Vagus Nerve Stimulation for Epilepsy

vagal nerve stimulation regulates physiology

Noninvasive Transcutaneous Vagus Nerve Stimulation for Epilepsy

Epilepsy Reconsidered

Vagus nerve stimulation (VNS) has been used for decades to treat epilepsy, but recent advances mean that effective forms of VNS are now available without the need for surgery. Today, VNS is safer, more accessible, and easier to use than ever before. At the same time, our understanding of epilepsy has advanced, leading to new approaches that can improve seizure control and quality of life. We are entering a new era in epilepsy treatment that offers renewed hope for many people living with seizures.

Allow me to explain. If you live with epilepsy, you may have been told that a seizure is like a “short circuit” in the brain. It’s a convenient analogy, and it captures something real—but it misses the true nature of the condition.

Importantly, epilepsy is much more than a disorder of abnormal electrical activity. Broader physiological processes, including sleep, neuroinflammation, autonomic function, and large-scale brain network dynamics, all shape seizure expression, as demonstrated by a substantial body of research. That perspective tells us that epilepsy is a disorder arising from dysregulated brain and body systems, rather than a purely electrical problem.

Brain connectome

Brain function depends on coordinated activity across complex, interconnected networks. In epilepsy, instability within these systems contributes to seizure vulnerability. This means that seizure occurrence is not determined solely by the presence of abnormal electrical activity, but by how stable and well-regulated the broader system is at any given time.

This leads to a different way of understanding seizures: Seizures are not simply events generated by abnormal activity, but expressions of a system that has lost its stability.

Beyond “Electrical Short Circuits”: Regulation, Sleep, Inflammation, and Seizure Control

There is much more to epilepsy than abnormal electrical activity in the brain. Most certainly the “electrical short circuit” idea is part of the picture, but it is incomplete. If we focus solely on the electrical problem, we miss multiple opportunities to treat epilepsy. That’s why the narrow electrical perspective is clinically limiting.

Epilepsy is also a disorder of regulation. Seizures emerge within a wider physiological context that includes sleep quality, circadian timing, autonomic function, inflammatory signalling, network stability, and the brain’s ability to maintain organised activity under stress. Furthermore, this broader understanding is important because it fits clinical reality. Patients recognise that poor sleep, physiological overload, and instability make seizures more likely. Contemporary research supports that intuition and shows that epilepsy cannot be understood adequately if it is reduced to “electrical short circuits” alone (Bonilla-Jaime et al., 2021). (See the complete reference list at the end of this page.)

Within that broader framework, vagus nerve stimulation (VNS) becomes easier to understand. It is not simply a device that suppresses seizures. It is a neuromodulatory intervention that acts on systems of physiological regulation. VNS influences autonomic function, engages central vagal pathways, modulates neurotransmitter systems, affects large-scale brain networks, and has documented anti-inflammatory benefits. In epilepsy, that matters because seizure control depends not only on reducing abnormal discharges, but also on restoring the stability of the system in which those discharges occur (Krahl, 2012; Krahl & Clark, 2012; Leung, 2017). In this sense, effective treatment is not only about suppressing abnormal activity, but about improving the conditions under which the brain can maintain organised, stable function.

Seizures are a symptom of problems within the brain. If treatment is going to be effective in the long-term, we need to do more than suppress the symptoms; we need to address the underlying causes. And doing so is a complex challenge that requires an expanded perspective on the problem.

Section 1: For Patients, General Readers and Doctors

Understanding epilepsy more fully

For many patients, anti-seizure medication works well. However, around 20–30% of patients develop drug-resistant epilepsy, meaning seizures continue despite appropriate treatment. For these individuals, it is often not enough simply to keep adding medication. A more layered and physiologically informed approach is required (Panebianco et al., 2022).

