 18 – SUDEP Action Day
  • October 31- November 1 – Epilepsy Awareness Day at Disneyland
  • November – Epilepsy Awareness Month
  • December 1-7 – Infantile Spasms Awareness Week


1 in 26 individuals will be impacted by epilepsy in their lifetime.
Each person has their own story.

Read Marc’s Story


Does ASM Polypharmacy Impact Injury Risk Among Older Adults With Epilepsy? 

Article published by Neurology Advisor


Most older adults with seizures receive an appropriate first prescription for antiseizure medication (ASM), and the risk for injury is associated with ASM polypharmacy. These are the findings of a retrospective cohort study published in Seizure: European Journal of Epilepsy. 


The prevalence of seizures roughly doubles between the ages of 50 and 80 years. More than 95% of patients with epilepsy are treated with ASMs as they are effective at preventing recurrent seizures; however, older adults may be vulnerable to the side effects of ASMs. 


Researchers from Icahn School of Medicine at Mount Sinai in the United States sourced data for this study from the MarketScan’s Commercial and Medicare Database. Adults (N=5,931) aged 50 years and older with newly diagnosed epilepsy or convulsion between 2015 and 2016, who received a minimum 30-day supply of ASMs within 1-year of diagnosis, were evaluated for injury within 1-year of ASM prescription. 


The exposure of interest was whether patients received guideline recommended (eg, gabapentin, lamotrigine, levetiracetam, zonisamide), neutral (brivaracetam, carbamazepine, eslicarbazepine acetate, pregabalin, lacosamide, oxcarbazepine, topiramate, valproic acid), not recommended (cannabidiol, felbamate, phenobarbital, phenytoin, primidone, rufinamide, vigabatrin), or benzodiazepine ASMs. 


Efforts to improve prescribing in older adults with epilepsy should consider both avoidance of potentially inappropriate therapies as well as avoidance of polytherapy.

New Clues Emerge About Possible Factors Behind Sudden Infant Death Syndrome

Article published by NBC

A new study finds that some infants who die of SIDS have abnormalities in a particular brain receptor that may be involved in helping them gasp for air.

Sudden infant death syndrome, the unforeseen and unexplained death of a baby younger than one year old, is by definition a mystery. But researchers are getting closer to understanding some of the risk factors and mechanisms that contribute to SIDS.

The prevailing theory points to three possible factors: First, the infant is at a critical stage of development during the first year of life. Second, the baby is exposed to a stressor, such as sleeping face down, which can lower the amount of oxygen in their blood while raising the level of carbon dioxide. And third, the infant has an underlying abnormality that makes it harder to survive that traumatic event.

A study published Thursday in the Journal of Neuropathology & Experimental Neurology points to one such abnormality.

Researchers from Boston Children’s Hospital and Rady Children’s Hospital in San Diego found that a particular brain receptor likely involved in helping babies gasp for air was altered in some infants who died of SIDS. The receptor in question is part of the serotonin system, which plays an important role in regulating involuntary body functions like heart rate, breathing and blood pressure.

SIDS usually happens during an infant’s sleep, and though it’s rare, it’s the leading cause of death among babies between one month and one year old in the U.S. The Centers for Disease Control and Prevention attributed nearly 1,400 infant deaths to SIDS in 2020.

To better understand the condition, the researchers behind the new study examined brain tissue from 58 infants who died of SIDS between 2004 and 2011, then compared those samples to the brain tissue of 12 infants who died of other causes, such as pneumonia or heart disease. The results showed that the babies who’d died of SIDS were more likely to have an altered version of the serotonin-related brain receptor than the control cases.

Seizures in Protracted CLN3 Disease Start Later, Delaying Diagnosis: Study 

Article published by Batten Disease

In rare cases, people with juvenile Batten disease may go years or even decades without developing seizures after the onset of vision problems, a new study highlights.

Findings suggest that diagnostic delays are common for this rare form of the disease, so researchers urge clinicians to consider it as a potential diagnosis for patients who develop vision problems in childhood and seizures in adolescence or adulthood.

The study, “Recognition and epileptology of protracted CLN3 disease,” was published in Epilepsia.

The most common form of Batten disease, juvenile Batten is a rapidly progressive disease caused by mutations in the CLN3 gene. Also called CLN3 disease, it is characterized by symptoms such as vision loss during childhood and seizures that typically start two to four years thereafter.

Early in the disease course, patients also develop neurological problems, such as cognitive impairments and movement issues, which progress rapidly. Most do not live beyond age 20.

