Summary: The brain may inadvertently treat seizures as important memories to be saved. A landmark study suggests that after a seizure, the brain enters a state of deep sleep that mimics memory consolidation. This “seizure-related consolidation” strengthens the neural pathways that generate seizures, essentially training the brain to have them more frequently.
This discovery identifies a critical post-seizure window—the hours and nights following an event—where targeted medical intervention could potentially disrupt this harmful “learning” process and stop the progression of epilepsy.
Key Facts
- Involuntary Learning: After a seizure, the brain uses the same biological processes it uses to store memories to instead reinforce seizure networks.
- Intensified Deep Sleep: Recordings from implanted brain devices showed that post-seizure nights are characterized by longer, more intense NREM (deep) sleep, specifically in the regions where seizures start.
- The REM Trade-off: While deep sleep increases, REM sleep (vital for emotional and cognitive health) is significantly reduced after a seizure.
- Disease Progression: This “hijacking” of memory consolidation explains why epilepsy often worsens over time and why memory and mood problems are common comorbidities.
- BIONIC Initiative: The findings support new “closed-loop” brain stimulation therapies that could sense a seizure and intervene during sleep to weaken, rather than strengthen, the seizure network.
Source: Mayo Clinic
The brain may inadvertently “learn” to have seizures by treating them like important memories to be stored, according to new research from Mayo Clinic.
The study, published in the Journal of Neuroscience, found that after a seizure, the brain enters a deep sleep state that mimics memory storage — and that this effect can persist into the following night’s sleep. In effect, this “saves” the seizure’s path like a normal memory, strengthening the disease.
The findings suggest new opportunities to prevent epilepsy from worsening by targeting brain activity during the hours immediately following a seizure and during the subsequent night of sleep — a critical period when harmful brain changes may occur.
“Sleep is one of the brain’s most powerful tools for learning and memory,” says Vaclav Kremen, Ph.D., a neuroscientist and engineer at Mayo Clinic and lead author of the study. “What we’re seeing is that after a seizure, the brain may be engaging the same biological processes used to consolidate memories, but instead reinforcing the networks that generate seizures.”
Epilepsy affects an estimated 50 million people worldwide, and many patients continue to have seizures despite medication. Understanding the relationship between seizures and sleep could help explain why epilepsy can worsen over time and why memory, mood and sleep problems are common in people with the condition.
The study analyzed long-term brain recordings from implanted devices in 11 people with epilepsy. Using these recordings, researchers compared sleep patterns on nights following seizures to nights when no recent seizures occurred.
They found that after a seizure, the brain consistently entered a prolonged and intensified state of deep sleep, known as non-rapid eye movement (NREM) sleep. During this period, slow brain waves became stronger and steeper — key features of memory consolidation — particularly within the specific brain regions where seizures originate.
At the same time, rapid eye movement (REM) sleep, which is important for emotional processing and cognitive health, was reduced. On average, patients slept longer and spent more time in deep sleep after seizures, but they experienced less REM sleep compared with seizure-free nights.
The researchers call this process seizure-related consolidation, a phenomenon in which seizures appear to hijack the brain’s normal learning mechanisms. Rather than helping the brain recover, this post-seizure sleep state may strengthen abnormal neural circuits, creating a vicious cycle in which each seizure increases the likelihood of future seizures.
“Instead of treating seizures as isolated events, this research shows they may actively shape the brain in ways that promote disease progression,” says Dr. Kremen.
Importantly, the findings point to a potential new window for treatment — the hours and nights after a seizure — when targeted intervention could disrupt this harmful learning process.
“If we can safely intervene during this post-seizure window, we may be able to weaken seizure networks rather than reinforce them,” says Gregory Worrell, M.D., Ph.D., a neurologist at Mayo Clinic and senior author of the study.
These insights support Mayo Clinic’s Bioelectronics Neuromodulation Innovation to Cure (BIONIC) initiative, which aims to devise personalized neuromodulation therapies to prevent, treat, and potentially reverse neurological disease.
By combining long-term brain sensing, advanced analytics and an understanding of how the brain adapts after seizures, the study highlights the potential for bioelectronic approaches to promote healthier brain function.
Future research will focus on translating these discoveries into BIONIC-enabled therapies, including adaptive closed-loop brain stimulation systems designed to respond to seizures and sleep states in real time. Mayo Clinic researchers have already begun designing next-generation approaches aimed at breaking this cycle and restoring normal brain activity.
Key Questions Answered:
A: In a biological sense, yes. The brain doesn’t distinguish between a useful skill and a harmful seizure. It sees the intense neural activity of a seizure and, during the following night’s sleep, “saves” that pathway just like it would save a new vocabulary word or a piano piece.
A: It’s not just physical exhaustion. The brain is literally forcing itself into an intensified deep sleep state to “consolidate” the seizure activity. This study shows the brain spends more time in NREM sleep post-seizure, often at the expense of restorative REM sleep.
A: That is the goal. By identifying this post-seizure sleep window, doctors hope to use personalized brain stimulation (neuromodulation) to “scramble” the consolidation process, preventing the seizure network from getting stronger.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- Journal paper reviewed in full.
- Additional context added by our staff.
About this epilepsy and sleep research news
Author: Emily DeBoom
Source: Mayo Clinic
Contact: Emily DeBoom – Mayo Clinic
Image: The image is credited to Neuroscience News
Original Research: Closed access.
“Post-Ictal Sleep Changes in Human Focal Epilepsy” by Vaclav Kremen, Vladimir Sladky, Vaclav Gerla, Yurui Cao, Filip Mivalt, Erik K. St. Louis, Mark R. Bower, Ben Brinkmann, Kai Miller, Jamie VanGompel, Mark Cook, Tim Denison, Kent Leyde and Gregory A. Worrell. Journal of Neuroscience
DOI:10.1523/JNEUROSCI.0303-25.2026
Abstract
Post-Ictal Sleep Changes in Human Focal Epilepsy
Bidirectional interactions between sleep, seizures, and epilepsy remain incompletely understood. Evidence from animal models and people with focal epilepsy suggest that seizures may engage mechanisms of memory consolidation during post-ictal sleep to reinforce and strengthen synaptic connections within the pathological networks that generates seizures, termed seizure-related consolidation (SRC).
Human studies of post-ictal sleep changes supportive of SRC, however, are limited by small sample size and restricted observations of post-ictal sleep. We investigated the interplay between seizures and sleep by analyzing sleep-wake and seizure catalogs derived from continuous local field potential (LFP) recordings in 11 people (6 males and 5 females) with drug-resistant focal epilepsy implanted with novel investigational devices and living in their natural environments.
Our findings demonstrate that post-ictal rapid-eye-movement sleep duration is reduced, whereas slow-wave sleep duration, slow-wave LFP spectral power and waveform slope are increased compared to inter-ictal nights without preceding seizures. The most significant changes localize to the epileptogenic networks generating the participants’ habitual seizures.
These results reveal parallels between SRC and physiological memory consolidation, providing novel insights into the potential role of post-ictal sleep in strengthening epileptic neural engrams, and may have implications for targeted disruption of post-ictal sleep and SRC in focal epilepsy.