One of the most important things to understand is that sleep is not a minor issue in epilepsy. It is central. Sleep disturbances are disproportionately common in people with epilepsy, and poor sleep quality is associated with increased seizure frequency, worsening disease course, and reduced quality of life. The scientific literature also makes clear that a substantial proportion of seizures occur during sleep, and that sleep-related mechanisms are relevant to epilepsy-related mortality as well (Bonilla-Jaime et al., 2021).

This is not a controversial or novel idea in the basic sense. Clinicians have long known that sleep deprivation can precipitate seizures. What is newer is the way we now understand this relationship. Sleep disruption is not merely a trigger that sits outside the condition. Sleep participates in the biology of epilepsy itself. The evidence suggests that neuroinflammation may be a key mechanistic link between disordered sleep and worsening epilepsy, helping to explain why unstable sleep can amplify seizure vulnerability and disease progression (Bonilla-Jaime et al., 2021). This is a crucial insight.

What is VNS?

Vagus nerve stimulation is a form of neuromodulation. It works by stimulating the vagus nerve, which is one of the major communication pathways linking the body and the brain. VNS has been an established treatment for drug-resistant epilepsy for many years. Surgically implanted VNS was approved by the FDA in 1997 and remains the only FDA-approved device-based treatment for epilepsy in this category (Krahl, 2012; Krahl & Clark, 2012).

There are two main forms of VNS relevant here. The traditional form is invasive VNS, in which a device is implanted surgically and attached to the left cervical vagus nerve. The newer form is transcutaneous auricular VNS, or taVNS, in which stimulation is delivered non-invasively through the auricular branch of the vagus nerve in the ear. The importance of taVNS is that it accesses central vagal pathways without requiring surgery (He et al., 2013; von Wrede et al., 2021).

How effective is VNS?

VNS is not a cure for epilepsy, but it is a meaningful treatment option in refractory cases, i.e. those patients with a poor response to medication. Reviews of invasive VNS show that approximately 20–40% of patients achieve a 50% or greater reduction in seizure frequency, and response often improves over time rather than appearing all at once (Krahl, 2012; Krahl & Clark, 2012). A Cochrane review found that high-level stimulation was more effective than low-level stimulation for drug-resistant focal epilepsy, with moderate-certainty evidence for improved responder rates (Panebianco et al., 2022).

Transcutaneous VNS is also increasingly promising. A randomized controlled trial in refractory epilepsy reported seizure reduction and improvement in quality of life with taVNS, while a separate randomized double-blind trial found the treatment was well tolerated and that the results justified further and larger trials (He et al., 2013; Bauer et al., 2016; Hamer & Bauer, 2019).

Particularly striking is a recent long-term retrospective cohort comparing invasive and transcutaneous VNS. In that study, response rates over five years were comparable, adverse effects were few and mild with both methods, and quality of life improved significantly. The authors concluded that both approaches were viable, well-tolerated, and were comparably effective as treatments for drug-resistant epilepsy (Weyand et al., 2025).

Why sleep matters so much

Sleeping person

If there is one idea that deserves to be made explicit, it is this: sleep is mechanistically central to seizure control. Sleep disruption is not just a nuisance. It affects neuronal excitability, inflammatory signalling, blood–brain barrier integrity, stress systems, and the stability of brain networks. A recent review makes this argument very clearly and shows that epilepsy patients with poor sleep quality have intensified seizure frequency and disease progression. The authors describe how neuroinflammation caused by sleep disruption seems to synergise with seizure-related neuroinflammation to worsen injury in the epileptic brain (Bonilla-Jaime et al., 2021).

That is exactly why a regulation-based approach matters. If a person’s sleep is unstable, if their physiology is chronically stressed, if inflammatory signalling is heightened, and if the brain is being repeatedly pushed toward dysregulation, then seizure control becomes more difficult. Conversely, when sleep is improved and the broader physiology is stabilised, the whole system becomes more resilient. This is not an alternative to medical treatment. It is part of a more complete, rational and scientifically credible understanding of epilepsy (Bonilla-Jaime et al., 2021).