In rarer cases, however, “seizures and other neurological manifestations do not typically develop until the third decade of life or later,” the researchers wrote, adding that the life expectancy of this milder form, referred to as protracted CLN3 disease, “is longer than that of classic CLN3 disease.”

To date, only a few dozen cases of protracted CLN3 disease have been documented.

Now, scientists in Australia have described the clinical and genetic features of 10 people (five men and five women) with protracted CLN3 disease. Patients were part of six unrelated families; there were three pairs of siblings and one pair of twins.

Sudden Unexpected Death in Epilepsy During Cenobamate Clinical Development

Abstract found on PubMed

Objective: We assessed mortality, sudden unexpected death in epilepsy (SUDEP), and standardized mortality ratio (SMR) among adults treated with cenobamate during the cenobamate clinical development program.

Methods: We retrospectively analyzed deaths among all adults with uncontrolled focal (focal to bilateral tonic-clonic [FBTC], focal impaired awareness, focal aware) or primary generalized tonic-clonic (PGTC) seizures who received ?1 dose of adjunctive cenobamate in completed and ongoing phase 2 and 3 clinical studies. In patients with focal seizures from completed studies, median baseline seizure frequencies ranged from 2.8 to 11 seizures per 28 days and median epilepsy duration ranged from 20 to 24 years. Total person-years included all days a patient received cenobamate during completed studies or up to June 1, 2022 for ongoing studies. All deaths were evaluated by two epileptologists. All-cause mortality and SUDEP rates were expressed per 1000 person-years.

Results: A total of 2132 patients (n=2018 focal epilepsy; n=114 idiopathic generalized epilepsy) were exposed to cenobamate for 5693 person-years. Approximately 60% of patients with focal seizures and all patients in the PGTC study had tonic-clonic seizures. A total of 23 deaths occurred (all in patients with focal epilepsy), for an all-cause mortality rate of 4.0 per 1000 person-years. Five cases of definite or probable SUDEP were identified, for a rate of 0.88 per 1000 person-years. Of the 23 overall deaths, 22 patients (96%) had FBTC seizures, and all 5 of the SUDEP patients had a history of FBTC seizures. The duration of exposure to cenobamate for patients with SUDEP ranged from 130-620 days. The SMR among cenobamate-treated patients in completed studies (5515 person-years of follow-up) was 1.32 (95% CI 0.84-2.0), which was not significantly different from the general population.

Significance: These data suggest that effective long-term medical treatment with cenobamate may reduce excess mortality associated with epilepsy.

CURE Epilepsy Discovery: Strides Made in the Understanding of Acquired Epilepsies by CURE Epilepsy Grantees

Key Points:

  • An acquired epilepsy can occur as a result of brain infection, tumor, or injury leading to spontaneous seizures.
  • Little is known about the mechanisms underlying epileptogenesis, the process by which the brain starts generating seizures following an insult or injury.
  • CURE Epilepsy grantee Dr. Annamaria Vezzani at the Mario Negri Institute for Pharmacological Research in Milan has made strides understanding the process of neuroinflammation as it relates to epileptogenesis in acquired epilepsy.
  • Her work on a molecule known as High Mobility Group Box 1 (HMGB1) gives clues as to a potential blood-based biomarker of epileptogenesis and pharmacoresistance (failure to respond to at least two anti-seizure medications (ASMs)).
  • Vezzani’s mentee and continued colleague, Dr. Teresa Ravizza, has also been funded by CURE Epilepsy and continues to drive research to understand the biological mechanisms of acquired epilepsy.


Deep Dive

Epilepsy (also referred to as a “seizure disorder”) is a group of conditions characterized by recurrent seizures. Epilepsy can be the result of many different underlying causes including through “acquired” physical injury, infection, brain tumor, or stroke.[1] In acquired epilepsy, spontaneous seizures start after the injury or insult to the brain has occurred. The process by which the brain starts generating seizures after a brain injury or insult is called epileptogenesis. Currently, there is no way to predict who will experience epileptogenesis, and there are no treatments that can prevent or halt epileptogenesis. If there was a way to know that epileptogenesis is taking place or predict who is at risk for it, it might be possible to gain valuable insights into treating and even preventing seizures.

CURE Epilepsy has awarded numerous grants to investigators examining diverse aspects of acquired epilepsies. A few examples of discoveries funded by CURE Epilepsy include Dr. Bruce Gluckman and Dr. Steven Schiff’s development of preclinical models to predict acquired epilepsy following a brain infection, Dr. Gerben van Hameren’s work looking at a particular part of the cell called the mitochondria as a target for post-traumatic epilepsy (PTE), and Dr. Asla Pitkanen’s work that aims to study changes in gene expression in brain tissue in a preclinical model of traumatic brain injury (TBI).

