Epilepsy affects about 1 in 26 people at some point in life. About two-thirds achieve seizure control with available medications, but one-third continue having seizures despite trying multiple drugs. Treatment options include more than 25 anti-seizure medications, surgery for drug-resistant cases, and devices like vagus nerve stimulators.
What's actually going on in research
Trials are testing new anti-seizure medications with different mechanisms, gene therapies for specific genetic epilepsies, neuromodulation devices, and cannabinoid-based treatments. Researchers are also studying precision approaches that match treatments to epilepsy type, surgical techniques for drug-resistant epilepsy, and ways to prevent epilepsy after brain injury.
Gene therapy
For rare genetic epilepsies like Dravet syndrome and CDKL5 deficiency, gene therapies aim to replace or silence the faulty gene causing seizures. Early trials show some children having fewer seizures after a one-time treatment.
Responsive neurostimulation
Devices that detect seizure activity and deliver electrical pulses to stop them are becoming more precise. Newer systems can track seizure patterns over years and adjust stimulation automatically.
Cannabinoid medications
Epidiolex, a purified CBD medication, is FDA-approved for certain rare epilepsies. Trials are testing whether it helps other epilepsy types and exploring other cannabinoid compounds.
What to know before you search
Eligibility typically depends on seizure frequency, number of medications already tried, epilepsy type, and whether seizure focus can be located on imaging.
What types of trials are currently open
- Medication trials — Testing new anti-seizure drugs, often as add-on therapy for people whose seizures aren't controlled. These trials measure seizure frequency and side effects over several months.
- Device trials — Studies of neurostimulation devices, responsive systems that detect seizures, or non-invasive brain stimulation methods.
- Gene therapy trials — Testing one-time genetic treatments for specific rare epilepsies caused by single-gene mutations.
- Surgical trials — Comparing surgical approaches for drug-resistant epilepsy, including laser ablation and traditional resection.
- Biomarker studies — Following people with epilepsy to identify genetic markers, brain imaging patterns, or blood tests that predict which treatments will work best.
Recently added Epilepsy trials
Bone Management in Pregnancy Outcomes in Epilepsy
This study is aimed to evaluate the efficacy of bone health management in improving pregnancy outcomes among WWE, and establish evidence-based vitamin D supplementation strategies for childbearing-age WWE.
Links Between Epileptic Activity, Sleep Disruption and Mental Content During Sleep
Interactions between epilepsy and sleep are numerous and bidirectional. Sleep can facilitate epileptic activity and seizures in several syndromes, while sleep deprivation increases cortical excitability and seizure susceptibility. Conversely, sleep disturbances are highly prevalent in patients with epilepsy (PWE). Using simultaneous stereoelectroencephalography (SEEG)-polysomnography, the investigators previously showed that sleep fragmentation in focal drug-resistant epilepsy is associated with both ictal and interictal epileptic activity, with increased interictal epileptiform discharges (IED) immediately before and during arousals. However, causality remains unclear, as sleep instability itself may promote epileptic discharges. Determining whether nocturnal seizures and IED directly induce awakenings is clinically important. Nocturnal epileptic activity is often considered less disabling than daytime seizures and rarely guides treatment decisions, yet demonstrating a direct impact on sleep continuity could support therapeutic strategies specifically targeting nocturnal epileptic activity to improve sleep quality. Beyond sleep continuity, epilepsy may also influence cognitive processes during sleep, including subjective sleep depth and dreaming. While the cognitive consequences of epilepsy during wakefulness are well established, relationships between epileptic activity, sleep architecture and subjective sleep experiences remain poorly understood. In a survey of 300 PWE, the investigators observed altered dream recall frequency and dream content, with seizure-related dreams associated with nocturnal seizures. However, retrospective morning reports cannot establish temporal relationships between epileptic discharges and dream phenomena, nor determine the influence of discharge localization or sleep stage. SEEG combined with direct electrical stimulation (DES) provides a unique framework to address these questions. DES is routinely used during presurgical evaluation to identify epileptogenic and eloquent cortex, but is mainly performed during wakefulness. Yet sleep modifies functional connectivity and facilitates epileptic activity, suggesting that DES during sleep may increase the sensitivity of stimulation-based localization of the seizure-onset zone. The EPIDREAM 3 study will investigate whether DES-induced epileptic activity during sleep provokes arousals, alters dream recall or content, and modifies perceived sleep depth. It will also assess whether sleep-related DES improves delineation of epileptogenic networks, particularly in sleep-related epilepsies. Detailed description: Patients with frontal or temporal drug-resistant focal epilepsy investigated with SEEG as part of presurgical evaluation will be included in the Department of Functional Neurology and Epileptology of the HCL, Lyon. The investigators will use intra-cranial DES performed during the SEEG investigation to explore the impact of focal induced epileptic activity on arousal and dreams. 1. DES will be first performed during wake as part of routine SEEG evaluation with the double purpose of localizing the seizure onset zone and providing a functional mapping. This step identifies channels: (i) in the assumed SOZ, where DES induces after-discharges with/without seizure symptoms; (ii) in the assumed SOZ, where DES induces no after-discharge/seizure but may induce clinical symptoms; (iii) in non-epileptic areas, where stimulation induces neither. For temporal lobe epilepsy, control channels will be selected in the frontal lobe; for frontal lobe epilepsy, in the temporal lobe 2. Stimulations will be repeated in REM and NREM sleep (N2/N3) during the first two sleep cycles of a single night with simultaneous PSG. The investigators will assess for each stimulation: (1) the precise location of the channel (2) the presence and characteristics of an induced after-discharge or seizure (3) presence of a spontaneous arousal (3-15 sec) or awakening (\> 15 sec) (4) presence of objective symptoms (5) in case of awakening: presence of subjective reported symptoms, sleep depth and mind content
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