Sleep apnoea: a common and treatable contributor to seizures

A particularly important and often under-recognised contributor to seizure burden is obstructive sleep apnoea (OSA). Sleep disorders are highly prevalent in epilepsy, and OSA appears to be significantly overrepresented compared to the general population. Estimates vary depending on the population studied, but approximately 30% of patients with epilepsy may have clinically significant sleep apnoea, with some studies reporting prevalence rates ranging from 10% to over 80% in selected cohorts (Foldvary-Schaefer & Grigg-Damberger, 2006; Malow et al., 2003; Manni & Terzaghi, 2010).

The mechanisms by which sleep apnoea influences epilepsy are well established. Repeated episodes of sleep fragmentation and intermittent hypoxia lead to autonomic instability, increased sympathetic activation, and heightened neuroinflammatory signalling. These changes increase neuronal excitability and reduce seizure threshold. In addition, disruption of normal sleep architecture impairs the restorative processes required for maintaining network stability.

Importantly, treatment of sleep apnoea has been associated with meaningful improvements in seizure control. In observational studies, patients with epilepsy and untreated OSA have significantly higher seizure frequency compared to those treated with continuous positive airway pressure (CPAP). One study reported that approximately 63% of patients treated with CPAP achieved a ≥50% reduction in seizure frequency, compared to only 14% of untreated patients (Malow et al., 2003). Another study found that seizure freedom was achieved in 42.6% of CPAP-treated patients compared to 15.4% of those who were untreated (Foldvary-Schaefer et al., 2008).

Taken together, these findings demonstrate that sleep apnoea is not merely an associated condition but a clinically significant and modifiable factor in epilepsy. Identifying and treating OSA represents a practical and evidence-based opportunity to improve seizure control, reinforcing the broader principle that regulation of physiological systems—particularly sleep—is central to effective epilepsy management.

This is why we actively target sleep apnoea at Ormond Neuroscience. These findings also provide a useful context for understanding interventions we use, such as VNS, which act on autonomic and regulatory systems that overlap with those systems affected in sleep apnoea.

Where VNS fits in this broader picture

This is where VNS becomes especially interesting. VNS should not be thought of narrowly as a seizure-suppressing device. VNS acts on the physiology of regulation. It engages afferent vagal pathways, influences the nucleus tractus solitarius, reaches neuromodulatory systems such as the locus coeruleus and raphe nuclei, alters network dynamics, and is linked to anti-inflammatory effects and restoration of vagal tone (Krahl, 2012; Krahl & Clark, 2012; Leung, 2017).

That means taVNS sits naturally inside a broader model of epilepsy management that includes sleep, autonomic regulation, inflammation, rehabilitation, and environmental stability. At Ormond Neuroscience, that broader model is what we call Neuroharmonics, our brain treatment programme. Within that framework, taVNS is not seen as a standalone cure. Instead, it is a powerful tool for helping the brain to become more stable, more adaptive, and more capable of regulating itself.

This reflects a shift in emphasis from targeting seizures as isolated events to supporting the physiological systems that determine whether those events occur in the first place.

Sleep and sleep apnoea are important treatment targets of the Neuroharmonics treatment programme. taVNS provides a means of directly stimulating specific nuclei in the brain, such as the nucleus tractus solitarius (NTS).

Safety and tolerability

The distinction between invasive and taVNS is especially important when discussing side effects. Invasive VNS can produce hoarseness, cough, dysphagia, throat discomfort, and dyspnoea. These effects are well known and arise because implanted stimulation at the cervical vagal trunk can influence branches related to laryngeal and other peripheral functions (Krahl, 2012; Panebianco et al., 2022).

taVNS is different. In the recent comparative cohort, hoarseness, cough, dyspnoea, and dysphagia were reported in the invasive group but not in the transcutaneous group, whereas taVNS adverse effects were mainly local and mild, such as paresthesia, pain, erythema (rash), skin irritation, or a feeling of pressure (Weyand et al., 2025). This is a legitimate clinical advantage of the non-invasive taVNS approach.