A subset of acquired epilepsies is called PTE, which develops in the months or years following a TBI.[2] TBI may be caused by blows to the head, blasts, penetrating head injuries, accidental falls, sports-related injuries, or motor vehicle accidents. It is currently not possible to predict who will develop PTE after a TBI.[3] Dr. Annamaria Vezzani, head of the Laboratory of Epilepsy and Therapeutic Strategies, Department of Acute Brain Injury at the Mario Negri Institute for Pharmacological Research in Milan, has been an important part of CURE Epilepsy’s efforts to understand acquired epilepsies for decades as an early (2002) and repeat (2015) grantee, and more recently, as part of the PTE Initiative. Dr. Vezzani’s work centers on the role of inflammation in epilepsy. Her work looks at neuroinflammation (i.e., the inflammatory response that is sustained by cells in the brain after insult or injury) and has shown that neuroinflammation can play an important role in the generation of seizures.[4] Through a study funded by CURE Epilepsy, Dr. Vezzani first studied a specific signaling pathway in the brain called interleukin-1 (IL-1) type 1 receptor/Toll-like receptor (IL-1R/TLR4). Her experiments in experimental animals showed that IL-1beta and an inflammatory molecule known as High Mobility Group Box 1 (HMGB1) are released from specific brain cells known as “glia” during seizures.[5] The levels of HMGB1 increased in the brain and the blood before animals developed epilepsy, and this increase in HMGB1 levels was maintained during the development of epilepsy.[6,7] These results gave her precise biological mechanisms that could be targeted to stop seizures.

In addition to showing that HMGB1 is closely involved with seizures, Dr. Vezzani’s work also showed that during an injury or seizures, HMGB1 moves from the nucleus to the cytoplasm of a cell, and this form of HMGB1 can also be measured in blood.[5,8,9,10] More specifically, Dr. Vezzani showed that there is a form of HMGB1 (the disulfide isoform of HMGB1) that contributes to seizures [11]; this finding may inform development of targeted therapeutic strategies. What makes this discovery on HMGB1 particularly exciting for the epilepsy community is its numerous applications: this work could lead to the development of novel drugs to target and halt epileptogenesis, and could also be a way to stop seizures once they have started. As a biomarker, increased levels of HMGB1 could be a sign that epilepsy is about to develop.[10,11] Dr. Vezzani’s work also found that a combination of anti-oxidant drugs that are already used in medical practice is capable of preventing the increase in HMGB1 and delaying the onset of seizures, as well as reducing seizure burden and the memory impairments that are seen in epilepsy.[7]

The role of HMGB1 has also been studied in people with epilepsy. Patients with epilepsy whose seizures were not adequately controlled by ASMs were found to have higher levels of HMGB1 when compared to those who responded to ASMs, and people who did not have epilepsy. Therefore, this work is evidence that HMGB1 can distinguish, with a high level of accuracy, those who respond to ASMs versus those who do not. This adds to the evidence that suggests that HMGB1 can be used as a biomarker for predicting how someone will respond to ASMs.[12] Dr. Vezzani’s more recent CURE Epilepsy-funded work looks at HMGB1 as a target and a mechanistic biomarker of epileptogenesis. HMGB1 is also being studied in people who have experienced TBI as a part of CURE Epilepsy’s PTE Initiative, which funded a diverse group of researchers, including Dr. Vezzani, to develop experimental models to study PTE and discover prediction methods to enable early intervention and eventual prevention.

In addition to her impact and contribution to epilepsy research, Dr. Vezzani is also passionate about mentorship and has guided many mentees who are now established epilepsy researchers in their own right. One of her mentees, Dr. Teresa Ravizza, also at the Mario Negri Institute for Pharmacological Research, received a Taking Flight Award from CURE Epilepsy in 2011. As part of her project, Dr. Ravizza focused on specific cells in the brain known as “astrocytes” and the role of these cells in acquired epilepsies.[13] She also looked at the mechanisms that may contribute to the breakdown of the blood-brain barrier, a network of cells that keep harmful substances from reaching the brain, as previous studies had shown that activation of inflammatory astrocytes along with a breakdown in the blood-brain barrier leads to the generation and sustaining of seizures.[14] Dr. Ravizza’s work hypothesized that the development of epileptogenesis followed by spontaneous seizures is dependent on the extent, duration, and location of blood-brain barrier breakdown. By using a host of techniques, including visualizing the brain by magnetic resonance imaging (MRI), studying the electrical activity of brain circuits, and looking at the behavior of animals, Dr. Ravizza examined whether blood-brain barrier breakdown and glia activation may predict the development of spontaneous seizures and cognitive deficits. Preliminary data support this hypothesis, suggesting that information obtained from these experiments may one day help predict the trajectory of seizures and serve as an effective therapeutic strategy for acquired epilepsies.

Drs. Vezzani and Ravizza continue their work to study neuroinflammation and the underlying mechanisms that may contribute to epileptogenesis. Their work is instrumental not only to understand why and how the brain generates and sustains seizures, but also to discover biomarkers that could predict if someone will have seizures, or how they may respond to a drug. The ultimate hope is that this work with CURE Epilepsy will lead to the ability to prevent or cure acquired epilepsies.



Literature Cited:

  1. Epilepsy. Available at: Accessed May 2.
  2. Verellen RM, Cavazos JE. Post-traumatic epilepsy: an overview. Therapy. 2010;7:527-531.
  3. Annegers JF, Coan SP. The risks of epilepsy after traumatic brain injury Seizure. 2000 Oct;9:453-457.
  4. Vezzani A, Aronica E, Mazarati A, Pittman QJ. Epilepsy and brain inflammation Exp Neurol. 2013 Jun;244:11-21.
  5. Maroso M, Balosso S, Ravizza T, Liu J, Bianchi ME, Vezzani A. Interleukin-1 type 1 receptor/Toll-like receptor signalling in epilepsy: the importance of IL-1beta and high-mobility group box 1 J Intern Med. 2011 Oct;270:319-326.
  6. Walker LE, Frigerio F, Ravizza T, Ricci E, Tse K, Jenkins RE, et al. Molecular isoforms of high-mobility group box 1 are mechanistic biomarkers for epilepsy J Clin Invest. 2017 Jun 1;127:2118-2132.
  7. Terrone G, Pauletti A, Pascente R, Vezzani A. Preventing epileptogenesis: A realistic goal? Pharmacol Res. 2016 Aug;110:96-100.
  8. Iori V, Maroso M, Rizzi M, Iyer AM, Vertemara R, Carli M, et al. Receptor for Advanced Glycation Endproducts is upregulated in temporal lobe epilepsy and contributes to experimental seizures Neurobiol Dis. 2013 Oct;58:102-114.
  9. Choi J, Min HJ, Shin JS. Increased levels of HMGB1 and pro-inflammatory cytokines in children with febrile seizures J Neuroinflammation. 2011 Oct 11;8:135.
  10. Pauletti A, Terrone G, Shekh-Ahmad T, Salamone A, Ravizza T, Rizzi M, et al. Targeting oxidative stress improves disease outcomes in a rat model of acquired epilepsy Brain. 2019 Jul 1;142:e39.
  11. Ravizza T, Terrone G, Salamone A, Frigerio F, Balosso S, Antoine DJ, et al. High Mobility Group Box 1 is a novel pathogenic factor and a mechanistic biomarker for epilepsy Brain Behav Immun. 2018 Aug;72:14-21.
  12. Walker LE, Sills GJ, Jorgensen A, Alapirtti T, Peltola J, Brodie MJ, et al. High-mobility group box 1 as a predictive biomarker for drug-resistant epilepsy: A proof-of-concept study Epilepsia. 2022 Jan;63:e1-e6.
  13. Vezzani A, Ravizza T, Bedner P, Aronica E, Steinhäuser C, Boison D. Astrocytes in the initiation and progression of epilepsy Nat Rev Neurol. 2022 Dec;18:707-722.
  14. Vila Verde D, de Curtis M, Librizzi L. Seizure-Induced Acute Glial Activation in the in vitro Isolated Guinea Pig Brain Front Neurol. 2021;12:607603.

CBD Use-Related Adverse Events Twice As Common in Patients With Epilepsy 

Article published by Neurology Advisor

Cannabidiol (CBD) use among patients with epilepsy is associated with an elevated risk for adverse events (AEs), including somnolence, decreased appetite, and pyrexia, according to findings from a systematic review and meta-analysis published in JAMA Open Network.

CBD is among a number of naturally occurring compounds, which are termed cannabinoids and are produced by the cannabis plant. CBD has been approved by the US Food and Drug Administration and the European Medicines Agency as an additional treatment for severe types of epilepsy, including Lennox-Gastaut syndrome (LGS) and Dravet syndrome (DS).

For the study, researchers assessed the frequency of and risk for AEs related to CBD use among individuals with epilepsy. They searched databases, including PubMed, Scopus, Web of Science, and Google Scholar for articles that reported at least 1 AE after CBD use among patients with epilepsy from database inception up to August 4, 2022.