Efficacy of taVNS

Transcutaneous auricular vagus nerve stimulation (taVNS) has emerged as a promising non-invasive approach to seizure reduction, particularly in patients with drug-resistant epilepsy. Randomised controlled trials and controlled studies have demonstrated that taVNS can produce clinically meaningful reductions in seizure frequency when used as an adjunctive therapy.

In a recent double-blind, controlled trial, active taVNS was associated with significant reductions in seizure frequency compared to control stimulation over a 20-week treatment period (Yang et al., 2023). Other studies have reported reductions in seizure frequency in the order of 30–40% over several weeks of treatment, with longer-term follow-up suggesting that a substantial proportion of patients may achieve ≥50% reduction in seizure burden (Zhang et al., 2024). Earlier controlled trials in drug-resistant epilepsy similarly demonstrated that taVNS can significantly reduce seizure frequency and severity compared to sham stimulation (Aihua et al., 2014).

While results across studies are not entirely uniform—reflecting differences in stimulation parameters, duration, and patient selection—the overall pattern is consistent: taVNS is associated with meaningful seizure reduction and has a favourable safety profile. These findings position taVNS as a clinically important adjunct in the management of refractory epilepsy, particularly when used within a broader framework that targets physiological regulation, such as Neuroharmonics.

The Ormond Neuroscience Experience

It’s worth mentioning our own experience at Ormond Neuroscience with taVNS. With one patient who was having 1-3 tonic-clonic epileptic seizures a week, we have been able to reduce his seizure frequency to approximately one seizure every 4-6 weeks using taVNS embedded within the Neuroharmonics treatment program.  Furthermore, the severity of the seizures has changed significantly.  When he first came to us, his seizures involved loss of consciousness and convulsions, whereas nowadays he experiences a transient loss of awareness and brief speech difficulties.  The convulsions are gone and the complete loss of consciousness is now history. 

Importantly, there was a stage when we thought we could reduce the daily duration of taVNS, but when we did this, his seizures returned. When we returned the stimulation duration and intensity to the original treatment regime, his seizures were again abolished. That was a tough learning experience but reinforced how effective taVNS can be. In his situation, the use of taVNS has been transformative and has made a massive difference to the quality of his life.

Section 2: For Healthcare Professionals

Epilepsy as a disorder of regulation

A purely electrical account of epilepsy is insufficient. While seizures are expressed electrophysiologically, the condition itself is embedded in a much broader physiology of dysregulation involving sleep-wake architecture, circadian timing, inflammatory signalling, autonomic balance, neuromodulatory tone, and network resilience. The sleep literature is particularly valuable here because it repositions sleep from a mere precipitant to a mechanistically relevant domain of disease progression. Bonilla-Jaime and colleagues argue that sleep disruption may worsen epilepsy via neuroinflammatory mechanisms and explicitly frame sleep intervention as clinically relevant to seizure management, mortality reduction, and quality of life.

This framing aligns well with lived clinical experience. Patients commonly identify sleep loss, sleep fragmentation, nocturnal seizure burden, and physiological stress as meaningful determinants of seizure control. The literature supports that perspective. Sleep disturbance is overrepresented in epilepsy, poor sleep quality is associated with intensified seizure frequency and progression, and neuroinflammation is a plausible common pathway linking disturbed sleep, seizure activity, and ongoing neurodegeneration (Bonilla-Jaime et al., 2021).

Mechanisms of VNS

The majority of vagal fibres are afferent and project primarily to the nucleus tractus solitarius, which functions as a major relay for visceral and sensory input. From there, the NTS projects directly or indirectly to multiple structures relevant to seizure modulation, including the locus coeruleus, raphe nuclei, hypothalamic nuclei, amygdala, thalamic regions, and distributed cortical systems (Krahl, 2012; Krahl & Clark, 2012). Thus, VNS targets include:

  • Nucleus tractus solitarius as the primary vagal relay and which modulates both excitatory glutamate pathways and inhibitory GABA pathways
  • Locus coeruleus and noradrenergic modulation
  • Raphe nuclei and serotonergic modulation
  • Limbic and thalamic projections
  • Distributed cortical and network-level effects

This matters because the clinical effect of VNS is not local but rather systems-level. In epilepsy, that includes altered excitability, seizure threshold modulation, network desynchronisation and stabilisation, and longer-term plastic effects. Recent imaging work has shown that structural and functional characteristics of the locus coeruleus, as well as its connectivity with the hippocampus, are associated with treatment response in drug-resistant epilepsy. These findings support the role of noradrenergic modulation and plasticity in the therapeutic effects of vagus nerve stimulation (Li et al., 2024).

EEG and network studies reinforce the same point. Responders to VNS have shown reduced interictal cortical synchrony, suggesting that desynchronisation may be part of the anti-seizure effect, while taVNS has been shown to induce stabilising modifications in large-scale functional brain networks consistent with greater resilience and stability (Bodin et al., 2015; von Wrede et al., 2021).

An extremely abnormal EEG
Example of highly abnormal EEG activity illustrating the complexity and instability of brain network dynamics in pathological states.

Autonomic and inflammatory regulation

Vagus nerve stimulation acts directly on systems of autonomic and inflammatory regulation. The vagus nerve is a central component of autonomic control, and its stimulation influences physiological state, including heart rate variability, neuromodulatory tone, and immune signalling. VNS engages pathways involved in the regulation of inflammatory responses, including modulation of cytokine activity and related immune markers. These effects are clinically relevant in epilepsy, where both seizures and associated physiological stressors are linked to inflammatory processes. Changes in autonomic function and inflammatory signalling therefore represent important components of the therapeutic effects of VNS (Leung, 2017).

The relationship between sleep, inflammation, and epilepsy further reinforces this perspective. Both seizures and sleep disruption are associated with increased neuroinflammatory activity, including activation of glial cells and the release of pro-inflammatory mediators. Emerging evidence suggests that sleep disruption may act as an additional “second hit,” amplifying seizure susceptibility and contributing to disease progression through inflammatory mechanisms (Bonilla-Jaime et al., 2021).

Within this framework, epilepsy is best understood as a condition in which multiple physiological systems interact to influence seizure vulnerability. From this perspective, seizure frequency and severity reflect the dynamic state of these interacting systems, rather than a fixed property of the underlying pathology alone. VNS is therefore relevant not only because it can reduce seizure frequency, but because it acts on core regulatory systems—autonomic state, neuromodulatory tone, inflammatory signalling, sleep stability, and large-scale network organisation—that together determine whether the brain moves toward instability or resilience.

Transcutaneous VNS in this framework

taVNS fits especially well within this model. Mechanistically, the auricular branch of the vagus nerve provides access to the NTS and therefore to central vagal circuitry. Researchers have proven the existence of the auriculo-vagal afferent pathway in rats (He et al., 2013). They showed that taVNS could suppress epileptiform activity via activation of the nucleus tractus solitarius (NTS), which is what we do with human patients. Then the clincher: they demonstrated that the anti-epileptic effect was weakened by a reversible cooling block of the NTS. That is powerful and convincing mechanistic evidence to support the biological plausibility of taVNS in epilepsy.

Clinically, taVNS also avoids the characteristic laryngeal side effects of implanted VNS (hoarseness, cough, dyspnoea, and dysphagia), while overall efficacy, quality-of-life impact, and patient willingness to choose treatment again were comparable over five years (Weyand et al., 2025).