Future research needs to investigate the therapeutic effects of CBD and AEs in the presence of various dosages of other antiepileptic dugs in order to achieve a safe and effective dose for treatment-resistant patients with epilepsy.

For Epilepsy Sufferers, Cutting-Edge Technology Offers Early Alerts Of Seizures 

Article published by Science Blog

People with epilepsy could soon get a one-minute warning of an impending seizure with the help of a new medical device.

An epileptic seizure can put a person at risk of injury in everyday situations that most other people take for granted. Often this leads sufferers to avoid common activities such as cycling, swimming or walking up steep inclines.

But wearers of the new device can be reassured that they will get an alert before the onset of a seizure and take necessary precautions. Dr David Blánquez, an engineer, was inspired to invent the earpiece for very personal reasons.

‘We started this project because of my daughter Marina, who has epilepsy,’ Blánquez said.

He had been a robotics researcher but saw the need for people like his daughter to wear a device that could warn them about an approaching convulsion.

The earpiece signals an app on the patient’s mobile phone that a seizure is likely. A family member or caregiver can also be alerted.

The device constantly monitors brain activity using an electroencephalogram, logging key medical information and building up an algorithm that over time gets better at spotting the signs of an impending seizure.

Multimodal Nocturnal Seizure Detection in Children with Epilepsy: A Prospective, Multicenter, Long-Term, In-Home Trial

Abstract found on Wiley Online Library

Objective: There is a pressing need for reliable automated seizure detection in epilepsy care. Performance evidence on ambulatory non-EEG-based seizure detection devices is low and evidence on their effect on caregiver’s stress, sleep and quality of life (QoL) is still lacking. We aimed to determine the performance of NightWatch, a wearable nocturnal seizure detection device, in children with epilepsy in the family home setting and to assess its impact on caregiver burden.

Methods: We conducted a phase 4, multicenter, prospective, video-controlled, in-home NightWatch implementation study (NCT03909984). We included children aged 4-16 years, with 1 weekly nocturnal major motor seizure, living at home. We compared a two-month baseline period with a two-month NightWatch intervention. The primary outcome was the detection performance of NightWatch for major motor seizures (focal to bilateral or generalized tonic-clonic (TC) seizures, focal to bilateral or generalized tonic seizures lasting >30 seconds, hyperkinetic seizures, and a rest category of focal to bilateral or generalized clonic seizures and ‘TC-like’ seizures). Secondary outcomes included caregivers’ stress (Caregiver Strain Index, CSI), sleep (Pittsburgh Quality of Sleep Index), and quality of life (QoL, EQ-5D-5L).

Results: We included 53 children (55% male, mean age 9.7 ±3.6years, 68% learning disability) and analyzed 2310 nights (28,173 hours), including 552 major motor seizures. Nineteen participants did not experience any episode of interest during the trial. The median detection sensitivity per participant was 100% (range 46–100%), and the median individual false alarm rate was 0.04 per hour (range 0–0.53). Caregiver’s stress decreased significantly (mean total CSI score 8.0 vs. 7.1; p=0.032), while caregiver’s sleep and QoL did not change significantly during the trial.

Significance: The NightWatch system demonstrated high sensitivity for detecting nocturnal major motor seizures in children in a family home setting and reduced caregiver stress.

Soft Robot Brain Implant Designed to Treat Epilepsy 

Article published by Informa


A new small-scale, soft robotic implant has been designed to help treat epilepsy.  


The flexible robot is inserted into a patient’s skull and sits between the skull and the surface of the brain.


Created by a team from Switzerland’s Ecole Polytechnique Fédérale de Lausanne (EPFL), the robot is a tiny, foldable electrode array that can be unfurled once inserted through a hole in a patient’s skull, applying consistent pressure to certain parts of the brain. 


This electrode array stimulates and monitors electrical activity in the brain for patients who suffer from neurological conditions such as epilepsy. 


“Minimally invasive neurotechnologies are essential approaches to offer efficient, patient-tailored therapies,” says Stéphanie Lacour, EPFL’s neurotechnology expert. “We needed to design a miniaturized electrode array capable of folding, passing through a small hole in the skull and then deploying in a flat surface resting over the cortex. We then combined concepts from soft bioelectronics and soft robotics.” 


The first prototype consists of an electrode array that fits through a hole 0.7 inches in diameter but can expand to cover a surface of the brain double the size. 


According to the team, the robot’s folding and expanding capabilities are achieved by the device being turned inside out and then extended once deployed in the brain using a pressurized liquid, a method known as eversion.