Mood, quality of life, and cognition

A balanced account remains important. Vagus nerve stimulation is associated with improvements in mood and quality of life, and some of these benefits may occur independently of seizure reduction. At the same time, evidence for cognitive improvement remains inconsistent. A recent systematic review and meta-analysis found no reliable overall improvement in cognitive function despite reductions in seizure frequency and improvements in broader clinical outcomes (Kong et al., 2024). This pattern is clinically informative, as it underscores that VNS is not a cure-all or general cognitive enhancer, but a meaningful intervention with a recognisable profile of benefits and limitations (Panebianco et al., 2022; Weyand et al., 2025).

Neuroharmonics and epilepsy

The Neuroharmonics framing helps to make the deep structure of the problem explicit. Epilepsy is not only about discharges. It is about dysregulation. Sleep instability, inflammatory burden, autonomic imbalance, physiological stress, and network fragility all influence whether a brain is pushed toward seizure expression or toward resilience. VNS belongs within this framework because it acts at the level of regulation. It modulates systems that stabilise the brain rather than merely suppressing symptoms in a narrow sense.

That is why the sleep story matters so much. It is not a side issue. It is one of the clearest windows into the physiology of epilepsy. Once sleep, inflammation, and autonomic regulation are brought into view, the condition becomes more intelligible, the patient’s experience makes more sense, and treatment moves beyond simplistic explanations toward a layered and scientifically credible model of care.

At Ormond Neuroscience, our approach to using vagus nerve stimulation for epilepsy uses a model with a rational and focused approach to neural regulation via multiple physiological systems. taVNS is a vital component of a broader treatment regime.

Learn More

If you’ve wondered about the terminology, “vagus” is a noun referring to the nerve itself, whereas “vagal” is an adjective referring to things related to the nerve, such as vagal pathways, vagal modulation, or the commonly used (but strictly incorrect) phrase “vagal nerve stimulation.”

For further information about vagus nerve stimulation and its clinical applications, please see the following pages:

Ormond Neuroscience Web Pages

Talks and Interviews

For those interested in a deeper exploration of the neuroscience and clinical application of VNS, the following talks and interviews provide additional context:

Get in Touch

If you would like to explore whether vagus nerve stimulation is appropriate for your situation, please get in touch to arrange an interview.

Frequently Asked Questions

What is vagus nerve stimulation (VNS)?

Vagus nerve stimulation is a form of neuromodulation that stimulates the vagus nerve, one of the major communication pathways linking the body and the brain. In epilepsy, VNS is used to help reduce seizure frequency and improve physiological regulation.

Traditional VNS involves surgical implantation of a device attached to the vagus nerve in the neck. Transcutaneous auricular VNS (taVNS) is a non-invasive form that stimulates branches of the vagus nerve through the ear.

Is epilepsy only an electrical disorder?

No. While abnormal electrical activity is central to seizures, epilepsy is increasingly understood as a disorder involving broader systems of regulation, including sleep, autonomic function, inflammation, stress physiology, and large-scale brain network stability.

This broader perspective helps explain why factors such as poor sleep, physiological stress, illness, and autonomic instability can strongly influence seizure frequency.

How does VNS help epilepsy?

VNS does not simply “block seizures.” Rather, it influences regulatory systems involved in autonomic function, arousal, inflammation, neuromodulation, and network stability.

Through pathways involving the nucleus tractus solitarius, locus coeruleus, raphe nuclei, and broader brain networks, VNS may help support the physiological conditions under which the brain becomes more stable and less vulnerable to seizures.

Is transcutaneous auricular VNS (taVNS) effective for epilepsy?

Research increasingly suggests that taVNS can reduce seizure frequency in some patients with drug-resistant epilepsy, particularly when used as part of a broader treatment approach.

Several controlled trials and longer-term cohort studies have reported meaningful seizure reduction, improvement in quality of life, and good tolerability. While results vary between individuals, the overall evidence supports taVNS as a promising adjunctive treatment option.

Does VNS replace anti-seizure medication?

Usually not. VNS is generally used as an adjunctive treatment rather than a replacement for anti-seizure medication.

However, some individuals may eventually reduce medication burden under specialist medical supervision if seizure control improves. Decisions regarding medication should always be made carefully with the treating neurologist or physician.

Why does sleep matter so much in epilepsy?

Sleep is deeply involved in seizure regulation. Poor sleep quality, sleep fragmentation, sleep deprivation, and sleep apnoea can all increase seizure vulnerability.

Research increasingly suggests that sleep disruption contributes to autonomic instability, inflammatory signalling, and impaired network regulation, all of which may make seizures more likely.

Improving sleep is therefore an important part of epilepsy management.

What is the relationship between sleep apnoea and epilepsy?

Obstructive sleep apnoea (OSA) is significantly more common in people with epilepsy than in the general population.

Repeated sleep disruption and intermittent oxygen deprivation can increase autonomic stress, inflammation, and neuronal excitability, lowering seizure threshold. Importantly, treatment of sleep apnoea has been associated with meaningful improvements in seizure control in many patients.

Is taVNS safer than implanted VNS?

taVNS avoids surgery and does not stimulate the cervical vagal trunk directly, so it generally avoids side effects such as hoarseness, cough, throat discomfort, and swallowing difficulties that can occur with implanted VNS.

Most reported taVNS side effects are mild and local, such as tingling, skin irritation, pressure, or temporary discomfort around the ear.

What is Neuroharmonics?

Neuroharmonics is the broader brain treatment programme used at Ormond Neuroscience. It approaches epilepsy as a disorder involving regulation across multiple physiological systems rather than purely abnormal electrical activity alone.

Within this framework, interventions such as taVNS, sleep optimisation, autonomic regulation, rehabilitation, behavioural intervention, and management of physiological stress are integrated into a broader systems-based approach to brain health and seizure control.

Selected References and Evidence Base

Aihua, L., Lu, S., Liping, L., Xiuru, W., Hua, L., & Yuping, W. (2014). A controlled trial of transcutaneous vagus nerve stimulation for the treatment of pharmacoresistant epilepsy. Epilepsy & Behavior, 39, 105–110.
Epilepsy & Behavior

Bauer, S., Baier, H., Baumgartner, C., Bohlmann, K., Fauser, S., Graf, W., Hillenbrand, B., Hirsch, M., Last, C., Lerche, H., Mayer, T., Schulze-Bonhage, A., Steinhoff, B. J., & Hamer, H. M. (2016). Transcutaneous vagus nerve stimulation (tVNS) for treatment of drug-resistant epilepsy: A randomized, double-blind clinical trial (cMPsE02). Brain Stimulation, 9(3), 356–363.
Brain Stimulation

Bodin, C., Aubert, S., Daquin, G., Carron, R., Scavarda, D., McGonigal, A., & Bartolomei, F. (2015). Responders to vagus nerve stimulation in refractory epilepsy have reduced interictal cortical synchronicity on scalp EEG. Epilepsy Research, 113, 98–103.
Epilepsy Research

Bonilla-Jaime, H., Zeleke, H., Rojas, A., & Espinosa-Garcia, C. (2021). Sleep disruption worsens seizures: Neuroinflammation as a potential mechanistic link. International Journal of Molecular Sciences, 22(22), 12531.
International Journal of Molecular Sciences

Foldvary-Schaefer, N., Andrews, N. D., et al. (2008). Sleep apnea and epilepsy: Who’s at risk? Epilepsy & Behavior, 13(3), 455–460.
Epilepsy & Behavior

Foldvary-Schaefer, N., & Grigg-Damberger, M. (2006). Sleep and epilepsy: What we know, don’t know, and need to know. Journal of Clinical Neurophysiology, 23(1), 4–20.
Journal of Clinical Neurophysiology

Hamer, H. M., & Bauer, S. (2019). Lessons learned from transcutaneous vagus nerve stimulation (tVNS). Epilepsy Research, 153, 83–84.
Epilepsy Research

He, W., Jing, X.-H., Zhu, B., Zhu, X.-L., Li, L., Bai, W.-Z., & Ben, H. (2013). The auriculo-vagal afferent pathway and its role in seizure suppression in rats. BMC Neuroscience, 14, 85.
BMC Neuroscience

Kaniusas, E., Kampusch, S., Tittgemeyer, M., Panetsos, F., Gines, R. F., Papa, M., Kiss, A., Podesser, B., Cassara, A. M., Tanghe, E., Samoudi, A. M., Perdikis, S., & Széles, J. C. (2019). Current directions in the auricular vagus nerve stimulation I – A physiological perspective. Frontiers in Neuroscience, 13, 854.
Frontiers in Neuroscience

Kong, Y., Zhao, K., Zeng, D., Lu, F., Li, X., Wu, Y., Jiang, Z., & Wen, W. (2024). Effects of vagus nerve stimulation on cognitive function in patients with epilepsy: A systematic review and meta-analysis. Frontiers in Neurology, 15, 1332882.
Frontiers in Neurology

Krahl, S. E. (2012). Vagus nerve stimulation for epilepsy: A review of the peripheral mechanisms. Surgical Neurology International, 3(Suppl 4), S47–S52.
Surgical Neurology International

Krahl, S. E., & Clark, K. B. (2012). Vagus nerve stimulation for epilepsy: A review of central mechanisms. Surgical Neurology International, 3(Suppl 4), S255–S259.
Surgical Neurology International

Li, M., Zhang, Y., Liu, H., et al. (2024). Locus coeruleus integrity and locus coeruleus–hippocampal connectivity predict response to vagus nerve stimulation in drug-resistant epilepsy. Brain Communications.
Brain Communications

Leung, H. (2017). The physiological and psychological effects of electrical vagus nerve stimulation in patients with refractory epilepsy (Doctoral thesis, University of Sheffield).

Malow, B. A., Weatherwax, K. J., et al. (2003). Identification and treatment of obstructive sleep apnea in adults and children with epilepsy. Neurology, 60(11), 1766–1771.
Neurology

Manni, R., & Terzaghi, M. (2010). Comorbidity between epilepsy and sleep disorders. Epilepsy Research, 90(3), 171–177.
Epilepsy Research

Panebianco, M., Rigby, A., & Marson, A. G. (2022). Vagus nerve stimulation for focal seizures. Cochrane Database of Systematic Reviews, Issue 7, CD002896.
Cochrane Database of Systematic Reviews

von Wrede, R., Rings, T., Schach, S., Helmstaedter, C., & Lehnertz, K. (2021). Transcutaneous auricular vagus nerve stimulation induces stabilizing modifications in large-scale functional brain networks: Towards understanding the effects of taVNS in subjects with epilepsy. Scientific Reports, 11, 7906.
Scientific Reports

Weyand, A. M., Cordes, N., Linka, L., Strehlau, S., Tsalouchidou, P.-E., Carl, B., Gjorgjevsky, M., Grote, A., Nimsky, C., Möller, L., Habermehl, L., Zahnert, F., Strzelczyk, A., Rosenow, F., Münchberger, C., Hakel, L., Menzler, K., Immisch, I., Krause, K., & Knake, S. (2025). Long-term effects of invasive and transcutaneous vagus nerve stimulation in patients with epilepsy: A retrospective cohort study. Clinical Epileptology.
Clinical Epileptology

Yang, H., Liu, Y., Liu, H., & Zhang, Q. (2023). Transcutaneous auricular vagus nerve stimulation for drug-resistant epilepsy: A randomized, double-blind clinical trial. Epilepsy Research, 197, 107185.
Epilepsy Research

Zhang, Q., Liu, Y., Yang, H., & Liu,H. (2024). Transcutaneous auricular vagus nerve stimulation for drug-resistant epilepsy: A randomized controlled trial. Epilepsy & Behavior, 153, 109613.
Epilepsy & Behavior

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